SMITHSONIAN CONTRIBUTION S TO ANTHROPOLOGY • NUMBER 28 

Identification 

of Pathological Conditions 

in Huma n Skeletal Remains 

Donald J. Ortner 

and Walter G. J. Putschar 

SMITHSONIAN INSTITUTION PRESS 

City of Washington 

1981 
ABSTRAC T 

Ortner, Donald J., and Walter G. J. Putschar. Identification of Pathological 

Conditions in Human Skeletal Remains. Smithsonian Contributions to Anthropology, 

number 28, 479 pages, 14 tables, 765 figures, 1981.—This reference work is an 

attempt to provide an integrated and reasonably comprehensive treatnient of 

pathological conditions that affect the human skeleton. The primary objective 

is to assist those who conduct research on archeological skeletal remains in 

interpreting abnormal conditions that they might encounter in the course of 

their research. However, there is much that ancient skeletal remains can reveal 

to the modern medical historian, orthopaedist, pathologist, and radiologist 

about skeletal diseases that are rarely encountered in modern clinical practice. 

All of the major categories of disease that affect bone are reviewed from the 

viewpoint of the pathologist. This review is followed by a discussion of the 

literature on the paleopathology of each condition and the presentation of 

paleopathological cases thought to represent each of the morbid categories 

affecting bone. 

This work is based on extensive individual and collaborative research by 

both authors on the known parameters of modern skeletal diseases and their 

expression in antiquity. The monograph provides essential text and illustrative 

materials on bone pathology, which will improve the diagnostic ability of 

those interested in human dry bone pathology. 

OFFICIAL PUBLICATION DATE is handstamped in a limited number of initial copies and is recorded 

in the Institution's annual report, Smithsonian Year. SERIES COVER DESIGN: Sioux Indian hide 

painting depicting mounted warriors. 

Library of Congress Cataloging in Publication Data 

Ortner, Donald J. 

Identification of pathological conditions in human skeletal remains. 

(Smithsonian contributions to anthropology ; no. 28) 

Bibliography: p. 

Supt. of Docs. no. SI 1.33:28 

1. Paleopathology. 2. Bones—Diseases. I. Putschar, Walter G. J., joint author. II. 

Title. III. Series. [DNLM: 1. Bone and bones—Pathology. 2. • Paleopathology. WI 

SM454 V. 28/Q Z 11.5 0771] 

GN1.S54 no. 28 [R134.8] 301s [616.7'107] 80-607929 
Contents 

Page 

INTRODUCTION 1 

Objectives of this Book 1 

Acknowledgments 3 

Abbreviations 4 

A Brief History of Paleopathology 5 

The Paleopathology Program at the Smithsonian Institution 6 

T H E BIOLOGY OF SKELETAL TISSUES 8 

The Development of Bone 8 

Cartilage 12 

The Cells of Bone 13 

Bone Growth 16 

Osteon Remodeling 19 

The Biology of Teeth 26 

METHODS USED IN THE ANALYSIS OF SKELETAL LESIONS 29 

Age Determination 30 

Race Determination 32 

Sex Determination 32 

Stature Determination 33 

Demographic Analysis 33 

Archeological Documentation 34 

Gross Study of Skeletal Lesions 36 

X-ray Film Study of Skeletal Lesions 45 

Chemical Analysis of Pathological Bone 51 

Microscopic Study of Skeletal Lesions 52 

TRAUMA 55 

Fracture 55 

Pathology 55 

Types of Fracture 55 

Fracture Healing 61 

Complications Arising from Fracture 64 

Paleopathology 72 

History and Examples 72 

Complications of Fracture 81 

Dislocation 85 

Pathology 85 

Paleopathology 87 

Deformation 90 

Pathology 90 

Paleopathology 90 

iii 
i v SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

Page 

Scalping "^ 

Pathology ^^ 

Paleopathology "*^ 

Mutilation 94 

Trephination "^ 

History "^ 

Paleopathology " " 

Types of Trephination " ' 

Complications of Trephination 97 

Traumatic Problems Arising from Pregnancy 100 

Pathology 100 

Paleopathology 101 

Sincipital-T Mutilation 102 

INFECTIOUS DISEASES 104 

The Inflammatory Response 104 

The Biology of Infection 104 

Osteomyelitis 105 

Pathology 105 

Hematogenous Osteomyelitis 109 

Changes in Individual Bones 116 

Paleopathology 121 

The Skull 123 

Postcranial Bones 123 

Periostitis 129 

Pathology 129 

Paleopathology 131 

Brucellosis 138 

Pathology 138 

Paleopathology 139 

Glanders 141 

Pathology 141 

Tuberculosis of Bones and Joints 141 

Pathology 141 

Statistical Data 142 

General Pattern of Bone and Joint Tuberculosis 144 

The Spine 145 

The Pelvis 149 

The Hip 150 

The Trochanter 153 

The Knee 154 

The Ankle and Tarsal Bones 154 

The Tubular Bones of the Hands and Feet (Spina Ventosa) . . 156 

The Shoulder 157 

The Elbow 157 

The Wrist and Carpal Bones 159 

The Shaft of Long Bones 159 
NUMBER 28 

se 

The Thoracic Cage l^'^ 

The Skull 162 

Paleopathology 1"" 

Leprosy 1' " 

Pathology 1^6 

Paleopathology 1' ' 

Treponemal Infections 1°0 

Pathology 180 

Yaws 180 

Endemic Syphilis (Treponarid) 181 

Venereal Syphilis 182 

Congenital Syphilis 198 

Paleopathology 201 

Congenital Syphilis 207 

Adult Treponemal Disease 210 

Actinomycosis and Nocardiosis 218 

Pathology 218 

Mycetoma (Maduromycosis) "^"^^ 

Pathology ^^^ 

Fungal Infections ^ 

Pathology 224 

North American Blastomycosis 224 

• 994 

Cryptococcosis 

• 924 

Paracoccidioidomycosis 

• 994 

Coccidioidomycosis 995 Histoplasmosis 

Sporotrichosis 

. 99fi 

Aspergillosis 

Mucormycosis (Phycomycosis) 227 

Paleopathology 

Viral Infections 

Pathology 227 

Smallpox 

Rubella 229 

Parasitic Infections (Echinococcosis) 229 

Pathology 229 

Paleopathology ^^ 

Sarcoidosis 

Pathology 

CIRCULATORY DISTURBANCES '^•^^ 

Blood Supply of Bones 235 

• 235 

Ischemia and Infarction 

Pathology ^;^^ 

Necrosis of Femoral Head 236 

Pathology 236 

Paleopathology 
VI SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

Page 

Perthes' Disease and Slipped Femoral Capital Epiphysis 238 

Pathology 238 

OQQ 

Paleopathology "^"^^ 

Other Vascular Disturbances of Epiphyses and Apophyses 242 

Kohler's Disease of the Tarsal Navicular Bone 242 

Pathology 242 

• • • 942 

Osteochondritis Dissecans ^^^ 

Pathology 242 

Paleopathology '^ ^ 

Osffood-Schlatter's Disease of the Tibial Tubercle 243 

Pathology ^^^ 

Paleopathology 243 

Freiberg's Disease of a Metatarsal Head 244 

Pathology 244 

Kienbock's Disease of the Carpal Lunate Bone 244 

Pathology 244 

Pulmonary Osteoarthropathy 245 

Pathology 245 

Aneurysmal Erosion 246 

Pathology 246 

RETICULOENDOTHELIAL AND HEMOPOIETIC DISORDERS 248 

Lipid Storage Diseases 248 

Pathology 248 

Gaucher's Disease 248 

Niemann-Pick's Disease 249 

Other Lipidoses 249 

Histiocytosis X 249 

Pathology 249 

Anemias 251 

Pathology 251 

Thalassemia 251 

Sickle Cell Anemia and Its Genetic Variants 254 

Hereditary Spherocytosis (Congenital Hemolytic Anemia) ... 257 

Iron-deficiency Anemia 257 

Erythroblastosis Fetalis 258 

Paleopathology 258 

Leukemia 263 

Pathology 263 

Myeloma 264 

Pathology 264 

Paleopathology 265 

METABOLIC DISORDERS 270 

Vitamin C Deficiency 270 

Pathology 270 

Infantile Scurvy (Moller-Barlow's Disease) 270 

Adult Scurvy 272 
NUMBER 28 vii 

Page 

Paleopathology 272 

Vitamin D Deficiency 273 

Pathology 273 

Rickets 273 

Rachitic and Postrachitic Changes in Individual Bones 274 

Late Rickets 280 

Osteomalacia 280 

Skeletal Changes Resembling Rickets and Osteomalacia 283 

Paleopathology 283 

Hypophosphatasia 287 

Pathology 287 

Starvation 287 

Pathology 287 

Fluorosis 288 

Pathology 288 

Osteoporosis 289 

Pathology 289 

Paleopathology 291 

Localized Hyperostosis 294 

Pathology 294 

Pregnancy Osteophyte 294 

Internal Frontal Hyperostosis 294 

Leontiasis Ossea 294 

Infantile Cortical Hyperostosis (Caffey's Disease) 294 

Generalized Hyperostosis with Pachydermia 294 

Pathology 294 

Paleopathology 297 

ENDOCRINE DISTURBANCES 298 

Pituitary Disturbances 298 

Pathology 298 

Pituitary Gigantism 298 

Acromegaly 298 

Hypopituitarism 300 

Pituitary Dwarfism 300 

Paleopathology 300 

Acromegaly 300 

Pituitary Dwarfism 302 

Other Endocrine Disturbances 304 

Pathology 304 

Hypothyroidism 304 

Hyperthyroidism 305 

Cushing's Syndrome 305 

Hypogonadism 306 

Hypergonadism 306 

Hypoparathyroidism 306 

Hyperparathyroidism 307 
SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

309 OTHER BONE DISEASES 

Paget's Disease ^ 

Pathology ^^^ 

Paleopathology 

Fibrous Dysplasia 

Pathology ^^^ 

Monostotic Fibrous Dysplasia 

Polyostotic Fibrous Dysplasia •^'-' 

Paleopathology 

Myositis Ossificans Progressiva •^^^ 

Pathology ^22 

NEUROMECHANICAL DEFORMITIES -^^^ 

Pathology 3^j 

Kyphosis ^'^'^ 

Scoliosis ^'^ 

Postparalytic Deformities 325 

Paleopathology 326 

Scoliosis 326 

Postparalytic Deformities 328 

SKELETAL DYSPLASIAS 329 

Achondroplasia 329 

Pathology 329 

Paleopathology 331 

Mucopolysaccharidoses 334 

Pathology 334 

Paleopathology 336 

Osteogenesis Imperfecta 337 

Pathology 337 

Paleopathology 338 

Dysostosis Cleidocranialis 338 

Pathology 338 

Osteopetrosis 340 

Pathology 340 

Pyknodysostosis 342 

Pathology 342 

Metaphysial Dysplasia (Pyle's Disease) 342 

Pathology 342 

Paleopathology 342 

Diaphysial Sclerosis (Camurati-Engelmann's Disease) 344 

Pathology 344 

Melorheostosis (Leri's Disease) 344 

Pathology 344 

Paleopathology 345 

Osteopoikilosis 345 

Pathology 345 

Osteopathia Striata 345 

Pathology ^ 
NUMBER 28 IX 

Page 

SKELETAL MALFORMATIONS 346 

Skull 346 

Pathology 346 

Paleopathology 346 

Spine 355 

Pathology 355 

Paleopathology 356 

Ribs 359 

Pathology 359 

Pelvis 359 

Pathology 359 

Paleopathology 360 

Extremities 362 

Pathology 362 

Paleopathology 363 

TUMORS 365 

General Discussion 365 

Pathology 365 

Paleopathology 365 

Primary Benign Tumors 366 

Pathology 366 

Cysts 366 

Osteoblastic Tumors 368 

Chondroblastic Tumors 370 

Fibroblastic Tumors 374 

Giant Cell Tumor 375 

Hemangioma 376 

Meningioma 378 

Paleopathology 378 

Osteoblastic Tumors 378 

Chondroblastic Tumors 380 

Meningioma 382 

Primary Malignant Bone Tumors 384 

Pathology 384 

Osteosarcoma 384 

Chondrosarcoma 385 

Ewing's Sarcoma 387 

Chordoma 388 

Paleopathology 389 

Metastatic Tumors 391 

Pathology 391 

Paleopathology 395 

LESIONS OF THE JOINTS 399 

Septic Arthritis 399 

Pathology 399 

Paleopathology 401 
SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

Page 

Rheumatoid Arthritis ^^^ 

Pathology 

Adult Rheumatoid Arthritis 

Juvenile Rheumatoid Arthritis (Still's Disease) "^05 

Psoriatic Arthritis 

Paleopathology 

Ankylosing Spondylitis (Marie-Striimpell's Disease) 

Pathology 

Paleopathology 

Metabolic Arthritis 

Pathology ^^^ 

Gouty Arthritis 

. 4.1 fi 

Ochronosis (Alkaptonuria) ^ " 

Hemophilic Arthropathy 

Hemophilic Pseudotumor 418 Paleopathology 

Gouty Arthritis '*^° 

Ochronosis (Alkaptonuria) ^^° 

Degenerative Arthritis '*1^ 

Pathology ^^9 

The Appendicular Skeleton 419 

Spondylitis Deformans (Spinal Osteophytosis) 420 

4 9 9 

Paleopathology ^'^'^ 

The Appendicular Skeleton 423 

The Axial Skeleton 4_9 

Other Lesions of the Joints 433 

Pathology 433 

Neuropathic Arthropathy (Charcot's Joint) 433 

Pigmented Villonodular Synovitis 435 

Synovial Osteochondromatosis 435 

LESIONS OF JAWS AND TEETH 436 

The Jaws 436 

Pathology 436 

Odontogenic Cysts 436 

Odontogenic Tumors 436 

Nonodontogenic Cysts 437 

Nonodontogenic Tumors 437 

The Teeth 438 

Dental Caries 438 

Pathology 438 

Paleopathology 439 

Periodontal Disease 442 

Pathology 442 

Paleopathology 443 

Disturbances in Dental Development 444 
NUMBER 28 xi 

Page 

Pathology 444 

Abnormal Quality of Teeth 444 

Abnormal Quantity of Teeth 446 

Abnormal Size and Shape of Teeth 447 

Dental Anomalies 447 

Dental Crowding 447 

Paleopathology 447 

Abnormal Quality of Teeth 447 

Abnormal Quantity of Teeth 448 

Abnormal Size and Shape of Teeth 451 

Dental Anomalies 451 

Dental Crowding 452 

Dental Trauma 452 

Pathology 452 

Paleopathology 453 

Dental Attrition 454 

Pathology 454 

Paleopathology 454 

Dental Discoloration 456 

Pathology 456 

Paleopathology 456 

LITERATURE CITED 457 
This book is dedicated 

to the memory of 

ERWIN UEHLINGER 

Emeritus Professor of Pathology 

of the University of Zurich (Switzerland) 

the dean of European bone pathologists 

whose continued interest and advice 

from the inception of this book 

was a great inspiration 
Erwin Uehlinger 

8 August 1899-1 8 April 1980 
Identification 

of Pathological Conditions 

in Huma n Skeletal Remains 

Donald J. Ortner 

and Walter G. J. Putschar 

Introduction 

Human biological history involves the interaction of countless individuals and their environment. This dynamic condition includes extraordinarily complex interrelationships, not only 

among peoples but between individuals and a 

host of physical and biological factors that affect 

their well-being. One of the major objectives of 

the biologist is to discover and record this history. 

However, any attempt to write even a partial 

biological history of man depends ultimately on 

our knowledge of the factors that influence it. 

Even the most superficial review of the history 

of disease reveals its enormous significance in 

human biological history. The terrifying plagues 

recorded in European history prematurely ended 

the lives of millions of people. The influenza 

epidemic after World War I resulted in the death 

of over twenty million people—far more than 

died as a direct result of that most devastating 

and bloody war. 

Why do some people survive a morbid condition and others die? Clearly chance factors operDonald J. Ortner, Department of Anthropology, National Museum of 

Natural History, Smithsonian Institution, Washington, D. C. 20560. 

Walter G. J. Putschar, Department of Pathology, Massachusetts 

General Hospital, Boston, Massachusetts 02114. 

ate. Genetics and its influence on several biological factors, including the immune response, must 

be significant. To the extent that heritable factors 

play a role in resistance to disease, morbid conditions influence the continuing process of human 

biological adaptation. Similarly the existence of 

cultural mechanisms that minimize the effect of 

disease may be of considerable biological importance. Thus, our understanding of man's cultural 

and biological response to disease through time 

becomes an important dimension of our understanding of human history. 

Objectives of this Book 

The genesis of this book began in 1970, at 

which time plans were developed for the first 

Paleopathology Seminar Series to be held in 1971. 

This seminar series brought several leading authorities on skeletal disease, paleopathology, and 

related subjects to the Smithsonian Institution to 

present lectures to a select group of scholars interested in skeletal paleopathology. 

The seminar series was held yearly through 

1974. By that time the logistics of obtaining funds 

to offer the series, arranging for students to come 

1 
SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

from many universities, including foreign ones, 

and assembling an outstanding faculty for the 

ten-week series became almost overwhelming. Dr. 

Donald J. Ortner, physical anthropologist and 

director of the series, and Dr. Walter G. J. Putschar, pathologist and the principal lecturer on 

skeletal pathology, decided that many more 

scholars interested in skeletal paleopathology 

would have access to the substance of the seminar 

series if the information were incorporated into a 

book. This book would reflect the content of the 

seminar series, which had included lectures on 

calcified tissue biology, methodology, pathology, 

and radiology, and laboratory sessions on paleopathology, all emphasizing the human skeleton. 

There are many sources of information on the 

history of disease including ancient medical documents, historical records, art, and the physical 

remains of ancient people, both soft tissues and 

skeletons. Undoubtedly human skeletons represent the most ubiquitous source of information on 

ancient diseases. Unfortunately this fact must be 

tempered with the knowledge that relatively few 

morbid conditions affect the skeleton in a way 

that leaves visible changes in the dry bones. In 

spite of this limitation, the study of skeletal pathology in archeological materials can provide 

time depth to our understanding of disease and 

contribute to our understanding of the role of 

disease in human adaptation. In addition, skeletal 

paleopathology may also broaden our understanding of disease as it affects bone at the present 

time. The paleopathologist generally has access 

to all portions of the skeleton, a situation rarely 

realized in modern pathology. This means that 

the gross pattern and distribution of the morbid 

condition in all areas of the skeleton can be 

studied in detail. A good example of such a study 

is the work by M0ller-Christensen (1967) on the 

medieval human skeletons from a leper cemetery 

in Denmark, which revealed hitherto not fully 

appreciated skeletal manifestations of the disease. 

Undoubtedly more careful analysis of paleopathological skeletons will reveal additional information on the biology of other bone diseases. 

It is against the background of the substantial 

literature in paleopathology (exceeding 3000 citations) and the scholarly needs revealed by this 

literature that we have formulated the objectives 

of this book. The most fundamental objective is 

to provide an integrated detailed discussion of the 

gross pathology of the human skeleton, emphasizing those conditions that can be seen in dry 

specimens regardless of whether or not they have 

so far been identified in archeological material. 

In order to provide reliable standard specimens 

for dry bone diagnosis, we had to concentrate on 

the period from about AD 1750 to 1930. Earlier, 

the medical data are too ambiguous and, later, 

the pathologic manifestations are too altered by 

surgery, chemotherapy, radiation therapy and, 

above all, by the use of antibiotics. For this 

purpose we had to turn to the great medical 

museums of Great Britain and of continental 

Europe. The British collections proved in many 

ways the most useful, because they were made by 

physicians and surgeons, who were at all times 

interested in documenting clinical and historical 

data. We realize that even this material, which 

represents as closely as possible the natural history 

of the affections at that period in time and which 

are not modified by significant therapeutic procedures, is not necessarily identical with previous 

manifestations seen in archeological specimens. 

However, it is the only documented material 

available for comparison. 

This book is mainly intended to serve as a text 

and atlas of dry bone pathology, regardless of 

whether or not each entity has been identified in 

paleopathology. For that reason, as many aspects 

as possible of documented, dry bone pathology 

have been illustrated, especially because the original skeletal collections can never be duplicated 

and may ultimately disappear. In the paleopathological discussions, emphasis is laid on careful 

and critical study of published reports and of 

actual specimens, bringing all types of evidence 

to bear on arriving at a reasonable diagnostic 

assumption. It hardly needs to be emphasized 

that, even so, multiple possibilities and uncertainties often remain. Not the least of these problems 
NUMBER 28 

is the ambiguous and confusing terminology 

about the chronology of archeological specimens 

in published reports. Chronological information 

on such specimens is reported in the following 

pages as it was reported in the sources. 

The different disease categories are treated in 

separate chapters as is the discussion of calcified 

tissue biology and methodology. Within the chapters on skeletal pathology the clinical background 

is presented first in condensed form. This is followed by a detailed discussion of bone pathology 

and of the differential diagnosis. Histologic detail, 

since not pertinent to the study of dry bones, is 

kept at a minimum. The paleopathological aspects, unpublished cases, and pertinent published 

reports follow the discussion of the pathology 

within each chapter. The introduction was written jointly. The chapters on skeletal biology, 

methods, trauma, and dental diseases (except the 

section "The Jaws") were written by D.J. Ortner. 

In all other chapters the pathology was written 

by W. G. J. Putschar and the paleopathology by 

D. J. Ortner. 

The book is written primarily with the needs 

of the anthropologist and archeologist in mind, 

with the hope that they will be able to recognize 

the abnormalities seen in human skeletal material. We are, however, interested in a broader 

readership with different backgrounds, including 

orthopaedic surgeons, radiologists, pathologists, 

and physicians who may be called upon to interpret skeletal lesions in dry specimens or who are 

interested in extending their understanding to the 

more detailed gross expressions of skeletal disease. 

Acknowledgments 

As a first step in preparing this book, Drs. 

Ortner and Putschar conducted, in 1974, an extensive survey of documented skeletal pathology 

in 16 of the European pathology and anthropology collections. This survey was supported by the 

Smithsonian Research Foundation and Hrdlicka 

Fund and took the authors to six countries. The 

following list of these institutions and the staff 

members who gave assistance to the survey of 

their collections is an inadequate recognition of 

the many courtesies extended during our work. 

However, we wish by this method to express our 

appreciation for the cooperation we received in 

studying and photographing the skeletal specimens: Austria: Federal Pathologic-Anatomy Museum, Vienna (Dr. Karl von Portele, Dr. Alexander Miiller); Pathology Museum of the University of Graz (Prof Dr. Max Ratzenhofer); 

Pathology Museum of the University of Innsbruk 

(Prof Dr. Albert Probst, Prof Dr. Josef Thurner 

(Salzburg, Austria)). Czechoslovakia: National Museum, Department of Anthropology, Prague (Dr. 

Emanuel Vlcek, Dr. Milan Stloukal, Dr. H. Hanakova). England: British Museum (Natural History), London (Dr. Theya Molleson, Miss Rosemary Powers); Guy's Hospital Medical School, 

Gordon Pathology Museum, London; The Royal 

College of Surgeons of England, Wellcome Museum, London (Dr. Martin S. Israel); The Royal 

College of Surgeons of England, Hunterian Museum, London (Miss Elizabeth Allen); St. 

George's Hospital Medical School, Pathology 

Museum, London; Westminster Hospital School 

of Medicine, Pathology Museum, London. France: 

University of Strasbourg, Department of Pathology, Museum (Prof Y. Le Gal, Prof Andre Batzenchlager). Scotland: The Royal College of Surgeons of Edinburgh (Prof Eric C. Mekie, Dr. 

Andrew A. Shivas, Mrs. Violet Tansy, Mrs. 

Turner, Mr. McKenzy). Switzerland: Anthropological Institute of the University of Zurich, (Dr. 

Wolfgang Scheffrahn); Historical Museum, Chur 

(Dr. H. Erb); Institute of Pathological Anatomy 

of the University of Zurich (Prof Dr. Erwin 

Uehlinger, Prof Dr. Christoph E. Hedinger, Mr. 

Aschwanden); Natural History Museum, Bern 

(Prof Dr. Walter Huber). Dr. Cecil J. Hackett, 

an associate of the Royal Orthopaedic Hospital, 

did much to expedite our work in London, England, and offered several helpful suggestions regarding collections in other countries that proved 

valuable to our study. 

The product of our survey was more than 1200 

photographs, in both black and white and color, 

taken by D. J. Ortner, of approximately 500 
SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

pathological specimens jointly studied. For some 

cases we were able to obtain X-ray films as well. 

W. G. J. Putschar described the specimens in 

detail on tape and included original autopsy and 

clinical data where available. This collection of 

photographs. X-rays, and the transcripts of case 

descriptions is available for study at the Department of Anthropology, National Museum of Natural History, Smithsonian Institution, Washington, D.C. Many of them are used as illustrations 

in this book. 

A number of people have made significant 

contributions in the preparation of the manuscript. Mrs. Paula Cardwell, Mrs. Eleanor Haley 

and particularly Mrs. Katharine Holland typed 

initial drafts. Mrs. Marguerite Brigida and Mrs. 

Elizabeth Beard typed the final draft. Mrs. Marcia Bakry prepared some of the drawings. To Ms. 

Jacqui Schulz goes a special note of appreciation 

for the many unpaid hours spent in preparing the 

remaining drawings and getting the photographic 

illustrations ready for publication. Photographic 

enlargements were prepared by Mr. H. E. Daugherty and Mrs. Agnes Stix. Mrs. Stix also assisted 

in editing and typing the manuscript. Mr. David 

Yong, Mr. Edward Garner and Mr. Dwight 

Schmidt provided valuable technical assistance. 

The staff of the library of the Smithsonian Institution, particularly Mrs. Janette Saquet, was 

most helpful. Drs. J. Lawrence Angel, T. Dale 

Stewart, and Douglas H. Ubelaker, Department 

of Anthropology, Smithsonian Institution, have 

made valuable suggestions, as have Dr. Saul Jarcho, New York City, USA, and Dr. George Armelagos, University of Massachusetts, Amherst, 

Massachusetts, USA. The staff of the Smithsonian Institution Press, particularly Mr. Albert L. 

Ruffin, Jr., Managing Editor, Series Publications, 

and Ms. Joan B. Horn, senior editor, deserve 

special recognition for their assistance from the 

conceptualization through publication of the 

book. 

Finally the wives of both authors have been 

intimately involved with the preparation of the 

book. Mrs. Florence Putschar has spent hundreds 

of volunteer hours organizing photographs, typing, preparing the bibliography, editing, and 

otherwise making her remarkable abilities available to the project. Mrs. Joyce Ortner has also 

assisted in obtaining illustrative material and 

skeletal specimens used in the book. 

Abbreviations 

The illustrations in this book are of specimens 

from many institutions. The following abbreviations are used in the legends to avoid repetition 

of lengthy institutional names and locations. 

AFIP Armed Forces Institute of Pathology 

Washington, D. C. USA 

AIAC Australian Institute of Anatomy 

Canberra, Australia 

AIUZ Anthropological Institute 

University of Zurich 

Zurich, Switzerland 

A NM National Museum of Anthropology 

Prague, Czechoslovakia 

BMNH British Museum (Natural History) 

London, England 

CGH Department of Pathology 

Charleston General Hospital 

Charleston, West Virginia 

DPUS Department of Pathology 

University of Strasbourg 

Strasbourg, France 

FM Field Museum of Natural History 

Chicago, Illinois, USA 

FPAM Federal Pathologic-Anatomy Museum 

Vienna, Austria 

GHP M Gordon Pathology Museum 

Guy's Hospital Medical School 

London, England 

H M Hunterian Museum 

The Royal College of Surgeons of England 

London, England 

HMCS Historical Museum 

Chur, Switzerland 

IPAZ Institute of Pathological Anatomy 

University of Zurich 

Zurich, Switzerland 

IPMI Pathology Museum 

Institute of Pathology 

University of Innsbruck 

Innsbruck, Austria 
NUMBER 28 

M G H Department of Pathology 

Massachusetts General Hospital 

Boston, Massachusetts, USA 

NHM B Natural History Museum 

Bern, Switzerland 

NMN H National Museum of Natural History 

Smithsonian Institution 

Washington, D. C , USA 

O M Odontological Museum 

The Royal College of Surgeons of England 

London, England 

PMES Pathology Museum 

The Royal College of Surgeons of Edinburgh 

Edinburgh, Scotland 

PMSG Pathology Museum 

St. George's Hospital Medical School 

London, England 

PMUG Pathology Museum 

University of Graz 

Graz, Austria 

PMW H Pathology Museum 

Westminster Hospital School of Medicine 

London, England 

UGPM Pathology Museum 

University of Gottingen 

Gottingen, Federal Republic of Germany 

V M Virchow Museum [destroyed WWII] 

Berlin, Germany 

W M Wellcome Museum 

The Royal College of Surgeons of England 

London, England 

A Brief History of Paleopathology 

Descriptions of dry bone lesions in anthropological or paleontological specimens go back at 

least two hundred years. The earliest work on 

paleopathology focused on nonhuman paleontological specimens (e.g., Esper, 1774; Cuvier, 

1820). Warren (1822) included a discussion of 

artificial cranial deformation in human skulls of 

indigenous North Americans in his book titled A 

Comparative View of the Sensorial and Nervous Systems 

in Man and Animals. In 1855, Gosse published, in 

Paris, another study of artificial cranial deformation. Toward the end of the nineteenth century the question of the origin of syphilis began 

to be debated with an intensity that continues 

today (e.g., Jones, 1876; Virchow, 1898). 

With the turn of the century there is a marked 

expansion of published reports on ancient disease. 

Particularly notable is the work of Sir Marc 

Armand Ruffer (1910) on Egyptian mummies, 

and the studies on Nubian skeletal material by 

Wood-Jones (1908a, 1910b) and Elliot-Smith and 

Wood-Jones (1910). In the United States, 

Hrdlicka (1914) published some observations on 

the pathology of ancient Peruvian skulls. In 1923, 

R. L. Moodie's introduction to the study of ancient disease, which emphasized nonhuman paleontological specimens, appeared. A brief, general review of human paleopathology was published by H. U. Williams in 1929. This review 

included observations on bones and teeth, as well 

as on mummy tissue and ancient art. Pales (1930) 

followed with his book on paleopathology and 

comparative pathology. Most of his cases and 

discussions concerned European human specimens. In the same year, Hooton (1930) published 

his classic study of the North American Indian 

skeletal material from Pecos, in which he included 

an extensive description of pathological specimens. Hooton's study is notable in its descriptive 

detail, in the statistical treatment of different 

types of disease in the skeletal population, and in 

his efforts to show trends in disease frequency 

through the time period of human occupation at 

the site. 

M0ller-Christensen's report (1953) on the skeletal material from a medieval leper cemetery in 

Denmark is perhaps unique in the history of 

paleopathology. The historical knowledge of the 

existence of a leper cemetery and its location led 

to excavation of the skeletons. The descriptive 

analysis of this material has provided important 

information about leprosy in ancient times. It has 

also expanded our knowledge of the effects of the 

disease on skeletal tissue. 

More recent general works on paleopathology 

include Calvin Wells' review of evidence of human paleopathology from skeletal material, 

mummies and art (1964a). Brothwell and Sandison (1967) brought together in a single volume 

many of the classic papers on paleopathology 
SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

with a broad range of new papers on numerous 

subjects related to the study of ancient disease. 

Morse's report (1969) on skeletal pathology in 

human archeological material from the midwestern United States provides excellent descriptive 

details on many types of skeletal diseases. 

Throughout the development of human skeletal paleopathology as a scholarly discipline, there 

have been recurring problems in both theory and 

methodology. In the early stages of this development most of the research was conducted by 

physicians who had little knowledge of archeology. In more recent times most of the studies of 

pathological skeletal specimens have been conducted by anthropologists whose background in 

gross bone pathology may have been inadequate. 

This has led to problems in which lesions of bone 

were incorrectly attributed to the pre-Columbian 

time period by those unfamiliar with the complexities of archeological dating and in which 

bone lesions were incorrectly diagnosed through 

ignorance of anatomy and the total range of 

diseases that affect bone (see Stewart's comments 

on this problem in Jarcho, 1966:43). 

Much of the emphasis in paleopathology until 

recently has been on descriptions of pathological 

specimens, and there has been little effort to relate 

the evidence of disease to the broader problems 

of human adaptation. Hints of such an emphasis 

exist in Hooton's Pecos Pueblo monograph (1930) 

and more recently in the consideration of epidemiological factors in evaluating the data on preColumbian tuberculosis in the New World 

(Morse, 1969) and in discussions on the origin of 

treponemal diseases (Hackett, 1963; Hudson, 

1965). The trend toward population studies of 

ancient disease undoubtedly will become increasingly important as descriptive data accumulate 

and the diagnostic criteria for skeletal disease are 

clarified. 

Much of the descriptive literature in skeletal 

paleopathology depends on the scholar's knowledge of gross bone pathology. Unfortunately, 

where this knowledge is inadequate there have 

been few reference sources that could be of assistance. Jarcho (1966) organized a symposium on 

human paleopathology, which addressed this 

problem among others. The participants called 

for the establishment of a paleopathology registry 

and improved diagnostic methodology to partially correct these problems. Steinbeck's recent 

textbook (1976) on diagnosis of ancient bone 

disease represents the first integrated attempt to 

establish diagnostic criteria for the paleopathologist. As such it represents an important step in 

improving the knowledge regarding the types of 

diseases that affect bone and the morphological 

features associated with the disease. 

The Paleopathology Program at the 

Smithsonian Institution 

Ortner (1976) has reported the development of 

a program at the Smithsonian Institution, which 

addresses the need for a registry and includes 

additional reference materials. This Paleopathology Program has as its major objective the 

identification and classification of all pathological 

specimens in the vast human skeletal collections 

of the National Museum of Natural History. 

Significant progress has been made toward this 

objective. Another objective is to build a reference 

collection of clinically documented cases of skeletal disease including gross specimens, photographs, and roentgen films. 

In the United States, Drs. George Huntington, 

College of Physicians and Surgeons in New York 

City, T. Wingate Todd, Western Reserve University in Cleveland, Ohio, and Robert Terry in 

collaboration with Mildred Trotter, Washington 

University in St. Louis, Missouri, developed major anatomical skeletal collections from anatomical, dissecting-room cadavers. Each of these collections contained about 2000 skeletons, among 

which were pathological specimens. Ales 

Hrdlicka, the founder of physical anthropology 

at the Smithsonian Institution and one of the 

pioneers of American paleopathology, obtained 

the Huntington skeletal collection for the National Museum of Natural History. This collection was accessioned in 1921, partially in the hope 

that it would become the nucleus of a reference 
NUMBER 28 

collection on pathology of the skeleton (Hrdlicka 

letter to J. H. Kellogg, 31 January 1921). More 

recently the Terry collection has also been transferred to the Smithsonian. The Todd collection is 

currently housed at the Cleveland Museum of 

Natural History, Cleveland, Ohio, USA. 

It is clear that collections of documented bone 

pathology will need to be added to these fine 

skeletal collections to supply adequate comparative material for the needs of the paleopathologist. 

In the United States, there are a few skeletal 

collections specifically devoted to pathological 

conditions including those of the Armed Forces 

Institute of Pathology in Washington, D. C , The 

Warren Anatomical Museum at Harvard University and the Mutter Museum of the College of 

Physicians of Philadelphia. However, direct comparison of material in these collections with archeological skeletons is awkward at best. Careful 

photographs and roentgen films of such materials 

are the most realistic vehicle for comparative 

studies. 

The final objective in the Smithsonian Paleopathology Program is to gather together bibliographic source materials from the literature on 

bone and joint pathology and on paleopathology. 

Much of this material is in older, rather inaccessible sources, and considerable effort has been 

expended to obtain originals or copies of much of 

the relevant literature. This bibliographic material, as well as the photographs and detailed 

descriptions of the cases studied in our joint European museum survey, are available for study at 

the Department of Anthropology at the National 

Museum of Natural History of the Smithsonian 

Institution in Washington, D. C , USA. 
The Biology of Skeletal Tissues 

The Development of Bone 

Early in the development of the fertilized human egg (zygote) the dividing cells form three 

distinct regions, which ultimately differentiate 

into the tissues and organs of the adult. These 

three layers are ectoderm, mesoderm, and entoderm. Of the three, ectoderm and mesoderm are 

relevant to our understanding of skeletal tissues. 

Ectoderm gives rise to structures that produce the 

enamel of teeth. Mesoderm differentiates into 

connective tissue including bone, cartilage, dentin, and cementum. 

In the embryo the tissue precursor of bone 

results from a condensation of mesodermal cells 

called mesenchymal cells. At this stage, these cells 

are undifferentiated and can become any one of 

several different types of specialized connective 

tissue cells. The factors that induce a mesenchymal cell to become or produce one of the specialized skeletal cells remain one of the intensely 

interesting problems in connective tissue biology. 

One of the important factors appears to be the 

immediate vascular and cellular environment resulting from the proliferation of blood vessels and 

adjacent cells in the embryo. This proliferation 

affects the accessibility of the cell to nutrients and 

oxygen. Changes in these factors are known to 

modulate the differentiation of cells. 

The specialized cells that are part of the biology 

of skeletal tissue induce cartilage cells and bone 

cells. There are two types of cartilage cells: (1) 

chondroblasts, which secrete cartilage matrix, 

and (2) chondrocytes, which maintain cartilage 

matrix and create conditions that lead to the 

mineralization of some cartilage tissue. There are 

three types of bone cells: (1) osteoblasts, which 

form bone matrix, (2) osteocytes, which maintain 

bone tissue, and (3) osteoclasts, which destroy 

bone tissue and calcified cartilage. 

Classically, two types of bone formation occur 

during the development of skeletal tissue. In one 

of these (endochondral ossification), cartilage cells 

are an important factor. In the second type of 

bone formation (intramembranous ossification) 

only bone cells are involved. These two types of 

bone formation produce tissue in different ways. 

During cartilage matrix formation, the new matrix is secreted within existing tissue matrix (interstitial development), whereas during bone matrix formation (except for limited interstitial development during embryonic life) the new matrix 

is laid down on an existing tissue surface (appositional development). 

Endochondral ossification is associated with 

the growth phase but may occur in the adult in 

abnormal situations, such as fracture healing. In 

the embryo the earliest centers of endochondral 

ossification are those areas that will become the 

major, long, tubular bones (the femur, tibia, fibula, humerus, radius, and ulna). All endochondrally derived bones begin as a condensation of 

mesenchymal cells which, in contrast to intramembranous ossification, develop into a cartilage 

model (anlage) of the future bone rather than 

directly into bone itself. 

The cartilage model consists of the cartilage 

cells (chondrocytes) and a protein matrix, the 

latter forming the bulk of the model. However, 

the entire model is surrounded by a connective 

tissue layer called the perichondrium. As the 

cartilage model grows, through the proliferation 

of cells (chondroblasts) in the germinative layer 

of the perichondrium, the oldest cells near the 

center of the model begin to swell (hypertrophy). 

As this occurs the perichondrium overlying this 

area takes on osteogenic properties and forms a 

sleeve of bone around the central region of the 

model (Figure 1). In contrast with the cartilage 

model, the sleeve bone is highly vascularized and 

8 
NUMBER 28 

v ,-j;;jV4|f|-f4 

.j^^'^:^i^.'! 

FIGURE 1.—Histological features in endochondral ossification. Cartilage (C) at the top of the field, the zone of 

hypertrophic and calcifying cartilage (CC) is near the middle 

level of the field. Bone formation (B) on calcified cartilage 

cores is taking place in the lower portion of the field. Sleeve 

bone (SB) marking the lateral margin of the growth plate is 

in the left portion of the field. The section is from the femur 

of a 5-month human fetus. (Approximately X 50.) 

with increasing hypertrophy of the cartilage cells, 

blood vessels invade the model. Vascularization 

of part of the model creates the conditions necessary for bone formation, but the initial process 

does not involve the synthesis of additional organic matrix as is the case in intramembranous 

osteogenesis. 

Cartilage has many of the same protein constituents as bone and apparently the cellular hypertrophy of the cartilage is associated with a 

process that makes it possible to mineralize the 

matrix that remains between the cartilage cells. 

During the early stages of long bone development, 

the constituents for mineralizing cartilage probably arrive at the site of mineralization by diffusion through the organic matrix (Ham, 1974: 

375). Vascularization makes the necessary constituents for mineralization much more accessible. 

As osteoblasts are adding bone to part of the 

mineralized cartilage trabeculae, bone destroying 

cells (osteoclasts) are frequently seen in histological preparations to be removing the mineralized 

cartilage (Figure 2). In a longitudinal section 

through a developing long bone of a 20-week 

FIGURE 2.—Fiber bone formation (FB) on calcified cartilage cores (CC). Osteoblasts (OB) are 

active in the left of the field. An osteoclast (OC) is destroying calcified cartilage near the right 

edge of the field. The section is from the femur of a 5-month human fetus. (Approximately 

X 1000.) 
10 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

fetus, it is apparent that mineralized cartilage is 

a very temporary tissue. Within 10 to 15 millimeters distance of the zone where the cartilage is 

mineralizing, most of such tissue has been replaced by the combined activity of osteoclasts 

and osteoblasts. 

The initial site of penetration by the blood 

vessels into the cartilage model of a long bone 

becomes the nutrient foramen of the mature 

bone. Bone growth takes place centrifugally from 

this site, although not necessarily in equal 

amounts in all directions. As the zone of mineralizing cartilage moves away from the initial 

center of ossification, the sleeve bone is also growing in both directions and forms the initial compact tissue or shaft of the developing bone. Because the shaft flares near the ends, the process of 

growth also involves a process of remodeling in 

which the flared end is reduced to the appropriate 

dimensions for the shaft. 

Toward the end of fetal life some of the long 

bones such as the femur establish secondary centers of ossification in the epiphyses. In these centers the process of cartilage mineralization, followed by vascular invasion and the addition of 

bone, in turn followed by the removal of trabeculae containing mineralized cartilage, is essentially the same as the growth of the diaphysis. 

In intramembranous ossification, mesenchymal 

cells differentiate (probably through one or more 

intermediate steps) into bone forming cells (osteoblasts). This process occurs within the mesenchymal cell condensation. As cell differentiation 

takes place, the cells become organized and form 

smooth, membranous sheets. Continuing development involves the synthesis of organic bone 

matrix by osteoblasts. This organic matrix is in 

close proximity to the cell and consists primarily 

of collagen but contains noncollagenous, organic 

materials as well. In its unmineralized state the 

organic matrix of bone is called osteoid. Normally 

the mineralization of osteoid proceeds rapidly (in 

a matter of hours) although full mineralization of 

bone matrix, particularly in the adult, may take 

months or years. 

As the long bones lengthen they also increase 

in diameter. Growth in diameter occurs by apposition as the result of intramembranous ossification. However, early in embryonic life most of 

the centers of ossification in the skull are of the 

intramembranous type. The development of the 

bones of the skull is complex and the reader 

should consult a standard reference on human 

embryology (e.g., Hamilton and Mossman, 1972) 

for a detailed discussion. For the purposes of this 

book, it is sufficient to note that the centers of 

endochondral ossification in the skull are primarily associated with the skull base including the 

sphenoid and part of the occipital (Figure 3). 

It might be well at this point to emphasize that 

the distinction between endochondral cartilage 

and membrane-formed bone is more than an 

academic exercise. As will be emphasized subsequently, some diseases focus on skeletal tissue 

formed in a cartilage model (e.g., achondroplasia). Other diseases also affect the process of 

membrane bone formation (e.g., osteogenesis imperfecta) . 

The embryological development of vertebrae is 

also complex. There are, however, congenital deFiGURE 3.—Midsagittal drawing of the skull of a 4-month 

human fetus. Stippled areas indicate approximate region of 

intramembranous ossification, horizontal lines indicate approximate regions of endochondral ossification. 
NUMBER 28 11 

fects of the vertebral column, which can best be 

understood in terms of defects in embryological 

development. Early in the development of the 

embryo, cell division results in the production of 

separate but similar segments in a process called 

segmentation. One product of segmentation is the 

somite, which is a paired condensation of mesodermal cells on each side of the embryonic precursor of the vertebrae (notochord) and the embryonic precursor of the spinal cord (neural tube). 

Each of the somites will give rise to a skin segment 

(dermatome), a striated muscle segment (myotome), and a sclerotome that forms a portion of 

a vertebra and, in the case of thoracic vertebrae, 

a rib. 

Cells in the sclerotomic condensations proliferate and completely surround the notochord, 

displacing the neural tube dorsally. In the dorsoventral axis the cells are distributed evenly. 

However, in a cranial-caudal axis this is not the 

case. The cranial mass of cells (the anterior sclerotome) is less condensed, while the caudal portion 

(the posterior sclerotome) is more condensed. The 

cells of a posterior sclerotome, at the boundary 

with the less dense cell condensation of the same 

sclerotomic condensation, differentiate into the 

intervertebral disc. The remaining cells of posterior sclerotome fuse with the anterior sclerotome 

of the adjacent sclerotome to form a vertebral 

body (Figure 4). 

Within the sclerotomic cell condensations, 

chondrification centers develop and form the cartilaginous vertebral body. Other cartilaginous 

centers on either side of the neural tube begin to 

proliferate and form the cartilaginous precursor 

of the vertebral arch and spinous processes. These 

centers fuse with the vertebral body. While the 

neural tube ultimately forms the spinal cord (and 

in the cranium, the brain), the notochord forms 

the nucleus pulposus of the intervertebral disc, 

but it degenerates in the region of the vertebral 

body. 

During the early growth phase, beginning with 

the fetus and continuing through early childhood, 

the growth rate is very high. For example, from 

the fifth fetal month to birth the length of the 

a> 

=Vi"''^if'\YiVfr'';-;'''frV'''''''4 

^(^0 

cD> 

FIGURE 4.—Schematic diagram of the embryonic development of vertebrae. The early stage of development is represented by the three sclerotomes on the left. The anterior 

sclerotome is represented by the lightly stippled areas. The 

more heavily stippled areas represent the posterior sclerotome. There is a blood vessel between each pair of sclerotomes. During embryonic development the posterior and 

anterior portions of adjacent sclerotomes fuse to form an 

embryonic vertebral body as seen on the right side of the 

diagram. 

femur doubles. However, from birth it takes approximately four years for the femur to double its 

length again and eight years to double a third 

time (Stewart, 1968:132-133). 

The bone tissue associated with very rapid 

growth is called fiber or woven bone and is not as 

dense or as well organized histologically as bone 

associated with slower growth. In a microscopic 

preparation, the bundles of collagen microfibrils 

are irregular in thickness and do not have the 

highly regular organization seen in later stages of 

the individual's life (Figure 5). However, fiber 

bone may be found in later life in abnormal 

conditions, such as fracture healing and neoplasms. 

The fiber bone of the early developmental 

stages is replaced by more organized tissue called 

lamellar bone. The histological characteristics of 

this type of bone are the layers (lamellae) of 

collagen of relatively uniform thickness and the 

alternating orientation of the fibers. These fea-
12 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

FIGURE 5.—Fiber bone in a 5-month human fetus. Note the 

irregular orientation of most of the fiber bundles. (Approximately X 100.) 

tures are easily seen in histological preparations 

using a polarizing microscope. The collagen of 

the protein matrix of bone has crystalline properties because of the periodic arrangement of the 

molecules of tropocoUagen, which make up the 

major component of the matrix. This arrangement results in an optical property called anisotropy (birefringence), in which the axis of light 

passing through the fibers is rotated. 

If two polarizing filters are adjusted so that the 

filter axes are perpendicular to each other, light 

cannot pass through the filters. If a histological 

specimen is placed between such filters, birefringent areas in the tissue will rotate the light permitting some of the rays to pass through the filter 

farthest away from the light source and be seen 

as a light area of tissue. Portions of the tissue that 

are not birefringent will not rotate light and this 

will appear dark in polarized light. In this context 

it may be well to emphasize that both fiber bone 

and lamellar bone have anisotropic properties in 

contrast with calcified cartilage, which does not 

rotate light and thus appears dark in a polarizing 

microscope (Figure 6). 

FIGURE 6.—Calcified cartilage (arrow) surrounded by developing bone in a 5-month human fetus. The light is partially 

polarized. Note that the calcified cartilage has optical properties similar to the background in contrast with bone, which 

is generally much brighter. This brightness is due to the 

anisotropic properties of bone. (Approximately X 1000.) 

Cartilage 

With this background on the early development of skeletal tissue let me review in greater 

detail the role of cartilage and bone in the function of skeletal tissue. Three types of cartilage 

tissue occur in human organisms: (1) hyaline, (2) 

fibrous, and (3) elastic. Of these three, hyaline 

cartilage is germane to our discussion of skeletal 

tissue because of its importance in bone growth. 

I have already discussed the role of cartilage in 

endochondral bone formation in which hyaline 

cartilage provides a temporary mineralized scaffold for bone formation. These endochondral ossification centers or zones persist throughout the 

growth period and are obliterated at varying ages 

in different bones; the last fusion occurs by about 

the age of 25 years with the fusion of the two 

growth centers of the iliac crest. 

In addition to its involvement in growth, hyaline cartilage provides the gliding surface of all 

true joints such as those between the long tubular 
NUMBER 28 13 

bones. Hyaline cartilage, like bone, has two basic 

components, cells and intercellular matrix. However, there are many features of hyaline cartilage 

that are in distinct contrast to bone. Although 

chondrocytes and chondroblasts are derived from 

mesenchymal cells, as are bone cells, the cartilage 

matrix secreted by chondroblasts contains less 

collagen (about 10 percent) but cartilage contains 

much more water and a higher concentration of 

chondroitin sulfate, a type of noncollagenous protein, than is found in bone. During the growth 

phase, chondroblasts are in direct contact with 

the enlarging cartilage and are contributing to 

the growth process by secreting protein matrix, 

which occasionally surrounds some chondroblasts. The chondroblasts that become surrounded by matrix differentiate into chondrocytes but retain many of the chondroblastic properties (Ham, 1974:372), such as the ability to 

divide, to produce new cells, and the ability to 

secrete matrix. Bone cells (osteocytes) do not divide and have only very limited ability to produce 

matrix. 

Cartilage tissue is similar to bone tissue in that 

it has the capacity to grow by adding cells and 

matrix to existing surfaces (appositional growth). 

However, unlike bone, cartilage can expand (interstitial growth) by multiplication of cells and 

interstitial secretion of matrix by its chondrocytes 

(Ham, 1974:372-374). Cartilage cells, both chondroblasts and chondrocytes, retain optimal ability 

to divide and secrete matrix only during the 

growth phase of the individual (Ham, 1974:374). 

Another contrast between hyaline cartilage and 

bone is that cartilage is poorly vascularized. The 

nutrients that are needed for chondrocyte function and the metabolites that result from cell 

activity must arrive and be removed while relatively isolated from vascular supply by the gellike matrix that surrounds the cell. The minimal 

vascularization and the reduced ability of cartilage cells to multiply after the end of longitudinal growth appear to be related factors in 

greatly limiting the capacity of cartilage to repair 

itself if damaged by injury or disease after maturity. This fact becomes important in interpreting a number of abnormal conditions seen in the 

joint surfaces of bone, particularly in the arthritides. 

The Cells of Bone 

Two cells of bone (osteoblasts and osteoclasts) 

are directly responsible for its gross appearance. 

The third bone cell, the osteocyte, is very much 

part of the histological appearance of bone and 

plays an important role in mineralization, bone 

tissue maintenance, and mineral physiology. The 

activity of all three bone cells may be divided 

into five functions: (1) protein matrix synthesis, 

(2) mineralization of protein matrix, (3) bone 

tissue maintenance, (4) resorption of mineralized 

tissue, and (5) involvement in general mineral 

physiology. 

The osteoblast itself contains the normal basic 

ingredients of a cell, a nucleus and cytoplasm 

containing organelles (mitochondria, endoplasmic reticulum, ribosomes, and Golgi bodies) involved particularly in the synthesis of protein 

matrix. The fluid phase of cytoplasm includes 

water, glycogen, and fat vacuoles. The cytoplasm 

is surrounded by a thin membrane, which has 

long, fine extensions filled with cytoplasmic fluid. 

These cytoplasmic extensions form an interconnecting network, with adjacent cells forming the 

main component of the germinative layer of the 

bone forming tissue (Figure 7). 

As the osteoblast sheets, applied to an existing 

surface of bone or calcified cartilage, begin to 

secrete osteoid, a matrix is formed, which becomes 

interposed between them and the bone surface 

(Figure 8). However, some of the osteoblasts become surrounded by the matrix in spaces called 

lacunae (Figure 9). The cytoplasmic extensions 

are maintained with other nearby osteoblasts, 

which are also being surrounded by osteoid, and 

with the osteoblasts, which remain at the protein 

secreting front. Surrounded osteoblasts are now 

osteocytes. The interconnections between osteocytes surrounded by matrix are maintained after 

mineralization and form the little canals (canaliculi), which are a prominent part of bone histology. The interconnections between the osteoid 
14 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

FIGURE 7.—Schematic representation of the different types 

of cells related to bone formation and bone maintenance. 

The fibroblastic layer consists of the very elongated, finely 

stippled cells at the top of the illustration. Adjacent to bone, 

the fibroblasts differentiate into osteoblasts seen as the 

coarsely stippled, interconnected cells on the bone surface. 

Osteoblasts secrete bone protein matrix and mediate the 

initial stage of mineralization. Some of the osteoblasts and 

their interconnecting processes are surrounded by bone matrix and differentiate into osteocytes represented by the finestippled cells. Osteocytes are involved in the physiological 

activities of bone including mineral exchange and final 

mineralization of the bone matrix. 

secreting osteoblasts and osteocytes are also maintained (Ham, 1974:419) as long as the osteoblasts 

are active. 

The protein matrix is fibrillar and in lamellar 

bone the collagen fibers have a highly specific 

orientation, with each subsequent layer having 

its fibers oriented at a varying angle to the preceding layer. There appears to be a fairly discrete 

number of osteoid layers secreted before mineralization takes place (Johnson, 1964:624). This may 

be related to the life span of the active osteoblast, 

which hypertrophies before the onset of mineralization. As with calcified cartilage, the initiation 

of bone mineralization is accompanied by increased alkaline phosphatase activity. With initial 

mineralization the death of some of the matrix 

forming cells occurs. With the completion of initial mineralization the organic bone matrix has 

achieved approximately 75 percent of maximum 

mineralization (Amprino and Engstrom, 1952: 

11). 

Former osteoblasts that were surrounded by 

protein matrix begin a process of differentiation 

by which they become osteocytes. While the osteocytes maintain the interconnecting network of 

cytoplasmic extensions (canaliculi) with other osteocytes, there is a marked reduction in the 

amount of cytoplasm. The space made available 

by this reduction appears to be filled with a 

special mineralized matrix, which is important in 

mineral physiology. The osteocytes may continue 

to function for years. 

During the initial stage of its life cycle, the 

osteocyte appears to be involved in the process of 

final or secondary mineralization of adjacent matrix. In part, because there are many fewer cells 

per cubic millimeter of tissue than was the case 

during osteoid formation, the process of secondary mineralization is much slower than mineralization mediated by osteoblasts. Another factor 

may be that mineral ions, cell nutrients, and cell 

metabolites must pass through the canalicular 

system. The process of secondary mineralization 

not only takes longer (many months versus hours 

to days for primary mineralization) but becomes 

even slower with increasing age. 

FIGURE 8.—Photomicrograph of bone cells during active 

matrix synthesis. The newly formed osteoid layer is indicated 

by the arrows. Two osteocytes are seen in the osteoid layer 

and osteoblasts are lining the surface of the osteoid. Fibroblasts are seen as dark elongated cells adjacent to the osteoblasts. (Approximately X 600.) 
NUMBER 28 15 

FIGURE 9.—Scanning electron micrograph of an osteocyte 

lacuna. Small holes at the bottom of the lacuna are opening 

into the canaliculi. The structure in the right portion of the 

lacuna may be the dried remnant of the osteocyte. (Approximately X 4000.) 

The second stage of the osteocyte life cycle 

marks a shift away from activity involving secondary mineralization to activity in mineral physiology. Thus far I have treated bone as a tissue 

with primarily mechanical functions. Here I need 

to introduce the reader to the concept that bone 

is an organ involved in the physiology of the 

human organism. There are several ionic concentrations in blood serum, which need to be maintained at virtually constant levels. One of these is 

calcium which, in a healthy individual, is maintained at a concentration of about 10 milligram 

percent. Physiologically calcium is, among other 

things, a cofactor in blood clotting and involved 

in the contractile mechanism of muscle (McLean 

and Urist, 1968:259). 

Serum calcium concentrations are maintained 

by a complex interrelationship among (1) dietary 

(intestinal) absorption of calcium, (2) renal (kidney) retention of calcium, (3) secretions by the 

parathyroid (parathormone) and thyroid (calcitonin) glands, (4) exchange with labile mineral in 

the skeleton (osteocyte activity), (5) bone resorption (osteoclast activity), and (6) direct exchange 

between bone crystal surfaces and serum. While 

the major factors in calcium physiology are dietary and renal, the skeleton through direct exchange and osteocyte activity provides a rapidly 

available (minutes to hours) finely controlled 

source of calcium (if there is some problem with 

the major mechanisms) to maintain serum calcium levels. 

The final stage of the osteocyte life cycle involves senescence and death. Precisely how this 

affects the metabolism of the organism and the 

mechanical and physiological functions of skeletal 

tissue is unclear. 

Throughout the life of the individual, there is 

a continuing need to remove and replace existing 

skeletal tissue. Earlier I have noted the need to 

change the contours of growing bone. The complexity of this process will become more apparent 

in the discussion of internal or osteon remodeling 

(p. 19). For the moment it is adequate to note that 

osteoclasts are the cells that are associated with 

the resorptive phase of skeletal remodeling and 

with bone loss in morbid conditions. 

Osteoclasts differ morphologically from osteoblasts and osteocytes in several zispects (Figure 

10). Two characteristics that are particularly noticeable are that osteoclasts are much larger than 

other bone cells and that they generally have 

more than one nucleus. There are no cytoplasmic 

extensions from the cell. Structures within the 

cytoplasm of the osteoclast also differ from the 

osteoblast. There are many more lysosomes in the 

osteoclast reflecting its destructive potential, 

while mitochondria and the endoplasmic reticulum are minimal reflecting a cell function in 

which protein synthesis is minimal. In a single 

day, a single osteoclast can destroy bone that took 

100 osteoblasts to form in the same time period. 

Grossly, all of the destructive lesions seen in skeletal disease are the direct result of osteoclastic 

action. Disease conditions resulting in bone destruction only stimulate osteoclastic responses and 

do not directly destroy bone. 

Histologically the osteoclast is always associated with bone resorption at an existing bone 

surface. One of the distinctive features frequently 
16 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

FIGURE 10.—An osteoclast in a Howship's lacuna. Arrows 

indicate three of the nuclei. Note the irregular edge of the 

resorbing bone in the lacuna. (Approximately X 1300.) 

seen in bone resorption is a deep concave depression in the surface known as Howship's lacuna. 

Osteoclasts may be seen occupying these depressions. The side of the cell in contact with the bone 

surface has a striated or "brush" border, which 

has been shown to be the folded cell membrane 

that is involved in the solubilization and removal 

of adjacent bone tissue including both organic 

matrix and mineral (Hancox, 1972:123, 127). 

Osteoclasts are very active cells, which are 

motile and thus do not necessarily resorb bone 

only in one place (Hancox, 1972:128). Furthermore, osteoclasts frequently form clusters of cells 

during resorption, such that the depressions or 

lacunae formed by one cell may be removed by 

the activity of another osteoclast leaving a relatively smooth surface. The point to be emphasized is that Howship's lacunae are always indicative of active resorption, but the absence of 

lacunae does not preclude the existence of resorptive activity. Since in archeological bone specimens the cells are gone, one microscopic bit of 

evidence of active bone resorption will be the 

presence of Howship's lacunae. 

Bone Growth 

There are two basic mechanical functions performed by bone. These are to provide a fulcrum 

for muscle activity and a counterforce to gravity. 

One should perhaps add a third function in a 

somewhat different context: providing space for 

blood-forming marrow. To accomplish these objectives it is necessary to (1) provide the surface 

area for joints, (2) provide attachment for muscles, (3) maximize compression, shear, and bending strength, and (4) minimize weight. All of 

these factors result in a general model of a long 

bone which is (1) hollow to minimize weight, 

maximize strength, and provide for space for 

marrow (both blood forming and fat storage), (2) 

flared at the ends to provide adequate surface 

area for joint movement, and (3) often provided 

with specialized areas for muscle attachment. 

While these criteria apply primarily to long tubular bones, to varying degrees they are also 

factors in the shape of other bones as well. I shall 

use the long bone as a model for the remodeling 

process. 

As I have implied earlier the typical growing 

long bone consists of a growing diaphysis, the 

ends of which are flared and are called the metaphyses, a cartilage growth plate, and finally an 

epiphysis at each end (Figure 11). There may be 

other secondary growth centers (apophyses), such 

as the greater and lesser trochanters of the femur. 

To demonstrate the principles of remodeling, I 

will limit the discussion to the diaphysis and 

metaphysis of a growing long bone. 

Bone growth occurs in both length and width 

with length growth predominating. Growth in 

width involves the addition of circumferential 

layers of bone to the external surface of the bone 

shaft. At the same time removal of bone is taking 

place on the internal or endosteal surfaces of 

bone. The latter is done to minimize the weight 

of the bone and provide space for hemopoietic 

(blood forming) and fatty marrow. 

Growth in length is more complicated. The 

flared ends of the bone are growing not only in 

length but also in width. As the flared ends grow. 
NUMBER 28 17 

EPIPHYSIS 

GROWTH J- \ 

PLATE )J 

METAPHYSIS^ 

DIAPHYSIS i 

METAPHYSIS 

GROWTH ^ 

PLATE \ 

EPIPHYSIS 

FIGURE 11.—Diagrammatic representation of the major components of a growing long bone. 

what was formerly part of the metaphysis must 

be converted to the narrower diaphysis, so that 

growth in length is accompanied by the removal 

of bone on the external surface of the metaphysis 

in the region not involved in active growth (the 

cutback zone). This must be accompanied by the 

formation of bone on the endosteal surface in 

order to maintain the mechanical strength of the 

bone. Thus, while growth in the diaphysis involves addition to the external surface and removal of the inner surface, growth in the flared 

ends involves the reverse with the exception of 

growth at the very end of the flare. Here growth 

is occurring in length and width simultaneously 

(Figure 12). 

FIGURE 12.—Remodeling dynamics at the end of a growing 

bone. The conical end represents the metaphysis and growth 

plate. Hatching indicates the earlier stage in growth. The 

cross hatching indicates bone that must be removed as the 

bone grows in length. Arrows indicate the direction of bone 

addition during the growth process. 
18 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

An understanding of the growth dynamics is 

very important to the paleopathologist. There are 

many disease conditions that produce inadequate 

or abnormal remodeling. Most of these are discussed in the chapter on congenital disorders 

(p.329). Furthermore, the very porous external 

appearance of the cutback zone in the growing 

bone can easily be misinterpreted as pathological 

by one who is unfamiliar with this process. 

The process of growth-related remodeling stops 

with the fusion of the epiphysis and the metaphysis. However, appositional growth (periosteal) 

and endosteal resorption continue throughout life 

although at a greatly reduced rate. This continuous growth of bone is more than offset by the 

degenerative changes that are associated with 

aging. Removal of compact and cancellous bone 

in the marrow cavity (endosteal) also continues 

at a diminished rate. In order to maintain the 

mechanical integrity of the bone, the processes of 

periosteal deposition and endosteal removal must 

be in balance with respect to the particular mechanical loading of the bone. In the case of 

compact bone, this does not mean that the thickness of the cortex must be maintained at the level 

found in the young adult, since a larger external 

diameter greatly increases the bending strength 

of a tube. This means that with an increase in 

the external diameter there can be a considerable 

decrease in cortical bone thickness while still 

maintaining about the same bone mass and adequate mechanical strength. 

However, with increasing age there is a tendancy for endosteal removal to exceed periosteal 

deposition. This condition is associated with a 

reduction in cancellous bone trabeculae with remaining trabeculae sometimes becoming thickened. The combination of abnormal thinning of 

compact bone and the loss of cancellous bone is 

called osteopofosis and is discussed in greater 

detail in the chapter on metabolic disorders 

(p.270). 

Garn (1970:29) has reported the importance of 

endocrine secretions in controlling cortical 

changes. Male sex hormone (testosterone) affects 

periosteal deposition whereas female sex hormone 

(estrogen) affects endosteal deposition. Clearly 

other factors are involved in cortical dynamics as 

well (e.g., men at the end of their growth period 

have thicker cortical bone than women at the 

same stage), but the marked reduction in secretion of sex hormones occurs 10 to 15 years earlier 

in females than in males and appears to be a 

major factor in the more severe bone loss seen in 

the aging female skeleton. 

It is important to emphasize that the process of 

cortical remodeling, which occurs during and 

after the cessation of growth, is not uniform. 

Enlow (1963:51-59) has documented the existence of a trend he calls drift, in which appositional growth is associated with only part of the 

external and internal surface. Figure 13 illustrates 

the process diagrammatically for the tibia. In the 

tibia, bone tends to be added to the anteromedial 

periosteal surface and the posterolateral endosteal 

surface. Bone is removed from the anteromedial 

FIGURE 13.—Diagrammatic representation of the process of 

bone drift. During growth, the load axis of long bones may 

change. To compensate for the change in the mechanical 

loading, as in the tibia, bone is added to the anteromedial 

periosteal and posterolateral endosteal surface while bone is 

removed from the anteromedial endosteal surface and the 

posterolateral periosteal surface. 
NUMBER 28 19 

endosteal surface and posterolateral periosteal 

surface. Histologically what is apparent is that 

surface parallel lamellar bone characterizes those 

areas where bone is being added, while internally 

(osteon) remodeled bone and partially resorbed 

osteons characterize areas of bone removal. The 

process of drift is a response to continuing changes 

in the load axis of the tibia during and to a lesser 

extent after the cessation of growth. As such it is 

analogous to the remodeling of bone in fracture 

healing (p.61), where alignment of the broken 

ends is poor. 

Osteon Remodeling 

During the growth phase, and to a greatly 

reduced extent throughout the remainder of life, 

compact bone is added to existing external surfaces of bone by apposition. Appositional bone is 

deposited in layers, which give rise to the characteristic histological appearance of circumferential lamellar bone. However, like most other 

tissues of the body, bone needs to be renewed. 

The process of renewal is called internal or osteon 

remodeling (Figure 14). All bone remodeling reflects an obvious but important biological property of bone, namely, it is hard. This means that 

it cannot grow by interstitial expansion as cartilage can, and it cannot be removed without destruction by cellular activity. Because of the hardness of bone this renewal process involves the 

removal of existing tissue and its replacement 

with newly formed tissue. Throughout the skeleton much of the lamellar bone formed during 

growth and remodeling remains at least through 

early adulthood. However, in compact bone, particularly in the diaphysis of long bones, the surface parallel lamellar bone is replaced by the 

osteons. 

The classic appearance of the osteon is seen in 

cross-sections of compact bone (Figures 15, 16). 

The basic structure of an osteon in such a preparation is circular, having a diameter that varies 

in size but averages approximately 300 microns. 

The thickness of this page of paper is about 100 

microns, so it is apparent that we are talking 

about a relatively large histological structure. The 

length of an osteon is problematical since osteons 

are not discrete units but divide, rejoin and interconnect with other osteons to form a complex 

network. The order of magnitude for the length 

of an osteon segment from where it splits off and 

forms a discrete unit to the point where it joins 

another similar structure or terminates is from 2 

to 5 millimeters. While osteons are most often 

viewed in two dimensions it is important to be 

aware of the three dimensional aspect of their 

morphology. 

Structurally, an osteon in cross-section has a 

histologically discrete, round boundary. Within 

this boundary are circular layers of bone tissue 

whose collagen fibers are aligned in alternating 

directions like the layers in circumferential lamellar bone. Osteocytes are distributed throughout these layers and are interconnected by canaliculi in the bone, which contain the cytoplasmic 

extensions of the osteocytes. All viable osteons 

contain a central (Haversian) canal averaging 

about 50 microns in diameter, which includes a 

FIGURE 14.—Photomicrographic field of osteons in adult 

human compact bone. The elongated white structures within 

an osteon are lacunae. The fine filament-like structure radiating out from the central canal are canaliculi. (Darkfield 

illumination, approximately X 100.) 
20 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

FIGURES 15, 16.—Microscopic field showing osteons in various stages of development: 15, A 

resorption space (RS) is seen in the lower right corner. A forming osteon (FO) is in the lower 

left corner. Most of the remaining osteons in the field have completed protein matrix synthesis 

as indicated by the small size of the central canals. (Approximately X 45.) 16, Microradiograph 

of field in Figure 15 showing variation in osteon density. Less mineralized osteons are darker. 

minimum of one blood vessel. At least some 

osteons contain a nerve. Some of the canaliculi 

containing cytoplasmic processes of the osteocytes 

open into the central canal thus providing a 

pathway for nutrients and for mineral ions 

needed for continuing mineralization or ion removal in mineral physiology. The canaliculi usually do not communicate between adjacent osteons. 

The process of osteon remodeling begins with 

the removal of bone, creating a circular tunnel 

(Haversian resorption space). The actual process 

is best visualized in its longitudinal axis (Figure 

17). As an advancing wedge of osteoclasts forms 

the tunnel, the osteoblasts generally begin the 

refill process. The initial layer of bone matrix 

deposited on the walls of the resorption space 

tends to be somewhat different histologically. It 

is more highly mineralized and the proportion of 

noncollagenous protein is somewhat greater. The 

term "reversal line" is used to distinguish this 

layer from the remaining layers of bone in the 

osteon. The space and time sequence between the 

osteoclast resorbing front and the osteoblast refilling front varies, but classically it is thought to 

be rather small. Therefore, both resorption and 

formation take place at the same time, although 

in different parts of the tunnel. The refill of the 

FIGURE 17.—Diagrammatic representation of osteon remodeling in longitudinal section. Osteoclastic resorption is seen 

to the left, with large multinucleated osteoclasts associated 

with the scalloped edge of bone. Osteoclastic activity is 

associated with active hyperemia represented by the interconnected network of capillaries adjacent to the osteoclasts. 

In the center and right portions of the illustration osteoprogenitor cells (spindle-shaped cells adjacent to the blood 

vessels) are differentiating into osteoblasts. Bone matrix synthesis and mineralization fill in the resorption space leaving 

an interconnected network of osteocytes seen as stellate cells 

in the layered matrix. 
NUMBER 28 21 

tunnel involves a process essentially identical to 

that described earlier for circumferential lamellar 

bone formation: (1) layers of protein matrix are 

secreted by osteoblasts; (2) cells and their cytoplasmic processes are incorporated in the protein 

matrix; (3) primary mineralization occurs; (4) the 

process is repeated in a centripetal direction leaving a central canal; and (5) osteocytes mediate 

continuing secondary mineralization. During osteonal refill of resorption spaces there may be 

temporary pauses in the refill process. This results 

in an arrest line, which is histologically similar to 

the reversal line. With the resumption of matrix 

synthesis and mineralization, these arrest lines are 

retained. The physiological factors in the temporary arrested development of osteons are not 

known, but could prove to be a valuable source 

of information on physiological conditions in archeological skeletons. The time needed for resorption and refill are important. Bone formation 

takes at least ten times as long as the destruction 

of an equal amount of bone (Johnson, 1966:127). 

This means that for formation-resorption to be in 

balance, there needs to be ten times as many sites 

of active bone formation as there are sites of 

active bone destruction. In osteon remodeling the 

theoretical equilibrium ratio in normal tissue remodeling is about ten osteons in the forming stage 

for each resorption space. 

In fact some studies have shown that in compact bone of present day populations the observed 

ratio is very close to the theoretical ratio (Blumberg and Kerley, 1966:159; Ortner, 1970:65). 

Deviation from this ratio may be indicative of 

inadequate nutrition or other morbid conditions. 

A study by Richman and Ortner (1978) of osteon 

remodeling in Eskimos, Arikara (Plains Indians), 

and Pueblo Indians (Southwest U.S.) indicated 

that the Eskimo sample has a formation-resorption ratio of 10 to 1. However, the two American 

Indian samples have a ratio of approximately 6 

to 1, indicating a substantial reduction in bone 

replacement after resorption. The meaning of this 

finding needs further clarification; however, nutritional factors seem a rather obvious possibility. 

Among the Eskimos meat constitutes the major 

source of food. The two American Indian groups 

and particularly the Pueblo Indians depended 

heavily on maize. Meat contains much more 

protein than maize and would thus be more likely 

to provide the amino acids needed for synthesis 

of organic bone matrix. Stout and Simmons 

(1979) review the application of histomorphometrical analysis in archeological bone specimens. 

During the growth phase appositional development of circumferential bone tends to be relatively rapid. Woven bone may be deposited on 

the cortex as fine, cancellous bone. Subsequently, 

the spaces in such woven, cancellous bone are 

filled in by lamellar bone, creating primary osteons (Enlow, 1963:63). Although similar in appearance to secondary osteons, such structures do 

not represent a remodeling event. Histologically 

they differ from secondary osteons, tending to be 

smaller in cross-section. Also, primary osteons do 

not have a clearly defined reversal line marking 

the termination of bone resorption (Figure 18). 

Primary osteons are generally replaced by secFIGURE 18.—Primary osteon (arrow) in the long bone of an 

infant about 6 months of age. This structure results from the 

fill-in of spaces in newly formed bone. In human bone it is 

primarily associated with the very rapid growth occurring 

during fetal and infant development. (Approximately 

X 100.) 
22 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

ondary osteons- which, in turn, are frequently 

replaced by additional secondary osteon formation. Exactly what the local factors are that initiate normal remodeling within a specific osteon 

is not known. However, changes in the direction 

of force (weight and muscle activity) and the 

death of osteocytes are thought to play a role. 

The tunneling activity of the osteoclasts disregards previous boundaries of an osteon so that 

encroachment on the walls of adjacent osteons is 

a frequent occurrence and may result in the 

destruction of the canal of an adjacent osteon. 

In addition to the classic osteon remodeling 

described above, which results in the typical appearance of the osteon, there is another type of 

osteon remodeling, which occurs entirely within 

an existing osteon. This type of remodeling (Figure 19) produces an "osteon-within-an-osteon" 

appearance shown in an early illustration by 

Tomes and de Morgan (1853, pi. 6: figs. 1,6) and 

is characterized by a reversal line like that found 

on the periphery of a classic osteon. This type of 

remodeling however, is intermittent along the 

longitudinal axis of an osteonal canal. Ortner 

(1975:29) has argued that the small, cross-sectional and longitudinal size of such osteons suggests a physiological rather than a mechanical 

function for such osteons. Richman, Ortner, and 

Schulter-Ellis (1979) have found differences in 

the frequency of this type of osteon in three 

archeological skeletal samples. They attribute this 

difference to variation in diet. 

The effect of this type of remodeling on tissue 

in the periphery of the antecedent osteon is not 

known. Normally bone tissue isolated from vascular supply by the reversal line will die. However, the intermittent distribution of this type of 

remodeling in the longitudinal axis might make 

it possible for such tissue to be adequately supplied via the anastomosing network of canaliculi 

from areas above and below the new osteon in 

the antecedent osteon. 

The various factors involved in osteon remodeling result in a diverse pattern in the normal 

cross-sectional histology of bone. The paleopathologist should be familiar with these factors in 

FIGURE 19.—A small osteon (arrow) entirely within a larger 

osteon. The remodeling that produces small osteons is intermittent along the longitudinal axis of an osteonal canal. 

Such osteons appear to be a response to physiological rather 

than mechanical conditions affecting bone tissue. (Adult, 

human compact bone, approximately X 150.) 

order to recognize abnormal histological patterns. 

This morphological diversity is illustrated in Figures 20 and 21. In Figure 20 we see a few osteons, 

but most of the field is unremodeled, circumferential lamellar bone. Typically the vascular supply in such tissue is poor with greater distances 

between blood vessels than in osteon remodeled 

bone. The microscopic field in Figures 15 and 20 

contain: (1) osteons, (2) interstitial bone left behind after osteon remodeling of circumferential 

lamellar bone, (3) osteon fragments remaining 

after partial destruction of an osteon, (4) small 

osteons entirely within an older osteon, and (5) 
NUMBER 28 23 

FIGURES 20, 21.—Cross-section of a compact bone from a young adult: 20, The right half of the 

field is primarily circumferential lamellar bone containing several primary vascular canals. The 

left portion of the field contains remnants of circumferential bone, but much of this bone has 

been replaced by secondary osteons. (Polarized light, approximately X 70.) 21, Microradiograph 

of field seen in Figure 20. Note that the circumferential lamellar bone is denser than that in the 

osteons. 

osteons in various stages of development. The 

distribution and relative proportions of these features will vary greatly within a single bone, from 

bone to bone, and with the age of the individual. 

However, most of these features can be seen in 

any normal cross-section of cortical bone. 

Trabecular bone is associated with the marrow 

and cancellous spaces of bone. In adult long bones 

it is found primarily in the ends of the bone. 

During fetal development and in infancy and 

early childhood, trabeculae may consist of woven 

fiber bone. By late childhood trabeculae are made 

of lamellar bone. This type of bone does include 

osteocytes like compact bone; however, vascular 

canals and osteons are rare (Figure 22). 

In addition to the histological variation that 

can be seen in a microscopic preparation of a 

cross-section of bone, there is often considerable 

variation in mineral density of the various osteons. This aspect of bone histology can be recognized with some experience in stained or polished sections; however, it is most easily seen in a 

microradiograph. Briefly, a microradiograph is a 

high resolution X-ray image that reveals variations in the mineral density of microscopic features in undecalcified bone sections. With the 

completion of matrix synthesis and initial mineralization, the osteon has achieved approximately 70 percent of maximum density. Secondary mineralization is mediated by the osteocytes 

and occurs much more slowly, typically achieving 

about 90 percent of maximum mineralization 

within a year or two. Osteons in various stages of 

mineralization are easily recognized in microradiographs. 

Figure 16 is a microradiographic image of the 

field seen in Figure 15. Several features may be 

seen in the microradiograph which supplement 

what is less apparent in the bone section itself 

Osteons in the forming phase are very dark, 

indicating low mineralization. Osteoid seams in 

forming osteons that are just beginning to be 

mineralized are almost black. Some osteons have 

several light (dense) bands, which are associated 
24 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

FIGURE 22.—Trabecular bone from the metaphysis of an 

adolescent human femur. Note the large spaces between the 

thin walls of the bone. (Polarized light, approximately 

X40.) 

with a temporary cessation of osteoblastic refill. 

Several osteons have a broad zone of denser bone 

adjacent to the central canal, which may represent a special, physiologically active, type of mineral. 

The process of matrix formation and mineralization in osteon remodeling is influenced by a 

number of factors, including age, physical activity, and disease. From childhood through early 

adulthood, the process of secondary mineralization is faster than at a later age. The microradiographic picture during this period is characterized by relative uniformity in the mineral density 

of osteons. With increasing age both the matrix 

refill and secondary mineralization slow down. In 

the microradiograph the result is increasing variability with age in central canal size and mineral 

density (Jowsey, 1960:215; Ortner, 1975:33). 

However, vigorous physical activity will tend to 

minimize the effect of aging on osteon remodeling 

and mineralization. 

The review of bone thus far has emphasized 

the mechanical and structural aspects. Earlier I 

have emphasized that bone should also be 

thought of as an organ with physiological functions analogous to those performed by any of the 

other organs of the body. However, to understand 

the physiological aspects of bone as an organ, the 

two basic components of bone, the protein and 

mineral phases, and their interrelationships need 

to be understood. 

Approximately 90 percent of the bone protein 

matrix is collagen. The remaining matrix consists 

of several proteins including those subsumed under the term "muccopolysaccharides" (sugar-protein complexes) and a small amount of lipoproteins (fat-protein complexes). More recently, additional knowlege regarding the chemistry of the 

sugar-protein complexes has indicated that the 

term "protein polysaccharides" would be more 

appropriate for this general category of noncollagenous protein. In addition to the noncollagenous proteins, amino sugars are found in the 

organic matrix of bone. 

It is important to emphasize that the components of the organic matrix of bone are not distributed uniformly throughout skeletal tissue. For 

example, the molecules of noncollagenous matrix 

are more highly concentrated at the boundaries 

of tissue, such as the reversal line and the border 

of the central canal in osteons. Furthermore, noncollagenous matrix is more highly concentrated 

during the forming and early mineralization 

phase of growing or remodeling skeletal tissue. 

Apparently the amount of collagen in bone matrix is constant once the tissue is formed. The 

variable components include (1) the noncollagenous organic material, (2) water (about 10 percent), and (3) the bone mineral. 

The mineral matrix of bone, like the organic 

matrix, is complex. This complexity is still not 

completely understood. However, it is now generally accepted that the major mineral component is hydroxyapatite, having a chemical formula of Caio(P04)6(OH)2. The atoms in a molecule of hydroxyapatite are arranged in such order 

to give crystal properties to the mineral. In addition to crystalline calcium-phosphate, there is 

growing evidence for the existence of an amorphous or noncrystalline mineral phase in bone 
NUMBER 28 25 

(Posner, 1969). The precise relationship between 

the two types of mineral is not known. However, 

the proportion of amorphous mineral decreases 

with increasing mineralization. This suggests that 

the amorphous calcium-phosphate might be a 

transitional phase existing predominantly during 

the early stages of mineralization, There is some 

evidence that there may be localized concentrations of amorphous mineral in discrete histological zones within bone tissue (Ortner and Von 

Endt, 1971). These zones may be important in 

mineral physiology by providing a more reactive 

or labile source of mineral ions. 

A detailed review of hypotheses regarding the 

chemical and structural relationship of bone protein and mineral is not pertinent here. However, 

bone protein precedes bone mineral and is involved in the mineralization process possibly by 

providing the initial site for mineralization. Two 

mechanisms have been proposed for this process. 

In one hypothesis collagen provides a template or 

pattern to which mineral ions are attracted and 

arranged in the appropriate spacial relationship 

for mineral crystallization. The second hypothesis 

involves chemical binding of one of the mineral 

components, such as phosphate to a reactive 

group of some of the amino acids of collagen. 

Lees (1979) has proposed a model with both interand intrafibril mineralization of collagen. 

Another view of initial bone mineralization 

implicates the noncollagenous protein. However, 

Hancox (1972:87) notes that much of the research 

supporting this hypothesis is based on mineralization in cartilage. He is of the opinion that bone 

mineralization is different from that occurring in 

cartilage and questions the validity of such research in explaining mineralization in bone. 

The mineral phase of bone includes calcium 

and phosphate. However, the crystal structure of 

bone mineral is such that substitutions by some 

elements (e.g., strontium, radium, and lead for 

calcium; fluorine for the hydroxyl group) can 

take place for elements and ions in the crystal 

lattice. Furthermore, many elements may be attracted to the surface of bone crystallites (adsorption) and the hydration shell surrounding the 

crystal. Given the small crystal size found in bone 

mineral, a few hundred angstroms in length and 

breadth and about fifty angstroms thick (Neuman and Neuman, 1958:55), there is an enormous 

amount of bone crystal surface and a high likelihood of considerable exchange of ions between 

bone and body fluids. This offers the potential for 

bone to contain a considerable variety of chemical 

elements. It has also been noted that bone mineral 

may be present in an amorphous phase, which 

may have particular significance in bone physiology. 

Johnson (1966:67-68) suggests that mineral 

ions are almost instantly available from the labile 

mineral lining the canalicular system. The next 

most accessible source of mineral would be from 

the osteocyte lacunae. Neither of these sources 

necessarily involves the dissolution of bone matrix. The surfaces of bone including trabeculae 

provide a second source of mineral ions, with the 

Haversian canals providing the least accessible 

source of mineral. Johnson appears to assume 

that ions from the last two sources must be released by osteoclastic activity. However, radioactive tracer studies suggest that exchange (including both uptake and loss of radioactive ions) 

can occur without matrix destruction by osteoclasts in the tissue surrounding the Haversian 

canal (Rowland, 1966:243). 

Regardless of the actual mechanisms involved, 

it is clear that bone acts as a mineral bank. 

Removal of mineral components from bone tissue 

is controlled systemically by parathyroid hormone. Jande (1972) has shown that increases in 

serum parathyroid hormone levels results in loss 

of mineral around the osteocyte. Parathyroid hormone also increases the activity of the osteoclasts 

in destroying bone. The hormone calcitonin is 

thought to act antagonistically to parathyroid 

hormone, although its action is less well understood and less obvious than parathyroid hormone. 

The major factor that affects the secretion of 

parathyroid hormone is the serum calcium level. 

The normal range for calcium in blood serum is 

from 8.5 to 10.5 milligrams percent (or 8.5 to 10.5 

milligrams per 100 cubic centimeters of serum). 
26 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

A drop in serum calcium levels below the normal 

range activates the parathyroids and increases 

hormone levels, resulting in rapid (minutes to 

hours) loss of calcium from canaliculi and lacunae 

(Jande, 1972). If the parathyroid hormone concentration remains at the activation level for 

longer periods of time, osteoclastic resorption 

takes place. In the disease state continuing resorption may result in severe osteoporosis. 

This brief review of the physiology of calcified 

tissue serves to highlight the complex relationship 

between bone structure, particularly at the microscopic and ultrastructural level, and the physiological function of bone. Abnormal physiological conditions will occasionally be associated with 

gross or microscopic features observable in archeological specimens. The specific details of skeletal 

responses to abnormal physiological conditions 

are treated later, particularly in the chapters on 

metabolic disorders (p. 270) and endocrine disturbances (p. 298). 

The Biology of Teeth 

The mature tooth consists of three components 

(Figure 23). The first of these is the very hard, 

exposed surface called enamel. Enamel has no 

vascular supply and no cells. Dentine is the second component and provides support for the 

enamel in the tooth crown and forms the hard 

tissue portion of the tooth root. Dentine is avascular but has cells (odontoblasts) lining its inner 

surface. Tubules extend from the odontoblasts to 

the outer surface of the dentine. The third component of a mature tooth is the pulp cavity and 

root canal, which contain the nerve, vascular 

supply, and pulp mesenchyme, which is the 

source of the odontoblasts. 

The following review of tooth development is 

based largely on the figures and text of Hamilton 

and Mossman (1972:572-575, figs. 549-554) and 

Sicher and Bhaskar (1972). About the sixth week 

of embryonic development, ectoderm begins to 

invade mesoderm in the region of the upper and 

lower jaw. This invasion consists of an outer arch, 

which will result in the gum and inner arch called 

Crown ^ 

N«ck 

EnanMl 

D*ntin« 

Pulp cavity 

Root 

- Comont 

Root canal 

Root foraman 

FIGURE 23.—Schematic representation of the major components of a human tooth. 

the dental lamina. Subsequently the dental lamina forms individual enamel organs with a lining 

of epithelial (ectodermal) cells called ameloblasts. 

FIGURE 24.—Schematic representation of a developing human fetal incisor with a crown-rump length of 100 mm, 

approximately 2V2 months fetal-life (Reprinted, with permission, from Hamilton and Mossman, 1972:574, fig. 552.). 
NUMBER 28 27 

This lining develops cup-like structures, which 

will form the enamel of each deciduous tooth. A 

branch of the lamina will similarly form the 

enamel for the permanent teeth. Filling the cuplike indentation in an enamel organ are proliferating mesenchymal (mesodermal) cells known as 

the dental papilla, which will produce the dentin 

(Figure 24). 

With the establishment of a connective tissue 

sheath around both the enamel organ and the 

dental papilla the two structures are called a 

tooth germ or bud. At this stage of development, 

the tooth bud consists of (1) an outer layer of 

ectodermal cells (epithelium), (2) an intermediate 

zone of stellate reticulum, (3) an inner layer of 

ectodermal cells, (4) highly vascularized mesodermal cells (mesenchyme) associated with the inner 

layer of ectodermal cells, (5) a capillary network 

surrounding both the enamel organ and the dental papilla, and (6) a connective tissue sheath 

around the capillary network. 

Later in the development of the embryo the 

inner layer of ectodermal cells (ameloblasts) will 

secrete the enamel of the tooth and is called the 

ameloblastic layer. Some of the mesodermal cells 

in the dental papilla become arranged along the 

FIGURES 25, 26.—Tooth bud in a 5-month human fetus: 25, Low magnification, the enamel is 

the dark layer of the apex of the tooth. (Partially polarized, approximately X 85.) 26, Higher 

magnification showing detail of dentin and enamel in tooth bud. Boundary between dentin 

and enamel is indicated by the arrow. Odontoblasts (OD) are seen with long processes extending 

into dentinal tubules. Ameloblasts (AM) line the outer surface of the tooth bud and are actively 

forming the enamel. (Approximately X 400.) 
28 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

ameloblastic layer. The cells in this layer are 

odontoblasts and will produce the dentin. The 

two layers of cells are separated by a membrane 

(membrana praeformativa) the shape of which 

directly defines the ultimate shape of the tooth. 

The formation of both dentin and enamel proceeds by addition (apposition) away from this 

membrane—dentin in a centripetal direction, 

enamel in a centrifugal direction (Figures 25, 26). 

The ameloblasts ultimately disappear after 

enamel formation is completed, leaving behind, 

on the enamel surface, a thin covering or dental 

cuticle. The odontoblasts persist throughout the 

life of the tooth as an inner lining of the dentin. 

The remainder of the mesodermal cells in the 

dental papilla become richly vascularized and 

form the dental pulp. The tooth root begins to 

form before eruption but is not completely formed 

until some time after eruption. The root surface 

consists of a specialized tissue (cementum), which 

provides attachment for connective tissue (the 

periodontal membrane), which in turn attaches 

to bone. The sequence of tooth formation and 

eruption provides a useful index of age through 

the adolescent years. For the present discussion it 

is sufficient to emphasize that the timing of eruption varies with the developmental age of the 

individual and the tooth type. 

During development, teeth require adequate 

nutritional input including protein, calcium, 

phosphate, trace elements, and vitamins A, C, 

and D. Inadequacies in these components may 

result in grossly abnormal teeth or in teeth more 

susceptible to wear and microbial invasion (caries). Abnormalities of teeth may also be the result 

of diseases occurring during development, such as 

rubella and syphilis, as well as of genetic problems. Various components, such as the enamel or 

dentin, may be differently affected by a morbid 

condition. 
Methods Used in the Analysis of Skeletal Lesions 

Today's physicians have at their disposal a vast 

array of data to assist them in diagnosing a 

morbid condition in a living patient. Most of 

these data are not available to the paleopathologist trying to diagnose a lesion in an archeological 

skeleton. In spite of the obvious limitations facing 

paleopathologists, it is well to remember that they 

have at least one significant advantage over a 

present day pathologist. If an archeological skeleton is recovered in a good state of preservation, 

the paleopathologist can examine an abnormal 

skeleton in its entirety and to a degree that would 

be quite impossible in a current patient, living or 

dead. In paleopathology the fundamental objective should be to obtain as much background 

information on the skeleton as possible and take 

maximum advantage of one's ability to evaluate 

the skeletal lesion itself by direct observation. I 

shall review the methods for obtaining background information on skeletal specimens first 

and then review the methods for analyzing a 

morbid condition in the skeleton. 

Basic to any evaluation of pathology in archeological specimens is the following data: (1) age, 

(2) race or human population, (3) sex, (4) geographic location, and (5) time period or archeological horizon. A knowledge of these factors can 

have a substantial influence on the probabilities 

of various types of morbid conditions. For example, if we are able to determine that a specimen 

was a young adult at the time of death, this fact 

would greatly reduce the probability that a diseased skeleton was affected by carcinoma, since 

this is primarily a problem of the aged. Likewise 

the knowledge that a skeleton, with multiple, 

disseminated, destructive lesions, was male would 

tend to rule out metastasis from breast cancer. 

It is clear that some diseases are associated with 

specific human populations. Sickle cell anemia 

primarily affects black populations while another 

anemia, thalassemia, is found in peoples from the 

Mediterranean area and in southeast Asia. While 

there is generally an association between racial 

distribution and geography, the factors affecting 

the individual in a specific geographic location 

may not be genetic as is the case in sickle cell 

anemia and thalassemia. For example, coccidioidomycosis is endemic mainly in dry, dusty regions 

of southwestern United States. This disease affects 

members of any human population living in this 

area although the incidence may vary (Miller 

and Birsner, 1949). 

Time should rarely be a crucial factor in the 

diagnosis of a skeletal lesion. However, it cannot 

be ignored. The significance of the time factor 

will be more apparent in the discussion of treponemal conditions (p. 180). The problem can be 

stated briefly for illustrating its importance. The 

question is whether syphilis was introduced by 

people from the Old World into the New World 

or vice versa. This is a very complex problem but 

the unambiguous identification of a case of syphilis in a specimen dated before 1492 in either the 

Old or New World would obviously be a significant bit of information. 

In evaluating all of the above factors with 

respect to a diseased archeological skeleton it is 

important to be open minded before eliminating 

a possible disease on the basis of any one element. 

For example, it would be unwise to eliminate the 

diagnosis of syphilis for a pre-Columbian New 

World skeleton simply because some scholars feel 

that syphilis originated in the Old World. While 

this is a rather obvious situation the principle 

applies to other variables as well, particularly 

since there is always a margin of error in determining any of these variables in an archeological 

skeleton. 

Many of the criteria for determining the above 

variables are available in published sources and 

29 
30 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

need not be discussed in detail here. The following review is derived largely from published 

sources and will provide a general summary of 

methods for obtaining background data on archeological specimens. However, the emphasis 

will be on those aspects of the variables that are 

significant for research in paleopathology. 

Age Determination 

The estimation of biological age in an archeological specimen is related to several biological 

processes, such as growth and skeletal remodeling, 

which result in age related changes in the morphology of skeletal components. These changes 

are seen at the gross, as well as at the microscopic 

level. All of the methods for age determination 

attempt to establish the relationship between 

morphological changes in the skeleton and the 

age of the individual at the time of death. Furthermore, the methods involve the establishment 

of procedures for estimating age on the basis of 

these changes. Methods for determining age vary 

significantly in terms of research design, statistical 

methodology, appropriate age range, etc. 

Through the age of 18 (subadult) three methods of aging are used. These are based on agerelated variations in (1) bone length, (2) dental 

eruption and root development, and (3) the appearance and fusion of secondary centers of bone 

development (epiphyses and apophyses). Excellent and readily available reviews of these methods are found in Krogman (1962) and Stewart 

(1968, 1979a). It is important to emphasize that 

estimates of age based on these methods reflect 

the usual problems in standardizing such procedures. One must assume that the research design 

of the original study was adequate, particularly 

with respect to sampling the entire age distribution and population and that the morphological 

features can be assessed objectively. Furthermore, 

in applying any method of aging to an archeological skeletal sample one assumes that the sample 

used to establish the prediction procedure and 

the unknown archeological sample are from the 

same statistical population of individuals. These 

conditions, particularly the latter, frequently are 

not met. In such situations one hopes that the 

approximation is close. 

There is evidence that different methods of 

determining age may reflect different statistical 

populations. Merchant and Ubelaker (1977) compared two different techniques of determining 

age in subadult material, both of which were 

based on the sequence of dental development. 

When both techniques were applied to a single 

archeological sample, they found considerable 

difference in the age as determined by each technique. With this and other limitations in mind 

let us review the various methods for estir. iting 

biological age in archeological samples. 

Fetal material in archeological skeletal series is 

relatively rare but may be very significant, as in 

a situation where the mother died and was buried 

with the fetus. Estimation of age in such material 

may be a factor in inferring whether problems in 

birth might have been a factor in the mother's 

death. Stewart (1968:132) provides a regression 

formula based on femur length for estimating age 

from the fifth fetal month through birth. At birth 

the bony femur is about 80 mm in length, which 

provides a convenient criterion for distinguishing 

fetal from postfetal material. 

Other criteria may be inferred, if the preservation and excavation has been very careful, by 

determining the presence or absence of centers of 

ossification. Standards for these features are published in Stewart (1979a) and Krogman (1962: 

56-68). However, these standards are for birth 

onward. The absence of bones, such as the calcaneous, talus, cuboid, and the epiphyses of the 

distal femur, proximal tibia, and proximal humerus, would be indicative of death before birth. 

In archeological material identification of such 

ossification centers may be difficult or impossible 

since they may bear little if any resemblance to 

the shape of the bone later in development and 

may not be preserved. Careful excavation may 

permit recovery of ossification centers in association with an identifiable bone. 

From birth through the growth phase, the criteria for estimating age are based on long bone 
NUMBER 28 31 

length (particularly femur), the appearance of 

ossification centers, the sequence of dental eruption and root development, and, during the late 

growth period, the fusion of secondary ossification 

centers. The methods of age estimation based on 

these variables are summarized by Krogman 

(1962), Stewart (1968, 1979a), and Ubelaker 

(1978:46-53). By the age of 18 years (earlier in 

females), significant growth has stopped in most 

individuals although some epiphyses will continue to fuse through about age 25 years. 

From 18 years onward, other aging criteria 

become more significant. These include the continuing metamorphosis of the pubic symphysis 

(Todd, 1920, 1921; McKern and Stewart, 1957; 

Gilbert and McKern, 1973), which provides age 

estimates to the age of 50 years. The fusion of 

skull sutures has been a traditional criterion for 

age determination. In their study of Americans 

killed in the Korean War, McKern and Stewart 

(1957:37) found that suture closure was poorly 

correlated with age and of little use in age estimation. Krogman (1962:89) supports this conclusion but notes that the skull may be the only part 

of the skeleton present and thus the only source 

for estimating age in an unknown specimen. 

While Krogman's observations are addressed to 

forensic modern specimens they are also appropriate for archeological skeletal collections. At the 

National Museum of Natural History, for example, more than half of the collection of about 

25,000 skeletal specimens consists of the skull 

alone. Another problem in archeological material 

is that the pubic symphysis and other age criteria 

are particularly vulnerable to destruction in the 

soil and may not be useable. Thus, age estimation 

based on suture closure may be the only criterion 

available, but its limitations should be recognized. 

Other aging methods have been developed including those based on tooth wear (Brothwell 

1965a:67-70) and the degree of arthritic degeneration (Stewart, 1958a). Without doubt these 

methods provide helpful corroboration for age 

estimates from other sources. However, they are 

limited by the influence of factors that are not 

part of the process of biological aging, such as the 

coarseness of the diet and the physical activity of 

the individual. 

A recently developed method for age estimation is based on the process of microscopic bone 

tissue renewal (osteon remodeling), which continues throughout life. Early studies by Amprino 

and Bairati (1936) and by Jowsey (1960) suggested the existence of age dependent changes in 

osteon remodeling. Kerley (1965) was the first to 

apply adequate statistical samples and procedures to this problem. In his research he used four 

histological features: (1) osteons, (2) fragments of 

former osteons, (3) the amount of unremodeled 

bone, and (4) the number of nonosteonal vascular 

canals. The first two of these criteria increase with 

age, while the last two decrease with age. The 

statistical association between age and frequency 

of these features is the basis for estimating the age 

of an unknown specimen. Kerley determined this 

relationship for three major bones: femur, tibia, 

and fibula. 

The error in estimating age using this method 

compares favorably with estimates based on 

changes in the pubic symphysis. However, microscopic aging methods can be applied to ages in 

excess of 50 years and thus, extends our ability to 

estimate age into the older age categories. Because 

there is an increasing discrepancy between biological and chronological age as one gets older, 

the factor of error is higher in the 50-plus age 

range. Regardless, this is the only method currently available that allows age estimation for 

skeletons over 50 years of age. Kerley and Ubelaker (1978) have published revised regression 

formulae for Kerley's earlier study. 

As with any method there are problems in 

using Kerley's method. Preparation of bone sections is a time consuming and delicate procedure 

and even more so in archeological specimens, 

where the bone may have to be strengthened with 

plastic to prevent crumbling during processing. 

Soil erosion and organisms may destroy microscopic features needed for such an analysis. The 

procedure also assumes a fairly sophisticated 

knowledge of compact bone microstructure. One 
32 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

modification of Kerley's method appears to offer 

a simpler procedure (Ahlqvist and Damsten, 

1969) but does not appear to be as accurate in 

the lower age ranges (Bouvier and Ubelaker, 

1977; Ubelaker, 1978:66). 

Race Determination 

Race (here used in the sense of a discrete 

human population) determination in archeological skeletons is rarely a significant problem for 

the paleopathologist, since the archeological 

provenience usually provides a reliable indication 

of at least the broad racial background. Occasionally, however, members of more than one human 

population will be buried in the same cemetery, 

and identification of this fact can provide relevant 

background data for the interpretation of skeletal 

lesions. Methods for distinguishing between 

broad racial categories (e.g.. White, Negro, Mongoloid) are well known and have been summarized in Krogman (1962) and Stewart (1968, 

1979a). 

The major differences between human populations are best seen in the skull. Traditionally, 

physical anthropologists have characterized these 

differences in terms of various complexes of the 

skull such as skull vault shape (long headed, 

round headed), relative projection of the jaws 

(prognathism), shape of the nose (long and narrow in Whites, short and broad in Negroes), and 

relative position of the cheek bones (prominent in 

Mongoloids). 

In the traditional approach to racial characterization, measurement of skull dimensions is important, but each measurement tends to be 

treated as a discrete feature. A more recent development has applied multivariate statistical 

procedures to broad racial classification (Giles 

and Elliot, 1962) and to more subtle skull variations within broad racial categories (e.g., Howells, 

1973, Ortner and Corruccini, 1976). A multivariate statistical approach to racial variation provides greater objectivity and a measure of racial 

distance, which is based on many measurements. 

The remainder of the skeleton does not provide 

unambiguous evidence of racial affiliation. Stewart (1962) has reported that the femora of Negroes 

tend to be straighter than those of other races. 

However, there is considerable overlap in the 

distribution of the data, making prediction of 

race difficult. Furthermore, the postcranial skeleton is greatly affected by nongenetic factors such 

as diet, making it unlikely that racial differences 

can be resolved on this basis alone, at least to the 

extent of being useful in paleopathology. 

Sex Determination 

Sex differences in skeletal specimens are probably the least ambiguous of all the factors basic 

to the paleopathologist. In the skeleton the best 

criteria for determining sex are in the pelvic 

bones. These bones reflect the fundamental differences in functions associated with reproduction, particularly childbearing, in the female. In 

the female pelvis the major factor influencing its 

shape is the necessity for the infant to pass 

through the pelvic canal during birth. Both the 

dimensions and the shape of the pelvic inlet and 

outlet reflect this function (Figure 27). Thus, the 

female inlet and outlet are relatively and usually 

absolutely larger and rounder than in the male. 

A more detailed review of the specifics of these 

differences is given in Krogman (1962) and StewFIGURE 27.—Comparative views of the male and female 

pelves. Although the male pelvis is larger overall, the female 

pelvic inlet is larger. The female sacrum is wider and the 

pubic bone is longer. The female subpubic angle is larger 

than the male. (Male, left, NMN H 320026; female, right, 

NMN H 320001.) 
NUMBER 28 33 

art (1968). The problem in applying these criteria 

to archeological specimens is that the most distinctive differences around the pubic symphysis 

are also the most likely to be damaged. 

Even if the pubic bone is damaged it may be 

possible to apply a method for determining sex as 

reported by Phenice (1969). This method is based 

on the sex differences that occur on the ischiopubic ramus involving three criteria: (1) the ventral aspect of the pubic symphysis region, which 

is an arch in females, (2) the subpubic portion of 

the ramus, which is concave in females, and (3) 

the medial aspect of the ramus, which is broad 

and flat in males, narrow and ridge-like in females. Phenice reports a remarkably good accuracy of about 96 percent in determining the sex 

of specimens from test samples where sex is 

known. The size of the angle of the sciatic notch 

is larger in females and is also useful in determining sex. 

The sex differences that occur in the rest of the 

skeleton, including the skull, generally reflect the 

fact that females are smaller, less muscular, and 

more gracile. Standards for sex determination for 

different bones from several human groups can 

be found in both Krogman (1962) and Stewart 

(1968). It is important to emphasize that the 

range or distribution of this type of sex variation 

differs between populations, with females tending 

to be more male-like in some populations and 

males more female-like in others. Ones experience 

in determining sex in one archeological population is not necessarily transferable to another 

population. Fortunately, this caution is less significant with respect to the pelvis. However, for 

many sex features it is essential for the paleopathologist to adjust his criteria for sex determination 

as he studies different skeletal populations, by 

comparing nonpelvic sex features, such as those 

seen in the skull, with sex-related traits in the 

pelvis. By studying skeletons that are fairly complete first, one can adjust the male-female sex 

criteria for nonpelvic features toward the male or 

female end of the range as appropriate and thus 

better estimate sex when pelvic features are missing. 

Stature Determination 

Stature (height) is a variable that is controlled 

largely by genetics. However, it is also clear from 

numerous studies that the health of the individual 

is also a significant component affecting stature. 

General health reflects many factors, including 

diet and disease, so that stature comparisons, 

particularly in combination with other types of 

analysis, can provide valuable data on the general 

health of skeletal samples. One should, however, 

carefully consider whether one's research objectives can be served equally well by comparing the 

long bone lengths themselves rather than converting lengths to stature estimates. 

Since stature is highly correlated with long 

bone length, it is possible to estimate stature by 

measuring one or several long bones and applying 

the appropriate regression formula. Numerous 

formulae for different long bones and human 

populations have been reported previously by 

Trotter and Gleser (1952, 1958). Both Krogman 

(1962) and Stewart (1968) summarize the work 

of Trotter and Gleser and other reports as well. 

Since the proportions of various parts of the 

skeleton vary in different human groups, it is 

important to use a formula that is based on a 

population similar to the archeological material 

being studied. 

Estimation of stature in archeological skeletons 

is limited by the same problem of damage and 

missing bones as in estimating other variables. 

Steele (1970) has developed regression formulae 

for fragmentary material, which are based on 

modern White and Negro specimens. However, 

this method may be helpful with archeological 

samples even if not from these populations provided that one is cautious regarding conclusions 

based on such estimates. 

Demographic Analysis 

It is important in studying ancient disease not 

to limit one's estimate of health in skeletal populations to direct evidence of morbidity or lack of 
34 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

it. Much can be learned by the analysis of mortality and the demographic aspects associated 

with it. Bogue (1969:549) notes that mortality 

exerts a varying force on different human populations. Clearly a major factor in this variation is 

the condition of health in these populations. 

Bogue (1969:549) also emphasized that "mortality has a very unequal impact on various age 

groups." The overall pattern of death rate in 

various age categories will also vary in different 

populations. This is clearly demonstrated in the 

marked reduction of infant deaths in highly developed societies as contrasted with developing 

societies (Bogue, 1969:556-557). Estimates of 

mortality in an American Indian skeletal population reveals high infant mortality but, in addition, another peak in mortality is present around 

adolescence (Ubelaker, 1974:60). Other estimates 

of mortality in ancient skeletal populations from 

the eastern Mediterranean have indicated higher 

mortality in females of childbearing age than 

males of the same age, which probably reflects 

the hazards associated with pregnancy and childbirth (Angel, 1969a; 1971:71). 

Of several statistical methods treating mortality, one of the most useful is the life table (e.g., 

Bogue, 1969:551-552; Swedlund and Armelagos, 

1976:47). In general, the life table summarizes 

the frequency of events and the probability of 

events happening within discrete intervals of time 

throughout the entire range of life within a population. Basically these events include (1) the 

number of deaths occurring per unit of population within specific age intervals and (2) the 

probable average number of years of remaining 

life for individuals in each category. Variations 

in these factors reflect many conditions, such as 

diet, disease, warfare, and other problems. As 

such, data in life tables may provide nonspecific 

but useful information on the relative health of a 

human population. 

A discussion of the methods and limitations of 

constructing life tables is given in several sources 

(e.g., Bogue, 1969:551-555; Swedlund and Armelagos 1976:63-64; Ubelaker, 1978:91-97). 

Such sources should be consulted before developing a life table for skeletal material. However, 

it is important that one be generally aware of the 

assumptions and hazards in applying such techniques to archeological populations. The most 

obvious problem arises from the fact that modern 

life tables are based on events (deaths) occurring 

in a living population, whereas archeological reconstructions of life tables are based on a population of individuals all of whom are dead. The 

characteristics of the two types of populations are 

not necessarily the same, although this must be 

assumed in such applications. Another problem 

is the extent to which skeletons recovered from a 

cemetery represent all the individuals who died 

in a given population. Cultural practices regarding formal interment in cemeteries vary and may 

not include burial of infants. Furthermore smaller 

skeletons may not be preserved as well as larger 

ones. This would, for example, adversely affect 

the proportion of infants recovered from the cemetery during excavation. Swedlund and Armelagos (1976:47) note that the validity of developing 

life tables for archeological populations depends 

on the degree to which the population is (1) 

sedentary and (2) large, and (3) provides a large 

number of recoverable skeletons. When these 

three conditions prevail, or are at least approximated, life table data provide a significant supplement to analysis of bone disease. 

Archeological Documentation 

I cannot overstress the importance of good 

archeological documentation of all skeletal specimens. Resolution of interesting and significant 

epidemiological problems may hinge on such 

data. For example, one archeological skeleton 

from Arkansas in the collection of the National 

Museum of Natural History, Washington, D.C, 

USA, probably represents one of the most convincing examples of treponemal infection that 

exists. This specimen (NMNH 258778) was excavated in the late nineteenth century using 

methods that make accurate archeological dating 

impossible without considerable destruction of 

the specimen (Figures 329-332). This skeleton, if 
NUMBER 28 35 

dated before Columbus, would provide valuable 

information toward resolving the problem of the 

origin of syphilis. Thus, the usual elements of 

archeological provenience, geographical location, 

archeological horizon or date, and cultural association, are important variables in paleopathologyIn most cases, data obtained during excavation 

of an archeological specimen will supply detailed 

information on provenience. Although it is conceivable that the geographical location of a specimen could be lost due to a mistake in museum 

cataloging, we assume that data or geographical 

location will almost always be readily available. 

Very often the archeolgist can determine the date 

or archeological horizon of the specimen on the 

basis of associated artifacts. In many areas of the 

world the evolution of artifacts has been carefully 

documented and associated with time. These time 

sequences of artifact series frequently provide the 

most accurate dating of associated skeletal material. Dates based on association of artifacts may 

be checked with dates obtained by absolute dating methods such as ^^C analysis, where appropriate material such as charcoal exists. Bone itself 

can be analyzed, but the methods currently available on a routine basis involve the destruction of 

a considerable amount of bone. 

Various methods of dating have been applied 

directly to bone including ^'*C, nitrogen, fluorine, 

and amino acid dating. However, all these methods may produce spurious results because of any 

one of several variables that can affect the analysis. There are several sources that review the 

methods of dating and their inherent problems 

(e.g., Zuener, 1958; Brothwell and Higgs, 1970; 

Ortner, Von Endt, and Robinson, 1972; Michels, 

1973; Hare, 1974; Von Endt, 1979). However, in 

view of the importance of dating in paleopathology it seems appropriate to provide a brief review 

of the problems with particular reference to the 

biology of bone as it affects dating methods. 

In ^"^C analysis of bone, the fundamental problem is bone's low carbon content, which requires 

the destruction of substantial quantities of bone 

for obtaining analytical data. Assuming that expendable skeletal material exists for such a purpose, there are many problems encountered in 

assuring that the ^'^C was part of the tissue at the 

time of death and not added later. 

Some of the carbon in bone is associated with 

the mineral phase of bone as carbonate. Hassan 

and Ortner (1977) have noted that carbonate 

exchange may occur after death and burial. Furthermore they point out that physical contamination with carbonaceous material also occurs. 

Thus, the mineral phase of bone is a poor source 

of ^^C because of contamination and recrystallization. 

The protein phase in bone also contains carbon, but it is much more stable than bone mineral 

after death and burial. Thus, bone protein is 

probably the best source of radioactive carbon. It 

is, however, essential to remove all contaminants. 

In the case of bone protein, it is very much 

simpler to do this than for bone mineral, since 

bone protein is more highly resistant to demineralizing agents. Such agents would tend to remove 

soil contaminants and leave behind the insoluble 

protein containing carbon incorporated in bone 

tissue during the life of the individual. 

In theory, at least, the protein matrix of bone 

should provide an accurate source for C analysis. However, keep in mind that varying soil 

conditions affect the stability of bone protein. 

Acid soils will hydrolyze bone protein over the 

years, destroying the protein, and breaking down 

the tissue in general. This results in the loss of 

nitrogen and this loss has been used as an index 

of time (Oakley, 1950, 1963a, 1963b; Cook, 1960; 

Doberenz and Matter, 1965). The effect of protein degradation on ^"^C analysis is unknown but 

cannot be ignored. 

Nitrogen analysis does provide supporting evidence of age. However, the degradation of bone 

protein, on which this method depends, is affected 

by several factors including soil pH, temperature, 

and water (Ortner, Von Endt, and Robinson, 

1972), which have not yet been fully clarified. 

Another dating method that is based on bone 

protein utilizes the ratio between natural amino 

acids (L form) and D amino acids, which gener-
36 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOG Y 

ally do not occur in biological tissue. Through 

time racemization occurs, in which L amino acids 

convert to D forms. This process is correlated 

with time (Hare, 1974) and has the advantage 

over nitrogen analysis of being affected by fewer 

variables. Regrettably, as of this writing, much 

remains to be done before amino acid dating 

provides a reliable method for dating archeological skeletons. 

Gross Study of Skeletal Lesions 

With this background on data basic to an 

analysis of a pathological specimen, we can focus 

on methods for analyzing specific morbid conditons in a skeleton. Fundamentally, there are four 

sources of information that may be relevant in 

paleopathology: (1) gross analysis of the skeleton 

itself, (2) analysis of X-ray images, (3) chemical 

analysis of bone, and (4) microscopic examination 

of bone. 

The gross appearance and X-ray images of an 

abnormal bone represent overlapping features of 

a disease process, and both should be part of any 

descriptive analysis of the morbid condition (see 

p. 45 ff). The ultimate goal of a descriptive 

analysis is the identification of the disease process. 

It is important to recognize that the specific cause 

or etiology of an abnormal bone condition cannot 

always be derived from even the most careful 

analysis of the paleopathological specimen. However, even when the specific disease cannot be 

identified, the description of the abnormal condition may, in itself, provide important data in 

paleopathological research by providing information on the frequencies of cases in the descriptive categories. I cannot overemphasize the importance of careful descriptive analysis of all 

paleopathological specimens. This is basic to the 

identification of disease, but it also represents 

significant data in and of itself 

In a descriptive system for abnormal bone conditions, there are several essential elements. These 

include (1) an unambiguous terminology, (2) precise identification of the location and distribution 

of abnormal bone, and (3) a descriptive summary 

of the morphology of the abnormal bone. The 

remainder of this chapter focuses on the descriptive system for paleopathological skeletal specimens. 

The most fundamental concept relating to the 

interpretation of abnormal bone conditions is 

that the abnormal morphology that results from 

pathological processes in bone is always the result 

of disturbances in the osteoblast and osteoclast 

cell populations (Schinz, Baensch, Friedl, and 

Uehlinger, 1951-1952:191). Shifts in the relative 

and absolute activity of these cells may be associated with abnormal activity by the osteocytes, 

but this is a minor component of any disease 

process in bone. Not only can there be shifts in 

the relative and absolute proportions of these 

cells, but, at least in the case of osteoblasts, the 

speed or metabolic rate of the cells may change. 

Thus, it is variation in the cell population balance 

and in cell activity that accounts for all the 

variation in the morphology of abnormal bone. 

In this sense then, one of the basic objectives of a 

descriptive analysis of abnormal bone is to determine the actions of the cells that produced the 

abnormal tissue. The importance of this perspective cannot be overemphasized. 

Both systemic and local factors can stimulate 

or inhibit the activity of osteoblasts and osteoclasts. Pathogenic organisms, including fungi, 

bacteria, viruses, and parasites, act on bone architecture by creating conditions that stimulate 

or inhibit the bone cells. While it is rather remarkable that the activity of only two types of 

cell can produce such a large variety of abnormal 

conditions in bone, it is important to remember 

that many distinctly different diseases produce 

very similar types of lesions. 

As we begin to think about the description of 

morbid conditions in the skeleton, it is important 

to be aware of the fundamental ways bone cells 

can respond to the stimulus of disease. Schinz, 

Baensch, Friedl, and Uehhnger (1951-1952:194-

220) provide an excellent summary of these responses, and their description has been used in 

the following review of bone cell reactions to 

disease. All abnormal conditions of bone can be 
NUMBER 28 37 

placed in one of the following general categories 

reflecting bone cell activity: (1) abnormal bone 

loss, (2) abnormal bone gain, (3) a combination 

of abnormal bone loss and abnormal bone gain, 

and (4) normal quality of bone but abnormal 

shape or contour. 

The first step in a descriptive analysis of a 

pathological specimen is to determine whether 

the abnormality consists of (1) a solitary lesion in 

which there is a single focus for the disease process, (2) multiple lesions in which there is more 

than one focus for the disease process, (3) diffuse 

abnormal bone in which there is no specific focus 

for the disease but a general change in bone 

quality, and (4) a local or generalized disturbance 

of normal size or shape in which the quality of 

the bone tissue is normal. If the abnormality is a 

solitary lesion one should identify the bone involved and its position on the bone, and then 

describe the lesion itself However, if the abnormality involves one of the other three categories 

the descriptive process is somewhat more complicated, largely because the distribution of abnormal bone in the skeleton is more complex. It is 

also important to remember that multiple lesions 

may not represent the same morbid process. 

Regardless of which of the above categories is 

appropriate for a specific abnormal specimen, the 

location of the abnormal bone in the skeleton is 

a crucial descriptive parameter. Various disease 

processes often affect preferentially groups of 

bones, specific bones, and specific locations in 

bones. Indeed, predilection, or lack of it, is an 

important aspect in itself 

Functionally the skeleton may be divided into 

two groups of bones. The first group is the axial 

skeleton and consists of the skull, mandible, vertebral column, ribs, manubrium, and sternum. 

The second broad group is the appendicular skeleton, which includes the pectoral girdle, the arms 

and hands, the pelvic girdle, and the legs and 

feet. Within the bones of the axial and appendicular skeleton specific disease processes vary in 

their distribution. A descriptive analysis of an 

abnormal skeleton should be specific regarding 

the bones involved and the location within the 

bone. The following outline can serve as a guide 

to the degree of precision that should be attempted. In the discussion of particular diseases 

in subsequent chapters we will identify, wherever 

possible, the sites in the skeleton affected preferentially by a disease. 

A. Location of abnormal bone(s) in skeleton 

1. Axial skeleton 

a. Skull 

(1) Vault 

(2) Face 

(a) alveolar 

(b) nonalveolar 

(3) Base (including entire sphenoid and temporal 

bones) 

b. Mandible 

(1) Body 

(a) alveolar 

(b) nonalveolar 

(2) Ramus 

(a) articular 

(b) nonarticular 

c. Vertebral column (except sacrum and coccyx) 

(1) Cervical 

(a) body 

(b) arch, transverse processes, and spinous 

process 

(c) joint surfaces 

(2) Thoracic 

(a) body 

(b) arch, transverse processes, and spinous 

process 

(c) joint surfaces 

(3) Lumbar 

(a) body 

(b) arch, transverse processes, and spinous 

process 

(c) joint surfaces 

d. Ribs 

(1) Near vertebrae (proximal) 

(2) Near sternum (distal) 

(3) Intermediate 

e. Sternum 

(1) Manubrium 

(2) Corpus 

(3) Xiphoid process 

2. Appendicular skeleton 

a. Pectoral girdle 

(1) Scapula 

(2) Clavicle 

b. Arm and forearm 

(1) Humerus 
38 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

(2) Radius 

(3) Ulna 

c. Hand 

(1) Carpals 

(2) Metacarpals 

(3) Phalanges 

d. Pelvic girdle 

(1) Innominate 

(a) Ilium 

(b) Ischium 

(c) Pubis 

(2) Sacrum 

(3) Coccyx 

e. Thigh and leg 

(1) Femur 

(2) Patella 

(3) Tibia 

(4) Fibula 

f Foot 

(1) Tarsals 

(2) Metatarsals 

(3) Phalanges 

B. Distribution of abnormal lesions within affected bones 

1. Long bones 

a. Longitudinal axis 

(1) Proximal joint surface 

(2) Proximal epiphysis 

(3) Proximal apophyses 

(4) Proximal metaphysis 

(5) Diaphysis 

(6) Medullary 

(7) Distal metaphysis 

(8) Distal epiphysis 

(9) Distal apophyses 

(10) Distal joint surface 

b. Cross-sectional axis 

(1) Extracortical 

(2) Periosteal (Parosteal) 

(3) Cortical 

(4) Endosteal 

(5) Medullary 

2. Skull/Mandible 

a. Outer table (Outer cortex) 

b. Diploe (Medullary) 

c. Inner table (Inner cortex) 

The above outline provides a systematic nomenclature for identifying the location of abnormal bone tissue. With the spatial parameters of 

the disease clearly identified, the next step is a 

careful description of the abnormal bone tissue 

itself. Keep in mind that the objective of any 

description of the abnormal conditions is to clarify the activity of bone cells with respect to the 

abnormal morphology. In the chapter on the 

biology of skeletal tissue (p. 13) I note that bone 

cell populations can destroy bone or form bone 

and may do both in fairly close proximity in some 

disease processes. Let me review the morphological manifestations associated with each of these 

possibilities. 

Abnormal bone loss can be the result of four 

types of cellular disturbances: (1) an abnormal 

increase in osteoclast activity with normal osteoblast activity, (2) an abnormal decrease in osteoblast activity with normal osteoclast function, (3) 

a combination of increased osteoclast activity and 

decreased osteoblast activity, and (4) normal osteoclast function with normal osteoblast matrix 

synthesis but an inability to mineralize the matrix. Since unmineralized protein matrix will 

rarely survive in archeological material the last 

category will probably appear as increased osteoclast activity. 

Abnormal bone loss is seen macroscopically as 

bone atrophy. Schinz, Baensch, Friedl, and Uehlinger (1951-1952:197-200) divide bone atrophy 

into two general categories: osteoporosis and osteolysis. Osteoporosis involves a loss of bone in 

which much of the spongy bone is resorbed, 

leaving behind a few, sometimes thickened, trabeculae and an increased porosity of compact 

bone. There may be a thinning of the compact 

bone as well. Osteolysis is localized bone destruction, which results in a specific defect in the 

morphology of bone. When osteolysis occurs in a 

limited area on the outer surface of bone it is 

called erosion; if erosion is more extensive the 

term "caries" is more appropriate. Osteolysis 

within compact bone or marrow may result in a 

bone cyst or cavity. 

While osteoporosis will usually involve more 

than one bone, osteolysis may be solitary or multiple, and, if multiple, it may be seen in one bone 

or several. Furthermore, the osteolytic lesions may 

be discrete or coalescent. At this stage of the 

discussion it is appropriate to introduce the concept of time in the development of an osteolytic 

lesion (Figure 28). If the lytic disease process is 
NUMBER 28 39 

FIGURE 28.—Schematic representation of bone tissue responses to osteolytic activity. If the lytic process is slow or 

stops after an acute phase, the bone tissue will circumscribe 

the lesion with dense, compact bone as seen in the left 

example. If the disease process is more active there will be 

little or no circumscribed, sclerotic reaction, but the boundary of the lytic lesion is sharply defined and there may be 

slight evidence of some bone formation. This type of lesion 

is associated with lytic processes having moderate destructive 

activity and speed as represented by the middle example. If 

the lytic activity is very rapid there tends to be a gradient of 

destruction at the margin of the lesion as represented by the 

right example. In such lesions the destructive boundary is 

not sharply defined. 

rather slow and chronic, there will be a tendency 

to circumscribe the disease process by surrounding it with newly formed bone, which is frequently normal in mineral density. As the speed 

of the disease process increases there is a decreased 

tendency to wall off the disease, resulting in 

sharply defined borders with very little or no 

bone circumscription in the lytic area. If the speed 

is very great, there is a zone of partial lytic activity 

surrounding the central lytic focus—in other 

words, a gradient of lytic activity from complete 

bone destruction to intact bone on the extreme 

periphery of the disease process. 

Bone hypertrophy contrasts with bone atrophy 

in that the activity of osteoblasts predominates in 

the reaction to disease. This means that abnormal 

bone formation and increased bone density are 

part of the gross and radiographic picture. Bone 

hypertrophy can occur in any part of the skeleton 

but the descriptive terminology associated with 

this process focuses on its cross-sectional distribution (Figure 29). Abnormal bone formation on 

the outer surfaces of bone is often referred to as 

periostitis in the American literature. This term 

means peripheral bone inflammation and as such 

implies more than is appropriate in the diagnosis 

of dry bone lesions. Periostosis means periosteal 

bone formation and precisely describes what is 

going on without implying the mechanism and is 

thus a more appropriate term. However, in view 

of current usage, both terms will be considered as 

synonyms. Abnormal bone formation can also 

occur on the endosteal, medullary surface of compact or cortical bone and is known as endostosis. 

Bone hypertrophy of cancellous bone is called 

spongiosclerosis. 

The morphological variants of bone hypertrophy are greater than for bone atrophy but are 

basically the result of an imbalance in the activity 

of osteoblasts and osteoclasts in which three relationships exist: (1) increased bone formation 

with increased bone resorption (2) increased bone 

formation with normal bone resorption, and (3) 

normal bone formation with decreased bone resorption. 

Periostosis is expressed in many ways and is 

frequently associated with changes in the endosteal and cancellous parts of bone (Figure 30). 

One of the most common examples of periostosis 

in archeological skeletons is fusiform bone hypertrophy on the diaphysis of long bones. This lesion 

involves an increase in the diameter of the cortex 

which may result from several abnormal conditions. In the paleopathological literature fusiform 

FIGURE 29.—Schematic representation of the basic types of 

abnormal bone formation. In the example to the left abnormal bone is added to the periosteal surface of bone. In the 

middle example, abnormal bone is added to the endosteal 

surface. The third possibility is depicted in the right example, 

in which abnormal bone is added to both periosteal and 

endosteal surfaces. 
40 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOG Y 

FIGURE 30.—Diaphysial, periosteal, and endosteal bone hypertrophy. Note the lamellar nature of the compact bone on 

the cut surface. Specimen of a left femur of a child about 12 

years of age. The lesion is attributed to syphilis. (12-year-old 

child, ANM 2999.) 

periostosis has been attributed most often to infectious diseases, such as osteomyelitis. Schinz, 

Baensch, Friedl, and Uehlinger (1952-1952:201) 

indicate that inflammatory reaction to a pusforming disease organism is a common cause of 

periostitis, but that trauma can result in periostosis. These fusiform lesions may be a solid mass 

of new bone or they may be layers of dense bone 

with intermediate, less dense or spongy layers in 

between, creating an onion skin effect in cross- or 

longitudinal section. 

While fusiform bone hypertrophy of a localized 

variety is very common in skeletal material, more 

extensive hypertrophy of diaphyseal bone is also 

often seen. These more extensive lesions frequently appear to be a more severe manifestation 

of the disease conditions that produce fusiform 

lesions. However, infectious disease rather than 

trauma is the most likely factor. Infectious disease 

may result from local conditions, such as an 

infected cut, but may be disseminated by the 

blood from a focus elsewhere in the body. The 

more extensive, diaphyseal, hypertrophic lesions 

of bone may also have the lamellar appearance 

seen in some fusiform bone lesions. 

The periosteal lesions described thus far are 

generally the reaction to low grade or chronic 

disease conditions in bone. Other morbid conditions can result in more exuberant development 

of abnormal bone. Neoplasms, both those that 

arise primarily in bone and those that metastasize 

to bone, may result in the most dramatic periostosis. Within neoplastic conditions of bone there 

is considerable morphological variation depending on the type of tumor. 

Some primary neoplasms of bone, that is those 

which arise in skeletal tissue, produce dramatic, 

exuberant growths of bone. The lesions tend to 

fall into two categories. The first of these lesions 

consists of spicules or plates of bone arranged 

perpendicular to the surface of the bone (Figure 

31). This arrangement creates a sunburst effect. 

These rays may fill in, ultimately creating a solid 

mass of bone, but the ray-like development of the 

periostosis is still apparent. The second type of 

lesion has the appearance of a head of cauliflower 

(Figure 32) and may reflect a more slowly developing course of the disease. 

The secondary neoplasms of bone, by which 

one means those resulting from metastasis from 

other parts of the body, may resemble the raylike conditions of some primary neoplasms but 

can also result in a fairly low-grade diffuse periostosis similar to that seen in infectious diseases. 

Endostosis results in partial to complete occlusion of the marrow space in some cases, with little 

or no change in the existing cortex (Figure 33). 

This type of bone hypertrophy illustrates an imbalance between osteoblasts and osteoclasts that 

results in increased bone. One of the diseases 

discussed in skeletal dysplasias (p. 340) is osteopetrosis (Albers-Schonberg's disease). This disease 

is the result of normal osteoblast activity and 

greatly depressed, or nonexistant osteoclast activity. Since osteoclasts do not enlarge the medullary 
NUMBER 28 41 

FIGURE 31.—Bone hypertrophy producing spicules or plates 

of bone that are perpendicular to the bone surface. Specimen 

is the right femur of a child about 7 years of age. Osteosarcoma, Ewing's sarcoma, and metastatic neuroblastoma are 

possible morbid conditions stimulating this bony reaction. 

(7-year-old child, W M S72 a.3.) 

cavity as the bone grows, the marrow space is 

filled with bone. Here we have endostosis in the 

sense that bone remains where it does not belong 

but there is no abnormal bone formation, only 

the retention of bone tissue that should have been 

removed. Both endostosis and periostosis may 

occur as responses to the same disease process 

(Figure 34). Osteomyelitis, in which the original 

focus of the disease is in the marrow, can be 

limited to the marrow and produce only endostosis or spongiosclerosis; more often, however, it 

also involves the outer surface of bone and stimulates periostosis. 

Abnormal bone formation can occur in response to an infectious disease process, such as 

osteomyelitis, in which newly formed bone tends 

FIGURE 32.—Bone hypertrophy in which the new bone has 

the appearance of cauliflower. The lesion is attributed to 

osteosarcoma, but periosteal chondrosarcoma should also be 

considered. (Distal right femur, 31-year-old male, WM 

S72 a.2.) 

to wall off the infectious focus. Neoplasms may 

stimulate spongiosclerosis and one can find this 

condition associated with other types of disease, 

such as osteopetrosis mentioned above. Radiologically, a bone with spongiosclerosis in its pure 

form will show relatively normal outer contours 

but increased radiodensity. 

Thus far in the descriptive review of bone 

lesions I have indicated that bone disease can be 

characterized as a process of abnormal bone destruction, bone formation, or both. I have further 

characterized bone disease by referring to the 

cross-sectional manifestations of disease. It is important to know that most bone disease involves 

several, if not all, of these descriptive categories. 

In osteomyelitis, for example, we may have general thickening of the compact bone and cortex 
42 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

FIGURES 33, 34.—Endostosis and periostosis of the midshaft of a left tibia: 33, Internal view. 

The arrow indicates the original cortex. 34, External view of periostosis in the diaphysis; note 

the porous nature of the thickened diaphysis. (PMWH W0721.) 

(bone hypertrophy) but with the compact bone 

becoming quite porous (bone atrophy) and have 

periostosis, endostosis, and spongiosclerosis in the 

same bone. Here, I have introduced one, new, 

descriptive element and that is the quality of the 

compact bone. 

Changes in periosteal, endosteal, or cancellous 

areas of bone are often associated with changes 

in the compact bone. In general, more bone tissue 

cannot be incorporated within existing compact 

bone since the only place for such addition would 

be vascular spaces. The increase in radiologic 

compact bone density is a function of new bone 

added to existing surfaces. Thus, the only abnormal development that can occur within previously normal, compact bone is rarefaction or 
NUMBER 28 43 

osteoporosis. This can be accomplished, as in 

hyperparathyroidism, by an increase in bone resorption by osteoclasts, in which the osteoblast 

cell population cannot keep up with abnormal 

resorption or, as in osteomalacia, the protein matrix produced during osteon remodeling is not 

mineralized. 

In Figure 33 we have seen that rarefaction is 

associated with the thickened cortex in one case 

of purported syphilis. Similar thickening of the 

cortex and increased porosity of the original cortex are associated with other disease conditions, 

such as Paget's disease. The point to be made is 

that the addition of new bone to existing compact 

bone is often associated with osteoporosis of the 

original compact bone. 

The mixed type of bone lesion involving both 

bone hypertrophy and bone atrophy can be found 

anywhere in the skeleton. A relatively common 

expression of this type of lesion is found on the 

skull vault and has been variously referred to as 

porotic hyperostosis, spongy hyperostosis, cribra 

cranii, and symmetrical osteoporosis. There are 

many manifestations of this general lesion and it 

provides a useful example of the complexity and 

pitfalls in the descriptive analysis of a bone lesion. 

For this reason I will review the morphological 

variants here although they will receive a more 

detailed treatment in the chapters on infectious 

diseases (p. 104), reticuloendothelial and hemopoietic disorders (p. 248), and metabolic disorders 

(p. 270). Porotic hyperostosis basically is characterized by bone hypertrophy of the skull vault. In 

some cases the abnormal bone is not found in the 

areas of major muscle attachment. In other cases 

this limitation does not prevail. Grossly the lesion 

results in thickened bones of the vault, but the 

added bone is not smooth (Figure 35). Its external 

gross appearance is usually porous but may also 

consist of labyrinth-like plates of bone. The porous nature of the abnormal bone varies from 

fine, pumice-like pores to large pores in excess of 

2 millimeters in diameter. A single lesion may 

contain all variations of porosity. 

The X-ray film appearance of porotic hyperostosis frequently suggests a ray-like arrangement 

FIGURE 35.—Porous hypertrophy of the right parietal bone 

in a 1-year-old girl. Arrows indicate the thickness of the 

porous hypertrophic bone. Note that orientation of the bone 

tends to be perpendicular to the surface of the skull. The 

outer table is almost completely remodeled away. (FPAM 

3874.) 

of the abnormal bone, which has been called the 

hair-on-end or hair brush appearance. Often, the 

original outer table of bone has been destroyed so 

that the bony rays are continuous with the diploe. 

Porotic hyperostosis also varies in its cross-sectional morphology. As suggested by the X-ray 

film appearance, the disease process may destroy 

the outer table creating the appearance of a 

greatly thickened diploe. However, in some examples of gross porotic hyperostosis the crosssectional morphology indicates that the lesion is 

entirely superficial to the outer table and thus is 

a periostosis. In such a case there is no significant 

change in the diploic space or the outer table. It 

seems likely that superficial, porous periostosis of 

the skull vault represents a disease process quite 

distinct from porous bone hypertrophy associated 

with enlargement of the diploe and destruction 

of the outer table. The above review illustrates 

the importance of careful descriptive analysis of 

gross lesions, which must include gross and X-ray 

film morphology, but also the cross-sectional ap-
44 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

pearance if this cannot be determined by the Xray film. The attempt should always be made to 

determine if the bone abnormality is the result of 

abnormal osteoblast or osteoclast activity or an 

abnormal combination of both. It is also important to indicate whether the disease process is 

accomodating some other body function, as is 

true in some cases where the development of 

abnormal bone tends not to affect areas of muscle 

attachment. 

In archeological skeletal material one is also 

confronted with abnormal-appearing bone tissue 

that is not the result of antemortem biological 

processes. Such conditions have been called pseudopathologies and considerable experience with 

pathological conditions may be necessary to make 

a distinction. However, an understanding of general principles of bone biology will help to resolve 

many such problems. 

Pseudopathologies are the result of postmortem 

destruction of bone tissue and result from two 

basic conditons: (1) the immediate burial environment and (2) careless excavation techniques. 

While the identification of pseudopathology as 

pathology is to be guarded against, it is important 

to remember that many pathological conditions 

will result in weakened bone tissue that may 

deteriorate more rapidly after burial than adjacent normal bone. Thus, destruction of bone tissue by components of the soil does not always 

mean that such abnormal bones represent only 

pseudopathologies. 

The preservation of bone tissue is generally a 

function of soil pH, temperature, and ground 

water volume. However, local conditions immediately adjacent to a specific bone may produce 

marked changes in bone preservation. Copper 

containing ornaments buried with the individual 

will greatly enhance the preservation of bones 

located next to the ornament. In contrast, bone 

resting on wood, as in a wooden coffin, deteriorates more rapidly than parts of the skeleton not 

in direct contact with wood. Earlier I have noted 

changes at the microscopic level, produced by 

fungi, which could be confused with osteoclastic 

activity. 

Damage by careless excavation can easily be 

confused with antemortem trauma. Indeed, the 

distinction between injury immediately before 

death and that occurring after death, including 

that occurring at the time of excavation, cannot 

always be made. In general, trauma will result in 

inflammation, within a few days, followed by 

bone remodeling, which is frequently apparent in 

archeological specimens. Depressed fractures occurring during life will generally have less sharply 

defined borders than those resulting from postmortem damage. There may be bone fragments 

still attached at the edge of the defect. This is 

almost certainly indicative of an antemortem lesion. 

Careless handling of a shovel can remove a slab 

of bone from a skull, the cut surface of which will 

resemble a sword wound. However, with sufficient experience with pathological specimens and 

the knowledge of how bone reacts to disease, the 

paleopathologist should be better able to identify 

pseudopathology in specimens. 

Assuming that paleopathological conditions 

can be described and classified in most cases, the 

information from such classifications needs to be 

integrated with the broader biological framework. In this context human group dynamics 

become the focus rather than individual cases of 

disease. Having determined the frequency of different types of disease in a group, such frequencies 

can be compared between groups. Inferences 

about demographic or environmental effects may 

be possible, as in Angel's research on malaria in 

the eastern Mediterranean areas (Angel, 1964, 

1966). 

In the broader paleopathological context of 

group responses to disease, we need to be careful 

in making inferences about the relative health of 

a population on the basis of the incidence of 

skeletal disease. Skeletal manifestations of morbid 

conditions tend to be associated with chronic 

responses to disease. Skeletal paleopathology, particularly infections, tend to be viewed as evidence 

of high morbidity and, indeed, this may be the 

case. The converse, however, is also possible. Skeletal paleopathology may indicate a better host 
NUMBER 28 45 

response to a disease since the host lived through 

the acute stage when other afflicted individuals 

may have died. Thus, absence of skeletal disease 

implies death due to acute conditions, while evidence of skeletal disease indicates a sufficiently 

adequate immune response to insure survival to 

the chronic stage. 

A final cautionary note is that skeletal diseases, 

particularly those caused by infectious agents, 

may not be the same today as they were in 

ancient times. Selection and adaptation undoubtedly improve the immune response to disease. At 

the same time infectious agents tend to become 

less virulent since the organism typically dies with 

the host making reduced virulence selectively advantageous. This means, of course, that an increase in the frequency of skeletal manifestations 

of disease after mutation of an existing disease 

organism or the introduction of a new infectious 

disease may mean only that the disease is becoming more chronic in nature and thus, is more 

likely to affect the skeleton. 

X-ray Film Study of Skeletal Lesions 

Analysis of X-ray films of gross pathological 

bone specimens is one of the most important tools 

for the paleopathologist and should be part of 

almost all descriptions of such material. The preparation of X-ray films has the advantage over 

many other methods in being completely nondestructive and thus, should always be used before 

chemical or histological methods are applied. In 

view of the importance of X-ray films in paleopathological studies I will review, in considerable 

detail, the methods involved in producing good 

X-ray films as well as the principles in interpreting such films after they are prepared. 

The correct exposure of an X-ray film depends 

on several factors including (1) electrical current 

flow measured in milliamperes, (2) energy of 

current measured in kilovolts, (3) time of exposure 

usually measured in seconds, (4) the distance 

between the source of X-rays and the film, (5) the 

speed of the film emulsion which may be enhanced by the use of phosphorescent screens, and 

(6) the density of the specimen. In actual practice 

most of the above variables are standardized, 

making the preparation of most X-ray films routine. Current, energy, and time are variables that 

are limited by the X-ray machine. In general, 

varying either current or time will produce the 

same result. Thus, if, as is often the case, the 

current is fixed on a particular machine, time is 

adjusted to meet the requirements of different 

exposures. The energy of the X-rays affects their 

potential to penetrate dense materials. The 

greater the energy the greater the penetrating 

potential. 

One tries to select a voltage that will penetrate 

the thickest or densest part of the specimen 

enough to expose the film somewhat, but not so 

high that it is not partially absorbed by the 

thinner or less dense areas of a specimen. For 

most archeological specimens the energy used to 

generate X-rays is between 60 and 80 kilovolts. 

However, if the specimen is fossilized, higher 

kilovoitages may be necessary. For delicate or 

small bones (e.g., hands, feet, ribs, or fetal bone) 

lower voltages may be needed. 

Radiology shares with photography many of 

the problems inherent in projecting the image of 

a three dimensional object onto a two dimensional plane. Like photography, it is possible to 

minimize the effect of inevitable distortion by 

keeping in mind certain principles. The first of 

these is primarily inherent in the X-ray equipment and is a function of the area of the target 

which produces X-rays (the focal spot). X-rays 

are generated from the entire surface of the focal 

spot and radiate out in a cone from each discrete 

point in the spot. For illustrative purposes I have 

taken the extreme edge of the focal spot, which, 

in effect, produces overlapping but slightly different images and results in reduced sharpness of the 

X-ray image (Figure 36). In selecting X-ray 

equipment it is important to obtain one with a 

small focal spot. Most manufacturers produce 

equipment with a focal spot of 0.5 millimeters or 

smaller. 

The effect of distortion produced by the geometry of the focal spot can be minimized by 
46 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

increasing the distance between the focal spot 

and the film plane. This also minimizes parallax 

distortion, which results when three dimensional 

objects are projected onto a plane (Figure 37). 

However, there are practical limits on the distance between the focal spot and film plane. Xrays, like light energy, diverge from the source so 

that the same number of X-rays are spread over 

a larger area as the distance increases. This principle is known as the inverse square law and 

means that one must increase the number of Xrays (by increasing time and/or current) if one 

increases the distance. In my experience an optimal distance from the focal spot to the film plane 

is between 3 and 4 feet (91-122 cm). However, 

for critical work on bones such as the skull, where 

parallax is a greater problem than in long bones, 

this distance may need to be increased. 

The orientation of the specimen with respect 

FIGURE 36.—Effect of focal spot size on X-ray image sharpness. X-rays are generated on the surface of a focal spot, 

represented by the solid bar at the top of the diagram. Xrays emanating from two different points on the focal spot 

(dashed lines) intercept the object, represented by the black 

disk, at different angles and project the images of the disk to 

overlapping but different areas of the film plane. The white 

area within the circle represents the area of reduced image 

sharpness resulting from the geometry of X-rays generated 

from different areas of the focal spot. 

\^o'^-^ 

FIGURE 37.—Variation in parallax distortion (D2) of X-ray 

images due to differences in focal spot to film plane distances 

(Di). 

to the X-ray source and the film plane is also a 

significant factor in image quality and accuracy. 

As a general rule one should be consistent in the 

placement of the specimen with regard to the 

source and film plane. Most often the film plane 

is perpendicular to the central axis of the X-rays. 

In routine roentgen procedures the specimen 

should be positioned to have the same anatomical 

relationship to the central axis. For example, in 

a lateral view of the skull one might wish to 

position the skull with external auditory meatus 

corresponding to the central axis of the X-rays; 

for long bones the midshaft might be appropriate. 

In producing an X-ray image of a specific 

lesion, we are generally less concerned in producing a relatively undistorted image of the lesion 

than in producing an image that helps us to 

characterize the pathology of the lesion. Thus, we 

may want to know if the marrow has been encroached upon or whether a lytic process has been 
NUMBER 28 47 

circumscribed by dense bone. In these and other 

related situations one positions the specimen so 

that these factors can best be visualized. In general one should have lateral and front views of a 

lesion on diseased bone, so that can at least 

partially reconstruct the three dimensional appearance of the lesion. It is important to try to 

avoid the superimposition of other parts of the 

bone on the diseased part if possible. In some 

bones, such as the skull, this may be very difficult, 

but an effort should be made to minimize the 

effect of superimposition. This can be done by 

careful positioning. 

There are several advantages in producing Xray films of archeological specimens in contrast 

with those of a living patient. Obviously, we are 

not concerned with radiation hazard to a skeleton, so long exposures and film speeds are not a 

critical consideration. Furthermore, if carefully 

positioned and supported, the bone specimen will 

not move. In addition, there are no soft tissue 

features to interfere with the image of the skeletal 

tissue. So many of the variables of concern to the 

clinical radiologist need not concern the paleopathologist. 

These advantages need to be considered in 

selecting a film. Film speed is, in general, inversely 

related to film resolution. Thus, the faster the 

film the poorer the quality of the image. Since 

high film speed is not an advantage with paleopathological specimens, image quality and convenience of processing become important factors 

in selecting a film. In my experience I have found 

Kodak Royal Blue Medical and Kodak X-Omat 

G film, to be satisfactory. I have evaluated some 

slower, high resolution industrial films, such as 

Kodak Industrex M film, and found them to 

produce excellent image quality. These should be 

considered in situations where fine detail is 

needed to bring out all the radiographic features 

of a lesion. 

X-ray film is available in many sizes. Many of 

these sizes are appropriate to specific applications 

in modern clinical radiology and only two are 

needed for general radiography in paleopathology. The most useful size for skulls is 24 X 30 

centimeters. In my experience, this size will accommodate the largest skulls, including the mandible, where this is desired. For the bones of the 

postcranial skeleton, film 35 X 43 centimeters is 

the largest standard size available from Kodak 

and is satisfactory for most applications. This size 

film is frequently not long enough to contain an 

entire femur on its long axis. In such a situation 

the diagonal position may be adequate. However, 

there will be femora for which even this orientation will be inadequate. In such situations one 

eliminates the least important end or exposes two 

films. Longer films are available commercially 

but create problems in processing and storage. 

In choosing a film one needs to keep in mind 

the method which will be used for processing. In 

most clinical laboratories. X-ray films are developed in high speed processors, which produce a 

dry film in one to two minutes. Special films have 

been created to accommodate this rapid processing. Such equipment has high initial and maintenance costs and will generally not be appropriate for the intermittent use needed by most paleopathologists. It may be possible to have film 

processed by a clinical facility, but frequently the 

more conventional and slower manual processing 

procedures will be used. Film not adapted for 

high speed processing must be processed by hand. 

However, the Kodak X-Omat G film can be 

processed manually or in a high speed processor. 

A decision on the method for processing should 

be made before X-ray film is purchased. 

While film can be purchased in a light proof 

envelope, it is considerably more expensive than 

film packed for loading in a film holder or cassette. For most applications in paleopathology a 

simple cardboard film holder, such as the Kodak 

X-ray Exposure Holder, is adequate. These holders are reasonable in cost. The purchase of several 

for each of the film sizes to be used will be a 

convenience. Film cassettes are much more expensive but last longer. Recent developments in 

cassette design, such as the Kodak X-Omatic 

cassette make loading very simple and offer the 

option of using phosphorescent screens to shorten 

exposure times. These screens are placed in close 
48 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOG Y 

contact with the X-ray film and are excited when 

exposed to X-rays. Those areas of screen that are 

excited by X-rays give off light (fluoresce), and 

since the film is sensitive to both X-rays and light 

the effect of the screen is to enhance the effect of 

the X-rays and decrease the exposure time. While 

shortened exposure times are not a crucial factor 

in paleopathology, they do have two advantages: 

(1) they lessen the effect of vibration on the Xray image, and (2) they lessen the risk of exposure 

to X-rays for persons exposing the X-ray film. 

Recently, I have begun the routine use of the 

Kodak X-Omatic cassette with fine, intensifying 

screens. There is a slight loss of resolution when 

these screens are used. However, the contrast may 

be enhanced and the overall X-ray film appearance of a lesion may be as good, or better, than 

the same film exposed without a screen. 

Basically, two types of situations exist in the 

radiology of paleopathological specimens. In the 

first of these we may have some external evidence 

of disease and want to clarify the nature of the 

lesion or see if there is any additional evidence of 

disease not apparent externally. To accomplish 

the latter objective we will need X-ray films of 

the bones of the entire skeleton. A second objective of radiology in paleopathology would be to 

conduct a general survey of nonspecific bone 

responses to disease (such as Harris' lines) in an 

archeological skeletal sample. In both these applications it is important to prepare a standard 

set of films for the entire skeleton with views that 

can be compared with X-ray films of normal 

skeletons. 

In doing this, attention to a few details will 

make comparison and interpretation much simpler. It is very important to include some type of 

identification number (museum catalog number 

or field number) on the film and to indicate from 

which side of the skeleton the bones are taken. 

Lead letters and numbers are available from 

distributors of X-ray supplies and should be part 

of an X-ray facility. If they are not available, 

process each film separately and write the information on the film when processed and dry. 

Common sense dictates that the orientation of 

the bones conform as much as possible to the 

anatomical position and relationships. It is frequently possible to group the bones of the arm 

and entire pectoral girdle (scapula and clavicle) 

on a single 35 X 43 centimeter film. The proximal 

end of the long bones should be positioned at the 

top of the film, bones from the right grouped 

together and, likewise, for bones from the left 

side. 

The vertebrae pose special problems for the 

paleoradiologist because of their irregular shape. 

One solution is to obtain some soft, flexible, polyurethane foam and cut it into strips about 2X 2 

X 35 centimeters long. After assembling the vertebrae in their correct anatomical relationship the 

foam can be threaded through the neural canal 

of the individual vertebrae. The vertebrae can be 

adjusted by sliding or twisting on the foam to 

achieve correct anatomical relationship. The 

foam will hold the vertebrae in the correct relationship and will have negligible effect on the Xray image. Since a complete vertebral column is 

usually too long for a single 35 X 43 centimeter 

film, I divide the vertebrae into anatomical 

groups: cervical, thoracic, and lumbar vertebrae. 

In the standard radiography of all bones it is 

important to orient the bones in the anteroposterior (A-P) axis or mediolateral (M-L) axis. To 

facilitate this, it is very helpful to have several 

wedge-shaped pieces of polyurethane foam. For 

most purposes these need not be large, the longest 

edge being about 5-8 centimeters long. A few 

pieces two or three times this size are useful for 

skull radiography. 

The skull poses the most difficult problems in 

the radiography of skeletal material. Because of 

the globular nature of the bone, it is impossible 

to avoid superimposition of images of one part of 

the skull on other parts. For this reason the 

positioning of the skull is more critical than that 

of other bones and should be done carefully. In a 

complete skull, the most useful landmarks for 

orienting the skull are the mastoid processes. In 

a lateral view the tips of the mastoid processes 

should be perpendicular to the film plane (Figure 

38). In an anteroposterior view the tips of the 

mastoid processes should be parallel to the film 

plane (Figure 39). The skull should be rotated on 
NUMBER 28 49 

an axis through the mastoid processes to minimize 

the superimposition of the occipital bone on the 

maxillary bones and teeth. 

The second type of problem in the radiography 

of paleopathological specimens is preparing films 

of specific lesions in order to get a better understanding of the gross lesion and to determine to 

what extent tissue that cannot be seen externally 

is involved in the disease process (e.g., medullary 

involvement in a periosteal lesion). In many cases 

the standard orientation, anteroposterior (A-P) 

and mediolateral (M-L) of the specimen will 

provide the information needed. However, with 

some lesions better results are obtained if the 

orientation point is the lesion itself rather than 

the whole bone. In such situations A-P and M-L 

views of the lesion, irrespective of the orientation 

of the rest of the bone, should be obtained. Generally, the lesion should be as close to the film as 

possible. For example, if a lesion is on the right 

parietal of the skull, this side should be placed on 

the film cassette or holder. 

In general radiography of a specific lesion one 

attempts to demonstrate two features: (1) involvement of bone tissue in areas that cannot be 

observed externally and (2) the pattern of bone 

density in the lesion and the area immediately 

surrounding the lesion. For illustrative purposes 

let me review the features of an expansive, diaFIGURE 38.—Orientation of the skull relative to the film 

plane. The axis through the mastoid processes should be 

perpendicular to both the x and y axes of the film plane 

when preparing a standard lateral X-ray film of the skull. 

FIGURE 39.—Orientation of the skull relative to the film 

plane in an anteroposterior view. The axis through the 

mastoid processes should be parallel to the x axis of the film. 

physeal lesion of a major long bone. The gross 

appearance of such a bone indicates that the 

diaphysis is abnormally thick. The bone tissue 

itself may be somewhat porous and have large 

openings or cloacae. We are unable, however, to 

determine from external inspection if the marrow 

space is normal, enlarged, or smaller than normal, 

if there are unusual features within the cortex, or 

if the abnormal tissue was laid down evenly or in 

alternating high and low density layers. 

An X-ray film, in which the axis of the X-rays 

is perpendicular to the plane of the lesion, may 

reveal increased bone density due to increased 

thickness but will not demonstrate marrow space 

encroachment or any lamellar arrangement of 

the abnormal tissue. Such information requires 

that the axis of the X-rays be parallel to the plane 

of the lesion. While the possible combinations of 

density patterns are almost infinitely large, common sense application of the above principle will 

permit optimal radiographic resolution of most 

abnormal conditions in skeletal tissue. A more 

comprehensive review of radiographic techniques 

is found in most radiology reference sources. The 
50 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOG Y 

first English edition of Roentgen-Diagnostics 

(Schinz, Baensch, Friedl, and Uehlinger 1951-

1952:3-72) and the first chapter in Anatomy Basic 

to Radiology (Meschan, 1975:1-23) are excellent 

examples of such sources. 

After exposure of the X-ray film, it must be 

processed to make the image visible. The principles involved are very similar to processing photographic film and involve immersing the film in 

(1) a developer solution that darkens the exposed 

silver halide crystals on the film and (2) a fixing 

solution that removes the unexposed crystals (Figure 40). The film must be washed to remove the 

processing solutions and then dried before view-

(C 

DEVELOPER 

WASH 

ONSTANT TEMPERATUR 

BATH) 

FIXER 

E 

FINAL 

WASH 

FIGURE 40.—The processing sequence in the preparation of 

X-ray films. The first solution is developer, which darkens 

the silver halide crystals in the exposed portions of the film 

emulsion. The developed film is washed for about two 

minutes before immersion in the fixer solution, which removes the unexposed silver halide crystals. A final wash 

removes all the processing solutions. 

ing and storage. A detailed review of these procedures is available from X-ray film suppliers 

(e.g., Eastman Kodak publication, Radiography in 

Modern Industry, 1969). 

In my brief discussion of film selection I have 

already noted that a decision regarding automatic 

versus hand processing needs to be made before 

the purchase of film. Using the automatic processing facility of a local clinical X-ray laboratory 

is a great convenience and saves a considerable 

amount of time. For most paleopathologists the 

number of X-ray films processed simply does not 

justify the establishment of a special laboratory, 

and arrangements to take and process films 

should be made with a clinical facility. Often this 

will be done as a professional courtesy, but even 

if charges are made for this service it is probably 

very much cheaper than establishing one's own 

laboratory. 

In the event that the volume of X-ray film 

preparation justifies the establishment of an Xray laboratory the major expenses will be (1) the 

construction of a special room to protect the 

technical staff from radiation during exposure, 

(2) the purchase of an X-ray machine, (3) the 

construction of a dark room, and (4) the purchase 

of film processing tanks. Many educational or 

research institutions have regulations regarding 

the safety of such a facility, and the official 

responsible for implementing these regulations 

should be consulted in the planning stage. The 

operator of X-ray generating equipment must 

minimize personal exposure to X-rays and insure 

that others in the vicinity are protected as well. 

Given the existence of an adequate facility for 

preparing X-ray films, one should consult standard sources for the specific details on taking and 

processing such films. I have already indicated 

the approximate parameters for exposing X-ray 

film. Hand processing the exposed film involves 

attention to the processing specifications that are 

appropriate for a given film. The most critical 

stage in processing is development, where time 

and temperature are the most important factors. 

In general, the temperature of the developer 

should be between 60° and 75°F. Exceeding this 
NUMBER 28 51 

temperature range on either end will result in 

poor image quality and should be avoided. In 

view of the importance of temperature the processing tanks should be in a water bath in which 

the temperature can be controlled. Cold tap water can be mixed with hot water to produce the 

optimum temperature by using a temperature 

control valve. This valve is generally part of a 

commercial hand processing tank system. Unfortunately, tap water temperature during the summer months may exceed the upper limit for development. If you anticipate processing film during such periods you will need to install a water 

cooling system as part of a processing system. 

Such equipment should be compatible with the 

water flow through the tank and can generally 

be purchased as part of the system. The temperature of the fixative is less critical, but since both 

developing and fixing tanks are usually in the 

same water bath, correct temperature for the 

developer automatically results in appropriate 

temperature for the fixer. Films such as Kodak 

X-Omat G are adapted for high temperature 

automatic processing and have greater temperature latitude when hand processed. 

In hand processing, the exposed film is attached to special, stainless steel wire, developing 

frames and immersed in the developing tank. A 

typical developing tank contains 5 gallons of 

reagent and can develop 5 X-ray films at one 

time. Practical experience has shown that the risk 

of scratching the film surface greatly increases if 

this number is exceeded. It is also important not 

to process different sizes of film at the same time. 

The almost inevitable result is scratches on some 

of the film surfaces. After development for the 

appropriate time (usually about 5 minutes) the 

film is washed for about 2 minutes. The film is 

then immersed in the fixer solution for about 5 

minutes, then washed for 30 to 45 minutes in 

running water and hung up to dry. Most X-ray 

films are made to be insensitive to a fairly bright 

amber light so that the work in the dark room is 

done in relatively light conditions. However, safelight specifications should be followed carefully. 

Once the film is dry, it should be stored in 

standard X-ray envelopes, available through any 

X-ray supply dealer. These envelopes have special 

areas for recording the specimen number and 

additional information that cannot be put on the 

film itself X-ray films are much more useful 

when this information is part of the record. Considerable care should be taken in handling the 

dry X-ray film. The image is part of a thin 

emulsion and is easily scratched. As with any 

photographic film. X-ray film should be handled 

by the edges both before and after processing. As 

the number of X-ray films accumulate, a wise 

investment is a film storage file that will keep the 

films in order and make them more accessible. 

Chemical Analysis of Pathological Bone 

In modern medical practice, tests of biological 

functions and products have become a routine 

part of diagnostic procedures. However, most of 

these tests utilize materials, such as blood or 

urine, which are not available in archeological 

material. Diseases that affect protein synthesis, 

such as osteogenesis imperfecta, may result in 

abnormal bone proteins. Eastoe, Martens, and 

Thomas (1973) have determined the amino acids 

in biopsy specimens from recent cases of this 

disease and found a relative increase in the neutral amino acids compared to normal bone protein. In research conducted in my laboratory 

(unpublished), I have found abnormal amino 

acid residues in a rare bone disease, known as 

fibrogenesis imperfecta ossium. 

In archeological skeletons the application of 

chemistry in the diagnosis of disease is very limited but should not be overlooked where appropriate. Such analyses will be limited to situations 

where bone preservation is very good, since degradation of bone protein by the soil introduces an 

uncontrolled variable making interpretation of 

data difficult, if not impossible. Von Endt and 

Ortner (1977) have applied amino acid analysis 

of bone to a suspected case of iron deficiency 

anemia in a prehistoric child's skeleton from the 

American Southwest. In this study, samples from 
52 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOG Y 

two prehistoric skeletons were analyzed. One 

specimen (NMNH 308697) had no evidence of 

disease affecting the skeleton. The other specimen 

(NMNH 327107) had marked, gross, porotic hyperostosis of the skull and in the postcranial 

skeleton, thinned compact bone and expanded 

marrow spaces. This combination of lesions is 

strongly suggestive of anemia. The amino acid 

residues from the abnormal skeleton were different from the normal skeleton and from bone of a 

modern child. These results are discussed in 

greater detail in the chapter on reticuloendothelial and hemopoietic disorders (p. 248) and suggest the potential for the study of protein chemistry in archeological specimens. 

The mineral phase of bone may also be affected 

by disease. In rickets, the protein matrix does not 

mineralize. In fluorosis, abnormally high levels of 

fluorine can result in gross and microscopically 

abnormal bone. It may also increase the concentration of fluorine in bone mineral. I have used 

the electron probe microanalyzer to investigate 

the toxic effects of fluorine on bone (unpublished 

data). This research demonstrated almost twice 

the normal concentration of fluorine in affected 

bone mineral. Analysis of strontium levels in bone 

have been used in dietary studies of archeological 

specimens (Schoeninger, 1979). Strontium levels 

in bone are lower with greater emphasis on meat 

in the diet and higher if plant sources account for 

more of the caloric intake. 

While chemical analysis of archeological skeletons may provide valuable data on a disease 

condition, considerable caution is needed in interpreting such an analysis. The process involves 

at least a small amount of destruction of valuable 

bone. Furthermore, one must insure that data 

from chemical analysis reflect conditions during 

the life of the individual and not one or more 

variable changes of bone in the soil. Data obtained by comparison of normal and abnormal 

tissue from the same site may not be reliable, 

since soil conditions may vary within a cemetery 

site. Indeed, a complete understanding of the 

chemical composition of normal and abnormal 

modern bone tissue remains an unachieved goal. 

Microscopic Study of Skeletal Lesions 

Microscopic study of bone, like chemical analysis, is limited in its application. As a general rule, 

in archeological skeletal material, microscopic 

data add little to what can be seen grossly or on 

X-ray films. Because microscopic examination 

does involve destruction of some of the bone, it 

should only be applied when diagnosis is likely to 

be aided. It should not be considered a routine 

procedure. 

If, after careful analysis of gross and X-ray film 

data, it seems likely that microscopic data would 

be valuable, several factors need to be considered. 

The first step in any analysis is the removal of a 

sample of the abnormal bone. Every effort should 

be made to minimize the amount of tissue taken 

for microscopic study. Very thin, dental sawblades are available, which destroy only a minute 

amount of bone in the cutting process. Furthermore, there is usually no need to remove a sample 

more than Vi centimeter thick since the sample 

will usually be reduced to a thinness that will 

permit transmission of light. 

In removing a specimen of tissue for microscopic analysis, include in the section some of the 

normal bone adjacent to the morbid tissue and 

enough of the abnormal tissue to insure that 

different aspects of the pathological process will 

be included. For example in some disease processes the edge of a lesion may reveal bone resorption while the more central part of the lesion may 

show bone formation. A clear understanding of 

the lesion requires that tissue from both areas be 

examined. 

Once an appropriate thin slab of bone has been 

removed for study it can be viewed in reflected or 

incident light using either a dissecting microscope 

or incident light optics on a research microscope. 

However, one of the cut surfaces of the specimen 

should be prepared to insure reasonable resolution. On most cut surfaces, microscopic detail is 

obscured by the irregular groves from the cutting 

action. If the bone is fragile it should first be 

infiltrated with or imbedded in some plastic material before cutting to strengthen it. Ubelaker 
NUMBER 28 53 

(1978:99-101) provides a brief review of this procedure. 

After strengthening, one surface can be ground 

on fine, water-resistant, carborundum paper to 

remove the rough scratches. It can then be polished slightly by rubbing the surface on good 

quality bond paper. Repeated microscopic inspection during processing will indicate when 

grinding and polishing is adequate but the order 

of magnitude is a few minutes. 

In most cases a bone section (75-100 microns) 

is the most satisfactory preparation for microscopic study. Elaborate equipment and procedures exist for making such preparations (e.g., 

Jowsey 1955; Moreland, 1968; Ortner and Yong, 

1975); however, a few inexpensive supplies will 

make it possible to produce a satisfactory thin 

section in most cases (Frost, 1958). 

In general the preparation is an extension of 

the procedure for polishing a single surface except 

that the grinding stage continues until the specimen is very thin (about 100 microns) before the 

polishing begins. Usually it is important to grind 

both cut surfaces and polish at least one surface, 

although the latter may not be needed if the 

section is mounted on a glass slide and coverslipped. If the specimen is large (2 cm or more) it 

may be difficult to grind the surface uniformly. 

Mounting one ground and polished surface on 

the glass slide and then grinding down the free 

surface to the appropriate thinness may help, but 

specially designed cutting and grinding equipment will produce the best results. Such equipment is available at many universities in the 

departments of geology or mineral sciences. 

Additional data may be obtained from a contact microradiograph of a bone section. Techniques for preparation of microradiographs are 

well-known (Amprino and Engstrom, 1952; Sissons, Jowsey, and Stewart, 1960; Ortner, 1975). 

In essence the technique involves placing a bone 

section on a high resolution X-ray film or plate 

and exposing the plate to low energy (10-15 Kv 

primary voltage) X-rays for a relatively long time 

(up to iy2 hours). Special equipment is necessary 

for this, and consultation with one of several 

laboratories doing such work would be appropriate. 

Having obtained a bone section and perhaps a 

microradiograph, the next step is to evaluate the 

findings. One should be familiar with the microscopic appearance of normal bone at different 

ages, for it is against this background that an 

understanding of the abnormal condition must 

be obtained. Given this background there are 

several aspects of disease that should be considered. However, with the exception of slight 

changes produced by osteocytes, all the abnormal 

changes seen in bone microstructure are the result 

of abnormal osteoclastic or osteoblastic activity. 

Microscopically, one can, in theory, see decreased, normal, or increased osteoblast activity 

in combination with either decreased, normal, or 

increased osteoclast activity. Within a single lesion there may be one or more combinations of 

cell activity, and multiple lesions may vary in 

their expression. 

In compact bone, disease is expressed as an 

abnormal quantity of resorption spaces and/or 

forming osteons. The latter can be identified by 

the presence of osteoid seams or, if these are 

missing in archeological bone, as low density 

osteons (in a microradiograph) with large central, 

or Haversian, canals. Let me illustrate these principles with a few concrete examples. I have already noted that Paget's disease involves an increase in the activity of both osteoclasts and 

osteoblasts with an increase in the internal or 

osteon remodeling of compact bone. This results 

in a microscopic appearance of many resorption 

spaces and many forming osteons and many osteon fragments. In hyperparathyroidism, there is 

a marked increase in osteoclast activity but little 

or no effect on osteoblasts. Here the microscopic 

picture is one of abnormal resorption occurring 

within existing bone. In compact bone there is a 

dramatic increase in the number of resorption 

spaces. The trabeculae of spongy bone will frequently be tunneled out by osteoclastic activity. 

This contrasts with severe osteoporosis, in which 

there is increased osteoclastic activity and/or possibly decreased osteoblastic activity in which the 
54 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOG Y 

overall cortex becomes thinned (involution) in 

addition to the increase in resorption spaces. 

Another aspect of the overall bone cell response 

to disease is the speed of the activity, particularly 

with respect to bone formation. If the process 

driving osteoblasts to produce bone is very rapid, 

the result will be poorly organized fiber bone 

rather than lamellar bone. Such bone will also 

tend to be poorly mineralized, a feature that 

would be apparent in a microradiograph. 

There is an additional problem to keep in mind 

in archeological specimens. Microorganisms in 

the soil have the ability to cause local destructions 

of bone and may give at least a superficial appearance of osteoclastic activity (Hamperl, 1966: 

82-83). Marchiafava, Bunocci, and Ascenzi 

(1974) report that fungi are one type of organism 

responsible for such activity. In general the spaces 

produced by destruction of bone microorganisms 

are much smaller than those produced by osteoclasts. 
Trauma 

Fracture 

PATHOLOGY 

Next to the almost ubiquitous degenerative 

changes seen in archeological specimens, the most 

common pathological condition affecting the 

skeleton is trauma. In the most general sense, 

trauma affects the skeleton in four ways: (1) 

partial to complete break in a bone, (2) an abnormal displacement or dislocation of bone, (3) 

a disruption in nerve and/or blood supply, and 

(4) an artificially induced abnormal shape or 

contour of bone. There are other traumatic conditions that occasionally can be inferred from 

circumstances of burial, such as death from complications of pregnancy. 

It is important to remember that trauma generally represents extrinsic influences on the skeleton, which result from many factors. Clearly the 

incidence and location of traumatic events is 

greatly influenced by culture. Hunters undoubtedly have a different pattern of traumatic conditions in the skeleton than sedentary farmers. 

Women generally differ from men, and children 

differ from adults. Of course, there are physiological factors to be considered as well, such as senile 

osteoporosis and other morbid conditions, which 

greatly increase the vulnerability of the skeleton 

to trauma. The various types of trauma that 

affect the skeleton include (1) fracture, (2) dislocation, (3) post-traumatic deformity, and (4) miscellaneous traumatic conditions, including those 

which do not affect the skeleton directly but can 

be inferred by the position or association of skeletal specimens. I will emphasize the biology and 

modern expression of each of these conditions and 

then review the archeological evidence for each 

type of trauma. 

In this discussion the term "fracture" is used in 

its broadest sense: any traumatic event that results in partial or complete discontinuity of a 

bone. Thus, traumatic conditions, such as a sword 

or axe wound, an injury to bone from a spear or 

arrow, or a surgical procedure such as trephination, are considered to be fractures, as well as the 

more conventional discontinuities of bone. If the 

break is incomplete, meaning that it does not go 

through the entire bone, it is called infraction; 

complete separation is called fracture. 

Fracture most often is the result of abnormal 

stress applied to one or more bones. This stress 

can be dynamic, meaning sudden high stress, or 

it can be static in which the stress is low initially 

but gradually increases until the break occurs. If 

a bone is exposed to excessive but intermittent 

stress over a fairly long time (several weeks), a 

fatigue fracture may develop. A final category of 

fracture occurs when bone is weakened by a 

morbid condition such that minimal stress results 

in a break. This is called a pathological fracture. 

Types of Fracture 

Stress in bone results from the application of 

one or more of the following types of force: (1) 

tension, (2) compression, (3) torsion or twisting, 

(4) flexion or bending, and (5) shearing. Figure 

41 illustrates the direction offeree for these types 

of stress. 

Dynamic stress fracture is the most common 

traumatic condition in skeletal material. Indeed, 

it forms the bulk of cases in modern orthopaedic 

practice. Each type of dynamic stress produces a 

different type of fracture. However, many fractures are the result of more than one type of stress. 

Although it is not always possible to identify the 

type of stress from the resulting fracture after 

callus formation and healing, attention to this 

aspect of fracture may provide significant insights 

regarding common traumatic stresses in archeo55 
56 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

FIGURE 41.—The types of stress in bone that can result in 

fracture: A, tension, B, compression, c, twisting, D, bending, 

and E, shearing. 

FIGURE 42.—Transverse, partially healed, fracture of the 

patella (arrow). This fracture is attributed to trauma to the 

patella resulting from a fall on the knee from a great height. 

The morphology of the fracture is also compatible with 

fracture resulting from sudden tension of the quadriceps 

tendon and the ligamentum patellae. (WM S33 Al.) 

FIGURE 43.—Multiple compression fractures of the thoracic 

(T) vertebrae. T6 (upper arrow) was fractured about one 

year before death. Callus is evident on the anterior portion 

of the vertebral body. TIO and T12 (lower arrows) were 

fractured in a fall occurring shortly before death. No callus 

is evident. (64-year-old male, IPAZ 8596.) 

logical skeletal samples. For this reason I provide 

a brief review of the relationships between a 

specific type of stress and the resulting fracture. 

A more detailed discussion is found in Schinz, 

Baensch, Friedl, and Uehlinger (1951-1952:270-

280). 

Tension fractures are generally associated with 

tendinous attachments to bone. In this type of 

fracture the tubercle or process to which the 

tendon is attached breaks off as a result of excessive tension from the tendon (Figure 42). This 

type of fracture is often associated with dislocation of a joint. 

Compression fractures are the result of sudden 

excessive impaction and result in a variety of 

patterns. Bone can split in the same axis as the 
NUMBER 28 57 

FIGURES 44, 45.—Healed fracture of the twelfth thoracic vertebra (second vertebra from the 

top): 44, Lateral view. The vertebral body has collapsed because of compression; however, the 

spinous process has separated from tension produced during the compression of the anterior 

portion of the body; the fracture resulted in angular deformity. 45, Anterior view. (24-year-old 

male, FPAM 5085.) 

direction of the force. In long bones excessive 

compression may produce a fracture in which the 

cortex buckles and bulges outward. Pure compression fractures are best illustrated in the spine 

where most fractures of the vertebral body are 

the result of compression (Figures 43-46). One 

also sees compression fractures resulting from a 

blow to the skull (Figures 47, 48). Many of the 

fractures of joint surfaces are the result of compression. 

In torsion fractures the force is directed in a 

spiral or twisting direction as when one end of a 

limb is fixed and the other rotates. In modern 

times this type of fracture is frequently associated 

with skiing accidents, in which the lower leg is 

rigidly fixed and the body twists during a fall. 

Because the stress occurs in a spiral direction the 

fracture line also spirals. Torsion fractures can be 

confused with compression fractures in long 

bones, which follow a natural spiral cleavage 

plane in the bone. Torsion fractures always involve abnormal rotation of the bone. 

Bending fractures are the most common type 

of bone separation and are often complicated by 

other types of stress. Abnormal stress can result 

when the bone is bent as the result of a fall or in 

response to a blow, as in the "parrying" fractures 

of the forearm. In either case the maximum stress 

often occurs at a discrete spot in the bone and 

may result in a simple transverse separation of 

the bone. The force can also radiate from the 

impact point in a conical shape with the fracture 
58 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOG Y 

FIGURE 46.—Healed compressed fracture of the twelfth thoracic vertebra (third vertebra from top). Both femora show 

marked, periosteal, bone hypertrophy over the trochanters, 

suggestive of myositis ossificans or a reaction to decubital 

ulcers secondary to the interruption of the spinal cord. A 

bone fragment had been pushed into the spinal cord adjacent 

to the fracture. (PMUG 4697a.) 

developing along the surface of the cone. This 

produces a triangular fragment of bone (Figure 

49). In a young person bending fractures may 

produce an incomplete transverse break in a long 

bone with longitudinal splitting. This condition 

is known as a "green stick fracture" (Figure 50). 

Shearing fractures result when opposite forces 

are applied to bone in slightly different planes. 

The opposing forces need not both be dynamic. 

The bone may be supported by a static force in 

one axis with dynamic force applied in the opposite direction (Figure 51). One example of 

shearing trauma is Colles' fracture of the distal 

radius. This is a fracture resulting from a fall 

FIGURES 47, 48.—Depressed fracture of the skull vault: 47, 

Some broken fragments are still attached to the skull, which 

is indicative of fracture occurring at or near the time of 

death. 48, Internal view. (Calvarium from a 19-year-old 

male, FPAM 2022.) 

forward, in which the individual reacts by extending the arms to minimize the impact. In this 

case the dynamic force is the falling body, the 

static force is the ground or floor. The result is a 
NUMBER 28 59 

fracture in which the distal end of the radius is 

sheared off and displaced backward. Schinz, 

Baensch, Friedl, and Uehlinger (1951-1952:276) 

note that in Colles' fracture the shearing stress 

rapidly changes to bending stress, and it may be 

impossible to distinguish the effects of the two 

types of stress in the resulting fracture. 

A fracture varies not only in terms of the type 

of stress but also with respect to its severity, which 

is related to the extent of the fracture. A simple 

fracture is one in which there is only one separation of the bone. This contrasts with a more severe 

fracture with many broken fragments, which is 

called a comminuted fracture. In either of these 

types of fracture the traumatic event may result 

in the broken bone being exposed through the 

skin. This is called a compound fracture and can 

greatly complicate healing because of the possibility of infection (Collins, 1966:50). 

While fractures brought about by sudden overwhelming stress are the most frequent of traumatic problems, other types of fracture occur in 

which other patterns of stress or pathological 

conditions are contributing factors. In modern 

populations unusual and continued stress over a 

period of weeks may result in a fatigue fracture. 

In fatigue fractures the stress applied to bone does 

not immediately result in fracture. In all cases 

such fractures are associated with the onset of 

intense physical activity of a type not engaged in 

previously. Fatigue fractures are often seen in 

military recruits during their initial training period (Schinz, Baensch, Friedl, and Uehlinger 

1951-1952:285). In fatigue fracture of the tibia, 

for example, the predilected site is the proximal, 

medial metaphysis, particularly in the region of 

active cutback, where cancellous support is poor. 

Such fractures are often incomplete, involving 

only a portion of the cross-sectional plane of a 

bone. They are also associated with unosteonized 

circumferential lamellar bone (Johnson, 1964: 

607). The physical activity triggers an attempt by 

the bone to increase its mechanical strength by 

osteon remodeling. However, the first step in 

FIGURE 49.—Schematic representation of bending fracture 

and the triangular fragment that may occur in such fractures. 

FIGURE 50.—Schematic representation of bending fracture, 

which produces ix green stick separation of part of a bone. 

Both transverse and longitudinal breakage may occur. 
60 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

FIGURE 51.—Depressed fracture of the skull of sufficient force 

to produce shear between the large fragment and the rest of 

the skull. (Calvarium of an adult male, WM S19.4.) 

osteonization is the formation of resorption 

spaces, which initially weakens the bone. Normally resorption space formation would be accomplished without a serious reduction in the 

mechanical integrity of the bone. Abnormal physical activity, however, greatly accelerates bone 

resorption and, if continued, results in callus formation and fracture. Part of the problem of 

increased osteon remodeling is the fact that osteonal refill of a resorption space occurs at about 

one-tenth the speed of resorption. 

Whether or not the somewhat unusual conditions of physical activity that result in fatigue 

fractures in modern populations could have existed in archeological skeletons is problematical. 

Detection of such fractures may also be more 

difficult since the bone may not be completely 

broken, and even when it is, good alignment of 

the broken ends is much more likely in fatigue 

fracture than in violent fracture. This means that 

the repair process may leave little trace of the 

fracture. It is, however, important for the paleopathologist to be aware of such fractures and 

attempt to make the distinction, since the stress 

involved is quite different from violent fractures 

and could contribute misleading data in frequency tables of violent fractures in various parts 

of the skeleton. 

The capacity of bone to resist stress depends on 

the quantity, quality, and architecture of bone. 

Conditions that adversely affect one or all of these 

factors can create a situation in which bone is 

unable to withstand a moderate force that normally would be tolerated easily. When fracture 

occurs in such situations it is called a pathological 

fracture meaning that some morbid process has 

weakened the bone to the point that it cannot 

resist relatively normal stress. Many diseases can 

produce abnormal bone loss and result in pathological fracture (Figure 52). Collins (1966:52) lists 

many of these which include congenital, metabolic, and infectious diseases, as well as neoFIGURE 52.—Pathological fractures of the left femur. Unhealed fractures are seen in the neck of the femur and the 

proximal metaphysis. The fracture of the upper diaphysis 

has healed but with angulation. (Adult female with carcinoma of the breast, W M H578.1.) 
NUMBER 28 61 

TABLE 1.—Distribution and types of fractures in cases 

reported by Hamilton (1853:33) 

Bone(s) affected 

Nose and face 

Clavicle 

Scapula 

Humerus 

Radius 

Ulna 

Radius and ulna 

Femur 

Patella 

Tibia 

Fibula 

Tibia and fibula 

Bones of the hand 

Ribs 

Vertebral column 

Pelvis 

Total number 

of cases 

Compound & 

comminuted 

6 

0 

0 

2 

0 

0 

0 

3 

0 

0 

1 

13 

1 

0 

0 

0 

26 

Compourul 

6 

4 

0 

1 

2 

2 

2 

1 

0 

6 

4 

19 

2 

0 

0 

0 

49 

Simple 

12 

37 

3 

36 

25 

20 

31 

67 

7 

13 

11 

40 

2 

4 

3 

1 

312 

Total 

no. of 

cases 

24 

41 

3 

39 

27 

22 

33 

71 

7 

19 

16 

72 

5 

4 

3 

1 

387 

plasms. Collins also reports that pathological fractures from different diseases are associated with 

rather specific age categories. To this list should 

be added aging, which is generally associated 

with gradual bone loss and which can contribute 

to pathological fracture (Schinz, Baensch, Friedl, 

and Uehlinger, 1951-1952:256). 

Previous studies have shown that the location 

of fractures in the skeleton varies with the age 

and sex of the individual (e.g., Buhr and Cooke, 

1959). Furthermore, there are differences in the 

frequencies of fracture in various locations in the 

skeleton (Table 1), which may be associated with 

cultural differences (Hamilton, 1853; Schinz, 

Baensch, Friedl, and Uehlinger, 1951-1952:249; 

De Souza, 1973; Iqbal, 1974). It is apparent that 

different cultural and environmental conditions 

create different fracture hazards. The potential 

fracture hazard of someone negotiating an icy 

sidewalk is quite different from a person living in 

the tropics. Similarly, the fracture hazard of the 

ancient hunter is likely to be different from that 

of the ancient city dweller. Differences in fracture 

pattern have considerable significance for paleopathology in part because of these cultural variations and the inferences that can be made regarding the characteristic hazards encountered 

by different groups. 

Fracture Healing 

The process of fracture healing in some respects 

recapitulates events associated with growth. 

There are, however, significant differences in 

which the conditions associated with the fracture 

event itself are significant. Traumatic, fatigue, 

and pathological fractures will also vary in the 

healing process. In the following review of fracture healing the major emphasis is on the biology 

of traumatic fracture repair. 

Several events occur with the fracture of a 

bone. Blood vessels are ruptured both in the 

cortex (in Haversian canals) and also in the periosteum and marrow. Blood vessels in overlying 

muscle may also be torn. With the rupture of the 

blood vessels, blood flows into the fracture region 

forming a hematoma, which coagulates. There is 

some debate regarding the value of the hematoma 

in the healing process. Collins (1966:50) suggests 

that the clot interferes with healing. More recent 

research (Schenk, 1973:xv) suggests that hematoma is not essential to fracture healing and 

indirectly supports Collins' opinion. Regardless 

of its value in fracture repair a hematoma is an 

almost inevitable result of fracture. The broken 

ends of the blood vessels contract and the open 

ends are sealed by clotted blood. However, the 

traumatic event stimulates an inflammatory reaction in which intact blood vessels and the undamaged portions of broken vessels dilate and 

release a plasma exudate, which adds to the fluid 

at the fracture site (Collins, 1966:44). 

The periosteum will usually be broken during 

fracture, although this is not inevitable, particularly in young individuals. The stress that breaks 

the periosteum also tends to strip it from the 

surface of the bone for a few millimeters adjacent 

to the fracture site. This appears to activate the 

bone-forming potential of the osteogenic layer in 

the periosteum and initiates the formation of 
62 SMITHSONIAIN CONTRIBUTIONS TO ANTHROPOLOG Y 

callus (Schinz, Baensch, Friedl, and Uehlinger, 

1951-1952:378). 

Breakage of the blood vessels at the fracture 

site also results in the death of tissue and cells 

including the osteocytes supplied by such vessels 

and any bone fragments resulting from the breakage. This bone will ultimately have to be removed 

and replaced. 

In classic fracture healing, the formation of a 

blood clot is followed by the second step in fracture repair, in which the blood clot is permeated 

by fibrous connective (granulation) tissue. Collins 

FIGURES 53, 54.—Healed fracture with slight angulation in an adult right femur: 53, Anterior 

view, arrow indicates callus. 54, Posterior view. (IPAZ 1780/62.) 
NUMBER 28 63 

(1966:50) notes that the hematoma, if not extensive, can assist in initial union by providing a 

matrix for the advance of granulation tissue. 

However, granulation tissue can penetrate hematoma only to a limited depth; thus, extensive 

hematoma between broken ends seems to delay 

the healing process. 

Schinz, Baensch, Friedl, and Uehlinger (1951-

1952:378) indicate that the fibrous callus that 

unites the ends of the fragments is derived from 

the granulation tissue. This fibrous union of the 

broken ends is the third stage of fracture healing. 

While the fibrous callus is unmineralized, it provides the matrix for the formation of fiber bone 

and the primary bony callus, which is the fourth 

stage in fracture healing. As I have indicated 

previously (p. 11), fiber bone is associated with 

rapid bone formation. In normal conditions it 

occurs only during the growth phase. Fiber bone 

is a temporary tissue, replaced by lamellar bone, 

which has much greater mechanical strength. 

Collins (1966:47) notes that primary callus formation generally begins about one week after 

fracture in human bone. Initially, primary callus 

consists of coarse, fibrillar trabeculae within the 

fibrous callus. Primary callus is associated with 

different areas of the fracture site and three basic 

types have been defined for conceptual purposes 

(Schinz, Baensch, Friedl, and Uehlinger, 1951-

1952:378). The intermediate or sealing callus 

joins the broken ends of the bone. The endosteal 

callus unites the opened marrow spaces forming 

a plug between the two ends, while the periosteal 

or bridging callus arches over the fracture site. 

The bridging callus provides the externally visible 

evidence of healed fracture in an archeological 

specimen. One other component of primary callus 

is the occasional occurrence of cartilage in the 

region of the callus. Collins (1966:48) expresses 

the opinion that cartilage is incidental to the 

overall process of fracture healing. In support of 

this conclusion, he cites the work of Ham (1930), 

who suggested that cartilage formation is associated with poor vascular supply. Aegerter and 

Kirkpatrick (1975:237) challenge this concept but 

offer no alternative. 

It is important to remember that bone formation requires an adequate blood supply. Intense 

vascular proliferation begins with the formation 

of granulation tissue and is associated with callus 

formation. The blood vessels supplying the formation of callus also create conditions in which 

resorption of bone fragments and dead bone ends 

at the fracture site can occur. 

The fifth stage in fracture healing involves the 

conversion of the fiber bone callus to lamellar 

bone. This includes the apposition of lamellar 

bone to existing fiber bone surfaces, the removal 

of fiber bone by osteoclasts, and internal osteon 

remodeling. The result is a much stronger union 

of the broken ends. This in turn means that less 

bone is needed for optimal mechanical strength. 

In the final, sixth stage of fracture healing the 

callus is reduced to a minimum (Figures 53, 54). 

If the orientation of the broken ends is good, the 

callus may no longer be apparent. If angulation 

has occurred there is compensatory remodeling 

(Figure 55). 

The time for fracture healing varies based on 

several variables including (1) the bone involved, 

(2) the severity of the fracture, (3) the apposition 

of the ends, (4) the stability of the fractured ends, 

(5) the nutritional state of the individual, and (6) 

the age of the individual. Collins (1966:52) indicates that in a typical bone under ideal conditions 

the primary callus takes about six weeks to develop. The secondary callus becomes significant 

after this time but bony union and return of 

adequate function is too variable to predict. 

Cruess and Dumont (1975:97), rather than 

assigning a specific timetable, indicate the approximate percentage of the total healing time 

spent in the three major phases of fracture healing. These phases include the inflammatory phase 

(10 percent), the reparative phase (40 percent) 

and, the remodeling phase (70 percent). The 

phases do not total 100 percent because of the 

overlap in time between the phases. In any case 

the time of reduced mechanical function is certainly a matter of weeks even in an ideal situation. 

The significance of this period of reduced activity is difficult to assess. Schultz (1939:978) 
64 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOG Y 

FIGURE 55.—Compensatory remodeling in angulated healed 

fracture of the right femur. Arrows indicate the thickness of 

new cortical bone added to the concave side of the angulated 

femur shaft. On the opposite side some of the cortical bone 

of the broken ends has been removed. (Adult, IPAZ 192/ 

60.) 

reports that the percentage of fracture cases for 

free-ranging nonhuman primates varies between 

12 and 34. Primates shot in the wild present 

numerous examples of well-healed fractures 

(Duckworth, 1912; Schultz, 1939), indicating that 

fracture need not be a serious threat to life. In 

human populations the threat is likely to be even 

less, but greatly dependent on the environment 

of the group. For an adult member of an Eskimo 

family, such an injury could be very serious indeed. 

Complications Arising from Fracture 

The complications of fracture include (1) infection, (2) tissue necrosis and loss of innervation, (3) 

inadequate fusion of the fracture, (4) bone deformity, (5) traumatic arthritis, (6) joint fusion, 

and (7) traumatic myositis ossificans. I shall provide a brief review of each of these conditions. 

Infection is a serious complication of fracture 

and can occur whenever infectious agents become 

associated with the fracture site. This event can 

occur if the soft tissue in the fracture area is 

penetrated by one or both of the broken ends of 

the bone. It can also occur if the agent producing 

the fracture also penetrates the skin, as would be 

the case with a bullet or other projectile. Infection 

is also possible if bone penetrates any portion of 

the digestive track, or any body cavity where 

infectious organisms exist. 

Bohler (1935:65) indicates that open (compound) fractures with direct injury to the skin 

(crushing or penetrating wounds) have a much 

greater risk of infection than those due to indirect 

injury (as when a broken bone penetrates the 

skin). Two major infectious conditions pose a 

serious threat to life. The first of the conditions is 

gas gangrene arising in necrotic tissue by action 

of organisms, such as Clostridium, which do not 

require oxygen (anaerobic). The other major 

threat to life is pus-forming (suppurative) organisms, which can spread from the fracture site 

and can produce general infection of the blood 

(septicemia) and ultimately death. Bohler (1935: 

64) reports statistics for 1887, in the pre-antibiotic 
NUMBER 28 65 

period, in which the estimated mortality from 

open fractures in German hospitals was 40 

percent. The data reported in Table 1 indicate 

that compound fractures (compound-comminuted and compound only) occur in about 19 

percent of all fracture cases. 

Another complication of local infection at the 

fracture site is disruption of the blood supply to 

bone leading to death of the tissue (necrosis). At 

the boundaries of the dead tissue osteoclasts may 

isolate the dead bone through osteoclastic resorption. Such an isolated segment of dead bone is 

known as a sequestrum. Often, if the blood supply 

to the bone itself is cut off, the periosteum remains 

intact and produces a new sheath of bone called 

involucrum around the necrotic tissue. A more 

detailed review of infection in bone is presented 

in the chapter on infectious diseases (p. 104). 

With respect to fracture the significant point is 

that infection, certainly in pre-antibiotic times, is 

a most serious complication, having a significant 

risk of mortality. However, in archeological skeletons it will require very careful and observant 

excavation technique to distinguish an unhealed 

fracture resulting in or associated with death from 

that of postmortem damage from soil movement 

or careless excavation. 

I have already noted that rupture of some 

blood vessels is an inevitable result of all fractures 

(p. 61). Damage to major blood vessels and nerves 

is not inevitable because of the flexible and relatively tough nature of these structures. Hazard to 

major blood vessels and nerves is greatest in 

crushing injuries resulting in fracture. However, 

even in simple fractures, the displacement of bone 

ends can compress or twist blood vessels or nerves 

(Bohler, 1935:73) and lead to ischemia and loss 

of nervous stimulation. Loss of blood supply will 

lead to delayed fracture healing and, if uncorrected, can result in bone necrosis. Loss of nerve 

supply does not appear to be as serious. However, 

if sensory nerve supply is lost to the fracture site, 

the lack of pain may allow continued use of the 

broken bone and prevent healing or, in the case 

of a fracture of an articular surface, lead to a 

neuropathic or Charcot joint, in which there will 

be exuberant bony response to unrelieved trauma 

to the joint (Figures 56, 57). 

In some cases the distribution of dynamic forces 

immediately after trauma may not break the 

bone but will disrupt the blood supply, lead to 

ischemia, and may result in tissue necrosis. Three 

such cases may be seen in the Hunterian Collection in London (Figures 58-60). All three cases 

are attributed to a blow on the head. If the blood 

supply in the immediate region of the blow is 

disrupted, the tissue becomes ischemic or necrotic, 

and there is an inflammatory response adjacent 

to the affected bone. 

Traumatic interruption of blood supply in a 

growing bone can produce abnormal shortening 

of bone. The growth plate in such bones is particularly vulnerable to trauma because of the relative weakness of calcified cartilage. Trauma to 

the ends of growing bone cannot only break the 

cortex but, also, can shear the epiphysis (Schinz, 

Baensch, Friedl, and Uehlinger, 1951-1952:422). 

In both cases, the blood supply is disrupted and 

growth is retarded. Such injuries to the epiphysis 

may also result in premature fusion of the growth 

plate. The result of any of these complications is 

a shortened bone. If only one of the two bones of 

the forearm or lower leg is involved, abnormal 

angulation of the hand or foot ensues. If both the 

radius and ulna or the tibia and fibula are affected the entire forearm or lower leg will be 

shortened. Similarly, fracture at the growth zone 

of other long bones can produce reduced length 

of the bone. 

Serious disruption of nervous supply to other 

parts of the body may be associated with fracture 

of the vertebral column, depending on the vertebrae involved, since either the spinal cord or 

spinal nerves can be affected. Bohler (1935:109-

145) reviews these fractures and their complications. The most serious complication occurs in 

complete severance of the spinal cord. The permanent paralysis below the level of the injury, 

which inevitably results, affects various parts of 

the body depending on where the break occurs. 

The comminuted fragments can put pressure 

on the spinal cord or spinal nerves producing 
66 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

^^H^^^3| '^1 

^^H^p-v. ^^i^P,,^^H 

^^^^B9v ~ '^ ^A^^^^^^^^H 

fc^^'a ^III^M.j;^^)' ^^^1 

1 '^^^AV 

% ^ j^^^^^^^^^^^^^^^^H 

FIGURES 56, 57.—Charcot joint resulting from traumatic fracture of the left femoral neck: 56, 

Anterior view of innominate and femur; note the large mass of bone over the acetabulum 

creating a new joint, which comes in contact with the greater trochanter. 57, Inferior-lateral 

view. (ANM 2243.) 

paralysis, which probably will not heal spontaneously. Since medical procedures are not likely 

to have been available in archeological populations, evidence of a partially occluded neural 

canal above the second lumbar vertebra should 

be suggestive of paralysis. Evidence of this should 

be sought in the limbs likely to have been affected 

(e.g., Figure 46). In general, paralysis prevents 

effective use of the paralyzed limb and will result 

in bone atrophy (p. 325). 

A less serious result of spinal fracture is a blood 

clot or callus producing pressure on the spinal 

cord or nerve root. The blood clot will disappear 

in time if the individual is kept quiet and the 

callus may be partially remodeled away after the 

break is healed. Dysfunction in the form of paralysis in such cases may be temporary. 

In some fractures the healing process is delayed 

or incomplete. This condition is almost always 

the result of inadequate immobilization of the 

fracture during the healing phase. Two complications can arise. In the first of these there is 

inadequate mineralization of the callus allowing 

the fractured ends continued movement. Such a 

condition is called pseudarthrosis. The second 

condition is called nearthrosis and differs from 

pseudarthrosis in that an actual joint space is 

formed (Schinz, Baensch, Friedl, and Uehlinger, 

1951-1952:425-430). In the American literature 

both these terms are frequently used synonymously and with the term "nonunion." However, 

each condition produces a slightly different result 

in bone and thus, should have distinguishing 

terms. 

The factors that produce nonunion remain 

somewhat obscure. Schinz, Baensch, Friedl, and 
NUMBER 28 67 

FIGURE 58.—Central bone necrosis surrounded by a zone of 

hypervascularity (arrows) following a blow to the head. 

(Portion of the left frontal bone, H M P626.) 

FIGURE 59.—A large area of bone necrosis (arrows) surrounded by a zone of hypervascularity following a blow to 

the head. (Frontal bone, H M P627.) 

Uehlinger (1951-1952:379) indicate that repeated disruption of the callus results in increased 

hyaline cartilage formation instead of the mineralizable osteoid normally expected in callus. This 

may be a response to reduced blood supply caused 

by breakage of developing vessels during movement of the broken ends (Schinz, Baensch, Friedl, 

and Uehlinger, 1951-1952:427). Another possibility is the interposition of other tissue (e.g., 

muscle) between the broken ends. 

In pseudarthrosis resulting from fracture, the 

ends of the broken bone are joined by connective 

tissue and, indeed, extensive callus may form. 

However, this tissue does not mineralize properly 

due to a lack of osteoid, and the union remains 

flexible. With time the broken ends of the bone 

will be sealed off by new bone formation and will 

be connected by flexible fibrocartilage. With continued movement, hyaline cartilage may develop 

near the middle of the fibrocartilage mass and a 

cleft develop forming a true joint. Ultimately, a 

joint capsule may surround the joint space, thus 

approximating the anatomy of a normal joint. 

The result is usually severely diminished function 

FIGURE 60.—A small area of bone necrosis surrounded by a 

zone of hypervascularity and bone resorption (arrows) following a blow to the head. The traumatic nature of the 

lesion is demonstrated by the partially healed bone fragment 

occurring internally. (Portion of the frontal bone, HM P628.) 
68 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

FIGURES 61, 62.—Healed diagonal fracture of the distal, left femur with marked mediolateral 

and longitudinal displacement of the broken ends: 61, Medial view. 62, Posterior view. The 

displaced ends are joined by abundant callus. There has been considerable cortical remodeling 

of the broken ends, which have been sealed off with compact bone. (WM S32.7.) 

of the limb. However, in the case of the forearm 

or lower leg, nonunion in one bone may be compensated by extensive hyperplasia of the other 

bone and adequate function can result (Schinz, 

Baensch, Friedl, and Uehlinger, 1951-1952:428). 

Problems in mechanical function can also be 

caused by misalignment of the broken ends. Two 

factors contribute to this. The stress producing 

the fracture may produce misalignment. At least 

equally significant, however, is the fact that the 

sensory stimuli triggered by the fracture produce 

a virtually instantaneous and powerful contraction of the muscles in the fracture area. Subsequent movement of the limb will repeat this 

stimulus if pain results (Bohler, 1935:58-59). 

With such muscle contraction the likelihood of 

misalignment is high. In modern clinical practice 

initial management of fracture involves minimizing muscle contraction and careful realignment 

of the broken ends so that the bone approximates, 

as near as possible, its original shape. 

Even when this procedure is attempted, however, misalignment can occur as is illustrated in 

a modern case (Figure 55). The effects of poor 

alignment vary with the bone involved and the 

severity of the fracture. Rarely, if ever, does it 

produce a direct threat to life. However, it can 

lead to premature and severe degeneration of a 

joint because of the abnormal stress on the joint 

brought about by misalignment. In the long 

bones this can result in reduced locomotion and 

manipulative ability. Misalignment of a vertebral 
NUMBER 28 69 

fracture can result in varying degrees of angulation in the spine since the vertebrae are all closely 

linked to each other in mechanical function. 

Fracture can, directly or indirectly, produce 

premature osteoarthritic degeneration of joints. If 

the joint surface is broken, the cartilage and 

subchondral bone are disrupted. Because of the 

absence of blood supply, the repair of cartilage 

depends on nutrients from the joint capsule, and 

any repair is a slow process. A break of the 

subchondral plate will usually result in permanent discontinuity of the bony joint surface. This 

complicates the healing process of the articular 

cartilage, since it results in poor contact between 

the gliding surfaces of the joint. This creates 

serious problems in dissipating the stress applied 

to the joint and results in premature deterioration 

of the articular cartilage. 

The fracture need not involve the joint itself to 

produce premature degenerative changes in the 

joint. As I have already noted (p. 68), a change 

in the axis of a long bone can shift the major 

focus of mechanical stress to a portion of the joint 

less well adapted for such stress. Similarly, abnormal shortening of a long bone after fracture 

(Figures 61, 62) can produce uneven locomotion, 

which results in unusual stress to the joint and 

premature degenerative change (Schinz, Baensch, 

Friedl, and Uehlinger, 1951-1952:430). In trying 

to distinguish between premature degenerative 

change resulting from fracture and degenerative 

change from aging, it is helpful to make a comparison with the joint of the corresponding limb. 

Fracture of the joint surfaces can also result in 

destruction and fusion of the joint. This problem 

is associated with comminuted fractures of the 

joint where more than one joint surface is involved and callus formation joins two or more 

bones. In the limbs this means loss of movement 

for the joint. In the vertebral column such a 

fusion is seen in Figure 46 and is a common 

sequela of compression fractures of one or more 

vertebral bodies (Bohler, 1935:142-143). In such 

cases, the mechanism is activation of the periosteum of the body with callus formation extending 

to adjacent vertebrae. The effect is a rigid segment of spine, perhaps associated with angulation, resulting in little overall loss of spinal movement. Fusion of fractured joints can easily be 

confused with fusion following infection of the 

joint (p. 113). In some cases a distinction may not 

be possible; however, traumatic fusion may retain 

evidence of the fracture line. 

The treatment of many fractures can be accomplished on the basis of intuitive knowledge and 

common sense. The frequent occurrence of wellhealed fractures in archeological skeletons testifies 

eloquently to this fact. Bohler (1935:566) lists 

three fundamental laws for fracture treatment. 

They are (1) reposition and realignment of the 

broken ends (reduction of the fracture), (2) immobilization (fixation) of the broken bone, and 

(3) maintenance of circulation and muscle tone 

through careful exercise of the affected limb. 

Obviously, in comminuted fractures, compound fractures, or simple fractures where 

marked displacement has taken place, proper 

reduction and restoration may be difficult, if not 

impossible, without modern techniques, including traction and surgical intervention. However, 

it is also apparent in archeological specimens that 

badly misaligned bones do heal and, judging 

from the lack of disuse atrophy, provide at least 

limited use of the limb. Perhaps such fractures 

heal spontaneously with the pain associated with 

movement being the immobilizing force. 

I have noted earlier (p. 61) that trauma to bone 

can also damage the overlying muscle. Johnson 

(1964:610) notes that muscle tissue can provide 

cells that contribute to callus formation around 

the fracture site. As with bone, the trauma to 

muscle tends to produce hematoma. With time 

the hematoma is usually dissolved. Occasionally, 

however, the muscle tissue will respond to the 

trauma by producing bone directly in the muscle 

tissue itself, often in association with the hematoma. This condition is known as traumatic myositis ossificans. This excessive formation of bone 

by muscle can be entirely separate from the bone 

(Figure 63) or it can become part of existing bone 

tissue (Figures 64, 65). The most common areas 

are the extensors and adductors of the thigh, the 
70 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOG Y 

FIGURE 63.—Traumatic myositis ossificans (arrow) within 

muscle tissue overlying a healed fracture of the left femur. 

(40-year-old male, FPAM 4751; scale in cm.) 

deltoid and the pectoralis. In paralyzed patients 

minor trauma of the insensitive muscles may lead 

to metaplastic bony bridging of joints, especially 

the hip. 

FIGURES 64, 65.—Traumatic myositis ossificans of the right 

innominate and proximal femur of an adult male: 64, Anterior view of hip; massive development of hypertrophic 

bone is seen in the area of the iliacus muscle (arrow) with 

exuberant bone development in the area of the intertrochanteric fracture of the proximal femur. 65, Inferior view showing the intertrochanteric fracture and development of hypertrophic bone in the region of the addilctor muscle insertions on the femur (arrow). (FPAM, no number.) 
NUMBER 28 71 

FIGURES 66, 67.—Saber wounds of the left parietal: 66, There is a large, displaced fragment on 

the lateral portion of the left parietal; the wound healed with the fragment in the displaced 

position leaving an opening in the skull; the second healed saber wound is seen superior to the 

large defect. Only the outer table was affected. 67, Internal view. (Adult male, ANM 2069.) 

Thus far in the review of fracture and its 

complications I have made only limited reference 

to the skull. Fracture of the skull presents an 

additional potential complication not associated 

with fracture in other bones. The most immediate 

problem in skull fracture is the hematoma and 

edema, both of which invariably result from such 

trauma. An unrelieved major increase in pressure 

on the brain from hematoma or edema will force 

the brain tissue into the foramen magnum, disrupting the blood supply to the brain and damaging the brain stem. If the skull is fractured by 

a blow, the pressure buildup may be relieved 

through the fracture site. Obviously if the blow is 

too severe, death will result from direct injury to 

the brain. 

The extent of injuries to the skull that an 

individual can survive is often remarkable. Figures 66 and 67 show views of a saber wound to 

the skull, in which a piece of the left parietal was 

completely dislodged with healing of the fragment in the displaced position. In this specimen 

(ANM 2069), currently located in the National 

FIGURE 68.—Healed wound from battle axe or saber in the 

left parietal of an adult male skull. Note the fracture lines 

radiating from the main defect. Evidence of healing and 

long term survival is seen in the smooth, rounded edges of 

the major defect. (FPAM 5719; scale in,cm.) 
72 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

Museum of Anthropology, Prague, the edges of 

the wound are well remodeled, indicating considerable time after the injury before death occurred 

due to an unrelated cause. In this specimen the 

glancing nature of the sword wound may have 

prevented any damage to the brain. Another case 

of severe trauma to the skull is seen in a specimen 

(FPAM 5719) from the Federal Pathologic-Anatomy Museum in Vienna (Figure 68). This specimen shows massive fracturing of the left parietal 

and occipital bones with fracture lines radiating 

from the major fracture site. The size of the gap 

is suggestive of a wound from a saber or axe. The 

edges of the break are well remodeled indicating 

a long-standing recovery. 

Surgical intervention in pathological conditions that affect the skull or its contents is a 

common practice today. Such a procedure carries 

with it the risk of infection and damage to the 

brain seen in traumatic injury of the skull. In 

view of the risk, evidence of surgical treatment of 

the skull (trephination) in antiquity is a remarkable phenomenon and will be discussed as part of 

the review of the paleopathology of trauma. 

PALEOPATHOLOGY 

History and Examples 

In the following review of fracture in archeological skeletal material I use published source 

materials but emphasize skeletal specimens from 

the collections of the National Museum of Natural History, Smithsonian Institution, Washington, D. C , USA, and my own experience and 

observations on paleopathology. It is important 

to emphasize, at the outset, that the advent and 

expansion of civilization has not eliminated 

trauma, either of the accidental or intentional 

type. What has happened is the introduction of 

new factors producing trauma, such as the substitution of the automobile for the horse in transportation, and the use of guns and bombs instead 

of clubs, axes, swords, arrows, and spears in warfare. 

While the human species is still subject to 

trauma, treatment has greatly improved. This 

improvement took a quantum leap forward with 

the development of antibiotics, which have 

greatly reduced the possibility of infection complicating the traumatic event. 

These introductory comments serve to highlight the importance of a reference point for the 

paleopathology of trauma, in which modern medical concepts and treatment, to a large extent, did 

not exist. It is important to add that, in the 

treatment of fracture, ancient populations often 

did a remarkably good job (e.g., Elliot-Smith, 

1908:734). 

Fracture and the complications arising from 

fracture most often provide the paleopathologist 

with easily interpretable lesions in archeological 

skeletons. However, there are some problems in 

the interpretation of this type of trauma of which 

the paleopathologist should be aware. First, evidence of healed fractures occurring in children 

can be completely obliterated by the skeletal 

remodeling that occurs with growth. Second, it is 

difficult and often impossible to make a distinction between fractures occurring at the time of 

death and those that occur subsequent to death 

and burial. Wood-Jones (1908b: 736) indicates 

that in Egyptian skeletons, fractures occurring at 

the time of death produced blood staining adjacent to the fracture site. However, such staining 

may survive only under conditions of minimal 

rainfall and soil water content, so that this criterion may be of little value in most geographical 

areas. 

In fracture occurring while the periosteum and 

other soft tissues are still intact, small bone fragments in the fracture site may still be adherent to 

adjacent bone (Figure 69). This condition is very 

helpful in distinguishing between fracture at the 

time of death and damage to the skeleton after 

interment resulting from shifting soil or damage 

during excavation. Also surfaces of bone tend to 

be stained a somewhat different color from bone 

not in direct contact with the soil. Thus, breaks 

occurring during excavation or in subsequent 

processing may have a surface coloration quite 

distinct from surfaces in contact with the soil for 

a long period of time. 

A third factor of significance to the paleopath-
NUMBER 28 73 

ologist is the distinction between accidental fracture, as from a fall, and fracture resulting from 

intentional violence either in single combat or 

warfare. Here, both the direct evidence in the 

skeleton and the circumstances of burial are significant variables. 

Occasionally one finds evidence regarding the 

causative agent in fractures or infractions imbedded in the skeleton. Metallic or mineral fragments 

of projectile points have been found in archeological skeletons (Figures 70-72). The injury may 

clearly indicate that a sword, axe, or similar 

cutting instrument produced the wound (Figure 

73). Similarly, a mass burial containing many, 

unhealed, broken bones may be evidence of warfare or massacre (e.g., Wood-Jones, 1908b; 

Turner and Morris 1970). 

One usually cannot be certain that a healed or 

unhealed fracture was caused by an accident. 

However, the location of the lesion in the skeleton 

is indicative. Wood-Jones (1910c:297) notes a 

high incidence of defensive (parry) fractures of 

the ulna in Egyptian materials in comparison 

with its low incidence in modern city populations. 

This contrasts with fractures of the humerus, 

which have virtually the same incidence, suggesting that fractures of the humerus are more likely 

FIGURE 70.—Stone projectile point embedded in the posterior portion of the body of the twelfth thoracic vertebra. 

(Adult male skeleton from an archeological site in Illinois, 

USA, NMNH 379841.) 

to be produced by accidental factors that are 

similar across cultural and time boundaries. 

There are distinctive accidental fractures (such as 

Colles' fracture of the distal radius) which are 

well known in modern clinical practice and are 

identifiable in archeological specimens (Figure 

74). 

FIGURE 69.—Adherent bone fragments at multiple fracture 

sites (arrows) in the left parietal of an adult skull. The 

adherent nature of the fragments is indicative of trauma 

occurring while the periosteum and other soft tissues are still 

intact. (NMNH 266571.) 

FIGURE 71.—Broken stone projectile point embedded in the 

anterior portion of the body of a fifth lumbar vertebra. 

(Adult female skeleton from an archeological site in Illinois, 

USA, NMNH 380118.) 
74 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

FIGURE 72.—Tip of stone projectile point embedded in the 

inner portion of a right innominate bone. (Adult male 

skeleton from an archeological site in Illinois, USA, NMN H 

380120.) 

FIGURE 73.—Healed sword wound in the posterior portion 

of the right parietal. (Adult male, BMNH CG69, XXXIX, 

280, Burial 1132.) 

FIGURE 74.—Healed Colles' fracture of the distal left radius 

(center), shown with the unaffected left ulna (right) and 

compared with the normal right radius (left). (Female skeleton excavated from an Eskimo burial ground in Alaska, 

USA, NMN H 345315.) 

A comprehensive review of the problems in 

identifying and interpreting traumatic lesions in 

archeological skeletons is beyond the scope of this 

book. However, the above observations should 

serve to make the paleopathologist aware of the 

types of variables that are important to consider 

in interpreting traumatic lesions. 

Fracture has been documented in some of the 

Early Paleolithic skeletal remains of Homo erectus 

from Choukoutien cave in China (Weidenreich, 

1939:37). Fracture has also been reported in Homo 

sapiens specimens from the Middle and Upper 

Paleolithic (Moodie, 1922:393; Weidenreich, 

1939:38; Roper, 1969). Angel (1974a) surveyed 

the incidence of fractures from the Neolithic to 

modern times in skeletal samples from the Eastern 

Mediterranean. Wood-Jones (1910c: 293-340) 

provides a very detailed report on fractures in 

ancient Nubian skeletal materials. These reports 

demonstrate, as one might expect, that fracture 

is as old as the vertebrates. It is significant, however, that the incidence and distribution of fractures in the skeleton appears to have changed. 

While accident undoubtedly was a significant 

cause of fracture in ancient times, it is clear from 

the high incidence of fractures attributable to 
NUMBER 28 75 

FIGURES lb-11.—Healed but malaligned fracture of the right 

humerus: 75, Posterior view. 76, Anterior view. 77, Detail of 

anterior callus; note remodeling of diaphysial ends. (Adult, 

female skeleton from Goat Cove, Texas, USA, NMN H 

372527.) 
76 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

FIGURE 78.—Healed, depressed fracture in an adult male 

skull. (BMNH Winchester-Saxon pathology collection, 

CG69, 697, 280 XXXIX.) 

violence that intentional violence was a major 

cause of fractures. Wood-Jones, for example, reports an incidence of fractures of 3 percent in a 

series of 5000-6000 Nubian skeletons (1910c:294). 

However, 31 percent of all fractures occur in the 

bones of the forearm. Wood-Jones found that the 

ulna is broken more often than the radius and the 

injury is more frequent on the left side. This led 

him to conclude that most of these fractures were 

the result of an attempt to fend off a blow using 

the forearm (1910c:297). In support of this conclusion he sites the modern habit in Nubia of 

using a heavy staff for offense and defense. This 

habit appears to have an antiquity at least going 

back through dynastic Egypt. Wood-Jones 

(1910c:295) also reports that the incidence of 

forearm fractures is about twice that found in 

FIGURE 79.—Two healed depressed fractures in the right 

parietal of an adult female skull (arrows). Note lateral 

fracture lines radiating from the medial depression. (Specimen from Cinco Cerros, Peru, NMN H 293818.) 

FIGURE 80.—Probable healed, glancing, sword wound of the 

right parietal bone from a Twelfth Dynasty rock tomb at 

Lisht in Upper Egypt. Note central area of partially fiUedin, spongy bone of the exposed diploe. Arrows indicate the 

porous, reactive margin of the wound (NMNH 256414a.) 
NUMBER 28 77 

early twentieth-century. Western city populations. Other comparisons indicate fewer fractures 

of the lower leg in the ancient Nubian material 

in contrast with modern city dwellers. WoodJones attributes this difference to modern footwear, which increases slipping and which was not 

worn by the Nubians (1910c: 296). Another 

marked contrast with modern populations is the 

incidence of hand fractures, which is about 10 

times greater in modern city populations. Injuries 

from machinery appear to be a major factor in 

this difference (Wood-Jones, 1910c:297). In the 

New World, Hooton (1930:312) found a rate of 

3.96 percent fractures of long bones or pelvis in a 

skeletal series of 503 pre- and post-Columbian 

skeletons from the Pecos site in the North American southwest. When fractures of the skull are 

added, the total percentage increases to 7.23. 

Angel's findings (1974a: 13) in skeletal material 

of various time periods from the Eastern Mediterranean suggest an inverse relationship between 

cultural level and fracture incidence. However, 

this trend does not occur in modern populations 

in the United States, where the fracture incidence 

is almost twice that of ancient Eastern Mediterranean peoples. Like Wood-Jones, Angel finds 

that the most common site of fracture is the 

forearm, which he also attributes to an effort to 

parry a blow. This suggests that intentional violence is a major causative factor of fracture in the 

Eastern Mediterranean, as well as in Nubia. 

Courville (1967:621) reaches a similar conclusion 

with respect to cranial injuries in antiquity, noting that most wounds and fractures of the skull 

are the result of "blows of malicious intent." 

Earlier (p. 69), I have indicated that the basic 

concepts of fracture treatment do not require 

sophisticated knowledge and indeed reflect common sense procedures. It is not surprising then to 

find that immobilization of fractured bones with 

a splint was practiced at least as early as the Fifth 

Dynasty in Egypt (Elliot-Smith, 1908). Although 

much later in time, there is evidence of similar 

sophistication in treating fracture among the Incas of Peru (Daland, 1935:550). Wells (1974a) 

finds evidence for both reduction and splinting in 

Anglo-Saxon England (ca. eighth century A.D.). 

While recognizing that fracture treatment may 

have been fairly sophisticated in regions of ancient high civilization, it is equally apparent that 

many fractures, even in these areas, received little, 

if any, helpful treatment (Wood-Jones, 1910c: 

294). The large number of badly deformed, 

healed fractures from many archeological skeletons testifies to this (Figures 75-77). The fact that 

fractures heal spontaneously, allowing at least 

some continued function of the affected bone, is 

not surprising in view of the reports of healed 

fractures in wild shot primates (Duckworth, 1912; 

Schultz, 1939, 1956) where, obviously, there was 

no treatment. 

Evidence on the methods for treating fractures 

in archeological populations is scanty. However, 

among primitive and peasant groups living in 

historic times, there are records of fairly sophisticated techniques to reduce fractures (bring about 

optimal realignment of the broken ends) and 

immobilize the broken bone until healing can 

take place (Elliot-Smith, 1908:734; Daland, 1935: 

550). There is convincing evidence for the use of 

splints, pads to absorb blood in compound fractures, and linen bandaging by the Fifth Dynasty 

(2730-2625 B.C.) in ancient Egypt (Elliot-Smith, 

1908:732-733). Freeman (1918:445) reports that 

manipulation and splinting of fractures occurs 

among the indigenous peoples of North America 

as well. Elliot-Smith (1908:733) notes one case 

where the splinting did little to stabilize the fracture. This is not a serious indictment of their skill 

since, without X-ray examination and in the 

presence of considerable pain, it could be very 

difficult to identify the location of the fracture. 

With or without effective reduction and immobilization, most often the healing of fracture was 

uneventful. Elliot-Smith (1908:733) notes evidence of infection in only one case out of 100 

fractures in ancient Egyptian material. 

Injuries to the skull are rather common in 

archeological specimens. One type of skull injury 

is trephination, but because of its importance 

in antiquity this topic will be treated as a separate category of the paleopathology of trauma 
78 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

FIGURE 83.—Extensive radiating fractures from a central 

impact point (arrow) in an adult female skull from Pachacamac, Peru. (NMNH 266584.) 

FIGURES 81, 82.—Sword or axe wound in an adult male skull 

from a rock tomb at Lisht in Upper Egypt dated between 

the Twentieth and Twenty-fifth Dynasty: 81, The point of 

contact is the left parietal near vertex; the blow produced a 

large bone fragment largely in the parietal. 82, Skull with 

bone fragment reflected. (NMNH 256384.) 

FIGURE 84.—Compression fracture of the second lumbar 

vertebral body in an adult male skeleton from the Hawikuh 

archeological site in New Mexico, USA. (NMNH 308653) 
NUMBER 28 79 

FIGURES 85, 86.—Partial fracture of the third sacral segment 

(arrow) of specimen from the rock tombs at Lisht, Upper 

Egypt, dated between the Eighteenth and Twenty-first Dynasty: 85, Posterior view. 86, Detailed view; note partial 

bony fill-in of fracture gap and porous reactive bone (arrow) 

adjacent to the fracture line. (NMNH 252874.) 

(p. 95), although fracture is often the event that 

initiates the surgical procedure of trephination. 

Most of the fractures to the skull appear to be 

related to intentional violence rather than accident. An example of a depressed fracture in an 

adult male skull vault is seen in Figure 78. This 

FIGURE 87.—Compressed fracture of a first lumbar vertebra 

in a male specimen from the Saxon period at Cathedral 

Green, Winchester, England. Anterior view of lumbar vertebrae and sacrum. Note evidence of periosteal reactive bone 

on vertebral bodies. (BMNH CG66, XXIII, layer IV.) 

specimen (CG69, 697, 280 XXXIX) is from the 

medieval site at Winchester, England, and is 

stored at the British Museum (Natural History). 

The lesion is well healed, indicating long survival 

after the injury. 

An example of a more massive, healed fracture 

is seen in an adult female skull from Cinco Cerros, 

Peru (NMNH 293818). The archeological age is 

unknown. There are two large, depressed fractures both of which are on the right parietal 

(Figure 79). One of these is located near the 

sagittal suture on the posterior portion of the 

right parietal. Radiating out from this lesion are 

two fracture lines, one of which crosses the sagittal 

suture well into the left parietal bone. The other 

depressed fracture is located in the central portion 
80 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

FIGURES 88, 89.—Early stages of fracture healing and callus formation in the midshaft of an 

isolated left humerus from an Eskimo cemetery on St. Lawrence Island, Alaska, USA: 88, Note 

the porous nature of the recently formed callus. 89, X-ray film; note the radiolucent line (arrow) 

indicating the fracture line. (NMNH 364816-32) 

of the right parietal, superior to the squamous 

portion of the right temporal bone. This lesion is 

deeper and more extensive than the first lesion, 

but it does not exhibit the long, radiating fracture 

lines. Both lesions are completely healed, indicating long survival after the injury. 

A right parietal bone (NMNH 256414a) from 

the rock tombs at Lisht in Upper Egypt exhibits 

a circular lesion suggestive of a healed, glancing, 

sword wound (Figure 80). This specimen is dated 

to the Twelfth Dynasty. The outer boundary of 

the lesion is pitted, perhaps indicative of an inflammatory response. The sword wound apparently removed the outer portion of the parietal in 
NUMBER 28 !1 

the region of the parietal boss, exposing the diploe 

in the central portion of the lesion and creating 

the porous appearance, which was partially filled 

in by subsequent remodeling. 

Another specimen from the rock tombs at Lisht 

and dated between the Twentieth and Twentyfifth Dynasty (NMNH 256384) illustrates a lesion 

resulting from a sword or axe wound, which 

occurred at the time of death. The wound penetrated the left parietal bone near vertex (Figure 

81). The blow removed a portion of the right 

parietal bone (Figure 82). No postcranial bones 

are associated with this adult male skull. 

An adult female skull from Pachacamac, Peru 

(NMNH 266584) has an extensive unhealed fracture of the left parietal bone (Figure 83). The 

archeological age of this skull is unknown. The 

focus of the trauma is the anterior portion of the 

left parietal, which exhibits a crushing injury 

with fracture lines radiating down the left parietal 

along the coronal suture. A fracture of the left 

zygoma could have occurred at the time of the 

skull fracture. Another fracture line proceeds posterolaterally across the sagittal suture and into 

the right parietal. There is no evidence of healing, 

indicating that the blow came at the time of 

death. 

Three examples of fracture of the vertebral 

column serve to illustrate the essential features of 

such trauma in archeological specimens. The first 

of these is seen in the second lumbar of an adult 

male from the Hawikuh site in New Mexico, 

USA. This is a multicomponent site dating from 

the late prehistoric to early historic period. The 

anterior portion of the second lumbar vertebral 

body is crushed (Figure 84). There is fusion with 

the left lateral and central portions of the inferior 

border of the first lumbar vertebra and contact 

between large, bony projections from the inferior 

L2 and superior L3 vertebral bodies. The second 

example of fracture of the vertebral column is a 

male sacrum from Lisht in Egypt dated between 

the Eighteenth and Twenty-first Dynasty 

(NMNH 252874). The fracture occurs in the third 

sacral segment and radiates laterally from the 

superior portion of the spinous process (Figures 

85, 86). The fracture involves only a portion of 

the posterior segment and was in the early stages 

of healing at the time of death. Evidence of early 

callus formation can be seen in Figure 86. The 

third example of vertebral fracture is from the 

Saxon period at an archeological site in Winchester, England (BMNH CG66, XXIII, layer IV). 

The first lumbar vertebra is wedge-shaped on the 

left portion of the body (Figure 87). There is bony 

bridging between the right sides of the first and 

second lumbar bodies and considerable rotation 

of the axis of LI. The fracture is well healed 

indicating survival after the trauma. 

Fracture in the remaining postcranial bones is 

common in archeological specimens and should 

offer few problems in correct diagnosis. Evidence 

of a fracture line seen in an X-ray film will 

confirm such a diagnosis. This line will often be 

seen as a rather sharply defined radiodense line 

in the fracture callus. However, in some cases, 

particularly if the individual died within a few 

months following the trauma, the line may be 

radiolucent. An example of the latter is seen in 

an isolated left humerus from an Eskimo burial 

on St. Lawrence Island off the coast of Alaska 

(NMNH 364816-32). The archeological age of 

this specimen is uncertain. The fracture is located 

near midshaft with evidence for the fracture seen, 

externally, as a porous bony callus (Figure 88). 

The X-ray film appearance shows a general increase in radiodensity resulting from the callus 

added to the cortical bone. However, the radiolucent fracture line is apparent in Figure 89. 

Complications of Fracture 

Severe pain undoubtedly accompanies any attempt to reduce a fracture. Thus, even in those 

time periods and areas where fractures could be 

treated, it is not surprising to find numerous 

examples of malaligned, but healed, fractures in 

archeological skeletons. Wood-Jones (1910c) reports many such examples in his review of fractures in ancient Nubian skeletons. Wells (1974a) 

finds similar evidence in Anglo-Saxon England. 

Perhaps the important point to be made regard-
82 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

FIGURE 90.—Nonunion of a midshaft fracture of an isolated 

left radius. Specimen is from an archeological site at Jones 

Point on Kodiak Island, Alaska, USA. (NMNH 363688; 

scale in cm.) 

ing these deformations is that individuals having 

them generally continue to live and somehow 

compensate for the dysfunction that results. 

The failure of the broken ends to unite at all is 

more serious than malunion, primarily because of 

even greater malfunction, particularly if this condition occurs in a major long bone. Stewart (1974) 

has summarized the evidence for nonunion in 

archeological populations and published five 

cases from the ancient New World. He concludes 

(1974:878) that in both Egypt and America the 

forearm is the most common site of nonunion. 

This probably reflects the high frequency of fractures at this site. He notes that ulnar nonunion is 

higher in Egypt but nonunion of the radius is 

more common in New World material (Figure 

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FIGURES 91, 92.—Fracture and nonunion of the left femoral 

neck in an adult male skeleton from an Eskimo archeological 

site on Golovin Bay, Alaska, USA: 91, The fractured femoral 

neck has been pushed into the proximal metaphysis. 92, 

Detail of sclerotic reaction of the broken femoral neck and 

the corresponding cavity of the femoral metaphasis in above 

specimen. (NMNH 333453.) 

90). In both geographical areas the incidence of 

nonunion is low. 

In Stewart's survey all the examples of nonunion are from the upper extremity. While this 

probably approximates real conditions, it is important to note that nonunion does occur in the 

lower limb. In two cases I have studied (NMNH 
NUMBER 28 83 

FIGURE 93.—Fracture and nonunion of the left femoral neck 

in an adult male skeleton from Lisht in Upper Egypt dated 

from the Twelfth Dynasty. The fragmentary remains of the 

femoral head and neck are seen to the left. Note the extensive 

development of callus and the sclerotic remodeling in the 

cavity of the proximal femur. (NMNH 256580.) 

FIGURE 94.—Healed compound fracture complicated by infection in the right femur from a young adult female skeleton 

excavated from an archeological site near Akron, New York, 

USA. Note the deviated axis of the distal shaft at the fracture 

site. There is a large cloaca and reactive bone (arrow) 

probably associated with a fistula. (NMNH 326853.) 

333453 and 256580) the fracture and nonunion 

occurred in the neck of the femur. In both cases 

there is evidence of continued use of the limb 

with the fractured end of the femoral head and 

neck becoming embedded in the marrow space of 

the greater trochanter and proximal shaft (Figure 

91). One of these two examples (NMNH 333453) 

is from an Eskimo site in Golovin Bay, Alaska. 

The skeleton is that of an adult male between 20 

and 25 years of age. The archeological age is 

uncertain. The fracture occurred through the 

neck of the left femur. The X-ray film of both 

femora reveals considerable osteoporosis of the 

left femur shaft and diminished density of the 

nonunited femoral head, particularly in the medial half of the femoral head. The latter is suggestive of impaired circulation. There has been considerable remodeling activity on both sides of the 

fracture site (Figure 92). The second specimen 

(NMNH 256580) is from the site of Lisht in Egypt 

and is dated to the Twelfth Dynasty. The fracture 

occurred in the femoral neck of the left femur. 

There is exuberant callus formation around the 

fracture site (Figure 93) with extensive remodeling in the bone adjacent to the fracture. The 

individual was an old male and exhibits excessive 

osteoporosis of the fractured femur. The nonunited femoral head is damaged by postmortem 

breakage. In these examples of nonunion the 

weight of the body tends to force the broken end 
84 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

FIGURE 95.—Bony fusion of the distal tibia and fibula following fracture. (NMNH 383010.) 

of the femoral neck into the proximal shaft of the 

femur. This condition and the fibrous connective 

tissue undoubtedly present in the living individual permitted some use of the limb, but some 

disuse atrophy is evident in both specimens. 

Of the fractures occurring in archeological skeletons, very few show evidence of infection. In 

part, this observation must reflect the low incidence of compound fractures that would permit 

the passage of infectious organisms to the fracture 

site. Hamilton's data (1853), from a 19th-century 

American city population, summarized earlier in 

Table 1 indicate that 19 percent of the fracture 

cases in his sample are compound. Of all the 

compound fractures of the bones 63 percent involve the tibia and fibula. Thus, the lower leg is 

by far most vulnerable to compound fracture in 

the population. 

FIGURE 96.—Hypertrophic bone development, probably due 

to traumatic myositis ossificans, on the left femur of a Homo 

erectus (Pithecanthropus) skeleton from Java. (NMNH 

362452, cast of original specimen.) 

Infectious complication of fracture is not limited to compound fracture nor will all compound 

fractures become infected. However, the incidence of compound fractures gives some idea of 

the probabilities for infection of fractures in archeological populations. Wood-Jones (1910c) 

cites two examples of fracture complicated by 

infection. One is a clavicle (1910c:306), the other 

an ulna (1910c:313). He makes no mention of 

infection in fractures of the tibia or fibula. Indeed, 

fractures of the tibia of any kind are less common 

in archeological populations than modern civilized groups. Hooton (1930:312) found, among 

the prehistoric Pecos skeletal sample from New 

Mexico, USA, that the humerus and femur were 

the most commonly fractured long bones. He 

states that some fractures show a lack of union, 
NUMBER 28 85 

although he does not indicate whether this is due 

to death occurring shortly after fracture or to 

nonunion. Hooton also indicates that some fractures seem to have suppurated, indicating that 

they were complicated by infection. In the collections of the National Museum of Natural History, 

Smithsonian Institution, USA, there are several 

examples of fracture complicated by infection. 

These cases tend to show marked deformation 

suggesting considerable traumatic force, possibly 

indicating penetration of the skin by the fractured 

bone. One example of this complication of a 

compound fracture is seen in the skeleton of a 

young adult female from an archeological site 

near Akron, New York, USA (NMNH 326853). 

The archeological age is uncertain. The fracture 

is located in the distal shaft of the right femur. 

There is considerable axial deviation, as well as 

some rotation. The callus is massive with considerable porosity. On the posterior portion of the 

callus there is a large, oblong cloaca measuring 

15 by 25 millimeters (Figure 94). There is bony 

evidence of a fistula, which would have extended 

to the skin surface. The tibia of the same leg was 

also fractured but with good alignment and no 

evidence of infection. 

In archeological populations one finds arthritic 

deterioration occasionally associated with fracture. Although not specifically addressing this 

problem, Wood-Jones (1910c:308, 312, 315, 317, 

318, 322) cites several examples of fracture contributing to the development of arthritis. Morse 

(1969:100, 104) cites similar conditions in archeological specimens from the midwestern United 

States. Making the distinction between traumatically induced arthritis and degenerative arthritis 

depends on two factors: (1) demonstration of 

fracture in the affected bone and (2) lack of 

bilateral symmetry in the pattern and degree of 

arthritis (Morse, 1969:13). 

Trauma to adjacent bones may also result in 

ankylosis. An example of this condition is found 

in an historic period archeological specimen from 

South Dakota, USA (NMNH 383010), in which 

the distal tibia and fibula are fused in the area of 

a fracture (Figure 95). Clearly such an injury and 

its sequelae could have affected locomotion. 

However, the long-standing callus and extensive 

remodeling indicate long survival and an active 

life after trauma. 

The last factor complicating fracture to be 

discussed in this review is myositis ossificans. Perhaps the most famous example of this condition 

is the bone excrescence on the fossil left femur 

from Java (Figure 96) associated with Homo erectus 

(Pithecanthropus). In this specimen there is an 

exuberant growth of bone on the posterior aspect 

of the femur extending from the insertion of the 

adductor muscles. Wood-Jones (1910c:317) has 

published a line drawing of a right femur from 

Nubia with fracture of the femoral neck. There is 

an extensive, bony spur projecting medially, 

which Wood-Jones attributes to extensive callus. 

The extent and shape of the bony mass suggests 

ossification in muscle tissue rather than exhuberant callus formation. However, the distinction 

between the two may be academic. While the 

Java and the Nubian specimens have the bony 

growth attached, the paleopathologist should be 

aware that ectopic bone can develop in muscle 

tissue and be completely unattached to any bone. 

Dislocation 

PATHOLOGY 

The second major category of trauma involving 

the skeleton includes luxation, in which the joint 

constituents are out of contact and the joint 

capsule is disrupted. Subluxation is a less severe 

condition characterized by partial loss of the 

contact between joint components, but no disruption of the capsule. Both these conditions can be 

associated with fracture but often occur without 

fracture. Luxation and subluxation can occur in 

most joints. However, to be detected in an archeological specimen there must be permanent 

change in the skeleton. This means that subluxation will rarely be identified and luxation will 

be seen most often in joints where the anatomy 

makes spontaneous correction of the problem difficult. The two joints particularly prone to 
86 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

FIGURE 97.—Morphology of the components of a normal left 

shoulder joint. (Specimen from the Terry Collection 

(NMNH 382085-1600). 

chronic or permanent luxation are the shoulder 

and hip and I will focus on these to illustrate the 

problems associated with this type of trauma. 

The anatomy of the shoulder joint permits 

maximal movement of the arm in virtually all 

axes (Figure 97). This degree of movement is 

highly useful for the manipulative functions of 

the arm and hand. However, the biological trade 

off for this mobility is a relatively unstable joint. 

Rockwood (1975:624) notes that the glenohumeral joint is the most commonly dislocated major joint in the body. 

The bony components associated with the 

shoulder joint are the scapula, humerus, and 

clavicle. The round head of the humerus articulates with the glenoid cavity of the scapula. However, unlike the acetabulum of the hip, the glenoid cavity is little more than a slight depression, 

so that the humeral head rests against the joint 

surface but receives little support from it. The 

major support for the glenohumeral joint is the 

ligament and capsule attaching the humeral head 

to the scapula. Overlying these are the muscles of 

the rotator cuff and the deltoid, which also help 

to stabilize the joint. However, all these supportFIGURE 98.—Long-standing inferior dislocation of the right 

hip. A new acetabalum has been formed in the area of the 

obdurator foramen. The original acetabulum (arrow) shows 

considerable atrophy. (FPAM 3939.) 

ing structures are loose to permit optimal movement and thus can do little to prevent traumatic 

dislocation. 

Rockwood (1975:641) indicates that indirect 

force is the most common cause of glenohumeral 

dislocation. The mechanism by which the force is 

applied involves sudden, extreme movement of 

the upper arm away from the body (abduction) 

in association with external rotation as could 

happen in a backward fall in which the hands are 

used to break the impact. The effect is to drive 

the humeral head into the anterior capsule. 

Forces associated with this traumatic effect frequently produce a compression fracture as the 

edge of the glenoid cavity is forced into the head 

of the humerus (Rockwood, 1975:642). According 

to Rowe (cited in Rockwood, 1975:641), 96 per-
NUMBER 28 87 

cent of dislocations were traumatic in origin, 4 

percent are nontraumatic. Congenital defects in 

the bony structure or supporting ligaments and 

muscles appear to play a minor role in traumatic 

and nontraumatic dislocations. 

Because of the anatomy of the glenohumeral 

joint, spontaneous reduction of the dislocation 

often will not occur. Rockwood (1975:625-627) 

notes that the methods for reducing shoulder 

dislocations go back at least to the time of Hippocrates (ca. 430 B.C.). Thus, it seems possible 

that the treatment of dislocations could have 

existed in many archeological populations. However, it is also clear that unreduced dislocations 

do occur in archeological populations. In such 

situations a new joint surface is created where the 

humeral head comes in contact with the scapula 

and provides clear evidence of dislocation. 

While the anatomy of the hip permits considerable movement, its structure is influenced by its 

major weight-bearing function. In contrast with 

the glenohumeral joint, the hip is a classic ball 

and socket joint with the head of the femur deeply 

extended into the hip socket or acetabulum. 

While the ball and socket arrangement of the 

bony components suggests a more stable arrangement than is found in the glenohumeral joint, it 

is important to remember that the ligaments and 

muscles associated with the hip joint provide 

relatively less support than analogous structures 

in the shoulder. 

Unlike the glenohumeral joint, the hip joint 

components are joined directly by a ligament 

(ligamentum teres), which also contains the vascular supply for that portion of the femoral head 

adjacent to the ligament. Dislocation of the femoral head thus threatens the vascular supply of 

part of the femoral head. 

In congenital hip dysplasia, the acetabulum is 

abnormally shallow, creating a tendency for the 

femoral head to slip out of the socket in response 

to slight trauma or even walking. Such a condition may be recognizable in skeletal material due 

to the abnormally shallow acetabulum, although 

the tendency for the acetabulum to be remodeled 

after traumatic dislocation may make it difficult 

to make this distinction. The mechanism for traumatic hip dislocation varies, depending on the 

position of the leg and the direction of the force. 

Depending on these factors, dislocation of the 

femoral head may occur in an anterior or posterior direction with the latter being the most common in modern orthopedic practice (H. Epstein, 

1973:116). Reduction of hip dislocations is more 

difficult than reduction of the shoulder. The failure to reduce the dislocation will result in the 

formation of a secondary articular surface on the 

innominate (Figure 98). Since spontaneous reduction is less likely, identification of this type of 

trauma to the hip in archeological material 

should be fairly easy and should more accurately 

reflect the actual incidence of dislocations in the 

archeological population than evidence of shoulder dislocation. 

I have reviewed dislocation of only two of the 

major joints for illustrative purposes. The student 

of paleopathology interested in this subject should 

consult the orthopaedic source materials for a 

more comprehensive treatment. However, these 

two examples of dislocation reveal several principles that are associated with all dislocations: (1) 

Although there may be congenital factors involved, trauma is by far the most common cause 

of dislocation; (2) dislocation may be associated 

with fracture; (3) unreduced dislocation creates a 

secondary joint surface; (4) the evidence for dislocation in archeological samples reflects only a 

portion of the actual incidence of this type of 

trauma; (5) the blood supply to the bony part of 

the joint may be disrupted by dislocation, resulting in tissue death (aseptic necrosis); and (6) the 

trauma associated with dislocation may also tear 

the ligaments and muscles associated with the 

joint. 

PALEOPATH O LOGY 

Dislocation of the shoulder and hip should 

come to the attention of the paleopathologist 

more often than other types of dislocation, because of high frequency and problems in reduc-
88 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

FIGURES 99, 100.—Anterior dislocation of the left shoulder 

in an archeological specimen from Norton Bay, Alaska, 

USA: 99, The humeral head articulates with a new joint on 

the anterior surface of the scapula; there is some degeneration of the anterior glenoid fossa. 100, Secondary joint 

formation on the scapula; note porous surface of new joint 

surface and arthritic degeneration including eburnation (arrow) on the humeral head. (NMNH 346205.) 

tion, which make permanent dislocation more 

likely. In his survey of the Nubian skeletal materials, Wood-Jones (1910c:341) reports that evidence of dislocation is rare, with only one hip 

FIGURE 101.—Anterior dislocation and secondary joint formation of the left scapula in a male skeleton from Kodiak 

Island, Alaska, USA. Part of the glenoid fossa has been 

remodeled away and a new joint surface has been formed on 

the remodeled surface (arrow). There is considerable degenerative arthritis on the humeral head. (NMNH 363615.) 

dislocation in several hundred skeletons. He cites 

other cases but admits that the diagnosis is dubious. One case described by Wood-Jones is of an 

abnormal forearm (case 7:6) but probably is not 

a dislocation but a congenital malformation. Elliot-Smith appends to Wood-Jones report (1910c: 

342) a case of a traumatic knee dislocation associated with a fracture. 

I have studied several cases of dislocation found 

in the collections of the National Museum of 

Natural History. Most of the shoulder dislocations involve anterior luxation. One example of 

this type of luxation is from an adult male skeleton from Norton Bay, Alaska, USA (NMNH 

346205). The archeological age is uncertain. The 

left humeral head is completely displaced and 

articulates with the anterior surface of the left 

scapula (Figure 99). Continued use of the arm 

has resulted in the formation of a secondary joint 

on the scapula and arthritic degeneration and 

eburnation of the humeral head (Figure 100). 

Another example is from an adult male skeleton 

from Kodiak Island off the coast of Alaska, USA 
NUMBER 28 89 

(NMNH 363615). The archeological dating is 

uncertain. The dislocation in this specimen also 

involves the left shoulder. However, the luxation 

was not as severe, having stimulated a secondary 

joint on the anterior portion of the glenoid fossa 

(Figure 101). There is considerable arthritic degeneration on the humeral head. One example of 

posterior dislocation of the shoulder was found in 

a disturbed burial from an Early Bronze Age 

cemetery associated with the town site of Bab 

edh-Dhra in Jordan (Figure 102). A secondary 

joint was created on the posterior half of the 

glenoid fossa. There is evidence of arthritic degeneration and eburnation on the secondary 

joint. The humerus was not recovered. 

Figures 103 and 104 illustrate fairly typical 

FIGURE 102.—Posterior dislocation of the right shoulder in 

an isolated scapula from the Early Bronze Age site of Bab 

edh-Dhra in Jordan. The arrow indicates the ridge between 

the original joint surface to the right and the new joint 

formed after luxation. The new joint is porous and eburnated. (NMNH, no number.) 

changes associated with hip dislocation. The skeleton is from Kodiak Island, Alaska, USA 

(NMNH 372897), its archeological age is uncertain. Figure 103 shows the effects of the dislocation on the right innominate, comparing it with 

the normal left innominate. In both innominates 

the acetabulum is somewhat shallower than normal, suggesting a possible congenital predilection 

for dislocation. Figure 104 provides a detailed 

view of the secondary joint on the innominate 

rsMic.i»'-':S",.«L*CdHr?«i«s;^.i:^iaiiff_ii:'^"':^* ^ 

FIGURES 103, 104.—Luxation of the right hip (left side of 

figure) with secondary joint formation in an adult male 

skeleton from an archeological site at Jones Point, Kodiak 

Island, Alaska, USA: 103, The acetabulum is shallower than 

normal in both innominates. 104, Detailed view of porous, 

secondary joint surface on the right innominate of above 

specimen; note arthritic change on associated femoral head. 

(NMNH 372897.) 
90 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

and the degenerative changes on the femoral 

head. 

Deformation 

PATHOLOGY 

Thus far, I have largely focused on the effects 

of sudden trauma on the skeleton. However, 

chronic, low-grade trauma over an extended period of time can also modify the normal shape of 

bone. Such deformities are often, but not always, 

intentional. The basic principal to be emphasized 

is that any long-term, deforming pressure brought 

to bear on a bone or group of bones can result in 

permanent deformity, particularly if it occurs 

during the growth period. 

In relatively recent times perhaps the best 

known intentional deformity was the foot-binding 

practice of upper class Chinese women. In this 

practice the feet of female children were bound 

in such a way that the metatarsals were bent 

downward and compressed toward the heel of the 

foot. This created abnormal angulation of the 

tarsal bones and abnormal relationships between 

all the bones and joints of the foot (Figure 105). 

FIGURE 105.—Lateral view of artificially deformed, right 

foot in an adult, Chinese female resulting from foot-binding. 

The arch of the foot is greatly exaggerated with major 

changes occurring in the metatarsals. (WM SI7.1.) 

In modern skulls one occasionally finds the 

skull vault to be asymmetrical or the occipital 

bone flattened; such deformation may be intentional. In the modern skulls, however, there is no 

evidence of intentional pressure on the skull. 

Probably this deformity is the result of the individual sleeping in the identical position on a 

relatively hard surface during infancy and childhood. Such deformation illustrates the fact that 

slight, intermittant pressure over a long time is 

adequate to produce a gross deformity in a bone. 

PALEOPATHOLOGY 

Dingwall's review (1931) of cranial deformation indicates that artificial modifications of the 

skull was one of the most ubiquitous cultural 

practices in antiquity, being found on every continent except Australia. A comprehensive review 

of cranial deformation and other forms of artificial modification of bony structure is beyond the 

scope of this book. It is important, however, that 

cultural deformation not be confused with pathological processes, such as osteomalacia, which also 

can result in bones of abnormal shape. 

While several methods of producing cranial 

deformation exist, most modifications of skull 

shape are the result of applying pressure to various areas of the skull, namely: (1) the occipital 

region, (2) the frontal region, (3) both frontal and 

occipital regions (Figure 106), and (4) along a 

transverse axis, approximately passing through 

vertex, the mastoid region, and the region just 

above the insertion of the nuchal ligament on the 

occipital bone. This last type of pressure, utilizing 

circular bands, produces the circular or Aymara 

type of deformity (Stewart 1941:343) and proportionately lengthens the skull (Figures 107, 

108). 

The reason for the practice of cranial deformation is universally cosmetic and is frequently 

associated with physical manifestations of high 

social status. The origins of such practices are 

buried in the unknown past of the people who 

induced the deformation. Snorrason (1946) hypothesizes that abnormal, artistic representations 
NUMBER 28 91 

FIGURE 106.—Fronto-occipital artificial skull deformation in 

an adult female skull from an archeological site near Chavina, Peru. (NMNH 293691.) 

of heads during the reign of Akhenaten was due 

to the abnormal shape of the pharoah's head, 

perhaps resulting from acromegaly. Dingwall 

(1931:102) reports that cranial deformity in 

Egypt is unknown prior to the Eighteenth Dynasty and the reign of Akhenaten. The purported 

skull of Akhenaten (Dingwall, 1931, pi. Via) does 

show a rather long, low profile, particularly with 

regard to other skulls of that period from Egypt. 

Dingwall (1931:104) cites the opinions of ElliotSmith and Ferguson that the skull shows signs of 

hydrocephaly. 

The suggestion is that the unusual morphology 

of the pharoah's head led to the establishment of 

a new and temporary fashion, and that people 

deformed their childrens' heads to conform with 

this fashion (Dingwall, 1931:110). It must be 

emphasized that the evidence for this cranial 

deformation is limited to artistic representations 

FIGURES 107, 108.—Circular or Aymara type of artificial skull deformation, which results from 

circular constricting bands wrapped around the posterior half of the skull during the early 

growth phase of the individual: 107, Lateral view. 108, Top view showing somewhat elongated 

aspect of the deformed skull. (Specimen from Ancon, Peru, archeological age unknown, NMNH 

242844.) 
92 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOG Y 

and not observed on skulls. In spite of the speculative nature of this hypothesis the general influence of Akhenaten's appearance certainly influenced at least the portrayal of people during his 

reign—a practice that soon disappeared after his 

death (Snorrason, 1946:601). 

The broader implication of this account is the 

possibility that leaders with unusual skull morphology from natural causes might have given 

rise to a fashion in some societies which, unlike 

the case of Akhenaten, became a permanent part 

of the cultural tradition. 

The complications of cranial deformation are 

mainly cosmetic. However, Stewart (1948:71) 

suggests that compression may disrupt the normal 

growth that takes place at the skull sutures and 

can give rise to a depression in the sagittal region. 

This depression creates a bi- or tri-lobed appearance in the skull and could be confused with the 

results of a therapeutic practice producing the 

sincipital-T deformation (p. 102). McGibbon 

(1912) and Moss (1958) report minor anatomical 

abnormalities that are associated with cranial 

deformation. However, Moss (1958:248) emphasized that the magnitude of growth is not reduced. 

This suggests that the practice probably did not 

produce any serious problems. 

Scalping 

PATHOLOGY 

Traumatic avulsion of the scalp may be the 

result of accident or intentional violence. A welldocumented case of accidental scalp avulsion illustrates the gross morphological features of this 

trauma. The specimen is from the Pathology 

FIGURES 109, 110.—Accidental scalping in a female industrial worker from the early twentieth century: 109, The 

irregular external surface of the parietal bones is the bony 

response to infection and proliferation of granulation tissue 

during a 8-month period after the accident and before death 

due to septic meningitis. The arrow indicates the anterior 

margin of the lesion. 110, The inner table showing the region 

of the sagittal suture. Note the porosity indicative of an 

inflammatory response in this area. (PMES l.EB.l.(6).) 

^, 

110 
NUMBER 28 93 

Museum of the Royal College of Surgeons of 

Edinburgh (PMES l.EB.l.(6)) and dates from 

the early twentieth century. The specimen consists of the skull and mandible of a female jute 

weaver, aged 55 years. Her hair had been caught 

in the machinery, tearing the scalp from the 

parietal region but leaving it suspended by its 

frontal attachment. The scalp was replaced and 

sutured but became infected, leading to extensive 

sloughing and proliferation of granulation tissue. 

The infection led to septic meningitis and death 

occurred eight months after the injury. The outer 

table of the skull exhibits the irregular surface 

typical of the bony response to granulation tissue, 

as well as marginal porosity indicative of hypervascularity and inflammation. These changes are 

more extensive on the left parietal bone (Figure 

109). On the inner table there are many small 

pores along the sagittal sulcus, reflecting hypervascularity in this region as well (Figure 110). 

This case provides evidence on the extent of 

changes that can occur in eight months. Thus, 

relatively short-term survival after scalping might 

be expected to produce changes in the skull that 

could be identified in paleopathological specimens. 

PALEOPATH O LOGY 

Reese's (1940) review of the history of scalping 

indicates considerable antiquity for this practice, 

with the earliest reference found in the fourth 

book of Herodotus (485-425 B.C). The second 

book of the Maccabees (ca. 67-37 B.C.) describes 

the practice of scalping of living captives in Palestine. Reese reports that the Visigoths, AngloSaxons, and Franks practiced scalping, and it is 

noted among the North American Indians in 

1520 just 28 years after the European discovery 

of the New World. 

The question of whether the practice of scalping was introduced into the New World by the 

European colonists remains unresolved. Neumann (1940) reports a skull from central Illinois 

dated around A.D. 1000-1500, which has cut 

marks suggestive of scalping. Hamperl and 

FIGURE 111.—Probable example of scalping in a pre-Columbian adult female skull from the Sea Island Mound in 

Georgia, USA. The irregular surface of the skull vault is 

virtually identical with that seen in Figure 109. The anterior 

margin of the injury is indicated by the arrow. (NMNH 

379000.) 

Laughlin (1959:81) conclude that "there is little 

evidence for the antiquity of the practice in the 

United States." 

Possible evidence for the practice of scalping in 

pre-Columbian North America is seen in an adult 

female skull from the Sea Island Mound in Georgia, USA (NMNH 379000). The mound from 

which this skull was excavated is dated about A.D. 

1000. Although the possibility that the burial was 

intrusive cannot be excluded, such a possibility 

does not appear likely. The skull is well preserved 

and normal except for a large lesion involving the 

frontal and both parietal bones (Figure 111). The 

boundaries of the lesion are most pronounced on 

the frontal and anterior parietals. There is no 

evidence of active inflammation. All aspects of 

the lesion suggest a response to granulation tissue, 

but with good recovery and no infection at the 

time of death. There is no evidence of inflammation on the inner table. The morphology of 
94 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOG Y 

the lesion is compatible with a diagnosis of scalping. 

Regardless of the origin of scalping, it is well 

documented for many of the Indian tribes in 

various geographical regions of North America in 

early Colonial times. Catlin (1844:239-240) reports that the Colonists would pay for scalps of 

enemies both White and Indian. Indeed, he notes 

that a knife commonly used for scalping was 

made in Sheffield, England, and traded to the 

Indians for horses (Catlin, 1844:236). 

The scalp was removed to provide evidence of 

having killed an enemy. Nadean (1941:181-182) 

indicates that some tribal variation existed regarding the amount of scalp taken. Catlin (1844: 

30-31, 238) indicates that the scalp taken from 

"the place where the hair radiates from a point" 

was most important but that scalp from other 

areas would be used to decorate clothing in some 

tribes (e.g., Blackfoot). In removing the scalp, the 

skin would be cut around the desired area and 

pealed off The initial cutting may have left 

marks on the skull whether or not the victim was 

dead (Owsley, Berryman, and Bass, 1977). 

Catlin (1844:239), Reese (1940:16), and Nadean (1941:193) report that survival after scalping did occur. Reese (1940:18-19) included in his 

paper a report by a physician who treated a case 

of scalping by Cheyenne Indians in 1867. The 

report indicates that the scalp was removed, the 

periosteum covering the skull cut and badly damaged. The outer table was exfoliated (shed), after 

which the wound healed. Hamperl and Laughlin 

(1959:88), in commenting on this case, suggest 

that the destruction of the periosteum deprived 

the outer table of its superficial blood supply. 

This resulted in necrosis with granulation tissue 

in the diploe eventually separating the necrotic 

tissue from the skull. An archeological specimen 

showing a lesion probably reflecting this same 

process is reported by Hamperl and Laughlin 

(1959). 

Mutilation 

Among historical preliterate groups mutilation 

of the body involves the soft tissues, teeth, and 

bone. In this section we shall only review mutilations of bone. Dental mutilations will be discussed, but soft tissue mutilations are beyond the 

scope of this book. 

Mutilation affecting bone may be voluntary, 

in which the victim either performs the mutilation on himself or willingly allows it to be performed by someone else. Involuntary mutilations 

are usually associated with punitive action 

against a criminal or a captive. Moodie (1920: 

1300) has published Aurignacian (ca. 20,000 B.P.) 

cave art from Gargas, Spain, suggesting finger 

amputations in that period. He further reports 

(1920:1303) the existence of finger mutilation 

throughout the world. In the Old World, the 

most commonly reported reason for finger mutilation is as a symbol of mourning. Among the 

North American Indians it was part of initiation 

rites. 

Major portions of one or more limbs have also 

been removed. Brothwell and M0ller-Christensen 

(1963b) report a case of amputation with subsequent healing of the stump of the distal right 

forearm from Egypt dated 2000 B.C. They offer 

three possibilities for the cause of the mutilation: 

(1) injury during warfare, (2) punitive action 

against a criminal or captive, and (3) surgical 

amputation for therapeutic reasons. While punishment for criminal behavior remains a possibility, Aldred (1964:56) challenges the likelihood 

that the Egyptians would have cut off the hand 

of a captive. He notes that to do so would have 

deprived the captors of a valuable spoil of war: 

the slave labor. He further notes that amputation 

of the hand was limited to the dead and dying 

victims of warfare and was used as a method of 

recording the dead from the field of battle. In 

another report Brothwell and M0ller-Christensen 

(1963a) described an amputation of the distal left 

forearm in a skeleton from Sicily dated to the 

seventh century A.D. The ends of the radius and 

ulna have fused, indicating healing. They conclude that the amputation was punishment for a 

criminal act—a practice common also in that 

age. Stewart (1950:43) reports the existence of 

bones showing amputations from Peru but does 

not indicate which bones are involved. 
NUMBER 28 95 

While there seems to be convincing evidence 

that both voluntary and involuntary mutilation 

of bony parts of the skeleton did occur in antiquity, a word of caution is appropriate regarding 

unequivocal interpretation. With respect to missing fingers or toes in an archeological specimen, 

at least two other conditions could be implicated. 

These are infectious disease (particularly leprosy) 

and frostbite. Amputation of the distal forearm 

or distal leg should also be reported with caution. 

Stewart (1974:889-890) calls attention to the 

morphological similarity between the skeletal 

manifestation of pseudarthrosis and what might 

be expected in an amputation. He suggests that 

bony fusion of the distal radius and ulna in the 

case reported by Brothwell and M0ller-Christensen (1963b) might be more reasonably explained 

by fracture and nonunion. Diagnosis in this case 

is complicated by the fact that the fused radius 

and ulna are isolated bones, raising the possibility 

that the distal portion of the specimen, if it was 

a case of nonunion, had not been recovered. 

Trephination 

HISTORY 

Perhaps the most remarkable trauma seen by 

the paleopathologist is trephination or the surgical removal of a portion of the skull. The earliest 

written accounts of trephination are found in the 

Hippocratic writings (460-377 B.C.). However, 

the evidence of trephining goes back at least to 

the Neolithic period (Moodie, 1919:484; Guiard, 

1930; Parry, 1931; Hrdlicka, 1939; Stewart, 

1958b:470; Oakley, Brooke, Akester, and Brothwell, 1959:93). It continues to be practiced among 

many recent, primitive peoples (Ruffer, 1918a: 

99-102; Freeman, 1918:445; Moodie, 1919:485; 

Hrdlicka, 1939; Oakley, Brooke, Akester, and 

Brothwell, 1959). The geographical distribution 

of the practice is extensive, including Europe, the 

Pacific, North Africa, the Middle East, and South 

America (Stewart, 1958b:470-480). Wood-Jones 

(1910c:299) states that trephining has not been 

reported in ancient Egyptian skulls. However, he 

saw no reason why trephined skulls should not 

have been found in Egypt in view of the contact 

with Greece where it was practiced in antiquity. 

Ruffer (1918a:95) published a photograph of a 

purported trephination from Egypt. Moodie 

(1919:485) has expressed reservations regarding 

Ruffer's case and further states (p. 494) that 

trephining did not occur among Greeks, Romans, 

Phoenicians, Babylonians, or Egyptians. More 

recently Oakley, Brooke, Akester, and Brothwell 

(1959:95) report a case of trephination from Tarkhan, Egypt, dated to early dynastic times. Clearly 

the Greeks of the Periclean Age performed trephination (Withington, 1927:3) and the strong 

evidence of trephination in Palestine suggests that 

the practice occurred in Middle East countries. 

Mallin and Rathbun (1976) have reported a case 

of trephination in ancient Iran. In any case, the 

practice in the Middle East appears to be relatively rare, certainly by comparison with South 

America, where over 1000 cases of trephining 

have been found (Stewart, 1958b:474). 

There is debate regarding the practice of trephination in pre-Columbian North America. 

Stewart (1958b:476-479) surveyed 17 purported 

cases and concluded that evidence for trephination in North America had not been demonstrated. One of the factors contributing to the 

controversy is the difficulty of conclusively identifying a trephination in an archeological specimen. Given a partial or complete hole in a skull 

there are several possibilities for the cause. Goldsmith (1945:348) suggests that some of the socalled examples of trephination are, in reality, 

cases of congenital, bilateral openings of the parietal bones (p. 352). This condition is a hereditary enlargement of the parietal foramina (Goldsmith, 1945:350). Other congenital conditions 

such as dysraphism (p. 351) can be confused with 

trephination. Both infection and neoplasm can 

produce holes in the skull, which might be confused with trephination. Injury such as a glancing 

sword or axe wound can remove a portion of the 

skull and produce a healed lesion similar to trephination. Furthermore, a trephine-like wound 

may not have been part of a surgical procedure 

on the living. Some groups apparently practiced 

postmortem removal of circular pieces of skull 
96 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOG Y 

(Ruffer, 1918a:91, Parry, 1931:1388-1389; Stewart, 1958b:475). Obviously, no healing would 

have occurred, but polishing of the edges by 

intentional or unintentional rubbing can create 

a superficial appearance of healing (Stewart, 

1958b:477). 

It is clear that the identification of the cause of 

holes in the skull cannot always be made. However, there are some criteria that will be important in any analysis. The first question to be 

resolved is whether the hole is the result of mechanical intervention. Evidence for cutting or 

scraping may still exist even if healing has taken 

place. The next problem to be clarified is if the 

cutting was done before or after death. The significant question here is whether we are seeing 

the product of a surgical procedure or the result 

of some postmortem ritual. Any evidence of healing or inflammatory reaction to the cutting is 

indicative of trephination. However, it is possible 

that a patient can die during the trephination or 

so soon after it that no reaction takes place. Such 

a situation in an archeological example of trephination may be indistinguishable from postmortem ritual removal. In such situations the 

demonstration of unambiguous trephination in 

the same geographical area would certainly be 

significant in interpreting the equivocal cases. 

Another important criterion is the presence of 

fracture in association with evidence of cutting. 

Many, if not most, trephinations occur in association with skull fracture. As with most other 

problems in paleopathology careful observation 

combined with a comprehensive knowledge of 

the options is the most important prerequisite in 

determining the presence of trephination. 

In trephination, four basic responses can occur. 

First, in those cases where trauma preceded the 

trephination procedure, death may be due to the 

initial trauma. Second, the surgical procedure 

itself may cause death. Third, the surgical procedure may not directly cause death but may 

introduce disease organisms that cause infection 

and possibly death. Fourth, there may be no 

complications resulting from surgery, in which 

case the individual survives with varying degrees 

of repair to the surgically induced defect. If there 

is no healing, as evidenced by the lack of remodeling of the cut edges or fill in of exposed, diploic 

spaces, the reasonable assumption is that death 

occurred at the time of, or shortly after, surgery. 

A zone of porous, reactive bone surrounding the 

surgical area suggests survival for some time after 

surgery, but with the possibility of infection complicating the healing process and causing death. 

Partial to complete refill of the surgical defect is 

indicative of recovery and long-term survival 

after surgery. 

PALEOPATHOLOGY 

Freeman (1918:445) remarks, somewhat whimsically, that trephination in ancient populations 

was probably no worse "than the torture occasionally inflicted on us by our dentist." Nevertheless, the pain involved, as well as the threat to life 

inherent in the procedure, raise inevitable questions regarding the biological or cultural reasons 

for trephination. Broca (1876:572) suggested that 

trephination was performed as a cure for mental 

disorders. Ruffer (1918a:91) states that in Europe 

until the Middle Ages, powdered cranial bone 

was thought to possess curative properties. He 

also states that roundels (circular pieces of human 

skull) were worn as ornaments as late as Gallic 

times. Parry (1931:1388) asserts that Neolithic 

man performed trephination "as a religious rite 

ridding an affected individual of some demon or 

demons "H e also indicates (1931:1388-1389) 

that amulets were made from the trephined skulls 

of deceased individuals, which included healed 

edges of the trephination. Stewart (1958b:481) 

suggests that this practice is limited mainly to 

Europe. More recently Oakley, Brooke, Akester, 

and Brothwell (1959:93) have supported the concept of the ritual significance of trephination, 

citing Albert Schweitzer's observation in modern 

African tribes that trephination is used to obtain 

a powerful fetish object. 

While the evidence for religious implications in 

trephination appears convincing, it is equally 

clear that trephination was also a surgical procedure done to correct a serious medical problem. 
NUMBER 28 97 

The Hippocratic writings (Withington, 1927:3, 

35) indicate that trephination was well known 

and practiced in the Golden Age of Greece (ca. 

500 B.C.) for relief of the effects of skull fracture. 

The expertise of the technique revealed in the 

discussion suggests even greater antiquity for trephination as a treatment of skull trauma. 

It should not be surprising to find trephination 

practiced for therapeutic treatment of skull fracture in other geographical areas and time periods. 

Moodie (1919:484) suggests that this is the reason 

for trephination in primitive societies. Hrdlicka 

(1939:175) notes that "a very large proportion of 

aboriginal trephinings in America were true surgical or curative operations for the relief of the 

effects of head wounds or for that of actual or 

supposed pathological conditions within the 

skull." Stewart (1958b:481) concludes that relief 

of pressure from skull fracture was the most frequent reason for trephination in Peru and Melanesia. Oakley, Brooke, Akester, and Brothwell 

(1959:93) indicate a similar rationale for trephination practiced by medicine men in Bolivia in the 

1950's. 

Types of Trephination 

Trephinations vary in terms of the extent of 

bone removed, the depth to which bone is removed, and methods used. The extent or area of 

bone removal varies with the size of the injury 

and the judgment of the surgeon. The depth of 

bone removal appears to reflect two possibilities: 

(1) the surgeon can remove the outer table of 

bone and diploe or (2) he can remove both tables 

of bone, exposing the dura. In ancient Greece, 

surgeons were conscious of the dangers of penetrating into the dura (Toole, 1964:91-92), and it 

is likely that such knowledge would quickly be 

acquired and disseminated. 

The methods of trephination have been reviewed by several scholars (e.g.. Parry, 1931, 

1936; Hrdlicka, 1939; Stewart, 1958b; Oakley, 

Brooke, Akester, and Brothwell, 1959). From 

these reports it is clear that the most widely used 

method was careful scraping through the bone 

with a sharp implement to the desired depth 

(Figures 112-114). This method undoubtedly involved the lowest risk of damaging the brain and 

is found in all geographical areas where trephination occurs. Other methods included drilling a 

circle of small holes and breaking or cutting the 

intervening bone and sawing or cutting directly 

into the bone (Figures 115, 116). Both these methods involved considerable risk to the brain. Eloquent testimony to this risk is seen in unhealed 

trephination of this type indicating that death 

occurred during, or shortly after, surgery (Figure 

117). Initially the direct cutting type of trephination was thought to occur only in the New 

World; however. Parry (1936:170-171) reports 

this type of trephination in Palestine. 

The surgical approach for trephination required that the overlying skin be cut, unless it 

was already cut by injury. Stewart (1958b:483) 

suggests that in some cases a portion of the scalp 

would be removed entirely. In modern cases from 

Melanesia the skin is reflected back, the bone 

removed and the skin replaced over the trephine. 

He notes that the incision into the scalp may 

produce scratches on the underlying bone and 

can occasionally be seen peripherally to the trephine indicating the extent of scalp removal. 

Complications of Trephination 

There are two major potential problems arising 

from trephination: (1) direct injury to the brain 

resulting from improper method or poor technique, and (2) infection. Either of these complications can cause death. Moodie (1919:481-485) 

estimates the total mortality rate from trephination at 50-75 percent as compared with a rate of 

15-18 percent in civilized modern populations in 

the early 1900's. Hrdlicka (1939:175) is much 

more optimistic regarding the outcome of trephination, expressing the opinion that complications, including infection, were rare. Piggott 

(1940:122) and Stewart (1958b:486) support this 

opinion. Stewart reports that of 214 operations he 

studied, 55.6 percent show healing, 16.4 percent 

show slight healing, and only 28 percent show no 
98 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

FIGURES 112-113.—Trephination by scraping in an adult 

male skull from Lupo, N. Huarochiri, Peru: 112, The lesion 

is confined to the frontal bone; note the marks of the scraping 

at the margin of the lesion (arrow) ) and that most of the 

inner table was left intact. 113, Detail of trephination. This 

case shows evidence for the association of trephination and 

previous trauma to the skull; note the edge of fractured bone 

(arrow). The large hole is probably due to the removal of a 

fractured fragment during surgery. There is no evidence of 

healing, indicating that the patient died during or shortly 

after trephination. (NMNH 293643.) 

FIGURE 114.—Healing after trephination by scraping in an 

adult female skull from Cinco Cerros, Peru. Arrow indicates 

the outer margin of the lesion. (NMNH 293794.) 

healing. With respect to the slightly healed and 

unhealed cases, it is important to note that they 

may have died from causes other than the surgery. This is particularly possible if the trephination was done to alleviate the complications of 

skull fracture. 

A case of partial trephination from Peru 

(NMNH 293782) illustrates the problem of determining the sequence of events that produced a 

specific condition on the skull. The large lesion is 

primarily on the left portion of the frontal bone 

(Figure 118). The lesion consists of a central bony 

sequestrum containing a single trephine cut, 

which extended through both tables. The sequestrum is surrounded by an almost purely lytic 

zone, which grades into the large porous area 

characterizing most of the lesion. On the left 

boundary of the lesion, the margin between normal and abnormal bone is sharply defined. In the 

remainder of the lesion the boundary is not well 

defined. The fundamental question is what produced the marked inflammatory reaction in the 

bone? The lesion could be a response to infection 

following the aborted attempt at trephination. In 

my opinion, a more likely possibility is an injury 

to the skull that resulted in tissue death and 
NUMBER 28 99 

FIGURE 117.—Extensive trephination by cutting in an adult 

male skull from Cinco Cerros, Peru. There seems to have 

been some indecision on the part of the surgeon about the 

appropriate place to cut. There is no evidence of healing, 

suggesting that the patient died during or shortly after 

surgery. The somewhat indecisive nature of the trephination 

suggests the possibility of experimentation, perhaps on a 

cadaver. (NMNH 293785.) 

FIGURES 115,116.—Trephination by cutting in a child of 

about 8 years of age from Cinco Cerros, Peru: 115, There is 

clear evidence of association with cranial trauma. Note the 

long circular fracture (arrow) adjacent to the trephine and 

the radiating fracture line extending inferiorly and posteriorly from the circular fracture. 116, Radiating fracture line 

in the base of the skull continuing the fracture line seen on 

the lateral aspect of the skull. There is no evidence of healing 

of the fracture or the trephination indicating death during 

or shortly after surgery. (NMNH 293315.) 

FIGURE 118.—Injury from blow to the skull followed by 

necrosis and sequestration of bone (arrows) near the point of 

impact. There is hypervascularity peripheral to sequestrated 

bone, which contains evidence of an aborted trephination 

with a single cut through the sequestrated bone. (NMNH 

293782.) 
100 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOG Y 

sequestration of bone near the point of impact 

and a marked, inflammatory reaction to the 

trauma in the surrounding tissue. This process 

may have been complicated by infection. Surgical 

intervention was not completed, perhaps because 

of the poor condition or death of the patient. 

Traumatic Problems Arising from Pregnancy 

PATHOLOGY 

Pregnancy and particularly traumatic complication of pregnancy that threatens the life of a 

mother is difficult to document in skeletal remains. Evidence for pregnancy, or at least parturition, is thought to be seen in the pitting and 

erosion of the pubic bones adjacent to the pubic 

symphysis (Putschar, 1931, 1976b; Angel, 1969a; 

Stewart, 1970; Gilbert and McKern, 1973). Even 

demographic data suggesting increased female 

mortality (e.g., Acsadi and Nemeskeri, 1970:251) 

does not provide unequivocal evidence of increased death directly due to pregnancy and 

childbirth. Wells (1975) argues that death due to 

pregnancy may have been high in Europe from 

the seventeenth to the early twentieth century 

when widespread rickets produced unusually 

high mortality from obstructed parturition. He 

states that rickets was not widespread before the 

seventeenth century and that complication from 

pregnancy may have been too rare to account for 

the high female mortality. Wells attributes differential female mortality to the cultural practice of 

males having nutritional needs met first, with 

females getting less and poorer quality food, particularly during periods of famine. 

In contemporary developing countries, death 

due to complications of pregnancy accounts for 

about 10 percent of female deaths during the 

childbearing period from 15 to 44 years of age 

(World Health Organization, 1976). Thus, while 

it may be inappropriate to attribute all the difference between male and female life expectancy 

to the hazards of pregnancy, it does constitute a 

significant threat to life today and probably did 

so in antiquity. 

Although death during pregnancy may occur 

due to any number of reasons, including obstructed labor, infection, or hemorrhage, it is 

difficult to estimate how these hazards relate to 

ancient populations. Indeed, it is likely that the 

knowledge and experience needed to minimize 

mortality varied significantly in ancient societies. 

In obstructed labor the problem may be the 

result of the pelvic outlet being too small for the 

infant or an abnormal presentation of the infant 

during delivery. In modern clinical practice the 

physician has several options available to alleviate this problem and complications arising from 

it, including surgical intervention and forceps 

delivery. These options were not generally available in populations whose skeletons are studied 

by the paleopathologist. Therefore, obstructed 

labor would have been a serious threat to life, 

although midwives or their analogue in modern 

primitive and peasant societies, show rather remarkable skill in successfully assisting a complicated delivery. 

Implantation and development of the fetus in 

any place other than the uterus is known as 

ectopic pregnancy. Willson, Beecham, and Carrington (1971:180) indicate population differences in frequency. However, in the general U.S. 

population incidence is one in about 80 normal 

intrauterine pregnancies. Termination generally 

occurs in 6 to 16 weeks and is accompanied by a 

rupture of the fallopian tube, where the fetus is 

most often implanted in ectopic pregnancy. The 

rupture is associated with profuse bleeding which, 

without surgery, almost always will cause death. 

In the early 20th century, the mortality was 

between 10 and 15 percent for such pregnancies 

(Willson, Beecham, and Carrington, 1971:188). 

However, much higher mortality would be expected in more primitive societies. If the fetus 

continues to full term there is a serious problem 

in delivery which must be done by surgical removal of the infant, an option not available in 

most ancient societies. 

Pregnancy increases the risk of infection, which 

represents a serious hazard to both mother and 

the developing fetus. There are, for example. 
NUMBER 28 101 

some urinary tract infections that seem to be 

exacerbated by pregnancy (Willson, Beecham, 

and Carrington, 1971:272). The childbed fever 

scourge, with its high mortality in the obstetric 

hospitals of the eighteenth and nineteenth centuries, may not have caused significant mortality 

in ancient populations (Wells, 1975:1240). However, women are particularly prone to infection 

through the genital area immediately following 

childbirth. 

Hemorrhage during pregnancy or childbirth 

can be caused by several conditions. I have already noted this problem in association with ectopic pregnancy. Postpartum hemorrhage occurs 

in about 5 percent of normal deliveries. It is also 

associated with improper implantation of the placenta in the lower region of the uterus (Willson, 

Beecham, and Carrington, 1971:318). 

Willson, Beecham, and Carrington (1971:306) 

report that 7 to 10 percent of all pregnancies in 

the United States are complicated by toxemias. 

One-half of these is due to high blood pressure, 

the other half is due to a poorly understood 

condition called preeclampsia and its more serious form eclampsia. Eclampsia is characterized 

by convulsions or coma. Mortality in the United 

States for advanced stages of preeclampsia and 

eclampsia is 10 percent, making it a fairly serious 

threat to pregnant women. Presumably the mortality would be even higher in populations that 

do not have access to modern therapeutic means. 

PALEOPATHOLOGY 

The conditions that cause death during pregnancy rarely leave any evidence in the skeleton. 

However, this brief summary of the more serious 

complications of pregnancy should alert the paleopathologist to these conditions when there is 

evidence of fetal or newborn skeletal materials in 

association with an adult female burial. 

Elliot-Smith and Wood-Jones (1910:260) report from ancient Nubia five cases of female 

skeletons with deformed pelves, in which death 

occurred during pregnancy and possibly labor. 

Acsadi and Nemeskeri (1970:253) report twelve 

similar cases from Hungary, although Wells 

(1975:1238) challenges their interpretation and 

suggests that only two of these cases were deaths 

resulting from childbirth itself Wells, however, 

does not rule out other complications of pregnancy, such as erysipelas or meningitis as a cause 

of death. Sj0vold, Swedborg, and Diener (1974) 

report a case of death due to childbirth in a 

woman having multiple exostoses blocking the 

birth canal. Hawkes and Wells (1975) report a 

case of a female burial with a baby's skeleton still 

partially in the pelvis. They conclude that death 

took place during childbirth. 

Unambiguous archeological examples leave little doubt that awareness of this problem and 

attention to careful excavating technique make it 

possible to reconstruct a traumatic event. However, Wells correctly cautions against the assumption that all examples of infants buried with a 

female skeleton or fetal bone lying inside the 

abdominal region are indicative of death due to 

pregnancy and childbirth. A pregnant woman 

can die of infectious diseases and several other 

conditions not necessarily related to pregnancy. 

One should also keep in mind that labor and 

childbirth may be traumatic to the infant even 

when delivery is completed. Evidence for such 

trauma will probably be uncommon in archeological materials, since severe trauma would result 

in the immediate death of the infant. In modern 

clinical practice difficult labor may be assisted by 

instrument delivery, in which the infant is physically drawn out of the mother with large forceps. 

Such intervention may injure the tissues of the 

infant and produce hematoma. When this occurs 

on the skull, the outer portion of the hematoma 

may ossify, creating a thin shell of bone. While 

the events leading to this specific problem are 

unlikely to occur in archeological popiilations, 

the morphological features seen in such problems 

serve to illustrate what might be seen if an infant 

were injured in some other way during delivery. 

Two cases from recent times provide examples 

of ossifying hematoma in infant skulls. Figure 119 

shows a large hematoma on the left parietal in a 

case from the Federal Pathologic-Anatomy Mu-
102 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

FIGURE 119.—Ossified hematoma on the left parietal of an 

infant who died several weeks after birth. Note that the shell 

of the hematoma does not cross the suture. (FPAM 5192.) 

seum, Vienna (FPAM 5192). The skull is from an 

infant who died shortly after birth in 1890. Note 

that the hematoma does not cross the suture lines. 

The second case is from the same museum 

(FPAM 5712). The skull is from an infant about 

four weeks of age at the time of death. The 

trauma giving rise to the ossifying hematoma 

over the right parietal occurred during delivery 

(Figure 120). The delicate nature of the ossifying 

outer shell is apparent. The underlying bone is 

porous, indicating change in the cortical bone in 

response to the injury and overlying hematoma. 

Sincipital-T Mutilation 

The skull lesions thought to be associated with 

cautery in the treatment of mental illness were 

first brought to the attention of anthropologists 

by Manouvrier (1895). He used the term "Tsincipital" to describe the lesion. What appears 

on the skull is a depressson in the shape of a T or 

a cross in which the vertical portion of the T is 

associated with the sagittal suture while the cross 

bar on top of the T is often associated with the 

lambdoid suture. 

FIGURE 120.—Ossified hematoma on the right parietal of an 

infant about 4 weeks of age. Hematoma is the result of 

trauma during birth. Note the delicate nature of the outer 

shell of bone and the porous appearance of the underlying 

cortical bone, (FPAM 5712) 

FIGURE 121.—Atrophy of the skull in the region of the 

sagittal and lambdoid sutures (arrows). The inner table is 

normal (NMNH, no number.) 
NUMBER 28 103 

In Europe, skulls with these lesions were found 

in skeletons of the Neolithic period (Manouvrier, 

1895). Zaborowski (1897) reports similar findings 

in central Asia. Moodie (1921) and Weiss (1955) 

report the sincipital-T pattern in ancient Peruvian skulls. However, Stewart (1958b: 480) cautions against interpreting any large bone scar as 

the result of cautery. 

Virchow (cited in MacCurdy, 1905:20) suggested that a tartar-emetic ointment smeared on 

the scalp could produce scarring and affect the 

bone. However, weight is lent to the hypothesis 

of cautery being the cause of the lesion by Avicenna's medieval prescription of melancholia in 

which "the head is to be cauterized in the form 

of a cross" (MacCurdy, 1905:23). Most often the 

lesion resulting from cautery did not expose the 

dura (MacCurdy, 1905:17-18), although at least 

one specimen exists in which the sincipital-T 

defect in part penetrated through both tables of 

the skull. 

There is also a possibility that senile atrophy 

can occur in the sagittal and lambdoid sutures. 

Atrophy in this location would produce a depression very similar to the changes reported for 

sincipital-T mutilation. One skull from a prehistoric site (Irene Mound) in Georgia, USA 

(NMNH unumbered) exhibits a depression in the 

posterior sagittal suture and much of the lambdoid suture (Figure 121). The inner table is normal. The skull appears to be that of a female over 

50 years of age with considerable antemortem 

tooth loss. There is evidence of senile atrophy 

medial to both temporal lines suggesting that 

senile atrophy is a likely explanation for the 

atrophy of the sutural areas. 
Infectious Diseases 

The Inflammatory Response 

The inflammatory response to infection begins 

as a vascular phenomenon. The capillaries dilate 

and their walls begin to allow the escape of large 

molecular proteins and cells normally retained in 

the circulation. Albumins, globulins, and fibrinogen enter the tissue where fibrinogen is converted into fibrin. This is followed by active 

emigration of neutrophilic leucocytes, which are 

capable of amoeboid motion and thereby can 

squeeze through moderately enlarged pores in the 

vascular wall. In the tissue they migrate, by 

chemotactic attraction, to the bacterial focus. It 

is these leucocytes, in connection with proteins 

and fibrin, which make up the pus of acute 

infections. Many leucocytes ingest bacteria by 

phagocytosis and may inactivate or destroy them; 

others succumb to bacterial toxins and disintegrate. The severity of inflammatory response is 

proportional to the number and virulence of infecting organisms. If the capillary leakage becomes gross, erythrocytes, which have no active 

mobility, may also enter the tissue in large numbers. Thus, it is customary to classify the inflammatory response by the type of exudate as serous, 

fibrinous, hemorrhagic, or purulent, reflecting the 

increasing severity of the infection. After the 

acute phase other cells, from the blood and from 

the tissue, participate in the inflammatory response. Lymphocytes and plasma cells particularly, involved in the cellular and humoral immune responses, appear in increasing numbers in 

and around the lesion in the subacute and chronic 

phases of infections. 

Histiocytes and macrophages of the tissue are 

mobilized and serve in cleaning up infected areas 

by means of phagocytosis of debris and of organisms. Multinucleated symplasts, so-called giant 

cells, may appear in this phase. The healing is 

mainly accomplished by proliferation of fibroblasts laying down collagen, which is the main 

constituent of scar tissue. In infections that have 

a component of allergic reactivity, as, particularly, in parasitic diseases, eosinophilic leucocytes 

may be prominent in the immediate inflammatory response. In viral infections, where the organisms propagate intracellularly and offer no 

opportunity for phagocytosis, the initial leucocytic response as well as the formation of pus is 

usually lacking. Lymphocytes, plasma cells, and 

macrophages dominate the picture even in the 

acute phase, mainly in response to the breakdown 

of infected tissue cells. 

Organisms that are difficult or impossible to 

control by the ordinary cellular defense mechanisms discussed above produce the so-called granulomatous response to infection. Such organisms 

are the acid-fast mycobacteria of tuberculosis and 

leprosy, many of the fungi, and treponemal infections. In these infections histiocytic proliferation 

around organisms form nodular foci. Multinucleated giant cells phagocytose organisms but often 

are not able to kill them. Thus, the center of the 

granuloma may undergo necrosis but harbor confined, viable organisms for a long time. Lymphocytes and plasma cells border the granulomas, 

indicating the continued response to the infection. 

The Biology of Infection 

In human populations of antiquity, generally 

about half the individuals born died during infancy or childhood. The major cause of this mortality was infectious disease, the single greatest 

threat to life. Of those living to adulthood, many 

died of the direct or indirect effects of infectious 

disease, but trauma becomes increasingly significant. Even among hunters and gatherers living 

today, infection of the digestive system results in 

the death of many of the infants and children. 

104 
NUMBE

R 28 105 

With the development of agriculture and its as-

sociated sedentary life many more infectious dis-

eases became endemic in human populations. 

Civilization, with its high concentration of people 

in a limited area, brought with it the spector of 

death on a massive scale, with epidemics killing 

half or more of the inhabitants of a city. 

For the paleopathologist, one of the great 

sources of frustration is the fact that infectious 

diseases, particularly those that result in death, 

rarely leave behind any direct evidence of their 

existence in the skeletons of the individuals who 

die of them. This places great restrictions on the 

ability to investigate the biological effects of these 

diseases on human populations. Despite these 

limitations, it is apparent that some infectious 

conditions do affect the skeleton and that careful 

analysis and appropriate investigations can reveal 

much about human adaptation in response to 

disease. It is important to emphasize that infec-

tious conditions affecting the skeleton tend to be 

subacute, chronic diseases and may not be the 

immediate cause of death. Many of the chronic 

infectious diseases produce morphologically over-

lapping responses in skeletal tissue. These re-

sponses make specific diagnosis difficult even in 

modern clinical cases where many more of the 

variables of the disease state are known. 

Osteomyelitis 

PATHOLOGY 

Osteomyelitis is the result of introduction of 

pyogenic bacteria into bone. The bacteria may 

reach the skeleton by several different routes: (1) 

by direct infection through traumatic or surgical 

wounds, (2) by direct extension from adjacent 

soft tissue infections, or (3) by the hematogenous 

FIGURES 122, 123.—Osteomyelitis of distal right femur: 122, 

Anterior view showing smooth total sequestrum with invol-

ucrum above and below. 123, Posterior view showing de-

struction of metaphysis and proximal diaphysis; notice the 

jagged border of the sequestrum at the junction with the 

living bone. (About 10 years, WM HS 44.5 from 1841.) 
106 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

FIGURES 124, 125.—Osteomyelitis of right femur with total 

diaphyseal sequestrum, involvement of both metaphyses and 

involucrum; epiphyses missing: 124, Anterior view. 125, 

Posterior view. (About 14 years, FPAM 837.) 

route from a remote septic focus. The causative 

organism, in close to 90 percent of the cases, is 

Staphylococcus aureus; the second in frequency is 

Streptococcus, with other cocci and bacilli making 

up a small percentage. 

The osteomyelitis secondary to wounds, compound fractures, or surgery obviously can occur 

at any age and in any part of the skeleton. 

However, since injuries to the limbs and, if not 

penetrating, to the skull are more likely to be 

survived than injuries to the thorax or abdomen, 

posttraumatic osteomyelitis will be found more 

often in the bones of extremities and the cranium 

than in those of the trunk. Although this route of 

FIGURE 126.—Chronic osteomyelitis of femur after fracture, 

10-years duration. Involucrum with large cloacal opening 

exposing cortical sequestrum. (33-year-old male, MG H autopsy 33172.) 
NUMBER 28 107 

FIGURE 129.—Osteomyelitis of left tibia with massive involucrum and numerous cloacal openings, anterior view, 3-

years duration. (20-year-old male, PMES l.E.B. 16(12) 

before 1931.) 

infection may result in the full blown picture of 

acute and chronic osteomyelitis, it may more 

often be more limited and localized. This is also 

true of osteomyelitis secondary to adjacent soft 

tissue infection. In such cases, infection may be 

limited to the periosteum and cortex and not 

spread through the medullary cavity. The result 

of such localized infections would be focal periosteal bone deposition around a partial cortical 

defect, with or without a small sequestrum, and 

with some sclerotic response in the vicinity. Such 

local infections may heal with sclerotic scarring 

FIGURES 127, 128.—Osteomyelitis of distal right tibia: 127, 

Massive involucrum exposing sequestrum (arrow) in large 

opening. 128, Porous involucrum with multiple cloacal openings (arrows). (HM P618.) 
FIGURE 130.—Osteomyelitis of left tibia following slight 

injury, 18-months duration. Notice massive hypervascular 

involucrum exposing large sequestra in large cloacal openings, periostitis of fibula. (Adolescent, W M HS44.6 from 

1851.) 

FIGURE 131 .—Chronic osteomyelitis of left tibia with involvement of the proximal epiphysis and partial bony ankylosis 

of knee in flexion. Notice cloacal openings, involucrum, and 

sequestrum. (12 years, FPAM 4948 from 1888; scale in cm.) 

FIGURE 132.—Chronic osteomyelitis of right tibia with ankylosis of ankle joint, involvement of talus and periostitis of 

fibula. Notice massive involucrum with multiple cloacae 

exposing sequestra. (About 20 years of age, FPAM 358 from 

before 1817.) 
NUMBER 28 109 

FIGURE 135.—Chronic osteomyelitis of right tibia with 

slipped distal epiphysis and ankylosis of ankle joint resulting 

in pes calcaneus deformity of the foot. (17-year-old female, 

PMUG 3239, autopsy 8278 from 1877.) 

around a depression. These scars may subsequently be greatly effaced by remodeling. 

Hematogenous Osteomyelitis 

Hematogenous osteomyelitis runs a fairly typical course and shows distinct variations in frequency and appearance in different age groups 

(Trueta, 1959:671-680; Putschar, 1976a:41-60). 

In Trueta's (1959) series of over 200 cases, 7 

percent were infants, 80 percent children, and 13 

percent adults. In preantibiotic days the hemaFIGURES 133, 134.—Chronic osteomyelitis of right femur 

with bony ankylosis of knee and disuse osteoporosis of tibia; 

two fistulae draining a large periosteal abscess were found at 

autopsy: 133, External view. 134, Cut surface. (58-year-old 

male, IPMI KM 180, autopsy 4802, annual 249 from 1898.) 
FIGURES 136, 137.—Chronic osteomyelitis of left femur: 136, 

Medial, outside view, showing remodeled periosteal reactive 

bone and cloaca. 137, Cut surface and lateral view, showing 

sclerotic remodeled involucrum, central sequestrum, and 

multiple cloacae. (ANM 2950.) 

togenous osteomyelitis of childhood and adolescence made up an even greater percentage of the 

total. In this age group there is a marked predominance of males over females at a ratio of at least 

3:1. The sex difference in infant osteomyelitis is 

not marked and in adult osteomyelitis is less than 

in the juvenile form. Hematogenous osteomyelitis 

greatly predilects the long bones of the extremities. It is limited to one bone in 80 percent of the 

cases; two or, rarely, more bones are affected in 

only 20 percent (Garre, 1893:276). The localization of juvenile hematogenous osteomyelitis is 

intimately related to the rate and time of growth 

of the various growth plates. The infection almost 

FIGURE 138.—Chronic osteomyelitis and periostitis of left 

femur, showing cancellous bone filling the medullary canal 

around residual abscess cavities. (34-year-old male, IPAZ 

3796, surgical specimen MB 1515 from 1936.) 
NUMBER 28 

FIGURE 139.—Chronic sclerosing osteomyelitis of left tibia, 

showing central lytic cavities and medullary sclerosis; 

marked, mostly anterior, periosteal bone deposition. Notice 

absence of sequestra and cloacal openings. (About 17 years 

old, IPMI K M 187; scale in cm.) 

always starts in the metaphysis near an actively 

growing plate. The greatest frequency involves 

the distal femoral metaphysis, the proximal tibial 

metaphysis, the distal tibial metaphysis, and the 

proximal femoral metaphysis in decreasing order. 

Femur and tibia together account for close to 80 

percent of locations, followed by the humerus 

with about 10 percent. Other long bones of the 

extremities are less often affected, especially those 

of hands and feet. The cancellous bones and the 

FIGURES 140, 141.—Sclerosing osteomyelitis and perostitis of 

left femur, probably nonspecific but, in absence of sequestra 

and cloacae, syphilis cannot be excluded: 140, Cut surface 

(KM 133c) and outside surface (KM 133c'). 141, Detail of 

periosteal surface (KM 133c'). (Adult, no data, IPMI.) 
112 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

FIGURES 142, 143.—Chronic sclerosing osteomyelitis of both femora; notice the similarity of the 

periosteal bone pattern to tertiary syphilis: 142, Anterior view. 143, Interior and medial view. 

(23-year-old male with periosteal abscess and skin fistula over both femora; died from amyloidosis; PMUG 1712 a and b, autopsy 3260 from 1869.) 

skull participate least in hematogenous osteomyelitis (Wilensky, 1934:276, 277). 

The acute hematogenous osteomyelitis begins 

with one or several purulent foci in a metaphysis, 

leading to lytic destruction of the newly formed 

spongiosa: The exudate spreads through the marrow cavity, increasing the pressure within the 

rigid confinement of the diaphysis and resulting 

in more or less extensive necrosis of the cortex by 

means of vascular compression. In the metaphysis, near the growth plate, the thin remodeling 

cortex permits easy extension of the exudate under the periosteum. The active osteogenic periosteum of the child readily strips from the cortex, 

permitting the formation of a subperiosteal abscess and depriving the diaphysial cortex of its 

external blood supply. This results in formation 

of large, often circumferential (Figures 122, 123) 

and sometimes total necrosis of the diaphysis 

(Figures 124, 125). The dead bone becomes the 

sequestrum, which can only be resorbed or remodeled if small. Large sequestra remain and 

maintain the infection if they are not extruded 

through fistulae or removed by surgical intervention. The elevated periosteum continues to produce bone, forming a shell of hypervascular bone 

surrounding the sequestrum (Figure 126). This 

enveloping reactive bone formation is called involucrum and serves as a scaffolding in ultimate 

repair. The metaphysial bone usually does not 

undergo total necrosis because of the easy escape 

of the exudate through the thin, porous cortex. 

The separation of living bone and sequestrum 

takes place in this area by means of osteoclastic 
NUMBE

R 28 113 

resorption (Figures 127, 128). The subperiosteal 

pus seeks escape through the involucrum and 

through the surrounding' soft tissue to the skin 

surface, causing a large, round cloacal opening in 

the involucrum (Figure 129), often exposing parts 

of sequestra to view (Figure 130). Skin fistulae, 

which discharge pus and fragments of dead bone, 

develop. The epiphysis in the growing child is 

relatively protected by the growth plate and by 

the fact that its vascular supply does not com-

municate with that of the metaphysis and dia-

physis. For this reason extension into the epiphysis 

and the adjacent joint is uncommon in that age 

group. An exception is the hip and, to a lesser 

extent, the shoulder joint, where part of the me-

taphysis is located within the articular space. 

However, in long standing or recurring osteomye-

litis the adjacent joint may become involved at 

any age and terminate with bony ankylosis (Fig-

ures 131-134). In the active phase of the disease 

the growth cartilage may be partly destroyed and 

epiphysiolysis (Figure 135) used to occur in up to 

15 percent of the cases (Garre, 1893:287). Patho-

logical fractures, mostly through the area of de-

marcation between living and dead bone, rarely 

through the involucrum, used to be observed in 

8 percent of the cases (Garre, 1893:293). The 

endosteal process of lytic destruction was followed 

by reactive sclerosis, limiting the intraosseous in-

fection to local areas (Figure 136-138). The com-

bination of these various phenomena over a pe-

riod of months, years, and, sometimes, decades 

results in a great variety of pictures, which defy 

detailed description. However, the common char-

acteristics are presence of sequestra, porous hy-

pervascular periosteal bone, and cloacal openings. 

Since dead bone is not easily attacked by osteo-

clasts, large sequestra may exhibit a smooth sur-

face but with a jagged border at the line of 

FIGURES 144, 145.—Osteomyelitis of femur with subperios-

teal abscess surrounded by a thick layer of reactive bone. 

The abscess cavity contained a cortical sequestrum: 144, 

Outside view, showing massive reactive bone with cloacal 

opening (arrow). 145, Cut surface, showing elongated abscess 

cavity (arrow). (20-year-old male, WM S.48.2 from 1882.) 

NUMBER 28 115 

FIGURES 150, 151.—Acute osteomyelitis of left tibia: 150, Tibial diaphysial sequestrum, extracted 

from the fistula. 151, X-ray one year later, showing complete regeneration of the tibia. 

(2-month-old African negro, WM S44.6, from 1963.) 

separation. The mortality of this disease used to 

be at least 20 percent. In many instances the 

disease remained active for a long time; in others 

FIGURES 146, 147.—Chronic recurring osteomyelitis of right 

tibia with involvement of the proximal epiphysis and elongation. Notice the low position of the proximal end of the 

fibula. Reactive periostitis of fibula: 146, Anterior view. 147, 

Cut surface; notice abscess cavities with perifocal sclerosis. 

(FPAM 4921, autopsy 86827 from 1888.) 

FIGURE 148.—Both lower legs. Chronic osteomyelitis of right 

tibia with elongation and with ankylosis of ankle joint, 

periostitis of fibula. (53-year-old female, FPAM 5217, autopsy 91835 from 1892.) 

FIGURE 149.—Squamous cell carcinoma of left tibia secondary to chronic osteomyelitis. Notice the extensive destruction 

and pathological fracture of the tibia and periostitis of fibula. 

(45-year-old male with osteomyelitis since childhood, PMES 

IVNa 16(4).) 

it healed temporarily to recur after years; others 

healed permanently. Other cases showed a less 

severe course with fewer or no sequestrations and 

more sclerotic response (Figure 139) (Garre, 1893: 

257-263). In the absence of sequestra and of 

cloacal openings entering the medullary canal, 

differentiation from tertiary syphilis is difficult or 

impossible (Figure 140-143). Some cases result 

only in a local abscess formation (Brodie's abscess) 

(Figures 144-147), usually near the growth plate, 

in the metaphysis, surrounded by sclerotic bone. 

The collateral hyperemia, not uncommonly, results in excessive, longitudinal growth of the affected bone if the growth plate (Figure 148) is not 

destroyed. In rare cases of chronic osteomyelitis, 

carcinoma may develop from the epithelium of 

the fistulous tract (Figure 149). 

INFANTILE OSTEOMYELITIS.—This disease exhibits some differences from juvenile osteomyeli-
116 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

tis. It used to be uncommon in the preantibiotic 

period, because most infants succumbed to the 

septicemia before osteomyelitis was established 

(Green and Shannon, 1936). In infantile osteomyelitis massive sequestration is unusual because 

the thin, loosely structured cortex permits escape 

of pus without raising the intramedullary pressure 

to critical levels. Involvement of the epiphysis 

and concomittant septic arthritis are common 

because, in this age group, the epiphysial blood 

supply is not yet separated from that of the 

metaphysis (Trueta, 1957:360-366). If the osteomyelitis heals, rapid remodeling removes much of 

the evidence of the disease, for, in the rapidly 

enlarging bone, the entire old cortex is removed 

as the bone grows in diameter. This is true even 

after elimination of a large sequestrum (Figures 

150, 151). 

ADULT OSTEOMYELITIS.—Adult hematogenous 

osteomyelitis is rare and may often represent 

continued or recurrent juvenile osteomyelitis. 

New infections also predilect the metaphysial 

areas of long bones, especially femur and tibia. 

The inflammation is less acute and less extensive. 

Sequestra tend to be small. The firm attachment 

of the periosteum prevents extensive stripping but 

local subperiosteal abscesses and fistulae are common. Since, after closure of the growth plate, 

communications of metaphysial and epiphysial 

blood vessels are reestablished to some extent, 

involvement of the epiphysis and of the adjacent 

joint is not unusual. 

Hematogenous osteomyelitis caused by bacteria other than Staphylococcus and Streptococcus 

should be briefly discussed. About one percent of 

patients with typhoid fever, regardless of age, 

develop osteomyelitis (Murphy, 1916). The main 

locations are ribs, tibia, and spine. The tibial 

lesion often is a diaphysial subperiosteal abscess 

involving the underlying cortex. The spinal lesion 

predilects the lumbar segment and often involves 

two adjacent vertebrae and the intervertebral disc 

between them. In various hemoglobinopathies, 

especially in sickle cell anemia, complicating salmonella osteomyelitis is not uncommon (Hook, 

Campbell, Weens, and Cooper, 1957:403-407; 

Golding, Maclver, and Went, 1959:711-718). 

Multiple bones are affected in about two-thirds 

of these cases. Long bones are predilected, but 

about 25 percent of the patients show involvement of bones of hands and feet. There are usually no major sequestra and the periosteal reactive 

bone is sparse (Putschar, 1976a:49). 

Changes in Individual Bones 

The overall description of hematogenous osteomyelitis given above mainly focuses on the 

changes in long bones of the extremities. A discussion of the pecularities of osteomyelitis in different other parts of the skeleton is therefore 

indicated. 

SHORT TUBULAR BONES.—Phalanges, metacarpals, and metatarsals are uncommon sites of osteomyelitis. In young children hematogenous infections in these rapidly growing bones do occur 

and lead to rapid destruction of the thin cortex 

and formation of a massive expanded involucrum, resembling the spina ventosa in tuberculosis and similar changes in congenital syphilis 

(Figure 152). In adults phalanges, especially of 

toes, are more often involved in cases of peripheral 

vascular disease secondary to skin ulcerations. 

These cases resemble the features of chronic adult 

osteomyelitis in other bones (Figure 153). 

T H E SPINE.—Vertebral osteomyelitis is uncommon, amounting to about 2 percent of all cases 

(Schmorl and Junghanns, 1971:389). It occurs 

more often in adults than in children (Kulowski, 

1936:343-344). In contrast to tuberculosis, only 

one vertebra is affected in 75 percent of the cases 

(Donati, 1906:1132-1133). The frequency of location in the spine increases distally. Lauche 

(1939:39) estimates that of cervical, dorsal, and 

lumbar involvement at a ratio of 1:2:3. The first 

and second cervical segments are very rarely affected. As far as the location within the vertebra 

is concerned, in contrast to tuberculosis, the spinous process and neural arch often participate in 

the lesion. The infection may even be limited to 

the neural arch and/or spinous process (66 percent (Donati, 1906:1133) 58 percent (Volkmann, 

1915:485)). The transverse process is rarely affected. In destructive spinal osteomyelitis, col-
NUMBER 28 117 

FIGURE 152.—X-ray of hematogenous staphylococcic osteomyelitis of first metatarsal, massive involucrum of diaphysis. 

(3-year-old male, surgical specimen 7637-1970, MGH.) 

lapse of a vertebra is not uncommon. In multiple 

involvement of adjacent vertebrae, some of the 

intervertebral discs are usually better preserved 

than in tuberculosis but may show bony bridging 

(Junghanns, 1939:325-326). Destruction of several adjacent vertebrae may result in an angulation of the spine, which may be indistinguishable 

from tuberculous gibbus. Paravertebral abscesses 

can occur and may elicit reactive periosteal bone 

formation. 

CANCELLOUS BONES.—These bones are rarely 

involved, but when they are affected, the process 

locates in the area with most cancellous bone: In 

the scapulae, in the spina (Figures 154, 155); in 

the pelvis, in the iliac crest (Figures 156, 157); in 

the sacrum, in the lateral wing. Pelvic osteomyelitis may localize in the acetabular roof, secondary 

to septic arthritis of the hip or around a ruptured 

symphysis pubis in puerperal septicemia (PutFIGURE 153.—Osteomyelitis of basal phalanx of right big toe 

with involucrum and sequestrum, periostitis of terminal 

phalanx, secondary to infected wound. (Adult, PMES 1 EB 

18 (100).) 

schar, 1931:91, 92). Ribs account for about 2 

percent of osteomyelitis. The infection is usually 

located near the junction with the cartilage or 

posterior, at the angle. There is usually no sequestration (Lauche, 1939:39). 

SKULL.—Primary osteomyelitis of the skull is 

rare (Figures 158, 159). The most usual is extension of an empyema of the frontal sinus into the 

frontal bone. The structure of the diploe with its 

interconnecting large vascular channels permits 

spreading of the infection through the cranial 

vault. Sutures may act as a temporary barrier, 

but extension into the parietal bone is not uncommon. The occipital bone is usually spared. Osteomyelitis of the skull base, originating from an 

empyema of the sphenoid sinus, is even more 

rare. Of more importance is traumatic osteomyelitis of the cranial vault following open wounds 
FIGURES 156, 157.—Chronic osteomyelitis of right ilium with 

right sacroiliac ankylosis and septic arthritis of right hip, 3-

years duration: 156, Frontal view. 157, Lateral view. (17-

year-old female, FPAM 5636.) 

FIGURES 154, 155.—Osteomyelitis of left scapula removed 

surgically, showing multiple cloacae over sequestral defects 

and massive involucrum: 154, Posterior view. 155, Anterior 

view. (14-year-old female, WM S45.1, from 1858.) 
NUMBER 28 119 

FIGURE 160.—Osteomyelitis of right parietal bone secondary 

to infected scalp wound and removal of sequestrum by 

trephining. (Adult, before 1850, PMES lE.B.l(l).) 

or blunt trauma, with or without fracture and 

surgical intervention (Figures 160, 161). This is 

particularly pertinent to the problems of archeological trephination and the custom of scalping. 

Infection, spreading from the intact scalp or 

through an open wound into the periosteum and 

bone of the cranial vault, tends to remain localized. The course is often protracted, eliciting a 

sclerotic response around a central, partly lytic, 

area around a sequestrum. The lesion usually is 

larger on the outer than on the inner table. Even 

direct infections of the opened diploe tend to 

remain circumscribed and take a chronic course 

with considerable perifocal sclerosis. Infected 

compound fracture may become the source of 

spreading osteomyelitis of the cranial vault, extending along the many venous channels of the 

diploe. In some instances, avascular necrosis of 

fracture fragments is followed by infection in and 

around the dead bone. For a detailed discussion 

of traumatic osteomyelitis of the skull, see AdelFiGURES 158, 159.—Osteomyelitis of skull vault, probably 

pyogenic, but syphilis with superimposed osteomyelitis cannot be excluded: 158, Outside view. 159, Endocranial view, 

showing marked involvement of inner table and sequestra. 

(WM S 43.1, from 1869.) 
120 

SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOG Y 

FIGURE 161.—Osteomyelitis of frontal bone with early sequestration, probably secondary to scalp infection. (Adult, 

H M P625.) 

Stein and Courville (1933). Localized, often 

chronic, and sclerotic osteomyelitis secondary to 

middle ear infections occurs in the mastoid process, the temporal, and the petrous bone. Occasionally ear infections spreading to the venous 

sinuses or meninges may lead to cranial osteomyelitis (Figures 162-164). The jaws of infants 

and small children, which are crowded with dental buds, may become infected from the mucosal 

surface or through the bloodstream. In the course 

of the infection, dental follicles may be sequestrated and extruded through mucosal ulcerations. 

Extension of the infection into the floor of the 

orbits before formation of a maxillary sinus is not 

uncommon. After 2 years of age, the infection is 

much more common in the mandible (Lauche, 

1939:37). Baranoff (1934) reports that the mandible is affected in 91 percent and the maxilla in 

9 percent of the cases in a Chinese series, most of 

which are in the young adult age range—16 to 

30 years. The preponderance of the mandibular 

infections remains throughout the adult period, 

due to extension from oral, dental, and periodontal infections. The course is usually very chronic, 

revealing little pus formation and no sequestrum. 

The condition is dominated by osteosclerotic condensation, with or without thickening of the manFIGURES 162, 163.—Osteomyelitis ofposterior portion of skull 

secondary to chronic left middle ear infection and streptococcic meningitis: 162, Internal view, showing lytic foci in 

sulcus transversus. 163, External view, showing corresponding small defect of outer table. (67-year-old male, PMES 

lE.B.l(2a).) 

dible (Panders and Hadders, 1970). The changes 

can simulate Paget's disease; however, the typical 

mosaic pattern of Paget's is not found microscopically. Other facial bones may be affected by 
NUMBER 28 121 

FIGURE 164.—Osteomyelitis of cranial vault secondary to 

chronic ear infection and streptococcic meningitis, showing 

disseminated lytic foci of the inner table along branches of 

both middle meningeal arteries. (67-year-old male, PMES 

1 E.B.I (2).) 

extension of infection of the paranasal sinuses or 

of the facial soft tissues. 

PALEOPATHOLOGY 

In historical times, before the availability of 

antibiotics, osteomyelitis was a common clinical 

condition well known to physicians of the period. 

This would suggest that osteomyelitis might be 

common in archeological skeletons as well. However, there are few references to this disease entity 

in the literature on paleopathology. Hooton 

(1930:309) reports four cases of osteomyelitis in a 

total sample of 503 pre- and post-Columbian 

New World Pueblo Indians (0.8 percent). WoodJones (1910b:283), in his report of disease in 

ancient Egyptian skeletons, states that inflammatory conditions of bones are very rare. Even in 

open compound fracture, where osteomyelitis was 

such a dreadful sequela in historical times, evidence for purulent infection in Egyptian skeletons 

is very limited. Wood-Jones (1910b:283) concludes that the ancient Egyptians had a much 

greater resistance to infectious diseases of bone 

than the Europeans of his day. However, this 

conclusion may reflect inadequate or biased sampling of the European population, because WoodJones, as an anatomist, probably would have 

based his observation regarding the incidence of 

European osteomyelitis on its frequency in dissecting room cadavers. This source does not provide a human sample comparable with the ancient Egyptian skeletal sample. Although osteomyelitis may have been a common ailment in 

early twentieth century medical practice, particularly in the poorer, working-class people, this 

does not mean that the incidence of the disease 

in the general population was high. This is evidenced by the League of Nations epidemiological 

report for 1921 (1922), which does not include 

osteomyelitis as a significant disease entity. Thus, 

in an archeological skeletal sample, the incidence 

of osteomyelitis might be low but not differ significantly from a primitive or peasant population 

of today. 

Both osteitis and periostitis are descriptive 

terms in the paleopathological literature to describe inflammatory conditions that could include osteomyelitis. By definition, osteomyelitis is 

an infection of bone involving the marrow. While 

this may be a helpful concept in the differential 

diagnosis of osteomyelitis in archeological specimens, it should be emphasized that clear evidence 

of marrow involvement may not be revealed in a 

gross specimen. It is due to such problems in 

diagnosis that scholars, reporting on lesions in 

archeological skeletons that could be osteomyelitis but are not clearly so, tend to avoid identifying 

a lesion as osteomyelitis, unless there is other 

evidence such as a cloaca or sequestrum to support this conclusion. Thus, many gross periosteal 

lesions possibly arising from osteomyelitis will not 

be attributable to this specific disease. 
122 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOG Y 

FIGURES 165-168.—Possible disseminated hematogenous osteomyelitis: 165, Large abscess of 

the first deciduous upper left molar in the skull of a child about 6 years of age; note the presence 

of a broad zone of reactive bone (arrow) on the maxilla peripheral to the abscess. 166, Periosteal 

reactive bone predominantly in the metaphyseal areas of the major long bones (scale in cm). 

167, A central lytic focus (arrow) surrounded by periosteal reactive bone in the proximal right 

ulna. 168, Extensive accumulation of periosteal reactive bone in the metaphyseal region of the 

posterior, distal, left humerus. (NMNH 379345.) 
NUMBER 28 123 

The Skull 

Wood-Jones (1910b:283) notes that dental disease accounts for almost all of the infectious 

conditions seen in the skull and mandible. This 

conclusion is supported in the clinical studies of 

Wilensky (1932:197) and Blum (1924:802). In 

ancient Nubian skulls, Wood-Jones (1910b:283-

284) reports a case of bony destruction in the 

nasal and palatal regions of a young female who 

had worn and carious teeth. He attributes the 

destructive process to chronic rhinitis. Hooton 

(1930:310) reports three crania with inflammatory lesions, in which osteomyelitis is possible; 

however, syphilis is also thought possible. Roney 

(1966:102) reports two cases of osteomyelitis in a 

sample of 44 skeletons recovered from the preColumbian Pueblo Indian site at Mesa Verde. 

The bones involved include the mandible, ulna, 

femur, and tibia. Infectious conditions of the 

mastoid region have been reported in ancient 

Nubian skulls by Wood-Jones (1910b:284). 

While a more detailed treatment of infection 

arising from dental disease is presented (p. 438), 

brief mention is appropriate here regarding complications of caries that can affect bone and possibly be a focal point for systemic infection. One 

possible example of this condition occurs in the 

skeleton of a young child in the skeletal collections 

of the National Museum of Natural History, 

Smithsonian Institution, Washington, D.C. 

(NMNH 379345). The specimen is from a site in 

Virginia, USA, and is dated about A.D. 1550. In 

the left maxilla there is a periapical abscess, which 

has destroyed bone adjacent to the root of the 

first deciduous upper left molar on the buccal 

side (Figure 165). A zone of periosteal, reactive 

bone extends beyond the lytic focus for 1-2 centimeters. There is clear evidence of caries in the 

deciduous second molar, leaving no doubt regarding the initial focus of the infectious process. The 

long bones of the skeleton show extensive development of periosteal, reactive bone indicative of 

a disseminated, inflammatory condition (Figures 

166-168). While it could be that the infectious 

condition of the maxilla and the inflammatory 

reaction in the long bones are unrelated, it is 

possible that the infectious condition in the maxilla was the initial focus for hematogenous dissemination of the infectious organism. Such a condition could have stimulated a general, periosteal 

response before the child succumbed to this or 

other problems. 

Postcranial Bones 

The best diagnostic evidence for osteomyelitis 

in skeletal material is a drainage canal in bone 

(cloaca) or sequestration in association with periosteal bone formation (involucrum). Lacking this, 

inflammatory lesions of the long bones are difficult to attribute to osteomyelitis. 

Wood-Jones (1910b:287) reports an ancient 

Nubian example of a humerus with a necrotic 

distal portion associated with a superficial layer 

of inflammatory bone. He attributed this to an 

infectious complication of an injury. 

Hooton (1930:308) found 13 out of 503 Pueblo 

skeletons that had nonspecific periostitis, some of 

which could have been osteomyelitis. However, 

he did identify four cases that he judged to be 

osteomyelitis (Hooton, 1930:309). Cressman and 

Larsell (1945:332) reported a case of probable 

osteomyelitis in a prehistoric Indian skeleton from 

Oregon, USA. The right arm was fused at the 

elbow and the left tibia, tarsals, and metatarsals 

were fused together. They attribute this condition 

to osteomyelitis acquired during childhood. The 

infection resulted in septic arthritis. Jarcho, Simon, and Bick (1963) have published their observations on a pre-Columbian, Pueblo skeleton 

from Arizona, USA, in which the left femoral 

head was fused to the innominate. They suggest 

the possibility that this condition is septic arthritis 

with ankylosis following infection, possibly of 

pneumococcal, gonococcal, staphylococcal, or 

streptococcal origin. 

In the skeletal collections of the National Museum of Natural History, Washington, D.C, 

USA, there are several archeological skeletons 

with lesions, which could appropriately be attributed to osteomyelitis. Perhaps the most clearly 

identifiable example is a case of a juvenile from 

Peru (NMNH 378243). All that was recovered of 
124 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

this skeleton is the right and left tibia, both of 

which are in an excellent state of preservation. 

The estimated age, based on the length of the 

normal, right tibia, is 9 years. Unfortunately, the 

archeological provenience is poorly documented. 

However, it seems likely that the specimen is preColumbian. 

Grossly the two tibiae differ dramatically in 

size (Figures 169-175). The measurements in Table 2 indicate the marked increase in size of the 

pathological left tibia in contrast with the normal 

right tibia. Osteomyelitis results in hyperemia, 

which may stimulate excessive growth in the 

affected bone. This effect of the disease is clearly 

seen in the two tibiae of this case. The excessive 

growth of periosteal involucrum is the result of 

pathological stimulation in response to the death 

of the cortex. This problem does not exist at the 

growth plate where excessive, longitudinal 

growth is stimulated by the general hyperemia. 

TABLE 2.—Metric comparisons of the right (normal) and left 

(pathological) tibia in osteomyelitis from a 9-year-old child 

from an archeological site near La Oroya, Peru (NMNH 

378243) 

Measurement 

Maximum length 

Maximum midshaft diameter 

Mediolateral diameter of 

proximal growth plate 

Left 

(mm) 

219 

34 

50 

Right 

(mm) 

196 

17 

45 

While the proximal growth plate of the pathological, left tibia is enlarged, the surface appears 

normal, although there is a postmortem break in 

the surface. There is a cloaca one centimeter 

below the growth plate, but it does not penetrate 

it. The distal medial cortex of this bone has a 

large, cloacal opening with a channel penetrating 

the distal growth plate. There is also some postmortem damage. The cloacal openings penetrate 

into the marrow space and are lined with smooth 

compact bone indicating a long-standing chronic 

condition. 

The proximal metaphysis of the left tibia contains a cloaca in the anterior cortex. There is a 

small, bony spur on the lateral anterior cortex, 

which is a localized periosteal reaction. The distal 

metaphysis has a cloaca on the medial aspect, 

which is continuous with the opening in the 

growth plate mentioned above. 

The diseased shaft contains a sequestrum, 

which projects through a large cloaca on the 

anterior shaft (Figure 170). There is a smaller (5 

mm diameter) cloaca inferior to the large cloaca. 

Both of these openings are part of a single channel 

that contains the sequestrum. There is a small, 

lytic pit near the sequestrum and a cloaca in the 

posterior portion of the distal shaft. 

The roentgen-film appearance of the diseased 

left tibia shows a greatly thickened, but porous, 

involucrum. The old sequestrated shaft is still 

apparent, although the cortex of the metaphyses 

has been removed by remodeling. The diameter 

of the shaft is compatible with an age of a 4- to 

5-year-old child. Since sequestration would most 

likely have occurred shortly after the onset of the 

disease, this suggests that the child suffered from 

osteomyelitis for about 5 years before death. 

In the lateral roentgen view of the osteomyelitic 

tibia, there appears to be another, much smaller, 

sequestrum in the distal anterior cortex (Figure 

175). Grossly, there is a bulge in this area but no 

cloaca. There are other roentgen features also 

suggesting sequestra; however, their identification on the X-ray film is less clear cut. 

A comparison of Harris' lines also offers some 

insight into the disease process. In the normal 

(right) tibia there are four distinct lines in the 

distal and three in the proximal ends. The osteomyelitic tibia contains two distinct Harris' lines 

and two much less distinct lines in the distal tibia, 

which may correspond to the four distal lines seen 

in the normal tibia. There is no evidence of 

Harris' lines in the proximal end of the pathological tibia. If they existed the disease has obliterated the roentgen evidence. 

Table 3 shows the distances between the Harris' lines in both distal tibiae. Since the distances 

between all Harris' lines are greater in the osteomyelitic tibia it would appear that accelerated 

growth has characterized all stages of the disease 

process. Table 4 shows the distances between the 

distal Harris' lines and the growth plate. In every 
NUMBER 28 125 

TABLE 3.—Distance (in millimeters) between the Harris' 

lines for the right (normal) and left (pathological) tibia of 

NMN H 378243 (lines 1 and 4 are indistinct in the left tibia, 

making the associated measurement somewhat speculative 

as emphasized by the question marks) 

Harris' line 

First to second 

Second to third 

Third to fourth 

Total 

Left 

(mm) 

20(?) 

27 

6(?) 

53 

Right 

(mm) 

18 

21 

3 

42 

TABLE 4.—Distance (in millimeters) between the distal 

Harris' lines and the distal growth plate of the right (normal) 

and left (pathological) tibiae of NMNH 378243 (lines 1 and 

4 are indistinct in the left tibia, making the associated 

measurement somewhat speculative as emphasized by the 

question marks) 

Hams' line 

First to growth plate 

Second to growth plate 

Third to growth plate 

Fourth to growth plate 

Left 

(mm) 

Right 

(mm) 

63(?) 

42 

15 

8(?) 

50 

32 

10 

3 

case the distance is greater in the pathological 

tibia. 

If we assume that growth in the distal tibia 

accounts for approximately two-thirds of total 

tibial growth, we can get an estimate of the age 

of the individual when the first Harris' line was 

formed. Doing this for the normal tibia only we 

find that there is 50 millimeters from the first 

Harris' line to the growth plate. This translates 

to about 75 millimeters total growth for the tibia 

from the first arrested growth line. Extrapolating 

from Stewart (1968:133) the tibia grows about 17 

millimeters per year between the ages of 4 and 9 

years. At this rate, it would take approximately 

4^2 years to add 75 millimeters to the total length 

of the tibia. Since the child was about 9 years old 

at the time of death, this suggests that the first 

Harris' line was formed between the ages of 4 and 

5 years. Because this age is in agreement with the 

age estimated on the basis of the midshaft diameter of the sequestrated tibial shaft, this first 

Harris' line may coincide with the time of onset 

of the osteomyelitis. 

The second case I shall review in considerable 

detail is an Eskimo specimen from Shishmaref, 

Alaska (NMNH 332611). This case is illustrative 

of the problems encountered in identifying the 

specific cause of an infectious condition. The 

archeological age is uncertain, but a bullet wound 

in the skull indicates a date in the postcontact 

period. 

The specimen is clearly male with an age at 

death estimated to be about 23 years on the basis 

of pubic symphysis morphology. The skull and 

long bones both suggest a muscular, robust individual. 

There are two pathological conditions in this 

specimen. Undoubtedly, the immediate cause of 

death was a bullet injury to the skull, in which 

the bullet entered the occipital region and exited, 

with a typical fracturing pattern, through the left 

parietal (Figure 176). The other pathological condition is a largely destructive process limited to 

the lumbar vertebrae and sacrum (Figures 177, 

178). 

The first lumbar vertebra is only slightly affected by the disease process with barely visible, 

lytic foci on the lateral parts of the vertebral 

body. The second lumbar vertebra has large, 

lytic, scalloped lesions in the posterior part of the 

vertebral body. These lesions are continuous with 

the spinal canal and on the right side extend into 

the transverse process. The proximal and distal 

endplates of the vertebral body and the true joints 

of the superior and inferior processes are unaffected in the first two lumbar vertebrae. There 

are three lytic depressions approximately one centimeter wide on the left lateral and anterior cortex 

of the second lumbar vertebra. In all of the lytic 

depressions there is a varying amount of bone 

remodeling in the spaces of the spongy bone in 

the vertebral body adjacent to the disease process. 

This is a typical response by bone, particularly 

spongy bone, to a destructive disease process. In 

slowly developing, chronic, destructive conditions, there may be a continuous wall of bone 

adjacent to the disease focus. There has been a 

limited, but incomplete, osteoblastic response to 

NUMBER 28 127 

FIGURES 169-175.—Osteomyelitis of the left tibia compared 

with the normal (right) tibia of a child about 9 years of age 

from an archeological site near La Oroya, Peru: 169, Anterior view; note the sequestrum (arrow) and cloacae. 170, 

Detail of sequestrum and cloaca (arrow) in left tibia. 171, 

Medial view of pathological and normal tibia. Large channel 

penetrates the distal growth plate (arrow). 172, Detailed 

view of channel penetrating the distal growth plate of the 

pathological tibia. 173, Posterior view of pathological and 

normal tibia. 174, Anteroposterior X-ray film of pathological 

and normal tibia; note the presence of Harris' lines in the 

normal tibia (arrows). 175, Medio-lateral X-ray film of 

pathological and normal tibia. The cortex, which was sequestrated at the onset of the disease, is apparent (arrows) 

but is completely surrounded by involucrum, which forms 

the externally visible cortex. (NMNH 378243; scales in cm.) 
128 SMITHSONIA

N CONTRIBUTIONS TO ANTHROPOLOGY 

FIGURES 176-178.—Possible osteomyelitis in a young adult 

male Eskimo skeleton with a bullet wound in the skull and 

destructive lesions of the lumbar vertebrae: 176, Postero-

lateral view of skull, showing entry (arrow) and exit wounds 

from a bullet. 177, Destructive lesions primarily affecting 

the third and fourth vertebral bodies in an anterior view of 

the lumbar vertebrae and first two segments of the sacrum. 

178, Right, lateral view of lumbar vertebrae and first seg-

ment of the sacrum showing virtually complete destruction 

of the third and fourth vertebral bodies. (NMNH 332611.) 
NUMBER 28 129 

the disease suggesting a somewhat chronic condition. In the third lumbar vertebra, the entire 

vertebral body, the left transverse process, and 

the left superior articular process have been entirely destroyed. There is a slight amount of 

reactive bone adjacent to the lytic areas. The 

spinous process is normal. Like the third lumbar, 

the vertebral body of the fourth lumbar vertebra 

has been completely destroyed. However, all articular processes are present, although the left 

articular facets have been partially destroyed. 

There are long spurs coming off the transverse 

processes with the most prominent one found on 

the right side. The anterosuperior plate of the 

body of the fifth lumbar vertebra is destroyed. 

However, the articular surface of the inferior 

body is largely intact. There is a large depression 

on each of the sides of the vertebral body and 

evidence of cavitation, mostly destroyed postmortem, on the anterior vertebral body. There has 

been some osteoblastic activity, which had begun 

to fill in spongy bone forming a new cortex. The 

vertebral processes are generally intact although 

the left superior articular facet is porous with fine 

reactive bone around the porous joint area. There 

is some periosteal reaction on the left dorsal lamina. In the first segment of the sacrum the anterosuperior portion of the body is destroyed as is 

the inferior body of the same segment. There are 

large, well-circumscribed cavities in the body. 

Both alae of the first segment have a lytic cavity 

extending into them. However, the articular surface with the innominate bone is normal. The 

articular facets, sacral canal, as well as spinous 

and articular tubercles, are unaffected. The second segment is affected only on the superior 

portion of the body. There are lytic lesions 1 to 2 

centimeters in diameter, some of which appear to 

be continuous with lesions in the body of the first 

segment. 

In this case the lesions are predominately lytic, 

but with some time for an osteoblastic response 

to the disease process before the individual died. 

The skeletal remains suggest a disease process 

with an initial, acute, destructive phase followed 

by a short but more chronic phase with an exclusive involvement in the lumbosacral vertebrae. 

Both osteomyelitis and tuberculosis are strong 

possibilities and neither can be ruled out. There 

are several factors, however, that more strongly 

indicate osteomyelitis. 

It has been noted that vertebral arches, joints, 

and spinous processes are almost never destroyed 

in tuberculosis (p. 145). In this specimen there is 

destruction of transverse processes, diarthrodial 

intervertebral joints and portions of the arch. 

Furthermore, the extent of osteoblastic response 

at this stage in the lytic process would be less 

likely in tuberculosis than in osteomyelitis. 

Periostitis 

PATHOLOGY 

Periostitis, as a disease by itself, is uncommon. 

It usually represents part of, or a reaction to, 

pathologic changes of the underlying bone. The 

inner layer of the periosteum retains osteoblastic 

capacity throughout life, even after termination 

of growth. It is, therefore, not surprising that the 

periosteum reacts to many different insults with 

formation of woven bone, which later may become incorporated into the underlying cortex and 

remodeled into lamellar bone. This periosteal 

bone formation is not always an expression of 

inflammation and certainly not restricted to infection. In most of the infections discussed in this 

chapter, periosteal bone formation is one of the 

significant changes. Of these changes, first and 

foremost, inflammatory periostitis plays a role in 

the infections of bone, specific and nonspecific. 

Obviously, transitory periosteal reaction, which 

neither leaves permanent bone deposition nor 

resorptive pitting of the underlying cortex, cannot 

be recognized on dry bone. This brings up the 

question: What are the characteristics of inflammatory periosteal bone? There are no unequivocal characteristics. Generally, inflammatory periosteal bone deposited over a long period of time 

tends to be unevenly distributed, not involving 

the entire bone. The surface tends to be irregular 

and the thickness often variable. The marked. 
130 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

FIGURE 179.—Periostitis and superficial osteomyelitis of right 

tibia beneath skin ulcers. Notice shield-like periosteal 

buildup under major ulcer. (WM S 47.2 from 1831.) 

uneven hypervascularity visible on dry bone in 

the form of smaller and larger pores in periosteal 

bone is often striking. In most cases, changes in 

the underlying bone will answer the question, but 

a purely subperiosteal bone deposit may be difficult or impossible to classify pathogenetically. 

In areas where the periosteum is close to the skin 

surface, as on the anterior surface of the tibia, 

localized ossifying periostitis can be observed secondary to trauma. Such longstanding periosteal 

bone deposition can be completely incorporated 

into the cortex in form of remodeled lamellar 

FIGURES 180, 181.—Periostitis and superficial osteomyelitis 

of tibia beneath leg ulcer. 180, Superficial cortical defect 

surrounded by reactive periosteal bone. 181, Sequestrum of 

reactive bone over cortical defect, beneath leg ulcer. (HM 

P673 and 674.) 
NUMBER 28 131 

FIGURE 182.—Ossifying periostitis of right tibia beneath leg 

ulcer, synostosis of tibia and fibula. (Adult, WM S 47.1 

before 1831.) 

bone. Large chronic ulcers on the skin, especially 

those due to venous stasis, not uncommonly produce a reactive, local, ossifying periostitis on the 

tibia (Figure 179). This may represent a plaquelike deposition of periosteal bone of considerable 

thickness, roughly copying the outline of the ulcer. Occasionally such deposits may separate as 

shallow sequestra (Figures 180, 181). In other 

cases, rough exostosis-like osteophytes, which flatten out below the ulcer, may occur. This is observed particularly in tropical ulcer, a skin ulcer 

over the shin, characterized by presence of fusiform bacilli and saprophytic spirochetes (Brown 

and Middlemiss, 1956). Occasionally, such reactive bone deposits may bridge the gap between 

tibia and fibula (Figure 182). Massive reactive 

periosteal bone formation of the mandible used 

to be observed in the nineteenth century in perFIGURE 183.—Phosphorus necrosis of mandible with involucrum. (IPAZ 1758, no date.) 

sons exposed to vapors of yellow phosphorus for 

a long period (Figure 183). 

PALEOPATHOLOGY 

While periostitis, as an isolated disease process, 

is uncommon in modern medical literature and 

clinical practice, undifferentiated, nonspecific, 

periosteal lesions of long bones are rather common in archeological skeletons. The main reason 

for this difference between clinical and paleopathology is that many of the periosteal reactions 

may be part of the expression of a specific disease 

process, which can be identified in a living patient, whereas in archeological specimens the 

pathological characteristics necessary to make a 

specific diagnosis are not available. This would 

have the effect of increasing the frequency of 

nonspecific periostitis in archeological skeletal series. 

It is important to emphasize that periostitis (as 

is also the case with osteomyelitis) has both a 

general descriptive usage as a term and a discrete 

usage. Thus, periostitis is part of a disease syndrome such as syphilis, but it is also a specific 

disease itself This varied usage of the term is well 

illustrated in Brothwell and Sandison's book. Diseases in Antiquity (1967). The index to their work 
132 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

lists six references to periostitis. Of these six, the 

term is used five times in the context of a syndrome associated with a specific disease, such as 

syphilis. Only once is the term applied to primary 

periostitis. Since we discuss secondary periostitis 

in the context of specific disease entities, the 

following discussion on the paleopathology of 

periostitis will focus on the primary type. However, the designation of primary periostitis in 

paleopathological skeletons may mean only that 

a more specific diagnosis is impossible and does 

not eliminate the possibility that the periosteal 

reaction is secondary to a specific disease process. 

Primary periostitis is most often the result of 

two pathological conditions, trauma and infection (Senn, 1886:5-6). Putschar (1966:60) notes 

that it is often impossible to determine which of 

these two conditions gave rise to a given lesion in 

an archeological skeleton. While the periosteum 

will always be activated in fracture, periosteal 

reactive bone can also be stimulated by injury 

that does not produce fracture. The latter may 

resemble periosteal reactions stimulated by localized infectious foci. 

Traumatic periostitis is brought on by sudden 

or chronic insult to bone. Wood-Jones (1910b: 

285-286) has described a periostitis of the skull 

common in Nubian archeological specimens. The 

initial lesion is characterized by hypervascularity 

either on or near the vertex of the skull. However, 

there are also small spicules of bone formed, and 

later stages may be characterized by hypervascularity and, in extreme cases, exfoliation of portions of the skull. Wood-Jones attributes this periostitis to chronic insult produced by women 

carrying water jars on their heads. This observation is supported by the fact that the lesion occurs 

much more often in female skulls. Periosteal reactions of the skull are occasionally associated 

with trephination; however, here the periostitis is 

probably due to complication of the surgical procedure by infection. 

Periostitis of long bones is often seen in the 

tibiae of archeological skeletons. The reasons for 

this localization remain obscure. It is, however, 

instructive to note that periosteal reaction in 

syphilis forms on bones that tend to be near the 

skin surface, such as the tibia and skull vault. 

Such bones may be somewhat cooler than bones 

like the femur, which are enclosed in a heavy 

mass of muscle and fat. It is also true that bones 

near the skin are more exposed to direct trauma 

than bones protected by overlying muscle. Perhaps both these factors are significant in localization of periostitis. 

The distinction between osteomyelitis and periostitis cannot always be made in dry bone specimens. However, in periostitis there will be no 

cloacae, involucrum, or changes in the marrow 

cavity. Furthermore, periosteal bone tends to be 

superficial to the normal cortex, at least in early 

stages of the disease condition. The superficial 

nature of periosteal lesions can be seen in a 

skeletal specimen from Ossuary II at the Juhle 

site near Nanjemoy, Maryland, USA (NMNH 

384380). The specimen is dated to the sixteenth 

century A.D. There is no evidence of European 

contact. The secondary nature of the burials 

makes it virtually impossible to obtain complete 

skeletons. However, the two long bones in question, the left ulna and tibia, exhibit similar periosteal lesions and both are from an individual 

between 14 and 18 years of age. Thus, the probability is high that the two bones came from the 

same individual. The periosteal, reactive bone is 

superficial to the intact cortex (Figure 184) and 

is porous fiber bone rather than compact bone. 

There is no evidence of a cloaca or marrow 

involvement. Thus, a diagnosis of primary periostitis is justified. 

In his study of pre- and post-Columbian Pecos 

Pueblo skeletal material, Hooton (1930:308-309) 

distinguished between periostitis and osteomyelitis. Although he does not indicate the criteria by 

which this distinction is made, Hooton diagnosed 

periostitis in 13 of 503 skeletons, an incidence of 

2.6 percent. There were four cases of osteomyelitis 

found in 503 skeletons indicating that periosteal 

reactions were more common. Morse (1969:17, 

106-111) presents four prehistoric cases of periostitis in his monograph on paleopathology in archeological skeletons from the midwestern United 
FIGURE 184.—Periosteal reactive bone on the left ulna of an 

individual between 14 and 18 years of age. Some of the 

periosteal reactive bone was broken away postmortem revealing the underlying cortex (arrow), which exhibits minimal changes. Specimen from an archeological site in Maryland, USA. (NMNH 384380; scale in cm.) 

States. With the possible exception of Burial 42 

from the Klunk site in Illinois, these cases would 

appear to be secondary reactions to infection. In 

the following cases from the collections of the 

National Museum of Natural History, Washington, D. C , USA, I illustrate a few examples of 

periostitis ranging from what would appear to be 

primary periostitis to those in which a distinction 

between primary and secondary periostitis cannot 

be made. 

One example of a nonspecific periosteal lesion 

is found in a skeleton (NMNH 308679) from the 

Hawikuh archeological site in New Mexico. The 

skeletons associated with the site are dated archeologically between A.D. 1200 and 1670. The individual was female and between 25 and 35 years 

of age. The preservation of the skeleton is excellent, with virtually all bones present except some 

FIGURES 185, 186.—Bilateral midshaft thickening: 185, Left 

and right tibiae of an archeological skeleton from the site of 

Hawikuh, New Mexico, USA. 186, A detailed view of the 

thickened midshaft of the left tibia; note the lack of any foci 

of active reaction. This lesion represents a healed periosteal 

lesion. (NMNH 308679.) 
FIGURES 187-189.—The right and left tibiae of a post-Columbian adult male skeleton from an archeological site in 

Florida, USA: 187, Lateral view; note the presence of a 

porous, thickened lesion below midshaft on the right tibia. 

The left tibia is normal. 188, A detailed view of the lateral 

aspect of the lesion on the right tibia. 189, The medial view 

of the right and left tibiae. The thickened area is less porous 

than the lateral aspect of the lesion. (NMNH 377457.) 
NUMBER 28 135 

of the hands and feet. The skull is normal except 

for a slight amount of occipital flattening, dental 

caries, and the loss of the lower left second molar 

antemortem. There is a supernumerary premolar 

in the left mandible. The postcranial skeleton is 

also normal except for a bilateral, diaphysial, 

cortical thickening of the tibiae (Figures 185, 

186). Grossly, the thickening takes place circumferentially. The lesions of both tibiae are remarkably similar. The bone surface of both lesions is 

smooth except for a medial focus, which has a 

slightly raised plaque adjacent to a region of 

longitudinal striations. The overall appearance of 

the lesions is one of a well-contained chronic 

process. There are no cloacae and no evidence of 

fracture. 

The original cortex of both tibiae has been 

partially remodeled near the main focus of the 

lesion. A somewhat greater amount of periosteal 

bone has been added on the lateral side, and it is 

on this side that the maximum cortical remodeling has taken place. The predominant lesion is 

periosteal and thus it is appropriately classified 

as periostitis. However, there is evidence of encroachment by bone reacting to the disease in the 

marrow cavity. This means that the focus of the 

lesion could have been the marrow cavity with 

secondary activation of the periosteum, as does 

occur in osteomyelitis. However, the superficial 

nature of the lesion and minimal medullary 

change make a periosteal origin somewhat more 

probable. 

Another example of periostitis is seen in an 

archeological skeleton from the Canaveral Peninsula of Florida, USA (NMNH 377457). The 

skeleton is an adult male approximately 30 years 

of age as estimated by pubic symphysis morphology. Arthritic degeneration elsewhere in the skeleton is suggestive of a somewhat older age. The 

presence of trade beads indicates a post-Columbian date for the site. The skull vault is normal, 

although the temporal portion of the temporomandibular joint exhibits considerable arthritic 

degeneration. The mandibular portion of the 

joint is much less severely affected. The dentition 

is considerably worn, as is typical of this population, and there is evidence of at least two abscessed teeth. The postcranial skeleton is incomplete. With the exception of severe arthritic degeneration of the right elbow, there is no evidence 

of pathology except for a lesion on the shaft of 

the right tibia (Figures 187-189). This lesion 

begins at midshaft and extends distally 10 centimeters. It involves both the medial and lateral 

sides of the shaft and encompasses most, but not 

all, of the circumference. On the medial side, the 

lesion consists of fine porous bone with a longitudinally striated appearance at the boundary 

with normal bone. Laterally the lesion has a more 

irregular surface but is still composed of fine 

porous bone. Posteriorly there are two small isolated plaques of fine periosteal bone located distally to the main lesion. The overall appearance 

of the lesion suggests an active, but chronic, 

inflammation limited to a single bone of the 

skeleton. The location, morphology, and circumscribed nature of the lesion is suggestive of the 

bony reaction to an overlying skin ulcer. The Xray picture of the two tibiae is of poor quality due 

to soil infiltration into the cortex and medullary 

cavity. There has been a slight degree of remodeling of the original cortex beneath the lesion, in 

which the lytic process predominates. There may 

have been slight encroachment into the medullary cavity by reactive bone, although the predominant disease process is periosteal. 

Another case from the same site in Canaveral, 

Florida (NMNH 377516) illustrates a periosteal 

reaction apparently resulting from a penetrating 

wound into the medial tibia just proximal to the 

midshaft. The main focus of the pathology on the 

tibia is a central, elongated, sharply outlined, 

traumatic defect (Figures 190-191), surrounded 

by a thickened periosteal lesion. There is a second 

periosteal lesion just inferior to the tuberosity. 

This lesion does not contain a central cavity. The 

skeleton is an adult male with an age estimated 

to be 24 to 30 years on the basis of pubic symphysis morphology. There is a hint of reactive 

periostitis on the skull near vertex and a small 

depression on the right frontal bone. The right 

humerus has a thickened periosteal lesion in the 

distal medial region. Adjacent to this lesion is a 

lytic focus. The left ulna has a slight swelling of 
136 SMITHSONIA

N CONTRIBUTIONS TO ANTHROPOLOGY 

the distal diaphysis with an irregular surface. 

There is no corresponding pathological involve-

ment on the radius. A comparison of the lateral 

roentgen images of the two tibiae suggests a slight 

reactive remodeling in the marrow cavity of the 

pathological right bone. However, the predomi-

nant lesion is periosteal. There is no apparent 

sclerotic reaction surrounding the central cavity 

in the most distal lesion. 

If the tibial lesion was the only lesion in the 

skeleton, a periosteal reaction to a local trauma 

(perhaps a sharp penetrating object embedded in 

the bone) would be the most probable diagnosis 

and, indeed, this remains a strong probability. 

However, the complications introduced because 

of the other bone lesions raises the possibility of 

a systemic disease affecting many parts of the 

skeleton, but producing a more pronounced lesion 

in a bone traumatized by a penetrating wound. 

In any case, we do have a lesion on the tibia, 

which is not bilateral and seems to be associated 

with a localized trauma. As such, it provides an 

example of what one might expect to find in 

periostitis resulting from injury to bone. 

There are several examples of periosteal reac-

tions to skin ulcers in the human skeletal collec-

tions of the National Museum of Natural History, 

Washington, D. C. One of these illustrates the 

distinctive external morphology associated with 

this condition. This specimen is a right tibia 

excavated from Ossuary II at the Juhle site near 

Nanjemoy, Maryland, USA (NMNH 384299). 

This site is dated to the sixteenth century A.D. 

There is no evidence of European trade contact. 

There is a large area of reactive thickening on the 

medial part of the bone just below the midshaft. 

This lesion measures 65 by 40 millimeters (Figure 

FIGURES 190, 191.—Right and left tibiae of a post-Colum-

bian adult male skeleton from an archeological site in Flor-

ida, USA: 190, Medial view; note the periosteal reactive 

bone proximal to midshaft. There is a central lytic focus that 

might have been traumatically induced. 191, Detailed view 

of the central lytic focus (arrow) on the right tibia. There is 

evidence of active periostitis surrounding the lytic area. The 

lytic depression does not penetrate to the marrow. (NMNH 

377516.) 
NUMBER 28 137 

FIGURES 192, 193.—Right adult tibia from the Juhle site in Maryland, USA. This site is dated 

to the sixteenth century. There is no evidence of European contact. 192, Anterior view; note the 

large area of reactive bone on the medial side just distal to midshaft (scale in cm). 193, A 

detailed view of the bony reaction to an overlying skin ulcer. Distal to this lesion is an additional 

periosteal reaction, which is not as well organized (arrow). (NMNH 384299.) 

192). There is a nodular thickening superior to 

this lesion and another area of reactive bone on 

the distal metaphysis (Figure 193). The sharply 

demarcated, thickened nature of the central lesion is characteristic of a bony response to a skin 

ulcer. This case appears to have been complicated 

by disseminated infection giving rise to the two 

other foci of periostitis. 

Periosteal skull lesions are also seen in archeological materials and present a challenge to the 

paleopathologist because of their resemblance to 

the expansive, porous bone seen in the anemias. 

An example of skull periostitis is seen in a skull of 

a young child (NMNH 377545). The dental age 

of the specimen is about 3 years. The presence of 

trade beads indicates a post-Columbian date for 

the site, located on the Canaveral Peninsula in 

Florida, USA. The major lesion on the skull 

involves the external surface of the skull and 

includes the contiguous portions of the frontal 

and both parietal bones (Figure 194). Less extensive lesions can be seen on the supraorbital region 

of the left frontal, lateral left parietal, and left 

temporal bones. These last two lesions may have 

been bilateral, although postmortem damage prevents confirmation on the right side. Porous lesions are also seen in the left orbital roof. A 

diffuse, porous lesion appears on the posterior 

part of the skull, primarily on the parietals near 

the lambdoid suture. The maxilla, both facial 

and palatine portions, is also affected, as is the 

anterior portion of the mandible. In the temporal 

bone, the maxilla, and the mandible, the lesions 

appear to involve the spongiosa. The other lesions, including the large lesion on the vault, are 

superficial. A cut section from the left parietal 
138 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

mil 

METR 

195 

IC 1 SYS T 

n. 

EM 

n 

FIGURES 194, 195.—An extensive periosteal lesion concentrated in the anterior region of the skull vault: 194, Top view 

of skull. 195, Detailed view of cut section of bone including 

areas of the lesion and normal bone. Note that the periosteal 

bone has been layed down on the intact cortex (arrow) and 

that there is no expansion of the diploe. (3-year-old child 

from a post-Columbian site on the Canaveral Peninsula, 

Florida, USA, NMN H 377545.) 

shows the outer cortex to be intact with abnormal 

bone, added in layers, superficially over the outer 

cortex (Figure 195). Unfortunately there are no 

postcranial bones associated with the skull. 

Brucellosis 

PATHOLOGY 

Brucella is a genus of gram negative rods (bacilli) containing three species pathogenic to domestic animals and through them to man: Brucella 

abortus, which causes miscarriage in cattle and 

horses; Brucella melitensis, mainly affecting goats 

in the Mediterranean area, transmitted to man 

through milk; and Brucella suis in domestic pigs, 

transmitted through infected meat. The human 

disease is a chronic infection of lungs and other 

organs, characterized by recurring bouts of fever 

(undulant fever) (Spink, 1956). In a number of 

cases the skeleton is involved by the hematogenous route. Skeletal involvement varies from 2-

70 percent of the cases and is especially high in 

B. melitensis infections (Jaffe, 1972:1048). Adult 

males are affected much more frequently than 

females; children are usually spared (Glasgow, 

1976). The most common skeletal lesion is on the 

spine or pelvis. Ganado and Craig (1958) observed 130 instances of spondylitis in 6300 patients with brucellosis. Long bones are rarely 

involved. Kelly, Martin, Schirger, and Weed 

(1960) observed in 36 cases the following localizations: spine 17, humerus 3, femur 2, ilium 1, 

hand 1, foot 1. The spinal lesion locates in the 

vertebral bodies, especially of the lower dorsal, 

lumbar, and lumbosacral areas, often involving 

more than one vertebra (Lowbeer, 1948, 1949). 

The lesion is a lytic cavitation. Grossly and on Xray, it frequently can be seen penetrating the 

vertebral end-plate and extending through the 

nucleus pulposus of the disc into the next vertebral body (Figure 196). The cancellous bone 

within the focus is destroyed without formation 

of significant sequestra. The cortex also may be 

perforated, leading to parosteal abscesses. There 

is usually very little, if any, reactive bone formation except in the healing phase (Glasgow, 1976). 

In contrast to tuberculosis, which it resembles in 

several ways, complete collapse of vertebrae with 

gibbus formation is usually not observed (Keenan 

and Metz, 1972) and paravertebral abscess is rare 

(Kelly, Martin, Schirger, and Weed, 1960; Glasgow, 1976). Lesions in the pelvis likewise show, 
NUMBER 28 139 

yj^jr^J^jjJtyBJ 

FIGURE 196.—Brucellosis of vertebral bodies, multifocal cavitating abscesses with perforation of intervertebral disc. (Histologic section. Courtesy Dr. L. Lowbeer, Tulsa, Oklahoma, 

USA). 

usually multifocal, cavitation of the spongiosa, 

occasionally with perforation of the overlying 

cortex. Monoarticular or polyarticular involvement in large joints occurs, but usually without 

significant destruction. 

PALEOPATHOLOGY 

Since the spread of brucellosis between humans 

is very rare (Glasgow, 1976:283), the presence of 

the disease depends on the presence of domestic 

vectors including cattle, horses, goats, sheep, pigs, 

and dogs. Clearly, if the disease was endemic in 

ancient times, it should be seen in archeological 

skeletons. However, brucellosis receives little attention in the literature on paleopathology. 

Brothwell (1965b:690, 692-693) reports a case of 

bone inflammation in Early Bronze Age remains 

from Jericho in the Near East, which he tentatively attributes to brucellosis. However, Brothwell, initially attributed the diseased lower lumbar vertebrae to infectious arthritis. Although the 

description of the Jericho specimen is incomplete, 

the disease involves the two fibulae and the lumbar spine. One fibula is irregular and has a 

somewhat thickened shaft, the other is also enlarged but has no evidence of active infection. 

One of the pathological skeletons in the National Museum of Natural History, Washington, 

D. C , has lesions that possibly can be attributed 

to brucellosis. This case (NMNH 227474) is a 

female Lapp skeleton from Norway accessioned 

by the museum in 1904. The estimated age at 

death on the basis of epiphysial fusion and pubic 

symphysis morphology is 20 to 25 years. The 

archeological date is unknown. The skull of this 

specimen is normal. Unfortunately, there is some 

mixture of bones from other skeletons. This problem is particularly apparent with the hand and 

foot bones, in which there are representatives of 

at least four individuals. However, there is no 

gross evidence of disease in any of these bones, so 

in all likelihood the hands and feet were not 

affected by disease in this case. Of the remaining 

bones of the upper extremity, only the left humerus is abnormal. Grossly only the head of the 

humerus is affected. Indeed, on superficial inspection the affected bone could easily be confused 

with postmortem damage due to burial conditions. However, the presence of periosteal, reactive bone peripheral to the destroyed area on the 

humeral head provides evidence of a pathological 

process. The humeral head itself has been eroded 

away, leaving exposed somewhat cavitated 

spongy bone, in which there has been no osteoblastic response to the disease process. However, 

the picture of the lytic process is obscured by 

what is undoubtedly some postmortem damage 

to the pathological bone. 

The glenoid cavity of the left scapula exhibits 

a similar destructive, pathological process obscured by postmortem damage. Here, again, there 

is a slight perifocal bony reaction. The left radius 

and ulna are normal. 

The X-ray film of the left humerus indicates 
140 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

much more extensive involvement than is seen 

grossly. The cortex is much thinner than in the 

right humerus and the appearance of the bone 

resembles a fairly coarse, net-like structure, suggesting multiple foci for the disease process. Virtually the entire left humerus is affected. 

The cervical vertebrae are all normal as are the 

first three thoracic vertebrae. An initial X-ray 

film of the thoracic and lumbar vertebrae indicated that the fourth through the sixth thoracic 

vertebrae were markedly osteoporotic. However, 

comparison of the corresponding articular facets 

and shape of the vertebral bodies revealed that 

these vertebrae were from another individual. 

Initially, this fact was not obvious since both the 

size and color of these vertebrae were appropriate. 

This problem serves to highlight the need to 

insure that all bones associated with a paleopathological specimen actually belong to a single individual and that great care is taken to prevent 

mixing bones during excavation and subsequent 

processing. 

The seventh and eighth thoracic vertebrae are 

normal. However, in T9 there is a large lytic 

process that has created a cavity in the body. The 

inferior plate of the body is largely destroyed, and 

there is a hole one centimeter in diameter into the 

neural canal. There is no marked gross evidence 

of bony reaction to the disease process. The tenth 

thoracic vertebra contains a similar lesion except 

that the superior plate of the body is involved. 

Thus the vertebral bodies adjacent to a single 

intervertebral disk are affected. The anterior cortex of the bodies of the tenth thoracic through the 

second lumbar vertebrae have enlarged vascular 

foramina but are otherwise normal. There is a 

suggestion of a lytic cavity on the anterior body 

of L3. On the anterior cortex of the body of L4 

there are four depressed lytic lesions, which are 

not confluent. In the largest of these there is slight 

scalloping, suggesting coalescence of two or more 

lytic foci. The fifth lumbar vertebra exhibits slight 

reactive bone on the lateral cortex of the body. 

In the sacrum, the anterior surface of the first 

and second bodies shows evidence of slight erosion 

and reactive bone. However, the left and right 

articular surfaces of the sacrum show a massive 

FIGURE 197.—Large circumscribed, lytic lesion in the sacroiliac joint surface of the innominate (arrow) with multiple 

lytic foci on the corresponding surface of the sacrum, possibly 

due to brucellosis. (Adult, female skeleton from Norway, 

NMN H 227474.) 

lytic process with multiple foci (Figure 197). The 

large cavities created by the disease process subsequently have been well circumscribed. There is 

corresponding circumscribed, lytic destruction on 

the articular portion of the innominate and adjacent bone as well. However, the cavities are 

somewhat larger than those in the sacrum. The 

major lesion on the left innominate measures 25 

X 40 millimeters, on the right 20 X 30 millimeters. 

Both cavities are at least 10 millimeters deep. 

The long bones of the lower extremities are all 

normal with the exception of the left femur. In 

this bone there is a well-circumscribed lytic lesion 

15 X 18 millimeters and approximately 5 millimeters deep, which is lateral to the lesser tubercle 

on the posterior diaphysis. Some of the edges of 

this lesion have been broken postmortem, suggesting that the lesion was a cyst rather than a 

shallow depression during life. 

Disease entities in differential diagnosis for this 

case must include, in addition to brucellosis, tuberculosis, osteomyelitis, mycotic infections, and 

cancer. The lesions of greatest significance in this 

case are the lytic cavities found in corresponding 
NUMBER 28 141 

endplates of the ninth and tenth thoracic vertebrae. The total bilobed appearance of the two 

cavities suggests an initial focus for the disease in 

the intervertebral disk. This is an unlikely focus 

for tuberculosis, osteomyelitis, or mycotic infections, but is typical for brucellosis (Glasgow, 1976: 

286). The fact that the vertebral bodies have not 

collapsed argues against tuberculosis. The roentgen appearance of the humerus has at least a 

superficial resemblance to patterns seen in multiple myeloma (plasmacytoma), although the irregular distribution of the lytic process argues 

against this disease. 

Glanders 

PATHOLOGY 

Glanders is an infectious disease of horses and 

donkeys, caused by the gram negative bacterium 

Malleomyces mallei. The disease is transmissible 

from animal to man and from man to man. In 

animals and man the nasal mucosa is frequently 

involved and often the portal of entry. Bone 

lesions in glanders are rare. The organism may 

affect the periosteum from adjacent soft tissue 

abscesses and skin ulcers. There can be marked 

periosteal reactive bone formation. Hematogenous osteomyelitis in glanders is very rare and 

inconspicuous (Beitzke, 1934c). The part of the 

skeleton most often affected is the skull, secondary 

to nasal and oral mucosal lesions. Involvement 

with defects of nasal bones, nasal septum, ethmoid, and sphenoid have been observed. Destruction of turbinates with perforation into the maxillary sinus and perforations of the hard palate 

occur. Cranial vault lesions, secondary to ulcerating glanders of the scalp, have been seen. Other 

bone lesions in glanders are almost exclusively 

limited to the lower extremities, particularly the 

tibia. The lesion may present as periostitis or 

osteomyelitis, occasionally with secondary infection by staphylococci, which modify the picture 

towards the appearance of ordinary osteomyelitis. 

The bone lesions in glanders are not diagnostic 

in dry bone. The main reason to mention them is 

to point out the similarity to tertiary syphilis and 

to some lesions seen in leprosy. Joint involvement 

in glanders is not rare, occurring mostly by extension from adjacent soft tissue lesions, and only 

occasionally secondary to an epiphysial bone focus. In 27 cases gathered from the literature, 

Beitzke (1934c) found distribution as follows: 

Knee 16, elbow 4, ankle 4, toes 2, fingers 1, tarsus 1. 

Tuberculosis of Bones and Joints 

PATHOLOGY 

Tuberculosis is a chronic infectious disease 

caused by Mycobacterium tuberculosis of the human 

or bovine type. The route of infection is usually 

through the respiratory tract, leading to the formation of a primary focus in the lung, followed 

by single or multiple foci in the regional hilar 

lymph nodes. Both lesions together form the primary complex. Much less common is the intestinal pathway with formation of a primary complex in the intestinal wall and mesenteric lymph 

nodes. The later course of the disease depends on 

the size of the inoculum, the virulence of the 

organisms, and the resistance of the host. In most 

instances (at least in Western populations of the 

nineteenth century), the primary complex heals 

without leading to a progressive disease. If the 

primary complex fails to heal, the lung lesion 

progresses and tubercle bacilli may be early disseminated through the bloodstream to other organs and tissues. Again, the number of organisms 

and the immunological capacity of the patient 

determine whether this early hematogenous dissemination will lead to fatal miliary tuberculosis 

and/or tuberculous meningitis or to isolated organ tuberculosis. Organ tuberculosis may not 

make its appearance until years after the early 

dissemination of organisms, and is precipitated 

by lowered host resistence due to malnutrition, 

other disease, or possibly local trauma. Since 

dormant primary pulmonary foci may harbor 

viable organisms for many years, late hematogenous dissemination also may become the source 

of organ tuberculosis. Skeletal tuberculosis is, 

with rare exceptions, the result of limited hematogenous dissemination. 
142 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

Statistical Data 

Although, obviously, statistical information is 

not available for earlier historic and prehistoric 

populations, data concerning the frequency and 

mortality of tuberculosis in the late nineteenth 

and early twentieth centuries, before chemotherapy and antibiotics, might serve as a guideline of 

limited value. The tuberculosis mortality in Germany in 1892 was 260 per 100,000 living inhabitants. For the beginning of the twentieth century 

(1901) statistics are only available for part of 

Europe and th6 United States and cover mortality of pulmonary tuberculosis only, ranging from 

111 to 289 per 100,000 population. The age and 

sex distribution of all tuberculosis deaths for 

Western Europe, the United States, and Canada 

for 1949 were published by the International 

Union Against Tuberculosis in 1964. All statistics 

show a predominance of male over female deaths 

at a rate of almost 2:1. One must also appreciate 

that the figures for 1892 and 1901 are already 

modified by successful surgery and the figures for 

1949 by the availability of effective antibiotics 

and chemotherapy. Therefore, these data represent less than a minimum of incidence which one 

should expect in earlier periods in areas involved 

by tuberculosis. The overwhelming majority of 

tuberculous infections affect the lungs. Skeletal 

tuberculosis comprises only about 3 percent of 

the total and about 30 percent of extrapulmonary 

tuberculosis (Kastert and Uehlinger, 1964:444, 

445). Even so, the official yearbook of tuberculosis 

for West Germany still reports 20,342 cases for 

1956, 3358 of them new. It is particularly noteworthy that not only the total tuberculosis mortality has steadily declined but, even more so, 

that in infants and children. 

Among 560 cases of fatal hematogenous tuberculosis autopsied in the 10-year period 1923-1932 

were 115 incidents of skeletal tuberculosis. Of 

these, 58 were limited to the skeleton while 21 

showed tuberculous foci in other organs, 12 

showed active pulmonary tuberculosis and 24 

organ and lung tuberculosis (Kastert and Uehlinger, 1964:447). 

The distribution and frequency of tuberculosis 

of bones and joints in a large clinical series (1752 

cases) before 1892 has been published by Alfer 

(1892) (Table 5). In addition to the tabulated 

cases, 91 patients presented with multiple tuberculous bone and joint lesions. The age distribution of the same series of cases is shown in 

TABLE 5.—Localization of skeletal tuberculosis listed in 

order of decreasing frequency (after Alfer, 1892) 

Location 

BONES 

Spine 

Tarsals and metatarsals 

Carpals and metacarpals 

Ribs 

Tibia and fibula 

Radius and ulna 

Phalanges of fingers 

Temporal bone 

Phalanges of toes 

Pelvis 

Sternum 

Femur 

Humerus 

Mandible 

Scapula 

Orbital margin 

Parietal bone 

Frontal bone 

Maxilla 

Sacrum 

Zygoma 

Patella 

Clavicle 

Occipital bone 

Coccyx 

JOINTS 

Knee 

Hin 

No. of cases 

239 

184 

109 

67 

49 

48 

38 

33 

31 

27 

21 

14 

10 

9 

8 

7 

5 

5 

5 

3 

2 

2 

2 

1 

1 

281 

941 

Elbow 

Ankle 

Shoulder 

Wrist 

Metacarpal phalangeal joints 

Metatarsal phalangeal joints 

Sternoclavicular joint 

Acromioclavicular joint 

113 

43 

28 

20 

5 

4 

4 

1 
NUMBER 28 143 

TABLE 6.—Age distribution of skeletal tuberculosis in bones and joints listed in order of 

decreasing frequency (after Alfer, 1892) 

Location 

BONES 

Spine 

Tarsals and 

metatarsals 

Carpals and 

metacarpals 

Ribs 

Tibia and fibula 

Radius and ulna 

Phalanges of fingers 

Temporal bone 

Phalanges of toes 

Pelvis 

Sternum 

Femur 

Humerus 

Scapula 

Orbital margin 

Frontal bone 

Maxilla 

Mandible 

Parietal bone 

Sacrum 

Patella 

Clavicle 

Zygoma 

Occipital bone 

Coccyx 

JOINTS 

Knee 

Hip 

Elbow 

Ankle 

Shoulder 

Wrist 

Metacarpal phalangeal joints 

Metatarsal phalangeal joints 

Sternoclavicular 

joint 

Acromioclavicular 

joint 

Multiple foci | 

LD 

1 

o 

89 

9 

16 

-

12 

6 

15 

6 

2 

1 

-

2 

1 

-

1 

-

-

2 

-

-

-

-

-

-

47 

58 

7 

5 

-

1 

-

-

-

19 

o 

1 in 

59 

20 

12 

4 

5 

9 

7 

4 

6 

1 

1 

2 

2 

-

2 

-

-

1 

-

-

52 

59 

14 

9 

2 

-

-

13 

m 

1 

o 

32 

26 

16 

9 

7 

6 

4 

2 

5 

3 

-

-

-

1 

-

-

-

-

-

-

47 

43 

14 

10 

2 

-

-

1 

1 

14 

-20 

m 

23 

38 

23 

8 

8 

8 

4 

3 

7 

7 

3 

1 

2 

2 

2 

1 

1 

1 

1 

-

-

-

-

-

37 

46 

21 

5 

6 

1 

1 

3 

-

-

11 

in 

CM 

1 

o 

CM 

9 

14 

12 

5 

3 

4 

1 

7 

1 

5 

1 

3 

1 

2 

-

1 

1 

3 

-

-

-

-

-

20 

9 

12 

2 

3 

5 

1 

-

I 

6 

-30 

in 

CM 

10 

10 

5 

9 

2 

2 

5 

1 

1 

2 

1 

3 

1 

1 

1 

-

1 

1 

-

-

1 

-

-

11 

11 

9 

1 

5 

1 

-

5 

m 

en 

1 

o 

CO 

3 

10 

1 

5 

1 

5 

2 

2 

2 

2 

1 

1 

-

-

-

1 

23 

6 

6 

1 

3 

-

-

-

-

4 

^ears -40 

m 

CO 

6 

7 

5 

5 

7 

1 

-

3 

1 

3 

3 

2 

1 

-

2 

-

-

1 

_ 

-

-

-

-

-

-

11 

-

5 

3 

1 

3 

-

1 

1 

3 

old* -45 

o 

3 

6 

3 

10 

_ 

2 

-

1 

2 

3 

2 

1 

1 

_ 

1 

-

-

-

1 

-

11 

4 

9 

2 

1 

1 

1 

2 

-50 

i n 

1 

8 

6 

-

1 

_ 

-

-

-

-

3 

-

1 

-

-

-

_ 

-

-

-

1 

-

-

3 

1 

8 

-

2 

3 

1 

-

-

-

1 

in in 1 

o 

in 

4 

11 

2 

7 

1 

2 

1 

1 

2 

1 

-

-

-

2 

-

-

-

-

1 

-

-

-

2 

1 

5 

3 

2 

2 

1 

5 

o 

1 

in 

•n 

_ 

9 

2 

2 

_ 

1 

1 

-

1 

-

3 

-

-

-

-

-

1 

1 

8 

3 

2 

-

1 

1 

-

-

-

-

4 

in 

1 

o 

9 

4 

2 

1 

2 

1 

-

-

-

1 

-

-

-

-

-

-

1 

-

_ 

-

-

-

-

-

6 

2 

2 

3 

-

-

3 

o 

1 

i n 

t£5 

_ 

5 

2 

1 

2 

_ 

-

2 

1 

-

-

-

-

-

-

-

-

3 

-

-

-

-

-

-

-

-

1 

i n 

1 

o 

2 

_ 

-

1 

_ 

-

-

-

1 

_ 

-

-

-

-

-

-

_ 

-

-

-

-

-

-

-

-

-

o 

00 

1 i n 

_ 

1 

-

-

-

-

-

_ 

-

-

-

-

-

-

-

-

-

-

-

* Overlap in age categories is from Alfer and is not resolved here. 
144 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

Table 6. It indicates the great preponderance of 

skeletal tuberculosis affecting infants and children. 

General Pattern of Bone and Joint Tuberculosis 

Tubercle bacilli circulating in the bloodstream 

locate within the skeleton, particularly in areas of 

hemopoietic (red) marrow, which has a high circulatory and metabolic rate. These are, essentially, the areas of cancellous bone rather than 

the cortex or medullary cavity. As far as long 

bones are concerned, this especially means metaphyses and epiphyses in adults. In infants and 

young children, the distribution of hemopoietic 

marrow is much wider so that tuberculous foci 

often occur in tubular bones of hands and feet 

and in ossification centers of tarsal and carpal 

bones in addition to occasional diaphysial lesions 

in long bones. At all ages, vertebrae, ribs, and 

sternum have hemopoietic marrow, which explains the frequent tuberculosis of the spine at all 

ages. The flat bones, particularly the cranial 

vault, are more frequently involved in infants and 

children than in adults. Joint tuberculosis is intimately linked to involvement of the adjacent 

bones and for that reason discussed here rather 

than separately. The process may begin in the 

synovial membrane or in the bone or simultaneously, in both. This is explained by the joint 

blood supply to the epiphysis and the joint capsule. In an advanced stage, the original focus 

often cannot be ascertained. 

The morphology of tuberculous lesions in dry 

bones is not specific and overlaps considerably in 

appearance with manifestations of other bone 

infections. However, there are some general characteristics of diagnostic value, in addition to the 

age-modified distribution of the lesions in the 

skeleton. 

The tuberculous process, in its exudative phase, 

permeates the marrow spaces, devitalizing areas 

of cancellous bone, thus leading to formation of 

centrally located sequestra of cancellous bone 

(caries). In its proliferative granulomatous phase, 

the process leads to local destruction and cavitation in the cancellous bone. In either case very 

little, if any, perifocal reactive bone formation is 

elicited, and often the involved bone shows perifocal or general osteoporosis. The process in long 

bones tends to remain localized, mostly to the 

metaphysial or epiphysial portion. In contrast to 

purulent osteomyelitis, massive sequestra, especially of cortical bone, are very uncommon. Periosteal reactive bone is very limited or absent with 

the exception of tuberculosis of small tubular 

bones in infants and children, characterized by 

destruction or sequestration of the cortex and 

formation of an expanded shell of periosteal reactive bone (spina ventosa). Similar changes affecting part of an involved long bone are observed 

also in the young age group. Perforation of the 

cortex with formation of an extraosseous abscess, 

with or without fistulous perforation of the skin, 

is common. Traces of such an abscess can sometimes be seen in the presence of reactive periosteal 

bone in the vicinity of the opening and, occasionally, ossification of portions of the abscess wall. 

In joints, destruction of the articular surface 

may be minimal if the process is limited to the 

synovium. Undermining and resorptive grooving 

of the articulating bones frequently occurs along 

the line of synovial or ligamentous attachments. 

If the process started in the bone or involves bone 

extensively, destruction of the articular surface 

and of the epiphyses with formation of cancellous 

sequestra and/or cavitation often occurs. Skeletal 

tuberculosis can heal without specific or surgical 

therapy. Small foci, particularly in infants and 

small children, may leave no trace, because the 

area is removed in the process of subsequent 

growth and remodeling. Foci destroying a growth 

plate will leave a growth deficit and/or deformity 

of the involved bone in the young age group. Foci 

in the vicinity of a growth plate may lead to 

excessive growth. This is not different from the 

effect of osteomyelitis. Joint tuberculosis may heal 

with obliteration of the joint cavity, often terminating in bony ankylosis with varying degrees of 

volume loss of the constituent bones. After healing, the spongiosa undergoes remodeling along 

altered stress lines but never reaches the original 

density of cancellous bone (Kastert and Uehlinger, 1964:467). 
NUMBER 28 145 

The Spine 

Vertebral tuberculosis is, in practically all of 

the clinical and autopsy series, the most common 

and most characteristic lesion. The disease begins 

usually in early childhood. A well-documented 

series of 1490 cases after 1920 has been published 

by Sorrel and Sorrel-Dejerine (1932). It shows the 

rapid decline in the number of new cases after 7 

years of age. The fourth, fifth, sixth, and seventh 

decades showed only 100, 50, 18, and 2 new cases, 

respectively. Since the disease takes a very chronic 

course, active and/or healed cases may be observed at any age. All studies indicate the predominant frequency of involvement of the lumbar vertebrae at all ages. Autopsy data concerning the frequency of involvement of individual 

vertebrae have been published by Uehlinger (in 

Kastert and Uehlinger, 1964:486) (Table 7). As 

far as the number of vertebrae affected is concerned, different statistics reported by Kastert 

and Uehlinger (1964:486) show that in about 80 

percent of the clinical and autopsy cases at least 

two adjacent vertebrae are involved, while three 

or more are affected in about 10 percent of the 

total. Multiple foci separated by intact vertebrae 

are observed in about 4 percent. 

The part of the vertebra involved is almost 

exclusively the vertebral body. Even after extensive destruction of one or several adjacent vertebral bodies, extension into the vertebral arches is 

uncommon and the true intervertebral joints and 

spinous processes are almost never destroyed. An 

exception from this rule is suboccipital tuberculosis involving the atlas and the axis. 

Because of the rudimentary bodies of these 

vertebrae, their intervertebral joints are not uncommonly involved (Oehlecker, 1924:242). Isolated tuberculous foci in posterior elements of 

vertebrae are extremely rare. Sorrel and SorrelDejerine (1932:500) observed only three cases of 

isolated spinous process and one case of lumbar 

transverse process tuberculosis in their large series. The destruction of the vertebral body is 

usually purely lytic, leading to cavitation. Central 

spongiosa sequestra can occur (Figures 198, 199). 

The vertebral collapse can be combined with a 

TABLE 7.—Distribution of lesions in 62 autopsied cases of 

vertebral tuberculosis (after Uehlinger, in Kastert and Uehlinger, 1964) (C = cervical, T = thoracic, L = lumbar, S = 

sacrum) 

NUMBER OF VERTEBRAE 

LLI 

z Q. 

CO 

z 

o 

o 

^ 

Q 

_J 

c / 

z 

3 

4 

5 

6 

7 

T 1 

2 

3 

4 

5 

6_ 

7 

8 

9 

10 

11 

12 

L 1 

Z 

3 

4 

5 

5 / 

2 

3 

4 

5 

1 2 3 4 5 6 7 8 9 10 II 12 13 14 15 16 17 Id 

pathologic fracture. Small wedge-shaped remnants of the affected vertebra often remain in 

contact with the end-plate and are displaced 

anteriorly or posteriorly by the collapse. Extension to adjacent vertebrae mostly occurs through 

the area of the nucleus pulposus of the intervertebral disc. 

A common complication of vertebral tuberculosis is the formation of uni- or bilateral paravertebral abscess or fistula (Figure 200). The presence of a paravertebral abscess on dry bone is 

characterized by flaring, shelf-like bony extensions from the affected vertebra (Figures 201, 

202). In Johansson's (1926:143) clinical material 

of 86 cases, 32 developed only abscess, 22 abscess 
146 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

FIGURES 198, 199.—Tuberculosis of spine, partly healed, 

involving thoracic (Th) vertebrae 7 and 8 and first lumbar 

(L) vertebra, with gibbus: 198, Lateral view, showing fusion 

of vertebrae and periosteal bone. 199, Cut surface, showing 

perforation of disc Th7-8 and sequestrum in LI. (52-yearold female, IPAZ autopsy S901 from 1948.) 

FIGURE 200.—Tuberculosis of the dorsolumbar spine with 

gibbus and large right psoas abscess. (Adult, PMUG, no 

number.) 
NUMBER 28 147 

FIGURES 201, 202.—Tuberculous spondylitis, healed with 

gibbus (thoracic vertebrae 6 to 9) and active with paravertebral abscess (thoracic 10 to lumbar 1): 201, Lateral view. 

202, Cut surface. (48-year-old female with visceral and miliary tuberculosis, IPAZ S 793 from 1936.) 

FIGURE 203.—Ossification in wall of right tuberculous psoas 

abscess extending to the femur, secondary to tuberculosis of 

the spine. (55-year-old male, FPAM 2894.) 
148 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

and fistula, and 2 fistula only. The abscess extends, usually downward, following the line of 

gravity, beneath the anterior longitudinal ligament and along the fascial plane of the psoas 

muscle, occasionally showing ossification of the 

abscess wall (Figure 203). The abscess may become an important source of contact infection of 

additional vertebrae, especially below the original 

focus. The tuberculous process erodes the cortical 

surface and slowly extends into the anterior portion of the vertebral bodies (Figures 204, 205). 

Such secondary extension into adjacent ribs is 

occasionally observed. 

Collapse of one or several vertebral bodies with 

remaining vertebral arches and spinous processes 

leads to a sharply angular kyphosis (gibbus). This 

deformity was observed in about 60 percent of 

the cases of spinal tuberculosis in the preantibiotic 

FIGURE 204.—Tuberculosis of lumbar vertebrae 2 and 3 and 

anterior excavation of lumbar vertebrae 4 and 5 by a prevertebral cold abscess; marked kyphotic angulation. (20-

year-old male, FPAM 3583.) 

FIGURE 205.—Lumbosacral tuberculosis with gibbus and 

presacral tuberculous abscess. Notice the almost complete 

destruction of the lumbar vertebral bodies and the excavation of the sacrum from without. (About 10 years old, FPAM 

1493.) 

era (Reinhart, 1932). The kyphosis is most 

marked in the thoracic spine (Figures 201, 202), 

while lumbar lesions may terminate with telescoping of the defect rather than severe angulation (Girdlestone, 1965:81-83). Healing may occur with permanent preservation of the deformity 

by means of bony fusion of the remnants of the 

involved vertebral bodies. New formation of spongiosa and of cortex is rather meager. Residual 

cavitary defects may remain. There is usually 

secondary bony ankylosis between the true intervertebral joints of the involved segment and often 

also ossification of the interspinous ligaments. If 

a sharp, angular gibbus develops in childhood, 

increased height of the vertebrae below, due to 

compensatory growth, is often observed. 

The differential diagnosis is mostly against osteomyelitis and healed fracture. In osteomyelitis. 
NUMBER 28 149 

the massive destruction of several vertebral bodies 

leading to the sharply angulated gibbus is uncommon. Paravertebral abscesses are also less frequently observed and, if present, may extend 

above the lesion as well as below because they 

form rapidly. In healed fracture with angular 

deformity, usually only one vertebra is involved 

with a diagonal break, and there is much less 

extensive destruction of the vertebral body. Besides, the predilected areas for fracture are the 

cervical and upper dorsal spine, a less common 

location for vertebral tuberculosis. 

Isolated tuberculosis of the sacrum and of the 

coccyx are rare (David, 1924). Abscess formation 

is a frequent complication, and in the case of the 

coccyx, total sequestration is not unusual (Konschegg, 1934:409). 

The Pelvis 

The acetabulum is most frequently involved by 

tuberculosis but, being part of the hip joint, it is 

discussed there. 

SACROILIAC JOINT—Of the pelvis in the stricter 

FIGURE 206.—Tuberculosis of the left hip with destruction 

of the femoral head and perforation of the acetabulum, 

tuberculosis of left ilium and of both sacroiliac joints. Notice 

minimal reactive bone in all affected areas. (15 years, FPAM 

5669 from 1895.) 

FIGURE 207.—Tuberculosis of spine and left ilium; reactive 

bone in wall of cold abscess in left inguinal area; notice 

round defect in ilium, erosion and bony buildup in inguinal 

area. (28-year-old male, FPAM 2488, autopsy 33582 from 

1853/54.) 

sense, the sacroiliac joint is most commonly involved (Figure 206), usually by extension of the 

lumbosacral focus unilaterally or bilaterally. This 

is observed more often in young adults than in 

children. Isolated sacroiliac tuberculosis is very 

rare. In their large series. Sorrel and Sorrel-Dejerine (1932:501) observed only two cases as compared with 114 cases secondary to lumbosacral 

involvement. There may be considerable destruction of the sacral wing with some reactive osteosclerosis (Kremer and Wiese, 1930:198). Healing 

with bony fusion may lead to asymmetrical pelvic 

deformity. 

ILIUM.—Isolated tuberculous foci in the ilium 

are rare, usually consisting of round or oval cav-
150 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOG Y 

ities with or without a central sequestrum, perforation of the cortex, or fistula (Konschegg, 1934: 

409-410). Extension of a psoas abscess into the 

ilium does occur (Figure 207). 

PUBIS AND SYMPHYSIS.—The pubis is rarely affected by tuberculosis. Both sexes participate 

about equally and most instances concern older 

children and young adults. The largest series 

published are 27 cases of Fares and Pagani (1966), 

of which about half showed other adjacent or 

remote tuberculous skeletal focj. There is apparently no relationship to trauma or parturition. 

The lesion in adults is usually close to the symphysis, which may be involved. In that case, both 

pubic bones may be affected (Kremer and Wiese, 

1930:195). The lesion is lytic and destructive, 

occasionally with formation of small sequestra. 

Abscess formation and fistula are common. In 

children, the lesion may be medial to the hip joint 

because of the incomplete ossification of the pubic 

area. 

ISCHIUM.—Similar lesions occur in the ischial 

ramus (14 ischial compared to 20 pubic lesions in 

the series of Sorrel and Sorrel-Dejerine, 1932:76). 

In addition, occasionally an isolated lesion can 

occur in the tuber ischii, similar to the more 

common lesion in the greater trochanter (Blankoff, 1927). 

The Hip 

Tuberculosis of the hip joint is the second most 

frequent skeletal lesion after tuberculous spondylitis. All statistical series agree that the majority 

of cases start in childhood and that onset of the 

disease after 25 years of age is rare (Johansson, 

1926:159; Sorrel and Sorrel-Dejerine, 1932:309). 

In the series of Sorrel and Sorrel-Dejerine, comprising 995 cases, the maximal incidence of onset 

is at 4 to 6 years of age with a second smaller 

peak around puberty. There were only 28 cases 

in the fourth, 11 cases in the fifth decade, and 4 

cases beginning after 50 years of age. In the 

majority, the lesion starts with an osseous focus 

(Konschegg, 1934:461-462). The anatomy of the 

hip joint allows early access to the joint space, not 

only to acetabular and femoral epiphysial foci 

but also to metaphysial foci of the femoral neck. 

In the Kastert series, one-third of the cases 

started from an extra-articular focus (Kastert and 

Uehlinger, 1964:508). In addition to the usual 

hematogenous route, direct extension to the hip 

joint can also occur by contact with long-standing 

abscesses from vertebral or pelvic tuberculosis. In 

advanced stages of the disease, the point of origin 

can no longer be determined. A series of 416 cases 

of tuberculous coxitis reported by Vacchelli in 

1922 (in Kremer and Wiese, 1930:202) gives the 

following breakdown: total destruction of femoral 

head and acetabulum 22, diffuse involvement of 

femoral head and acetabulum 220, diffuse synovial tuberculosis 52, isolated osseous tuberculous 

foci 122. The isolated foci were distributed as 

follows: femoral head 60, femoral neck 24, acetabulum 30, greater trochanter 8. The foci in the 

femoral head or neck may be small cavitating 

lesions or larger triangular foci with a spongiosa 

sequestrum in the center. These foci may represent territories of terminal arteries. Acetabular 

foci predilect the posterior superior rim and the 

cartilage-free center around the origin of the 

round ligament (Figures 208, 209). Foci in the 

neck of the femur are often adjacent to the medial 

inferior cortex (Girdlestone, 1965:44,45). Extension of primarily synovial tuberculosis into the 

bone occurs along the synovial attachment on the 

neck of the femur. The weight-bearing articular 

surfaces are longest preserved. Ultimately, destruction of the bones may be very extensive with 

sloping upward extension of the acetabulum, 

leading to upward partial or complete dislocation 

of the remnant of the femoral head and/or neck 

(Figures 210, 211). If the dislocation is complete, 

a neo-acetabulum is formed on the lateral surface 

of the iliac wing. In contrast to the appearance in 

congenital dislocation of the hip, the head of the 

femur is more eroded and there is no groove for 

the round ligament, which is destroyed by the 

infection before the dislocation occurs. The old 

acetabulum is not rudimentary and the neo-acetabulum shows evidence of infection. If there is 

extensive necrosis and destruction of the acetab-
NUMBER 28 151 

FIGURE 210.—Tuberculous arthritis of right hip with upward 

subluxation, partly healed. Notice restoration of subchondral 

bone plate on the partly destroyed femoral head. (16-yearold male, died of tuberculous meningitis, IPAZ S325 from 

1936.) 

FIGURES 208, 209.—Tuberculous arthritis of left hip, three 

months after resection of femur; evidence of upward subluxation: 208, Lateral view. Periosteal buildup on ischium 

probably secondary to cold abscess. 209, Medial view, hypervascularity of acetabular base. (66-year-old female with 

chronic pulmonary tuberculosis; DPUS 7641, autopsy 880 

of 1912.) 
152 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

FIGURE 211.—Destructive arthritis of right hip with upward 

subluxation, probably tuberculous. Note severe osteoporosis 

of femur and ilium and iliac shelf secondary to subluxation. 

(88-year-old female with pulmonary and lymph node tuberculosis, IPAZ autopsy 1445 from 1954, museum no. 5947.) 

ulum, its pelvic aspect shows lytic defects (Figures 

212, 213); perforation of its floor with central 

dislocation of the remnants of the proximal femur 

can occur (Figures 214, 215). Menard (1900) 

observed 105 acetabular perforations in the 

course of 268 hip resections. Tregubow (1929) 

reported 12 acetabular perforations in a series of 

500 radiologically studied cases of tuberculous 

coxitis. In healed cases, bony ankylosis usually 

occurs. Growth deficit also may be observed. 

Differential diagnosis is mainly between tuberculous and septic arthritis. The septic process is 

rapid and bone destruction is much more limited. 

Dislocation upward or centrally is not observed. 

Bony ankylosis as final outcome usually reveals 

little, if any, bone loss of the joint constituents. 

Only in infants with septic arthritis is complete 

FIGURES 212, 213.—Tuberculosis of the left hip: 212, Anterior view. 213, Medial view. Notice 

destruction of femoral head with exposure of porotic spongiosa and perforations of the involved 

acetabulum. (Adult, IPMI K M 352.) 
NUMBER 28 153 

destruction of the femoral head seen. But this 

condition is usually accompanied by osteomyelitis 

of the shaft. Statistically tuberculous coxitis was 

much more common than septic arthritis. 

FIGURES 214, 215.—Tuberculous arthritis of right hip with 

complete destruction of the acetabulum and central dislocation of the remnant of the femoral head; notice sparsity of 

reactive bone: 214, Lateral view. 215, Medial view. (Male 

about 30 years old, IPAZ 1940, old no. 2167.) 

The Trochanter 

Chronic tuberculosis of the greater trochanter 

of the femur is an uncommon but characteristic 

lesion. Sorrel and Sorrel-Dejerine (1932:70) observed, in a series of 6578 cases of skeletal tuberculosis, 32 instances of tuberculosis of the trochanter (11 in children and 21 in adults). McNeur 

and Pritchard (1955) reported 38 clinical cases 

treated at the Royal National Orthopaedic Hospital (London, England) in a period of 35 years. 

The age distribution was as follows: 30 of the 

cases were between 10 and 40 years, only 3 cases 

concerned children below 10, and 5 patients were 

above 40 years. The infection may start in the 

trochanteric bursa or in the bone. It takes a very 

chronic course and has a great tendency to recur 

FIGURE 216.—Chronic tuberculosis of right greater trochanter with fistulating abscess, hip joint free. Notice scalloped 

destruction of greater trochanter exposing porotic cancellous 

bone. (54-year-old female with pulmonary tuberculous focus, 

FPAM, Jubilaumspital 857, autopsy from 1924.) 
154 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

over many years. This has also been the experience with three cases followed at the Massachusetts General Hospital in Boston. The lesion tends 

to remain localized to the trochanter area, which 

is progressively destroyed (Figure 216). The cavity 

often contains a sequestrum of cancellous bone 

(Sorrel and Sorrel-Dejerine, 1932:70). Abscess 

and fistula formation are common. This actually 

represents the most identifiable tuberculous bone 

lesion of the adult with exception of tuberculous 

spondylitis. This entity is relatively little known 

except to orthopedists, but a number of similar 

series have been published (Meyerding and Mroz, 

1933; Wassersug, 1940; Alvik, 1949; Ahem, 

1958). 

The Knee 

Tuberculosis of the knee joint occurs about as 

often or even more frequently than tuberculous 

coxitis. Again, the majority of cases begin in 

infancy, childhood, and adolescence. Johansson 

(1926:177) observed 50 percent before the age of 

5 years, with about an equal distribution between 

the sexes. The series of Sorrel and Sorrel-Dejerine 

(1932:247) comprises 558 cases, of which 34 occurred in the first year of life and only 51 cases 

began after age 20. The majority of cases start as 

synovial tuberculosis and may remain so. Extension of the synovial infection occurs along the 

capsular insertions of the femur and tibia and 

along the attachments of the cruciate ligaments. 

Linear cortical erosion and undermining destruction of the adjacent portion of the articular surface occurs. Significant amounts of localized destruction of femoral condyles or of the tibial 

plateau are observed only if a primary or simultaneous hematogenous osseous focus, with or 

without sequestrum, is present (Figure 217). Such 

foci are more often found in the femoral condyles 

or in the tibial epiphysis, rarely in the patella or 

fibula. Konig (1906:112) observed, in a series of 

720 cases, 50 with involvement of the patella. In 

33 of these the patella was the only focus, with or 

without secondary extension to the knee joint. In 

healing, fibrous or bony ankylosis results. If bone 

destruction was absent or limited, differentiation 

FIGURE 217.—Tuberculosis of knee, recurrent after previous 

surgery. Notice the destruction of subarticular bone and the 

minimal reactive bone formation. (13-year-old female, 

DPUS 3921 from 1899.) 

from the end-stage of rheumatoid or septic arthritis may be impossible. Both rheumatoid and 

tuberculous gonitis are usually accompanied by 

osteoporosis of the involved limb. Tuberculous 

and septic arthritis are more often unilateral than 

rheumatoid arthritis. In severe cases, particularly 

in children, dislocation and valgus or varus deformity of the knee is observed, depending on the 

relationship of the osseous focus to the growth 

plate. Generally, the adult cases are less destructive than the infantile ones (Sorrel and SorrelDejerine, 1932:267). 

The Ankle and Tarsal Bones 

Tuberculosis of the ankle most commonly involves the tibiotalar joint (Figure 218), much less 
NUMBER 28 155 

FIGURE 218.—Tuberculous arthritis of right ankle with extensive destruction of distal tibial epiphysis and partial 

ankylosis with remnants of talus; histologically proven, 9-

years duration. Initiated by crushing trauma. (25-year-old 

male, PMES 2 FT 16(1) from 1930.) 

commonly the talocalcaneal joint. The lesion is 

most common in children. In the large series of 

Sorrel and Sorrel-Dejerine (1932:210), the tibiotalar joint was involved in 185 cases of which, 

121 cases were below 13 years of age and only 64 

were adolescents or adults. The maximum incidence is at 3 years of age. In most cases the 

process seems to start with an hematogenous 

osseous focus. In the majority, the primary bony 

focus is in the talus, less commonly in the distal 

tibia and rarest in the fibula. The ossification of 

the talus begins at birth and essentially fills the 

cartilage model at 2 years of age, leaving only the 

articular cartilage between the ossification center 

and the adjacent joints. This explains why isolated tuberculosis of the talus without involvement of the adjacent joints is not observed (Sorrel 

and Sorrel-Dejerine, 1932:210), but early extension into the tibiotalar, and, less often, into the 

talocalcaneal joint as well, is the rule. In tibiotalar 

tuberculosis of talar origin, the talus is cavitated 

and often ultimately destroyed. In the cases of 

tibial origin, there is significant destruction of the 

distal tibial epiphysis and sometimes also of the 

metaphysis. Healing always leads to tibiotalar 

bony ankylosis. In advanced cases of tuberculosis 

of the ankle, the talocalcaneal joint frequently 

becomes involved at any age. If the talus was 

completely destroyed, tibiocalcaneal bony ankylosis develops with uptilted position of the calcaneus. This would not be the case in ankylosis 

following juvenile rheumatoid arthritis. Since the 

ankle is a weight-bearing joint, limited perifocal 

osteosclerosis does occur. 

Isolated involvement of the talocalcaneal joint 

usually is due to secondary extension of a calcaneal focus. This tuberculosis, limited to the lower 

ankle joint, is observed only in older children 

between ages of 7 and 16 (Sorrel and SorrelDejerine, 1932:207). Healing terminates with 

broad bony fusion of talus and calcaneus. 

Of the tarsal bones, after the talus, the calcaneus is most frequently affected by tuberculosis. 

Sorel and Sorrel-Dejerine (1932:207) observed 

131 cases of calcaneal tuberculosis but only 29 

cases in all other tarsal bones. The explanation 

for the frequent and often isolated involvement 

of the calcaneus rests with its development. An 

ossification center usually appears as early as the 

last trimester of intrauterine life and ossification 

is not completed until 17 to 18 years of age. This 

makes a highly vascular area available for tuberculous seeding in infancy and early childhood, 

while thick layers of the cartilage still separate 

the focus from the adjacent joint cavity (Sorrel 

and Sorrel-Dejerine, 1932:268). In early childhood, central tuberculosis of the calcaneus is fairly 

frequent and may heal without permanent traces, 

because of the effect of growth and remodeling. 

At age 7 to 9 years an apophysial ossification 

center appears on the posterior portion of the 

calcaneus, and during later childhood tuberculous foci adjacent to the anterior surface of the 

posterior growth plate appear. The lesion usually 
156 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

shows a cavity with a central spongiosa sequestrum and often some perifocal osteosclerosis. After 

termination of growth in the adult, tuberculous 

foci of the calcaneus readily breaks through or 

around the articular cartilage into the talocalcaneal joint and from there spread to the tibiotalar 

joint (Sorrel and Sorrel-Dejerine, 1932:59-60). 

The cuboid is much less often involved and 

most of the patients are children (11 children, 2 

adults). The ossification of the cuboid begins at 

3 months of age and terminates at 9 to 10 years. 

Occasionally the navicular also is involved in 

older children (6 cases in children, 1 adult). The 

ossification of the navicular begins at 2V2 to 5 

years of age and terminates between 10 and 12 

years. The cuneiformes are rarely involved; if 

destroyed, medial deflection of the foot may occur. Foci like these may remain isolated in children and may heal without joint involvement. 

All these data are taken from the discussions of 

Sorrel and Sorrel-Dejerine (1932:63-65). In 

adults, tarsal bones not uncommonly participate 

in extensive tuberculosis of the ankle. The differential diagnosis between tuberculosis and subacute osteomyelitis on isolated tarsal lesions may 

be impossible on dry bone. 

The Tubular Bones of the Hands and Feet 

(Spina Ventosa) 

The most frequent localization of skeletal tuberculosis in infancy and early childhood is the 

often multiple involvement of phalanges, metacarpals, and metatarsals (spina ventosa). Sorrel 

and Sorrel-Dejerine (1932:2) reported that among 

4660 children with skeletal tuberculosis, there 

were 649 cases of spina ventosa with 1 to 10 foci 

in individual patients. Bailleul (1911:4) reported 

that in 274 patients, there were 495 lesions of 

spina ventosa, of which 381 were located in the 

hands and 114 in the feet. The age distribution 

in Johansson's (1926:144) material is as follows: 

15 percent in the first year, 62 percent below 3 

years, and 77 percent below 5 years. The lesion 

rarely occurs after 10 years of age. Of his patients 

50 percent showed solitary lesions. The localizations in his cases were fingers 108 times, metacarpals 68 times, metatarsals 32 times, and toes 11 

times. 

In infancy and early childhood these short 

tubular bones still have hemopoietic marrow 

throughout the shaft. In these small bones a focus 

will readily occupy the whole diaphysis, leading 

to ischemic necrosis and/or penetration of the 

thin cortex. The cortex may be rapidly resorbed 

or form a sequestrum. The elevated periosteum 

forms a new bony shell, which accounts for the 

ballooned appearance of the involved bone (Figure 219). These lesions often accompany other 

skeletal manifestations of tuberculosis. If the child 

does not die from tuberculosis located elsewhere, 

the lesion usually heals. Destruction of the growth 

plate in metacarpals and metatarsals, and, less 

commonly, of phalanges, may lead to marked 

shortening of the digit after healing. If this is not 

FIGURE 219.—Tuberculous dactylitis (spina ventosa) of the 

basal phalanx of the finger of a child. Notice expanded 

involucrum surrounding remnant of diseased phalanx; epiphysis spared. (PMES 1 FT 12(1).) 
NUMBER 28 157 

the case, evidence of the healed lesion will disappear in remodeling. Very similar lesions are 

produced by osteomyelitis and by congenital 

syphilis. However, those lesions are usually singular, and expansion of the involved bone is 

usually much less marked. 

In children, tuberculous dactylitis spares the 

interphalangeal joints. In adults, rarely, phalanges may be involved, the lesion extending into the 

joint and not giving the distended appearance of 

the bone (Girdlestone, 1965:183). 

The Shoulder 

Tuberculosis of the shoulder is much less common than that of the hip or knee. Kastert observed 77 cases in a series of 2457 skeletal tuberculosis patients (in Kastert and Uehlinger, 1964: 

517). It is seen at any age, but in adults more 

often than in children. There is prevalence of 

male cases and in both sexes the right side is three 

times more affected than the left (Kremer and 

Wiese, 1930:291). The complicated relationships 

FIGURE 220.—Tuberculosis of humeral head with cavitation, 

sequestrum removed; resection specimen. Note exposed porotic hypervascular bone with little reactivity. (17-year-old 

female, PMWH W0709.) 

FIGURE 221.—Cavitating tuberculosis of the lateral portion 

of a right clavicle. Notice the sparsity of reactive bone. (From 

an adult with tuberculous arthritis of the shoulder, PMES 

1 FT 5(2) from before 1920.) 

of the shoulder joint to the synovial sheath of the 

long biceps tendon and to the subdeltoid bursa 

favor extensive synovial involvement. If osseous 

foci are present, they are more frequently found 

in the head or proximal metaphysis of the humerus than in the scapula (Figure 220). In children, cavities with sequestra occur in the epiphysis and metaphysis of the proximal humerus 

(Sorrel and Sorrel-Dejerine, 1932:165-168). In 

the synovial form, the extension to the humerus 

is along the capsular attachment, creating a resorption groove on the lateral aspect of the humeral head. In children, shoulder tuberculosis 

may heal. In adults, ultimate extensive destruction of the humeral head and of the glenoid fossa 

are common. Occasionally the acromion and 

clavicle may also be involved (Figure 221). Abscess formation and fistula are less frequent than 

in other large joints. In the differential diagnosis, 

septic arthritis is the main consideration. In that 

condition bone destruction is usually much less 

extensive and the lateral grooving and undermining defect on the humeral head is not observed. 

The Elbow 

Tuberculosis of the elbow is in many series the 

most frequent joint tuberculosis of the upper 

extremity (50 percent, Kremer and Wiese, 1930: 

304). The majority of the lesions develop between 
158 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

FIGURE 222.—Tuberculosis of right elbow with bony ankylosis between radius, ulna, and humerus. Notice marked 

involvement and enlargement of the distal humerus. The 

defect of the olecranon process is artificial. (Amputate from 

a child, PMES 2 FT 7 (4).) 

1 and 20 years of age (Konig, 1906:141, Cheyne, 

1911:328). Sorrel and Sorrel-Dejerine (1932:121) 

observed, in the 10 years preceding 1928, tuberculosis of the elbow in 164 children and 72 adults. 

Osseous foci, if present, are most common in the 

distal humerus, second in the proximal ulna, and 

least common in the proximal radius. Konig 

(1906:141-142) found bony foci in 91 of 128 

patients. The distribution was as follows: distal 

humerus 43 (mostly in the lateral condyle), ulna 

(olecranon) 36, proximal radius 2. In advanced 

cases, several of the adjacent bones may be involved. In very young children a central tuberculous focus in the olecranon is not uncommon 

as part of multiple skeletal foci (fingers, toes, 

calcaneus, zygoma). This is a cavitary lesion with 

central sequestrum and reactive periostitis resembling spina ventosa. The joint may not be involved (Sorell and Sorrel-Dejerine, 1932:121). 

After 6 years of age, the joint is often involved by 

extenstion of the ulnar focus through the joint 

cartilage. This leads to deeper excavation of the 

semilunar incisure of the ulna with elongation of 

its coronoid process. In children, the process may 

heal with fibrous ankylosis. In adults, destruction 

of the adjacent bones may be extensive, usually 

least and last of the head of the radius. Healing 

usually terminates in bony ankylosis (Figure 222). 

Ankylosis without major bone loss may be impossible to differentiate from rheumatoid or septic 

arthritic sequelae. Periarticular osteophytosis can 

occur in extensive capsular involvement (Figure 

223). 

FIGURE 223.—Tuberculosis of right elbow. Notice exposure 

of subchondral porotic spongiosa on all joint surfaces and 

partial destruction of the radial head. The periarticular 

osteophytosis suggests massive capsular involvement. (68 

years, IPAZ 1969, old no. 253.) 
NUMBER 28 159 

The Wrist and Carpal Bones 

The wrist consists of three partly separated 

joints: the radiocarpal joint, the intercarpal joints, 

and the carpometacarpal joint. Any one or all of 

them may be involved in tuberculosis. The following discussion is mainly based on the detailed 

study of Sorrel and Sorrel-Dejerine (1932:91-

120). They observed 63 instances in children and 

51 in adults. The location and manifestation of 

the lesions vary greatly in different age groups. 

In children, the carpometacarpal joint is mainly 

involved and the radiocarpal joint is spared. In 

adults, the process usually begins in the radiocarpal joint and spreads rapidly throughout the joint 

compartments of the wrist (Figure 224). The 

difference is explained by the anatomy and matFIGUPE 224.—Tuberculosis of the left wrist. Wet preparation 

with soft tissue attached, showing extensive destruction of 

distal radius, ulna, carpal bones, and carpometacarpal joints 

of 1-year duration. (56-year-old male with pulmonary tuberculosis, WM S82.1 from 1876.) 

uration of the constituent bones. In children below 4 years of age, the carpus is mainly a block of 

cartilage with minimal focal ossification. At this 

stage carpal tuberculosis is not observed. From 4 

to 12 years of age, carpal ossification centers 

become larger and more numerous. At this time, 

localized carpometacarpal involvement is observed, since adjacent bones are still protected by 

thick layers of unossified cartilage. The carpometacarpal joint is uncommonly involved by extension of a spina ventosa of an adjacent metacarpal. In general, an active growth plate serves 

as a barrier for spread to the adjacent joint. The 

metacarpals two to five are devoid of a proximal 

growth plate. These localized joint lesions may 

heal along with the healing of the accompanying 

spina ventosa, leading to bony fusion between 

individual carpals and metacarpals. With increasing age, the cartilage cover diminishes and extensive joint involvement becomes the rule. In children and adults, the joint lesion may originate 

directly in the synovium or by contact with tuberculous tenosynovitis. In the adult, osseous destructive foci are not infrequently present in the 

distal radial epiphysis and/or metaphysis. The 

disease rapidly spreads through the entire wrist 

and, in contrast to the infantile type, the proximal 

row of carpal bones is more severely involved. In 

healing, with various degrees of bone loss, the 

entire carpus becomes a solid bone block, fused 

to the radius and often to the base of the metacarpals as well. 

The Shaft of Long Bones 

Tuberculosis of the shaft of long bones is uncommon. It is almost exclusively observed in children and frequently as a manifestation of multiple skeletal foci, particularly spina ventosa. Sorrel 

and Sorrel-Dejerine (1932:2 and 21) observed 

about 100 cases in infants and children compared 

with 649 cases of spina ventosa. The lesion consists of eccentric cavitation, usually in the metaphysis, with a small sequestrum (Figure 225), 

and often marked reactive periosteal bone formation over the overlying cortex (Figure 226). 

Thus, in children, there is considerable resem-
FIGURE 225.—Tuberculosis of lateral epicondyle of right 

humerus. Notice smooth cavity with porotic sequestrum and 

minimal reactive bone in vicinity. (Adult, DPUS 5989, 

French catalog no. 834.) 

FIGURE 226.—Tuberculosis of medial epicondyle of right 

humerus. Notice porotic destruction with moderate periosteal reactive bone. The joint is not involved. (Adult, DPUS 

5982, French catalog no. 827.) 

FIGURE 227.—Tuberculosis of proximal left ulna (spina ventosa) with extension to the elbow joint and humerus, posterior view. Notice the bulbous expansion of the new ulnar 

cortex with single cloaca, destruction of olecranon, and 

erosion of humerus. (From a child, PMES 2 FT 7(6).) 

blance to the appearance of spina ventosa (Figures 227, 228). In adults, the lesion is extremely 

rare; periosteal bone formation is meager (Figure 

229, 230). Perifocal osteoporosis may be followed 

in long-standing cases by perifocal osteosclerosis. 
NUMBER 28 161 

FIGURE 228.—Tuberculosis of proximal radius (spina ventosa) with bulbous enlargement of new cortex and multiple 

cloacal perforations; epiphysis and articular surface spared. 

(6-year-old female with tuberculosis of cervical lymph-nodes, 

PMES 1 FT 10 (2) from before 1900.) 

FIGURES 229, 230.—Healed tuberculosis of distal femur with 

partial ankylosis of knee and severe osteoporosis due to 

disuse: 229, External view; note periosteal hyperostosis. 230, 

Cut surface; note cavitation in femur metaphysis and severe 

osteoporosis. (68-year-old male, IPAZ 6052, surgical specimen MB 6936 of 1955.) 

A certain differentiation from osteomyelitis and 

Brodie's abscess may be impossible on the dry 

bone. 

The frequency of involvement is: tibia, ulna, 

radius, humerus, femur, and fibula, respectively 

(Konschegg, 1934:422). 
162 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

The Thoracic Cage 

RIBS.—Tuberculous involvement of one or several ribs is not rare. Sorrel and Sorrel-Dejerine 

(1932:84-88) observed 93 instances, of which 56 

concerned children and 37 adults. The infection 

is usually hematogenous, but direct extension 

from paravertebral abscesses and other adjacent 

tuberculous foci can occur (Kremer and Wiese, 

1930:283). The hematogenous foci predilect the 

area near the osteocartilaginous border and may 

involve the cartilage secondarily (Kastert and 

Uehlinger, 1964:515). The process creates a lytic 

lesion with fusiform enlargement of the involved 

area and often perforations of the cortex lead to 

chest wall abscesses. Periosteal reactive bone formation is usually rather meager. The middle ribs 

FIGURE 231.—Tuberculosis of sternum (posterior view) probably by direct extension from visceral tuberculosis. Note 

excavation of manubrium and corpus sterni from without 

with moderate amount of reactive bone. (PMWH WO 706.) 

are more often affected than the upper or lower 

ones and secondary involvement of adjacent ribs 

can occur (Konschegg, 1934:407). Differentiation 

from osteomyelitis, fibrous dysplasia, and eosinophilic granuloma may be very difficult on dry 

bone. 

STERNUM.—The sternum is much less frequently involved than the ribs. Konig (1906:155) 

observed that ribs are five times as often affected 

as the sternum. The most frequent location is in 

the manubrium (Figure 231). These lesions may 

extend into the sternoclavicular joint and involve 

the medial portion of the clavicle. The sternal 

lesion is mostly lytic and may perforate the anterior or posterior cortex or both. In the differential diagnosis, erosion of the manubrium by an 

aortic aneurysm must be considered. 

SCAPULA.—The scapula is very rarely involved 

except by extension of tuberculosis of the shoulder 

joint into the glenoid fossa or the acromion. In 

hematogenous tuberculosis of the scapula, the 

vertebral margin is predilected (Kremer and 

Wiese, 1930:301). 

The Skull 

The skull is a rare area of involvement except 

in young children. Tuberculosis of the skull has 

to be separated into three areas: cranial vault, 

cranial base, and face. 

CRANIAL VAULT.—This is the most common 

location of cranial tuberculosis. Sorrel and SorrelDejerine (1932:78) saw 21 cases, of which 16 were 

children and 5 adults. The localization in the 

different bones, in a statistical survey by Straus 

(1933), is as follows: frontal 86, parietal 86, occipital 18, temporal 16. The majority of the cases are 

infants and children below 10 years of age. The 

infection usually is through the hematogenous 

route. In children, the lesions are often multiple 

and secondary to or coexistent with other active 

tuberculous skeletal foci (Sorrel and Sorrel-Dejerine, 1932:79-80). Apparently the presence of 

hemopoietic marrow and the growth activity of 

the cranium at this age determine the frequency 

of involvement. The most characteristic lesion is 

a round lytic focus of not more than 2 centimeters 
NUMBE

R 28 163 

in diameter, with or without a "moth-eaten" 

central sequestrum, terminating in complete per-

foration of the inner and outer tables (Figures 

232, 233). There is often abscess formation and 

fistula with transcutaneous elimination of the 

sequestrum. The lesion does, not uncommonly, 

cross suture lines. The margin of the lesion shows 

active resorption, but no reactive bony wall. 

Spread along the internal periosteum, with peri-

focal bone resorption and hypervascularity, is 

often observed. In this age group, the lesions have 

to be differentiated from eosinophilic granuloma 

and metastatic neuroblastoma. Solitary lesions of 

eosinophilic granuloma usually do not contain a 

central sequestrum and do not cross suture lines. 

Multiple lesions of reticulosis usually do not spare 

the skull base. Metastatic neuroblastoma often 

shows marked osteoblastic reaction. In adults, the 

cranial vault lesion is almost always solitary and 

often much larger than in infants and children. 

In addition to the hematogenous route, extension 

from tuberculoma of the brain or dura does occur 

(Figures 234-236). The process is characterized 

by a chronic progressive destruction of the cranial 

vault with irregular margins. Major sequestration 

is uncommon, in contrast to osteomyelitis, and 

bony reaction is very limited or absent, in contrast 

to tertiary acquired syphilis. The defect of the 

inner table is usually larger than that of the outer 

(Figures 237, 238), while in tertiary syphilis the 

greater defect is usually outside, and the inner 

table may be completely intact (Erdheim, 1932: 

355). 

CRANIAL BASE.—The base of the skull is rarely 

involved in tuberculosis. Tuberculous otitis media 

is not rare in infants, representing 50 percent of 

middle ear infections in the first year of life and 

about 3 percent at all ages (Eraser and Stewart, 

1936; 402). There is occasional destruction and 

sequestration of the petrous bone and mastoid 

process by secondary extension of mucosal middle 

FIGURES 232, 233.—Tuberculosis of cranial vault: 232, Ex-

ternal view; notice little reactive bone around frontal defect 

and porous sequestrum in parietal lesion. 233, Endocranial 

view; the frontal lesion is broader based on the inner table. 

(Adult, DPUS 4584.) 

.-^ 
164 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

1 r^^oer^'' 

234 w. 

''I^^^W -k T 

FIGURES 234-236.—Tuberculosis of the cranial vault secondary to tuberculous external pachymeningitis: 234, External 

view showing small perforation of the outer table. 235, 

Endocranial view; notice the lesions are much larger on the 

inside. 236, Left lateral view, showing plaque-like healing. 

(12-year-old female, FPAM, Jubilaumspital 40, from 1914.) 

ear tuberculosis (Krause, 1899:54) (Figures 239, 

240). Occasionally the base of the occipital bone 

in the vicinity of the foramen magnum may 

participate in suboccipital tuberculosis of the atlas and axis (malum suboccipitale) (Figure 241). 

FACIAL BONES.—In small children focal tuberculosis of the inferior lateral orbital margin is not 

uncommon, involving the maxilla, especially at 

the junction with the zygoma. Involvement of the 

zygoma itself also is seen frequently. Chronic 

tuberculosis of the zygomatic arch may lead to 

an abscess, which typically ascends on the temporal squama along the temporal muscle (Figure 

242). Most of these cases show multiple skeletal 

tuberculosis elsewhere. The lesions are superficial, 

leading to small sequester formation eliminated 

through a fistula (Krause, 1899:54-55; Kremer 

and Wiese, 1930:153-155). 

The bony walls of the nasal cavity may be 

secondarily affected by extension of mucosal tuberculosis (Figures 243-246). The facial bones 

also can be secondarily involved by long-standing 

tuberculosis of the facial skin and soft tissues 

(lupus vulgaris), which often leads to destruction 

of the nasal bones, as in leprosy (Figures 247-

249). 
NUMBER 28 165 

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t 

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238 ^ 

FIGURES 237, 238.—Tuberculosis of right parietal bone: 237, 

External view; notice small perforation in exposed diploe. 

238, Endocranial view, showing larger defect on inner table 

sloping to smaller perforation on outer table. (55-year-old 

female died of tuberculosis, ANM 2480, autopsy 658-(16) 

from 1896.) 

FIGURES 239, 240.—Cranial tuberculosis with lesion in right 

frontal bone and left middle ear: 239, Lateral view, showing 

exposed diploe and posterior penetration of the inner table. 

240, Basal exterior view, showing involvement of the left 

middle ear, necrosis of mastoid process and extension to base 

of sphenoid. (About 8 years old, DPUS 5266, French catalog 

779 from 1837.) 
166 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

FIGURE 241.—Tuberculosis of cranial base and atlas with 

superficial erosion of anterior surface of cervical vertebrae 

suggestive of prevertebral abscess. Sudden death by compression of the medulla. (55-year-old male with chronic 

pulmonary tuberculosis, PMWH W O 702.) 

In infants the mandible occasionally also shows 

hematogenous foci, near the angle. These lesions 

may be very similar to foci of eosinophilic granuloma. In adults, in advanced stages of open 

pulmonary tuberculosis, extension of oral mucosal lesions into the alveolar process of the mandible uncommonly and, even less often, of the 

maxilla has been described (Zandy, 1896). 

PALEOPATHOLOGY 

The earliest report on presumptive tuberculosis 

in ancient Old World human remains is an article 

by Bartels (1907) on a neolithic skeleton found 

near Heidelberg, Germany. The fourth and fifth 

thoracic vertebrae have collapsed and fused with 

the somewhat abnormal sixth vertebra creating 

an angulation often, but not exclusively, seen in 

spinal tuberculosis. There are several reports of 

lesions attributed to tuberculosis in Egyptian skeletal material (Derry and Elliot-Smith, 1909; Elliot-Smith and Dawson, 1924; Derry, 1938b). Elliot-Smith and Ruffer (1910) reported a case of 

probable tuberculosis in an Egyptian mummy 

FIGURE 242.—Cranial tuberculosis with destruction of left 

zygomatic arch and involvement of temporal bone and 

mastoid process with periosteal reaction to subtemporal cold 

abscess. Separate foci in frontal and left parietal bone. 

(Adolescent, DPUS 5268, French catalog 778a from 1837.) 

dating from the Twenty-first Dynasty (ca. 1000 

B.C.). This specimen shows extensive destruction 

of the last four thoracic and first lumbar vertebrae. There was some bony reaction to the disease 

process on the first lumbar vertebra. Inferior to 

the lesion on the lumbar is a swelling in the soft 

tissue, which Elliot-Smith and Ruffer judged to 

be a psoas abscess. Although no tubercle bacilli 

were found in any of the soft tissue lesions, the 

morphological evidence for tuberculosis is strong. 

Indeed, while discounting much of the purported 

evidence for tuberculosis in the ancient Egyptian 

material, Williams (1929: 869-873) concluded 

that the evidence for tuberculosis in the Egyptian 

skeletal and mummy remains was convincing. 

Morse, Brothwell, and Ucko (1964) reached a 

similar conclusion. Although Hrdlicka (1909:1) 

claimed that there were no pre-Columbian skeletal lesions attributable to tuberculosis, there 

have been several authors who subsequently have 

reported cases. Hooton (1930:319) reported a case 

of possible vertebral tuberculosis among the preand post-Columbian Pecos Pueblo skeletal series. 

Ritchie (1952) coordinated a study of three pre-
NUMBER 28 167 

Columbian kyphotic Indian spines from New 

York state. In this study he submitted photographs and roentgen filrns of the three specimens 

to 17 specialists. The majority opinion of the 

medical specialists was that in all three abnormal 

cases the lesions were the result of tuberculosis, 

although there were some dissenting opinions. 

Lichtor and Lichtor (1957) published their observations on a pre-Columbian kyphotic spine 

from Tennessee. The tenth thoracic through the 

fourth lumbar were involved with vertebral body 

destruction followed by collapse, angulation, and 

fusion. The authors conclude that the lesion is 

characteristic of spinal tuberculosis. Roney (1966: 

103) reports a case of thoracic vertebrae destruction followed by kyphosis in a spine from an 

archeological site in California. 

Morse (1961, 1967) reviews the evidence for 

prehistoric tuberculosis in America. He bases his 

review on artistic representations of abnormal 

human figures suggestive of tuberculosis and on 

a critical evaluation of 15 cases of Indian skeletons 

that have vertebral lesions, possibly attributable 

to tuberculosis. Nine cases were from published 

reports and six were based on original observations by Morse. Of these 15 cases, Morse considered only four to be sufficiently typical to allow 

a strong presumption of spinal tuberculosis. One 

of these four cases could not be dated to the preColumbian period with certainty. Despite the 

strong evidence of pre-Columbian tuberculosis in 

the other three, Morse concluded that the existence of the disease among the prehistoric American Indians had not been demonstrated. 

It would seem appropriate to review critically 

the criteria on which Morse bases his judgment. 

The following are the characteristics that he attributes to classic vertebral tuberculosis: (1) One 

to four vertebrae are usually involved, rarely 

more. (2) Bone destruction occurs with little or 

no bone regeneration. (3) Angular kyphosis of the 

affected spine is a frequent sequela. (4) Neural 

arches, transverse and spinous processes are rarely 

involved. (5) Cold abscesses drain mostly along 

the anterior surface of the vertebrae; they almost 

never drain posteriorly through the skin. (6) Massive regeneration is a great rarity; even spontaneous fusion of affected vertebrae is uncommon. 

In addition to these criteria, Morse argues that 

the rarity of lesions in pre-Columbian skeletal 

material argues against the disease being present. 

He bases this conclusion on the following argument. In his survey of American Indian groups 

living in the American Southwest around the 

turn of the twentieth century, Hrdlicka (1909) 

found the incidence of bone tuberculosis to be 7 

cases in every 100 cases of tuberculosis. Since one 

of every 3 deaths among the Indians was due to 

this disease, Morse (1961:493) suggests that about 

22 of every 1000 burial specimens should show 

some evidence of tuberculosis. Morse (1961:493) 

concludes that if tuberculosis was endemic among 

the prehistoric Indians, we should see more evidence of it than we do. Since lesions that might 

be attributed to tuberculosis are rare, paleopathological cases of such lesions are more likely to be 

one of the several other pathological conditions 

that can produce similar lesions. One problem 

with this argument is that social and environmental conditions in the post-Columbian period were 

very much worse for the American Indians. Both 

these factors adversely affect the incidence and 

course of tuberculosis. Thus the incidence reported by Hrdlicka (1909) may not be indicative 

of the incidence in pre-Columbian times. 

In his review of the 15 purported cases from 

the Western Hemisphere, Morse (1961) most often argues against the diagnosis of tuberculosis 

on the basis of two criteria: (1) destructive lesions 

extending to more than four vertebrae and (2) 

significant amounts of bone regeneration. However, Morse (1961:489) himself, notes that the 

skeletal response to the tubercle bacilli is dependent on the virulence of the organism and the 

host response. If the host had little ability to 

defend himself, then tuberculosis could cause a 

rapidly progressive type of acute osteomyelitis 

and early death. "If the host's resistance was 

considerable, it is presumed that the disease then 

would be extra-chronic with the possibility of 

extensive healing and bone regeneration." 

It is significant to note that in only one of the 
168 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

244 

' "f^K^'ff'--:'^:'--^\^>: 
FIGURES 243-246.—Tuberculosis of cranium with right frontal and basal lesion: 243, External view showing small sievelike perforation of outer table. 244, Endocranial view showing large dura-based lesion crossing the coronal suture. 245, 

Destructive lesion of sphenoid-ethmoid area, endocranial 

view. 246, Exterior view of skull base. (10-year-old female, 

ANM 2439 from 1870.) 

FIGURE 247, 248.—Craniofacial tuberculosis in lupus vulgaris 

with destruction of nose: 247, Anterior view, showing porotic 

erosion around nasal aperature and maxilla; extensive destruction of mandible. 248, Left lateral view, showing multiple superficial erosive lesions of cranial vault and extensive 

destruction of mandibular angle. (12-year-old male with 

visceral tuberculosis and meningitis, FPAM 5001, autopsy 

87916 from 1888.) 

FIGURE 249.—Cranial tuberculosis in lupus vulgaris, with 

partial destruction of nasal bones, conchae, nasal septum, 

maxilla, and palate; periostitis of mandible. 10 years duration. (15-year-old male, PMES 1 FT 2(1) from before 1920.) 
170 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

nine cases does Morse indicate age and it is that 

of a child. Furthermore, it is this case that provides the most typical expression of vertebral 

tuberculosis, implying that the acute or subacute 

cases do not survive to adulthood. As a result 

acute or subacute cases show the primarily lytic, 

bony response typical of spinal tuberculosis. As 

has been stated, vertebral tuberculosis begins 

most often in early childhood (p. 145). This means 

that the vertebral tuberculosis occurring in the 

adult probably reflects a chronic condition in 

which the host response is at least sufficiently 

adequate to insure survival through childhood 

and adolescence. In such long-term, chronic, 

adult cases the criteria of no more than four 

vertebrae being involved with little bone regeneration may be less applicable. 

Morse's (1961:489) caution about attributing 

a specific bone lesion in an archeological specimen to tuberculosis is understandable and, indeed, commendable, particularly at a time when 

unequivocal evidence for tuberculosis in the 

Western Hemisphere during pre-Columbian 

times does not exist. Allison, Mendoza, and Pezzia (1973) have published a report of a case of 

tuberculosis in a naturally preserved body of a 

child from southern Peru. The case appears to be 

well-dated to about A.D. 700, clearly long before 

European contact. The child was a male between 

8 and 10 years of age. The roentgen and gross 

appearance of the lumbar spine indicates partial 

destruction of the first three lumbar vertebrae. 

The authors indicate that the burial position was 

unusual and suggest that the position of the legs 

of the burial is commonly seen in living individuals with paralysis of the lower limbs. 

At autopsy, the mummy had a psoas abscess 

overlying the lumbar vertebrae and nodules resembling tubercles in the right lung. By rehydrating some of the recovered tissues it was possible to prepare stained histological sections, 

which revealed acid-fast bacilli in the tubercles. 

The evidence from the roentgen, gross, and histological sources leave little doubt that the child 

suffered and probably died from tuberculosis. 

This study would seem to provide unambiguous 

evidence regarding the presence of tuberculosis in 

the Western Hemisphere during pre-Columbian 

times. 

The existence of valid evidence for tuberculosis 

in the New World in the prehistoric period has 

considerable significance for the diagnosis of lesions in skeletal remains that could be attributed 

to tuberculosis. Morse (1961:491) lists 13 diseases 

that produce lesions that can be confused with 

tuberculosis. The most serious problems in differential diagnosis arises in distinguishing between 

pyogenic osteomyelitis, perhaps the mycotic infections, and tuberculosis. Brucellosis should be 

added to this list. Assuming that all of these 

infectious conditions are endemic, tuberculosis, 

because it is the most frequent morbid condition, 

becomes the most likely diagnosis on the basis of 

probability. Thus, the unequivocal demonstration of tuberculosis in the pre-Columbian New 

World means that the disease was endemic and 

acceptance of this diagnosis in more questionable 

cases becomes a more acceptable conclusion. 

Three cases of possible bone tuberculosis in 

archeological specimens are presented to illustrate 

the morphology of bone lesions associated with 

this disease. The first of these cases is a child's 

skeleton from Pueblo Bonito, New Mexico 

(NMNH 327127). The archeological date for cultural materials from this site is A.D. 828-1130. 

The right femur of this specimen measures 265 

millimeters (without the epiphyses) which indicates an age at death of about 9 years. This 

estimate is in good agreement with age based on 

dental eruption. Determination of sex in a child's 

skeleton of this age is not reliable. 

While some of the bones are damaged or missing, the majority are present including some of 

the hands and feet. There is no grossly observable 

evidence of disease in any of the bones except the 

vertebrae. The first through the fifth cervical 

vertebrae are missing, although the sixth and 

seventh are normal. The first through the tenth 

thoracic vertebrae are normal. The pathological 

process begins with the eleventh thoracic (Figures 

250, 251). The superior surface of the body of this 

vertebra is normal, as are the transverse, spinous. 
NUMBER 28 171 

FIGURES 250, 251.—Slight to pronounced destruction of the vertebral bodies of the eleventh 

thoracic through first lumbar vertebrae probably due to tuberculosis: 250, Destruction of the 

thoracic and lumbar (arrow) vertebrae has resulted in kyphosis; there has been a limited 

amount of healing. 251, The right lateral view of the lower vertebrae; note the large cavity 

(arrow) on the remnant of the body of T12. (9-year-old child from the pre-Columbian site of 

Pueblo Bonito in New Mexico, USA, NMNH 327127; scale in cm.) 

and articular processes. Cavitation is seen on the 

anterior and left portion of the vertebral body. 

An enlarged canal resembling a cloaca occurs in 

the left sector of the body. The inferior surface of 

the body is eroded from the central to the left 

side. All vertebral processes are normal. 

The anterior body of the twelfth thoracic vertebra is destroyed leaving a scalloped spongy 

surface in the remaining bone. There is no bony 

fusion and the spinous, transverse, and articular 

processes are normal. 

The first lumbar vertebra is the most extensively affected bone with almost complete destruction of the body. The left pedicle is fused 

with the body of L2. All vertebral processes are 

normal; however, there is slight deformation apparent in the lamina. This suggests the possibility 

of compensatory remodeling after the destruction 

of the vertebral body. 

The superior surface of the body of L2 is eroded 

and fused with the remnant of Ll. The inferior 

body is intact but has slight exostoses on the left 

side. All processes are normal. The third through 

the fifth lumbar vertebrae are all normal except 

for slight evidence of deformity on L5, which, like 

the deformation seen in the lamina of Ll, may be 

a reaction to the kyphosis produced by the collapse and fusion of Ll and L2. 

X-ray films of the vertebrae demonstrate the 

anterior angulation (kyphosis) of the normal axis 

NUMBER 28 173 

of the spine. The collapse of the vertebrae produced an angle of about 110 degrees (170°-180° 

normal). The film also shows evidence of bony 

response to the deformity in the form of reinforced 

trabecular bone in the affected vertebrae. X-ray 

films of the femur suggest two, and possibly three, 

Harris' lines indicative of acute disease episodes 

at various times before death. The skull is badly 

broken and deformed by actions subsequent to 

death and burial. However, there is no evidence 

of disease on the skull. The erupted teeth are 

normal. The age of the individual and the morphology of the lesion are compatible with a diagnosis of tuberculosis, although other diseases 

are possible. Morse (1961:500) provides a brief 

descriptive summary of this case (his No. 10) and 

concludes that it is "quite typical of tuberculosis 

with destruction of vertebral bodies, angular deformity, and very little bone regeneration." 

The second case (Figures 252-255) is a skeleton 

from Illinois, USA (NMNH 381853), whose archeological provenience cannot be accurately determined. In his brief report of this specimen, 

however, Morse (1961:502) indicates that it was 

probably late Hopewell or post-Hopewell Woodland (A.D. 200-1000). The age at death of this 

individual was about 22 years and the sex is male. 

Only a few of the bones of the hands and feet 

are present. None of these bones show any evidence of disease. The bones of the upper extremity are normal. In the pelvis the sacrum is missing. 

There are no gross lesions of the innominates. 

FIGURES 252-255.—Probable spinal tuberculosis in an archeological specimen from Illinois, USA: 252, The right 

lateral view of the vertebral column. The entire vertebral 

body of T8 is destroyed and the posterior remnant is fused 

with T9 (arrow). 253, Anteroposterior X-ray film of the right 

and left femora, the fibulae, and the right tibia. Compare 

the left femur with the right, noticing the diminished diameter of the midshaft and the increased neck-shaft angle of 

the left femur. 254, Detailed view of the major lytic and 

kyphotic focus in the vertebrae. The body of T8 is completely 

missing and the partially eroded body of T7 is resting on the 

partially destroyed body of T9 (arrow). 255, Lateral X-ray 

film of the area of angulation of the spine. Osteosclerosis is 

apparent in the partially destroyed remains of the T9 body 

(arrow) and in the body of TIO. (NMNH 381853.) 

although the left ilium is visibly less flared than 

the right. 

In the lower extremities, the left tibia is missing, 

although the right is normal, as are both fibulae. 

Comparative measurements of the two femora 

are presented in Table 8 and suggest significant 

differences. 

TABLE 8.—Comparative measurements of the left and right 

femur in possible case of skeletal tuberculosis of archeological 

specimen from Illinois, USA (NMNH 381853) 

Measurement 

Maximum length 

Maximum midshaft diameter 

Minimum midshaft diameter 

Neck-shaft angle 

Left 

(mm) 

428 

27 

18 

152° 

Right 

(mm) 

421 

29 

21 

136° 

The left femur is grossly more gracile than the 

right. The neck and head of the left femur are 

more nearly in line with the long axis of the shaft 

than the right (Figure 253). This condition (coxa 

valga) is typical when partial to complete paralysis of the limb occurs during the growth phase. 

The abnormally large neck-shaft angle of the left 

femur, the reduced size of the shaft diameters, 

and the diminished flare of the left ilium suggest 

partial paralysis of the left limb perhaps caused 

by the collapse of the vertebrae. 

In the vertebral column (Figure 252) the first 

cervical is missing. The remaining cervical vertebrae are normal, as are the first three thoracic 

vertebrae. On T4 there is a lytic lesion on the 

anterior inferior surface of the vertebral body, 

with a similar but smaller lesion on the right 

portion of the body. T5-T7 have a slight periosteal bony reaction on both sides of the posterior 

portion of the body. The inferior articular surface 

of the body of T7 is eroded but shows evidence of 

circumscription, although there is no exuberant 

bone formation. The body of T8 is destroyed with 

the posterior remnant fused with T9 (Figures 254, 

255). Both inferior articular facets are fused with 

their corresponding facets on T9 producing an 

anterior angulation. The superior plate of the 

body of T9 is destroyed. There is some peripheral 
174 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

reactive bone formation with a large, bony spur 

on the right lateral portion of the vertebral body. 

In TIO the articular surface of the vertebral body 

is intact. There are bilateral bony spurs on the 

vertebral body with slight cavitation on the anterior surface. TI 1 and T12 are missing. 

The first lumbar vertebra has slight erosion of 

the superior articular surface of the body and 

lateral bony spurs with anterior cavitation. The 

inferior articular surface of the vertebral body is 

normal. Both L2 and L3 show evidence of destructive lesions on the anterior part of the body. 

There is a reactive spur joining L2 and L3 on the 

right portion of their respective bodies with a 

draining sinus affecting primarily the body of L3. 

L4, L5, and the sacrum are normal. The skull 

and mandible were badly crushed and not available for study. 

In his review of this case Morse (1961:502) 

expresses the opinion that such an extensive, destructive process would have resulted in rapid 

death and that the bony fusion of T8 and T9 

must have occurred early in the disease process. 

Initially he suggests a type of acute osteomyelitis 

of short duration as the cause of the lesion. However, he did not rule out tuberculosis and later 

(1967:257-258) included this case as one of four 

cases "considered typical enough to give a strong 

presumption of spinal tuberculosis." An alternative opinion is that the destruction is suggestive 

of an acute initial condition. However, the bony 

spurs, fusion, and draining sinuses are all suggestive of limited recovery and a more chronic response with life prolonged for some time (a year 

or two) beyond the acute stage. The abnormality 

of the left femur suggests a longer time. 

The third case (Figures 256-258) is a skeleton 

of an Eskimo from the Yukon River in Alaska 

(NMNH 345394). The archeological age of the 

specimen is uncertain. The estimated age on the 

basis of epiphysial union and pubic symphysis 

morphology is 20 years. The sex appears to be 

male, although the small size for the long bones 

and the abnormal shape of the pelvis make sex 

determination difficult. The skull, which does not 

exhibit any gross pathology, is male in appearThe upper extremities are normal although 

small and suggest robust muscle activity. The 

bones of the hands are small but appear normal. 

There is no evidence of disease in the vertebrae 

either grossly or on the X-ray film. 

The sacrum is normal, although small. The 

right innominate is small and somewhat deformed in response to the pathological condition 

in the left hip. The left innominate is grossly 

deformed, but the major focus of the infection is 

the acetabulum. The acetabulum is very shallow, 

an effect created by the destruction of the acetabular rim and articular surface with subsequent 

remodeling and healing. There are large, wellorganized osteophytes in the posterior rim area 

and a pronounced cavity in the inferior rim area. 

A well-developed bony ridge on the anterior-superior margin of the acetabulum is suggestive of 

upward migration and subluxation of the joint. 

There is a large hole through the acetabulum in 

the region of the fovea. The overall gracility of 

the innominate is exemplified by the very delicate 

ischial ramus. 

The left femoral head is destroyed with subsequent cavitation. Apparently this destruction 

took place in late childhood with diminished 

growth of the bone following the acute phase of 

the disease. The measurements of the two femora 

highlight the differences in growth occurring after 

the onset of the disease (Table 9). 

TABLE 9.—Comparative measurements of the left and right 

femur and tibia in a possible case of tuberculosis of the hip 

(NMNH 345394) 

ance. 

Measurement 

FEMUR 

Length from medial condyle 

to greater trochanter 

Maximum midshaft diameter 

Minimum midshaft diameter 

TIBIA 

Length from lateral condyle 

to medial maleolus 

Maximum midshaft diameter 

Minimum midshaft diameter 

Left 

(mm) 

332 

20 

15 

299 

18 

13 

Right 

(mm) 

340 

22 

20 

290 

20 

15 
NUMBER 28 175 

257 

FIGURES 256-258.—Possible tuberculosis of the left hip in 

an archeological skeleton: 256, X-ray film of the major long 

bones of the lower extremity, anteroposterior view; note that 

the bones of the left leg are more gracile. 257, The anterior 

view of the right and left femora. The femoral head of the 

left femur has been destroyed. The lesser trochanter is elongated and the shaft diameter of the left femur is much 

smaller. 258, A detailed view of the left hip joint; note that 

the lytic process has produced a hole (arrow) completely 

through the wall of the acetabulum. (NMNH 345394.) 

The measurements of femora length do not 

include the diseased femoral heads and thus reflect the diminished growth of the pathological 

left femur. Notice that the left tibia has undergone accelerated growth, perhaps in an attempt 

to compensate for the shortened left femur. Indeed, the total lengths of the femur plus the tibia 

for the two sides are virtually identical. This, 

however, would have left the left leg somewhat 

shorter due to the destroyed femoral head and 

the pathological superior subluxation of the hip 

joint. The resulting abnormal gait undoubtedly 

contributed to the deformity of both innominates. 

In addition to diminished growth in length (endochondral ossification) there is reduced appositional growth (intramembranous ossification) of 

the shaft diameter. While the left tibia has undergone compensating growth in length exceed-
176 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

ing that of the right side, its development in 

midshaft diameter is relatively deficient, suggesting only limited use of the limb in locomotion. 

The powerful development of the arms may be 

the result of using some type of crutch to assist in 

locomotion. 

The developmental difference between the legs 

is also seen in the bones of the feet. The left 

metatarsals have attained the same length as the 

right, but have visibly narrower shafts. Curiously, 

there is a lytic lesion in the right talocalcaneal 

joint, which has affected the medial articular 

surface of both bones. The lesion is somewhat 

circumscribed, indicating containment of the disease process. The relationship of this lesion to the 

disease process in the left leg remains problematical. 

It has been noted that differential diagnosis of 

distinctive lesions in major joints is difficult (p. 

144). Morse (1961:489) indicates that bone lesions 

from tuberculosis in locations other than the spine 

are indistinguishable from many other diseases. 

In view of the obvious problems in differential 

diagnosis it is, of course, appropriate to avoid 

dogmatic assertions. However, with this caution 

in mind, let us review the evidence presented thus 

far and seen in the illustrations of this case. 

In addition to tuberculosis, osteomyelitis and 

septic arthritis are important entities in the differential diagnosis. In tuberculosis, it has been 

noted that the active phase leads to destruction 

and cavitation in the cancellous bone with little 

perifocal reactive bone. This description certainly 

applies to the destructive process in the femoral 

head of this case. There is no evidence of sequestration or involucrum as would tend to occur in 

osteomyelitis, nor is there fusion of the joint, 

which is a common sequela in both septic arthritis 

and tuberculosis of the hip. 

Furthermore, tuberculosis of the hip is second 

in frequency to the involvement of the spine in 

bone tuberculosis and is the most common destructive lesion of the hip. Dislocation and perforation of the acetabulum in the region of the 

fovea are also associated with hip tuberculosis. 

Although ankylosis is a common sequela if healing occurs, the early death of this individual 

would have precluded this effect. Furthermore, 

subluxation is not typical in septic arthritis. While 

other diseases obviously cannot be ruled out, this 

case does provide an example of what tuberculosis 

of the hip could look like in an archeological 

specimen. 

Leprosy 

PATHOLOGY 

Leprosy is a very chronic granulomatous infection of man caused by Mycobacterium leprae, which 

is acid-fast and Gram-positive. There is no known 

animal reservoir for the organism. Leprosy used 

to be worldwide in distribution with the arctic 

regions the only exception. Presently, the most 

affected areas are the tropical and subtropical 

regions of Asia (India, Thailand, Indonesia, Philippines), Africa, and of the Americas. There is a 

predominance of male over female in a ratio 2:1 

(Faget and Mayoral, 1944). The infection mainly 

involves skin, mucous membranes, soft tissues, 

and nerves. The disease manifests itself either as 

lepromatous, with abundant bacteria in the lesions, or as tuberculoid, with scanty organisms, or 

an intermediate type. Peripheral, especially sensory, nerves of the extremities are often involved 

(neural leprosy) leading to loss of sensory perception in affected areas. The development and progression of the disease extends over decades. Various skeletal changes can be observed, based on 

three different pathogenetic mechanisms: (1) lepromatous osteomyelitis and periostitis, (2) neurotrophic bone and joint lesions, in neural leprosy, 

and (3) ordinary osteomyelitis and septic arthritis 

due to secondary infection. In a series of 483 

lepers, 306 showed bone lesions radiologically 

(Esguerra-Gomez and Acosta, 1948). 

Lepromatous osteomyelitis is an uncommon 

and frequently insignificant lesion, which may 

take decades to develop and involves only a small 

portion of a bone. Only 5.6 percent of the lepromatous type showed specific lepromatous bone 

disease (Faget and Mayoral, 1944). Small bones 

of the extremities (fingers and metatarsals) are 
NUMBER 28 177 

predilected, mostly the epiphysis (Beitzke, 1934d: 

595). These lesions appear as lytic destructive 

foci, which may extend into the adjacent joint. 

There is no periosteal reaction on the phalanges, 

and no sclerosis is observed in the healing phase 

(Paterson and Job, 1964:430). The bone may be 

infected by the hematogenous route or, more 

commonly, by direct extension from adjacent skin 

or mucosal lepromas. On the skull, destruction of 

nasal bones, nasal septum, turbinates, and of the 

hard palate does occur (Job, Karat, and Karat, 

1966). Erosions of the cranial vault, secondary to 

lepromatous scalp lesions, can be observed. 

M0ller-Christensen (1953) has described the socalled facies leprosa, which he observed on skeletons with neurotrophic lesions from a medieval 

Danish cemetery of a leprosarium. The characteristic features frequently found were the disappearance of the anterior nasal spine, the rounding 

and widening of the nasal aperture, and the 

partial resorption of the premaxillary alveolar 

process with or without loss of the upper incisors. 

He usually found the bony nasal septum and, in 

most cases, the hard palate intact. Similar lesions 

occur in tertiary syphilis and in lupus vulgaris. 

Periostitis with subperiosteal new bone deposition is not uncommon (de la Camp, 1900; Riordan, 1960). M0ller-Christensen (1953) frequently 

found finely, longitudinally striated, subperiosteal bone deposits on the tibia and/or fibula on 

skeletons of medieval Danish lepers. 

Neurotrophic changes in advanced leprosy are 

the most common bone and joint lesions observed 

in this disease. Faget and Mayoral (1944) found 

such lesions in 66 percent of neural and 33 percent 

of mixed cases. Destruction of the sensory nerves 

with ensuing anesthesia, circulatory alterations, 

and local pressure (Coony and Crosby, 1944) lead 

to slowly progressive concentric atrophy of terminal phalanges of fingers, metatarsals, and toes. 

Anesthesia often begins in the distribution of the 

ulnar nerve and, therefore, the terminal phalanx 

of the fifth finger is usually involved first (Hopkins, 1928). In the hands, the resorption begins in 

the distal phalanges and progresses proximally, 

occasionally including the metacarpals. In the 

foot, the concentric resorption starts in the proximal phalanges and distal metatarsals, often sparing the subluxed distal toes. The difference is 

probably due to the effect of local trauma (Faget 

and Mayoral, 1944). At all times, one observes a 

complete cortex on these tapered pointed remnants of involved bones. Similar changes, with a 

similar pathogenic mechanism, are seen in advanced cases of rheumatoid arthritis, but in leprosy no primary arthritic changes are seen. Severe 

degenerative arthritis and even neuropathic arthropathy, similar to Charcot's joint, can be seen 

in weight-bearing joints of ankles and feet in 

advanced cases of leprosy. In addition, the existing anesthesia facilitates traumatic mutilations 

and secondary infections. 

Osteomyelitis and septic arthritis may modify 

the appearance of the skeletal lesions of leprosy 

in the terminal phase. In mutilating leprosy, 

hands or feet may be almost completely destroyed. Even secondary tuberculous arthritis is 

not uncommon (Beitzke, 1934d:611). In seven of 

eight autopsied lepers, active pulmonary tuberculosis was found (Brutzer, 1898). The specific 

granulomatous bone lesions, especially in the phalanges of hands and feet, resemble very closely 

those observed in sarcoidosis (Paterson and Job, 

1964:432). Mutilations also occur in both diseases. Differentiation of these lesions on dry bone 

alone may be impossible (see also page 233). 

PALEOPATHOLOGY 

Leprosy is one of the diseases in which features 

identified in archeological specimens have been 

of value in modern diagnosis (M0ller-Christensen, 

1965:603). It has been noted in the discussion of 

the clinical aspects of leprosy that its distribution 

was virtually worldwide until recently. However, 

while the evidence of leprosy in the ancient Old 

World is convincing, its presence in pre-Columbian New World populations is doubtful (Cochrane, 1964:10). 

The earliest purported evidence of leprosy is 

from a Canaanite jar from Beth-Shan in Palestine 

(Yoeli, 1955:331). The vessel is dated between 
178 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

1411 and 1314 B.C. and shows features of the face 

that resemble those associated with leprosy. Cochrane (1964:2) questions Yoeli's interpretation but 

indicates that there are references to a disease like 

leprosy in China dating to 600 B.C. The disease is 

first reported in Europe around A.D. 150, increasing to its most serious intensity between A.D. 1000 

and 1400. By 1798, the disease had died out in 

Great Britain, although it continued to be a 

minor problem in continental Europe (Cochrane, 

1964:7). It was present in Norway through the 

nineteenth century. Andersen (1969:123) suggests 

that the disease may have been introduced into 

the Western World by the soldiers of Alexander 

the Great on their return from the campaign in 

India in 327-326 B.C. 

One of the problems in using historical documents in studying the history of leprosy is the 

vagueness of the descriptions and imprecision of 

terms. MacArthur (1953:8) suggests that the term 

"leprosy" was used for nonspecific skin diseases, 

elephantiasis, small pox, bubonic plague, mange, 

etc. He further suggests that many of the people 

relegated to lazar houses in medieval times may 

have been suffering from diseases other than leprosy. However, Chapman Binford (1965), responding to a scientific paper read by M0llerChristensen (1965), emphasized that the work by 

M0ller-Christensen on the cemeteries of leper 

houses or hospitals in Denmark showed that most 

if not all of the people buried there could have 

had leprosy. This suggests greater precision in the 

diagnosis of leprosy than MacArthur (1953) proposes. 

M0ller-Christensen's research (1952, 1953, 

1961, 1965, 1967, 1978) has provided empirical 

evidence for the presence of leprosy in Denmark 

during the Middle Ages. Wells (1962a) reports a 

probable case of leprosy in a sixth-century A.D. 

Saxon burial in Great Britain. Brothwell (1958: 

287) found lesions in a post-Conquest skull from 

Scarborough in England, which he attributes to 

leprosy. Wood-Jones (1910b:283) describes an ancient Nubian skull in which the nasal bones, 

including the turbinates and nasal septum, were 

destroyed. In the same specimen the major portions of the hard palate were also destroyed. 

M0ller-Christensen and Hughes (1966:243) concluded that this destructive process was probably 

the result of leprosy. They also found an additional Nubian skull from the same series, in which 

leprosy was a probable diagnosis. GladykowskaRzeczycka (1976) attributes to leprosy the lesions 

seen in an adult male skeleton (her No. 20) from 

a medieval cemetery located in Suraz, Lapy 

County, Poland. There is atrophy of the anterior 

nasal spine, evidence of truncated metatarsals, 

and extensive periostitis of the long bones. 

If, as seems probable, leprosy was introduced 

into the New World during the colonial period, 

archeological examples of leprosy should be rare 

and limited to the post-contact period. I know of 

no reports suggesting the presence of leprosy in 

the New World before Columbus. Indeed, leprosy 

remains a condition rarely mentioned in the New 

World paleopathology in the post-contact period 

as well. This is not too surprising, since leprosy is 

one of the least contagious of transmissible infectious diseases (Browne, 1970:640). Thus, its introduction into the New World would not have had 

nearly the impact of other infectious diseases, 

such as small pox, malaria, and measles. M0llerChristensen and Inkster (1965:12) have a reference to an Indian skull from Vancouver Island, 

off the coast of Canada, found in 1866, which 

they suggest had the facies leprosa syndrome 

associated with leprosy. 

M0ller-Christensen's experience with many 

skeletons from leper cemeteries having lesions 

presumably produced by leprosy provides significant insight regarding the bone changes to be 

expected from this disease (M0ller-Christensen, 

1961). The major foci for the disease are the face 

and the small bones of the hands and feet, although other bones may be affected. The skull 

lesions include the destruction of the nasal bones, 

particularly the anterior nasal spine and hard 

palate. He also found a high incidence of cribra 

orbitalia (usura orbitae) in leprous specimens 

(1953:134-135; 1961:29). Henschen (1961:729) 

observed that cribra orbitalia may result from 

insufficient nutrition and chronic inflammation. 

This suggests that cribra orbitalia may not be a 

primary lesion of leprosy but arise from the poor 
NUMBER 28 179 

nutrition and other problems that may attend the 

disease. 

The postcranial lesions are most pronounced in 

the extremities, particularly the hands and feet, 

with concentric atrophy and truncation of the 

phalanges (M0ller-Christensen, 1961:15). The 

bony destruction appears to affect the subarticular, more highly vascularized, bone in the epiphysis adjacent to the articular surface. This process compromises the joint leading to collapse and 

a cupping deformity of the joint. 

M0ller-Christensen (1961:13) states that atrophy of the anterior spine and destruction of maxillary alveolar bone are pathognomonic of leprosy. However, my experience with anatomical 

specimens of syphilis indicate that very similar 

conditions are found in syphilis. M0ller-Christensen (1965:604) indicates that in leprosy, pathological changes are not found on the skull vault. This 

contrasts with syphilis where changes on the vault 

predominate. This is certainly a helpful criterion 

but should not be considered absolute. I have 

studied pathological cases of purported syphilis 

in recent materials in which there was nasal 

destruction with no vault involvement (see Figures 274, 275, 277, 278, 279). The facies leprosa 

syndrome, in combination with atrophy and truncation of the fingers and toes, would appear to be 

almost pathognomonic for leprosy, although it is 

conceivable that combinations of other diseases 

(e.g., syphilis and frostbite) might cause this condition. 

Probably the best documented, archeological 

examples of leprosy are those skeletons excavated 

by M0ller-Christensen at Naestved, Denmark. 

This town was the site of a medieval leper hospital 

and was part of a complex called the St. Jorgen's 

Hospitals, which were built throughout Denmark 

(M0ller-Christensen, 1953:14-15). Most of the 

200 individuals excavated showed bone changes 

attributable to leprosy and formed the basis for 

the classic work by M0ller-Christensen on such 

changes. 

One of the specimens recovered during these 

excavations was presented by M0ller-Christensen 

to the British Museum (Natural History). This 

specimen (BMNH 1962.1.1.2) is the cranium of 

FIGURES 259, 260.—Female leper from the medieval leper 

cemetery at Naestved, Denmark: 259, The nasal aperature 

is enlarged with evidence of an inflammatory response in the 

bone adjacent to the aperture. Note the lytic lesion in the 

palate seen through the aperature (arrow). 260, The palate 

of the female leper showing a possible lytic focus (arrow) and 

the porous bone adjacent to the lytic lesion indicative of an 

inflammatory condition. (BMNH 1962.1.1.2.) 

an adult female leper dated to between A.D. 1250-

1550. The destructive lesions focus on the nose, 

whose lateral margins have been eroded, producing an oval rather than the normal elongated 

opening (Figure 259). The anterior nasal spine is 

destroyed, and there is a suggestion of alveolar 

resorption, although postmortem destruction 

complicates the picture (Figure 260). There is a 

rounded, penetrating defect in the left portion of 

the hard palate, which extends slightly across the 

midline. The central, lytic lesion is surrounded by 

hypervascular, partly resorbed bone. Neither the 

mandible nor the postcranial skeleton was avail-
180 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

able for study. However, M0ller-Christensen 

(1953) does provide descriptions of bone lesions 

in the extremities of other skeletons from the 

Naestved cemetery, which resemble those discussed earlier (p. 176). One possibly significant 

diagnostic feature is that the metacarpals are not 

as severely affected in leprosy as the metatarsals 

(M0ller-Christensen, 1953:141). 

Treponemal Infections 

PATHOLOGY 

Treponemal infections occur in four clinically 

different diseases having a worldwide distribution 

through the tropical and temperate zones of all 

continents. They are venereal syphilis, endemic 

syphilis (treponarid), yaws, and pinta, of which 

only the first three may affect the skeleton. 

Whether they are caused by four different species 

of treponema or by variants of the same species 

is still unresolved and does not concern us here. 

The important feature is that bone lesions of 

venereal syphilis, endemic syphilis, and yaws are 

so similar that diagnostic differences of individual 

lesions cannot be elicited with certainty (Hackett, 

1976). However, there is no evidence that yaws 

produces the "worm-eaten" appearance of the 

outer table of the skull that is seen in syphilis 

(Williams 1935:613). The geographic distribution 

before antibiotic eradication was very characteristic. Yaws was a worldwide disease of tropical 

indigenous populations. Pinta was restricted to 

tropical America. Endemic syphilis was widespread among indigenous populations of subtropical North Africa, the Near East, and temperate 

Asia, but not found in the Americas. Venereal 

syphilis is a sporadic disease following the habitations and colonizations of urbanized white 

races. In all treponematoses, the infecting organisms enter the body through the skin or mucous 

membrane near the skin surfaces. In venereal 

syphilis, Treponema pallidum enters mostly in areas 

of sexual contact, especially the genitals. In endemic syphilis and yaws, the infection may locate 

anywhere on the body surface by intimate contact, mostly already occurring in childhood. In 

all three treponematoses affecting bone, the organisms are disseminated throughout the body 

and reach the skeleton by the bloodstream. 

Yaws 

Bone lesions in yaws occur in about one percent 

of the patients (Wilson and Mathis, 1930). The 

location of such lesions in 101 cases observed by 

Goldmann and Smith (1943) was as follows: tibia 

46, fibula 20 (19 times with tibia), femur 13, ulna 

10, humerus 9, radius 7 (6 times with ulna), spine 

5, clavicle 4, hand 4, foot 4, skull 3, ribs 3, pelvis 2. • 

Since yaws is mostly acquired in childhood, the 

most active lesions are seen in children and in 

adolescents. Many are similar to those seen in 

congenital syphilis. This is particularly true of the 

often symmetrical dactylitis of the spina ventosa 

type and of the periostitis (Hackett, 1957:14-15). 

However, since it is not a disease of the newborn, 

osteochondritis is not seen in yaws. The early 

bone lesions of yaws may completely heal without 

leaving permanent bone changes. Another finding frequently observed in yaws is bending of the 

tibia (boomerang leg) (Figure 261), which is very 

similar to the saber tibia of congenital syphilis 

and usually begins before 15 years of age (Wilson 

and Mathis, 1930). Hackett (1936:54-56) describes disseminated radiologic lucencies in the 

anterior cortex in the early stages followed by 

anterior cortical thickening and bending. In the 

late stage, the posterior concave cortex is thickened and the anterior cortex thinned, as in late 

rachitic deformities. Rarely, the fibula participates in the deformity and occasionally radius 

and ulna show similar bending (Hackett, 1936: 

52-54). These changes are indistinguishable from 

postrachitic deformities and may not be due to 

yaws alone. 

Late yaws show destructive dactylitis of single 

phalanges. The long bones, especially the tibia 

and bones of the forearm, show gummatous periostitis and osteomyelitis, very similar to tertiary 

syphilis. In contrast to early yaws, the overlying 

soft tissues frequently ulcerate and thus open the 

way for secondary pyogenic infections (Hackett, 

1957:16). 

Skull changes mainly consist of destruction 
NUMBE

R 28 181 

around the nasal cavity, particularly extensive in 

gangosa (nasopharyngitis mutilans), a rare com-

plication of yaws in Africa and South America. 

Destruction of the nasal bones, the nasal septum 

and the hard palate are much less frequent in 

ordinary tertiary yaws than in syphilis. The same 

is true of the involvement of the cranial vault. If 

the frontal bone is involved in tertiary yaws, it 

shows shallow, pitted defects rather than the char-

acteristic appearance of syphilitic caries sicca. 

Endemic Syphilis (Treponarid) 

This treponemal infection occurred in Syria, 

Bosnia, and certain areas of Africa. In a survey of 

25,000 persons in Bechuanaland, 26 percent 

showed latent and 1.4 percent active treponemal 

infections (Murray, Merriweather, and Freed-

man, 1956:991). In this study the predilected 

skeletal locations were tibia and ulna. Bone le-

sions were not seen in children less than 2 years 

old (Murray, Merriweather, and Freedman, 

1956:1000). In a study from Syria, the changes 

observed resemble those of acquired or late con-

genital syphilis. They consisted mostly of perios-

teal bone deposits causing fusiform swelling but 

little, if any, medullary changes. Intracortical, 

sharply lytic, rounded gummas are occasionally 

found. Saber tibia does occur (Rost, 1942:321-

323). Periostitis and gummas in short bones of 

hands and feet have been observed in Bosnia by 

Grin (1935:482). Charcot's joint is not observed 

in endemic syphilis (Rost, 1942:323; Murray, 

Merriweather, and Freedman, 1956:1001). De-

structive nasal lesions leading to perforation of 

the hard palate are not uncommon (Grin, 1935: 

482; Murray, Merriweather, and Freedman, 

1956:1000). 

The detailed discussion of the bone lesions is 

FIGURE 261.—X-ray of saber tibia in yaws. Notice the bowed 

and elongated tibia with anterior cortical osteoporosis and 

posterior cortical thickening. Compare with the normal fibula. (48-year-old Javanese male with yaws since childhood; 

studied by W. Putschar at Orthopedic Rehabilitation Cen-

ter, Solo, Java, Indonesia.) 
182 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

essentially based on cases of venereal syphilis, 

with the understanding that similar or identical 

lesions can occur in yaws and in endemic syphilis 

(treponarid). 

Venereal Syphilis 

Venereal syphilis is transmitted through sexual 

contact. This type is called "acquired syphilis." 

However, the actively infected female can pass 

the organisms transplacentally to a fetus, so that 

the infant is born with the disease. This type is 

called "congenital syphilis" and will be discussed 

separately (p. 198). In view of the mode of transmission, it is obvious that, as a rule, acquired 

syphilis commences beyond the age of puberty. 

After an incubation period of several weeks following the infective contact, a distinct primary 

lesion (chancre) usually develops at the point of 

entry. The ensuing long lasting disease is customarily divided into three stages. 

The primary stage begins with the appearance 

of the chancre and ends with the involvement of 

the regional lymph nodes, to which the organisms 

migrate. The secondary stage begins with dissemination of the organisms through the blood 

stream, characterized by transitory skin rash and 

mucous membrane lesions. The borderline between the secondary and the tertiary stage is not 

as clearly defined. However, the tertiary stage is 

mostly characterized by progressive syphilitic involvement of different organs, as, for instance, the 

skeleton. It is in this stage that the tissue reaction 

may assume a distinct granulomatous appearance 

of nodular foci with central liquifying necrosis 

(gumma). The character of the inflammation at 

all stages is more chronic, with lymphocytes and 

plasma cells predominating. Neutrophilic leucocytes are not prominent and there is no significant 

formation of pus. Hypervascularity is usually 

marked. In the secondary stage periostitis is not 

uncommon, producing some periosteal bone. 

These changes are usually transitory and leave no 

characteristic permanent alterations on the bone. 

Our main interest centers on the bone lesions 

of the tertiary period. For the study of these one 

has to go back to specimens collected before the 

advent of effective chemotherapy and antibiotics. 

which means, approximately before 1910. It is 

estimated that at that period about 10 percent of 

inhabitants of European cities gave positive serological reactions for syphilis, which is not identical with active disease (McElligott, 1960). In a 

survey of 2000 cases of syphilis in Norway covering the three decades from 1890 to 1920, Gjestland (1955) found that approximately one percent of the patients showed bone lesions. The 

combination of these figures would result in the 

frequency of syphilitic bone lesions in about one 

in 1000 Europeans in the time period before 

effective treatment was discovered (Hackett, 

1976:114). 

The tertiary syphilitic bone lesions usually develop between 2 and 10 years after the infection, 

but may occasionally occur earlier or much later. 

Often more than one bone is affected. Although 

any bone can be occasionally the seat of a syphilitic lesion, there are a few areas that are greatly 

predilected: the tibia, the bones surrounding the 

nasal cavity and the cranial vault. These three 

locations combined represent about 70 percent of 

all tertiary syphilitic bone lesions. These are followed in decreasing frequency by the cancellous 

bone, rich in hemopoietic marrow (ribs, sternum), 

and the long bones of the extremities. A survey of 

frequency from the greatest series of Fournier 

(1906, as cited in Beitzke 1934a:471) is given in 

Table 10. The spine is an exception to the behavior of other cancellous bones, rarely being involved by syphilis. 

Tertiary syphilitic bone changes are the result 

of either chronic nongranulomatous inflammation or granulomatous (gummatous) processes. In 

many cases a combination of the two is present. 

Either one of these changes can affect only a 

localized area of the bone or the entire bone. The 

inflammation may begin on the periosteum or in 

the bone. Ultimately, however, periosteum and 

cortex, more rarely the medullary cavity, are 

involved. All tertiary syphilitic bone lesions are 

characterized by an excessive osteosclerotic response to the infection. In many instances adjacent mucosal surfaces, as in the nasopharyngeal 

area, and overlying skin, as on the scalp or shin, 

or soft tissue are involved and ulcerated. The 
FIGURE 262.—Tertiary syphilis of cranial vault, outside view. 

These are relatively early lesions with central destruction 

and peripheral reactive bone. The inner table shows only 

minimal diffuse reactive bone deposition. (Adult, ANM FIGURE 264.—Syphilis of cranial vault with considerable 

2232.) healing; top view. (HM P717.) 

FIGURE 263.—Tertiary syphilis of cranial vault, external 

view, multiple small cavitating lesions with advanced and 

partly complete healing; inner table unchanged. (Adult, 

ANM 2468.) 

FIGURE 265.—Extensive syphilis of cranial vault with advanced sclerotic healing. (Adult, WM S50a.2 from 1828.) 
184 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

FIGURES 266-268.—Syphilis of cranial vault (caries sicca): 

266, Top view, showing advanced healing with nodular 

sclerotic bone (scale in cm). 267, Endocranial view, showing 

only slight bony buildup with hypervascularity. 268, Cut 

surface, showing marked thickening of vault with sclerotic 

and porotic areas alternating. (Adult, PMSG 9/1.372E.) 
FIGURE 269.—Infectious defect of frontal bone covered by 

scarred soft tissue, probably syphilis with superimposed osteomyelitis, 25 years duration. (58-year-old male, PMES 

1 E.B.I(4) from 1899.) 

TABLE 10.—Localization of 945 tertiary syphilitic bone lesions in order of decreasing frequency (after Fournier, 1906) 

Bone 

Tibia 

Nose and palate 

Skull 

Ulna 

Ribs 

Sternum 

Clavicle 

Metacarpals 

Humerus 

Radius 

Femur 

Mandible 

Fibula 

Spine 

Nasal bone 

Fingers 

Pelvis 

Metatarsals 

Scapula 

Ribs and sternum 

Tarsals 

Toes 

Maxilla 

Patella 

Carpals 

No. 

248 

238 

179 

37 

35 

29 

27 

21 

20 

17 

16 

14 

12 

9 

9 

7 

5 

4 

4 

3 

3 

3 

3 

1 

1 

FIGURES 270, 271.—Tertiary syphilis of cranial vault: 270, 

Surface view, wet preparation, showing multiple scalp ulcerations exposing the affected bone. 271, Endocranial view, 

wet preparation, showing multiple perforations of the dura 

over the affected bone. (GHPM 3914 from 1914.) 
186 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

FIGURES 272, 273.—Tertiary syphilis of cranial vault (caries 

sicca): 272, Surface view, showing extensive sclerotic healing 

between areas of active destruction. 273, Endocranial view, 

showing only small perforations and slight deposition of 

reactive bone on the inner table. (Adult, ANM 2011.) 

FIGURES 274, 275.—Syphilis of nasal cavity: 274, Frontal 

view, showing widening of the nasal cavity, complete destruction of the nasal septum and large perforation of the 

hard palate. 275, Exterior basal view, showing eroded hypervascular bone at margin of defect. (Old female, ANM 

2423.) 
FIGURE 276.—Syphilis of nasal cavity with destruction of 

hard palate and perforations of ossa palatina; exterior basal 

view. (24-year-old male syphilitic, WM H R 4.1 from 1848.) 

FIGURE 277.—Nasomaxillary syphilis with extensive endonasal destruction and some sclerotic healing, destruction of 

the palate and involvement of the maxilla. (43-year-old 

female, ANM 2221 from 1889.) 

FIGURE 278.—Cranionasal syphilis, mostly healed. Notice 

scarring of nasal and frontal bones; also preservation of the 

inferior nasal spine. (43-year-old male, ANM 2000 from 

1893.) 

FIGURE 279.—Frontonasal syphilis with active destruction of 

the nasal bones and medial orbital walls, healed margin of 

enlarged nasal aperture and completely healed lesions of 

frontal bone. (Adult, WM HS 50a.2 from 1841; lines on 

forehead are shadows from plastic box containing skull.) 
188 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

FIGURE 280.—Syphilis of calvarium and nose. Notice extensive sclerotic healing combined with active destruction, especially frontal, sequestration of the nasal septum and perforation of the palate. (30-year-old female syphilitic, WM S 

50a.3 from 1869.) 

FIGURE 281.—Craniofacial syphilis, showing endonasal destruction with perforation into both orbits, perforation of 

palate, and sequestration of anterior portion of maxilla. 

(Adult male, four years after syphilitic primary lesion, PMES 

l.GD. 1(136) from before 1824.) 

FIGURE 282.—Cranionasal syphilis, external basal view, 

showing active destruction of palate, sclerotic scarring of 

nasal roof with extension to sphenoid; frontal exterior lesions 

almost healed. (30-year-old male syphilitic, FPAM 1552, 

autopsy 8826 from 1834.) 

most characteristic lesions are those with a gummatous destruction and perifocal osteosclerotic 

reaction involving the periosteum and the underlying bone. (For a detailed analysis of morphologic features and their relative diagnostic specificity, see Hackett, 1976.) 

T H E SKULL.—The most common location of 

tertiary syphilitic lesions is in the skull, particularly in the perinasal area and in the cranial 

vault. Furthermore, calvarial lesions represent the 

most specific diagnostic features. 

Transient cranial periostitis is common in the 

earlier stages of syphilis, and chronic syphilitic 

nongummatous periostitis probably contributes 

to the cranial hyperostoses designated as leontias-
FIGURES 283, 284.—Syphilis of left tibia: 283, Medial external view with marked periostitis and 

two small round defects. 284, Cut surface, showing sclerotic obliteration of medullary cavity. 

Autopsy showed also gummatous periostitis of right tibia and cranial syphilis. (40-year-old 

male, IPMI KM229, autopsy 2922 from 1892, annual no. 2; scales in cm.) 
190 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

FIGURE 285.—Tertiary syphilis of left tibia complicated by 

skin ulcer. Notice the mid-diaphysial involvement and the 

erosion at the ulcer base below. The medullary cavity was 

blocked by reactive bone. (27-year-old female, ANM 2914 

from 1872.) 

sis ossea. However, these are not diagnostic etiologically. The main interest concentrates on the 

tertiary gummatous, osteoperiostitic lesions of the 

cranial vault, the majority of which begin in the 

frontal bone from where they may spread across 

sutures to the adjacent parietal and facial bones. 

Less commonly, the first lesion in the cranial 

vault begins in a parietal bone. The occipital 

bone is usually spared, even if the process extends 

to the lambdoid suture. The characteristic lesion 

has been classically described by Virchow (1858, 

1896) under the term of "caries sicca." Hackett 

(1976:30-49) has revived this term, added more 

detail to the sequential events of this lesion, and 

designated it as the most diagnostic feature in dry 

bone. The lesion begins at or near the osteoperiosteal border, usually of the outer table, eliciting 

hypervascularity which, on inspection of the outer 

table of a dry skull, reveals itself in the form of 

grouped, enlarged vascular foramina. This initial 

change is shared with the reaction to tuberculous 

foci and to metastatic cancerous deposits. However, in the latter two the inner table is predilected and ultimately shows the larger defect. In 

osteolytic metastatic cancer, due to its frequently 

rapid growth rate, full thickness destruction of 

both tables and the intervening diploe is common, 

resulting in a hole with crenelated nonreactive 

border. In tuberculosis, in addition to the broadbased involvement of the inner table, there is 

usually little reactive bone formation perifocally. 

The syphilitic lesion leads to a destruction of 

the outer table and part of the diploe by the 

syphilitic granulation tissue but often spares the 

inner table almost completely. It elicits strong 

sclerotic response of the surrounding bone, forming a sclerotic base and an elevated sclerotic 

margin around the defect in the table (Figure 

262). Microscopically, focal bone necrosis is common and may well be a major stimulant to reactive sclerosis in the process of remodeling (Axhausen, 1913). However, pus formation is not significant and large sequestra usually do not form. In 

the chronic course of syphilis, even if untreated, 

individual foci will heal, but new foci will form 

in the vicinity. The healed individual focus of 

caries sicca of the skull leaves a depressed, slerotic, 

radially grooved stellate scar (Figure 263). This is 

somewhat less obvious in confluent healed areas 

(Figure 264). The continued process leads to confluent pitting in circinate arrangement surrounded by ivory-hard reactive bone, partly with 

smooth, partly with hypervascular surfaces (Figure 265). In advanced confluent caries sicca, the 

diploe may be markedly thickened and sclerotic 

while the inner table exhibits only minor reactive 

FIGURES 286-289.—Tertiary syphilis involving multiple 

bones: 286, Distal left femur (P374) with periostitis and 

sclerotic placquing. 287, Right ulna (P372) with periostitis 

and slight pitting. 288, Left clavicle (P369), with diffuse 

periosteal bone and focal pitting. 289, Left scapula (P370) 

with enlargement and erosion of the acromion and spine. 

(HM 372.) 

192 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

bone (Figures 266-268). Full thickness destruction and perforation of the cranial vault does 

occur (especially in cases with secondary pyogenic 

osteomyelitis), but even then the changes on the 

inner table are less pronounced (Figure 269). 

Major sequestra are seen in European syphilitic 

skulls, often showing darker discoloration of the 

necrotic bone. This is due to exposure of the 

affected bone in scalp ulcerations and probably 

largely represents the result of secondary pyogenic 

infection, presumably from without (Figures 270, 

271). In contrast to the sequestra in pyogenic 

osteomyelitis, these sequestra show a "worm-eaten" appearance, indicating their involvement in 

the disease process before becoming necrotic (Figures 272, 273). Hackett (1976:57) did not find 

sequestra in skulls of Australian aborigines affected by endemic syphilis or yaws. He attributes 

this to the presumed absence of pyogenic infections in these populations. 

The facial bones most often affected by tertiary 

syphilis are the nasal bones, the bony nasal septum, the hard palate, the turbinates, and the 

medial walls of the maxillary antrum. These 

bones are involved secondary to common syphilitic lesions of the nasal mucosa. The thin bones 

are often destroyed, resulting in perforation of the 

nasal septum, the hard palate, and of the medial 

walls of the maxillary sinuses (Figures 274-277). 

The nasal cavity appears enlarged and empty in 

the dry skull. However, in contrast to neoplastic 

destruction in this area, the margins of the defect 

are bordered by smooth sclerotic bone. In contrast 

to leprosy, the frontal bone is usually involved, 

the perforation of the nasal septum and hard 

palate is common, the sclerotic response is marked 

and the inferior nasal spine may be spared (Figure 

278). The zygoma, the ossa nasalia, and medial 

orbital walls may be affected by direct extension 

of the process in the frontal bone (Figure 279). 

Destruction of the bony support of the bridge of 

FIGURES 290, 291.—Syphilis of left femur with fusiform 

hyperostosis and medullary osteosclerosis: 290, Anterior 

view, showing snail-track pitting, especially on the metaphysis. 291, Cut surface, showing extensive sclerotic obliteration 

of medullary cavity. (Adult, WM S 506.1 from 1831.) 
NUMBER 28 193 

FIGURES 292, 293.—Tertiary syphilis of cranium and right 

femur: 292, Skull, frontal view; active superficial lesions on 

frontal bone with hyperostosis. 293, Right femur, frontal 

view; massive gummatous periostitis with typical snail-track 

pattern. (55-year-old male, PMUG 3466.) 
194 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

FIGURES 294-296.—Syphilis of cranial vault and of long 

bones: 294, Frontal view, showing quiescent external defect 

with sclerotic healing. 295, To p view, showing more active 

destructive lesions in both parietal bones. 296, Left arm 

bones; notice absence of sequestra and cloacas (scale in cm). 

(45-year-ol J female, PMUG 2647, autopsy 6262 from 1874.) 

FIGURES 297-299.—Tertiary syphilis of skull and extremities: 

297, Total skeleton, frontal view. 298, Both arms, posterior 

view, showing especially massive symmetrical involvement 

of both humeri. 299, Both legs, anterior view, showing 

especially marked symmetrical involvement of both tibiae. 

(Adult male, DPUS 5527 from before 1820.) 
NUMBE

R 28 195 
FIGURES 300-304.—Details from a total skeleton with numerous syphilitic bone lesions: 300, 

Lateral view of skull showing three unusual features: involvement of the mandible, lesions on 

the inferior portion of the occipital bone, and fusion of the diarthrodial joints including the 

occipital condyles through the sixth cervical. 301, Severe involvement of clavicles and sternum. 

302, Extensive destruction right scapula and ribs. 303, Lateral view, right femoral diaphysis, 

showing penetrating defect surrounded by periosteal buildup. 304, Posterior view, right tibial 

diaphysis, showing fusiform swelling and multiple defects with isolated bone fragments. 

(51-year-old male with visceral and cerebral syphilis, DPUS 4479, autopsy 697 from 1907.) 
NUMBER 28 197 

the nose results in the syphilitic saddle nose (Figure 280). Major sequestration may be the result 

of secondary infection (Figure 281). 

The skull base is rarely involved, but extension 

of the nasopharyngeal process into the sphenoid 

does occur, resulting in marked sclerosis of the 

area (Schinz, Baensch, Friedl, and Uehlinger, 

1951-1952:627)(Figure 282). 

T H E LONG BONES.—The tibia is approximately 

10 times more often the site of syphilitic lesions 

than any other long bone of the extremities (Figures 283, 284). The syphilitic lesions of long bones 

can be separated into nongummatous and gummatous osteoperiostitis. The nongummatous lesions are suggestive but probably not diagnostic 

of treponemal infection (Figure 285). Hackett 

(1976:87-90) puts them into his "on trial" category of diagnoses. The localized form of nongummatous syphilitic periostitis may leave elevated, 

placque-like exostoses on the cortex of bones with 

a large muscle mantle (as the femur or 

humerus) (Figures 286-289), or circumscribed 

buildup of surface parallel lamellar bone of varying thickness and density on bones immediately 

beneath the subcutis (as the anterior surface of 

the tibia). Extensive periosteal thickening is often 

combined with cortical thickening, including the 

endosteal surface. Diffuse nongummatous osteoperiostitis tends to leave the bone thick and 

heavy. The entire surface, with exception of the 

cartilage-covered articular facets, may be involved. The periosteal bony buildup may be thick 

and becomes firmly fused with the old cortex. 

The outer surface is rough and markedly hypervascular. In late stages of nongummatous osteoperiostitis, the medullary canal may be completely obliterated by sclerotic trabeculae, while 

the old cortex may be loosened up by Haversian 

resorption so that, on cross-section, the bone appears uniformly coarsely cancellous with loss of 

the distinction of cortex and medulla. Differential 

diagnoses from Paget's disease can be made microscopically by the absence of the typical Paget 

mosaic patterns in syphilis, in which bone deposition is not interrupted by many phases of active 

resorption. 

Gummatous osteoperiostitis is a much more 

characteristic lesion. In its localized form it may 

result in tumor-like enlargement of the affected 

bone area (Axhausen, 1913). In dry bone, the 

marked hypervascular periosteal bony buildup 

surrounds a scooped-out defect, extending into 

the cortex. This corresponds to the location of a 

destructive gumma in the fresh specimen. At 

times the scooped-out lesions are smaller and 

grouped, resembling the picture of cranial caries 

sicca, but individual gummatous defects tend to 

be larger than on the skull. The underlying cortex 

is hyperostotic and endosteal bone formation may 

encroach upon the medullary canal (Figures 290, 

291). Diffuse gummatous osteoperiostitis resembles closely the surface appearance of cranial 

caries sicca (Figures 292, 293). In some cases 

larger defects are seen in the mantle of hypervascular periosteal bone, exposing to view deep cortex (Figures 294-296) and sometimes small sequestra. These lesions must not be confused with 

cloacal openings of hematogenous osteomyelitis. 

In contrast to that condition, major sequestra are 

missing, and the margins of the defects are rough 

and thin, and not smooth and sclerotic as on the 

cloacas of pyogenic osteomyelitis. Hackett (1976: 

82, 93-97) accepts this form of osteoperiostitis as 

diagnostic of treponemal infection. Central gummas of the medullary cavity occur in the form of 

larger lytic lesions surrounded by a marked perifocal reactive sclerosis. This lesion may not be 

differentiated with assurance from a Brodie's abscess, although the sclerosis is more marked than 

in the latter. Pathologic fractures in bones weakened by syphilitic osteoperiostitis are not uncommon. 

T H E SPINE.—Syphilitic osteomyelitis of the 

spine is rare (Whitney and Baldwin, 1915) and 

the changes in dry bone would not be diagnostic 

in themselves. The outcome may be gibbus, after 

destruction of adjacent vertebrae, similar to tuberculosis. In contrast to tuberculosis, a paravertebral abscess is missing; however, this may not 

be obvious on dry bone. Also, in contrast to 

tuberculous spondylitis, the cervical spine is affected three times as often as any other segment 
198 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

(Beitzke, 1934a:510). This may suggest extension 

from nasopharyngeal mucosal lesions rather than 

hematogenous origin. 

T H E JOINTS.—Syphilitic arthritis occasionally 

occurs in the large joints (knee, shoulder, elbow) 

during the secondary stage (Glutton's joint). This 

affection is transitory and leaves no changes visible on dry bone. Occasionally an epiphysial 

gumma may perforate into a joint and lead to 

gummatous arthritis (Axhausen, 1913). The perforation into the joint predominantly occurs near 

the margin of the articular cartilage (Freund, 

1933). Subsequent bone changes, if present, are 

not significantly different from other forms of 

arthritis, particularly degenerative arthritis. Only 

the presence of the gummatous bone lesion may 

be a clue to the treponemal etiology. 

Indirect suspicion of syphilitic infection may 

be aroused by observation of pressure erosions of 

sternum, ribs, or thoracic vertebrae or from findings of a Charcot joint. However, it should be 

realized that not all aneurysms of the thoracic 

aorta are syphilitic and not all neuropathic arthropathies are the result of tabes dorsalis (nerve 

degeneration associated with syphilis). 

The multiplicity and complexity of tertiary 

syphilitic bone lesions is illustrated in selected 

views from two complete skeletons of the Pathology Museum of the University of Strasbourg, 

France (Figures 297-304). 

Congenital Syphilis 

Congenital syphilis was a common disease with 

high mortality before the possibility of effective 

treatment of the infected mother during pregnancy. Among 4500 consecutive autopsies at 

Johns Hopkins Hospital before 1933, there were 

189 fatal cases of congenital syphilis, only two of 

which were older than 4 years of age (Smith, 

1933). In congenital syphilis the treponemal infection is transmitted transplacentally from the 

actively infected mother to the fetus. The result 

is fetal death followed by abortion in the first half 

of pregnancy, fetal death with delivery of a premature or mature diseased stillborn fetus, or delivery of a living infected infant. If the infection 

is mild it may not manifest itself for several years 

(syphilis congenita tarda). In massive infections, 

all organs and tissues of the fetus are permeated 

with numerous treponemal organisms. Since the 

immune capacity to mount an inflammatory response is not yet developed in the first half of 

pregnancy, such aborted fetuses show no tissue 

changes. Furthermore, such fetuses are obviously 

subject to rapid disintegration and, therefore, do 

not concern us here. In premature and full-term 

stillborns, as well as in actively infected newborn 

living infants, characteristic skeletal changes are 

almost always present in form of syphilitic osteochondritis. This is the result of hematogenous 

dissemination of Treponema pallidum throughout 

the fetus in utero. It affects all areas of enchondral 

growth in the entire skeleton but is most marked 

in the fastest growing metaphyses (distal femur 

and proximal tibia). The lesions are symmetrical. 

They consist of accumulation of calcified cartilage adjacent to an area of lucency due to poor 

bone formation (Figure 305). This may represent 

merely a toxic effect on the enchondral ossification ("passive osteochondritis" of Schneider, 

1923-1924:205) or be the result of formation of 

syphilitic granulation tissue in this area ("active 

osteochondritis" of Schneider, 1923-1924:205). 

Similar disturbances of enchondral growth are 

seen in a variety of conditions and are not diagnostic of syphilis (Caffey, 1939). It is appreciated 

that these fetal and neonatal alterations will have 

very little chance of recognition in archeological 

material. In the surviving infants, transverse metaphysial pathologic fractures through this weakened area of the metaphysis not uncommonly 

occur (Parrot's pseudoparalysis). Since, in the 

infant, before walking, the arms are more mechanically stressed than the legs, the distal humerus is the predilected site of such fractures. 

This osteochondritis heals in the infant even if 

untreated. Syphilitic periostitis often develops 

during infancy, mostly following the osteochondritis. Occasionally it has already begun in intrauterine life and is present at birth. It consists of 

multiosseous, usually symmetrical, circumferen-
NUMBER 28 199 

FIGURE 305.—Syphilitic osteochondritis of distal femur, wet 

preparation. Notice the broadened and irregular area of 

provisional calcification at the meta-epiphysial junction. 

(2-month-old male, W M S 51.2 from 1910.) 

FIGURE 306.—Humerus with subperiosteal bone formation 

on the shaft in congenital syphilis. Most long bones showed 

the same changes. (3y2-month-old infant, WM S 51.1 from 

1880.) 

FIGURE 307.—Congenital syphilis of cranial vault with 

periosteal bony buildup on both frontal and parietal bones. 

The mother had extensive ulcerated nasofacial syphilis. 

(1 year, PMWH WO 734 from 1886; lines on skull vault are 

shadows from box containing specimen.) 

tial deposition of subperiosteal bone on the shafts 

of long bones. The trabeculae of this bone deposit 

often shows a radial arrangement. This change is 

frequently transitory but may be recognizable on 

infant bones under conditions of ideal preservation (Figure 306). Similar periosteal bone deposits 

may occur on the cranial vault (Figure 307). 

Gummatous periostitis and osteomyelitis occasionally occur, especially in older children who 

have passed through mild, unrecognized, and 

untreated manifestations in infancy (syphilis congenita tarda) (Wimberger, 1925:307-370). In this 

age group the bone involvement is neither so 

frequent nor so generalized as in the infant period 

but comes closer to the distribution and appearance of acquired syphilis (Figures 308-

310)(Pendergrass, Gilman, and Castleton, 1930). 

Only 32 of 462 patients of over 13 years of age 

with late congenital syphilis showed active syphilitic bone changes (Smith, 1933). Such lesions in 

the long bones predilect the tibia, ulna, and 
200 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

FIGURES 308-310.—Tertiary congenital syphilis involving 

multiple bones of about a 12 year old: 308, Left femur, 

external view, showing periosteal buildup with scooped-out 

defects and snail-track pattern. 309, Bisected left femur with 

cortical resorption and medullary reactive bone; notice absence of medullary penetration and sequestrum (AMN 

2999). 310, Fibula, ulna, and radius (bisected), showing 

similar lesions (ANM 3163, 3166, 3185). 
NUMBER 28 201 

FIGURE 311.—Tertiary congenital syphilis of radius and ulna, 

bilateral (all bones bisected longitudinally); notice pitting 

destruction and marked hyperostosis without cloacas or sequestra. (About 6 years, ANM 3386.) 

radius (Figure 311). Skull lesions occur but usually appear as multiple, rounded, destructive foci 

without the characteristic features of the caries 

sicca sequence (Figures 312, 313). Syphilitic saddle-nose in congenital syphilis may be mainly the 

result of disturbed enchondral ossification of the 

base of the skull. In adolescents, tertiary syphilitic 

bone lesions may more closely simulate those 

observed in adults, and differentiation of a late 

stage of congenital from venereal syphilis may be 

impossible without clinical data (Figures 314, 

315). Occasionally extensive involvement of facial 

bones can occur in congenital syphilis (Figures 

316,317). 

Nongummatous periostitis results in osteosclerosis with ultimate fusion of the subperiosteal 

bone deposits and the underlying cortex. The 

most characteristic lesion of this type is the socalled saber tibia of Fournier (1886:265-269). 

This apparently represents the combination of 

stimulated growth and layered bone deposition 

on the anterior surface. The tibia is longer than 

normal and shows a true forward curve, while the 

fibula remains of normal length and configuration. As previously mentioned, similar bony 

buildup on the anterior tibial surface occurs in 

nongummatous periostitis of acquired syphilis 

(Figures 318, 319). In that case, however, the tibia 

is not truly elongated and curved, and the posterior contour remains straight. 

Syphilitic dactylitis used to be more frequently 

observed in congenital than in acquired syphilis. 

It concerned the fingers more often than the toes 

and predilected the basal phalanges. The condition often affected more than one finger, not 

infrequently bilateral but not symmetrical. The 

appearance, especially in small children, may 

closely simulate that of tuberculous spina ventosa with widening of the diameter and formation 

of a thin, bony shell. In adults there is less expansion and more reactive osteosclerosis. 

Hutchinson's and Moon's teeth, although present in a variable number of individuals with 

congenital syphilis, also have been questioned in 

their specificity (Kranz, 1927:263). 

Although there are a variety of skeletal changes 

occurring in different phases of congenital syphilis, the findings are more indicative than diagnostic and must be critically evaluated in the 

entire context of the skeletal findings. Individual 

lesions may not be distinguishable from tuberculous or other infectious changes. 

PALEOPATHOLOGY 

In the history of disease, probably no single 

pathological condition has generated more 

scholarly debate than treponemal infections and, 

in particular, syphilis. The debate has focused on 

the origin of syphilis, with some scholars arguing 

that the disease was introduced into the Old 

World by Columbus and his crew after their 

discovery of the New World. Another possibility 

is that syphilis existed in the Old World before 
202 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

FIGURES 312, 313.—Congenital syphilis with destructive lesion of right frontal bone involving 

both tables: 312, Outside view. 313, Endocranial view. (8-month-old female, ANM 2233 from 

1865.) 

Columbus and may have been introduced into 

the New World by Columbus. A third point of 

view is that treponemal diseases existed in both 

the Old and New World before Columbus. 

These different and conflicting opinions are 

based on three distinct, but not necessarily mutually exclusive, sources of information: (1) historical documents, (2) pathological remains, and 

(3) speculation based on evolutionary theory. The 

relative dependence of a scholar on one of these 

sources appears to have considerable influence on 

his subsequent conclusions. The problem, of 

course, is that so far there is no source that can 

provide overwhelmingly convincing evidence for 

any of the three hypotheses. 

While a comprehensive review of the basic 

literature on the subject of the history of treponemal diseases is beyond the scope of this work, 

a brief summary of the major concepts is essential 

to our subsequent presentation of paleopathological specimens. It also serves to highlight the 

pitfalls of uncritical reliance on published sources. 
FIGURE 314.—Tertiary cranial syphilis (congenital?). Notice 

active and healing lesions in frontonasal area, widened nasal 

aperture, loss of nasal septum and inferior nasal spine, and 

perforation of palate. (16-year-old male, ANM 2009 from 

1870.) 

FIGURE 315.—Frontofacial syphilis with destruction of nasal 

bones and involvement of zygomas, the frontal lesion partly 

healed. The young age raises the question of tertiary congenital syphilis. (17-year-old female, ANM 2427.) 

FIGURES 316, 317.—Congenital syphilis of maxilla, right 

orbit, and right frontoparietal area: 316, Frontal view, showing sclerotic healing of frontal and nasal bones; teeth normal. 

317, Lateral view, showing active frontoparietal lesion. 

(8 year old, with history of syphilis, O M F 133.) 
204 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

FIGURES 318, 319.—Syphilitic saber tibia: 318, Right tibia, 

lateral view, showing massive anterior periosteal bone deposition. 319, X-ray of lateral view, showing anterior cortical 

thickening and preservation of the medullary cavity. (Adult 

Caucasian male; Pathology Department of the University of 

Otago, New Zealand, courtesy of Dr. B. Ragsdale, Armed 

Forces Institute of Pathology, Washington, D.C, USA.) 

Bruhl (1880) cites many primary historical 

sources, including early chroniclers of colonial life 

in the Americas, such as Oviedo and Las Casas, 

who supported the view that syphilis existed in 

the New World at the time of its discovery by 

Europeans. He also cites Diaz de Isla, the physician who treated Columbus' men for presumed 

syphilis. Bloch (1901, 1911) provides a review of 

older, relevant source material on the subject. In 

another report (1908:4), he concludes that "all 

available statements and facts point to the last 

decade of the fifteenth century—particularly the 

years 1493-1500—as the time when syphilis first 

appeared in the Old World. There is not a particle of evidence to show that the disease existed 

in Europe before that time." Dennie (1962:61-

63) notes that syphilis was particularly virulent 

after its initial introduction from the New World 

and subsequently became milder. Dennie argues 

that this reflects the normal progress of a newly 

introduced disease and thus supports the theory 

of New World origin for syphilis. 

In contrast with the above opinions, Holcomb 

(1941) cites early descriptive medical reports of a 

disease process attributed by the early writers to 

leprosy. However, Holcomb (1941:151-152) indicates that many of these purported cases of 

leprosy were clearly syphilis, both in terms of 

appearance and the venereal mode of transmission. He concludes (1941:167) that "syphilis in a 

congenital and acquired form certainly prevailed 

in Europe long before the discovery of America." 

This conclusion is supported by a description 

reported by Thorndike (1942:474) on a disease 

process resembling syphilis dated 1412. 

Elsewhere in the Old World, Hyde (1891:117) 

states that the ancient medical literature of 

China, India, Greece, and Italy contains unmistakable proof that early in the world's history 

genital lesions were known to occur from sexual 

contact. However, Crosby (1969:219) offers an 

opposing opinion that there is no unequivocal 

description of syphilis in the ancient Old World 

medical literature. In particular, Crosby cites 

Wong and Wu (1936:218), who state that no 

Chinese writer has ever described a case that 

could be attributed to syphilis. 

There is one, final, historical argument pertaining to the origin of syphilis that bears noting. 

Bloch (1908:8) suggests that the presence of syphilis would have led to its widespread prevalence 

had it existed in the ancient Old World. In view 

of the "unbridled licentiousness of Imperial Rome 

and the excesses of the Middle Ages," he argues, 

there should be considerable evidence for syphilis 

in ancient skeletons. Bloch found no such evidence in European skeletal material of pre-Columbian age. There is, unfortunately, no indication regarding the sample size of pre-Columbian 
NUMBER 28 205 

European skeletons on which this conclusion was 

based. Undoubtedly, Bloch's reference to unnumbered thousands of skeletons of pre-Columbian 

age refers primarily to the work of Elliot-Smith 

and Wood-Jones on Egyptian material, where 

other epidemiological considerations need to be 

considered before one eliminates the possibility of 

syphilis in that population. 

In discussing evidence for pre-Columbian syphilis in the New World we are primarily limited to 

human remains and most of the evidence is from 

the skeleton. With skeletal material there are 

two fundamental requirements: (1) unambiguous 

identification of treponemal disease and (2) unambiguous determination of pre-Columbian archeological age. Several purported cases of preColumbian syphilis have foundered on one or 

both of these factors. 

The earliest reference to syphilitic lesions in 

New World skeletons is Jones' (1876:66) report 

on archeological skeletons from Tennessee. Indeed, this early report appears to have been the 

basis for subsequent reports in which the authors 

concluded that syphilis was in the New World 

before Columbus (e.g.. Lamb 1898). Morgan 

(1894) challenges Jones' conclusions calling into 

question both the diagnosis of syphilis and the 

pre-Columbian date. 

Many other purported cases of skeletal syphilis 

have been reported in New World specimens. 

One of the most respected scholars studying this 

material was H. U. Williams, a pathologist, who 

concluded on the basis of a critical review of 

published material and his own observations that 

the case for pre-Columbian syphilis was probable 

beyond reasonable doubt (Williams, 1932:978). 

He found the evidence for Old World skeletal 

syphilis before 1490 to be much less convincing. 

After a careful study of Eskimo and Aleut skulls, 

Holcomb (1940:189) concluded that syphilis 

probably did not exist in these northern regions 

of the New World until after contact with Russian 

sailors and traders. 

The third source of speculation on the history 

of treponemal diseases is based on theoretical 

reconstructions with evolutionary theory as the 

major integrating concept. In essence this concept 

of treponemal diseases suggests that they have 

evolved with man and migrated with him 

throughout the world and thus were endemic in 

both the Old and New World long before Columbus (Hudson, 1968; Cockburn, 1961; Hackett, 

1963). Although not phrased in evolutionary 

terms, the concept of treponemal diseases being 

endemic in both Europe and the Americas goes 

back to an early report by Krumbhaar. He states 

(1936:232): "Personally, I regard as most convincing the theory of the existence of syphilis in 

both continents as far back as prehistoric times." 

Similarly, Stewart and Spoehr (1952) speculate 

that treponemal diseases existed in the Old and 

New World but had developed different strains 

while isolated from each other. When contact 

between the European explorers and indigenous 

Americans occurred, they traded strains of treponemal organisms to which neither had developed any immunity. This they suggest is the 

reason for the syphilis epidemic in Europe after 

Columbus and the increase in bony lesions possibly attributable to syphilis in post-Columbian 

Indian skeletons in the New World. Stewart and 

Spoehr's (1952) observations on the increase in 

syphilitic type lesions in post-Columbian indigenous American skeletons is significant, because of 

Stewart's extensive experience with New World 

skeletal material. 

Hudson, in several papers, has attempted to 

reconstruct the evolutionary history of the treponemal organism. In one of his earlier papers 

(1958:23) he suggests that the treponeme evolved 

from a saprophyte (a microorganism that is 

closely related to the treponemal organism) early 

in man's evolutionary history through the introduction of such an organism into a break in the 

skin. He further speculates that this event may 

have taken place in Central Africa in an environment similar to the rain forest of today (Hudson, 

1965:890-891). Such an early disease would probably have been similar to yaws of today, in which 

the organism survives on the moist skin. 

Crucial to an understanding of Hudson's evolutionary history of treponemal diseases is the 
206 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

concept that treponemal organisms represent a 

"biological gradient" rather than separate species. In this scheme the various treponemal diseases reflect adaptations by the same microorganism to varying epidemiological conditions. Thus, 

when man moved to more temperate regions the 

organism migrated to the more moist regions of 

the body (the mouth, axillae, and the crotch), 

creating a new disease syndrome called endemic 

syphilis by Hudson (1965:891). 

Hudson (1965:895) argues that the development of venereal syphilis was the result of development of the cities with the improved hygiene 

associated with city life. Also the increased use of 

clothing prevented the frequent skin contact in 

children necessary for transmission of endemic 

syphilis. After man's migration to the New World, 

the development of the South American treponemal disease, pinta, was, in Hudson's reconstruction, the result of a local adaptation, in which the 

treponeme was again introduced to environmental conditions similar to those found in Central 

Africa (Hudson, 1965:892). 

Hudson recognizes the inherent question in his 

theory which is, why did venereal syphilis not 

develop sooner in the evolutionary process if all 

treponemal diseases are the result of adaptations 

in a single species? In response to this question he 

notes that immunity to the treponeme would be 

acquired during childhood as the result of exposure to nonvenereal syphilis so that venereal 

transmission after sexual maturity was not possible until children no longer contracted the disease 

(Hudson, 1965:892). 

Hackett (1963) takes a somewhat different approach in reviewing the origin and history of 

treponemal diseases. While recognizing that the 

organisms associated with the four contemporary 

treponemal diseases are indistinguishable microscopically, he continues to distinguish the diseases 

as clinical entities (Hackett, 1963:9). In Hacketts's 

evolutionary scheme, treponemal diseases began 

in the Afro-Asian landmass about 15,000 B.C. The 

syndrome was pinta, which spread throughout 

the world, subsequently becoming isolated in 

America. Yaws, also, developed in the Afro-Asian 

landmass as a mutant of the pinta treponeme and 

spread throughout the Old World. Endemic syphilis evolved from yaws during the drying trend 

following the last Pleistocene glacial period. As in 

Hudson's reconstruction, Hackett associates the 

development of venereal syphilis with the emergence of cities. However, he suggests that the 

disease was mild until a virulent mutation toward 

the end of the fifteenth century A.D. gave rise to 

the European epidemic attributed to the return 

of Columbus from the New World. Subsequent 

to this event venereal syphilis was spread throughout the world during the European colonial expansion in the sixteenth and seventeenth centuries (Hackett, 1963:38). Like Hudson, Hackett 

does find a likely association between the evolution of treponemal diseases and environment, 

particularly climate. However, these two scholars 

differ in the evolutionary mechanism. Hudson 

supports the concept of a pluripotential organism; 

Hackett evokes multiple mutations and different 

organisms. 

While these arguments may seem rather arcane, scholarly debates that are probably unresolvable, it is important to stress that these speculations do have a bearing on the interpretation 

of skeletal lesions or the lack of skeletal lesions. 

The historical and contemporary expression of 

treponemal diseases suggests some variation in 

the organ systems affected (Hackett, 1963:8-9) 

and the virulence of the disease. These basic 

principles apply to the effect of treponemal disease on the skeleton. Thus, the absence of skeletal 

evidence of treponemal disease is necessary but 

not sufficient support for the absence of the disease in an archeological population. Indeed, the 

arguments presented, particularly by Hudson 

and Hackett, should make one cautious about 

assumptions of the absence of treponemal diseases 

on any continent at any point in man's history of 

the last 10,000 years. 

Crosby's observation (1969:219) that the typical evolutionary development of some infectious 

diseases is characterized by decreasing virulence 

is a well-known epidemiological principle and is 

based on the fact that those organisms that kill 
NUMBER 28 207 

the host generally die as a result, while organisms 

that are less virulent or infect individuals with a 

more effective immune response tend to survive. 

Where a disease has been endemic for centuries, 

as Hudson and Hackett suggest was the case for 

treponemal diseases, milder forms of the disease 

and improved host-response could have developed in which the skeleton was not affected, as is 

the case with pinta today. 

Congenital Syphilis 

Because of the problems in differentiating various expressions of treponemal disease in paleopathological specimens, most of the following case 

descriptions will not be attributed to a specific 

syndrome. An exception to this is an archeological 

example of probable treponemal disease in a 6-

to 7-year-old American Indian child from Virginia (NMNH 379177). The sex of the child is 

unknown. There were no European trade goods 

found at the site. Both the pottery types and the 

presence of stone pipes suggest a date before 1400. 

While a later date cannot be ruled out, the evidence points to the pre-Columbian period. 

Lesions on the skull appear to be confined to 

the face and forehead (Figure 320). There is some 

postmortem damage to the skull, which complicates the picture somewhat. The lesion on the 

forehead is located near the midline and measures 

about 35 millimeters by 45 millimeters. It may 

extend to the left of the frontal bone, but postmortem damage precludes confirmation. The lesion itself consists of periosteal bone, which shows 

only slight evidence of porosity (Figure 321). The 

most markedly abnormal bone tissue occurs 

around the nose. The nasal bones and the maxillary bone adjacent to the nasal bones and nasal 

aperture have thickened, porous, periosteal bone 

on their external surfaces (Figure 323). The remaining portions of the maxilla appear to be 

normal. There is a slight degree of porosity of the 

orbital roof (cribra orbitalia). There are plaques 

of porous periosteal bone on the inferior and 

anterior portions of the mandibular body. This is 

accompanied by a slight expansion in the thickness of the body on the left side. The maxillary 

deciduous incisors are missing on the left. However, both right maxillary incisors have marked 

hypoplastic enamel defects (Figure 322). Indeed, 

the defect was so severe that the lower portion of 

the right lateral incisor appears to have broken 

off antemortem. There is a less severe hypoplastic 

defect on the left deciduous maxillary canine. 

The enamel of the right canine has been damaged 

postmortem, although there is a slight vestige of 

a defect on this tooth as well. The deciduous and 

first permanent molars are normal, as is the 

emerging permanent left central incisor. 

The dentition of the mandible is less severely 

affected. The central incisors are hypoplastic with 

antemortem loss of the superior portions of the 

crown. The lateral incisors have a very slight 

enamel defect. The remaining teeth appear to be 

normal, although the severe caries of both deciduous second molars suggests weakened enamel. 

Caries of the lower left first deciduous molar has 

resulted in an abscess on the left side. 

All of the major bones of the postcranial skeleton exhibit porous periosteal lesions. The severity and thickness of these lesions varies and is 

significant in reaching a preferred diagnosis. Both 

scapulae are normal, as is the manubrium. Both 

clavicles have periosteal bone deposits on the 

anterior medial aspect of the diaphysis; the metaphyses are normal. Both humeri have patchy, 

periosteal bone deposits, which are limited to the 

diaphysis. Involvement is slight and there is no 

appreciable expansion of the cortex. The radii are 

somewhat damaged but clearly indicate a general 

deposition of periosteal bone on the diaphysis, 

which is more severe distally. There is a slight 

expansion of the diaphysis, and the metaphysis is 

normal. A similar distribution of periosteal bone 

occurs on the ulnae, but the diaphysial expansion 

is more marked. This expansion occurs through 

the apposition of periosteal bone, but this is also 

associated with an expansion of the marrow 

space, although there appears to be a net increase 

in the thickness of the cortex. 

Many of the smaller bones of the hands were 

not recovered during excavation, although all the 
208 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

FIGURES 320-327.—Probable congenital syphilis in a 6 to 7-year-old child from an archeological 

site in Virginia, USA (artifacts associated with the burial suggest a pre-Columbian date): 320, 

Facial view showing abnormal periosteal, reactive bone (arrows) on the frontal, nasal, and 

maxillary bones. 321, Detailed view of the frontal lesion. 322, Detailed view of the hypoplastic 

development of some of the deciduous dentition. Note the hypoplastic enamel lines and the loss 

of a portion of the crowns of some of the defective incisors (arrows). 323, Detailed view of the 

periosteal reactive bone on the nasal and maxillary bones. 324, The anterior view of the femora, 

tibiae, and left fibula. Note that the diaphyses of the tibiae (arrows) are much thicker than the 

diaphyses of the femora. 325, A detailed view of the expansive periosteal bone on the left tibia. 

326, The laterosuperior view of the right fifth metatarsal; note the thickened porous nature of 

the periosteal reactive bone. 327, The mediosuperior view of the right fifth metatarsal; note the 

diminished amount of reactive bone on the medial aspect (arrow). (NMNH 379177.) 
NUMBER 28 209 

/•I i,'.VJ 

'•'. ' .^.;•';••.>*, ' • '.:.... ' 

mr • • 
210 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

FIGURE 328.—Upper incisors and canines of a 3-year-old 

child with congenital syphilis. Note that the crowns are 

partly to completely missing from the incisors. (Redrawn 

from Hutchinson, 1909, plate 31, figure 3, facing page 460). 

metacarpals are present. In general they exhibit 

a low-grade, diaphysial periostitis, which is somewhat expansive. All bones appear to be affected 

to approximately the same degree except the 

fourth metacarpal, which is only slightly affected 

on the right and normal on the left. 

The vertebrae and pelvis are normal, as are the 

existing fragments of ribs. There is slight periostitis on the femora, which is limited to the anterior 

distal diaphysis and metaphysis with involvement 

extending almost to the growth plate. Both tibiae 

exhibit a marked, expansive, porous periostitis 

with the major focus being the anterior proximal 

portion of the diaphysis (Figures 324, 325). However, the entire shaft is abnormally thickened. 

The fibulae are less severely affected with a similar lesion. The major focus is the mid- to distal 

portion of the shaft with the right fibula somewhat more affected than the left. 

Many of the smaller bones of the feet are 

missing. Both tali are normal, although the calcanei exhibit periostitis. The involvement is more 

severe on the right calcaneus. The metatarsals 

show a bilateral pattern of involvement, in which 

the first and fifth metatarsals are most severely 

affected. The fifth metatarsal, in particular, exhibits a much more severe condition than that 

seen on the other metatarsals (Figures 326, 327), 

and both the first and fifth metatarsals are more 

severely affected than any of the metacarpals. 

The overall pattern in this case is that the 

bones, which have minimal overlying or adjacent 

tissue, are most severely affected. These bones 

include the frontal, nasal and adjacent maxillary 

bones, the ulnae, tibiae, and first and fifth metatarsals. The position of the marked hypoplastic 

defect on the incisors could only have occurred in 

utero, since that portion of the tooth was developing at about the seventh fetal month. This 

indicates a congenital disease and, in combination with the pattern of relatively severe lesions 

in the skeleton, suggests congenital syphilis. 

Hutchinson (1909, pi. 31: fig. 3) illustrates the 

upper incisors and canines of a 3-year-old child 

with congenital syphilis. The canines were normal 

but the incisors have hypoplastic defects, which 

resulted in part, or all, of the crown breaking off 

(Figure 328). 

Adult Treponemal Disease 

The second case of probable treponemal disease 

is the skeleton of an adult female Indian from 

Arkansas, USA (NMNH 258778). This skeleton 

was excavated by Clarence Moore during field 

work conducted in 1909 and 1910. Moore (1910: 

258) believed that the burial was pre-Columbian. 

However, the date remains uncertain since documentation is poor. The bones that were recovered include a fragmentary skull, the right 

clavicle, both humeri, the left radius and proximal ulna, the distal right radius, the proximal 

right tibia, the shaft of the right fibula, and the 

right talus and calcaneus. Of these bones, the 

skull, left ulna, both femora, and the left tibia 

have obvious lesions. The right calcaneus has a 

slight periostitis of the superior and lateral cortex. 

The other bones are normal. 

The lesions of the skull (Figures 329, 330) are 

most pronounced on the vault and are much less 

developed on bone underlying the temporal muscle mass. However, both temporal bones show a 

thickened, irregular, and slightly porous surface. 

The major focus for the lesions is the external 

table, although some of the lesions penetrate to 

the inner table and others seem to originate there. 

However, inner table involvement is much less 
NUMBER 28 211 

FIGURES 329-332.—Probable acquired syphilis in an adult female Indian from Arkansas, USA: 

329, Right lateral view of skull; note that the reactive bone is minimal below the area of the 

temporalis muscle. 330, Detailed view of the irregular, lumpy outer table of the right parietal. 

This is a typical bony reaction to gummatous lesions. 331, Anterior view of the femora and 

tibiae. 332, Detailed view of medial side of right femur near midshaft; note the bony bridging 

that took place over blood vessels (white arrows) and the undercut periosteal bone (black 

arrow). Such lesions are typical of bony reactions in treponemal disease. (NMNH 258778.) 
212 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

FIGURES 333-335.—Probable acquired syphilis in a young 

adult female skull from Alaska, USA: 333, Facial view, 

exhibits an active, bony reaction typical of a gummatous 

condition. 334, Left lateral view. 335, Detailed view of the 

reactive bone on the left parietal showing mixed active and 

healing condition. (NMNH 372956.) 

extensive. Broken sections of the frontal and the 

parietals reveal a thickening of the skull with 

almost complete fill-in of the diploe by compact 

bone. The lesions of the external table are typical 

gummatous lesions characterized by a mixture of 

bone formation and destruction, creating an irregular lumpy appearance. In this case, the 

smoothed surfaces of the lesions indicate a longterm chronic condition. The left orbital roof was 

not recovered; however, the right orbital roof 

exhibits a slight labyrinthian periostitis, which 

may or may not be associated with the disease 

process affecting the rest of the skeleton. 

The proximal left ulna is the only long bone of 

the upper extremity that exhibits a morbid condition. The lesion consists of an expansion of the 

proximal metaphysial cortex with slight porosity. 

Because of the rotation of the biceps tendon and 

the biceps tubercle of the radius, the superior 

lateral portion of the metaphysis could not par-
NUMBER 28 213 

FIGURES 336-338.—Probable acquired syphilis in an adult 

female skull from Alaska, USA: 336, Left, lateral view; note 

that the more active lesions are on the posterior part of the 

skull. 337, Facial view showing mostly healed lesions on the 

frontal bone. 338, Detailed view of the lesions on the left 

frontal bone. Healing was taking place in the central portions 

of the lesions with porous reactive bone on the periphery of 

many lesions. (NMNH 280095.) 

338 'i 

ticipate in this expansion, creating a depression 

in this region of the ulna. The insertion of the 

brachialis muscle is markedly rough with spicules 

occurring on the periphery of the insertion area. 

The joint surface itself shows a slight degree of 

breakdown on the coronoid portion, which may 

reflect an expansion of the disease process into 

the joint. However, the joints of the affected bones 

of the lower extremity are normal. 

The abnormal bone of the left femur is restricted to the proximal shaft and metaphysis 

(Figure 331). The lesion does not extend to the 

trochanters or the femoral neck. The disease process has resulted in concentric thickening of the 
214 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

FIGURES 339, 340.—Probable treponemal disease in a skull 

from the Cook Islands: 339, Facial view; note the extensive 

but largely healed lesions of the frontal bone and resorption 

of the alveolar bone. 340, Right lateral view, showing active 

lesions on the parietal and occipital bones. (WM S 50 A5.) 

cortex, which is most pronounced on the posterior 

aspect. The surface is generally smooth with isolated regions of slight porosity. Muscle attachments in the affected area are noticeably rugose. 

The entire shaft of the right femur is abnormal, 

somewhat more so distally than proximally (Figures 331, 332). The gross lesion consists of thickening with isolated patches of porosity. Proximal 

muscle attachments appear normal. However, 

there has been considerable thickening of bone 

with a very irregular surface in the distal region 

of the linea aspera. The anterior surface shows 

raised plaques and bony spicules, which appear 

to be bridging over superficial blood vessels. 

There are no cloacae. The last three features are 

very typical of conditions occurring in long bones 

of known cases of syphilis, and in my experience 

are not found together in nontreponemal infectious diseases. 

A very similar pattern of abnormal bone is seen 

on the left proximal tibia. The abnormal bone is 

expanded and has isolated foci of porosity. There 

are occasional, slightly raised plaques and bony 

bridges over superficial blood vessels. The attachments of the proximal posterior muscles and ligaments, including the soleus, popliteus, and the 

tibial collateral ligament, are markedly rugose. 

The surface appearance suggests that the periosteal bone grew around the ligament attachments 

but did not affect the attachment area. 

The roentgen picture on both femora and the 

left tibia reveals the thickening of the cortex. The 

original cortex is still apparent but has been 

significantly cancellized in focal areas of disease 

in the three bones. Endosteal surfaces of the 

cortex do not encroach on the marrow cavity as 

often happens in osteomyelitis and occasionally 

in periostitis. 

An isolated Eskimo skull from Mud Bay in the 

Alaska Peninsula (NMNH 372956) demonstrates 

a more active phase of probable treponemal disease. The skull is adult and is labeled female. The 

age is unknown, but minimal wear of the teeth 

suggests young adult. The archeological age is 

uncertain. 

The lesions are distributed extensively over the 
NUMBER 28 215 

FIGURES 341-343.—Probable treponemal disease in an adult 

aboriginal Australian: 341, Facial view of the skull; note the 

healed nature of the frontal lesions and the sclerotic diploe 

in the sectioned portion of the frontal bone. 342, Lateroposterior view, showing active lesions on the occipital and 

posterior parietal bones. 343, Top view of the skull showing 

the more active nature of the lesions toward the posterior 

portion of the skull. (PMES 1GD1(116).) 

skull, sparing only part of the outer table underlying the temporalis muscle, the alveolar portion 

of the maxilla, the base of the skull, and most of 

the occipital bone (Figures 333, 334). In general, 

the lesions are almost purely lytic, coalescing foci, 

which leave more or less intact projections of 

bone between the foci. This creates the very 

irregular surface seen on the frontal bone and on 

the posterior portion of both parietals. The destructive process was sufficiently severe to expose 

the frontal sinuses. The bones of the face are 

affected as well, including the nasal spine, which 

has been destroyed. At the edges of the large 

coalescing lytic lesions one sees fine, porous, periosteal, reactive bone (Figure 335). The lesions are 

largely confined to the outer table, although slight 

porosity is apparent on the inner table, particularly in association with the most extensive lesions 

on the outer table. There is very little evidence of 

healing and this is largely restricted to a slight 

remodeling (smoothing) of remaining bone projections. The penetrating damage on both parietals and the frontal appears to be postmortem. 

The lesions in this specimen have a distribution 

and morphology compatible with treponemal disease, although the predominantly active nature 

of the lesions is less commonly seen in such skeletons. The young age of the specimen, along with 

the active nature of the lesions, suggests that the 

individual died during the active phase of the 

disease. 

The above specimen contrasts with another 

Eskimo skull (Figures 336-338), St. Lawrence 

Island, Alaska (NMNH 280095). The mandible 
216 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

FIGURES 344-346.—Probable treponemal disease in an adult 

aboriginal Australian: 344, Facial view of skull; note the 

large, confluent, lytic lesions of the frontal bone. 345, Posterior view of the skull showing an active, lytic morbid 

process. 346, Top view of the skull showing a large area of 

bone loss. This is the result of extensive necrosis followed by 

sequestration and possible exfoliation of the sequestrated 

bone. (WM HS 50a.4.) 346 

and postcranial bones were not recovered. Regrettably, the archeological age is unknown, but 

other specimens collected at the same time were 

thought to be post-Russian contact. The skull is 

female and the teeth in the maxilla, except the 

right canine, have been lost before death. The 

canine is badly worn which, with the loss of teeth, 

suggests an older age than the previous case. The 

lesions are largely confined to the skull vault, 

although there is a focus on the left parietal bone 

superior to the mastoid process, which also involves the adjacent temporal bone (Figure 336). 

While the most obvious lesions are confined to 

the outer table, the external lesions penetrate to 

the inner surface in the region of the left mastoid, 

the right parietal, and the posterior sagittal suture. There is considerable fine porosity on the 

inner surface of the vault with some lytic depressions about 0.5 centimeter in diameter, particularly on the right parietal. 

The lesions in the frontal region of the outer 

table reveal a fairly typical, coalescing, lytic-blastic response associated with the chronic, less active 

phase of treponemal disease. In the posterior portion of the skull, the lesions appear to be more 

active and are largely lytic in nature. However, 
NUMBER 28 217 

FIGURES 347, 348.—Tibial lesions attributed to yaws or treponarid (endemic syphilis) in a 

specimen from Australia prior to European contact: 347, Posterior view of tibiae. 348, Medial 

view of tibial lesions. (AIAC SF 19:27, in Hackett, 1978; photograph courtesy of Dr. C. J. 

Hackett and the South Australian Museum.) 
218 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

there is a slight development of reactive bone at 

the margins of the more active lesions. 

The general picture in this case is that of a 

more chronic course of the disease process with 

considerable healing in the frontal region but 

with active lesions elsewhere. The more active 

lesions on the younger specimen from Mud Bay, 

Alaska, may reflect a more aggressive course of 

the disease, an earlier infection by the disease, or 

death occurring during the active phase of the 

disease and before any healing could occur. The 

specimen from St. Lawrence Island may have 

acquired the disease later in life or the disease 

may have taken a less aggressive course. 

The pattern of healing lesions on the frontal 

bone with more active lesions in the posterior 

portion of the skull is also seen in three specimens 

located in the European pathology collections. 

The first of these is a specimen now located in 

the Wellcome Museum in London, but found on 

Atui in the Cook Islands (WM S 50 A5). The 

skull probably dates to before 1850. Age and sex 

are unknown, but the condition of the teeth 

suggests fully adult age and the skull morphology 

is female. There is considerable destruction of the 

nasal bones and the hard palate (Figure 339). 

The frontal bone shows extensive confluent lytic 

foci, which have been remodeled and healed. 

More active lesions are seen in the right parietal 

bone (Figure 340). 

The second specimen is the skull of an adult 

aboriginal Australian. The skull appears to be 

female and judging from toothwear was over 30 

years of age. It dates to before 1920 and probably 

is much older. Currently the specimen is in the 

Pathology Museum of The Royal College of Sugeons of Edinburgh (PMES 1GD1(116)). The 

frontal bone exhibits extensive, but mostly 

healed, lesions (Figure 341). However, the lesions 

become more active in appearance toward the 

occipital region (Figures 342, 343). The most 

active lesions are seen in the occipital bone but 

extend up into the left parietal (Figure 342). The 

skull has been sectioned and reveals a sclerotic 

diploe similar to that seen in the archeological 

specimen from Arkansas described earlier. 

The third case of probable treponemal disease 

is also the skull of an Australian aborigine (Figures 344-346) currently located in The Royal 

College of Surgeons of England Wellcome Museum (WM HS 50a.4). The date in the catalog is 

1811; thus the skull dates to before that year. In 

contrast to previously described specimens, this 

shows much more extensive destruction, particularly in the posterior portion of the parietals and 

the superior occipital bone (Figure 346). On the 

frontal bone there are large carious defects with 

porous reactive bone on the boundary with normal bone and evidence of some healing (Figure 

344). However, the occipital bone exhibits an 

active destructive process, which could be active 

syphilis or possible secondary pyogenic osteomyelitis (Figure 345). Again, the lesions exhibit a 

pattern of increasing activity toward the posterior 

portion of the skull. 

Hackett (1978) describes several cases of bone 

lesions in pre-European skeletons from Australia. 

He attributes these lesions to yaws or treponarid 

(endemic syphilis), since venereal syphilis is not 

thought to have been present until European 

contact. The long bone lesions of one of these 

cases is shown in Figures 347 and 348. The lytic 

lesions in this case are quite different from bony 

reaction seen in the femur of the specimen from 

Arkansas, USA (Figures 331, 332). 

Actinomycosis and Nocardiosis 

PATHOLOGY 

Actinomyces israelii is a higher bacterium, rather 

than a true fungus, and is a common saprophyte 

of the human oral cavity. Infections with this 

organism are uncommon and occur mainly in 

three areas of the body: cervicofacial, thoracic, 

and abdominal. The organism enters through the 

oral mucosa in the first area, by aspiration into 

the lungs in the second, and by the gastrointestinal route in the third. The cervicofacial location 

is the most common (Nathan, Radman, and Barton, 1962). Of 60 clinical cases reported by Baracz 

(1902), 55 involved head and neck, 3 thoracic. 
NUMBER 28 219 

and 2 abdominal lesions. The distribution of the 

disease is worldwide. The great majority of the 

human infections is restricted to the soft tissue 

and organs (lungs, liver, intestines). It consists of 

a protracted purulent infection with great tendency for local invasion and extension and frequent fistula formation. Bone involvement is uncommon. In a study including statistics of 486 

cases of human actinomycosis, Grassner (1929) 

reported 73 incidents of skeletal involvement (15 

percent). The bone or bones are usually affected 

by direct extension of the infection from an adjacent soft tissue focus. This means that, in most 

instances, the bone infection starts on the periosteal surface and frequently remains limited to it. 

Hematogenous dissemination, especially to the 

long bones of the extremities, rarely occurs. The 

frequency of actinomycotic lesions in the different 

FIGURE 349.—Actinomycotic periostitis of lumbosacral spine and left ilium, secondary to 

actinomycosis of sigmoid colon, left ovary, and presacral soft tissue. (21-year-old female, FPAM 

5315, autopsy 93144 from 1891.) 
220 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

FIGURE 350.—Actinomycosis of cervical spine. Notice periosteal reactive bone including transverse processes and superficial erosion of vertebral bodies from without. (53-yearold male with actinomycosis of cervical soft tissues and both 

lung apices, UGPM autopsy 203 from 1907.) 

bones in Grassner's study is as follows (quoted 

from Beitzke, 1934b:540): vertebrae 37 percent, 

mandible 25 percent, ribs 10 percent, maxilla 8 

percent, extremities 5 percent, skull base 4 percent, pelvis 4 percent, sternum 3 percent, zygoma 

3 percent, and clavicle 1 percent. 

The periosteal involvement usually leads to 

hypervascularity, which is noticeable on the dry 

bone by the increased number and size of vascular 

channels and foramina. In addition, there is usually a varying degree of reactive subperiosteal 

bone formation of porous or solid character. 

There is superficial erosion of the cortex and a 

varying degree of destruction of the adjacent 

cancellous bone, with little or no endosteal sclerotic response, in contrast to bacterial osteomyelitis. Sequester formation also is uncommon. 

FIGURE 351.—Actinomycosis of fifth lumbar vertebra and 

sacrum. Notice pitted transcortical erosions based on periosteum. (46-year-old female, FPAM 5649 from 1897.) 

The most characteristic lesion is that of the 

spine (Young, 1960). The segmental location, in 

decreasing frequency, is as follows: Thoracic, 

lumbar, cervical, and sacral (Beitzke, 1934b:554). 

Since the spine is usually infected from spreading 

pleural, abdominal, or cervical soft tissue lesions 

in broad contact with its anterior surface, the 

anterior periosteum of several or many vertebral 

bodies is involved (Figure 349). Transverse processes and, in the thoracic portion, attached ribs 

often participate in the lesions (Figure 350). The 

involvement of the vertebral bodies, if present, 

starts anteriorly and seldom extends very deeply 

(Figure 351). Vertebral collapse and gibbus formation hardly ever occur. The neural arches and 
NUMBER 28 221 

FIGURES 352, 353.—Actinomycosis of lumbar spine and left pelvis, showing mainly periosteal 

reactive bone deposition and hypervascularity with focal erosion of cortex: 352, Interior view. 

353, Exterior view. (18-year-old male, FPAM 5686, autopsy 130155-1353 from 1909.) 

spinous processes are usually spared. The intervertebral discs are usually preserved. Lumbosacral actinomycosis may spread to the pelvic bones 

(Figures 352, 353). 

The mandibular lesions are mostly limited to 

periosteal reactive bone formation of moderate 

extent with occasional destruction and focal necrosis of the underlying bone, especially of the 

alveolar process. A central involvement of the 

mandible, possibly through a dental alveolus. 

leading to cavitation and expansion of the bone, 

is very rare in the human. By contrast, this is the 

most frequent type observed in bovines and 

equines infected with Actinomyces bovis, which is 

usually not pathogenic for humans. In the rare 

actinomycosis of the maxilla, adjacent paranasal 

sinuses, facial bones (zygoma), and middle and 

inner ear may become involved. Destruction of 

mastoid process and petrous bone have been observed. 
222 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

In small and flat bones (ribs, sternum, pelvis), 

the destruction may be more extensive, creating 

a "worm-eaten" appearance and large cortical 

perforations. Actinomycosis of long bones is 

rather rare and probably mostly the result of 

hematogenous dissemination from a pulmonary 

focus. The area most frequently affected is the 

metaphysis. Extensive destruction of the cortex 

with reactive periosteal bone formation may be 

observed, but large cortical sequestra, as in coccal 

osteomyelitis, do not occur. Focal cavitation may 

closely resemble a Brodies's abscess, but perifocal 

osteosclerosis is usually slight or wanting. 

Joint involvement may occur, secondarily, to 

lesions in adjacent bones. This is most often the 

case in costovertebral and less commonly in intervertebral joints (Beitzke, 1934b:563). Pelvic 

actinomycosis can extend to the hip joint and 

proximal femur. Periosteal reactive bone is seen 

in such areas. If actinomycotic arthritis heals, 

bony ankylosis results. 

Nocardia asteroides is a bacterium of the actinomycetales group which, in contrast to actinomyces, grows aerobically and stains acid-fast. Infections occur through the pulmonary route and 

mostly are confined to the lung and pleural cavity 

(Pizzolato, 1971:1064-1066). In rare instances 

hematogenous spread to bones occurs. The lesions 

predilect cancellous areas and mainly consist of 

FIGURE 354.—X-ray of nocardia osteomyelitis of pubis with 

fistula, proven by culture. (27-year-old female with pulmonary cavity, MGH 1293348.) 

lytic cavitation, often complicated by fistula (Figure 354). There is little, if any, reactive bone 

formed. 

Mycetoma (Maduromycosis) 

PATHOLOGY 

Mycetoma or maduromycosis is a clinicopathological entity, caused by a variety of different 

higher bacteria {Actinomyces, Nocardia, Streptomyces) 

and different true fungi of various genera that 

occur in the soil (Winslow, 1971:591). The infection almost always is located in the foot (Madura 

foot), much less commonly in the upper extremity 

(Oyston, 1961)(Figures 355, 356). The disease is 

practically limited to tropical and subtropical 

areas. The geographic distribution illustrates this 

point. In Asia, the disease is common in India, 

particularly in the south, in Ceylon, and in the 

Philippines. In Africa, the affected areas are Madagascar, Zanzibar, East Africa, Senegal, Tunis, 

Algiers, Morocco, and southwestern Africa. In the 

Americas, the disease is not uncommon in Cuba, 

Nicaragua, Costa Rica, Guyana, Brazil, Argentina, and Chile. In the United States, 30 cases 

had been observed before 1921, mostly in the 

southwestern states. In Oceania, cases were reported from Yap (Carolines). In Europe, mycetoma was observed in Sardinia, southern Italy, 

and Greece (Plehn, 1928). The infection occurs 

through skin lacerations in barefoot-going populations, producing long-lasting, progressive, soft 

tissue lesions with formation of multiple fistulae. 

The bones become secondarily infected through 

the periosteum. The tarsal and metatarsal bones 

usually show multiple lytic foci and progressive 

osteoporosis (Figure 357). The tarsal and ankle 

joints frequently participate in the process. The 

distal tibia and fibula as well as the metatarsals 

are involved in advanced cases, showing multiple 

cortical perforations and destructions with very 

little reactive bone formation. If the process heals, 

bony ankylosis of the affected joints is to be 

expected (Figure 358). 
FIGURES 355, 356.—Actinomycosis (maduromycosis) of left hand: 355, Volar view; notice 

extensive periosteal involvement of carpals, metacarpals and phalanges. 356, X-ray; notice 

subcortical involvement and cloacal openings on some bones. (Adult Iranian male, AFIP 

859604.) 

FIGURE 357.—Maduromycosis of right foot, plantar view, 

showing extensive lytic destruction of most bones. (Adult 

Asian Indian from India, WM S 52.1 from 1875.) 

FIGURE 358.—Infection of right ankle and foot, with ankylosis of ankle, tarsal and tarsometatarsal joints. Notice the 

extensive destruction of the tarsal bones and the large cloacas, suggestive of actinomycosis or fungal infection, but 

ordinary osteomyelitis cannot be ruled out. (HM P948.) 
224 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

Fungal Infections 

PATHOLOGY 

Of the numerous fungal infections of man, only 

those capable of involving bones concern us here. 

There is a variety of yeast-like, budding fungi 

with different geographic distributions causing 

human infections. This group of fungi all enter 

through the respiratory tract with the principal 

internal lesion usually in the lung. Occasionally, 

in systemic cases, hematogenous dissemination to 

the skeleton occurs. The bone lesions produced 

are similar to and not distinguishable from each 

other on X-ray or dry bone specimens. Therefore, 

the geographic location becomes a key factor in 

attempted identification. 

North American Blastomycosis 

North American blastomycosis is caused by 

Blastomyces dermatitidis, which usually enters the 

body through the respiratory tract. It can manifest itself as a skin infection, but frequently presents as a systemic disease (Witorsch and Utz, 

1968:169-171). Its main distribution is in North 

America, especially in the Mississippi and Ohio 

valleys and North Carolina, but presently it has 

worldwide distribution to some extent. In Canada, Ontario and Quebec have a significant number of cases. The male:female ratio in disseminated cases is at least 5:1. There is no distinct 

racial predilection. The highest incidence is between 30 and 50 years of age (Chick, 1971:466-

468). Two-thirds of the disseminated cases show 

bone involvement. The predilected areas are vertebrae and ribs (often multiple), skull, tibia, and 

tarsus. The lesions are usually purely lytic with 

sharp borders (Boswell, 1959). In contrast to tuberculosis, vertebral collapse is rare. Paravertebral abscesses occur. In long bones the focus can 

mimic an infarct. The foci in long bones predilect 

subarticular epiphysial and metaphysial areas. 

Periosteal reactive bone can be found (data from 

Chick, 1971:485-486). 

Cryptococcosis 

Cryptococcosis is the result of infection by Cryptococcus neoformans, mainly in the form of a systemic 

disease. The main distribution of cases is through 

Europe, with occasional cases occurring in all 

continents. The disease often develops in debilitated patients, especially in leukemia and lymphoma. There is no age, sex, or race predilection 

(Salfelder, 1971:385-390). About 10 percent of 

the disseminated infections show bone involvement. The predilected areas are bony prominences, cranial bones, and vertebrae, but any 

bone may be affected occasionally (data from 

Salfelder, 1971:420-421). The lesions usually appear lytic and well circumscribed on X-ray (Collins, 1950). 

Paracoccidio idomycosis 

Paracoccidioidomycosis is due to infection with 

Paracoccidioides brasiliensis. This American fungus 

disease mainly occurs in Brazil, Venezuela, and 

Colombia but is found from Mexico to Argentina 

with the exception of Chile, San Salvador, and 

Panama. The disease mainly affects middle-aged 

persons with a male:female ratio of at least 12: 1. 

About half of the patients are farmers. Whites are 

most often involved and Negroes least (Angulo 

and Pollak, 1971:511-513). Bone involvement is 

not rare in disseminated cases. The lesions are 

round and lytic, single or multiple, or may mimic 

ordinary osteomyelitis (Emmons, Binford, and 

Utz, 1970:336). The predilected locations are 

clavicles, ribs, vertebrae, and extremities (Angulo 

and Pollak, 1971:555-556). 

Coccidioidomycosis 

Coccidioidomycosis is the result of inhalation 

of spores of Coccidioides immitis. This disease is 

heavily concentrated in parts of Southern California (San Joaquin Valley) but occurs in the dry 

areas of adjacent southwestern states and Mexico 

with additional foci in Central America, Venezuela, Bolivia, and Argentina (Huntington, 1971: 
NUMBER 28 225 

FIGURE 359.—X-ray of coccidioidomycosis of right carpal 

bones. Notice round lytic focus in os triquetrum and os 

pisiforme (arrows). (38-year-old male from California with 

pulmonary lesion, MGH admission no. 1187633.) 

172-174). About 25 percent of the fatal disseminated cases show bone lesions (Huntington, 1971: 

184). The mortality is considerably higher in 

Negroes and Filipinos than in Whites and Mexican Indians in California (Huntington, 1959). 

(For clinical and radiological reviews, see Miller 

and Birsner, 1949; Dykes, Segesman, and Birsner, 

1953; and Birsner and Smart, 1956.) 

The bone lesions of all these fungus infections 

are very similar. Cancellous bone areas are predilected and multiple lesions are not uncommon. 

In the spine, the lesion may be indistinguishable 

from tuberculosis, although in these conditions 

the posterior elements are not spared and vertebral collapse with gibbus formation usually does 

not occur. In general, the bone lesions tend to be 

lytic on X-ray and show central cavitation, usually combined with osteoporosis, in the gross. 

Perifocal reactive sclerosis can be found, making 

the differentiation from Brodie's abscess difficult 

or impossible. Fistula formation is common. The 

most characteristic aspect of these systemic fungus 

lesions is that they predilect areas of the skeleton 

usually spared by other infections. Such areas are 

bony prominences such as the acromion, coracoid 

process, styloid processes of radius and ulna, condyles of the humerus, ends of clavicles, malleoli 

and tibial tuberosity. There is also involvement 

of small bones: carpals (Figure 359), tarsal bones, 

and patella. Marginal destructive lesions of ribs 

and destructive lesions of the skull, limited to the 

outer table, do occur (Carter, 1934). In carpal 

and tarsal lesions, adjacent joints are often implicated. 

Histoplasmosis 

Histoplasmosis is a common infection of the 

respiratory tract, caused by Histoplasma capsulatum. 

Infections are usually slight and self-healing and 

are most common in the Mississippi and Ohio 

valleys. A few cases occur, sporadically, worldwide. Bone lesions are uncommon even in the 

systemic cases but, if present, resemble those in 

other systemic fungal diseases (Schwarz, 1971:95-

97). There is, however, a different species {Histoplasma duboisii), which causes severe systemic infections in young Negroes in tropical West Africa 

(Nigeria). In this disease, multiple round lytic 

lesions usually are present in the cranial vault 

(Figure 360) and in long and small bones of the 

extremities (Figure 361)(Cockshott and Lucas, 

1964). Such lesions in long bones may lead to 

expansion of the shaft (Edington, 1971:131-138). 

Sporotrichosis 

Sporotrichosis mainly manifests itself as a skin 

and soft tissue infection, caused by Sporotrichum 

schenkii entering the body through skin lacerations. The disease has a worldwide distribution 

between latitudes of 50° north and south. There 

is a male:female ratio of 3:1. The majority of 

cases are children and young adults (Lurie, 1971: 
226 SMITHSONIA

N CONTRIBUTIONS TO ANTHROPOLOGY 

616-621). In about 10 percent of the cases, 

mostly hematogenous osseous lesions occur 

(DeBeurmann and Gougerot, 1912:329). The 

majority of cases described are in the French 

literature. Bone lesions represent the most fre-

quent extracutaneous foci in sporotrichosis. The 

bones affected, in decreasing order of frequency, 

are tibia, hands and feet, ulna and radius, skull 

and facial bones, ribs, clavicles and vertebrae. 

The process may extend into joints, terminating 

in severe destruction (Altner and Turner, 1970). 

The joints involved, in decreasing frequency are 

knee, elbow, wrist, and sternoclavicular joints 

(data from Lurie, 1971:629-630). Bone lesions 

may be mild, healing without residual alterations. 

Localized bone abscesses and ossifying focal or 

extensive periostitis have been observed. Sponta-

neous fractures can occur (Zeiliger, 1911:13-28). 

The lesions are probably too rare and too un-

characteristic to be identified without recovery of 

the causative organism. The bone lesions most 

frequently affect the tibia and the skull. Hands 

and feet, especially metacarpals and metatarsals, 

are more often involved than long bones of the 

extremities. The spine and bones of the thorax 

seem to be spared. The prevailing lesion is peri-

osteal rather than a deep lytic bone abscess or 

osteomyelitis ( The above data are from Beitzke, 

1934e:616-619). 

Aspergillosis 

Several species of Aspergillus, especially Aspergillus fumigatus, may act as opportunistic invaders in debilitated individuals. Aspergillosis occurs 

worldwide, without predilection of sex or race 

(Pena, 1971:766-767). Destruction and necrosis 

of bone between affected paranasal sinuses and 

FIGURES 360, 361.—Bone lesions in Histoplasma duboisii infec-

tion: 360, X-ray of lateral view of skull; notice multiple 

round lytic lesions of cranial vault. 361, X-ray of right hand; 

notice multiple lytic lesions in bones of forearm and hand, 

partly with sclerotic border. (Adolescent negro, courtesy Dr. 

Stanley Bohrer, Ibadan, Nigeria.) 
NUMBER 28 227 

orbit or anterior cranial fossa can be observed. 

Hematogenous dissemination is rare but may 

involve ribs or vertebrae. In vertebral aspergillosis, collapse and gibbus occurs, which may 

mimic tuberculous lesions (Pena, 1971:807-812). 

Mucormycosis (Phycomycosis) 

Several genera of Mucoraceae {Rhizopus, Mucor, 

and Absidia) can occasionally become invasive 

opportunistic pathogens. Most of the patients 

affected are diabetics in the acidotic state 

(Straatsma, Zimmerman, and Gass, 1962). Extension into bone is seen in the cranial form of 

mucormycosis, starting from the nasal cavity with 

involvement of the paranasal sinuses and their 

walls. The main reason for discussing this lesion 

here is that perforation of the hard palate, with 

or without sequestrum, occurs, which may be 

confused with a tertiary syphilitic lesion. Since 

only one maxillary sinus is usually affected by 

mucormycosis, the perforation of the hard palate 

is more often unilateral (Baker, 1971:835-860). 

PALEOPATHOLOGY 

Fungal infections and their effect on human 

bone have received little attention in the literature on paleopathology. Poswall (1976) has called 

attention to the presence of both coccidioidomycosis and blastomycosis in North America. She 

suggests that skeletal lesions from these fungal 

diseases may be distinguishable from other infectious diseases of bone and may be a more probable diagnosis for bone lesions seen in skeletal 

remains of some American Indian groups. Morse 

(1969:45) had included both blastomycosis and 

coccidioidomycosis as diseases that must be considered in the diagnosis of destructive lesions of 

the spine. Similarly, Buikstra (1976) has called 

attention to the need to differentiate fungal infections from other infectious conditions that affect 

bone. She indicates the importance of epidemiological factors, as well as the morphology and 

location of the lesions in the skeleton, as helpful 

diagnostic features. 

There are, however, no published cases of bone 

lesions in paleopathological specimens attributed 

to fungal infections. Clearly in geographical regions where such diseases are known to have been 

endemic in the historic period, it is probable that 

they existed in ancient times as well. Lesions in 

skeletal material recovered from such areas, such 

as the American Southwest, should be studied 

with an awareness that fungal diseases represent 

a significant cause of conditions that can produce 

skeletal lesions. 

Viral Infections 

PATHOLOGY 

Of the viral infections involving the skeleton, 

only smallpox and rubella need to be discussed. 

In chickenpox, bone and joint participation is 

extremely rare, and vaccinia osteomyelitis, representing a rare complication of prophylactic vaccination, does not fall within the scope of this 

book. 

Smallpox 

Smallpox was a worldwide common viral infection, especially in infants and children, before 

the use of vaccination. Until recently, large areas 

of Africa had a high incidence of smallpox. As 

late as 1958, Cockshott and MacGregor reported 

a series of 2500 cases observed in 18 months in 

Nigeria, and Davidson and Palmer (1963) report 

400 cases from southern Rhodesia. During my 

w^ork in India and Indonesia in the 1960's I had 

ample opportunity to study the radiological 

changes of smallpox osteomyelitis and arthritis. 

The skeletal involvement varies in different series 

from 2 to 5 percent (Cockshott and MacGregor, 

1958:377, 1959:57; Middlemiss, 1962:11-13) to 

about 20 percent (Davidson and Palmer, 1963: 

687). The skeletal infection starts between one 

and four weeks after onset of the disease; 80 

percent of the patients in the series of Davidson 

and Palmer (1963) were less than 5 years of age. 

Skeletal involvement is not seen in the adult. 

Variola osteomyelitis, in contrast to most other 
228 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

FIGURE 362.—X-ray of smallpox osteomyelitis of both arms 

and hands; notice the involvement of humerus, radius, and 

ulna and of most metacarpals and phalanges. (2-year-old 

female Indonesian; courtesy Dr. L. A. Tamaela, Djakarta, 

Indonesia.) 

skeletal infections, predilects the upper extremities, especially the elbow areas. The lesion usually 

starts in the metaphysial area near the growth 

plates and often spreads to the adjacent joint. 

There is destruction of metaphysial bone, leading 

to separation of the epiphysis and, in severe cases, 

to pathological fracture. There is no massive sequestration, in contrast to bacterial osteomyelitis, 

but pronounced formation of reactive periosteal 

bone attached to the cortical surface is usually 

present. In about 80 percent of the 81 patients of 

Davidson and Palmer (1963), the elbow was affected and very frequently bilaterally, which is 

uncommon in any other infection. Often all three 

bones (humerus, ulna, and radius) participated, 

while in most other infections, including tuberFIGURE 363.—X-ray of growth deformity of forearms 7 years 

after onset of smallpox osteomyelitis. (13-year-old male Asian 

Indian; courtesy X-ray Department, All India Institute of 

Medical Sciences, New Delhi, India.) 

culosis, the radius is usually spared. Second to the 

elbows, the wrists, knees, and ankles are most 

often affected, but any joint may be involved. In 

a review of 124 published cases of variola arthritis, 

Cockshott and McGregor (1958:376) report the 

following locations: elbows 97, wrist and hands 

25, knees 17, ankle and foot 16. In more than half 

of the cases more than one area was affected. In 

carpal and tarsal bones, which are often involved, 

uneven, patchy, lytic destruction is seen on X-ray 

(Figure 362). Lesions in the calcaneus are common (Davidson and Palmer, 1963:692). In fingers 

and toes dactylitis occurs. Ribs, spine, pelvis, and 

cranium are usually spared in smallpox. During 

the active disease, the bones may be sufficiently 

weakened to permit bending deformities to arise 

in weight-bearing areas. Permanent changes are 

mainly deformities due to arrested growth, sec-
NUMBER 28 229 

ondary to destruction or slipping of the growth 

plate (Figure 363). Dactylitis may lead to short 

stubby digits for the same reason. Joint involvement may terminate in bony ankylosis. 

Rubella 

Rubella is a relatively harmless viral infection 

of children and adults which, however, often has 

serious effects on the fetus, if acquired by the 

mother during the first trimester of pregnancy. In 

addition to the triad of congenital cataract, heart 

defects, and mental retardation, frequent skeletal 

changes have been appreciated only recently. In 

a series of 81 infants with a history of maternal 

rubella during pregnancy, 34 showed skeletal involvement (Singleton, Rudolph, Rosenberg, and 

Singer, 1966). The most characteristic lesions are 

seen on X-ray in the metaphysial areas of the 

long bones of upper and lower extremities of the 

newborn. The changes affect all metaphysial 

areas but are most obvious on the distal femoral 

and proximal tibial metaphysis, reflecting the 

greatest growth rate in these areas. These changes 

consist of poor mineralization adjacent to the 

growth plate and coarsening of the reduced trabecular pattern. The diaphyses are not involved. 

The lesion is similar to that of congenital syphilis, 

but in contrast to syphilis, ossifying periostitis is 

not observed in rubella (Highman, 1967). There 

is general retardation of growth, and the skull 

may show enlargement of the anterior fontanel 

and poor mineralization. If the infant survives, 

the bone changes disappear at about 3 months of 

age without leaving residual irregularities of architecture; but the mortality rate in this group 

with skeletal involvement was 32 percent (Singleton, Rudolph, Rosenberg, and Singer, 1966). 

Parasitic Infections (Echinococcosis) 

PATHOLOGY 

The only parasitic infestation of the human 

causing significant bone changes is the Echinococcus. Echinococcus granulosus is a tapeworm, which 

inhabits the small intestine of canines. The larval 

stage causes echinococcosis in humans and domestic animals (sheep, cattle, and pigs), which 

serve as intermediate hosts. This circumstance 

gives this disease a special paleopathological interest, since human involvement would depend 

on the domestication of the dog and the herding 

of domestic animals. The present and recently 

past geographic distribution of the disease is 

closely tied to the use of dogs in cattle and sheep 

herding by people living under primitive hygienic 

conditions. The disease occurs in two different 

manifestations, probably caused by two different 

but closely related parasites. The common manifestation is the hydatid cyst, which has worldwide distribution. The European areas presently 

or previously involved are Iceland (with the greatest frequency in the past), Mecklenburg, Pomerania, Friesland, Spain, Sardinia, Sicily, Yugoslavia, Hungary, Bulgaria, Rumania, Greece, 

Russia, parts of France and Switzerland, and 

England. Outside of Europe, the areas of highest 

incidence are Australia and Argentina, followed 

by New Zealand, South Africa, Uruguay and 

Chile. In my own experience, even presently, 

cystic echinococcosis is a common disease in Iran. 

The alveolar type of echinococcosis is much rarer 

and occurs in a more limited area: in Europe, 

particularly in the Alps and their forelands (Bavaria, Austria, eastern France, Switzerland, 

northern Italy) and, to some extent, the Balkans 

and southern Russia. I have seen one case in 

northern Iran. In the areas where the alveolar 

form occurs, the hydatid form is rare (Posselt, 

1900:238, 314). 

In the heavily infested areas, echinococcosis is 

a major health problem and a significant cause 

of death. As recently as 1935, Racic reported that 

in Split (Yugoslavia) 70 to 100 percent of the 

animals coming to the slaughterhouse were infected with hydatid cysts and that he, alone, in 

20 years operated on 269 cases of human echinococcosis, including five involving the skeleton. 

Ivanissevich (1934) surveyed the problem in Argentina and found that 1 percent of all hospital 

patients and 3 percent of all operated patients in 

a large hospital in Buenos Aires suffered from 

hydatid cysts. Similar figures are reported from 
230 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

Australia. In Concepcion (Chile), hydatid cysts 

were found in about 1 percent of all autopsies 

and over 0.5 percent of all surgicals (Behn, 1938). 

Slightly lower autopsy figures were reported from 

Virchow's Institute in Berlin (Boecker, 1868). In 

this series of 33 cases, none were found in individuals below 15 or above 70 years of age. 

The infection occurs either by direct contact 

with dogs or by contamination of pasture, crops 

and drinking water with dog feces containing the 

ova of the parasite. Domestic animals form the 

reservoir, reinfecting dogs through their eating of 

or contact with the offal of slaughter. The embryonated ova, ingested, lose their shells by digestive 

action of the stomach and penetrate with their 

six hooks the intestinal blood capillaries of the 

portal system. Through the portal blood they 

most commonly infect the liver but may, with 

varying frequency, settle in any part of the body. 

In the organ or tissue involved, the larva forms a 

cyst, which consists of laminated chitin and is 

usually surrounded, by the host, by a fibrous 

capsule. The inner layer of a fertile cyst forms 

many little tapeworm heads (scolices), each with 

a crown of hooks. If such a cyst ruptures, each 

scolex can form a new cyst. Hydatid cysts are 

usually well tolerated by the affected tissue. In 

contrast, the rare alveolar Echinococcus continues 

to invade and destroy the infected tissue in the 

form of a microcystic invasion, producing extensive necrosis of the tissue and giving the gross 

appearance of a malignant neoplasm. It was Virchow (1856) who first recognized the parasitic 

origin of this lesion. 

The behavior of the hydatid type of echinococcosis in the skeleton is different from that in 

organs and soft tissues. Usually, no major cysts 

are formed, but small cysts rupture and disseminate between the bone trabeculae, causing osteoclastic resorption. There is often foreign body 

giant cell reaction around ruptured cysts but no 

inflammatory reaction or fibrous encapsulation 

(Ivanissevich, 1934). Extensive permeation of the 

marrow spaces may cause local ischemic necrosis 

of the bone with formation of sequestra. By contrast, in the few instances of alveolar echinococcosis involving bone, the microcysts may not be 

recognizable grossly but, as in other tissue, the 

parasite shows a more aggressive growth and 

produces extensive necrosis and inflammatory response (Klages, 1930:141). The main difference 

between the two types is that the hydatid form 

resumes its macrocystic patterns when it escapes 

from the confines of the bone into the soft tissue, 

while the alveolar form always maintains its microcystic destructive growth. There are very few 

cases of alveolar echinococcosis of bone on record 

and this type of bone lesion has never been found 

in Africa, Australia, or America. 

The frequency of skeletal involvement in echinococcosis of the hydatid type is about 2 percent 

in the statistics of Ivanissevich (1934:17) from 

FIGURE 364.—Echinococcus granulosus cyst of left scapula 

showing ballooning of the inferior angle and the lateral 

margin with sparse reticulated new cortex. (Adult, specimen 

provided by Lord Joseph Lister's collection, before 1912, 

WM S 54.1.) 
NUMBER 28 231 

Argentina and other series give similar data. According to collective worldwide statistics of 406 

cases of skeletal echinococcosis published by Pasquali (1930:369), the distribution through the 

skeleton is as follows: vertebrae 41.6 percent, hip 

bone 22.1 percent, humerus 9.4 percent, tibia and 

fibula 8.9 percent, femur 8.1 percent, skull 5.2 

percent, sternum and ribs 2.2 percent, scapula 1.5 

percent, phalanges 0.7 percent. All bones are 

occasionally involved, with the exception of the 

carpal and tarsal bones and the ulna (Ivanissevich, 1934:21). The vertebral lesions form close to 

one-half of all cases, followed in frequency by the 

pelvic bones. The segments of the spine most 

often affected are the middorsal and sacral region 

(Ivanissevich, 1934:21). 

The parasites most often settle in areas of cancellous bone with hemopoietic marrow. This 

means predilection, in the long bones, of the 

metaphysis and, in the spine, of the vertebral 

bodies. The infection progresses very slowly over 

decades and may remain asymptomatic for a long 

time. The changes in different bones are different. 

In the spine, progressive destruction of one or 

several vertebral bodies may lead to angular kyphosis, similar to a tuberculous gibbus. Transverse processes and posterior elements are more 

often involved in echinococcosis than in tuberculosis. In flat bones, the outer contour is often 

expanded by slow destruction of the old cortex 

and formation of a new bony shell (Figure 364). 

The progressive destruction, especially of pelvic 

bones (Doebbelin, 1898), may be extreme, leading 

to multiple large cystic cavities separated by residual bony septa (Figures 365, 366). The large 

cavities do not contain large parasitic cysts but 

FIGURES 365, 366.—Echinococcus granulosus cysts of left pelvis with secondary infection and 

destruction of acetabulum, 18 years duration: 365, Lateral view. 366, Medial view. (Adult male, 

GHP M 4196.) 
232 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

numerous small cysts and tube-like membranes. 

Destruction of the floor of the acetabulum with 

central dislocation of the head of the femur has 

been observed (Racic, 1935). On X-ray, the 

polycystic transformation and great reduction of 

bony density is apparent. In the differential diagnosis on dry bone, fibrous dysplasia has to be 

excluded. In this latter condition, the destruction 

of the bony structure between the fibrous foci is 

much less pronounced. The cystic form of hyperparathyroidism can give a similar picture but 

would not be limited to one area. The rest of the 

skeleton would show other evidence of hyperparathyroidism. 

In long bones, the parasitic small cysts starting 

in the cancellous bone of the metaphysis may 

ultimately occupy the entire marrow cavity. Articular or epiphysial cartilage forms a barrier, 

which is not penetrated by the parasite. This 

explains the absence of joint involvement. The 

outer contour of the involved bone may not be 

altered, but scalloping of the endosteal cortical 

surface may be apparent on X-ray. Pathological 

fractures occur frequently in the late stage of the 

disease. Gangolphe (1894:675) observed in 25 

cases of long bone involvement 14 pathological 

fractures (humerus 5, femur 5, tibia 4). Ultimately, even long bones may be extensively destroyed if the cortex is transgressed and the parasites extend into the soft tissue. Reactive osteosclerosis and periosteal new bone formation is 

uncommon except in cases complicated by superimposed bacterial osteomyelitis. 

PALEOPATHOLOGY 

Paleopathological evidence of echinococcosis 

may occur in the skeleton, but it may also be 

inferred from the presence of mineralized outer 

shells of hydatid cysts occurring in the thoracic 

or abdominal cavity. Wells and Dallas (1976) 

found a probable example of such a cyst in the 

thoracic cavity of a woman about 45 years of age. 

The skeleton of this woman was excavated from 

a site at Orton Longueville, Cambridgeshire, 

England. The site was dated to the late first or 

early second century A.D. and is part of a Belgic 

and early Romano-British farmstead. In the left 

side of the thoracic cavity, the excavators found 

a mineralized shell approximately ellipsoid in 

shape measuring 47 X 35 millimeters. The object 

was not attached to bone. Wells and Dallas conclude that the specimen is the mineralized shell 

of a hydatid cyst produced in response to infestation by the tapeworm Echinococcus granulosus. 

Similar cyst-like structures are associated with 

an adult female skeleton from Jones Point, Kodiak Island, Alaska, USA (NMNH 374623). The 

skeleton is associated with what Hrdlicka called 

FIGURES 367, 368.—Three cyst-like structures associated with 

an adult female skeleton from Kodiak Island, Alaska, USA. 

These structures may be the mineralized outer shells of a 

hydatid cyst resulting from infestation by Echinococcus: 367, 

External view. 368, Internal view. (NMNH 374623.) 
NUMBER 28 233 

the intermediate, pre-Koniag period, which 

would have been before Russian contact. The 

skeleton is incomplete and fragmentary, but the 

skull and postcranial bones exhibit no external 

evidence of disease. X-ray films of the major long 

bones, vertebrae, and innominates do not reveal 

any cystic changes with the exception of a partial 

cyst-like structure in the cancellous bone of the 

right iliac crest. The postmortem damage of this 

bone makes firm identification impossible. There 

are, however, three fragmentary, ovoid structures 

associated with the skeleton but not attached to 

any bones (Figures 367, 368). These fragmentary 

structures appear to represent three different mineralized cysts. The external surfaces of the cysts 

are irregular with calcified spurs and holes in the 

surface, indicating that the external shell of the 

cyst was not completely mineralized. Internally 

there is no evidence of bony divisions in the cyst. 

Wells and Dallas (1976) note that hydatid cysts 

of Echinococcus typically are unilocular and may 

range in size from a pigeon's egg to as large as a 

human skull. The mineralized cysts from this 

specimen are very similar to the cyst illustrated 

by Wells and Dallas (1976, pi. 6). I would agree 

that the most likely diagnosis is that they represent the mineralized partial outer shell of a hydatid cyst resulting from Echinococcus infestation. 

Sarcoidosis 

PATHOLOGY 

Sarcoidosis is a granulomatous disease of unknown etiology affecting mainly lymph nodes, 

lungs, and skin. The disease is more often observed in adolescents and young adults than in 

children and is even rarer in infants. There is a 

marked racial predilection for Negroes. About 14 

percent of the cases show bone involvement 

(Mayock, Bertrand, Morrison, and Scott, 1963: 

76). The bone lesions are usually multiple and 

often bilateral. 

The bone lesions are most commonly located 

in the fingers and toes, less often in metacarpals 

and metatarsals. The second and third phalanges 

are most frequently involved. Within the phalanges, the lesions predilect the distal epiphysis but 

do not break through into the interphalangeal 

joints. The granulomas cause purely lytic, round, 

or slightly lobulated defects in the spongiosa, 

varying from one millimeter to one centimeter or 

more. If the granuloma is located in the diaphysis, 

the cortex is markedly thinned and the shaft may 

be slightly widened, with loss of the dumbbell 

shape of the bone. There is usually no significant 

perifocal sclerosis. There is no sequestra formation. Perforations of the thin diaphysial cortex by 

the granulomas are not uncommon and create 

round defects. There is usually only minimal or 

no reactive periosteal bone formation. Occasionally phalanges, especially terminal, may be completely destroyed. Destruction of nasal bones occurs secondary to granulomas of the skin of the 

bridge of the nose (Holt and Owens, 1949). 

Lesions of similar lytic character have occasionally been described in other bones, such as skull, 

pelvis, long tubular bones, especially in the metaepiphysial spongiosa, and vertebrae. The vertebral lesions are located in the vertebral bodies 

and usually spare the intervertebral discs and the 

pedicles. Vertebral collapse may occur. Lesions 

usually involve multiple, sometimes widely separated, vertebrae and may show sclerotic rimming. 

In differential diagnosis, the hand and foot 

lesions have to be differentiated from leprosy, 

spina ventosa, and from osteochondromatosis 

(Ollier's disease). In tuberculous and syphilitic 

spina ventosa the widening of the affected bone 

is more pronounced; there is marked periosteal 

new bone formation and a central sequestrum is 

often present. In Ollier's disease the enlargement 

and distension of the involved phalanges is much 

more marked. There is also usually similar involvement of large tubular bones of the same 

extremity while bilaterality is uncommon. The 

greatest similarity exists between the bone lesions 

of sarcoidosis and those of lepromatous leprosy 

(Paterson and Job, 1964:432). Both show the 

same predilection of the phalanges of fingers and 

toes, the lytic character of the lesions, and absence 

of reactive bone formation. A differentiation of 

individual lesions may be impossible on dry bone 

alone. The cranial lesion may be more character-
234 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

istic, since sarcoidosis mainly affects the nasal 

bones but not particularly the inferior nasal spine 

and maxilla. The mutilating lesions have to be 

differentiated from leprosy, which would not usually show simultaneously lytic lesions in other 

phalanges. The vertebral lesions have to be differentiated from those of tuberculosis and of osteomyelitis. Osteomyelitis usually does not spare 

the intervertebral space, and, therefore, often involves two adjacent vertebrae, while discontinuous involvement of vertebral bodies is less common. The sarcoid lesions also have to be distinguished from metastatic lytic neoplastic lesions 

which, by contrast, usually involve the pedicles 

and spinous processes multifocally. 
Circulatory Disturbances 

Blood Supply of Bones 

For the present purpose we are mainly interested in the arterial supply of the long bones of 

the extremities. There is a separate arterial supply 

for the diaphyses, for the metaphyses, and for the 

epiphyses. The one or several larger nutrient arteries enter the bone through a grossly visible 

nutrient canal on the posterior aspect and branch 

into an ascending and descending ramus in the 

medullary cavity. The metaphyses have several 

smaller nutrient vessels entering through the cortex around the circumference. The epiphyses receive several smaller arteries, which branch from 

a vessel that also supplies the joint capsule and 

synovium. During the growing period, the growth 

plate completely separates the vascular territories 

of the metaphysis and the epiphysis. After closure 

of the growth plate, some connections between 

the two systems are reestablished, but the circulation, to a large extent, remains separate. The 

intraosseous arteries, being enclosed in a rigid 

compartment shielded from external pressure, are 

usually thin-walled. This is particularly true of 

the arterioles. The diaphysial cortex is, in part, 

supplied by ramifications of the nutrient vessels, 

in part by the periosteal vessels. The relative 

contribution of these two systems varies in different portions of the same bone. The epiphysial 

vessels, which form a system of arcades beneath 

the articular cartilage, contribute to the nutrition 

of the cartilage during the growing period, before 

formation of a more or less solid subchondral 

bony plate. The cortical bone has vascular supply 

through the Haversian and the Volkmann canals, 

which connect Haversian canals and also enter 

directly from the periosteum. Cancellous bone 

trabeculae are usually avascular, depending on 

the vasculature of the marrow spaces for nutrition. The sinusoidal veins of the marrow are 

.numerous, thin-walled, and, in hemopoietic marrow, wide. They collect into a large, thin-walled 

vein, running lengthwise in the medullary canal. 

The venous return in part follows the nutrient 

artery, in part exits through multiple, circumferentially located, venous outlets in the metaphysial 

area. The epiphysial venous return drains into 

that of the adjacent joint capsule. On smaller and 

cancellous bones the blood supply is less complicated, except for those with growth plates, which 

always lead to separate epiphysial and apophysial 

vascular territories, at least during the growing 

period. The vertebral bodies show a radiant arrangement of larger veins, which converge medially and emit on the posterior surface of the 

vertebral body through two foramina, close to the 

midline. These segmental veins join the longitudinal vertebral plexus in the spinal canal, which 

is of some significance in the dissemination of 

infection or malignancy. The diploe of the cranial 

vault likewise shows large interconnecting venous 

channels, which drain through the parietal and 

mastoid emissary foramina but also have some 

connection with the large intracranial venous 

sinuses through small openings in the inner table. 

Ischemia and Infarction 

PATHOLOGY 

Continued cortical remodeling during adult 

life leads to formation of more osteon fragments 

and interstitial lamellae, which are devoid of vascular channels. With increasing age more and 

more of these fragments become necrotic (Miiller, 

1926). In arteriosclerotic peripheral vascular disease, extensive portions, especially of the cortex, 

can become necrotic (Jaffe and Pomeranz, 1934; 

Sherman and Selakovich, 1957). Although microscopic study of the intact fresh specimen will 

reveal these changes, they are demonstrable on 

X-ray and on dry bone only if reaction in the 

235 
236 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

adjacent living bone, in the form of bone resorption or bone formation, has occurred. In many 

instances, such reactions to cortical necrosis do 

not occur and therefore will not be recognizable 

in an archeological specimen. 

In infarction, larger areas of the fatty bone 

marrow and the intervening bone trabeculae undergo necrosis, presumably due to interruption of 

the circulation. The lesion is almost exclusively 

observed in the long bones of the extremities, 

mostly in adults. The areas involved are principally the diaphysial and metaphysial marrow of 

the femur, tibia, or humerus. The epiphyses, particularly the head of the femur or, less commonly, 

of the humerus are also the sites of avascular 

necrosis. 

An infarction in the shaft of a long bone undergoes calcification, particularly at the interface 

between living and dead marrow, due to conversion of the liberated fat into calcium soaps. In 

fact, it is this change that makes the lesion visible 

on X-ray as a circumscribed lesion, often of up to 

10 centimeters in length, showing a radiodense 

shell around the whole lesion and between its 

individual components. There is little or no 

change in the overlying cortex. It is questionable 

whether calcium deposits could be preserved in 

archeological material. Also, the sifting in of mineral particles into the marrow cavities of interred 

bones may mimic infarction on X-ray. 

In the majority of present cases a definite cause 

for the infarction cannot be stated. Some known 

causes of circulatory impairment are blood sludging in hemoglobinopathies, nitrogen gas embolization in decompression disease, and arteritis in 

systemic lupus erythematosus. Circulating lipase, 

a fat splitting enzyme, in extensive pancreatic fat 

necrosis may also cause necrosis of medullary fat 

tissue (Scarpelli, 1956). 

Necrosis of Femoral Head 

PATHOLOGY 

Subcapital or transcervical fracture of the neck 

of the femur frequently is complicated by aseptic 

necrosis of part or all of the femoral head (Figures 

369, 370). This is due to the peculiarity of the 

blood supply to the femoral head, which consists 

of three groups of vessels: (1) the artery of the 

ligamentum teres, supplying a portion of the 

upper part around the fovea; (2) the inferior 

metaphysial vessels coursing beneath the synovium on the inferior aspect of the femoral neck 

FIGURES 369, 370.—Aseptic necrosis of femoral head: 369, 

Proximal right femur, anterior view, showing collapse and 

cavitation of femoral head with sequestrum of necrotic bone 

(arrow). 370, X-ray, showing reactive osteosclerosis on the 

border of living and dead bone. (69-year-old male with 

bilateral aseptic necrosis of femoral head for several years; 

USPHS surgical specimen 2427 of 1975, courtesy of Dr. B. 

Ragsdale, Armed Forces Institute of Pathology, Washington, 

D. C., U.S.A.) 
NUMBER 28 237 

and supplying the inferior portion of the head; 

and (3) the lateral epiphysial vessels, which enter 

the head within one centimeter distal to the 

margin of the articular cartilage, supplying most 

of the femoral head and communicating especially with the vessels of the ligamentum teres 

(Trueta and Harrison, 1953). These are, apparently the most important vessels. If they are severed by the fracture, aseptic necrosis always develops, whereas the common severance of the 

inferior metaphysial vessels bears no consistant 

relationship to necrosis (Claffey, 1960). The area 

around the fovea is often spared if the ligamentum teres is intact. 

If the fracture is survived for a long time, 

inactivity osteoporosis characteristically will be 

present in any surviving part of the femoral head 

and in the femoral neck, while the necrotic portion maintains the trabecular pattern as of the 

time of fracture, if no revascularization and new 

bone deposition has occurred. The necrotic portion appears dense on X-ray for several reasons: 

(1) the above-mentioned inactivity atrophy and 

osteoporosis in the adjacent surviving bone, (2) 

the deposition of calcium into the necrotic tissue 

of the fatty marrow, (3) the compression of dead 

bone trabeculae into a smaller area during collapse, and (4) the deposition of new bone on deadbone in the process of repair. 

Traumatic dislocation of the hip also can be 

followed by aseptic necrosis. This is seen more 

frequently in posterior dislocations, especially if 

they are complicated by acetabular fractures. In 

traumatic dislocations the ligamentum teres is 

usually torn, and it is particularly an area on the 

top of the femoral head that may become necrotic 

and demarcated as a sequestrum surrounded by 

a sclerotic rim on its base, resembling a focus of 

osteochondritis dissecans. 

The so-called idiopathic aseptic necrosis of the 

femoral head is not common. About 50 percent 

of the cases are bilateral. Approximately 80 percent of the cases occur between 30 and 60 years 

of age, and approximately 80 percent are in males 

(Jaffe, 1972:634). 

The necrosis usually begins in the weight-bearing area of the femoral head, beneath the articular cartilage. Its further development and gross 

and radiologic appearances are not different from 

those of known etiology, such as sickle cell anemia 

or Gaucher's disease. In systemic lupus erythematosus, a disease of the connective tissue of the 

body, unilateral or bilateral necrosis of the femoral head is not uncommon (Dubois and Cozen, 

1960). 

PALEOPATHOLOGY 

In the paleopathological literature, circulatory 

disturbances have received little attention. Gray 

(1968) describes two possible cases of bone infarction in Egyptian archeological material. The first 

of these is a mummy (his No. 6) dated to the 

Greek period (ca. 330 B.C.). The mummy is currently located in the Horniman Museum in London. Gray found radiodensities in the distal femora and proximal and distal tibia, all of which he 

attributes to bone infarction. The figures of the 

X-ray films show radiodense lines circumscribing 

normal or radiolucent areas. The remainder of 

the skeleton is normal. The second case is a 

mummy (his No. 7) dated to the Roman period 

(first to second century A.D.). The distal portion 

of the femur has a large, oblong radiodensity 

aligned with the long axis of the bone. Gray 

attributes this condition to a solitary bone infarct 

or enchondroma. While these may very well be 

examples of bone infarction, all of the lesions 

illustrated in the published figures are suspicious. 

All the changes seen on the X-ray film could be 

due to dried overlying soft tissues or, depending 

on burial conditions, to infiltration of the tissue 

by soil constituents. Final judgment on these cases 

should be postponed until these possibilities are 

eliminated. 

A possible case of necrosis of the femoral head 

is seen in a proximal fragment of a left femur 

(Figures 371-374) excavated in an American Indian site ih Arkansas, USA (NMNH 255142). 

The archeological age is uncertain. Most of the 

superior portion of the femoral head was destroyed antemortem creating two large confluent 
238 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

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FIGURES 371-374.—Necrosis of the femoral head of left femur fragment: 371, Anterior view. 

372, X-ray of anteroposterior view; note the radio-dense sclerosis inferior to the necrotic defect. 

373, Anterosuperior view of reactive bone. 374, Detailed view of reactive bone showing the 

thickened trabeculae. (NMNH 255142.) 

depressions. The smallest of these is superior, 

lateral, and continuous with the femoral neck. 

The largest depression involves about one-half of 

the area of the femoral head. There has been 

considerable bony reaction in the depressions, in 

which the exposed trabeculae have become 

greatly thickened indicating a long-standing condition. On the anteroinferior margin of the articular surface there is a bony projection about one 

centimeter square extending inferiorly. There is 

noticeable periosteal bone deposition on the femoral neck, suggestive of a low grade inflammatory 

condition. This raises the possibility of a septic 

condition contributing to the necrosis of the femoral head. However, periosteal reaction to an 

aseptic inflammation arising from trauma is also 

possible. 

Perthes' Disease and Slipped Femoral 

Capital Epiphysis 

PATHOLOGY 

Perthes' disease is represented by extensive 

aseptic necrosis of the epiphysis of the femoral 

head. It is an uncommon disease occurring unilaterally in 90 percent of the cases. It usually 

begins between 5 and 9 years of age and involves 
NUMBER 28 239 

boys four times as often as girls (Jaffe, 1972:566). 

The condition has been found in different races 

but is rare in Negroes. 

In the course of the disease the necrotic epiphysis increases in radiodensity, contrasted with 

focal radiolucency of the area of the femoral neck 

bordering the growth plate. Later the head flattens, due to a combination of compression fracture and lack of enchondral growth. The basal 

bulge of the flattened head leads to subperiosteal 

and enchondral bone formation, thickening the 

neck of the femur. The end result, after revascularization, is a mushroom shaped femoral head 

with overhanging margin but without significant 

dislocation of the center of the femoral head from 

the axis of the shortened femoral neck. Early 

severe degenerative arthritis modifies the appearance and can make the differentiation from the 

endstage of slipped femoral epiphysis difficult or 

impossible. In the acute stage, the differentiation 

from tuberculous coxitis and from aseptic necrosis 

in Gaucher's disease may be uncertain in dry 

bone. 

Although slipped femoral capital epiphysis is 

not primarily an aseptic necrosis, it is best to 

discuss it in this connection. The primary pathology of this lesion is a stress fracture between the 

metaphysial side of the growth plate and the neck 

of the femur. This allows medial posterior and 

downward displacement of the head of the femur 

and, not uncommonly, leads to some degree of 

aseptic necrosis in the epiphysial bone. The disease is uncommon and occurs more frequently in 

boys than in girls. The age of manifestation 

ranges from 10 to 16 years in boys, 9 to 14 years 

in girls (Jaffe, 1972:577). Kelsey, Keggi, and 

Southwick (1970) found Negroes almost twice as 

often affected as Whites. 

Since the growth plate remains with the epiphysis, the bone of the epiphysis is little altered, 

except in cases with extensive aseptic necrosis. 

The proximal end of the femoral neck, however, 

shows irregularities due to the fracture with subsequent abrasion and resorption. In dry bone, 

since the joint capsule and the cartilage are missing, the appearance of the proximal surface of the 

femoral neck would be the main clue. In the 

healed stage, the head, united with the neck in 

the slipped position, shows some dislocation of 

the center of the head towards the axis of the 

neck. The neck is always short and thick, reflecting both the attrition in the fracture area and the 

loss of enchondral growth for several years. As in 

Perthes' disease, early and severe degenerative 

arthritis complicates the picture. Occasionally, 

upward dislocation of the femur is observed, creating a new "acetabulum" on the lateral aspect 

of the ilium, while the slipped head is held in the 

anatomical acetabulum by the ligamentum teres 

(Schinz, Baensch, Friedl, and Uehlinger, 1951-

1952 (l):450-454). 

PALEOPATHOLOGY 

A right femur from the Valley of Chicama in 

Peru provides a possible example of Perthes' disease. This case is from a miscellaneous group of 

femora all accessioned as NMNH 265331 at the 

National Museum of Natural History, Washington, D. C. The archeological age is unknown. The 

epiphyses of the femur are fully fused indicating 

full adulthood. The femur is 383 millimeters in 

length and gracile, suggesting female sex. The 

diaphysis, distal metaphysis, and the joint surface 

are normal. The maximum diameter of the femoral head is 60 millimeters, much larger than 

expected for a female. Part of the femoral head 

was damaged postmortem, although enough remains to indicate the nature of the pathology. 

There is a large circumscribed porous lesion 

covering more than half of the remaining joint 

surface of the femoral head (Figures 375-377). 

This porosity has completely obliterated the depression for the ligamentum teres. There is a 

depressed groove at the boundary with normal 

bone. The margins of the joint surface are characterized by exuberent bony overgrowth creating 

a mushroom-like appearance. This overgrowth 

extends well over the femoral neck. There are 

some bony outgrowths on the superior portion of 

the neck, but otherwise the neck appears normal. 

The X-ray film shows considerable thickening 

of the trabeculae under the porous lesion. This is 

indicated by a radiodense zone on the medial 
240 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

FIGURES 375-377.—Perthes' disease in a right femur: 375, 

Posterior view; notice extensive development of periarticular 

lipping. 376, X-ray of anteroposterior view; note the relatively normal length of the femoral neck. 377, Medial view 

of the femoral head; note the enlargement in diameter and 

extensive porous degeneration. (NMNH 256331.) 

aspect of the femoral head. There are small radiolucent areas in the lateral head region and in the 

femoral neck. There has been considerable reduction in the mediolateral diameter of the head. 

This added to the marked overgrowth at the joint 

margins creates the false impression of the head 

having been forced into the femoral neck. However, the normal length of the neck and the 

overgrowth of the joint margins make it clear that 

the pathological process involves collapse of the 

superior medial portions of the femoral head 

followed by bony overgrowth on the articular 

margins. 

The criteria for differentiating Perthes' disease 

and slipped femoral capital epiphysis can be seen 

in a right femur from the miscellaneous femora 

from Chicama, Peru (NMNH 265331). The maximum length of this femur is 370 millimeters, 

although this is misleading due to the inferior 

displacement of the femoral head. The bone is 

moderately robust, suggesting male sex. The diaphysis, distal metaphysis, and the joint surface 

are normal except for a moderate degree of middiaphysial, anteroposterior flattening. This is due 

in part to the abnormal gait induced by the 
NUMBER 28 241 

FIGURES 378, 379.—Slipped femoral capital epiphysis in a 

right femur: 378, Anterior view showing inferior displacement of capital epiphysis. 379, X-ray of anteroposterior view 

demonstrating shortened femoral neck. (NMNH 265331.) 

FIGURES 380, 381.—Slipped femoral capital epiphysis in a left femur: 380, Anterior view; note 

that the superior articular surface is below the level of the greater trochanter. 381, Posterior 

view. (HMCS GR 1582.) 
242 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

defective femoral head. The femoral head is displaced inferiorly (Figures 378, 379) so that the 

superior margin is about 15 millimeters lower 

than the greater trochanter. There is no evidence 

of porosity. Indeed the joint surface is smooth and 

intact. The depression for the ligamentum teres 

is well defined, unlike that of the head in Perthes' 

disease. Its position relative to the joint surface is 

much nearer the inferior, posterior margin of the 

joint surface than normal. The ligament attachment was maintained after the epiphysis slipped. 

Growth continued in the epiphysis but predominantly on the anterior and superior aspects. Ultimately, the head reunited with the neck. The 

femoral neck is abnormally short and thick resulting from the loss of the growth plate activity 

when the epiphysis slipped. 

The X-ray film shows an even, well-organized, 

trabecular structure with no unusual radiologic 

abnormalities. It is possible to identify the growth 

plate of the femoral head in the film and see that 

the mediolateral diameter of the head is relatively 

normal. In marked contrast with Perthes' disease, 

the femoral neck is almost nonexistent on the 

superior aspect and greatly shortened inferiorly. 

Another example of slipped epiphysis is seen in 

a left femur of a specimen from the Historical 

Museum in Chur, Switzerland (HMCS GR 

1582). The specimen is from the archeological site 

at Bonaduz in Canton Grissons, Switzerland. The 

epiphysis has slipped inferiorly and the femoral 

neck is shortened (Figures 380, 381). 

Other Vascular Disturbances of Epiphyses 

and Apophyses 

There are a number of skeletal areas that are 

subjected to severe mechanical stress, which may 

lead to vascular disturbances of chronic trauma 

or a combination of both. This is particularly true 

of the skeletons of growing children and adolescents. 

Kohler's Disease of the Tarsal Navicular Bone 

PATHOLOGY.—This bone is in such a key position in the vault of the foot that its blood supply 

to the ossification center may be impaired in the 

growing child, leading to aseptic necrosis, usually 

with flattening of the bony center and increased 

density on X-ray. This flattening may be due in 

part to compression of the necrotic bone, in part 

merely an effect of arrested enchondral ossification in the necrotic area. Over the years more or 

less complete repair can be observed, secondary 

to revascularization. The disease is uncommon 

and occurs four to five times as often in males as 

in females. The onset of the disease is around 3 

years of age, usually several months earlier in 

females in whom this ossification center develops 

correspondingly earlier (Jaffe, 1972:606). 

Osteochondritis Dissecans 

PATHOLOGY.—Osteochondritis dissecans is a 

type of aseptic necrosis characterized by the formation of a small, in profile triangular, sequestrum consisting of articular cartilage on one surface and necrotic subchondral cancellus bone. 

The disease occurs in the adolescent and young 

adult and is much more common in males than 

in females. Familial occurrence has been observed 

(Stougaard, 1964). The knee is the affected joint 

in 90 percent of the cases, and the most frequent 

location is the lateral portion of the articular 

surface of the medial femoral condyle. Other 

large joints are only rarely involved. 

In the course of the disease, the necrotic fragment is extruded into the joint cavity and becomes a loose osteocartilaginous body, which often enlarges due to circumferential growth of the 

surviving cartilage. The cartilage may calcify, but 

the bone fragment remains dead and unaltered 

in size and shape. The subchondral osseous defect 

of the condyle closes over with a thin layer of 

bone but always remains a depression on the 

bony articular surface. 

PALEOPATHOLOGY.—Wells (1961) describes an 

archeological skeleton from a Bronze Age cemetery (1600 B.C.) at Long Crickel, Dorset, England. 

The skeleton is that of a young female about 16 

years of age. The abnormality consists of deficient 

bone on the anterosuperior margins of the third 

and fourth lumbar vertebral bodies. About onethird of the affected body is missing. Wells attributes this condition to adolescent osteochondritis. 
NUMBER 28 243 

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FIGURE 382.—Osteochondritis dissecans of the medial right 

femoral condyle with severe arthritic degeneration of the 

joint. Specimen is a Late Saxon period burial from Thorpe 

St. Catherine, Great Britain. (Photograph reproduced from 

Wells 1974b, fig. 4, with permission from Mrs. Calvin Wells.) 

However, a congenital malformation of the Morquio or Hurler type should be considered, as 

should trauma. 

Wells (1962b) reports a case of osteochondritis 

dissecans in a Late Saxon burial excavated near 

Norwich, England. The specimen is male and the 

abnormality occurs on the medial condyle of the 

left femur. The defect is a large circumscribed 

depression in the joint surface about one centimeter in depth. Additional evidence of osteochondritis dissecans is reported in skeletons of Romano-British date from the leklingham cemetery 

in England (Wells, 1976). Several additional purported cases of osteochondritis dissecans in ancient British skeletal material are described by 

Wells (1974b). Figure 4 of his report shows a 

fairly certain example of osteochondritis dissecans 

of the distal femoral joint surface (Figure 382). In 

this report Wells expresses the opinion that osteochondritis dissecans is more common in RomanoBritish and Anglo-Saxon skeletons than skeletons 

of Bronze Age people in the British Isles. 

Osgood-Schlatter's Disease of the Tibial Tubercle 

PATHOLOGY.—The tibial tubercle is the site of 

the insertion of the patellar tendon. It develops 

from one or several apophysial ossification centers 

which, during the growing period, are separated 

from the proximal tibial metaphysis by a cartilage 

plate. There is considerable variation in this process but the powerful pull of the quadriceps may 

lead to partial avulsion of the tendon insertion 

with fragmentation of the apophysial center and 

ultimate marked nodular irregularity of the tibial 

tubercle after fusion with the metaphysis. This 

condition is essentially of traumatic origin and 

aseptic necrosis plays a minor, secondary part, if 

any. It is more common in boys than in girls. It 

does not occur before 8 years of age in girls and 

10 years of age in boys and does not commence 

in either sex after 14 years of age (Jaffe, 1972: 

599). More than 20 percent of the cases involve 

both knees. 

PALEOPATHOLOGY.—Wells (1968) reports a possible case of Osgood-Schlatter's disease in a Late 

Saxon (ninth or tenth century A.D.) burial in 

Norwich, England (Norwich Castle Museum No. 

15, 953 [9]). The affected bone is a left tibia from 

a male skeleton containing a defect of the tibial 

tuberosity. The defect consists of an oblong depression 30 millimeters long, 20 millimeters wide, 

and 10 millimeters deep. 

Another possible case of Osgood-Schlatter's disease is found in the miscellaneous long bones 

from Chicama, Peru (NMNH 265330-661). This 

specimen is a right tibia (Figures 383, 384) of a 

fairly small adult, probably a female. The archeological age is unknown. The diaphysis, distal 

metaphysis, and distal joint surface are normal. 

In the region of the tibial tubercle there is a large 

irregular spur, which projects toward the knee 

joint. Both medial and lateral to the spur are 

zones of periosteal reactive bone. These are well 

healed indicating that the condition was not active at the time of death. The proximal joint 

surface of the tibia is abnormal. The bony surface 

for the attachments of the cruciate ligaments is 

poorly defined. The lateral and medial joint surfaces are poorly delimited. The medial joint surface extends posteriorly creating an irregular surface. There is a sharply defined narrow depression 

11 millimeters long by 3 millimeters wide and 4 

millimeters deep on the anterior lateral edge of 
244 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

FIGURES 383, 384.—Possible Osgood-Schlatter's disease of 

the tibial tubercle in a right tibia: 383, Anterolateral view 

showing bony spur; note defect (arrow) inferior to joint 

surface, which may have been the result of a crushing injury. 

384, X-ray of mediolateral view of proximal tibia. (NMNH 

265330-661.) 

the lateral joint surface. Grossly this defect appears to have resulted from a crushing injury to 

this portion of the joint. Reactive bony spurs in 

the region of the tibial tubercle and reactive bone 

deposition are compatible with Osgood-Schlatter's disease. 

the head broadened transversally, and the distal 

portion of the diaphysis thickened, with disappearance of the usual necklike constriction (Kohler, 1923). There is a corresponding change in the 

configuration of the articular surface of the adjacent basal phalanx. 

Freiberg's Disease of a Metatarsal Head 

PATHOLOGY.—This lesion involves the head of 

the second, less commonly the third, metatarsal. 

The lesion consists of subchondral necrosis and 

infarction of the metatarsal head, which may 

separate from the shaft, similar to the fragment 

in osteochondritis dissecans. The second metatarsal is usually the longest and bears the burden of 

pressure against the ground, especially when the 

heel is unduly elevated. 

The lesion usually occurs in adolescents but 

may be observed in adults. Bilateral involvement 

occurs. There is a concave defect in the articular 

bony surface of the metatarsal head with a sclerotic base. The metatarsal is somewhat shortened. 

Kienbock's Disease of the Carpal Lunate Bone 

PATHOLOGY.—The carpal lunate forming the 

center of the proximal carpal chain bears the 

brunt of the mechanical impact transmitted to 

the radius. The disease consists of necrosis and 

fragmentation of this bone, mainly on a basis of 

chronic trauma. The condition is not rare, more 

common in males, occurring between 20 and 40 

years of age, with predilection of the right hand. 

Radiologically, areas of increased density and 

lucency alternate, and in the dry state bone areas 

may actually be fragmented after disappearance 

of interposed fibrous and cartilaginous tissue. 

More rarely the carpal navicular bone may be 

similarly affected (Preiser's disease). 
NUMBER 28 245 

Pulmonary Osteoarthropathy 

PATHOLOGY 

Pulmonary osteoarthropathy is a somewhat obscure affection of the skeleton in persons with 

inflammatory or neoplastic, primary or metastatic, pulmonary lesions. Rarely pleural, cardiac, 

or mediastinal lesions may also lead to this condition. Although the skeletal involvement is initiated by a lymphocytic infiltration of the periosteum, it is presently thought that altered neurocirculatory reflexes are probably the underlying 

cause. In the living patient, the skeletal changes 

often disappear after removal of the pulmonary 

lesion. The concomitant arthritic changes and the 

clubbing of the fingers and toes only affect 

FIGURES 385, 386.—Pulmonary osteoarthropathy: 385, Right radius and ulna showing marked, 

diffuse periosteal hyperostosis with pronounced vascular grooving. 386, Right foot, dorsal view; 

note periosteal hyperostosis of metatarsals and phalanges. (58-year-old female with large, 

solitary metastasis of breast cancer in lung; IPAZ 6649, autopsy 1259 of 1961.) 
246 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

FIGURES 387, 388.—Pulmonary osteoarthropathy: 387, 

Cross-section of tibia. 388, Cross-section of fibula, enlarged 

to show periosteal bone deposition and cortical bone resorption. (58-year-old female with large, solitary metastasis of 

breast cancer in lung; IPAZ 6649, autopsy 1259 of 1961.) 

the soft tissues and, therefore, need not be discussed here. 

The skeletal lesion consists of a strictly symmetrical periosteal bone deposition on the shafts 

of the long bones of the extremities. The new 

bony shell is usually thickest at middiaphysis, 

tapering towards the metaphysis and sparing the 

bony ends and tendon insertions. The bones most 

frequently and most severely involved are the 

bones of the forearms (Figures 385-388) and 

lower legs (radius, ulna, tibia, and fibula). Femur 

and humerus show less involvement. Of the small 

tubular bones of hands and feet, the metacarpals 

and metatarsals are more affected than the phalanges (Figure 386), usually leaving the terminal 

phalanges, in spite of the clubbing, unchanged. 

The bones of the trunk rarely are affected and 

the skull is unchanged, except, infrequently, for 

bone deposition on the inner table (Jaffe, 1972: 

290). The new bone is first fibrous, later remodeled into lamellar bone. It may be separated 

from the old cortex by a thin, fibrous layer. Its 

surface, on the dry bone, presents a rough aspect 

resembling a tree bark. It may be several millimeters thick at middiaphysis. In the late stages, 

the underlying cortex shows resorption with 

widening of the Haversian canals (Figures 387, 

388) and, at times, endosteal resorption with 

widening of the medullary cavity. The carpal and 

tarsal bones merely show osteoporosis (Schinz, 

Baensch, Friedl, and Uehlinger, 1951-1952 (1): 

485). 

Aneurysmal Erosion 

PATHOLOGY 

Bone is very sensitive to closely applied, pulsating pressure, as indicated by normal and abnormal vascular grooves on bony surfaces. An 

extreme case in point is the effect of the longstanding proximity of a large saccular dilatation 

of an artery (aneurysm) to bone. 

The aortic arch is located immediately behind 

the manubrium of the sternum. Aneurysms in 

this area, mostly of syphilitic origin, can cause an 

erosion of varying depths on the posterior surface 

of the manubrium. Complete round perforation 
NUMBE

R 28 247 

FIGURES 389, 390.—Erosion of vertebral bodies by aortic 

aneurysm, probably arteriosclerotic; note the multiple deep 

scalloping defects partly showing a thin layer of reactive 

bone: 389, Lateral view. 390, Anterior view. Note the resist-

ance to erosion of the areas adjacent to discs. (FPAM, 

Jubilaumspital 593.) 

of the manubrium can occur. The descending 

aorta is closely attached to the vertebral column. 

Aneurysms of this portion, usually of arterioscle-

rotic etiology, may erode several vertebral bodies 

anteriorly. Since cartilage is not resorbed as read-

ily as bone in response to pulsating pressure, 

deeply scalloped resorption defects are seen on 

several adjacent vertebral bodies while the end-

plates adjacent to the intervertebral discs are 

better preserved (Figures 389, 390). 

The internal mammary arteries are closely at-

tached to the posterior surface of the ribs, near 

the osteochondral junction. In congenital extreme 

narrowing of the aorta below the left subclavian 

artery (coarctation), the internal mammary arter-

ies show marked compensatory dilatation. In this 

condition deep pressure grooves are seen on the 

ribs, near the osteochondral junctions. 
Reticuloendothelial and Hemopoietic Disorders 

In various disorders of the reticuloendothelial 

system, bone changes occur either due to accumulation of abnormal metabolites or abnormal 

proliferation of histiocytic cells. 

Lipid Storage Diseases 

PATHOLOGY 

Gaucher's Disease 

Gaucher's disease represents an inborn, genetically controlled, abnormality of lipid metabolism, in which abnormal cerebrosides are increasingly accumulated in histiocytes of the reticuloendothelial system, especially in the spleen, liver, 

lymph nodes, and bone marrow. The disease 

manifests itself in about one-third of the individuals in affected families. Both sexes are equally 

involved. The frequency of Gaucher's disease is 

about 30 times as high in Jews of central or 

eastern European descent as in Mediterranean 

Jews or in other populations (Jaffe, 1972:508). 

Although the disease may start in a family as a 

mutation, usually it seems to be transmitted as 

an autosomal recessive trait. Although the main 

involvement is extraskeletal, we are here only 

concerned with the bone changes. 

The bone changes are due to continued accumulation over many years of cerebroside-laden 

histiocytes in the bone marrow. This accumulation may be diffuse or in the form of nodular 

aggregates. The deposition, although widespread 

throughout the skeleton, does not involve all 

bones equally. Diffuse infiltration in hemopoietically active bones (vertebrae, sternum, ribs, pelvis, and cranial vault) leads to widening of the 

marrow spaces and reduction of the number and 

diameter of bone trabeculae, giving a coarse, 

spongy appearance on X-ray and in dry bone. 

The cortices also appear thinned, but the periosteal surface remains smooth. This osteoporosis 

has no specific characteristics. The weakened porotic bone is subject to compression fractures in 

weight-bearing areas. This is especially observed 

in the lower thoracic and lumbar portion of the 

vertebral column. Anterior wedging with collapse 

and resulting kyphosis occurs (Pick, 1927:20-21). 

In severe cases, changes in the femoral head are 

common. These manifest themselves as flattening 

of the curvature of the articular surface with 

lateral bulging and diminished height. This 

change may be brought about by interference 

with the precarious blood supply by pressure of 

accumulated Gaucher cells or by infractions of 

the porotic spongiosa or both. The head may be 

actually driven into the neck, which then appears 

shortened on external inspection. This deformity 

of the femoral head later leads to early development of degenerative arthritis in the hip joint 

because of incongruity of the two articular surfaces. These changes are very similar to other 

forms of aseptic necrosis of the femoral head, 

especially that due to Perthes' disease. Pathologic 

fractures also occur, mainly in the proximal femur, vertebrae, and ribs (Greenfield, 1970). The 

shafts of long bones, most often of the femur, may 

become the seat of nodular and diffuse infiltration 

with Gaucher cells, resulting in widening of the 

marrow space with increased diameter of the 

bone. This most characteristic change is often 

observed on the distal femoral rrietaphysis. Instead of the usual concave flare, it shows a straight 

contour or even slightly bulging outline (so-called 

Erlenmeyer flask deformity). This can be due, in 

part, to inhibited remodeling during the growth 

period or actual expansion of the thin metaphysial cortex in adult life. 

The nodular infiltration, in addition to coarse 

porosis, may also lead to complete trabecular 

resorption in the affected area, giving a lytic 

appearance on X-ray and a cystic defect in dry 

bone. Characteristically, the diaphysial cortex 

248 
NUMBER 28 249 

may show lamination and thinning, secondary to 

invasion of the Haversian canals by Gaucher cells 

(Pick, 1927:23). If this process is severe, a minimal 

amount of subperiosteal bone deposit can be 

observed, but usually the external cortical lamellae, although thin, remain smooth. Similar 

changes may be observed on the proximal tibial 

metaphysis or on the humerus, albeit less often. 

In long-standing cases, severe destruction of the 

proximal humerus with varus deformity is not 

uncommon. In these late cases, lytic skull and 

mandibular lesions and focal reactive sclerosis 

may occur (Rourke and Heslin, 1965). Bone marrow infarcts have been observed in various long 

bones (Arkin and Schein, 1948). 

Niemann-Pick's Disease 

Niemann-Pick's disease is a rare, congenital, 

familial disorder of the phospholipid metabolism, 

leading to progressive storage of phospholipids 

(mainly sphingomyelin) in the reticuloendothelial 

cells of the liver, spleen, lymph nodes, and bone 

marrow. There is no sex predilection and the 

inheritance seems to be recessive. About 50 percent of the affected individuals are Jews. The 

majority of the individuals die in infancy but 

survival to young adult age has been observed 

(Crocker and Farber, 1958:2-4). 

Bone changes are mostly limited to reduction 

of number and size of trabeculae and cortical 

thinning of long bones. Occasionally, moderate 

widening of the distal femoral metaphysis is observed, not reaching the extent often seen in 

Gaucher's disease (Crocker and Farber, 1958:82). 

The generally poor health of affected infants may 

manifest itself in delayed appearance of secondary ossification centers. Superimposed deficiency 

in Vitamins D and C may add features of rickets 

and scurvy to the picture. In contrast to Gaucher's 

disease, collapse of the femoral head and focal 

lytic lesions do not occur (Gildenhorn and Amromin, 1961). 

Other Lipidoses 

Essential familial hypercholesteremia is a disorder of the cholesterol metabolism, inherited as 

a Mendelian dominant. The condition is characterized by elevated blood cholesterol levels and 

often leads to tumor-like deposits of cholesterol in 

subcutaneous and periarticular connective tissues 

or tendons (xanthoma tuberosum). There is no 

predilection of sex or race. 

There seems to be no deposit of cholesterol in 

the bone marrow. Observed bone changes mainly 

consist of pressure erosions of phalanges of fingers 

and toes by adjacent xanthoma nodes (Merrill, 

1920). This is apparently caused by the tightness 

of space in the subcutaneous compartments of 

digits, whereas much larger xanthomatous deposits in the vicinity of larger bones and joints do 

not usually indent the bones. The scooped-out 

cortical erosions may cross interphalangeal joints 

and simulate defects caused by gouty tophi (Gaal, 

1933). 

Lipid (cholesterol) granulomatosis (ErdheimChester's disease) is a rare disorder characterized 

by massive cholesterol deposition in the bone 

marrow and occasionally in other organs, but 

sparing the spleen. The condition remains asymptomatic into adult life. The reason for mentioning 

it here is that distinct bone changes have been 

demonstrated radiologically and anatomically 

(Chester, 1930-1931:577-592; Jaffe, 1972:537-

541). The most marked lesions were found in the 

long bones of the forearms and lower legs, symmetrically. The changes consist of spotty and 

diffuse osteosclerosis, most pronounced in the 

metaphysial area but often also involving the 

epiphysis. The shaft cortex may be thickened but 

shows widened Haversian canals. The changes 

extend into the bones of hands and feet, most 

markedly so in the talus and calcaneus. Femur 

and humerus are less affected and the skull is 

normal. The sclerosis observed is due to both 

trabecular thickening and ossification of medullary cholesterol granulomas. 

Histiocytosis X 

PATHOLOGY 

Histiocytosis X (Lichtenstein, 1953) is a term 

introduced to unite three different clinical mani-
250 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

festations of a non-neoplastic histiocytic lesion of 

unknown etiology: Letterer-Siwe's disease, eosinophilic granuloma of bone, and Schiiller-Christian's disease. Although the clinical courses of 

these conditions are very different, transitions 

have been observed and the bone lesions are very 

similar, radiologically and histologically. The 

common denominator between the three conditions is proliferation of histiocytes in various tissues and organs. This may be diffuse or nodular, 

generalized or local, with varying admixture of 

eosinophilic leucocytes, lymphocytes, and plasma 

cells. Fibrosis and granulomatous aggregates of 

histiocytes, laden with neutral fat and some cholesterol, are present or dominant in chronic cases. 

Letterer-Siwe's disease affects infants and children, mostly below 2 years of age. It involves 

most organs and tissues of the body and frequently takes an acute course with fatal outcome. 

Eosinophilic granuloma of bone represents the 

most common histiocytosis developing in children 

and young adults and is characterized by solitary 

or multiple bone lesions. The course is often selflimiting and benign. Schiiller-Christian's disease 

is characterized by multiple bone lesions often 

occurring subsequently over periods of years in 

children, adolescents, and young adults. Lipid 

granuloma and fibrosis are an essential part of 

this condition. The ultimate prognosis is often 

unfavorable because of involvement of the brain, 

pituitary, lungs, or heart in some cases. Encroachment upon the pituitary often leads to severely 

retarded growth, approaching dwarfism (Chiari, 

1931:430). 

Although, as stated, the bone lesions are very 

similar in all three conditions, their distribution 

may be somewhat different. Any bone may be 

involved, but skull lesions are most common. 

Second in frequency are lesions in flat bones. 

Vertebrae, ribs, and long bones are not uncommonly involved. The small bones of hands and 

feet are usually spared. The lesion generally presents as a central, purely lytic, lesion without 

sclerotic margin or reactive bone formation. The 

small lesions are round or oval, later acquiring 

undulating or "geographic" borders. 

FIGURE 391.—Histiocytosis X, cranial vault with multiple 

penetrating defects showing geographic contours and little 

reactive bone. Multiple destructive lesions were found in 

many bones. (3V2-year-old male, 1^/^ years known duration, 

IPAZ autopsy 1328 of 1955.) 

In Letterer-Siwe's disease multiple skull lesions 

are usually present, involving the cranial vault 

and base, especially the sphenoid. In some cases 

facial bones are involved. In eosinophilic granuloma the most common lesion is a solitary, purely 

lytic, round or oval defect in an area of the cranial 

vault, showing a beveled edge and, occasionally, 

a central sequestrum. In Schiiller-Christian's disease, large, multiple, confluent cranial defects are 

often seen (geographic skull) (Figure 391). The 

lesions of the cranial vault, even after destruction 

of both tables, are usually devoid of periosteal 

reactive bone. In eosinophilic granuloma, destructive focal involvement of the mandible is not 

uncommon, elevating the teeth above, creating 

the appearance of "floating" teeth on X-ray. 

Lesions of the vertebral bodies, especially in 

small children, often lead to collapse, giving the 

picture of a vertebra plana. 

The involvement of long bones is also primarily 

subcortical, mostly metaphysial, less common 

middiaphysial, and rarely epiphysial. If the overlying cortex is destroyed, subperiosteal reactive 
NUMBER 28 251 

bone formation does occur. Rib lesions may circumferentially erode the old cortex and expand 

the diameter, eliciting some sclerotic response in 

the new cortex. Pathological fractures can occur 

in long bones and ribs. 

Anemias 

PATHOLOGY 

In various, mostly hemolytic, anemias bone 

changes occur secondary to the need for expansion of the spaces occupied by hemopoietic marrow (Caffey, 1937:293, 294). 

Thalassemia 

Thalassemia is a hemolytic anemia caused by 

a genetic defect in the hemoglobin structure. The 

severe manifestations of thalassemia major are 

usually restricted to homozygotes as regards the 

abnormal gene. Heterozygotes show thalassemia 

minor with little or no clinical, and certainly 

without skeletal, manifestations. Moderately severe cases occur (thalassemia intermedia), which 

may be due to a different abnormal gene. Recent 

advances in hemoglobin chemistry have shown 

that there are two major and several minor genetic abnormalities producing thalassemia. The 

classical thalassemia, affecting mainly central and 

eastern Mediterranean populations (Italians, 

Greeks, North Africans, but not French and Spaniards) is of the beta-type, characterized by the 

limited ability to synthesize the beta-chain of the 

globin molecule. The other large area of the world 

affected by thalassemia is India, Thailand, Malaysia, China, and the Philippines. In these areas, 

beta-thalassemia, but probably of a different genetic background, and alpha-thalassemia, in 

which the alpha chain synthesis is genetically 

inhibited, occur side by side. Less frequent instances of various types of thalassemia occur in a 

worldwide distribution in almost all ethnic and 

racial groups. The North and South American 

Indians, who apparently completely lacked a 

thalassemia gene, are an exception. All American 

Indian instances are due to admixture of White 

or Negro genes. A detailed discussion of the 

geographic, ethnic, and genetic problems of this 

disease complex has been given by Rucknagel 

(1966). Although extremely interesting, it is of 

little significance to the present problem since, 

regardless of genetic background, the clinical and 

skeletal changes are the same. A geographic distribution in different populations is given in Table 11 from Rucknagel (1966). The percentages 

TABLE 11.—World distribution of alpha and beta thalassemia in indigenous populations (from Rucknagel, 1966) (dash 

= no data; ? = questionable data) 

Geographic area 

SOUTHERN EUROPE 

Italy 

Sicily 

Sardinia 

Greece 

Portugal 

Turkey 

AFRICA 

Algeria 

Morocco (Jews) 

Egypt 

West Africa 

MIDDLE EAST 

Israel (Samaritans) 

Lebanon and Syria 

ASIA 

India (Madras, Castes) 

Thailand (Valley) 

Thailand (Hill tribes) 

South Vietnam 

China (southern) 

Malaysia 

Indonesia 

SOUTH PACIFIC 

New Guinea 

New Britain 

Philippines 

Saipan 

AMERICA 

North and South 

American Indians 

Alpha 

{%) 

0.2 

-

1 

4-7 

-

•> 

2-10 

-

3-5 

-

-

-

1.5-2 

0.5 

-

-

? 

0 

Beta 

{%) 

0-20 

3-13 

4-38 

6-14 

0.6 

? 

1-15 

3 

0.3 

2 

14 

5 

15 

5 

1-10 

2 

3-5 

-

0-8 

4-6 

1 

1 

0 
252 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

FIGURES 392-394.—Thalassemia major; frontoparietal segment of cranial vault: 392, External view. 393, Endocranial 

view. 394, Cross-section showing widening of the diploic 

spaces and honey-combed buildup of subperiosteal bone 

replacing the outer and inner tables. (8-year-old Thai, studied by Putschar in 1962 at Department of Pathology, Medical School, Chiengmai, Thailand.) 

quoted include homozygotes and heterozygotes, 

and it is understood that there is more than one 

genetic type of beta-thalassemia. 

Thalassemia major results in a very high mortality in infancy and childhood and a limited 

adult life span in the few survivors. The heterozygote without anemia presumably has a selective 

advantage in malaria-infested areas, which would 

explain the geographic distribution. However, the 

evidence is more circumstantial and less clear-cut 

than in sickle cell anemia (Rucknagel, 1966). In 

thalassemia major, bone changes always develop 

and become radiologically obvious after the first 

year of life. Intermediate thalassemia may show 

skeletal lesions; thalassemia minor does not. The 

bone lesions in thalassemia are entirely due to 

increased spatial demands for the hyperplastic 

erythropoietic marrow. In keeping with the general distribution of hemopoietic marrow, the entire skeleton of the child is affected, more or less 

uniformly, while, in the adult, characteristic bone 

changes remain only in areas of permanent hemopoietic activity. 

The most severe changes are in the skull. In 

children, the diploe of the cranial vault expands, 

leading to marked thickening of the cranial vault, 

usually beginning in the upper portion of the 

frontal bone (Figures ,392-394). The trabeculae 

of the diploe are reduced in number with thickening and later radial rearrangement of the remaining trabeculae. The external table is progressively eroded and later completely destroyed. 

This is accompanied by honeycombed compartments of subperiosteal new bone, harboring hyperplastic marrow. The destruction of the inner 

table comes much later and is always much more 

limited than that of the outer table. On X-ray, in 

these severe cases, the honeycombed compart-
NUMBE

R 28 253 

395 

'^^^HB-' 

ments give the appearance described as "hair on 

end." The facial bone, especially the maxilla and 

zygoma, are expanded in their external dimen-

sions, showing thin cortices and loose spongiosa, 

causing a mongoloid appearance with prominent 

cheek bones. Development of maxillary and 

sphenoid sinuses as well as of the mastoid cells is 

inhibited and delayed (Caffey, 1957a, 1972 (1): 

89). Ethmoid sinuses are better developed, since 

there is little marrow in these bones (Baker, 1964). 

The involvement of the maxilla and, to a lesser 

extent, of the mandible leads to disorderly erup-

tion of the teeth and malocclusion of the jaws. In 

general, the reduction of the total mass of trabe-

cular and cortical bone leads to arrangement of 

residual trabeculae along stress lines to give max-

imal mechanical stability with minimal encroach-

ment on marrow space. This is most pronounced 

in ribs, where the cortex can be completely miss-

ing and the trabeculae show diagonal arrange-

ment with right angle crossings (Figures 395, 

396). There is a linear reinforcement on the con-

cave surface in response to respiratory bending 

stresses. The diameter of the ribs is expanded. 

Similar expansion and alteration of the trabecu-

lar pattern are seen in flat bones (pelvis, scapulae) 

showing a fan-like pattern on X-ray. 

In addition to porosis, the vertebrae show de-

creased height, increased width, and cupping of 

the end-plates. Actual compression fractures oc-

cur, especially in the lower dorsal and lumbar 

areas (Caffey, 1972 (2): 1393). In children, meta-

carpals, metatarsals, and phalanges show expan-

sion, diagonally crossing trabeculae, and reticu-

lated thin cortices. 

Long bones of the extremities show marked 

widening of the medullary cavity accompanied 

FIGURES 395-396.—Thalassemia major: 395, Longitudinal 

cut (left) of proximal tibia showing widening of epiphysial 

and metaphysial marrow spaces and of medullary cavity, 

marked thinning of cortex, and lines of arrested growth. 

External view (right) of distal radius with lace-like reduction 

of metaphysial cortex. 396, Rib, endothoracic surface, show-

ing extreme lacey cancellization of cortex. (8-year-old Thai, 

studied by Putschar in 1962, Department of Pathology, 

Medical School, Chiengmai, Thailand.) 
254 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

by thinning of the cortex, most pronounced in 

the femur. In the metaphysial area, the cortex 

may assume a reticulated appearance with markedly enlarged vascular foramina, harboring hyperplastic marrow. There is often inhibited remodeling of the distal femoral metaphysis, leading to a widened contour without the usual concave flare, closely resembling the so-called Erlenmeyer flask deformity seen in Gaucher's disease. 

Multiple "lines of arrested growth" are frequently 

present, in keeping with the usual inhibited 

growth and delayed epiphysial closure observed 

in this disease. In a smaller percentage, premature 

and irregular fusion of the growth plate occurs, 

especially of the proximal humerus, leading to 

significant medial tilting of the humeral head. In 

the series published by Currarino and Erlandson 

(1964), 12 of 79 thalassemia patients showed premature fusion of growth plates beginning after 10 

years of age and producing shortening and deformity. Of these, nine concerned the proximal 

humerus (three bilateral), three the distal femur 

(one bilateral). The general reduction of growth 

may lead to an infantilistic, dwarfed skeleton 

(Caffey, 1972 (2): 1284). 

In adults, the tubular bones of hands and feet 

resume normal contours and may develop some 

osteosclerosis subsequent to the replacement of 

erythropoietic by fatty marrow (Caffey, 1972 (2): 

1284). The widening and reticulation of the ribs 

remains mostly in the posterior portions and 

rarely may lead to a tumor-like expansion of 

erythropoietic marrow covered by a thin, expanded, cortical shell, projecting into the thoracic 

cavity. Changes in the vertebrae and, to a lesser 

extent, in the cranium remain. Pathological fractures, especially of the femur, occur in adults 

more frequently than in children. 

Double heterozygous combinations with other 

hemoglobin abnormalities occur, but only in thalassemia-hemoglobin S combinations are bone infarctions observed (Middlemiss and Raper, 1966: 

698). Pure thalassemia creates no circulatory obstructions and does not have an increased rate of 

osteomyelitis. In the differential diagnosis of dry 

skeletal parts, other hemoglobinopathies, congenital spherocytic anemia, and iron deficiency anemia have to be considered. The skull changes of 

thalassemia occasionally resemble those in sickle 

cell anemia but the extensive lesions of the rest of 

the skeleton do not. Cyanotic congenital heart 

disease (Ascenzi and Marinozzi, 1958) and, 

rarely, polycythemia (Dykstra and Halbertsma, 

1940) can mimic the skull changes in thalassemia. 

Congenital hemolytic anemia and iron deficiency 

anemia never show bone changes of such severity. 

Sickle Cell Anemia and Its Genetic Variants 

A variety of normal and abnormal hemoglobins can be identified by electrophoresis. At birth, 

fetal hemoglobin F amounts to about 60-80 percent of the total and remains in significant 

amounts until about 6 months of age. It is rapidly 

replaced by adult hemoglobin A to a level below 

one percent, but there exists genetic abnormal 

persistence of hemoglobin F. Hemoglobin S is an 

abnormal hemoglobin, responsible for the sickling 

phenomenon. Another abnormal hemoglobin is 

C. A further abnormality of hemoglobin is caused 

by the thalassemia genes (Thai). All these genetic 

factors are realized in the various genotypic combinations of any two of them. 

Sickle cell anemia patients have a genotype SS 

while individuals with sickle cell trait have genotype SA. The gene for hemoglobin S is almost 

exclusively limited to the Negro race with a slight 

scattering in adjacent Mediterranean populations 

(southern Italy, Greece, Armenia). Other genetic 

combinations (SC, and SThal) represent the genetic variants of sickle cell anemia. In persons 

with two abnormal hemoglobin genes, hemolytic 

anemia will develop in intermittent crises, and 

the erythrocytes will assume sickle shape under 

hypoxemic stress, due to crystallization of the 

abnormal hemoglobin within the cell. The result 

is constantly increased demand for red cell production to compensate for the cell loss in hemolysis. During crises, the misshapen red cells conglutinate and cause vascular obstructions, leading 

to areas of ischemic necrosis. Although the genetic 

abnormality is present at birth, the clinical man-
NUMBER 28 255 

ifestation is prevented before 6 months of age due 

to the protective effect of the high concentration 

of fetal hemoglobin F before that age. The mortality of infants and children with sickle cell 

anemia is high. 

In persons with sickle cell trait (SA), only extreme hypoxemic stress can produce hemolysis 

and infarctions. Persons with the genetic combination of sickle cell trait and persistent fetal 

hemoglobin (SF) are usually free of anemia. Of 

considerable interest is the fact that hemoglobin 

S is more resistant to attack by malaria parasites. 

This offers survival advantage to carriers of hemoglobin S, which in turn leads to increasing 

frequency of hemoglobin S in inhabitants of the 

malaria infested areas of tropical Africa. The 

frequency of hemoglobin S varies in different 

Negro populations. In North American Negroes, 

7.5 percent show the sickling trait but only 1 in 

40 (2.5 percent) of these suffers from sickle cell 

anemia (Lewis, 1942:234-235). Of course the 

American Negroes are a dislocated group of 

mixed genetic background. In Panama, Tomlinson (1945) found at autopsy that 9 percent of 

individuals with sickling trait actually showed 

clinical sickle cell anemia. The sex distribution 

rate of the sickling trait in 3000 determinations 

in Panama (representing autopsies, hospital patients and village populations), was 7.2 percent 

in males and 11.4 percent in females. In spite of 

a high frequency of hemoglobin S in African 

Negroes, clinical sickle cell anemia is uncommon. 

A survey of over 2000 Yorubas in Ibadan (Nigeria) showed the following distribution of hemoglobin genes: normal 70.9 percent, carriers of 

AS 23.9 percent, AC 4.3 percent, SC 0.7 percent, 

and CC 0.2 percent (from Cockshott, 1958). 

The skeleton may be involved in sickle cell 

disease in three different ways: (1) changes secondary to increased demand of space for hemopoietic marrow; (2) sequelae of vascular obstruction of smaller and larger blood vessels; and (3) 

secondary infections superimposed on ischemic 

areas. Although a variety of bone changes have 

been described in sickle cell anemia, it should be 

emphasized that, as a rule, they are neither common nor obvious nor specific. The most careful 

and detailed study of bone changes in this disease 

has been published by Diggs, Pullian, and King 

(1937) in a series of their own cases. Their series 

comprised 39 Negro patients with active severe 

sickle cell anemia, ranging from 1 to 51 years of 

age. This includes eight autopsies at which special 

attention was paid to bone changes. The frequency and degree of bone involvement increased 

with age beginning in children past 5 years of 

age. The bones most likely to reveal alterations 

are the skull, vertebrae, tibia, and fibula, with the 

skull changes appearing the earliest. They found 

in their series that the majority of patients showed 

no alteration in size, shape, and density of their 

bones on X-ray. There is general agreement 

among all observers that bone changes are not 

related to the severity of the disease. 

The first and most conspicuous changes are 

observed in the skull. The diploe may be thickened, and there may be diminished definition of 

the outer table on X-ray. The radiation density 

is diminished, sometimes with coarsened trabeculation arranged perpendicular to the inner table. 

Complete destruction of the outer table with socalled "hair on end" arrangement of bony septa 

is uncommon. It was present in only 1 of 39 cases 

in the series of Diggs, Pullian, and King (1937). 

They found the thickening of the diploe to be 

bilateral, symmetrical, and usually limited to the 

parietal bones, less often involving the frontal 

and occipital bones. The maximal thickness occurs in the vertex, tapering to normal towards the 

temporal area. Skull changes are most often observed in older children and in young adults. 

Occasionally the osteoporosis may lead to small 

focal lytic lesions resembling myeloma. The facial 

bones showed normal appearance on X-ray in 

their cases. Sarjeant (1974:166) states that the 

zygoma may be enlarged and the orbital roof 

tlTickened, but the frontal sinuses develop normally, although the other sinuses may be delayed 

and hypoplastic. In the mandible, reduction and 

coarsening of trabeculae is observed, accompanied by prominence of the lamina dura of the 

alveoli and thinning of the cortex. The vertebrae 
256 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

show rarefaction of the spongiosa in the vertebral 

bodies. In adults, depression of the central portion 

of the end-plate with intact peripheral portion is 

observed, which is somewhat different from the 

"fish vertebra" appearance in postmenopausal 

osteoporosis. Widening and flattening of vertebral 

bodies, especially in the lumbar area, is seen in 

about 30 percent of adult patients (Jaffe, 1972: 

700). The ratio of height to width of vertebral 

bodies in anterior-posterior views on X-ray 

ranged from 1:1.4 to 1:2.8 with a normal of 1:1.4 

for Negroes of comparable age (Diggs, Pullian, 

and King, 1937). 

The scapula, sternum, pelvic bones, and ribs 

(flat bones) may show increased lucency and 

coarsening of the trabeculation. However, in the 

series reported by Diggs, Pullian, and King 

(1937), only slight osteoporosis without widening 

of the bones was observed. 

In long bones, the most marked changes occur 

in the tibia and fibula. Hemopoietic marrow may 

occupy Haversian resorption spaces in the cortex, 

especially near the medullary canal (Diggs, Pullian, and King, 1937). In adults with advanced 

disease, endosteal reactive lamellar bone and occasional bony plugging of segments of the marrow 

cavity can occur (Diggs, Pullian, and King, 1937). 

In these cases neither the medullary cavity nor 

the diameter of the shaft is widened. On the 

contrary Diggs, Pullian, and King (1937) found 

the cortex thickened and the medullary cavity 

actually narrowed. In their series they found 11 

cases, mostly adults, with marked changes of long 

bones. The hyperplastic marrow also may produce multifocal spotty radiolucency in the metaphysial areas. The medullary cavities of metacarpals may be widened and vascular foramina enlarged (Cockshott, 1958). The changes produced 

by sickling and blocking of blood vessels are 

essentially ischemic infarctions, which may be 

large and located in the medullary cavity, small 

and spotty in the metaphysis, or involving portions of shaft cortex due to blockage of Haversian 

vessels. Generally, the large medullary infarcts 

are indistinguishable from those produced by 

other causes. As in those, they also tend to collect 

calcium salts around the necrotic focus, which is 

readily visible on X-ray. The metaphysial foci 

may appear as focal increased densities alternating with spotty lucencies of hyperplastic marrow. 

In fact, some of the bony plugging of the medullary cavity, as described by Diggs, Pullian, and 

King (1937), may well represent healed infarctions. The cortical infarcts may reveal a lytic 

intracortical separation on X-ray. Infarctions of 

the cortex of short tubular bones of hands and 

feet are not uncommon in infants and small 

children. These may elicit moderate periosteal 

reactive bone formation and spotty densities and 

lucencies in the course of repair (Jaffe, 1972:697-

703). However, Diggs, Pullian, and King (1937) 

found no bone changes in hands and feet in their 

cases, but in some instances epiphysial necrosis 

may lead to shortening of individual fingers (Sarjeant, 1974:175-177). 

Of special significance is the occurrence of 

aseptic necrosis in the head of the femur in sickle 

cell anemia and its genetic variants. This is the 

most common site of infarction. Apparently, it is 

even more common in the variants, particularly 

in SC patients, than in classical SS anemia (Cockshott, 1958). Golding, Maclver, and Went (1959) 

reported from Jamaica only 5 instances in 51 SS 

patients, but 13 in 19 SC and in 1 of 2 SThal 

patients. Chung and Ralston (1969:38) quote the 

incidence of aseptic necrosis of the femoral head 

from a literature survey as 0-12 percent in SS but 

20-60 percent in SC disease. The lesion occurs 

mostly in adolescents near the time of fusion of 

the proximal growth plate. It resembles Perthes' 

disease, however with two differences: The lesion 

occurs several years later and it lacks metaphysial changes adjacent to the growth plate. Furthermore, Perthes' disease is uncommon in Negroes (Chung and Ralston, 1969:51). If the necrotic focus is small, hugging the base of the 

articular cartilage, it may simulate an unusually 

large osteochondritis dissecans or Perthes' disease 

(Middlemiss and Raper, 1966:695). In a series of 

13 cases reported by Chung and Ralston (1969: 

38), four showed bilateral hip lesions and six of 

these patients also showed aseptic necrosis of the 
NUMBER 28 257 

FIGURE 397.—X-ray of right humerus, of sickle-cell anemia 

with Salmonella osteomyelitis. (Nigerian negro, courtesy Dr. 

Stanley Bohrer, Ibadan, Nigeria.) 

humeral head; others had infarcts in long bones. 

These additional necrotic foci mostly concerned 

older patients with classical (SS) sickle cell anemia rather than genetic variants. Occasional unusual locations of aseptic necrosis, such as elbow, 

knee, sacroiliac joint, and ankle, have been observed in SS disease (Chung and Ralston, 1969: 

40). Secondary infections are not uncommonly 

superimposed on ischemic necrotic foci, which 

permit colonization of bacteria if circulating in 

the blood stream in only small numbers. In these 

infections, intestinal pathogens, especially strains 

of Salmonella, make up an unusually large percentage (Figure 397). As in ordinary types of 

osteomyelitis, the metaphyses of growing long 

bones are predilected. In contrast to purulent 

osteomyelitis, there is often destruction of the 

growth plate, which may lead to Coxa vara at the 

hip joint (Middlemiss and Raper, 1966:696). 

Pathological fracture through the osteoporotic 

bone also occurs. 

In general, sickle cell anemia diminishes the 

rate of growth and frequently delays the closure 

of growth plates. For additional statistical and 

anatomical details consult Diggs (1967) and the 

recent survey of Sarjeant (1974:165-192). 

Hereditary Spherocytosis 

(Congenital Hemolytic Anemia) 

This is a genetically determined hemolytic disorder, characterized by the globular shape of the 

erythrocytes. It is uncommon in Negroes (Kline 

and Holman, 1957). The disease manifests itself 

at various ages. Bone changes are uncommon and 

slight, usually limited to the cranial diploe, rarely 

affecting long bones. The cases with onset in 

infancy or early childhood may show the most 

marked changes (Moseley, 1963:10-11). 

Iron-deficiency Anemia 

Bone changes in iron-deficiency anemia are 

uncommon. If such changes occur, they are usually limited to the skull vault, showing expansion 

of the diploe, vertical striation and occasional 

"hair on end" appearance on X-ray (Moseley, 

1961, 1963, 1966; Lanzkowsky, 1968). The patients reported as showing the bone changes mentioned have been Indonesian (Eng, 1958), Negroes (Burko, Mellins, and Watson, 1961), or 

prematures and twins (Shahidi and Diamond, 

1960). The facial bones and long bones are usually spared and pneumatization of the paranasal 
258 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

sinuses is not delayed (Moseley, 1963:5). However, in some Turkish patients, enlargement of 

the facial bones, delayed pneumatization, and 

coarse porotic trabeculation around elbows, 

hands, and feet have been observed (Aksoy, 

^amli, and Erdem, 1966). 

In other conditions, such as cyanotic congenital 

heart disease with secondary polycythemia (Ascenzi and Marinozzi, 1958) or in polycythemia 

vera (Dykstra and Halbertsma, 1940), expansion 

of the cranial diploe due to hyperplasia of the 

hemopoietic marrow has been described. 

Erythroblastosis Fetalis 

In some infants with this disorder, usually 

based on RH incompatibility between the RH 

negative sensitized mother and the RH positive 

fetus, bone changes have been described. They 

consist of alternating band-like areas of increased 

and decreased radiodensity, especially in the metaphysis of the most rapidly growing bones (distal 

femur and proximal tibia). These changes were 

present in 20 of 110 cases (Brenner and Allen, 

1963) but are not specific. They reflect disturbances of the late fetal enchondral ossification 

with delayed resorption of calcified cartilage cores 

in primary trabeculae (Follis, Jackson, and 

Carnes, 1942). The only reason to mention this 

finding is that similar changes can be seen in the 

newborn in congenital syphilis. 

PALEOPATHOLOGY 

Because of the problems in differentiating various types of anemia in dry bone specimens, I 

shall discuss here the paleopathology of all the 

anemias. This, of course, does not preclude an 

attempt to establish a probable specific diagnosis 

for a given case but does serve to emphasize the 

importance of other variables, such as ethnohistorical data on diet and endemic disease, in reaching a diagnosis. 

An important basic distinction in the anemias 

is between genetic and acquired anemia. Some of 

the genetic anemias, such as sickle cell anemia 

and possibly thalassemia tend to be influenced by 

the distribution of malaria, since the abnormal 

hemoglobin in such anemias reduces the severity 

of the symptoms of malaria. Acquired anemia is 

a response to one or more of several variables 

including nutrition and debilitating diseases and 

thus occurs in any human population irrespective 

of the presence of malaria. 

Most of the inferences made about the presence 

of anemia in paleopathological specimens are 

based on lesions of the skull thought to be associated with this disease. The lesions are found on 

the skull vault, primarily the outer surface of the 

parietal bones, and on the orbital roof (Figure 

398). They consist of porous periosteal bone deposition in these areas of the skull. Henschen (1961: 

724) attributes the earliest awareness of these 

lesions in clinical cases to Rokitansky (1844) and 

Virchow (1848). Several descriptive terms have 

been used for this condition including cribra 

crania, symmetrical osteoporosis, and spongy hyperostosis. I shall use the term "porotic hyperostosis" introduced by Angel (1966). 

The relationship between the calvarial and orbital lesions has never been clear. Virchow (1874: 

61-62) believed that both lesions are part of the 

FIGURE 398.—Porous, reactive bone on the orbital roof 

(Child about 12 years of age from Pachacamac, Peru, 

NMN H 266599.) 
NUMBER 28 259 

same disease process. Hrdlicka (1914) indicated 

that the calvarial lesions begin in the orbit. M0llerChristensen and Sandison (1963:180) note the 

possibility of lacrimal gland involvement in orbital lesions and suggest mumps as a possible 

cause. Local inflammation of the orbital roof 

from such a cause probably would not affect the 

cranial vault. The implication of this opinion is 

that orbital lesions are not necessarily associated 

with calvarial lesions. My own experience is that 

one often finds both types of lesion in a single 

skull, but one also finds each type of lesion occurring by itself and occasionally in association with 

morbid conditions other than anemia. 

Several morbid conditions other than anemia 

have been proposed as the cause of porotic hyperostosis. Williams (1929:854-855) suggested 

rickets as the most likely cause but also suggested 

that abnormal conditions created by artificial 

deformation of the skull could produce similar 

lesions. Earlier, Hrdlicka (1914:58) expressed the 

opinion that the condition was not rachitic but 

more likely a "toxic" rather than a nutritive or 

degenerative disorder. Henschen (1961:724, 729) 

examined 2000 modern skulls from Sweden and 

found no evidence of porotic hyperostosis. However, he did find four such lesions in some midnineteenth century Swedish skulls. He suggests 

that the lesions may have been caused by nutritional conditions or chronic infection. 

While infectious and metabolic disease may be 

implicated in porotic hyperostosis of the skull, 

anemia has received much more attention in the 

paleopathological literature as a possible cause of 

this condition. Vyhnanek, Kolar, and Stloukal 

(1963) describe two medieval skulls of children 

from central Europe with porotic hyperostosis. 

The authors conclude that they are examples of 

hemolytic anemia but are not more specific. 

Zaino (1964:403) proposes that the porotic hyperostosis, which is common in pre-Columbian 

skulls from Peru, is due to thalassemia. 

Jarcho, Simon, and Jaffe (1965) report a case 

of porotic hyperostosis from a Pueblo Indian site 

in the American Southwest. The authors conclude that bone changes suggest the presence of 

some type of hemolytic anemia, probably thalassemia, in the pre-Columbian New World. The 

problem in inferring the presence of thalassemia 

in the ancient New World from skeletal lesions 

is that there is no evidence of this gene in 

post-Columbian unmixed .American indigenous 

-populations. 

Moore (1929) summarizes the modern clinical 

findings in sickle cell anemia, which include the 

thickened hair-on-end appearance in roentgen 

films. He briefly describes a modern skull with 

similar lesions. He attributes this example of porotic hyperostosis to sickle cell anemia and offers 

the opinion that the morbid condition was widespread. As with thalassemia, however, there is no 

evidence of this genetic blood abnormality in 

modern unmixed indigenous populations in the 

New World. 

In the Old World, Angel (1964, 1966) has 

proposed that porotic hyperostosis found in ancient Greek skulls is evidence for the presence of 

thalassemia in antiquity. Here, however, the evidence for the genetic variant in modern ethnic 

groups is unquestioned, making such an inference 

much more plausible. 

Moseley (1965) added acquired anemia to the 

list of possible morbid conditions producing porotic hyperostosis. On the basis of his clinical 

experience as a radiologist he proposed to differentiate thalassemia major from other genetic and 

acquired anemias because of its involvement of 

the face and long bones. He expressed the opinion 

(1965:141) that porotic hyperostosis seen in skulls 

from Peru and Yucatan is due to iron-deficiency 

anemia. This diagnosis was also applied to a 

Bronze Age (1650-1550 B.C.) skull of a 6-year-old 

child from Wales with porotic hyperostosis, described by Cule and Evans (1968). Sir Arthur 

Keith, who also saw the skull, attributed the 

lesions to rickets (in Wheeler, 1923:21). The published photographs, as well as Keith's description, 

also suggest congential syphilis as a possibility. 

The presence of hypoplastic enamel defects in the 

teeth is also compatible with a diagnosis of congenital syphilis but could also occur in anemia, 

particularly if related to poor nutrition. 
260 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

El-Najjar, Lozoff, and Ryan (1975) studied the 

expression of porotic hyperostosis in archeological 

skeletal samples from the southwestern United 

States. In their study they found an association 

between presumed dietary factors and the frequency of skeletons having porotic hyperostosis. 

The authors conclude that acquired anemia due 

to inadequate iron absorption is the most likely 

causative factor for porotic hyperostosis in skeletons from the southwestern United States. Mensforth, Lovejoy, Lallo, and Armelagos (1978:38) 

report an association between evidence of infectious disease and the occurrence of porotic hyperostosis in prehistoric skeletons from Ohio, USA. 

They suggest that illness and nutritional stress 

are important factors stimulating iron-deficiency 

anemia. 

Two specimens from the National Museum of 

Natural History, USA, provide useful insight into 

the expression of porotic hyperostosis. The two 

cases are both from the American Southwest 

(NMNH 327074 and 327107) and are skeletons 

of young children from the Pueblo Bonito ruin, 

Chaco Canyon, New Mexico. This site is associated with the Pueblo III cultural period and 

dated between A.D. 919 and 1130 (Seltzer, 1944: 

25), thus making it clearly precontact. During 

this period skulls show marked artificial deformation characterized by occipital flattening. The 

dental age of the first specimen (NMNH 327074) 

is about iy2 years (Figures 399-402). The lesions 

in this specimen are primarily porous but with 

some labyrinth-like lesions as well. The affected 

area involves the frontals including the orbital 

roofs but predominantly involves the outer table 

of the parietal bones. The inner table is not 

affected. The specimen is characterized by severe 

occipital flattening and the lesion encroaches only 

slightly on the deformed part of the skull. The 

facial bones and mandible are not markedly affected, although the region surrounding the zygomaticofacial foramen on the zygomatic bone 

suggests an inflammatory reaction. The lateral 

X-ray film shows the perpendicular striations 

found in many examples of porotic hyperostosis. 

A postmortem break through the lesion in the 

right parietal reveals an intact inner table, greatly 

enlarged diploe with the virtual elimination of 

the outer table. 

An X-ray film was prepared of the extant long 

bones including major portions of both femora, 

right tibia, both humeri, and ulnae. This film 

reveals a relatively enlarged marrow cavity and 

greatly diminished thickness of the cortex in all 

long bones. 

The second specimen (NMNH 327107) has a 

dental age of about 2 years. The state of preservation is not as good. Like the previous specimen 

the most severely affected region is the external 

table of the parietals (Figures 403, 404). The 

lesion does not cross the sagittal suture. The left 

frontal bone is also affected, with the disease 

process continuous across the coronal suture. 

Only portions of the right orbit are present. They 

reveal no evidence of porotic hyperostosis. The 

left temporal bone is abnormal with an irregular 

surface, which is thickened and slightly porous. 

Two features distinguish this specimen from 

the preceding one. First, the lesion does occur in 

the region of deformation. This may be related to 

the fact that the occipital deformation is not as 

severe. Second, unlike the preceding specimen, 

there appears to be slight deposition of reactive 

bone on the inner table. The abnormal bone is 

concentrated in the region of the anterior fontanel 

with reactive tissue apparent at its sutural borders. There is a solitary lesion on the left parietal 

boss. A lateral X-ray film of the skull reveals the 

vertical striations in the area where porotic hyperostosis is most pronounced. 

Also apparent in the film is the absence of the 

outer cortex in the porous area. The lesion itself 

is slightly different from the first specimen in 

being more variable in appearance. Beginning on 

either side of the sagittal suture, the parietal 

lesion has a narrow zone of finely porous bone. 

This quickly merges with bone that is labyrinthian in gross appearance. Continuing in a lateral 

direction the lesion is characterized by a circular 

porosity, which becomes finer and less pronounced in the area below the temporal muscle. 

Here the bone takes on the lumpy quality like 

that seen in the left temporal bone. 

Like the first specimen, the long bones are 
NUMBER 28 261 

FIGURES 399-402.—Porotic hyperostosis of skull vault: 399, 

Facial view. 400, Porous lesions of skull vault. 401, Lateral 

view of skull. 402, X-ray of skull, lateral view. (1- to 2-yearold child from pre-Columbian site of Pueblo Bonito, New 

Mexico, USA, NMNH 327074). 

affected by the disease process. An X-ray film of 

the complete right femur and the partially complete tibiae, left femur, and humerus reveals a 

generalized enlargement of the medullary cavity 

with the cortex much thinner than normal. Comparison of the abnormal femur with normal femora (Figure 405) of similar size from the same 

population reveals a cortical thickness of less than 

1 millimeter for the abnormal specimen, while 

the normal femora are between 2 and 3 millimeters. 

As El-Najjar, Lozoff, and Ryan (1975) argue, 

if some porotic hyperostosis is caused by nutritional anemia in which iron is deficient, one 

might find evidence of other metabolic problems 

resulting from iron deficiency. Von Endt and 
262 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

Ortner (1979) hypothesized that dietary iron deficiency might also affect the production of two 

amino acids, hydroxylysine and hydroxyproline, 

which are found in bone protein. They reason 

that, since iron is a factor in the synthesis of 

FIGURES 403-405.—Bone marrow reactions in a skeleton 

with porotic hyperostosis: 403, Porous labyrinth-like lesions 

of the skull vault. 404, Broken section of parietal demonstrating expansion of diploe. 405, X-ray of femur of specimen 

(center) compared with the femora of two normal children. 

Note the expanded marrow space and thinned cortex. (2-

year-old child from the pre-Columbian site of Pueblo Bonito, 

New Mexico, USA, NMN H 327107.) 

hydroxylysine and hydroxyproline, these two 

amino acids might be deficient in the bone protein of children suffering from iron-deficiency 

anemia. Von Endt and Ortner (1981) evaluated 

this possibility using one of the specimens described above (NMNH 327107). They compared 

the amino acid residues of bone protein from an 

archeological skeleton of a child having porotic 

hyperostosis with a similar skeleton that did not 

have porotic hyperostosis. A bone protein sample 

from a modern child who died from accidental 

causes was used as an additional control. The 

hydroxylysine and hydroxyproline residues of the 

ancient and modern skeletal samples that did not 

have porotic hyperostosis were virtually identical. 

In the bone of the child having porotic hyperostosis there was 5 percent less hydroxyproline and 

25 percent less hydroxylysine. The authors argue 

that these reduced concentrations support a diagnosis of iron-deficiency anemia in the skeleton 

with porotic hyperostosis. 

Certainly a diagnosis of some type of anemia is 

a strong probability in the two cases described 

above. However, the specific type of anemia is 

more problematical. Moseley (1963:6, 1966:128) 

reports that the long bones are not affected in 
NUMBER 28 263 

iron-deficiency anemia. This conclusion is not 

supported by Lanzkowsky (1968:24), who found 

widened medullary spaces and thinned cortices 

in the postcranial bones, particularly the metacarpals and phalanges. This difference of opinion 

clearly indicates that differential diagnosis of 

anemia in dry skeletal specimens may not be 

possible without considering other variables, including biochemistry and paleoepidemiology. 

There is the further problem of differentiation 

between porotic hyperostosis from anemia and 

similar lesions seen in infectious disease and metabolic disease. I have already discussed porous 

expansive lesions of the skull in infectious disease 

(p. 137). Similar lesions in scurvy and rickets will 

be reviewed in the section on metabolic disorders 

(p. 270). Briefly, porous lesions of the skull in 

infectious diseases tend to be periosteal. They 

tend not to involve an expansion of the marrow 

space or destruction of the outer cortex. The 

lesion typically is superficial to normal bone. In 

scurvy the bony reactions thought to occur could 

easily be confused with those of anemia or infectious disease. It is possible that in scurvy the outer 

cortex remains intact and no expansion of the 

diploe would be expected. The porous, expansive 

lesions in rickets are morphologically distinct 

from anemia. Although the lesion is porous and 

expansive, the pores in the skull are much finer 

and could not be confused with porotic hyperostosis associated with anemia. Indeed one should 

keep in mind that lesions attributed to metabolic 

diseases may, in fact, be due to undiagnosed anemia, perhaps associated with metabolic disease. 

Leukemia 

PATHOLOGY 

Leukemias are cancers of the myeloid and 

lymphoid hemopoietic cells of the bone marrow 

and occur in acute and chronic form in children 

and adults. The tumor cells extensively replace 

the normal bone marrow throughout the skeleton. 

As far as bone changes are concerned, only the 

acute leukemias of childhood need to be considered here. 

FIGURE 406.—Acute lymphatic leukemia; distal femur showing metaphysial cortical erosion due to leukemic deposits. 

(6V^-year-old female, MGH autopsy 26137.) 

FIGURE 407.—Sarcomatosis of cranium and many bones in 

lymphoma; frontal view of skull. Notice the destruction of 

the frontal and periorbital area. (About 20-year-oId male, 

with generalized lymphadenopathy, ANM 2039 from 1883.) 
264 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

In the growing bone of children, the replacement of the normal marrow cells by tumor cells 

and their subsequent proliferation lead, not 

rarely, to recognizable alterations of the bone 

structure. The most frequent lesion is a narrow 

radiolucent line on the metaphysial side of the 

growth plate. This change is not specific and 

resembles, to some extent, the lucent metaphysial 

zone in scurvy. Another alteration seen in acute 

childhood leukemias concerns the cortical surface 

of the metaphyses. Normally, in these areas, osteoclastic resportion of the modelling process creates a rough and somewhat grooved or porous 

cortical surface. In acute leukemia, these areas of 

the periosteum may be colonized by tumor cells 

emanating through the vascular foramina. This 

leads to widening of the vascular foramina and 

exaggerated grooving and porosity of the metaphysial cortical surface (Figure 406). This may be 

the most characteristic bone lesion of acute leukemia. Occasionally, widespread nonspecific subperiosteal bone deposits are observed over 

thinned cortices of long bones and ribs. Bone 

changes in adult leukemias are too uncommon 

and uncharacteristic to warrant discussion in this 

context. 

In malignant lymphoma, bone lesions, if present, resemble lytic or sclerotic metastases of carcinoma. Occasionally diffuse subperiosteal involvement with cortical erosion occurs (Figure 

407). 

Myeloma 

PATHOLOGY 

Myeloma is a highly malignant tumor of 

plasma cells, usually arising in an area of hemopoietic bone marrow and, after varying time intervals, involving extensive portions of the skeleton. 

The disease is relatively rare. There is a great 

prevalence of males over females affected. The 

tumor rarely occurs below 40 years of age with a 

maximal frequency between 50 and 70 years of 

age. There is no known racial or geographic 

prevalence. 

The initial lesion usually arises in that part of 

the skeleton that contains hemopoietic marrow 

which, in the older adult individual, is the trunk 

skeleton and the proximal metaphyses, especially 

of the femur and the humerus. Single tumor cells 

disseminated through the blood colonize mostly 

in the areas of hemopoietic marrow. In the cranial 

vault and in portions of the long bones of the 

extremities, reactivated hemopoietic marrow appears, secondary to massive marrow involvement 

in the trunk. The facial bones and the small bones 

of the extremities are usually spared. 

The initial lesion may remain localized and 

solitary for months or years, but ultimately dissemination to other parts of the skeleton almost 

always occurs. A typical location for this type of 

lesion is the proximal metaphysis of the femur 

and humerus (Schinz, Baensch, Friedl, and Uehlinger, 1951-1952:1947). The solitary lesion is 

slow-growing, creating an osteolytic defect, ultimately eroding the cortex but permitting the new 

formation of an expanded bony shell with ridgelike internal reinforcements, giving the so-called 

soap bubble pattern on X-ray. Pathological fractures through the lesion are not uncommon. The 

lesion usually does not extend into the head of 

the femur. This distinguishes it from giant cell 

tumor and chondroblastoma. In dry bone, the 

solitary lesion could not be differentiated with 

certainty from unicameral bone cyst, chondromyxoid fibroma or nonossifying fibroma, except 

for the fact that these would usually occur in a 

younger age group. The differentiation of the 

lesion from solitary lytic metastasis of renal or 

thyroid carcinoma may be impossible. The most 

frequently observed and most characteristic manifestation is the disseminated form (multiple myeloma). The lesions start within bone marrow but 

ultimately scallop and destroy cortex. In most 

affected bones (vertebrae, ribs, sternum, clavicles, 

scapulae, pelvis, calvarium, and long bones) the 

individual lesions create punched out, purely lytic 

defects without reactive bony margins (Figure 

408). Most are round, 3 to 10 millimeters in 

diameter. Individual large lesions are rare, with 

exception of the original ones; but small lesions 

can become confluent, often showing scalloped 
NUMBER 28 265 

FIGURE 408.—Multiple myeloma. Endocranial view of cranial vault showing multiple lytic lesions destroying the internal table. (65-year-old male, MGH autopsy 33606.) 

margins. In vertebral bodies this confluence of 

individual lesions is particularly common. The 

spinous processes are often involved. The destruction of the vertebral spongiosa often leads to 

collapse of multiple vertebrae, frequently with 

deep cupping of the end-plates due to expansion 

of the intervertebral discs (Figure 409). Wedgeshaped vertebrae, kyphosis, and scoliosis are common. The ribs also frequently show multiple 

transverse fractures and a coarsely reticulated 

irregular pattern of the few remaining trabeculae. 

Pathological fractures on long bones are also not 

uncommon. The differential diagnosis between 

disseminated multiple myeloma and osteolytic 

metastatic cancer, particularly of the breast, may 

be impossible. The male prevalence in myeloma 

and the female predominence in breast cancer 

are helpful in the differentiation. Furthermore, in 

metastatic carcinoma, even if predominantly 

lytic, some of the lesions usually show osteoblastic 

response, at least in the vicinity. Multiple myeloma frequently involves the glenoid fossa of the 

scapula and the lateral portion of the clavicle and 

disseminates into radius and ulna, a condition 

which is uncommon in metastatic carcinoma 

(Schinz, Baensch, Friedl, and Uehlinger, 1951-

1952:951). The presence of a larger, older lesion 

also helps in the differentiation from metastatic 

carcinoma. Rarely, multiple myeloma may leave 

the bone structure unchanged or produce only a 

FIGURE 409.—Multiple myeloma. Bisected spine and ribs 

with severe osteoporosis, compression fractures, kyphosis. 

Notice disseminated small lytic lesions in ribs and spinous 

processes. (77-year-old female, IPAZ autopsy 1703 of 1954.) 

pattern of diffuse osteoporosis without distinct 

lytic lesions. These cases cannot be recognized on 

the dry bone. 

PALEOPATHOLOGY 

The identification of myeloma in paleopathological specimens is complicated by the close 

resemblance between bone lesions of myeloma 

and those of some types of metastatic carcinoma. 

All the accounts of myeloma in the paleopathological literature are of the multiple type, and I 

shall limit the following discussion to that expression of the disease. 

Ritchie and Warren (1932) report a case of 

multiple lytic lesions in a skeleton of a pre-Columbian Indian (ca. A.D. 800-900) from New York 
266 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

State, USA. The skeleton is that of an old male. 

The roentgen films show multiple lytic lesions of 

the skull, which vary from a few to 25 millimeters 

in diameter. Other postcranial bones show similar 

lesions, with the long bones less affected then the 

axial skeleton. They suggest that prostate carcinoma is a possible cause but indicate that multiple myeloma is more likely, citing the opinions of 

H. U. Williams and R. M. Moodie in support of 

this diagnosis. The age and sex of the individual 

is compatible with a diagnosis of multiple myeloma. However, the large variation in the size of 

the lytic foci is more compatible with metastatic 

carcinoma. 

Williams, Ritchie, and Titterington (1941) report a case of multiple lytic lesions in the skeleton 

of a 10-year-old pre-Columbian child excavated 

near Rochester, New York, USA. The lesions vary 

between 3 and 10 millimeters in diameter in 

almost every bone recovered. The authors suggest 

multiple myeloma as a probable cause, but this 

is unlikely because of the young age. A more 

likely cause would be one of the histiocytoses, 

such as Schiiller-Christian's disease. 

Fuste (1955) describes a neolithic human skull 

from the Pyrenees that had multiple, lytic lesions. 

The lesions were roughly circular with irregular 

borders associated with reactive bone. Either multiple myeloma or metastatic carcinoma is possible, although the presence of reactive bone is 

more likely in metastatic carcinoma. 

Nemeskeri and Harsanyi (1959) describe the 

skeletal remains, from the tenth to eleventh century site of Kerpuszta, of a male about 50 years 

of age (burial no. 38, catalog no. 5293) which 

contain multiple lytic lesions. Their figures 9-

12 show longitudinal sections of humerus, femur, 

and innominate bones, all of which have lesions 

including a fairly large lytic lesion in the innominate. Although a scale is not provided, this lesion 

appears to be in excess of 2 centimeters in largest 

diameter. Roentgen films of the skull show multiple lytic lesions of fairly uniform size, none 

appearing to be in excess of one centimeter. There 

seems to be evidence.of bony reaction surrounding some lytic foci, although sand infiltration 

could be the cause. The large size of some lesions 

and the possibility of bony reaction would, in my 

opinion, tilt the scale in favor of a diagnosis of 

metastatic carcinoma rather than myeloma. Indeed, Brothwell (1967a: 337), in commenting on 

this and other similar cases, offers the opinion 

that skeletons with multiple lytic lesions should 

be considered cancer metastases, until more convincing evidence can be provided for a diagnosis 

of multiple myeloma. 

Wells (1964b) reported on two medieval skulls 

with multiple lytic lesions. The skulls were from 

Kent and Suffolk, England, and both were adults 

of unknown age. Wells was reluctant to offer a 

firm diagnosis but suggested metastatic carcinoma and multiple myeloma as likely, with myeloma the more probable. 

Brooks and Melbye (1967) describe a pre-Columbian skeleton from Missouri, USA, with multiple lytic lesions. The skeleton is that of a female 

over 40 years of age. Photographs of skull and 

femora reveal considerable variation in the size 

of the lesions. Some on the femora are at least 

half the diameter of the femur (about 15 mm). 

They attribute the probable cause of the lesions 

to multiple myeloma. The age and sex of this 

specimen is more compatible with a diagnosis of 

metastatic carcinoma, such as breast cancer, but 

certainly multiple myeloma is a strong possibility 

as well. 

Morse (1969:25, 144) briefly discusses a possible 

case of multiple myeloma from a site on Santa 

Cruz Island, California, dated between A.D. 300 

and 1450. The specimen is in the Lowie Museum 

(No. 12-4356), University of California, Berkeley, 

USA. There are multiple, coalescing, lytic lesions 

on the skull and postcranial bones, features that 

are compatible with multiple myeloma. The skeleton is reported to be a female with an estimated 

age of 45. 

Morse, Dailey, and Bunn (1974) published a 

report on four paleopathological specimens from 

Florida and Mississippi, USA, with lesions that 

they attribute to multiple myeloma. All were 

dated to the pre-Columbian period. The first of 

these is a skull (their specimen number 1) from 
NUMBER 28 267 

the Sowell Mound thought to be a male about 45 

years of age. A photograph shows a large circular 

lytic lesion 24 millimeters in diameter on the 

occipital bone. There are other lytic lesions in the 

skull ranging from 2 to 8 millimeters in diameter. 

The age and sex of this case are compatible with 

a diagnosis of multiple myeloma; however, metastatic carcinoma is equally possible and is more 

compatible with the large variation in the size of 

the lesions. 

Burials 1 and 2 from the Calico Hills mounds 

in Jefferson County, Florida, USA, both show 

multiple lytic lesions of the skeleton. Burial 1 is 

reported to be a female about 25 years of age. 

The lytic lesions range in size from 1 to 13 millimeters. The published roentgen picture reveals 

some lesions on the skull, but major involvement 

is on the innominates and the distal femur. The 

latter in particular shows multiple coalescing lytic 

lesions with some evidence of bony circumscription, although sand infiltration could be creating 

the appearance of reactive bone around the lesion. The age and sex of the individual, as well as 

the possibility of bony reaction to the disease 

process, argue more for metastatic carcinoma 

rather than multiple myeloma in this case. 

Burial 2 from the Calico Hills site consists of 

several postcranial bones and fragments of the 

skull. The authors report that the skull appears 

to be female and 25 years of age or less. A 

roentgen film of the skull shows multiple lytic 

lesions with no evidence of bony reaction. However, a photograph of the skull (Morse, Dailey, 

and Bunn 1974, fig. 4) shows considerable porous 

bony reaction of the external skull surface in areas 

surrounding lytic foci. In this case the lytic lesions 

are compatible with multiple myeloma, but the 

age and sex favor a diagnosis of metastatic carcinoma. Infectious disease should be considered 

as well. 

The fourth case of purported multiple myeloma is from the Magnum Mound in Clarbourne 

County, Mississippi, USA. Burial 4 from this site 

is a female postcranial skeleton of about 35 years 

of age. The vertebrae, ribs, pelvis, and right scapula show multiple lytic foci. The skull (4) thought 

to be associated with the postcranial bones shows 

a normal outer cortex (Morse, Dailey, and Bunn, 

1974, fig. 6). The roentgen film reveals lytic lesions in the diploic space sometimes penetrating 

through the inner table. There is a large eroded 

surface on the inner table, which the authors feel 

is antemortem. They suggest a large myelomatous 

area could have destroyed the inner table. However, they indicate that this large lesion is not 

typical of myeloma. The long bones are unusually 

light suggesting osteoporosis. 

Three paleopathological specimens from the 

National Museum of Natural History, Washington, D.C, provide further insight into the problems of differentiating between multiple myeloma 

and osteolytic metastatic carcinoma. The first of 

these is a female skeleton (NMNH 290064) from 

the Indian Knoll site in Kentucky, USA. Most of 

the artifacts from this site are dated in the Late 

Archaic period (ca. 3000-1000 B.C); however, 

some components date to the Late Woodland 

period (ca A.D. 800-1700). Thus the archeological 

age of this specimen remains obscure but with a 

strong probability of being Archaic. The age of 

the individual cannot be determined precisely. 

The skull sutures had just begun to fuse on the 

endocranial side, there is little evidence of arthritis, and tooth v^ear is marked. However, in this 

population tooth wear typically is marked in 

adults. These criteria suggest an age in the 30- to 

40-year range. The disease process consists of 

multifocal, mostly lytic lesions distributed in the 

skull, mandible, axial skeleton, and the proximal 

left femur (the right femur is missing). The bones 

of the hands and feet are unaffected except for a 

slight, superficial osteoporosis of the superior surface of the calcanei. The gross lesions vary in size 

from being barely detectable to about 15 millimeters in diameter. Most of the cranial lesions 

(Figure 410) penetrate both tables, with no clear 

pattern regarding which table is most extensively 

affected. The lytic process is more extensive in the 

diploe, suggesting that the marrow was the focal 

point for the disease process. The roentgen films 

of the skull and long bones reveal additional lytic 

foci that are not visible from the outside. The 
268 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

scapulae are present and both show multiple lytic 

foci (Figure 411), although the glenoid fossa is 

normal. However, unlike lesions elsewhere in the 

skeleton, there is a slight osteoblastic response 

adjacent to several of the lytic foci. With this 

exception, there is no osteoblastic reaction to any 

FIGURES 410, 411.—Multiple lytic lesions of the skull and 

postcranial skeleton: 410, Left lateral view of the skull and 

mandible. 411, Posterior view of left scapula with lytic lesions 

and porous bone hypertrophy (arrow) adjacent to lytic focus. 

(Adult female from Indian Knoll, Kentucky, USA, NMN H 

290064.) 

of the other lytic lesions in the skeleton. This 

suggests a rather acute disease process. Steinbock 

(1976:381-384) has reported on this case and 

concludes that "the size, location, and appearance 

of the destructive lesions in this Archiac Indian 

are highly indicative of multiple myeloma rather 

than metastatic carcinoma." While conceding 

that multiple myeloma is a strong possibility 

based on some aspects of the gross and roentgen 

film morphology of the lesions, I feel that an even 

stronger case can be made for metastatic carcinoma. The lesions are somewhat more variable 

in size than typical for multiple myeloma. Peripheral bone reaction on the scapulae is more 

characteristic of metastatic carcinoma as is the 

age and sex of the skeleton. 

Another possible case of multiple myeloma is 

a female skull from Peru (NMNH 242559). This 

specimen is fully adult and probably in the 30- to 

40-year age range. The archeological age is unknown. The external gross aspect of the entire 

skull, except the face, is characterized by several 

scalloped, lytic lesions (Figure 412), which vary 

in size from pin holes to 15 millimeters in diameter. There is no evidence of bony circumsciption 

(Figure 413) either by inspection or on roentgen 

films. The lesions are characteristic of both myeloma and metastatic carcinoma and, again to the 

extent that age and sex are useful variables in 

differential diagnosis, metastatic carcinoma 

would appear slightly more probable. 

The third case from the National Museum of 

Natural History, Washington, D.C, USA, is also 

a female skull from Peru (NMNH 242578). Age 

at death is, like the two previous cases, in the 

range of 30 to 40 years. The archeological age is 

unknown. Unlike the lesions in the preceding two 

cases, the external appearance of the lesions is 

much less obvious. The lytic lesions, which do 

penetrate the surface, are small holes typically 1-

2 millimeters in diameter. On the internal table 

the lesions are somewhat more pronounced. All 

bones of the skull are affected, but the facial 

bones and occipital bone show much less involvement. The greater wings of the sphenoid and the 

body of the sphenoid are markedly affected with 

much of the latter totally destroyed. In the X-ray 
NUMBER 28 269 

FIGURES 412, 413.—Multiple scalloped lesions of the skull: 412, Left lateral view of the skull 

with lytic lesions of varying size. 413, Detail of lytic lesion demonstrating the presence of spongy 

bone which indicates a lack of circumscription. (Adult female from Caudivilla, Peru, NMNH 

242559; scale in cm.) 

FIGURE 414.—X-ray of mediolateral view of multiple lytic 

lesions of the skull. Note the lack of sharply defined boundaries of the lytic foci. (Adult female from Peru, NMNH 

242578.) 

(Figure 414), it is apparent that the major focus 

of the lytic process is the diploe. There is no 

evidence of any osteoblastic reaction in any of the 

lesions. On the film a typical lesion consists of a 

lytic focus ranging in diameter up to 2 centimeters. Many of the lesions coalesce. The overall 

picture presented by this case is not typical of 

either multiple myeloma or metastatic carcinoma. However, Schinz, Baensch, Friedl, and 

Uehlinger (1951-1952:947, 949) briefly describe 

a case of atypical multiple myeloma in which 

"rather numerous individual foci are distinctly 

delimited, and a moth-eaten, finely mottled kind 

of osteolysis develops. ... " This description and 

their published roentgen film views closely match 

the appearence of the Peruvian skull. However, 

Schinz, Baensch, Friedl, and Uehlinger caution 

that the case they describe is not easily distinguishable from metastatic carcinoma. Provisionally, however, it is useful to consider this skull as 

an example of atypical multiple myeloma. 
Metabolic Disorders 

Vitamin C Deficiency 

PATHOLOGY 

Scurvy is a disease caused by prolonged inadequate intake of vitamin C (ascorbic acid). It 

affects many organs and has a high mortality in 

severe cases. Ascorbic acid is essential in the 

formation of the collagen fibril polypeptide precursors. Since the organic matrix of bone consists 

mainly of collagen, scurvy manifests itself in diminished or absent bone matrix formation, most 

marked in the rapidly growing skeleton of the 

infant. Ascorbic acid also plays a role in the 

formation of the cement substance between vascular endothelial cells and of basement membrane. This explains the great tendency to hemorrhage in scurvy, occurring spontaneously and 

on minor traumatization. The skeletal manifestations, which alone concern us in this discussion, 

are most marked in infants and rather minor in 

degree in adults. 

Adult scurvy has been recognized worldwide as 

a serious disease with high mortality. It occurred 

throughout history in populations deprived of 

fresh vegetables and meats due to war, famine, or 

prolonged trips at sea (e.g., voyages of discovery 

and polar explorations). Infantile scurvy, however, was not appreciated until well into the 

nineteenth century (Moller, 1862; Barlow, 1883). 

Since vitamin C is destroyed by boiling temperature, its deficiency is prone to manifest itself 

in populations consuming mainly cooked foods, 

rather than in primitive peoples, who eat considerable amounts of raw food. 

Infantile Scurvy (Moller-Barlow's Disease) 

Since ascorbic acid freely passes from the 

mother through the placenta to the fetus, vitamin 

C deficiency does not exist at birth. Even if no, or 

almost no, vitamin C intake occurs after birth it 

takes several months before the deficiency manifests itself as a recognizable disease. Infantile 

scurvy is seldom observed before 4 months of age 

and reaches its maximum of occurrence between 

8 and 10 months of age (Wimberger, 1925:288-

307). 

The skeletal changes are most marked in the 

areas of most rapid growth: costochondral junctions of ribs, distal metaphysis of femur, radius 

and ulna, and proximal metaphysis of humerus. 

The skeletal changes in scurvy are twofold: 

those caused directly by the vitamin C deficiency, 

and secondary changes due to traumatic effects 

on the vulnerable scurvy bone. The primary lesion consists of the combined effect of severely 

diminished osteoblastic activity and continued 

osteo- and chondroclastic activity. This leads to 

a piling up on the metaphysial side of the growth 

plate of calcified cartilage septa, which are not or 

incompletely covered by bony matrix ("scorbutic 

lattice" of Park, 1954). The resulting mechanical 

instability of this metaphysial zone usually results 

in transverse fracture through this area with fragmentation of the lattice and of the sparse trabeculae, producing hemorrhage and dislocation of 

the epiphysis. Since not only enchondral but, 

equally, periosteal bone formation is inhibited, 

the cortex is thinner than normal, especially on 

the metaphysis of long bones. 

The vascular vulnerability often leads to subperiosteal hemorrhages of varying degree and 

location. The most massive subperiosteal hematomas are usually observed in the weight-bearing 

long bones of the legs, especially the femur and 

tibia (Figure 415). Such hematomas usually begin 

at the level of a fractured metaphysis but may 

strip the entire shaft periosteum (Figure 416). 

270 
NUMBER 28 271 

FIGURE 415.—Infantile scurvy with subperiosteal hematomas 

and transmetaphysial fractures of both distal femora and 

tibiae. Wet specimen with periosteum opened. (11-monthold infant, 6 months duration, PMWH W 3530.) 

FIGURE 416.—Infantile scurvy, right bisected femur. Wet 

preparation showing massive subperiosteal hematoma and 

pathological fracture near the distal growth plate. (6- to 12-

month-old infant, PMSG 9/856A.) 

The elevated periosteum begins to produce reactive bone which, in the course of resorption of the 

hematoma, becomes attached to the cortical surface. 

The changes observed in scurvy in different 

parts of the skeleton are as follows: 

RIBS.—The bone adjacent to the osteochondral 

junction is often transversely fractured, causing 

an inward dislocation of the sternum and the rib 

cartilages, thus forming the palpable scorbutic 

"rosary." 

LONG BONES.—In addition to the metaphysial 

fractures already described, the marked cortical 

thinning and deposition of reactive periosteal 

pumice bone, up to one centimeter in thickness 

(Schmorl, 1901:217), can occur. The proximal 
272 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

metaphysis of the femur, if severely affected, caves 

in only beneath the head of the femur but not 

beneath the greater trochanter, because of the 

weight-bearing stresses transmitted through the 

hip joint (Erdheim, 1931b). This leads to a depressed angle of the neck of the femur. In healing, 

usually no major deformities remain, but collapsed metaphyses and dislocated epiphyses may 

become reunited in abnormal position. The secondary ossification centers of the epiphyses likewise show marked osteoporosis circumferentially 

surrounded by a layer of increased calcified cartilage at the growing periphery. This radiodense 

layer represents Wimberger's ring on the X-ray. 

FLAT BONES.—Subperiosteal hemorrhages also 

occur rarely on pelvic bones and scapulae (Fraenkel, 1929:228). 

SKULL.—Subperiosteal hemorrhages are common on the frontal bone and particularly on the 

portion forming the orbital roof. These hemorrhages are found more often on the orbital rather 

than on the endocranial surface and may lead to 

deposition of vertically arranged trabeculae of 

subperiosteal bone, covering the thin, partly resorbed cortex. 

Fraenkel (1929:228-229) found involvement of 

the orbital roof in 4 of 34 autopsied cases of 

infantile scurvy. Hemorrhages also occur over the 

cranial bosses and over the maxilla and mandible 

(Fraenkel, 1929:229-230). 

HEALED SCURVY.—The fragmentation zone of 

the metaphysis undergoes slow remodeling, while 

normal new bone increasingly separates it from 

the growth plate. This shows on X-ray as a 

coarsely structured transverse band, which remains demonstrable for several years (Wimberger, 1925:288-307). Similarly, a double ring of 

radiodensity appears on secondary ossification 

centers in healing (Wimberger's ring). 

Unfortunately, most of the changes of acute 

infantile scurvy have little chance of preservation 

in grave material due to the loss of the cartilage 

and soil disintegration of the infant bones. Possibly the changes of the orbital roof and remnants 

of incompletely remodeled fragmentation bands 

of healed scurvy may be of help in recognizing 

the disease. 

Adult Scurvy 

Already in older children, skeletal changes in 

scurvy are of a minor nature reflecting the slowed 

growth rate. In adults, skeletal changes are restricted to transverse fractures at the osteocartilaginous junctions of ribs (Aschoff and Koch, 

1919:53). 

PALEOPATHOLOGY 

In view of the problems in diagnosing scurvy 

in dry skeletal specimens, it is not surprising that 

the paleopathological literature contains little evidence of this disease. Wells (1964a: 118-119) 

states that edentulous jaws associated with alveolar osteitis often found in European medieval 

cemeteries are examples of scurvy. He further 

states that ossified subperiosteal hematomas of 

the long bones are often found in such cemeteries 

in association with exfoliation of teeth. Both these 

conditions, in Well's opinion, point to a high 

incidence of scurvy in European medieval populations. 

Wilson (1967:193, 194) finds evidence of scurvy 

in some of the ancient texts of Mesopotamia and 

Palestine. The description of a disease known as 

"the stinking disease" combined with the loss of 

teeth, as well as the possible use of wine as a cure, 

certainly support a diagnosis of scurvy whose 

clinical features include foul breath and loss of 

teeth. 

In the New World, early explorers suffering 

from scurvy encountered Indian tribes who 

treated the disease with a drink made by boiling 

bark and leaves in water (van Wersch, 1954:10-

11). The extent to which this knowledge was 

widespread is not known. However, the existence 

of a treatment certainly suggests the presence of 

the disease. 

Paleopathological evidence of scurvy in the 

New World has been reported by Saul (1972:56-

66), who attributes the existence of expansive 

lesions of the diaphysis of long bones and the 

antemortem loss of teeth to scurvy. The skeletal 

material is from the pre-Columbian Mayan site 

called Altar de Sacrificios in Guatemala. Saul 
NUMBER 28 273 

supports his conclusion by citing sources that 

indicate that the amount of vitamin C in contemporary Maya Indian diet is deficient and in the 

past many Indians died from scurvy. 

The lesions in Saul's figures are nonspecific and 

are more compatible with a diagnosis of infectious 

disease or trauma. The antemortem tooth loss 

seen in Saul's figures 40 and 41 is from a specimen 

whose age he estimates to be 60+ years. The 

pattern of alveolar resorption is more typical of 

tooth loss due to caries and abscess. The anterior 

teeth of the mandible are present as well, a condition that would be unlikely if the molar tooth 

loss was due to scurvy. 

Hooton (1930:317) suggested that porotic hyperostosis found in the Pecos skeletal material 

from the American Southwest is due to scurvy or 

rickets. Cranial involvement in scurvy is not as 

common as that found in the long bones. Barlow 

(1883:169) however, noted porous lesions of the 

external skull vault in association with at least 

one case of scurvy and reported (1883:168) abnormal conditions in the crania of 8 cases in a 

sample of 31 scorbutic infants and children. 

There remains a problem in ascribing porous 

lesions of the skull to scurvy. It is a well-documented fact that scurvy and rickets frequently 

occur in the same case (Follis, Jackson, and Park, 

1940:745). The presence of one disease does seem 

to have an inhibiting effect on the expression of 

the other disease. The question of which disease 

is dominant is unresolved. Based on histological 

evidence, Follis, Jackson, and Park (1940:746) 

suggest that "vitamin D deficiency certainly inhibits vitamin C deficiency from expressing itself .. . "I n contrast Park, Guild, Jackson, and 

Bond (1935:286) offer the opinion that, since 

vitamin C deficiency inhibits osteoid formation, 

the expression of rickets would be inhibited by 

scurvy. It is also possible that scurvy could be 

found in association with anemia (Goldberg, 

1963:51) and that porous lesions of the skull are 

caused by anemia rather than scurvy. 

The experimental evidence suggests that hemorrhage from scurvy with the associated bone 

formation is seen only following trauma (Park, 

Guild, Jackson, and Bond, 1935:276; Follis, 1943: 

580). In a subsequent publication Follis (1948: 

140) states that "subperiosteal hemorrhages develop as a result of trauma and normal stress and 

strain." Whether the normal stresses and strains 

to which the head is subjected in the infant or 

young child is sufficient to trigger bleeding, which 

could give rise to a large porous lesion, must 

remain an open question. Although Fraenkel did 

not note skull vault lesions in his report of scorbutic autopsied cases, he did note the development of porotic, hypertrophic bone in the orbital 

roof (Fraenkel, 1929:228-229). The association of 

both these features with scurvy needs further 

confirmation. However, it would seem prudent to 

consider scurx^^ as a possibility when such a lesion 

is encountered in archeological specimens. 

Vitamin D Deficiency 

PATHOLOGY 

Rickets 

Rickets is a systemic disease of early childhood 

extensively affecting the skeleton, but without 

direct mortality. It is caused by inadequate availability of effective vitamin D, which is essential 

in the mineralization process of the organic matrix of bone (osteoid). Dietary vitamin D is transformed in the liver into the active compound. 

Precursors of vitamin D taken with the food 

are transformed in the skin under the influence 

of the ultraviolet fraction of sunlight. This explains the prevalence of rickets in populations 

climatically (high latitudes) or mechanically 

(crowded cities, occlusive clothing) deprived of 

sunlight. However, it should be appreciated that 

the darkly pigmented races are not fully benefited 

by tropical sunshine, because most of the ultraviolet rays are absorbed by the skin melanin 

pigment. The main causative factor remains the 

inadequate intake of vitamin D and its precursors. 

Rickets was not well documented by written 

descriptions until the sixteenth or seventeenth 

century. From then on, increasing attention has 

been paid to this common disease of early childhood, especially in northern Europe and North 
274 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

America. There was a marked increase of frequency with industrialization and metropolitan 

crowding. Figures for autopsy material in Dresden, Germany, show that 89 percent of all children between 2 months and 4 years of age exhibited evidence of active or healed rickets 

(Schmorl, 1909:437). Clinically, 97 percent of 

young children had evidence of rickets in Vienna 

(Escherich, 1899, cited in Hess, 1929:48) and, as 

late as 1921, Hess found 75 percent of the children 

in New York City affected by rickets (Hess, 1921: 

697). The disease occurs worldwide with varying 

frequency. 

Rickets rarely begins before 4 months of age 

because vitamin D passes from the mother to the 

fetus through the placenta and is stored in the 

liver of the infant. The highest frequency is observed between 6 months of age and 2 years in 

the sunless winter months. Only a few new cases 

develop after 4 years of age. The manifestations 

are earliest seen and most marked on the rapidly 

growing areas of the skeleton: osteocartilaginous 

junctions of ribs, distal metaphysis of femur, radius and ulna, and proximal humerus (Wimberger, 1925:269-288). The changes at the growth 

plate consist of lack of preparatory calcification 

of the columnar cartilage and of the newly deposited bone matrix (osteoid). Since the proliferation of cartilage and the formation of bone 

matrix by osteoblasts continues at close to normal 

levels, both uncalcified cartilage, which cannot 

be resorbed, and unmineralized osteoid pile up 

next to the growth plate. In the ribs this results in 

a rounded nodular swelling of the osteocartilaginous junction, the "rachitic rosary," and, in long 

bones, in a broadening and cup-shaped depression of the metaphysial areas. Since the intramembranous bone formation is affected equally 

to the enchondral one, the rapidly growing and 

expanding cranial vault of the infant becomes 

increasingly replaced by nonmineralized osteoid 

giving rise to areas of thinning and softening 

(craniotabes). This actually precedes recognition 

of the changes in the long bones in acute rickets 

(Hess, 1929:208). 

The changes observed in rickets are threefold: 

direct effects of the metabolic disturbance, deformities secondary to the vulnerability and pliability of the poorly mineralized skeleton, and 

retardation of growth. 

Rachitic and Postrachitic Changes 

in Individual Bones 

SKULL.—In active infantile rickets the cranial 

vault may develop thin and soft areas, especially 

in the posterior lateral portions of the parietal 

bones and of the occipital squama (craniotabes). 

This is due to the rapid remodeling of the infant 

skull to accommodate the growing brain, replacing mineralized bone with osteoid. This is not to 

be confused with the incomplete ossification of 

the entire cranial vault in premature infants or 

with the congenital lacunar skull often complicating spina bifida, in which sharply marginated 

multiple defects in various areas of the cranial 

vault are present. Craniotabes may lead to permanent posterior flattening or lateral and asymmetrical deformities of the skull, due to pressure 

of the head against the supporting surface in the 

lying position. The closure of the fontanels is 

delayed in rickets. In cases where long-standing 

thickening of the cranial vault is seen, especially 

in older children, mainly due to external (occasionally also internal), subperiosteal bone deposition, the external deposition often spares the 

center of the parietal and frontal tubera 

(Schmidt, 1929:32) (Figures 417-420). In this process of remodeling, the outer and often the inner 

table as well disappears, so that the entire thickness of the cranial vault has the porous appearance of diploe (Figures 421-423). The weight of 

the head may cause the bone surrounding the 

foramen magnum of the softened skull base to be 

pushed upward, diminishing or effacing the angle 

of the clivus (Schmidt, 1929:60). Similar subperiosteal deposits can occur on the facial bones 

(Figures 424-426). 

LONG BONES.—The frequent combination of 

hypovitaminosis D and general malnutrition 

leads to a combination of rickets and osteoporosis, 

resulting in the so-called porotic form of rickets, 
NUMBER 28 275 

FIGURE 417.—Moderate rickets of cranium showing fine 

porotic bone deposition on frontal and parietal bosses. (7-

month-old female, PMUG 2465, autopsy 6115 of 1874.) 

characterized by brittle thin cortex and sparse 

cancellous trabeculae. In otherwise well-nourished infants, however, the deposition of massive 

osteoid, periosteally and endosteally, results in 

the plump bones with narrowed medullary spaces 

of the hyperplastic form of rickets. In the porotic 

form, stress fractures, especially in the diaphysis, 

are common, leading to axial deformities (Wimberger, 1925). In this type, bending deformities 

due to the flexibility of the undermineralized 

bones, with or without additional stress fractures, 

are common. 

The growth is slowed down in active rickets, 

but the development of secondary epiphysial ossification centers is not delayed (Wimberger 

1925). The most marked shortening is seen on the 

femur (Schmidt, 1929:73). The most characteristic change of a long bone is the flaring of the 

frayed metaphysial cortex and cupping of the end 

of the metaphysis. 

Periosteal deposition of osteoid, which is mineralized in the healing process, is common. GenFIGURES 418. 419.—Rachitic skull: 418, Outer table, parietal 

bone, showing porous periosteal bone. 419, Cut surface, 

showing subperiosteal fine cancellous bone externally and 

internally. (About 1-year-old female, FPAM 3874 from 

1881.) 

erally, these deposits are thickest at middiaphysis, 

giving the shaft the appearance of a column, 

without the usual tapering to the middle 

(Schmidt, 1929:33). These subperiosteal bone deposits show some characteristic distribution in 

different bones (Pommer, 1885). On the ribs, they 

are limited to the anterior surface and the margins, leaving the pleural surface free. On the 

femur, the deposits are heavier on the posterior 

than on the anterior surface. On the tibia, the 
276 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

FIGURE 420.—Cranial rickets, left lateral view, showing porous subperiosteal bone deposition, mainly of parietal boss, 

focally transformed into a new outer table. (About 6- to 8-

month-old female, DPUS 5216.) 

FIGURE 422.—Rachitic calvarium, cut surface, showing external and internal deposition of subperiosteal cancellous 

bone. (About 2 years of age, FPAM 5051 from 1889.) 

FIGURE 421.—Rachitic calvarium showing subperiosteal 

bone deposition with pronounced vascular pattern on right 

parietal boss. The dried periosteum appears dark. (7-monthold female with rickets and scarlet fever, DPUS 5212 from 

1904.) 

FIGURE 423.—Rachitic calvarium, cut surface, showing porous hyperostosis with obliteration of outer and partial obliteration of inner table. (2-year-old male, FPAM 2694 from 

1858.) 
NUMBER 28 277 

FIGURES 424, 425.—Rachitic skull with slight hydrocephalus: 

424, Frontal view, showing slight deposition of periosteal 

bone on glabella, maxilla, and mandible. 425, Top view of 

calvarium, showing periosteal bone focally consolidating 

into a new outer table on the parietal bosses. (3 to 6 years of 

age, ANM 2126 from 1866.) 

FIGURE 426.—Rachitic cranium, frontal view, showing fine 

subperiosteal bone deposition on glabella, facial bones, and 

orbital roofs. (3 to 6 years of age, ANM 2127 from 1866.) 

deposits locate on the posterior and on the medial 

surface, leaving free the lateral surface that faces 

the fibula. 

In severe and protracted or recurring cases, 

characteristic deformities develop, secondary to 

the static and dynamic stresses. After healing, 

these bending deformities largely remain for the 

rest of the life of the individual (Figure 427). 

When the deformities develop in the active phase, 

an alteration of the distribution of subperiosteal 

bone is observed. This alteration consists of increased deposition on the concavity of the deformity, in response to the altered stresses. These 

deposits may be locally accentuated by addition 

of callus over stress fractures, forming ridges or 

lumpy projections (Recklinghausen, 1910(1):213-

215). Such fractures occur most often in the dia-
278 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

FIGURE 427.—Postrachitic deformity of left leg. (Adult, 

V M 106 from 1876.) 

physis, seldom in the metaphysis (Wimberger, 

1925) (Figure 428). They often transect only the 

cortex on the concave side and their margins may 

project into the medullary canal (Recklinghausen, 1910(1):213-215). 

In the infant, before walking, bending deformities of the humerus and forearm occur, depressing the humeral head medially downward and 

bending the shaft laterally and forward (humerus 

varus) (Figures 428, 429). Later, after assumption 

of upright gait, deformities of the long bones of 

the lower extremity prevail. The femur usually 

shows downward bending of the neck (coxa vara), 

seldom the opposite increase of the neck angle 

(coxa valga). The femoral shaft usually bends at 

the lower metaphysis with an anterolateral convexity. The tibia also usually shows anterior bowing at the lower metaphysis, and the fibula has to 

follow with a similar deformity because of its firm 

fixation to the tibia. Rarely medial bending of 

the lower tibial metaphysis occurs (Schmidt, 

1929). 

Minor deformities can disappear due to corrective postrachitic growth. Major deformities become permanent and are followed by characteristic remodeling changes. The bent bones show a 

decreased transverse and increased anteroposterior diameter. The cortex of the convexity is 

markedly decreased and the cortex of the concavity is greatly increased. There is complete alteration of the trabecular pattern with new trabeculae 

crossing the medullary cavity in a radial arrangement, CO verging to the concavity of the curve 

(Putschar, 1937:695-700). At this final stage it 

cannot be recognized whether the deformity was 

mainly caused by bending or by stress fractures 

or whether it occurred in the metaphysial or 

diaphysial portion. 

RIBS.—The ribs may show flattening of their 

curves, secondary to bending of the rib cartilages 

at the osteocartilaginous junction. This leads to 

a forward bending of the sternum, giving the 

pigeon breast deformity (pectus carinatum). In 

severely malacic rickets, lateral depression of the 

rib contour may occur, secondary to the pressure 

of the arms (Putschar, 1937:600). 

VERTEBRAE.—In severe rickets, the vertebrae 

may appear of decreased height due to compression, often combined with a deeper scalloping of 

the end-plate. Although kyphoscoliosis may develop after rickets, major abnormal curvatures 

are usually lacking in the active phase. 

PELVIS.—The pelvis is more affected by altered 

growth than by mechanical deformation. The 

typical rachitic pelvis, during the active disease, 

is smaller and plumper than normal but does not 

show the disproportions of the adult postrachitic 

pelvis (Breus and Kolisko, 1900-1911(1) :440-

441). The typical postrachitic flat pelvis is characterized by an anteroposterior narrowing of the 

pelvic canal, mainly due to deficiency of growth 

of the iliac portion of the pelvic ring (Figure 430). 

The maximal growth period of this portion, especially from its posterior growth cartilage, falls 

into the infant period and is not made up later 
NUMBER 28 279 

FIGURES 428, 429.—Severe malacic rickets with very light, porous bones: 428, Both arms and 

shoulder girdle with bending deformities and healing stress fractures of all bones. 429, Close-up 

of left hand. (About 2 years of age, ANM 3334 and 3335.) 

FIGURE 430.—Rachitic flat pelvis. (32-year-old female, 

VM 2 from 1860.) 

while the maximal growth of the pubic bones 

falls into later childhood and adolescence. Therefore, the transverse diameter of the pelvic canal 

is not diminished and the pelvis appears flattened. 

Posteriorly also, the transverse diameter of the 

sacrum is not significantly affected (Breus and 

Kolisko, 1900-1911(1) :469-476; Putschar, 1939: 

483-492, 509-512). The sacrum tends to protrude 

more into the pelvic canal and the acetabula face 

more forward than normally. 

In surveying all described findings, it seems 

obvious that many of the features of active rickets 

will not be recognizable in skeletal material after 

loss of the cartilage and disintegration of unmineralized osteoid. Craniotabes and the flaring 

distortion and cupping of metaphysial ends of 
280 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

long bones and sternal ends of the ribs would 

have the best chance of being preserved. However, postrachitic deformities of the various bones 

of the skeleton would be readily recognizable. 

Late Rickets 

Rickets developing or recurring in later childhood and adolescence, at a time when bone 

growth has slowed down greatly, is more characterized by severe mechanical deformities than by 

changes at the growth plate resulting in deficient 

or altered growth. These deformities are essentially identical with those of adult osteomalacia. 

Osteomalacia 

The etiology of osteomalacia is identical with 

that of rickets—vitamin D deficiency. The difference in the manifestations is due to the fact that 

in the adult the skeleton is no longer growing; 

therefore, various changes on the cartilage and 

bones of the growth plate, which dominate the 

picture of rickets, are no longer present. As in 

rickets, the bone matrix formed during the disease 

remains uncalcified (osteoid). The first radiological changes are a diffuse diminished density of 

the otherwise normal-appearing skeleton, not distinguishable from osteoporosis. In dry bone the 

light weight and cardboard-like consistency is 

noted (Figure 431). Depending on the remodeling 

rate, it takes considerable time before the skeleton 

is sufficiently weakened to show radiolucent zones 

in mechanically stressed areas, due to replacement of the mineralized bone with osteoid 

(Looser, 1920; Milkman, 1930). In severe and 

protracted cases, mechanical deformation of the 

skeleton, due to fractures and pliability, dominate 

the picture (Figures 432, 433). 

In the causation of osteomalacia, in addition 

to vitamin D deficiency, general malnutrition, 

especially deficiency of protein and fat, and low 

intake or loss of calcium and phosphorus, play an 

important role. This explains the great prevalence 

of the disease in the female, particularly between 

20 and 40 years of age. Numerous closely spaced 

pregnancies and protracted lactation are a heavy 

drain on the mother of bone mineral and vitamin 

D. This loss to the fetal skeleton and, through the 

milk, to the infant is a significant factor in the 

pathogenesis of puerperal osteomalacia. 

The disease used to be common in Europe in 

crowded cities and under poor economic conditions. Numerous cases have been reported from 

China and I have seen, even recently, many cases 

in India. There, skin pigmentation, shrouding 

clothing, and seclusion of women indoors (purdah) still contribute to the prevalence of the 

disease, in addition to the other factors enumerated above. 

Although the deficiencies affect the entire skeleton, the most marked changes are observed in 

the bones that contain mostly cancellous bone 

and, therefore, have the highest remodeling rate. 

These are the ribs, sternum, vertebrae, and pelvis 

(Figures 434, 435). The skull and the solid cortices 

of the long bones of the extremities have a low 

remodeling rate. Therefore, deformities of osteomalacia rarely occur in these bones except in 

young, still growing individuals (late rickets and 

juvenile osteomalacia). 

The specific change of osteomalacia is the deposition of unmineralized osteoid on the trabeculae 

of old bone and the replacement of resorbed old 

bone with osteoid. However, in contrast to rickets, 

subperiosteal deposits do not occur. 

Looser-Milkman zones of great radiolucency, 

often followed by stress fractures only transecting 

the overburdened cortex, occur in characteristic 

locations and often symmetrically. The predilected areas are the ribs, the medial cortex of the 

neck of the femur and of the humerus, the pubic 

rami, and the lateral margin of the scapula. In 

many instances multiple such stress fractures occur in each area. In healing, internal and external 

callus is formed, which ultimately mineralizes. 

The osteomalacic deformities are usually restricted to the trunk skeleton. The vertebrae are 

flattened with accentuated cupping of the endplates and dense trabeculae. There is angular 

kyphosis in severe cases, often at the level of the 

eighth or ninth dorsal vertebra, occasionally combined with a scoliotic curve (Jaffe, 1972:401). The 
NUMBER 28 281 

spinal deformity alters the shape of the thorax, 

which becomes deep and laterally narrowed. The 

ribs show a decreased curvature and the sternum 

is angulated and pushed forward. In very severe 

cases the ribs may, in addition, show inward 

bending, laterally, due to the pressure of the arms 

(Figure 436). 

The most marked and most characteristic deformation is observed on the pelvis in puerperal 

osteomalacia (Figure 436). The fourth or fifth 

lumbar vertebral bodies descend and protrude 

into the pelvic canal. The iliac wings are rolled 

and folded inward. The pubic rami are pushed 

together with the symphysis pubis projecting, 

beak-like, forward. The ischial tubera are bent 

medially and the acetabular floors protrude inward. The sacrum is bent angularly forward in 

the lower portion (Figure 437). All these deformities narrow and partly obliterate the pelvic canal, 

reducing it to a cloverleaf-shaped space (Breus 

and Kolisko, 1900-1911(2) :50-62; Putschar, 

1939:535-540). Deformities of the long bones of 

the extremities are much less common. They 

consist most often of downward bending of the 

neck of the femur (coxa vara) or of the humerus. 

Deformities of the shafts of these bones are rare 

and due more to fractures than to pliability. 

FIGURE 431.—Skull with severe active osteomalacia. Notice 

the diffuse porosity of the cortical surface; cardboard-like 

bones of very low weight. (20-year-old Italian male with 

multiple fractures, ANM 2125 from 1865.) 

FIGURES 432, 433.—Angulated healed stress fracture in osteomalacia of right femur: 432, Surface view showing the 

unbroken cortex on the convexity and callus on the concavity. 433, Cut surface showing thin cortex and sparse cancellous bone. (ANM 3292.) 
282 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

FIGURE 436.—Osteomalacic skeleton with severe pelvic and 

thoracic deformity. Notice the rib deformities caused by the 

weight of the arms, the angulated protruding sternum and 

the folded iliac wings. (Adult female, died after seventh 

pregnancy, PMES 1 (QAM(l).) 

FIGURES 434, 435.—Active osteomalacia: 434, Pelvis and 

lumbar spine, showing maximal malacic deformity of the 

cardboard-like bones and delayed fusion of growth plates. 

435, Calvarium, showing fine pitting and slight periosteal 

bone formation on the outer table. (18-year-old male with 

bending deformities of most bones, DPUS 7664c and 7664d 

from 1896.) 

FIGURE 437.—Severe osteomalacia with angular kinking of 

sacrum from sitting. (43-year-old female, FPAM 5676.) 
NUMBER 28 283 

Although the osteoid of the active phase would 

not survive burial, the characteristic deformities 

that remain, even after healing and restored mineralization, will be readily recognizable. 

Skeletal Changes Resembling Rickets and Osteomalacia 

Excessive loss of dietary vitamin D due to 

inability of resorption from the intestines will lead 

to the changes of rickets or osteomalacia, depending on the age of the patient. Such conditions are 

celiac disease and nontropical sprue, chronic biliary stasis and biliary fistula. In the first, the fatsoluble vitamin D is eliminated with the fatty 

diarrheic stools; in the others, the bile salts necessary for the resorption of vitamin D are not 

present in the gut. 

A group of syndromes characterized by various 

congenital defects in the renal tubules concerning 

excretion and reabsorption of different substances 

also, ultimately, affect the metabolic integrity of 

the skeleton (refractory or vitamin D-resistant 

rickets). The changes, when they occur, are essentially identical with rickets or osteomalacia, the 

only difference being that they do not develop 

until later childhood or adulthood. In those conditions in which various amino acids are lost 

through faulty renal excretion on a genetic basis, 

in addition to and preceding the manifestation of 

rickets or osteomalacia, one may observe severely 

inhibited growth (dwarfism) and severe osteoporosis leading to pathological fractures because of 

the inability to produce adequate amounts of 

organic bone matrix. 

PALEOPATHOLOGY 

Wells (1964a: 116-117) expresses the opinion 

that medieval European towns and the "perpetual twilight of dark tenements," in the city slums, 

which were a prominent feature of cities during 

the Industrial Revolution, were the major factors 

in the marked increase of rickets associated with 

this phase of human history. Evidence of rickets 

in other geographical areas and other time periods is not common. 

Hrdlicka (1907:540) stated that in North 

America rickets did not occur in prehistoric indigenous groups. Snow (1948:508) describes a 

possible case of rickets in an 8-month-old infant 

(Burial 633, Indian Knoll site, Kentucky, USA). 

However, the description of features that lead to 

this conclusion is not convincing. Snow does not 

report any evidence of deformity in the long 

bones. He bases his conclusion on the presence of 

"swollen spongy extremities" in the smaller long 

bones and abnormal sternal ends of ribs. Since 

these are areas of active growth and consequent 

remodeling, they would normally appear somewhat spongy. In view of the lack of evidence of 

rickets in other North American skeletal series, 

this case should be reevaluated. 

In the Old World, Wood-Jones (1910b:263) 

found no evidence of rickets in ancient Egyptian 

skeletal material. Virchow (cited in Pales, 1930: 

40) thought that the distinctive features of European Neanderthal skulls were due to rickets. This 

possibility has not, however, received serious consideration by subsequent scholars who have studied the Neanderthal skeletons. In the Winchester 

Saxon collection of paleopathological specimens 

(BMNH CG 1966, no number) is a case of medieval healed rickets in a child about 6 years of 

age. The specimen consists of the right femur, 

tibia, and fibula. Anterior bowing is most pronounced on the femur and tibia (Figure 438). 

Another example of healed rickets is from the 

Royal College of Surgeons of England pathology 

collection at the British Museum (Natural History). The case is from the Ludgate Hill site in 

England (No. 1961, 5, 12, 5). The specimen is a 

right femur from an adult. There is marked anterolateral bowing with anteroposterior flattening 

and a buildup of bone along the linea aspera 

(Figure 439). 

An example of rickets is found in the skeletal 

collections of the Historical Museum in Chur, 

Switzerland. The specimen is from the medieval 

archeological site of Bonaduz in canton Grissons, 

Switzerland. The skeleton in question is a male, 

probably over 50 years of age. The only evidence 

of deformity is seen in the tibiae. Both the right 

and left tibiae show bowing with an increased 
284 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

FIGURE 438.—Healed rickets in the right leg of a child about 

6 years of age. Note that the interosseous line of the tibia is 

curved. (BMNH CG 1966, no number; scale in cm.) 

FIGURE 439.—Healed rickets in an adult femur. (BMNH, 

Ludgate Hill No. 1961, 5, 12, 5.) 

anteroposterior diameter of the midshaft and a 

very prominent anterior edge (Figure 440). 

Osteomalacia must certainly have occurred in 

ancient times although the evidence for it is 

scarce. A probable example of osteomalacia is 

seen in an isolated sacrum from the Twelfth 

Dynasty, rock tombs at Lisht, Upper Egypt 

(NMNH 256470 PI). The sacrum is small in size 

and unusually light in weight. It appears to be 

from an adult female skeleton. There is a 90 

degree angle between the lower and upper portion of the sacrum (Figure 441) with the angulation primarily at the third sacral segment (cf 

Figure 437). 

Rowling (1967:275-278) describes a remarkable specimen from the Royal College of Surgeons of England pathology collection, which is 

stored at the British Museum (Natural History) 

(BMNH 178A). The specimen is from a predynastic Nubian and consists of the major bones of 

the arms and legs, the pelvis, and three lower 

lumbar vertebrae. The most striking feature of 

the specimen is the very extensive hypertrophic 

bone development on the femora. Rowling attributes this development to paraplegia with possible complications of rickets. 

The authors have also studied this specimen 

during our survey of pathological specimens in 

1974. In addition to the extensive hypertrophic 

bone associated with the femora, these bones 

show anterolateral bowing (Figures 442, 443). On 

the right femur, bowing is complicated by a 
NUMBER 28 285 

FIGURE 440.—Healed rickets in adult male tibiae. (HMCS 

GR 1352; no data.) 

fracture with displacement and overlap of the 

broken ends. Both tibiae and fibulae show anterolateral bowing of a severe degree with extreme 

flattening, particularly of the fibulae, and partial 

synostosis between the fibula and tibia in the 

distal portion of the right side. 

The humeri are straight but show a pronounced buildup of the deltoid insertion. Both 

radii and ulnae show severe lateral and anterior 

bowing with marked flattening and partial ossification of the interosseous membrane. Articular 

surfaces of all the long bones are normal. The 

pelvis is that of an adult male with a moderate 

deformity of the pelvic entrance, marked superior 

bulging of the acetabula, and greatly reduced 

subpubic angle (Figure 444). There is significant. 

FIGURE 441.—Abnormally angulated sacrum probably due 

to osteomalacia. Isolated specimen from Twelfth Dynasty, 

rock tombs, Lisht, Upper Egypt. (NMNH 256470 PI.) 

periosteal, bony buildup, particularly on the lateral aspects of both iliac bones. The sacrum is 

angulated in its midportion anteriorly with a 

pronounced, smooth, bony ridge below the second 

intrasacral foramina. 

The deformity of the long bones and pelvis 

illustrate typical changes in osteomalacia. The 

relationship of this disease with the exuberant 

development of bone, particularly on the femora, 

is not clear but is certainly not typical of osteomalacia. However, if Rowling's (1967:277) conclusion that the added bone is a result of paraplegia, osteomalacia could easily be a secondary 

effect of restricted outdoor activity due to paralysis. The unresolved problem with this hypothesis 

is that the bones of the leg show deformity indicating weight-bearing, which implies at least 

some ambulation involving the legs. While the 

sequence of events leading to this skeletal manifestation of disease may not be resolved, it is clear 

that osteomalacia did occur in geographical areas 

where it was theoretically unexpected. 
286 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 
NUMBER 28 287 

Hypophosphatasia 

PATHOLOGY 

This is a rare condition, only fairly recently 

recognized (Rathbun, 1948), in which alkaline 

phosphatase is deficient in varying degrees on a 

genetic basis. Since alkaline phosphatase is an 

essential factor in the calcification mechanism, 

changes indistinguishable from ordinary rickets 

ensue in this condition. In severe cases, this deficiency is operative in the fetal period, resulting in 

the birth of a dwarfed infant with deformed long 

bones, a poorly mineralized cranial vault, and all 

the appearances of active rickets. These children 

usually live for only a few days or are stillborn. If 

the deficiency is of a lesser degree, rachitic 

changes may not develop until later childhood. 

These individuals survive with minor skeletal 

changes, of which osteoporosis is more obvious 

than rachitic stigmata. However, occasionally 

they do develop craniosynostosis (Jaffe, 1972: 

440). (For a comprehensive discussion of this 

condition see Currarino, Neuhauser, Reyersbach, 

and Sobel, 1957). 

444 

FIGURES 442-444.—Deformed long bones and pelvis from 

osteomalacia with hypertrophic bone development of long 

bones perhaps developing as a complication of paralysis: 

442, Deformity of ulnae, femora, and tibiae. The humeri are 

not bent. 443, Posterior view of femora. 444, Superior view 

of pelvis; note the deformity of the iliac bones and the 

greatly reduced subpubic angle. (BMNH 178A, Nubian 

Pathology Collection; scales in cm.) 

Starvation 

PATHOLOGY 

Extreme prolonged malnutrition, especially 

protein deficiency, leads to a complete arrest of 

growth in the young individual that cannot adequately be made up later, resulting in stunted 

stature (Follis, 1948:9). In the adult, severe dietary restrictions can result in "hunger osteopathies," as observed after the First World War 

(Edelmann, 1919; Partsch, 1919; Beninde, 1920; 

Dalyell and Chick, 1921) and in inmates of European concentration camps in the Second (Maratka, 1946). The changes mainly affected the 

spine and occurred in both men and women, 

mostly in the second half of life. Such changes 

consisted of severe osteoporosis with some overlay 

of osteomalacia. 
288 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

FIGURE 445.—Fluorosis, showing severe generalized periosteal hyperostosis of fibula, lumbar vertebrae, rib, talus, first 

metatarsal, and right femur, which shows a healed pathological fracture. (Adult Asian Indian male, studied by Putschar in 1965 at Department of Pathology, Guntur, India.) 

FIGURE 447.—Severe fluorosis. X-ray of cross-section of femur, showing massive subperiosteal bone deposition and 

some intracortical resorption. (Adult Asian Indian male, 

courtesy Dr. Niranjan Das Aggarwal, Rajendra Hospital 

and Medical College, Patiala, India.) 

FIGURE 446.—Fluorosis with generalized periosteal hyperostosis. Notice the almost complete bony bridging of the 

interosseous membrane of the right forearm. (Adult Asian 

Indian male, studied by Putschar in 1965 at Department of 

Pathology, Medical School of Guntur, India.) 

Fluorosis 

PATHOLOGY 

In certain areas of the world (Texas, USA, 

Iran, India, Taiwan) the surface water may have 

an unusually high fluorine content. The longstanding intake of high levels of fluorine can 

affect the structure and appearance of bone and 

teeth (Johnson, 1965). Fluorine can assume the 

position of the hydroxyl radical in the apatite 

crystal of mineralized tissues. In addition to the 

formation of abnormal apatite, fluorine has a 

toxic effect on the cells. The first noticeable effects 

of fluorosis are abnormalities of dental enamel, 

which, like bone, is mineralized by apatite crystals. It is mostly teeth of the second dentition, 

which are being formed during childhood, that 
NUMBER 28 289 

are affected. Such teeth show spotted enamel 

consisting of small, round, discolored and pitted 

areas in the otherwise shiny and white enamel 

surface. Bone changes are only observed in longstanding and severe cases (Flemming M0ller and 

Gudjonsson, 1932; Sankaran and Gadekar, 1964). 

Fluorine stimulates periosteal and endosteal bone 

formation, but the bone produced is microscopically and mechanically abnormal. Externally, exaggeration of insertions of muscles and ligaments 

are noted by addition of bone-forming irregular 

excrescences (Figure 445). There is marked accentuation of the linea aspera of the forearm and 

lower leg (Figure 446). The ribs and vertebrae 

show ridges and icicle-like, bony excrescences into 

the intercostal muscles and paraspinal ligaments. 

There is considerable subperiosteal and endosteal 

bony accretion, often accompanied by increased 

resorption in the old cortex on long bones (Figure 

447). The fluorosis bone is mechanically inferior 

and pathological fractures occur. 

Osteoporosis 

PATHOLOGY 

Senile osteoporosis represents a condition of 

significantly diminished bone mass due to longstanding imbalance between bone resorption and 

bone formation. With increasing age, bone formation lags more and more behind bone resorption thus diminishing the entire bone mass. This 

leads imperceptibly into osteoporosis, which most 

observers arbitrarily define as a loss of 30 percent 

of bone mass or more. Osteoporosis usually does 

not manifest itself before the fifth decade and is 

more frequent and more severe in the female than 

in the male. This, at least in part, reflects the 

sharp drop in estrogens at menopause as compared with the slow steady decrease of testosterone in the aging male. However, comparative 

statistical studies between affluent industrialized 

populations and primitive populations requiring 

strenuous physical activity from both sexes, indicate that the mechanical forces play a great role 

in the development of senile osteoporosis. Severe 

osteoporosis, as measured by the incidence of 

fractures of the femoral neck, was highest overall 

and showed the greatest female prevalence in 

Sweden and the least in the Bantus (Chalmers 

and Ho, 1970). 

Osteoporosis does not affect the entire skeleton 

evenly. Since the greatest physiological turnover 

of bone occurs in cancellous bone, the bones rich 

in spongiosa are most involved in osteoporosis. 

The bones of the trunk, such as the spine, ribs, 

sternum, and pelvis, are most severely affected by 

osteoporosis. Of the large bones, the heavily burdened femoral neck, which also mainly depends 

for its integrity on the trabecular architecture, 

shows the most characteristic changes. The skull, 

especially the calvarium, participates very little 

in senile osteoporosis. This may be, at least in 

part, due to the continued mechanical stresses of 

chewing. 

T H E CANCELLOUS BONES.—The vertebral bodies usually show osteoporosis first and most severely. The normal dense vertical and transverse 

trabecular system becomes reduced. In this process the transverse trabeculae are more affected 

than the vertical ones. The trabeculae are not 

only diminished in number but also in size. In 

late stages of osteoporosis the few remaining vertical trabeculae may become reinforced (sclerotic 

atrophy). Although the bone is normal in matrix 

structure and mineralization, the diminished 

quantity creates mechanical instability. If the 

intervertebral discs retain their normal turgor, 

they will bulge the thinned vertebral, bony endplates, creating the picture of so-called "fish vertebrae" (Figure 448). If the intervertebral discs 

are degenerated, this deformity of the vertebral 

body does not occur in spite of severe osteoporosis. 

Compression fractures resulting in flattened or 

wedged vertebrae are common, the latter resulting in secondary kyphosis. The other cancellous 

bones show similar changes characterized by rarefaction of the spongiosa and pronounced cortical 

thinning. The ribs also often exhibit multiple 

osteoporotic fractures which, however, heal with 

good callus response. 

T H E LONG BONES.—Since the physiological 

turnover in cortical bone is much slower and less 

than in cancellous bone, the long bones, with 

predominantly cortical bone, are later and less 
290 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

FIGURE 448.—Severe osteoporosis. Sagittal section of "codfish" vertebra (left) compared with normal vertebra (right). 

(Department of Pathology, MGH, no number.) 

affected by senile osteoporosis. The resorption of 

the cortex proceeds in two patterns: the endosteal 

resorption, which leads to increased diameter of 

the medullary cavity, and the intracortical resorption, resulting in increasing numbers of unfilled or only partly filled Haversian resorption 

spaces. The latter process results in increasing 

porosity and lamination of the cortex which, in 

extreme cases, may assume a cancellous appearance, especially in advanced arteriosclerotic peripheral vascular disease. 

The frequency of pathological fractures of the 

neck of the femur (subcapital or transcervical) in 

advanced osteoporosis requires a discussion of the 

underlying structural changes in this area. The 

normal trabecular architecture of this eccentrically loaded, weight-bearing bone shows three 

trajectorial systems to distribute and absorb static 

and dynamic mechanical stresses: (1) The one 

system arising from the lateral cortex and (2) the 

system from the medial cortex (calcar), cross each 

other at right angles and terminate in the femoral 

head; (3) the third system, crossing the other two, 

arises from the area of the lesser trochanter, and 

terminates in the greater trochanter. It is particularly this third structure that first disappears in 

osteoporosis, accompanied by resorption of some 

of the other two trajectorial systems. This results 

in a roughly triangular area of the neck of the 

femur with sparse or absent bony trabeculae 

(Ward's triangle). This structural weakening precedes the pathological fracture, which often terminates in nonunion (pseudarthrosis) and aseptic 

necrosis of the femoral head. Impacted fractures 

may heal with shortening and widening of the 

neck of the femur. 

Widespread osteoporosis may also be a secondary phenomenon in other conditions affecting the 

formation and resorption of bone. In osteogenesis 

imperfecta, inhibited osteoblastic activity but 

normal osteoclastic activity results in generalized 

osteoporosis. In Cushing's syndrome, the overproduction of adrenal corticosteroids likewise suppresses protein synthesis and, thus, bone matrix 

production. These conditions are discussed elsewhere (pp. 305, 337). 

Localized osteoporosis is a frequent result of 

removal of mechanical stresses because of disuse, 

pain, trauma, infection or disturbed innervation 

(Figures 449, 450). In some cases posttraumatic 

osteoporosis can develop rapidly and out of proportion to the trauma (Sudeck's atrophy). This 

condition is, at least in part, caused by neurovascular changes affecting the circulation in bone, as 

demonstrated by the fact that the symmetrical 

uninjured area of an extremity may also show 

increased bone resorption. 

Brief mention should be made of the occurrence of a peculiar symmetrical bilateral atrophy 

of the parietal bones. In this condition a large flat 

depressed area covered by a thin external table is 

observed. It is mainly the diploe that is diminished or absent. The outer and inner tables may 

be contiguous and the cranial vault transparent 

on transillumination. In a few cases the resorption 

is complete, creating a large defect surrounded by 

inward-sloping exposed diploe. This must not be 

confused with unusually large parietal foramina 

that show a smooth cortical margin (Goldsmith, 

1922; Pepper and Pendergrass, 1936). The significance of the symmetrical parietal atrophy is not 

clear but is often thought to be related to senile 

osteoporosis (B. Epstein, 1953; Steinbach and 

Obata, 1957), while other observers attribute it 

to a developmental abnormality (Camp and 

Nash, 1944). 
NUMBER 28 291 

FIGURES 449, 450.—Extreme osteoporosis of right femur due to disuse and malnutrition. 449, 

External posterior view; notice reticulated perforations of metaphysial cortex. 450, Cut surface; 

notice paper-thin cortex and sparse trabeculae. (28-year-old female with tuberculosis of hip 

died in extreme cachexia, FPAM 4433, autopsy 81477 from 1884.) 

PALEOPATH O LOGY 

Osteoporosis, as manifested in the skeleton, 

involves two factors. The first of these is a reduction in the number and diameter of trabeculae 

accompanied by a thinning of cortical bone. The 

second factor is a change in osteon remodeling, 

in which the rate of refill of resorption spaces is 

diminished and the thickness of the osteon wall is 

reduced, leaving a larger central canal. Either 

one or both of these factors may be involved in 

what is seen as osteoporosis in dry bone specimens. 

In an archeological case of osteoporosis the 

external appearance of the bone may be normal. 

Often the first indication that the disease is present in a skeleton is the greatly reduced weight of 

the bones. However, more subtle forms of bone 

loss have been studied by obtaining data on the 

relative amounts of bone marrow space and cortical thickness. Dewey, Armelagos, and Bartley 

(1969) studied bone loss in three Nubian skeletal 

samples. The authors found that osteoporosis in 

women began earlier in life among the ancient 

Nubians than in modern Western samples. They 

suggest that inadequate calcium intake and extended lactation, rather than hormonal conditions, were major factors in explaining the differences in the onset of osteoporosis. 

Ericksen (1976) compared age-related changes 

in cortical thickness in three North American 

indigenous skeletal samples. In all three groups. 
292 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

bone loss in females was much greater than in 

males. She also found a difference between populations in the rate of bone loss with age. She 

concludes that environmental factors, rather than 

genetics, is the major factor in the differences, 

and she speculates that nutrition and physical 

activity may be important. 

Although the skull normally participates in 

osteoporosis to a lesser degree than other bones, 

alveolar resorption and thinning of the parietal 

bones do occur with increasing age. Lodge (1967) 

has described this condition in early Egyptian 

skeletal samples. He reports some support for an 

association between biparietal thinning and osteoporosis but concludes that other factors, such 

as a congenital predisposition, are probably involved. Stress from chewing may be another factor. 

An interesting case of female osteoporosis was 

found in an Early Bronze Age shaft tomb (3150-

3000 B.C.) at the site of Bab edh-Dhra in Jordan 

(NMNH, no catalog number. Tomb A lOOE, 

Burial 2). The estimated lifespan of the individual 

was in excess of 50 years. The skeleton is from a 

secondary burial and many of the smaller bones 

are missing. The remaining bones are very delicate and fragments have been broken off 

The most noticeable changes are in the pelvis 

and vertebrae. The sacrum, for example, weighs 

42 grams while another sacrum almost identical 

in size and from the same tomb chamber weighs 

68 grams. This indicates a loss in bone mass in 

the osteoporotic sacrum of about 38 percent. 

The gross size and shape of the vertebrae and 

pelvis are normal although there is a slight bulge 

in the pelvic canal from the femoral heads. The 

surface of the bone has patches of porous bone, 

particularly in areas adjacent to muscle or ligament attachments. 

Although the long bones are less severely affected, roentgen films of the humeri show cortical 

thinning and loss of density characteristic of osteoporosis. An additional complication in the 

bones of the lower legs is the presence of osteomyelitis. This condition is severe on the left tibia 

and fibula, where there is also evidence of an 

FIGURE 451.—Biparietal atrophy of the external table and 

diploe in an adult male skull from Peru, top view. (NMNH 

294027.) 

overlying ulcer on the distal shaft of these two 

bones. 

The bones of the skull and mandibles are normal given the age and sex of the skeleton. There 

has been little if any alveolar resorption and no 

biparietal thinning of the skull vault. Most teeth 

were lost or broken postmortem. Those that remain show unusually little wear but some evidence of caries. 

Biparietal atrophy is not common in archeological skulls. Two examples from the collections of 

the National Museum of Natural History, Washington, D.C, USA, serve to document the presence of this condition in both the New and Old 

World. The first of these (NMNH 294027) is a 

male skull from near Santa Lucia in Peru (Figure 

451). The archeological age is unknown. On the 

posterior portions of the parietals there is a large 

oblong depression in the outer table, measuring 

55 by 40 millimeters on both sides. The inner 

surface of the inner table is unaffected. The edges 

of the depressed lesion are smooth although there 

is still evidence of the exposed spongy bone. This 
NUMBER 28 293 

FIGURES 452-454.—Biparietal atrophy in an old male skull 

from the Twelfth Dynasty near Lisht, Upper Egypt: 452, 

Facial view. 453, X-ray of anteroposterior view. 454, Posterior view. (NMNH 256186.) 

suggests that the atrophic condition involves the 

outer table and diploe with, in extreme cases such 

as this one, some thinning of the inner table. 

There is no evidence of abnormal loss of bone 

thickness or density in other parts of the skull. 

The second example is a skull from the Twelfth 

Dynasty site near Lisht in Upper Egypt (NMNH 

256186). The skull appears to be from an old 

male. The oblong atrophic lesions are located in 

the posterior region of the parietals (Figures 452-

454). The depressions are smooth but show remodeled spongy bone. The lesions are even larger 

than those in the skull from Peru. The morphology of the atrophic depressions suggests a process 

that primarily involves the outer cortex and the 

diploe. The remainder of the skull is normal. 
294 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

Localized Hyperostosis 

PATHOLOGY 

Pregnancy Osteophyte 

There are a variety of syndromes characterized 

by formation of mostly periosteal bone. The first 

of these is pregnancy osteophyte. During and 

shortly after pregnancy, one commonly observes 

a thin, chalky layer of surface parallel periosteal 

bone on the inner surface of the internal table of 

the cranial vault, especially in the frontal area, 

and to a lesser extent on the cranial base. This 

layer does not exceed 0.5 millimeter in thickness 

(Henschen, 1949:62-64). Concomitantly, there 

may be osteosclerosis of the diploe (Haslhofer, 

1958). Burkhardt (1970:166-167) observed that 

the cranial vault is dense and heavy in pregnancy. 

These changes are apparently the result of altered 

pituitary hormone secretion. 

Internal Frontal Hyperostosis 

This is a common finding almost only occurring in aging females, particularly after menopause. Henschen (1949:85) estimates the female 

to male ratio of incidence close to 100:1. The 

lesion is usually restricted to the endocranial surface of the frontal bone but occasionally involves 

the temporal and parietal bone. The changes 

consist of marked thickening of the frontal bone, 

presenting a ridged buildup on the inner surface 

of considerable thickness. On cross-section much 

of the new bone is cancellous and has become 

part of the diploe. The inner surface shows a thin, 

but continuous, cortical layer. This alteration, 

which also is the result of changes in pituitary 

hormones after menopause, is frequent enough to 

serve as a means of sexing and aging in archeological material. (For a detailed discussion, see 

Henschen, 1949, and S. Moore, 1955.) 

Leontiasis Ossea 

This is a rare condition in which long-continued excessive bone formation on the cranial and 

facial bones leads to marked distortions of the 

normal features. The periosteal buildup and diploic sclerosis may be uniform (Figures 455, 456) 

or nodular and lead to narrowing of the orbits 

and of the paranasal sinuses (Figure 457). The 

changes would be obvious on dry bone and the 

only differential diagnosis would be Paget's disease. However, Paget's disease of such severity 

would not likely be limited to the skull. Microscopically, the characteristic mosaic pattern of 

Paget bone is not present in this condition. (For 

detailed discussion, see Knaggs, 1923-1924, and 

Jaffe, 1972:276-281.) 

Infantile Cortical Hyperostosis (Caffey's Disease) 

This is a disease affecting the skeleton of infants 

in the first year of life (Caffey and Silverman, 

1945; Caffey, 1957b, 1972(2): 1210-1222). The 

cause is unknown. It occurs sporadically or occasionally in several siblings. The lesion is characterized by massive deposition of layered periosteal 

woven bone on one or several bones. It is not a 

systemic disease. The bone deposits usually disappear spontaneously after weeks, months, or 

rarely years. The disease is rarely fatal. The most 

frequently involved bones are the mandible and 

the clavicle, followed in frequency by the long 

tubular bones of the extremities and ribs. The 

small tubular bones, most of the cancellous bones, 

and the skull are usually spared. The periosteal 

bone deposits on long bones are mainly over the 

diaphysis, less over the metaphyses, and spare the 

epiphyses. They are usually distinctly separated 

from the underlying cortex, which may become 

osteoporotic. The deposits can be so massive that 

they exceed the normal diameter of the involved 

bone. The surface of the deposits is rough and the 

contour uneven. If both bones of the forearm or 

lower leg are involved, the bony mantles of both 

may become fused. 

Generalized Hyperostosis with Pachydermia 

PATHOLOGY 

This is a rare familial disorder characterized by 

excessive formation of dermal collagen and of 

periosteal bone. The disease usually begins 
NUMBER 28 295 

FIGURE 457.—Leontiasis ossea of cranium and facial bones, 

frontal view. Notice the massive deposition of periosteal 

bone. The paranasal sinuses were obliterated by bony overgrowth. (Adult Peruvian, WM S65.a from 1828.) 

FIGURES 455, 456.—Leontiasis ossea. Notice thickening of 

cranial vault and ivory-like sclerosis of the diploe without 

encroachment on the cranial cavity; skull weight 2500 g. 

455, Endocranial view of calvarium. 456, Endocranial view 

of base. (56-year-old female, FPAM, Jubilaumspital 511, 

from 1919.) 
296 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

FIGURES 458, 459.—Generalized hyperostosis with pachydermia: 458, Anterior view of skeleton, showing excessive 

periosteal bone; notice sparing of joint ends and preservation 

of medullary cavities. 459, Vertical section of vertebral body, 

showing thickened, coarse trabeculae. (55-year-old male, 

IPAZ autopsy 1146 of 1940.) 
NUMBER 28 297 

around puberty and progresses through adult life. 

The outstanding feature in advanced cases is the 

markedly increased diameter of long bones, without alteration of the joint ends (Figure 458). The 

surface of the bones shows a rough irregular 

texture. On cross-section the new bone blends 

into the old cortex, which may show considerable 

porosis. The medullary canal is not obliterated. 

The skull usually shows only sclerosis of the skull 

base and of the diploe. The cancellous bones are 

less thickened and their trabecular architecture 

becomes coarse and exaggerated (Figure 459). 

The pelvis shows rough osteophytes and exostoses. 

In late stages spinal ligaments and interosseous 

membranes may be ossified. Large and small 

joints may become ankylotic. Carpal and tarsal 

bones may be transformed into solid bony blocks. 

(For a detailed discussion see Uehlinger, 1941.) 

PALEOPATHOLOGY 

Allison, Gerszten, Sotil, and Pezzia (1976) have 

described an archeological case of generalized 

hyperostosis with pachydermia in an adult female 

skeleton. The case is from a Huari-culture cemetery, which is dated about A.D. 1000 and is located 

in the Ingenio Valley, lea, Peru. The bones of the 

skeleton are thickened and have greatly diminished marrow spaces. This has resulted in the 

bones being as much as '2}h times heavier than 

normal. Histologically the bone tissue, while 

thicker than normal, has good lamellar bone with 

normal osteon remodeling. 
Endocrine Disturbances 

The skeletal growth and maturation is 

mainly controlled by an intricate interrelationship between pituitary and thyroid. This interrelationship can be separated only in the animal 

experiment, revealing that the pituitary mainly 

controls growth and the thyroid maturation 

(Asling and Evans, 1956). Estrogens and androgens of testicular or adrenal origin stimulate longitudinal growth but hasten epiphysial closure. 

(For a general discussion of endocrine-skeletal 

relations see Putschar, 1960:405-414.) 

Pituitary Disturbances 

PATHOLOGY 

The anterior lobe of the pituitary produces 

somatotrophic (growth) hormone, with direct action on skeletal growth, and thyrotropic hormone, 

which stimulates the production of thyroxin by 

the thyroid. Excessive production of growth hormone by hyperplasia or adenoma of the anterior 

pituitary produces characteristic skeletal changes 

besides effects on other tissues and organs not 

discussed here. Depending on the age of the 

individual affected by hyperpituitarism, either 

pituitary gigantism or acromegaly will result. 

Pituitary Gigantism 

This is a very rare condition in which the 

continued excessive production of somatotrophic 

hormone during the growing period and beyond 

leads to gigantic proportions of the skeleton by 

overstimulation of the growth cartilages. In this 

condition, not only the total body height but also 

the length and diameter of all bones are enlarged. 

If the underlying cause was a tumor, the sella 

turcica is usually markedly enlarged with thinning or destruction of the anterior and posterior 

clinoid processes and, occasionally, with perforation of the bony floor of the sella. This condition 

results in an open communication between the 

sella and the cavum sphenoidale in the dry skull. 

In pituitary hyperplasia the contour of the sella 

may not be significantly altered. Continued hyperpituitarism beyond the growing period leads 

to a superposition of acromegalic features onto 

the giant skeleton (Figure 460). 

Acromegaly 

This condition is much more common than 

pituitary gigantism and is usually the result of an 

acidophilic adenoma of the pituitary occurring in 

an adult (Figures 461-464). After closure of the 

FIGURE 460.—Pituitary giant. (42-year-old Iranian male exhibiting giant stature and massive periosteal, especially cranial, bone apposition, Pahlavi University Medical School, 

Shiraz, Iran.) 

298 
^ ^ ** 

FIGURES 461-464.—Acromegaly: 461, Skull, lateral view, showing prominent chin, malocclusion of teeth and prominence of inferior and superior nasal spine. 462, Skull base, showing 

enlarged frontal sinuses, enlarged sella (arrow) with resorption of anterior and posterior clinoid 

processes. 463, Right hand, showing extreme arrowhead tufting of terminal phalanges, and 

periosteal hyperostosis. 464, Lumbar vertebrae, showing marked subperiosteal apposition. (39-

year-old male with pituitary adenoma, FPAM, Jubilaumspital 610.) 
300 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

epiphysial plates, only the remaining cartilages 

and the periosteum can respond to stimulation 

by growth hormone. Therefore, there is no gigantism in acromegaly. The reawakened growth 

mainly affects the cartilages of the mandibular 

condyle, the rib cartilages, the synchondroses of 

sternum and pubis and, to some extent, the articular cartilages and intervertebral discs. The periosteal bone deposition is most marked at terminal 

points of bones and at normal prominences and 

insertion of tendons and ligaments. Usually, the 

skull shows enlargement of the sella, as described 

above, as a result of the pressure erosion of an 

intrasellar tumor (Figure 462). There is exaggeration of the supraorbital ridges and of the posterior occipital protuberance. The facial bones are 

enlarged and so are the paranasal sinuses. The 

cranial vault is thickened. The most marked 

changes affect the mandible. Since the cartilage 

of the mandibular condyle is a growth cartilage, 

marked elongation of the mandible with elongation of the ramus leading to pronounced prognathism and dental malocclusion result (Figure 

461). 

There is marked periosteal bony buildup on 

the chin, adding to the distortion of the mandible. 

Marginal buildup of bone on the alveolar process 

of the mandible and of the maxilla leads to 

separation between the teeth. The ribs show 

marked elongation, increasing the diameters of 

the thorax. The external relief on the bones is 

exaggerated on all prominent points, such as 

trochanters and linea aspera. The periosteal 

buildup is slow and consists of lamellar bone, 

intimately welded to the old cortex. The tufts of 

the terminal phalanges are characteristically enlarged with an arrowhead appearance (Figure 

463). The changes of the articular cartilages are 

not directly visible on dry bone but the complicating degenerative arthritis is. The spine may 

show marked periosteal buildup with anteroposterior and lateral enlargement of the vertebral 

bodies, complicated by degenerative arthritic lipping (Erdheim, 193la:203-210) (Figure 464). 

There is often kyphosis, mainly secondary to muscular weakness. 

Hypopituitarism 

Hypopituitarism only affects the skeleton significantly if the functioning pituitary is destroyed 

during the growing period. This is most often due 

to a tumor of developmental remains of Rathke's 

pouch (craniopharyngioma) developing within or 

above the sella in a child. Malformation or traumatic destruction of the pituitary is rarely the 

cause. Hypopituitarism in the adult produces no 

demonstrable skeletal changes beyond nondescript osteoporosis. 

Pituitary Dwarfism 

Deficiency of growth hormone in early life 

leads to pronounced inhibition of longitudinal 

growth, resulting in dwarfism of infantile proportions (Priesel, 1920). The synergism between pituitary and thyroid is demonstrated by the concomitant hypothyroidism secondary to the deficiency of thyrotropic hormone. Therefore, growth 

is not only stunted but the development of secondary ossification centers is markedly delayed, 

and the epiphysial and apophysial growth plates 

remain open long into adult life (Erdheim, 1916: 

338-344, 356), although they do ultimately close 

in old age (Priesel, 1920:252). The cranial sutures 

also remain widely open into adult age. The sella 

may show widening, if the tumor was intrasellar, 

or an aperture at the floor as a remnant of a 

persistent craniopharyngeal canal. The skeleton 

is gracile in dimensions, the cortices are thin, and 

the spongiosa porotic and sparse. Although 

growth plates may remain, the metaphysial surface is usually closed by a thin layer of bone, 

indicating arrested growth. (For detailed bone 

measurements in hypopituitary dwarfs, see Priesel, 1920.) 

PALEOPATH O LOGY 

Acromegaly 

Brothwell (1965a: 158) describes an ancient 

Egyptian skull in which the face is unusually 

long. The photograph of the skull (Brothwell, 

1965a, pi. 4c) shows an enlarged mandible and 
NUMBER 28 301 

an apparent overgrowth leading to prognathism 

and malocclusion. Brothwell's diagnosis of acromegaly is almost certainly correct. 

Morse (1969:26, pi. 22b) provides a brief summary of features associated with acromegaly accompanied by a lateral photograph and roentgen 

film of the skull and mandible of a Late Woodland (ca. A.D. 900) burial from Dick's mound in 

Illinois, USA. He describes the long bones as 

elongated and thickened and the lower jaw as 

lengthened. The photograph of the roentgen film 

and description of the long bones support a diagnosis of acromegaly. 

The almost complete skeleton of an indigenous 

North American from the Midwest, USA 

(NMNH 227508) provides another possible example of acromegaly. The skeleton is from the 

historic period and is remarkable because of the 

massive size of both skull and postcranial bones. 

The maximum length of the skull is 201 millimeters, maximum breadth is 144 millimeters. The 

cranial capacity is estimated to be 1865 cubic 

centimeters, which is well within the normal human range but about 400 cubic centimeters 

greater than average. The gross morphology of 

the skull is rugged (Figures 465, 466) with pronounced and unusually high markings (near the 

sagittal suture) for the origin of the temporalis 

muscle. The mandible has slightly overgrown the 

development of the maxilla and has prominent 

bony projections on the anteroinferior border of 

the chin. The roentgen film demonstrates clearly 

the additional growth of the mandibular condyles 

and the increased angle between the ramus and 

mandibular body. The roentgen film (Figure 467) 

reveals a large but not abnormal pituitary fossa; 

thus the presence of a pituitary tumor is problematical. 

The long bones are long and heavy. The right 

femur, for example, is somewhat damaged postmortem, but the estimated length is 545 millimeters. Stature estimates based on this length are 

FIGURES 465-467.—Possible acromegaly: 465, Comparative 

facial views of normal (left) and possible acromegalic (right) 

skulls from the same skeletal sample. 466, Left, lateral view; 

note the projection of the chin in the skull on the right. 467, 

X-ray of lateral view of possible acromegalic skull. (Normal 

skull, NMNH 243703; possible acromegalic skull, NMNH 

227508.) 
302 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

189.75 centimeters (ca. 75 inches). This is certainly at the upper end of the normal range 

among American Indians but not abnormal. This 

suggests somewhat greater pituitary function during growth but with major morphological 

changes, as in the skull, occurring after the normal growth period had ended. 

The skeleton appears to be fully adult and 

male with estimated age, based on the morphology of the fragmentary pubic symphysis, about 

35 to 45 years of age. The ends of the ribs show 

evidence of secondary growth as would be expected in acromegaly. The bones of the hands 

and feet are large but of normal proportions, 

although the phalanges, particularly the terminal 

phalanges, show evidence of secondary growth 

and remodeling on the distal ends (tufting). The 

abnormal features of this skeleton are compatible 

with a diagnosis of acromegaly. However, the 

disease process does not appear to be as severe as 

cases encountered in the European pathology 

collections. 

Pituitary Dwarfism 

I know of no references on pituitary dwarfs in 

the literature on paleopathology; however, there 

is a probable case of this condition in the collections of the National Museum of Natural History, 

Washington, D.C, USA (NMNH 314306). This 

remarkable case is from the Hawikuh site in New 

Mexico, USA, which includes late precontact and 

early historical components. The skeleton is fragile and damaged but includes most of the bones. 

The features of dental and skeletal maturation 

used in estimating age are affected by a deficiency 

of pituitary hormone. Therefore, the age of the 

skeleton cannot be determined with certainty. 

However, the second permanent molars have 

erupted. There is no evidence of a third molar in 

the left mandibular fragment; however, this absence might be due to agenesis rather than young 

age. All the teeth that are present are normal in 

size, which has created severe crowding in the 

small jaws. 

In the postcranial skeleton most epiphyses are 

unfused. The primary elements of the innominate 

have fused, indicating an age in excess of 12 years. 

The ischiopubic ramus is unfused. The distal 

epiphysis of the humerus has fused. These features 

added to the dental eruption clearly indicate an 

age in excess of 12 years in a normal individual. 

Because of the delayed development and fusion 

of epiphyses in pituitary dwarfism, a minimal age 

in the twenties would seem more likely for this 

case. 

The skull is somewhat deformed postmortem 

but is obviously much smaller than normal (Figures 468, 469). Maximum length is 145 millimeters, maximum width is 108 millimeters. Typical 

skull measurements for a 12-year-old child from 

the same site would be maximum length 160 

millimeters and maximum width 127 millimeters. 

The relative proportions of the skull are normal 

although more typical of a child than a 20 year 

old. Unfortunately, the base of the skull has been 

damaged and lost, making observations on the 

pituitary fossa impossible. 

The postcranial long bones are very slender 

and shorter than normal (Figures 470,471). Stewart (1968:133) indicates that the approximate 

femoral length (without epiphyses) of a 12 year 

old is 310 millimeters. The femoral length of the 

dwarf is about 280 millimeters or 90 percent of 

the expected length of a 12 year old. If, as I think 

likely, the dwarf was fully grown the expected 

femur length would be about 370 millimeters and 

thus would have been only three-fourths as tall 

as normal. The torsion angle of the left femur is 

unusually large and probably would be associated 

with an abnormal gait during life. 

The vertebrae are small but of normal proportions, although the bodies of thoracic vertebrae 

T5-T11 show a slight eccentric development to 

the right, which might be associated with a slight 

scoliosis. The sacrum and innominates are small 

but of fairly normal proportions, although the 

anteroposterior dimension of the pelvis is longer 

than would be expected. The pubic symphysis is 

poorly formed lacking the normal features of the 

symphysial face and the ridge formation. The 

bones of the hands and feet are of normal shape 

although very small. 

The overall appearance of the skeleton conveys 
NUMBER 28 303 

FIGURES 468-471.—Pituitary dwarf: 468, Comparative facial views of normal (left) and dwarf 

(right) skulls: normal skeleton selected on basis of comparable dental and epiphyseal development and closure. 469, Right lateral view of skulls; note the prognathism of the dwarf skull. 

470, Compartive anterior views of a right normal and abnormal femur and tibia. 471, X-ray of 

same long bones. (Normal bones, NMN H 308611; dwarf, NMNH 314306.) 
304 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

FIGURE 472.—Possible congenital idiot skull (left) compared 

with pituitary dwarf skull (right), right lateral view. Note 

the different contour of the frontal bones. (Congenital idiot, 

NMN H 379510; pituitary dwarf, NMNH 314306.) 

the impression of diminished growth and development. The features of the face, particularly the 

large but depressed nasal aperature, are suggestive of features seen in achrondroplasia. The general morphology of the skull and long bones, 

however, would rule this possibility out. In general there has been diminished growth and delayed fusion of epiphyses, both of which are conpatible with a diagnosis of pituitary dwarfism. 

Another specimen in the collection of the National Museum of Natural History, USA, is of 

interest in the context of pituitary dwarfism. The 

specimen consists of only the skull from Chilca, 

Peru (NMNH 379510). The archeological age is 

unknown. The skull was initially obtained by 

J. R. Wells who published his observations (1942). 

He reports that the skull was a microcephalic 

with a cranial capacity of 485 cubic centimeters. 

He concludes that the skull does not resemble 

that of a congenital idiot as described in the 

clinical literature. 

Wells contributed the specimen to the National 

Museum of Natural History, USA, and Hrdlicka 

(1943) added additional data and observations in 

a subsequent report. Hrdlicka (1943:77) concluded that except for its small size, "the skull is 

unquestionably a 'normal' specimen, i.e. it shows 

nothing of any pathological nature." 

The profile of the Peru skull reveals diminished 

development of the frontal region of the skull 

(Figure 472). A measure of this feature is the 

length of the arc from nasion to bregma. On the 

Peru skull this arc is 76 millimeters. This arc on 

the New Mexico pituitary dwarf is 100 millimeters. To the extent that diminished frontal bone 

development is indicative of brain abnormality, 

the Peru skull would appear to be a congenital 

idiot rather than a pituitary dwarf or microcephalic. 

Other Endocrine Disturbances 

PATHOLOGY 

Hypothyroidism 

Thyroxin, the thyroid hormone, is secreted by 

the follicular epithelium under stimulation by the 

thyrotropic hormone of the anterior pituitary. 

The effects of thyroxin are, in addition to the 

general stimulation of the metabolism and local 

effects on the skeletal maturation, a stimulating 

feedback on the pituitary to secrete somatotrophic hormone. The main skeletal alterations 

are seen in severe thyroxin deficiency. 

The severe deficiencies occur on the basis of 

congenital absence of the thyroid (sporadic cretinism) or of suppressed thyroid function in infants of goiterous mothers who are hypothyroid 

themselves (endemic cretinism). This is mainly 

observed in mountainous areas of the world, 

where endemic goiters occur due to iodine deficiency. 

Since in either form of cretinism the deficiency 

already operates through intrauterine life, the 

skeletal effects are similar to but more severe than 

those in primary hypopituitarism. Sporadic cretins show the most severe degree of drawfing 

because of complete absence of thyroxin. This is 

accompanied by great delay in formation of secondary ossification centers and permanently open 

epiphysial plates, resulting in a great discrepancy 

between radiological and chronological bone age. 

In endemic cretins there exists a gradient of deficiency leading to a subnormal stature of childlike proportions (de Quervain and Wegelin, 1936: 

35-41). In these individuals the epiphysial plates 
NUMBER 28 305 

FIGURE 473.—Dysplastic femoral head with multiple ossification centers and short, plump neck, markedly delayed 

epiphysial closure in a 37-year-old female hypothyroid dwarf 

with nodular goiter; body length 114 cm. (FPAM, Jubilaumspital 869.) 

ultimately close, albeit beyond middle age. The 

last to close is the spheno-occipital growth plate, 

resulting in a brachycephalic configuration. The 

cranial sutures also remain open longer than normal. Continued growth at the mandibular condyle may ultimately result in some degree of 

prognathism. The marginal ossification centers of 

the scapula and the ilium may form only incompletely and remain open (Looser, 1929). 

Most epiphyses show multifocal irregular ossification centers, which later fuse (for details see 

Wilkins, 1941) (Figure 473). These abnormalities 

of the ossification centers are specific. The development of the ossification center of the head of 

the femur is not only delayed but often abnormal. 

The lack of bony support of the femoral head 

leads to deformation of the cartilage model, secondary to static and dynamic stresses. The end 

result is a misshapen flattened head with a mushFiGURE 474.—Skeleton of a cretin showing typical hip deformation with mushroom-shaped femoral heads, coxa vara, 

and secondary degenerative arthritis, bilateral. (67-year-old 

female, IPAZ 65 from 1940.) 

room-like deformity (not unlike the endstage of 

Perthes' disease), which fits badly into the acetabulum. However, in contrast to Perthes' disease, 

there is no aseptic necrosis. This misshapen "cretin hip" leads to early and severe degenerative 

arthritis (de Quervain and Wegelin, 1936) (Figure 

474). 

Hyper thy ro idism 

Excessive amounts of thyroxin, as observed in 

Graves' disease or toxic goiter, mostly occur in 

adults. Skeletal changes in this condition may be 

absent or limited to increased bone resorption, 

producing osteoporosis. Occasionally, these 

changes may mimic those in mild hyperparathyroidism and result in stress fractures (Askanazy 

and Rutishauser, 1933; Uehlinger, 1957). These 

findings would not be diagnostic of hyperthyroidism in dry bones. 

Cushing's Syndrome 

Of the different hormones produced by the 

adrenal cortex under stimulation of pituitary 

adrenocorticotropic hormone (ACTH), only the 

glucocorticoid cortisone needs to be discussed 

briefly in regard to its skeletal effects. 

Cushing's syndrome may be caused by any of 
306 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

the following: hyperplasia, adenoma, carcinoma 

of the adrenal cortex, or, less commonly, adenoma 

of the basophilic pituitary cells. The excessive 

secretion of cortisone leads to suppression of protein synthesis, including production of collagen. 

The ensuing osteoblastic suppression and scarcity 

of bone matrix production results in severe osteoporosis. The osteoclastic resorption is not increased, but it is not balanced by a corresponding 

amount of bone formation. The condition may 

be observed at any age. The severe osteoporosis is 

most marked in bones rich in trabeculae where 

the normal turnover is rapid. The vertebral column and ribs are most severely affected. The 

vertebral bodies show marked cortical thinning 

and severe reduction in the number and size of 

the trabeculae (Figure 475). The end-plates bulge 

inward due to the pressure exerted by the resilient 

intervertebral discs, creating the picture of biconcave, so-called "codfish" vertebrae. The vertebral 

bodies lose height and compression fractures are 

common. Anterior wedging with kyphotic deformity on the vertebral column occurs. The ribs 

become severely osteoporotic and may exhibit 

multiple pathological fractures (Sissons, 1956). 

The long tubular bones also show trabecular 

osteoporosis and endosteal cortical resorption, but 

the changes are less obvious and the outer cortical 

FIGURE 475.—Cushing's syndrome. Vertebra with extreme 

osteoporosis after 10 years of cortisone therapy. (51-year-old 

female, MGH autopsy 20884.) 

surface appears normal. Although this osteoporosis is not specific, severe changes of this kind 

and severity, particularly in a child or young 

individual, are very suggestive of Cushing's syndrome. 

Hypogonadism 

Estrogen and testosterone both stimulate enchondral growth and skeletal maturation. In both 

sexes subnormal production of gonadal hormones 

will delay the appearance of secondary ossification centers and postpone the closure of epiphysial discs and sutures. Periosteal bone formation is 

also inhibited, resulting in a gracile skeleton with 

thin cortices. Since the period of enchondral 

growth is markedly lengthened, the normal skeletal proportions are altered due to disproportional 

length of the upper and lower extremities 

(eunuchoid stature) and elogation of the mandible, producing some degree of prognatism. Since 

castration of the male was practiced in various 

cultures, it is worth mentioning that in the early 

castrate (eunuch) the above-mentioned changes 

are present in a most marked degree, resulting in 

a tall, long-legged, gracile skeleton. Cessation of 

production of gonadal hormones in the adult, 

either by involution (menopause) or pathologic 

destruction of the gonads will often ultimately, 

over a period of about one decade, result in trunk 

osteoporosis in either sex (Nowakowski, 1955). 

Hypergonadism 

Excessive amounts of gonadal hormones produced by various neoplasms or other abnormalities will result in precocious puberty in affected 

children. Although the enchondral growth is 

stimulated, the early closure of the epiphysial 

plates results in a short but stocky skeleton (Wilkins, 1950:230; Prader and Maassen, 1953:148). 

Hypopara thyroidism 

The parathyroids control the level of ionized 

calcium in the blood plasma. This is accomplished by increased secretion of parathormone 
NUMBER 28 307 

in response to lowered blood calcium. Parathyroid hormone acts on the skeleton by stimulation 

of osteoclastic resorption, liberating calcium from 

the bone matrix. 

Inadequate production of parathormone, due 

to congenital absence or acquired impairment of 

the parathyroids, results in hypoparathyroidism. 

In this rare condition, suppression of osteoclastic 

remodeling can lead to a degree of nondiagnostic 

osteosclerosis as a result of the continued osteoblastic endosteal and periosteal bone formation 

(Figure 476). 

Hyperparathyroidism 

Hypersecretion of parathormone leads frequently to marked skeletal changes. It occurs as 

a primary condition or secondary to renal impairment. 

PRIMARY HYPERPARATHYROIDISM (osteitis fibrosa cystica generalisata).—This condition, first 

described by Recklinghausen (1891), is the result 

of hypersecretion by either a parathyroid adenoma of one gland or by diffuse hyperplasia of 

all parathyroids. The continued overstimulation 

of osteoclastic resorption results in osteoporosis 

and the continued loss of the liberated calcium 

through the kidneys in a negative calcium balance. The early changes are demonstrable only 

microscopically. They consist of osteoclastic intratrabecular resorption (Figure 477) accompanied 

by fibrous conversion of the bone marrow ("dissecting bone atrophy"). Only advanced cases will 

show significant radiologic and gross skeletal 

changes. As a direct effect of continued bone 

resorption exceeding bone formation, general osteoporosis develops. This resorption may be radiologically and grossly demonstrable, particularly on the cortical surface of phalanges, forming 

scalloped depressions. Similarly, the normally 

present thin layer of lamellar bone (lamina dura) 

lining the dental alveoli undergoes resorption, 

visible on X-ray and by direct inspection of the 

dry jaws. The osteoporosis of the spine may lead 

to biconcave deformity of the vertebral bodies. 

Cranial osteoporosis tends to diminish the distinction of an outer and inner table. There is 

FIGURE 476.—Hypoparathyroidism. Frontally bisected proximal right tibia showing marked cortical thickening, some 

periosteal hyperostosis, and increased strong spongiosa. The 

femur showed the same findings. (62-year-old female hypothyroid with postsurgical hypoparathyroidism of 10 years 

duration, IPAZ 6168, autopsy 1265 from 1955.) 

FIGURE 477.—Hyperparathyroidism. Vertebral spongiosa 

showing centrotrabecular resorption (dissecting atrophy). 

(70-year-old female, IPAZ autopsy 1204 from 1970; courtesy 

Prof E. Uehlinger.) 
308 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

FIGURE 478.—Hyperparathyroidism (osteitis fibrosa cystica) 

in bisected femur. 

transformation of the diploe into fine trabecular, 

poorly mineralized, cancellous bone. The major 

gross abnormalities observed are the result of the 

continued and repeated minor traumas acting 

upon the vulnerable, demineralized skeleton. 

These changes consist of cyst formations and 

proliferations of fibrous marrow ("brown tumors") secondary to hemorrhage and microfractures. These lesions appear on dry bone as cystic 

lytic defects with one or several cavities separated 

by bony septa and ridges (Figure 478). They may 

expand the affected area of the bone remarkably 

and lead to pathological fractures and deformities. These lesions can appear in any bone but 

predilect the mandible, the long and short tubular bones of the extremities, and the pelvis. In 

extreme cases the demineralized skeleton may 

become more pliable and deformed than in osteomalacia or fibrous dysplasia. The preservation of 

these changes in archeological material is unlikely. 

SECONDARY HYPERPARATHYROIDISM.—In a variety of chronic renal diseases, parathyroid hyperplasia occurs as a response to disturbance of the 

metabolism of calcium and phosphorus. The majority of these cases concern children and will 

show, in addition to rickets-like changes (p. 273) 

and stunted growth, features of hyperparathyroidism. In adults, of course, alterations of growth 

no longer can occur and, therefore, the picture of 

renal osteopathy is a combination of hyperparathyroidism and osteomalacia. In rare instances of 

longlasting renal impairment in adults, all features of primary hyperparathyroidism, including 

skull changes (Figure 479), cysts, and brown tumors, can be observed (Jaffe, 1972:326). 

FIGURE 479.—Secondary hyperparathyroidism. X-ray of 

skull, showing "cotton-wool" appearance of cranial vault. 

(62-year-old female, IPAZ surgical specimen 12807154.) 
Other Bone Diseases 

Paget's Disease 

PATHOLOGY 

Osteitis deformans (Paget, 1877) is a chronic 

bone disease, which may affect a single, several, 

or many bones but never involves the entire 

skeleton. The etiology is completely unknown. It 

occurs commonly in populations of European 

descent but is very rare in Asians. The disease 

seldom appears before 40 and mostly not before 

50 years of age. The frequency and extent of 

involvement increases with age. Males are more 

often involved than females. The disease is not 

rare in a limited form but widespread multiosseous involvement is uncommon. Schmorl (1932: 

698-699) found an incidence of 3 percent of 

Paget's disease in a series of over 4600 autopsies 

of individuals above 40 years of age. The lesions 

of the 138 cases found in this study show the 

following distribution in the skeleton (in rounded 

off percentage figures listed in decreasing frequency): sacrum 57 percent, spine 50 percent 

(lumbar segment 26 percent, thoracic 17 percent, 

cervical 7 percent), femora 46 percent, skull 39 

percent, sternum 32 percent, pelvis 30 percent, 

clavicle 18 percent, tibia 11 percent, ribs 10 percent, humerus 6 percent. These figures indicate 

the great predilection for the axial skeleton, which 

often is the only area involved. 

The disease process can be best characterized 

as a pathological speedup and distortion of the 

normal remodeling mechanism. It always begins 

as a local process but may spread through an 

entire bone, including the epiphyses, clear up to 

and involving the subchondral bone plate of the 

joint. In the skull the process extends readily 

across suture lines. The initial change is excessive 

osteoclastic resorption accompanied by fibrous 

conversion of the bone marrow and hypervascularity. This is followed by osteoblastic overstimulation, producing irregular and excessive 

amounts of woven and lamellar bone. In the long 

protracted course of the disease osteoclastic and 

osteoblastic activities occur simultaneously, leading to excessive remodeling in affected areas, 

which results in the characteristic mosaic pattern 

in the microscopic picture. This picture consists 

of increased numbers of fragments of lamellar 

bone separated by cement lines. This pattern is 

present in trabecular and cortical bone. Since it 

is a feature of the microarchitecture of mineralized bone, it is recognizable in ground sections of 

dry bone (Figure 480). This is one instance where 

microscopic examination of archeological bone 

will be of great diagnostic significance. 

The early lesions are predominantly lytic and 

osteoporotic; later, thickening of the cortex by 

endosteal and periosteal bone deposition and enlargement of the bones is observed. The trabecular architecture becomes accentuated and its usually smooth outline assumes irregular surface contours on X-ray. This alternation of resorptive and 

sclerotic areas gives a mottled picture on X-ray. 

The changes of the bone at different stages of the 

disease and at different locations in the skeleton 

present a variety of different pictures, necessitating the following, more detailed discussion of 

various areas. 

T H E SKULL.—The early Paget lesion of the 

skull is represented by the so-called osteoporosis 

circumscripta (Erdheim, 1935). This single, or 

sometimes multiple, lesion of the cranial vault is 

characterized by prevailing bone resorption, resulting in reduction of the trabeculae in the diploe 

and marked thinning of the inner and outer table, 

and creating an area of markedly increased radiolucency on X-ray. The thinned tables may 

exhibit a porous surface. The outline of the lesion 

is somewhat wavy, may cross suture lines and has 

a sharp interphase against adjacent uninvolved 

309 
FIGURE 480.—Mosaic pattern with numerous cement lines 

in Paget's disease, femoral cortex. Ground polished section 

of undecalcified bone. Polarized light, approximately XlOO. 

(Specimen courtesy Prof E. Uehlinger.) 

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'1 • 1 

t'.'i'. »•«- • M 

I. * Jl 1 ^ if. j 

FIGURE 481.—Paget's disease of calvarium (original case), 

showing extreme thickening and sclerosis of cranial vault 

with nodular bony masses in the diploe. (68-year-old male, 

duration 22 years, WM H.S.62.1 from 1876.) 

FIGURES 482, 483.—Paget's disease: 482, Cranial vault, endocranial view, showing thickening, especially of frontal 

bone, with nodular bony masses in the diploe. The bone is 

soft and pumice-like. 483, Close-up of frontal area with 

nodular diploe. (65-year-old female, polyostotic Paget, IPAZ 

4566, autopsy 46 from 1940.) 
NUMBER 28 311 

FIGURE 484.—Paget's disease of frontal bone with circumscribed nodular densities in diploe. (66-year-old female, 

MGH autopsy 34336.) 

bone. Although this lesion may remain for a 

number of years, ultimately, characteristic blastic 

lesions of Paget will develop either in the skull or 

in other areas of the skeleton (Kasabach and 

Gutman, 1937:598). 

The location and appearance of this lesion is 

distinct enough to make one suspect early cranial 

Paget's disease on a dry bone specimen. Changes 

of fully developed Paget's disease of the cranial 

vault may exhibit distinct thickening of the calvarium by endocranial and external bone formation. Such calvaria may reach several centimeters in thickness and there may be considerable 

encroachment on the intracranial space (Figure 

481). The cross-section of the calvarium shows 

areas of laminated thickening of the tables and 

alternation of porotic and sclerotic areas in the 

diploe, presenting the characteristic appearance 

of finely porous pumice bone (Figures 482, 483). 

In the diploe, ball-shaped masses of sclerotic Paget bone occur, exhibiting greatly increased radiological density (Figure 484). These masses are 

more common and much more dense than those 

seen occasionally in fibrous dysplasia. 

The skull base may be involved (Figure 485). 

Thickening takes place mostly on the endocranial 

surface with encroachment upon the cranial cavity. The cranial air sinuses may also be impaired 

by the transformation and thickening of their 

FIGURES 485, 486.—Skull in advanced Paget's disease: 485, 

Cranial base, showing massive endocranial hyperostosis and 

sclerosis of thickened cranial vault. 486, Frontal view, showing diffuse hyperostosis of facial bones with porous subperiosteal bone deposition. (75-year-old female, FPAM, Jubilaumspital 510, from 1917.) 
312 SMITHSONIA

N CONTRIBUTIONS TO ANTHROPOLOGY 

FIGURE 487.—Early Paget's disease. Bisected tibia showing 

lytic transcortical lesion (dark) with wedge-shaped progres-

sive margin. (77-year-old female, MGH surgical specimen 

4149 of 1963.) 

walls. The cortex of the petrous bone may partici-

pate in Paget's disease but the otic capsule is 

usually spared. This is in keeping with its lack of 

remodeling. The facial bones are usually spared. 

If the facial bones are involved, subperiosteal 

deposition of pumice-like bone may disfigure the 

face and resemble leontiasis ossea (Figure 486). 

The jaws also ordinarily do not participate in the 

disease, although abnormal deposits of radiodense 

cementum around some dental alveoli is not un-

common in Paget's disease. 

T HE LONG BONES.—The femur and the tibia 

are the most common sites of involvement. The 

FIGURES 488, 489.—Left femur, Paget's disease: 488, external 

view, showing bowing and thickening. 489, Cut surface, 

showing cortical thickening, narrowing of the medullary 

canal and irregularly coarsened cancellous bone. (64-year-

old male, 10 years duration, WM HS62.3) 
NUMBER 28 313 

FIGURE 492.—Paget's disease of lumbosacral spine, complicated by secondary hyperparathyroidism. Midline cut showing the characteristic coarse trabeculation of Paget's disease 

and the fine pumice bone deposition along the endplates, 

particularly of the fifth lumbar and first sacral vertebra, 

characteristic of hyperparathyroidism. (71-year-oId female, 

IPAZ autopsy 358 of 1960.) 

early lesion in these bones also is represented by 

a purely lytic osteoclastic resorption involving the 

entire thickness of the cortex and showing a sharp 

wedge-like border against uninvolved bone (Figure 487). This lesion alone is not diagnostic in dry 

bone and can, even on X-ray, be mistaken for a 

tumor metastasis. The later blastic phases show 

marked thickening and lamination of the cortex. 

The bones become plump by periosteal bone 

formation. Bowing, especially of the weight-bearFiGURES 490, 491.—Paget's disease of tibia showing pumice 

bone subperiosteally and transcortically: 490, Surface. 491, 

Cut surface. The spongiosa is normal. (Studied by Putschar 

in 1940 at Charleston General Hospital, Charleston, West 

Virginia, USA.) 
314 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

ing bones, occurs mainly due to complete or 

incomplete transverse pathological fractures, 

demonstrating the mechanical inferiority of Paget 

bone (Figures 488, 489). The spongiosa of the 

epiphyses and metaphyses shows characteristic 

coarsening and focal deposition of pumice bone 

(Figures 490, 491). The medullary cavity is preserved. Secondary degenerative arthritis over severely affected epiphyses is common. Although, 

occasionally, any bone may be affected by Paget's 

disease, the fibula and the small tubular bones of 

hands and feet are usually spared. The same is 

true of the tarsal and carpal bones. 

T H E SPINE.—The axial skeleton is most often 

FIGURE 493.—X-ray of Paget's disease of vertebra with adjacent normal vertebra (above). Note increased density and 

coarsening of the spongiosa of the involved vertebra. (European X-rays show densities as black and lucencies, white; 

studied by Putschar.) 

FIGURE 494.—Osteosarcoma in Paget's disease of right distal 

femur. (80-year-old female, MGH surgical specimen 13584 

from 1963.) 

the site of Paget lesions. The frequency of involvement decreases steadily from the sacrum to the 

cervical spine. Within a vertebra, the body is 

most markedly affected. The lesion may extend 

into the neural arches but often spares their posterior portions and the spinous process. The vertebral bodies show laminated thickening of the 

end-plates and the cortex, with porotic reduction 

of the trabeculae in the center (Figure 492). These 

trabeculae are reduced in number but thickened 

with uneven surfaces (Figure 493). Compression 

fractures of severely affected vertebrae are not 

uncommon. Frequently, although several vertebrae show the disease, they are separated by 

completely normal vertebrae. 

T H E FLAT BONES.—The ilium is often involved 

if there are lesions in the sacrum. The sternum 

rates high in the Schmorl (1932) series. The disease usually involves the manubrium or the body 
NUMBER 28 315 

but does not cross the synchondrosis. Ribs are not 

uncommonly affected and may become markedly 

thickened. 

PAGET SARCOMA.—In longstanding active Paget, especially of the long bones and calvarium, 

a sarcoma may arise in one or several areas 

(Figure 494). 

PALEOPATHOLOGY 

The earliest reference to Paget's disease in archeological human remains is a report by Pales 

(1929:263-267), which includes a brief discussion 

of a femur from the Neolithic site at Lozere in 

France. The specimen is part of the collections of 

the Museum of Natural History of Paris. There 

has been some postmortem damage to the joint 

surfaces, but otherwise they appear normal. 

There is considerable anterior curvature of the 

diaphysis with a marked expansion of the cortex. 

The X-ray film indicates that the cortical bone 

in the diaphysis is reduced in density. The line 

drawings, published in Pales (1929) as figures 1 

and 2, portray a gross morphology compatible 

with a diagnosis of Paget's disease. No histology 

was reported, making this diagnosis probable but 

not certain. The antiquity of this specimen would 

certainly make restudy with appropriate histology desirable. 

Five purported cases of Paget's disease in prehistoric skeletons from the Illinois River Valley 

in the United States were published by Denninger 

(1933). In all cases the long bones have a thickened cortex. In some of the cases the skulls were 

thickened. In no case was there any report of the 

histology. In view of the many disease conditions 

that can produce the lesions described by Denninger, including periostitis and osteomyelitis, 

these specimens would need to be restudied before 

the diagnosis of Paget's disease can be accepted. 

Fisher (1935) reports a purported case of Paget's disease in a skeleton from a prehistoric 

mound in Crawford County, Wisconsin, USA. 

The specimen consists of portions of both tibiae 

and a part of the lower jaw. Morse (1969:57-58) 

also discusses this case noting that the jaw fragment is normal. He also notes that one of the 

tibiae was sent for study to Dr. Lent C. Johnson 

at the Armed Forces Institute of Pathology in 

Washington, D.C. Johnson found no histological 

evidence of Paget's disease in the bone. 

Wells and Woodhouse (1975) report a case of 

Paget's disease in a skeleton from an Anglo-Saxon 

burial ground (A.D. 950) in Durham, England. 

The skeleton is male with an estimated age of 65 

years. The authors indicate that the skull is unusually thick. The surface of most bones is rough 

and pitted. The spine exhibited kyphoscoliosis 

with evidence of osteoarthritis. The pelvis has the 

appearance of a slight osteomalacic deformity. 

The major bones of all the extremities are bowed. 

The left femur was fractured antemortem with 

poor alignment and considerable deformity with 

healing. The poor quality of the bone prevented 

the preparation of microscopic sections; thus the 

presence of the mosaic histological pattern could 

not be determined. However, the generalized distribution of abnormal bone, the long bone deformity, and the roentgen film appearance of the 

femora and vertebrae are compatible with a diagnosis of Paget's disease. The vertebrae show 

coarse vertical striations and discontinuity of affected vertebrae. 

Fibrous Dysplasia 

PATHOLOGY 

Fibrous dysplasia is a bone disease of unknown 

etiology characterized by faulty differentiation of 

portions of the osteogenic mesenchyme into fibroosseous tissue. It manifests itself in a single or in 

multiple bones, often limited to one limb or one 

side of the body (Lichtenstein and Jaffe, 1942: 

814). The entire skeleton is never involved even 

in widespread manifestations, and there is no 

basic metabolic disorder (Figures 495, 496). The 

disease, especially the polyostotic form with widespread manifestations, usually begins in childhood and often stops progressing at the termination of the growth period (Uehlinger, 1960:283). 

Females are more often affected than males and 

may exhibit endocrine disturbances leading to 

precocious puberty and premature termination of 
316 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

FIGURES 495, 496.—Polyostotic fibrous dysplasia showing "shepherd crook" deformity of both 

proximal femora and deforming involvement of many bones: 495, Anterior view. 496, Posterior 

view. (40-year-old female, DPUS 4016, French catalog 323a from before 1891.) 

growth (Albright's disease) (Albright, Butler, 

Hampton, and Smith, 1937) (Figures 497-499). 

The bone lesion consists of dysplastic proliferation of endosteal fibrous tissue, in which fine 

trabeculae of woven bone arise by direct fibroosseous metaplasia, without differentiation of osteoblasts. Depending on the amount of bone and 

the degree of mineralization, the lesion may appear purely lytic, ground-glass, or dense on Xray. It may ultimately involve most parts of a 

bone, sparing some portions and practically always sparing the epiphyses. In small bones, tumor-like expansion is observed after pressure resorption of the old cortex. However, at least a 

thin shell of newly formed periosteal bone surrounds the lesion at all times. This results in a 

cyst-like lesion confined by a ridged, thin, bony 

shell, particularly in small and flat bones, such as 

ribs and pelvis. The weakened bony structure 

permits mechanical deformities with or without 

major pathological fractures (Figure 497). The 

recognition of the lesion in dry bone would depend on at least partial preservation of the fine 

or coarse woven bone trabeculae (Figure 500). 

Admittedly such preservation may be unlikely 

and differentiation from various other lesions, 

especially giant cell tumor, unicameral cyst, and 

nonossifying fibroma may be impossible in a 

single lesion. Hyperparathyroidism should be possible to rule out on the basis of absence of metabolic bone disease in uninvolved parts of the 

skeleton. 
NUMBER 28 317 

Monostotic Fibrous Dysplasia 

This condition occurs most frequently in a rib, 

the proximal femoral metaphysis, the jaws, or the 

tibia. Other bones are less frequently involved 

(Schlumberger, 1946a, 1946b). In dry bone, dif 

ferentiation from eosinophilic granuloma and enchondroma may be impossible, especially in the 

rib. In the mandible, or less often in the maxilla, 

giant cell reparative granuloma or eosinophilic 

granuloma may give a similar picture. Probably 

the most characteristic solitary lesion is that of 

the proximal femoral metaphysis. The dysplastic 

focus often weakens the subtrochanteric area resulting in the typical "shepherd crook" deformity, 

while the head and neck of the femur are more 

nearly normal. 

Polyostotic Fibrous Dysplasia 

In involved limbs the disease affects the proximal bones earlier and more severely than the 

distal ones. The proximal femoral metaphysis is 

the most frequent location (Figures 501-503). In 

36 cases of polyostotic fibrous dysplasia, the involvement of different bones was as follows: femur 

36, tibia 24, fibula 10, metatarsals 10, toes 8, 

humerus 12, radius 9, metacarpals 8, fingers 6, 

pelvis 15, skull base 6 (Schinz, Baensch, Friedl, 

and Uehlinger, 1951-1952(2): 1199). 

The lesions in the cranial vault and face are 

asymmetrical and often unilateral (Figure 498). 

Rounded masses of woven bone can be found in 

the diploe, similar to those seen more frequently 

in advanced Paget's disease. Lesions of the skull 

base tend to be sclerotic and inhibit pneumatization of the paranasal sinuses (Figure 499). 

The skeletal distribution of the lesions, especially in the limbs, is similar to that of Ollier's 

enchondromatosis; but, in the latter the distal 

tubular bones of the extremities (metacarpals, 

metatarsals, and phalanges) are most frequently 

and more severely involved. The presence of the 

cranial changes discussed above would also rule 

out enchondromatosis. 

PALEOPATHOLOGY 

Denninger (1931) provides a description of a 

probable case of polyostotic fibrous dysplasia in 

an adult male skeleton from a pre-Columbian site 

in Illinois, USA. The disease affected the bones 

of the left side of the body. The left side of the 

skull was deformed and there was the characteristic shepherd's crook deformity of the left femur. 

The cortex of the bowed upper end of the left 

femur is thin. This region has multiple cyst-like 

lesions revealed in the roentgen film. Postmortem 

breakage reveals the poorly organized bone partially filling the marrow space. The right femur 

is not deformed but exhibits some pathological 

changes on the proximal end. In the region of the 

greater trochanter, there are perforations of the 

cortex with poorly organized, spongy bone apparent through the perforations. Similar lesions 

are found on both tibiae and fibulae. The bones 

of the left foot show increased porosity of the 

cortical surface with cortical perforations and 

spongy bone apparent in the first and second 

metatarsals. Perforations and spongy bone development are also seen in the bones of the pelvis 

primarily on the left side. The ribs of the left side 

are similarly affected as is the seventh cervical 

vertebra and many of the thoracic vertebrae. 

Denninger's description of this case leaves little 

doubt that this pre-Columbian Indian skeleton is 

an example of polyostotic fibrous dysplasia. 

Wells' (1963b) report of an adult skeleton from 

an Anglo-Saxon site in Britain, dated in the 

seventh century A.D., provides another example 

of probable fibrous dysplasia. Of the bones recovered, only the left humerus shows evidence of 

the disease. The normal axis of the bone has been 

deformed producing anterior bowing. The cortex 

of the diaphysis is enlarged with the focus being 

near midshaft. The longitudinal cut section reveals extensive development of fine spongy bone 

in this region with cystic cavities between the 

spongy bone and the cortex. 

A possible case of fibrous dysplasia in a young 

adult female skull from Egypt (NMNH 256360) 

was brought to my attention by Dr. Eugen Strou-
318 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 
NUMBER 28 319 

FIGURES 497-499.—Polyostotic fibrous dysplasia with precocious puberty and skin pigmentations (Albright's disease): 

497, Both lower extremities with multiple deformities and 

fractures. 498, Skull showing left-sided involvement and 

deformity. 499, Skull base shows massive frontal involvement, somewhat resembling Paget's disease. (16-year-old 

female, 161 bones were affected, FPAM 5807, autopsy 331 

from 1949, St. Polten Hospital, Austria.) 

FIGURE 500.—Polyostotic fibrous dysplasia of bisected distal 

tibia, showing finely porous abnormal bone replacing cortex 

and spongiosa. (40-year-old Chinese male; studied by Putschar in 1960 at Department of Pathology, National University, Taipei, Taiwan.) 
FIGURES 501-503.—Polyostotic fibrous dysplasia: 501, Right 

femur, posterior view, showing typical "shepherd crook" 

deformity. 502, Cut section, showing cystic changes and 

pumice bone filling the medullary cavity. 503, Right lower 

leg, showing marked involvement of fibula. (63-year-old 

male, with involvement of many bones, IPAZ autopsy 953 

from 1938, skeleton 80.) 

FIGURE 504.—Fibrous dysplasia in the region of the frontal 

sinus. Note roughened texture and nodular fiber bone proliferation (arrows). (NMNH 256360.) 
NUMBER 28 321 

hal during his research on the Egyptian skeletal 

collection in the National Museum of Natural 

History, USA. The skull is from the rock-tombs 

at Lisht, a Twelfth Dynasty site near Matanieh 

in Upper Egypt. The skull is fragmentary but 

includes much of the vault and face. The abnormality is limited to the frontal bone in the region 

of the frontal sinus. Indeed it was a postmortem 

break in the skull in this region that revealed the 

presence of dense round nodules of bone near the 

frontal sinus and coarse bony spicules covering 

the internal bony surface of the sinus cavity (Figure 504). 

The gross morphology of the lesions is compatible with a diagnosis of either Paget's disease or 

fibrous dysplasia. The young adult age estimate 

would, however, make Paget's disease unlikely. A 

ground section through one of the circular nodules of bone reveals a mixture of well-organized 

lamellar bone and poorly organized woven bone. 

There is no evidence of the characteristic mosaic 

pattern associated with Paget's disease. The combination of fiber bone proliferation, the lack of 

mosaic pattern in the histology, and the young 

age of the specimen support a diagnosis of fibrous 

dysplasia, although a very mild expression of this 

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FIGURES 505, 506.—Myositis ossificans progressiva: 505, 

Thorax, lateral view, showing bony bridging along fascial 

planes. 506, Pelvis and right thigh, anterior view, showing 

extensive fascial ossification. (48-year-old female, IPAZ autopsy 2406 from 1968.) 
322 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

disease. Greenfield (1975, fig. 3:106) has published a documented case of fibrous dysplasia 

showing similar nodular proliferation of bone in 

the frontal sinus revealed by the roentgen films. 

Myositis Ossificans Progressiva 

PATHOLOGY 

This is a rare hereditary and familial disease 

(Uehlinger, 1936). The name is really misleading 

because it is not an inflammatory disease and it 

does not primarily affect the muscles but the 

fascias, tendons, and ligaments. Although the 

disease may not manifest itself until a child is 

several years of age, its congenital nature is attested by frequent concomitant congenital anomalies. These are shortness, usually bilateral, of the 

first metatarsal and/or the first metacarpal. At 

times the second phalanx of the fifth finger is 

missing. The disease usually begins to manifest 

itself in the neck-shoulder area and progresses 

distally. It begins as fibroblastic proliferation followed by metaplastic ossification of the fibrous 

tissue. The end result is formation of bony prongs 

and spicules following the outline of muscles from 

origin to insertion and immobilizing intervening 

joints. The ossification of spinal ligaments may 

be followed by ankylosis of spinal and costovertebral joints. The disease progresses into adulthood, resulting in almost complete skeletal immobility (Figures 505, 506). The limitation of 

respiratory motion and the bridging of the temporomandibular joint may contribute to death. 
Neuromechanical Deformities 

PATHOLOGY 

Kyphosis 

Kyphosis is the pathological increase of the 

normal slight anterior concave curvature of the 

thoracic spine. The deformity is caused either by 

changes in the intervertebral discs (primary kyphosis) or of the vertebrae themselves (secondary 

kyphosis) (Putschar, 1937:675-681). The primary 

kyphosis separates into two groups: the juvenile 

and the senile form. 

JUVENILE KYPHOSIS (Scheuermann's disease).— 

This deformity develops in adolescents with great 

predilection ofthe male sex (Scheuermann, 1921). 

The apex of the curvature in this deformity usually falls in the area ofthe eighth to tenth thoracic 

vertebra. The underlying cause is probably extrusion of nucleus pulposus material, mostly into the 

adjacent vertebral bodies (Schmorl's nodes) followed by anterior narrowing ofthe disc space and 

subsequent growth disturbance in this area ofthe 

end-plate, resulting in some degree of wedging 

(Schmorl, 1930; Schmorl and Junghanns, 1971: 

345-354). The location of the wedge vertebrae 

usually coincides with the apex of the curvature. 

Since, of course, the curvature cannot be appreciated on the skeleton, the presence of one or 

several adjacent wedge vertebrae and of round or 

oblong defects near the center of the vertebral 

end-plate, corresponding to the location of the 

disc herniation, would be the main findings. If 

this type of deformity is long survived, secondary 

sclerotic changes and marginal anterior lipping 

may be added to these findings. 

SENILE KYPHOSIS.—This is a very common 

spinal deformity, developing in the fifth decade 

and increasing in frequency and degree with age. 

The underlying cause is degeneration and attrition of the intervertebral discs, particularly of 

their anterior portions, in the physiologically 

kyphotic thoracic segments. The apex of the curvature in senile kyphosis is in the upper thoracic 

spine, and wedging of vertebral bodies is either 

absent or slight. The main features recognizable 

on skeletal material are osteosclerosis of the anterior portions, especially the end-plates, of affected vertebrae with marginal lipping and, sometimes, anterior fusion of several segments (Figure 

507, left). Disc herniations are not a characteristic 

part of this condition. The anterior marginal 

lipping, in contrast to spondylosis deformans, 

arises directly from the vertebral end-plate and is 

usually of rather moderate dimension. In advanced cases the anterior portions of the interverFiGURE 507.—Kyphosis. Two bisected spines. Left: Senile 

kyphosis with anterior compression of intervertebral discs 

and bony bridging. Right: Severe postmenopausal osteoporosis with kyphosis, showing biconcave '"codfish" vertebrae. 

(IPAZ 6017: left, 71-year-old female, autopsy 385 from 1955; 

right, 65-year-old female, autopsy 403 from 1955.) 

323 
324 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

tebral disc may be replaced by continuous bone 

trabeculae and the lipping may be completely 

smoothed down by modeling resorption. 

SECONDARY KYPHOSIS.—This deformity is secondary to lowered mechanical resistance of the 

vertebrae. A variety of conditions, especially osteoporosis (Figure 507, right), osteomalacia, hyperparathyroidism, and Paget's disease, may present this complication. In this condition wedge 

vertebrae, due to compression fractures, are common. The intrinsic changes of the underlying 

bone disease would help in recognition of the 

deformity as secondary. This is especially true of 

kyphosis due to a congenital anomaly ofthe spine, 

such as dorsal hemivertebra. 

Scoliosis 

The vertical position of the spinal column in 

the human depends on a precarious balance of 

neuromuscular control and fibrous supportive 

structures. Scoliosis is the term used for lateral 

deviations of the spinal column from the midsagittal plane. The factors leading to this deformity 

are various and usually not obvious. An exception 

to this is scoliosis due to congenital maldevelopment of one or several spinal segments, especially 

lateral hemivertebra or segmental disarrangement. However, the pathogenesis need not concern us here since the observable bone changes, 

which develop secondary to the deformity, are all 

essentially the same. Scoliosis, with or without a 

significant kyphotic component, often starts in 

childhood and progresses throughout the growing 

age and early adult life. This factor is of importance because the bone changes are, to a large 

extent, the result of altered growth and modeling 

under abnormally directed static and dynamic 

stresses (Putschar, 1937:649-675). 

The deformity usually shows a double curvature, which permits the position of the head close 

to the midsagittal plane despite the lateral deviation of the spinal column. These deviations are 

not purely lateral but include a considerable element of rotation toward the convexity (Figure 

508). This, as well as abnormal pull of tendons 

and ligaments, accounts for the bone changes by 

means of modified growth and modeling. Since, 

in the dry skeleton, the continuity ofthe vertebral 

column is not maintained, alterations of individual vertebrae are important for the recognition of 

the deformity. The transverse processes of the 

thoracic vertebrae are deflected backwards on the 

convex and forwards on the concave side. The 

transverse processes of the lumbar spine are short 

and plump on the convex side and long, slender, 

and pointed on the concave side. The spinous 

processes usually are deflected towards the concavity in the lumbar spine. The vertebral bodies 

show lateral wedging at the apex of the curvature 

in addition to rotation and torsion. The latter is 

reflected in a diagonal pattern of the vertebral 

cortex, secondary to the altered course of the 

fibers of the anterior spinal ligament. The spongiosa architecture of the laterally wedged vertebrae usually shows sclerotic reinforcement on the 

overburdened concave side and reduction in 

number and size of trabeculae on the unburdened 

convex side. The areas of the neural arch and of 

the diarthrodial intervertebral joints show the 

least degree of deformation. In long-standing 

severe scoliosis, additional bone changes may occur secondary to degenerative processes in the 

eccentrically stressed intervertebral discs. These 

changes are most marked laterally on the concave 

side of the wedged vertebrae and follow the same 

pattern as described in senile kyphosis. Bony fusion across the narrowed intervertebral space occurs in the apex of the curvature. The overexpansion of the disc on the convex side may lead to 

bony replacement of the disc itself Ossification 

of various spinal ligaments and, occasionally, ankylosis across the diarthrodial joints can occur, 

especially on the concave side of the apex of the 

curvature. 

The ribs, which are firmly attached to the spine 

by two joints and to the sternum through the rib 

cartilage, must adapt their shape and curvature 

to the spinal deformity. Generally, they are 

spread on the convexity and pressed together on 

the concavity of the spinal deformity. These 

changes include alterations of the size and loca-
NUMBER 28 325 

FIGURE 508.—Severe thoracic and lumbar kyphoscoliosis. 

Notice the structural torsion of the vertebrae, the fusion on 

the concavity and the new joint formations between compressed ribs. (VM, no number.) 

tion of the costovertebral articular facets and of 

the angulation of the neck of the ribs. Length, 

width, and curvature are altered by modified 

growth and modeling. If the curvature is extreme, 

ankylosis of costovertebral joints and formation 

of new, joint-like, irregular areas between compressed ribs can occur (Figure 508). 

A special type of kyphoscoliosis can occur in 

neurofibromatosis, a condition characterized by 

formation of multiple nerve sheath tumors on 

spinal and peripheral nerves. In this disease, the 

maximal scoliotic deformity more frequently involves the cervical spine. The tumors of spinal 

nerves in this condition lead to smooth widening 

of interspinal foramina in the affected area. This 

feature would permit recognition of such a scoliosis as due to neurofibromatosis even on the dry 

skeleton. 

Postparalytic Deformities 

Neuromuscular paralysis occurring in childhood and adolescence can affect the skeleton in 

various ways. Paralysis of different muscle groups 

can unbalance the spinal column and cause postparalytic scoliosis. The examination of such a 

spine will not reveal the pathogenesis of the deformity. Since the growth and surface modeling 

of a bone are influenced by muscle pull and 

weight-bearing, the lack of either or both will 

alter its size and shape. Paralysis of an extremity 

results in smooth and slender shafts because of 

reduction of periosteal bone formation (Figure 

509). The lack of muscle pull and weight-bearing 

is most pronounced when it affects the hip joint. 

FIGURE 509.—Femora from individual with poliomyelitic 

paralysis of left leg. Notice small diameter and minimal 

surface relief of the affected left femur. (19-year-old male, 

died 15 years after onset of paralysis, IPAZ 4429, autopsy 

468 from 1939.) 
326 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

FIGURE 510.—Postparalytic deformity of proximal right femur showing extreme coxa valga, flattened, elongated lesser 

trochanter, slender femoral shaft and small femoral head. 

(14y2-year-old female, 9 years after acute poliomyelitis, IPAZ 

4337, autopsy 1372 from 1938.) 

The paralyzed hip develops a much steeper angle 

of the femoral neck, which is slender and elongated (paralytic coxa valga) (Figure 510) (Putschar, 1937:701-705). The most common postparalytic foot deformity is a clubfoot (pes equinovarus), which may be combined with an exaggerated pla.ntar arch and uptilted calcaneus (pes 

cavus) (Figures 511, 512). 

PALEOPATHOLOGY 

Scoliosis 

References to spinal deformities in the literature on paleopathology are rare. This is due, in 

part, to the fact that vertebrae are not as well 

preserved as many other parts of the skeleton. 

FIGURES 511, 512.—Postparalytic deformities of distal skeleton, showing lumbosacral scoliosis, flaring ischia from sitting, 

flexion contracture of both knees, bilateral clubfoot with 

paralytic pes cavus deformity: 511, Overall view. 512, Dorsal 

view of left foot. (24-year-old male, many years after poliomyelitis, FPAM 5013, autopsy 88103 from 1880.) 

Another problem is that kyphosis and scoliosis 

are most noticeable in an articulated spine and 

thus would tend to be overlooked in archeological 

specimens unless the defect was noticed during 
NUMBER 28 327 

excavation. (For some examples of kyphosis induced by infectious destruction of vertebral bodies, see pages 125, 145, 166). 

Brothwell (1961:327-328) reviewed five published and unpublished cases of scoliosis in British 

skeletons. One of these is from the Beaker period 

(ca. 2000 B.C.). Brothwell attributes the scoliosis 

in this specimen to congenital problems in which 

additional centers of ossification developed as 

semi vertebrae. The anterior view shown on 

Brothwell's plate 8d clearly shows the lateral 

deviation that resulted from this abnormal development. 

An interesting case of scoliosis comes from the 

archeological site of Hawikuh located near the 

modern village of Zuni in New Mexico, USA. 

The site includes pre-Columbian and historic 

components. During the early historic period the 

site was used as a base of operations for the 

Spanish explorer Francisco Vasquez de Coronado 

and a Franciscan mission was established there in 

1630 (Smith, Woodbury, and Woodbury, 1966: 

1). The site, including the cemetery, was excavated between 1917 and 1923. Skeletal material 

from both the pre- and post-contact period was 

recovered from the cemetery. 

The skeleton in question (NMNH 314297) is 

from that portion of the cemetery associated with 

the historic period. However, the skull is morphologically different from the Indian Christian burials. J. Lawrence Angel (personal communication) suggests that the ethnic affinity of the skull 

is Spanish and that this skeleton may be the 

remains of one of the priests massacred during 

the Pueblo Revolt of 1680. 

The estimated age of the skeleton is between 

25 and 35 years. The sex is clearly male. There is 

no evidence of deformity on the skull although 

there is considerable antemortem tooth loss, including all incisors. The upper right canine was 

FIGURES 513, 514.—Scoliosis: 513, Spinal column exhibiting 

an S-shaped lateral curve. 514, Second and tenth ribs showing asymmetrical development in response to scoliosis. 

(Adult male, NMNH 314297.) 
328 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

lost shortly before death as evidenced by the 

reactive bone still in evidence in this part of the 

maxilla. Caries is well advanced in the upper left 

first molar although the corresponding molar on 

the right is worn but not decayed. Only the lower 

right third molar is present in the mandible, with 

clear evidence that most of the molars were lost 

antemortem. 

The upper extremities have a slight lateral 

deviation of the distal humeri and considerable 

bowing of both radii and ulnae. The major abnormality is seen in the vertebrae, which exhibit 

an S-shaped scoliosis (Figure 513). The ribs (Figure 514) and manubrium are also abnormal reflecting the conditions on the vertebrae. The cervical vertebrae and first two thoracic vertebrae 

are normal. The first lateral deviation to the right 

begins at T-3 and continues to T-8 where the 

lateral deviation begins to be oriented toward the 

left, continuing until L-2 when the lateral orientation shifts back toward the right. The sacrum 

shows minimal evidence of abnormality and the 

pelvis appears normal. The major long bones of 

the lower limbs have a slight lateral bowing of 

the distal tibiae and fibulae. The combination of 

scoliosis and slight deformity ofthe limbs suggests 

the possibility of rickets in early childhood as the 

cause of scoliosis. 

Postparalytic Deformities 

Wells (1964a:92) reports the presence of a left 

humerus and radius, which is shorter and lighter 

than the right humerus and radius in a Neolithic 

skeleton from Sussex, England. He notes a similar 

deformity in a Bronze Age skeleton from Norfolk, 

England. Both of these cases are probable examples of postparalytic deformity. 

Mitchell (1900) has described a predynastic 

Egyptian skeleton in which the left femur is 

shorter than the right. He attributes this condition to poliomyelitis. Elliot-Smith (1912) noted 

the existence of a deformity of the left foot in the 

Nineteenth Dynasty Egyptian mummy of Pharaoh Siptah. Initially he attributed the deformity 

to poliomyelitis but in a subsequent publication 

(Elliot-Smith and Dawson, 1924:100, 157) he refers to this specimen as an example of clubfoot. 
Skeletal Dysplasias 

The skeletal dysplasias can be grouped into 

two categories: (1) those affecting the proliferation and biology of cartilage and (2) those affecting the formation and/or resorption of bone. 

As far as the group of cartilage dysplasias is 

concerned, a great number of syndromes have 

been described. Most of them are very rare and 

terminate fatally during infancy or early childhood. Others are survived but fail to show diagnostic features in the macerated skeleton that 

would permit classification beyond the term "dysplasia." For these reasons only classical achondroplasia, with typical disproportional dwarfism and 

some mucopolysaccharidoses will be discussed 

here in some detail. The dysplasias of bone formation and resorption, however, are better characterized and, in most instances, due to the tissue 

involved, exhibit identifiable skeletal changes. 

For this reason, even rare entities have been 

included in this discussion. 

Achondroplasia 

PATHOLOGY 

Achondroplasia is a familial or sporadic congenital disorder of cartilage growth. This condition is the cause of the most common form of 

dwarfism. In many cases, affected persons can 

reach adult age. The basic defect is a severe 

inhibition of cartilage proliferation, thereby limiting the enchondral growth in all areas of the 

body. The enchondral ossification of the limited 

amount of proliferated cartilage proceeds normally and so does the intramembranous and 

periosteal bone formation. Adult achondroplastic 

dwarfs usually reach a height of 130 centimeters 

or less (M0rch, 1941:118). The dwarfism is disproportionate (Figure 515). This is due to the fact 

that the bones with the fastest growth and the 

least number of growth plates are most severely 

shortened. Thus, the trunk, although shortened, 

is least affected because of the great number of 

growth plates in the spine. The extremities are 

much more severely shortened and, in the extremities, the fast growing long bones, which have 

only two growth plates, are most markedly affected. The femur is more shortened than any 

other bone, followed by the humerus, and the 

bones of the lower legs and forearms. The fingers 

and toes with their numerous growth plates are 

less affected. The body disproportions in the 

achondroplastic newborn are about the same as 

in the adult. The discrepancy between longitudinal growth, controlled by cartilage proliferation, and circumferential growth, controlled by 

periosteal bone formation, results in changes in 

the shape ofthe bones (Figure 516). The diameter 

of the diaphyses and the cortical thickness are 

close to normal. The epiphyses and metaphyses 

are usually disproportionately wide as compared 

to the length of the bones (Figure 517). The 

degree of penetration varies from case to case and 

milder forms are observed. For details the reader 

is referred to the monograph of M0rch (1941), 

who studied more than 100 achondroplastic individuals. The skull typically is brachycephalic 

but large and bulbous. This is due to the discrepancy of the short skull base, which depends on 

enchondral growth at the intersphenoidal and 

spheno-occipital synchondroses, and the normal 

sized cranial vault, which is intramembranous in 

its development. The more normally large cranial 

vault over the short skull base exhibits an increased curvature, which is responsible for the 

bulging forehead. On the other hand, the shortness of the skull base is responsible for the markedly depressed bridge ofthe nose. M0rch (1941: 

118) found this typical skull deformity in 80 

percent of his cases. However, the characteristic 

shortness of all four limbs was present in all cases. 

329 
330 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

FIGURE 515.—Achondroplastic dwarf Notice the short and 

thick bones; the rudimentary development of humeral and 

femoral heads with varus deformity is unusual. (Skeleton of 

adult female, who died in childbirth; PMUG 2668, autopsy 

15050.) 

FIGURE 517.—Hyperplastic achondroplasia of right femur. 

Notice the short and thick diaphysis and the enlarged flaring 

metaphyses. (Newborn, W M S 59.3 from 1880.) 

All patients also showed limitation of the extension of the elbow joint to 150 degrees and increased lumbar lordosis. About one-third showed 

lower thoracic kyphosis and approximately onehalf revealed the typical "trident" hand, in which 

the fingers tend to be of more equal length than 

normal, with tapering terminal phalanges. The 

pelvis can be severely narrowed in all dimensions, 

particularly in the diameter between symphysis 

pubis and sacral promontory (Figure 516). This 

may create an insurmountable obstetric difficulty 

in the female achondroplastic dwarf in primitive 

populations, resulting in the death of the mother 

and the fetus (Figure 515). 

FIGURE 516.—Achondroplasia, showing narrow pelvis with 

flaring iliac wings and thick, short femora with accentuated 

muscular insertions. (Adult, probably female, FPAM 5680.) 
NUMBER 28 331 

PALEOPATHOLOGY 

Seligmann (1912) published photographs and 

a brief description of a skull found by Sir Flinders 

Petrie in the temple of Thotmes IV at Thebes in 

Egypt (Eighteenth Dynasty). He states that the 

abnormality seen in this skull could be the result 

of cretinism or achondroplasia. In Seligmann's 

opinion the skull had poorly developed nasal 

bones, which led him to conclude that cretinism 

was the cause of the skull abnormality. Keith 

(1913:195-200), in his general discussion of 

achondroplasia, includes a description of this 

skull concluding that it was achondroplastic. The 

skull was from a female individual about 25 years 

of age. Keith's profile drawing shows shortening 

of the skull base with otherwise relatively normal 

development of the cranium, a condition that is 

characteristic of achondroplasia. 

Bleyer (1940) concludes that a predynastic (ca. 

5000 B.C.) skeleton from the Budari district in 

Egypt was achondroplastic. He also attributes the 

FIGURES 518-520.—Achondroplastic skull from the Fourth 

Dynasty Egyptian tomb of King Mersekha: 518, Facial view. 

519, Left, lateral view; note the depression in the region of 

the nose. 520, Skull base; note the abnormal shape of the 

foramen magnum and the short basioccipital. (BMNH 

AF. 11.4/427.) 
FIGURE 521.—Achondroplastic long bones (left humerus, 

right femur, and both tibiae) from the Fourth Dynasty 

Egyptian tomb of King Mersekha. Notice the short length 

but relatively normal diameter of the shafts and epiphyses. 

(BMNH AF. 11.4/427; scale in cm.) 

abnormality of a humerus found in the First 

Dynasty Egyptian tomb of King Zer to achondroplasia. 

Brothwell (1967b:433) briefly describes two 

achondroplastic skeletal specimens from the 

Fourth Dynasty Egyptian tomb of King Mersekha. The first case consists of long bones only. 

The second specimen (BMNH AF. 11.4/427) includes the skull, the left humerus, right femur, 

and both tibiae. I have studied and photographed 

the latter specimen, which exhibits the classic 

features of achondroplasia. The skull vault is of 

normal size (Figures 518-520). However, the skull 

base is shortened as evidenced by the very short 

basioccipital (Figure 520). The shortened skull 

SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

base contributes to the appearance of a depression 

in the middle third of the face. The nasal bones 

and the frontal processes ofthe maxilla are broad, 

and the short face is accentuated by the prognathism ofthe alveolar portion ofthe maxilla. All 

adult teeth have erupted but have little wear, 

suggesting that the individual was a young adult. 

The long bones are very short (Figure 521) with 

the femur about 235 millimeters in maximum 

length. The epiphyses and apophyses are all 

fused, indicating adulthood. The tibiae have 

slight medial bowing of the distal half The humerus is robust with the abnormal joint morphology associated with achondroplasia. The diaphyses of all the long bones have near normal 

diameters, indicating virtually normal periosteal 

bone formation. 

In the New World, Fowke (1902:372) describes 

a skeleton, less than 152 centimeters (5 feet) in 

stature (undated but probably pre-Columbian) 

from mound number 4 near Waverly, Ohio, USA. 

The long bones were thick with extraordinary 

development of the areas of muscle attachment. 

The skull was thick and had a full and high 

forehead. Snow (1943:10) concluded that the features in Fowke's description were compatible with 

achondroplasia, and I would agree that such a 

conclusion is reasonable. 

Snow (1943) provides unequivocal evidence of 

achondroplasia in indigenous New World skeletal 

material. Two dwarf skeletons were recovered 

during excavations of thousands of skeletons from 

the cemetery of an Indian village site at Moundville, Alabama, USA. No European or Colonial 

American trade goods were recovered during excavations indicating that the site was pre-contact. 

The first of the two dwarf skeletons to be 

excavated was an adult female with a stature 

estimated to be about 125 centimeters. The posterior portion of the skull was not recovered. The 

forehead is prominent. The region around the 

nose is depressed, and the maxilla and mandible 

are prognathous. All the adult teeth had been lost 

antemortem. The postcranial bones exhibit the 

classic features of achondroplasia. The vertebral 

column, because of the multiple growth centers. 
NUMBER 28 333 

523 

is less affected than the long bones. The bones of 

all limbs are short but robust. 

The second skeleton is a male dwarf excavated 

five years later but from the same area of the 

FIGURES 522, 523.—Achondroplastic male skeleton from a 

pre-Columbian archeological site at Moundville, Alabama, 

USA: 522, Front view of skeleton (scale in cm and inches). 

523, Left lateral view of skull. (Photograph from Snow, 1943, 

figs. 4, 6; courtesy Dr. Joseph Vogel and the Natural History 

Museum, University of Alabama.) 

mound (Figure 522). The reported stature ofthe 

male dwarf is about 150 centimeters, but this 

estimate is probably too large. The skull (Figure 

523) is virtually complete and exhibits abnormal 
334 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

features similar to the female dwarf The cranium 

is large (Snow estimates cranial capacity to be 

2011 cc), but the skull base is short, creating a 

midfacial depression. The individual was an adult 

FIGURES 524, 525.—Achondroplastic skull from ossuary IV, 

Accokeek, Maryland, USA: 524, Left lateral view; note the 

concave profile of the face. 525, Base of skull; note the 

abnormal foramen magnum and short basioccipital. 

(NMNH 379527.) 

but had lost many teeth to decay antemortem. 

The long bones are short but robust. The humeral 

and femoral heads are abnormally displaced distally. In the femora, the greater trochanter is at 

the same level as the femoral head. The morphological features of both dwarf skeletons are compatible with a diagnosis of achondroplasia. 

Hoffman (1976) provides a description of an 

archeological achondroplastic skeleton from Sacramento County, California, USA. The specimen 

is dated between A.D. 1500 and 1800. The skeleton 

is nearly complete and is currently part of the 

Lowie Museum of Anthropology skeletal collection (University of California, Berkeley, California, USA). The cranium is large and bulbous. 

The midfacial region is depressed and the cranial 

base shortened. The vertebrae are small and 

kyphotic at Til and T12. Vertebral bodies of 

TlO-Ll have projecting osteophytes creating a 

beak-like lateral appearance. The long bones are 

very short but robust exhibiting an external morphology common in achondroplasia. The kyphosis associated with the lower thoracic and 

upper lumbar vertebrae is also suggestive of 

Hunter's disease. 

An isolated skull from ossuary IV at the Ferguson Farm, Accokeek, Maryland, USA, is probably another New World example of achondroplasia. The site is Late Woodland with no evidence of European trade goods associated with 

the ossuary. This suggests a pre-contact date. The 

skull vault is of normal size. The face is fragmentary, although there is little doubt that the region 

of the nasal bones was depressed (Figure 524). 

The base of the skull exhibits an abnormal foramen magnum and an abnormally short basioccipital (Figure 525). 

Mucopolysaccharidoses 

PATHOLOGY 

The mucopolysaccharidoses are a group of diseases characterized by biochemical abnormalities 

in the mesenchymal cells, mainly fibroblasts and 

chondrocytes elaborating mucopolysaccharides. 

In these abnormal conditions, various mucopoly-
NUMBER 28 335 

saccharides are, in part, accumulated in these 

cells, interfering with their normal function. Since 

mucopolysaccharides form a large part of cartilage matrix, cartilage proliferation and, therefore, 

skeletal growth and development are variously 

affected in these conditions. The base of these 

conditions is an inborn, genetically controlled, 

biochemical abnormality, which often manifests 

itself in several members of one family. Presently, 

six different mucopolysaccharidoses have been 

recognized (McKusick, 1972:521-686), of which 

only three are sufficiently well characterized in 

their skeletal manifestations to warrant a brief 

discussion here: Hurler's syndrome (gargoylism), 

Hunter's syndrome, and Morquio-Brailsford's 

syndrome. 

HURLER'S SYNDROME (mucopolysaccharidosis 

type I).—This syndrome is transmitted as an 

autosomal recessive trait affecting children of 

either sex. The time and degree of its manifestations vary. Often it becomes apparent in infancy 

or early childhood and few individuals live beyond 10 years. Skeletal changes have even been 

observed in the newborn (Caffey, 1951, 1952). 

The main substance accumulated in fibroblasts 

and cartilage cells is chondroitin sulphate B. The 

abnormality involves many tissues and organs of 

the body, but we are here only concerned with 

the bone changes. In typical cases the affected 

growth cartilages lead to markedly stunted 

growth or dwarfism. Also, the development of 

secondary ossification centers is delayed and morphologically abnormal (Jaffe, 1972:545). Among 

the many deviations from the normal size and 

shape of bones observed, the changes ofthe spine 

and of the hands are the most typical. The spine 

shows a characteristic ossification defect at the 

dorsolumbar junction. This may affect the twelfth 

thoracic but usually involves the first and often, 

to a lesser degree, the second lumbar vertebral 

body. The cartilage model of any involved vertebra is ossified only in the posterior and inferior 

portions, giving the impression of a beak-like 

inferior projection on the lateral view of the Xray or of the dry bone. This lack of anterior 

ossification at the dorsolumbar junction leads to 

a sharply angulated kyphosis at this level. The 

hand shows marked widening of the metaphyses 

of metacarpals and phalanges adjacent to the 

growth plate, with tapered narrowing on the 

other end. Thus, the enlarged metacarpals taper 

proximally, the phalanges distally. As usual, the 

first metacarpal behaves like a phalanx. The 

distal phalanges are hypoplastic. The changes are 

less marked in the corresponding bones of the 

feet. 

Early in the disease, the long bones show periosteal bone deposition followed by increased endosteal cortical resorption, leading to widening of 

the marrow space and cortical thinning (Caffey, 

1951, 1952). The humeri often show varus deformities of the head. Other deformities are coxa 

valga with plump femoral necks, shallow acetabula and genu valgum due to lateral tilting ofthe 

maldeveloped distal femoral epiphysis (Jaffe, 

1972:542-552). 

The skull frequently shows premature closure 

ofthe sagittal suture, giving a laterally narrowed, 

anteroposteriorly elongated, configuration. The 

skull base in the area ofthe sella is elongated; the 

mandibular condyles are flattened or even concave (Aegerter and Kirkpatrick, 1968:138-152). 

The skull bones are thick and dense. The scapulae 

are often broad and thick, as are the ribs, with 

exception of their misshapen necks and their narrow osteocartilaginous junctions. 

HUNTER'S SYNDROME (mucopolysaccharidosis 

type II).—In this syndrome, which was only recently differentiated from Hurler's syndrome, the 

skeletal changes are practically identical with 

those of Hurler's syndrome. The inheritance is 

sex-linked so that only males are affected. Survival into adult age occurs. 

MORQUIO-BRAILSFORD SYNDROME (mucopolysaccharidosis type IV).—This syndrome is transmitted as an autosomal recessive trait. Both sexes 

are involved equally and there are usually multiple siblings affected in one family. The syndrome is not apparent at birth but begins to 

manifest itself in early childhood. The progressive 

accumulation of a mucopolysaccharide, probably 

mostly keratan sulfate, leads to skeletal changes 

and growth disturbances. The outstanding bone 

change is the flattening of all vertebrae with 
336 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

widening of the transverse and anteroposterior 

diameter. There is anterior wedging, especially at 

the dorsolumbar junction, leading to severe kyphosis. Subsequent to this deformity, the ribs 

show an altered configuration and the thorax is 

enlarged in its anteroposterior diameter. The sternum is angulated at the junction of the manubrium and corpus and protrudes forward. Growth 

is generally stunted, resulting in dwarfed stature. 

There is disproportionate shortening of the neck 

and trunk due to general flattening of the vertebral bodies (platyspondylia). The skull is normal 

and, therefore, relatively too large. The primary 

dentition is usually normal, but the permanent 

teeth are abnormal in shape and position (Aegerter and Kirkpatrick, 1968:141). 

Secondary ossification centers are delayed and 

show abnormal configuration. The long bones 

may be significantly shortened and often show 

flaring of the metaphyses with lipping at the 

junction with the epiphysis. Similar spike-like 

projections occur on tarsal bones (Jaffe, 1972: 

220). Hip deformities are common, consisting of 

large deep acetabula with irregular contour and 

delayed ossification of the femoral head (Jaffe, 

1972:219). 

PALEOPATHOLOGY 

In the Maclvor collection stored in the British 

Museum (Natural History), there is a pair of 

deformed humeri (BMNH AF.l 1.3/75). There 

are no other bones associated with this specimen 

which is from early dynastic Egypt. Both humeri 

are abnormally short (Figure 526). The diaphysis 

is normal in diameter with a well-developed delFIGURES 526, 527.—Possible mucopolysaccharidoses in the isolated right and left humeri of an 

early dynastic Egyptian specimen: 526, Anterior view, showing the shortened ,'ength and 

abnormal development ofthe humeral heads. 527, Medial view, showing porosity and abnormal 

development of humeral heads. (BMNH AF. 11.3/75; scales in cm.) 
NUMBER 28 337 

toid tuberosity. This combination of features is 

suggestive of achondroplasia. However, the humeral heads exhibit severe malformation of the 

articular surface with pitting of the subchondral 

plate particularly on the right (Figure 527). The 

left humerus is about 2 centimeters shorter than 

the right. Brothwell (1965a: 164) includes an illustration of the right humerus in his discussion 

of congenital defects but does not attempt a 

specific diagnosis. The general appearance of the 

humeri is undoubtedly indicative of a chondrodysplasia, although the extreme abnormality of 

the humeral heads is not typical of achondroplasia. The external morphology of the humeral 

heads suggests an almost complete failure in the 

development of the epiphysis. This aspect is more 

compatible with conditions seen in the mucopolysaccharidoses. While the age cannot be determined, the fusion of the distal humeral epiphyses and apophyses indicate a minimum age of 

about 14 with a good probability of at least being 

a young adult. The age of the individual makes 

Hurler's syndrome a less likely possibility than 

either Hunter's syndrome or Morquio-Brailsford's 

syndrome. 

Osteogenesis Imperfecta 

PATHOLOGY 

Osteogenesis imperfecta is based on an inborn 

deficiency of the mesenchymal cells in the production of mature collagen fibrils. It is often a 

familial disorder but also occurs as a spontaneous 

mutation. In severe manifestations of this disorder 

the collagenous fibrous tissue throughout the 

body is poorly developed. However, since the 

organic bone matrix almost entirely consists of 

collagen, skeletal changes dominate the picture. 

The disease expresses itself in two forms: osteogenesis imperfecta fetalis (Vrolik type) and osteogenesis imperfecta tarda (Lobstein type). 

OSTEOGENESIS IMPERFECTA FETALIS.—In this 

condition the disease fully manifests itself in intrauterine life. Osteoblastic inhibition results in 

great reduction of enchondral and intramembraneous bone formation. The condition is often 

fatal at birth or in early childhood. Already in 

the uterus the fetus suffers numerous fractures, 

which show various stages of callus formation at 

birth. The newborn reveals markedly shortened 

extremities because of the accordion pleating of 

numerous transverse fractures of the long bones. 

The trunk is also shortened because of compression fractures of the vertebral bodies. Numerous 

transverse rib fractures exhibit multiple knobby 

swellings of fracture callus. The skull is soft and 

may show only very rudimentary ossification centers in the cranial vault. If the condition is survived for a longer time, multiple ossification centers may form, giving rise to Wormian bones. The 

bones show an extremely thin cortex and very 

sparse and thin cancellous trabeculae. Recognition of this type in skeletal remains would depend 

on ideal conditions of preservation. However, 

since the condition affects the entire skeleton, it 

could be surmised even from single bones. 

OSTEOGENESIS IMPERFECTA TARDA.—This condition is not manifest at birth but reveals itself 

during childhood and adolescence. The continued deficiency of bone formation results in frequent fractures, particularly of the long bones. 

Although normal bone formation is inhibited, 

trauma can overcome the osteoblastic inhibition 

and fractures heal. In some instances callus formation can be so excessive that it may be mistaken for an osteosarcoma. In these individuals, 

enchondral growth is normal, but periosteal bone 

formation is very limited. This results in bones of 

normal length but subnormal diameter of the 

shafts. The cortex is very thin and the cancellous 

bone sparse. The inhibited osteoblastic activity is 

also reflected in the delay of cortical remodeling. 

This can be demonstrated microscopically in undecalcified ground sections, revealing persistence 

of surface parallel lamellar bone and scarce osteonization. Multiple fractures may lead to severe 

deformities, especially of the weight-bearing 

bones of the lower extremities and the pelvis. 

However, some of the severe deformities are also 

due to bending by muscle pull and static forces, 

which the defective skeleton cannot resist (Figure 

528). Any bone except the skull may be deformed. 

The tendency to develop new fractures usually 
338 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

FIGURE 528.—Osteogenesis imperfecta tarda. Notice the severe bending deformities of both legs and the narrow pelvis. 

From a woman who died in childbirth. (PMES 1QAL(2).) 

diminishes in adult age. Since odontoblasts produce the collagenous matrix of dentin, they are 

subject to the same suppression as osteoblasts. 

Teeth of the first and second dentition show 

deficient and discolored dentin, while the ectodermal enamel is normally formed. However, 

inadequate support of the enamel leads to chipping and early dental loss. 

PALEOPATHOLOGY 

Wells (1965b) describes a burial from an AngloSaxon cemetery at Burgh Castle in Suffolk, England, dated about the seventh century A.D. The 

abnormality occurs in the left femur and consists 

of a 90-degree angulation of the proximal diaphysis. Wells estimates the age to be at least 18 

years. The femur appears to have been fractured 

twice at the point of the angulation. Wells states 

that possible causes are rickets, fibrous dysplasia, 

and osteogenesis imperfecta. He rejects rickets, 

since that disease is unknown in other AngloSaxon burials, and fibrous dysplasia for unstated 

reasons, concluding that osteogenesis imperfecta 

is most likely. The age of the individual would 

indicate the tarda manifestation if osteogenesis 

imperfecta is the cause. 

A more certain example of osteogenesis imperfecta is described by Gray (1970). The skeletal 

specimen is that of an infant from the cemetery 

of Beni Hassan on the east bank of the Nile at a 

site known as Speos Artemidos in Egypt. This site 

is dated to the Twenty-first Dynasty (ca. 1000 

B.C.). The skeleton was found in a coffin and is 

currently stored in the British Museum, Department of Egyptian Antiquities (Registry No. 

41603). The bones are friable and extremely light. 

The skull has an enlarged vault with vertically 

elongated eye orbits and multiple ossification centers. The teeth are also abnormal with poorly 

developed roots. The long bones are deformed. 

The bones of the lower extremities show wellmarked anterolateral bowing. The cortex is thin 

and the spongiosa poorly developed. All of these 

features are compatible with a diagnosis of osteogenesis imperfecta. 

Dysostosis Cleidocranialis 

PATHOLOGY 

This is a congenital disorder of skeletal development mainly affecting intramembranous bone 

formation. The condition is usually familial but 

sporadic cases occur. The most marked changes 

concern the cranial vault and the clavicles (Figures 529, 530), both areas of intramembranous 

ossification. The skull is brachycephalic with increased transverse diameter and accentuated 

frontal and parietal bosses (Figure 531). The 

fontanels are large and persist long beyond the 

normal time for closure. The sutures are widely 

separated and remain open, including the metopic suture. The space between the sutures may 
NUMBER 28 339 

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FIGURES 529, 530.—Dysostosis cleidocranialis: 529, Frontal 

view, showing enlarged frontal skull with wide-open anterior 

fontanel and rudimentary clavicles; notice delayed dental 

eruption. 530, Posterior view, showing Wormian bones. (25-

year-old male, FPAM 5701 from 1909.) 

FIGURES 531, 532.—Dysostosis cleidocranialis: 531, Frontal 

view, showing enlarged skull vault and delayed eruption of 

teeth. 532, Skull base, showing open intersphenoidal and 

spheno-occipital growth plates (arrows). (25-year-old male, 

FPAM 3766 from 1879.) 
340 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

ultimately be occupied by numerous Wormian 

bones (Figure 530). The skull base may be slightly 

shortened and the basal growth plates fail to fuse 

(Figure 532). The facial bones may be small and 

the mandible may not be fused at the chin. 

Clavicles, which develop from three ossification 

centers, of which at least the middle one is intramembranous, are usually defective, unilaterally 

or bilaterally. They may be completely missing 

or, more often, only the lateral or only the medial 

third is developed. Failure to unite different portions of the clavicle may be observed (congenital 

pseudoarthrosis). In the rest ofthe skeleton, late 

and rudimentary ossification of the femoral head 

and neck may result in severe coxa vara deformity. The pelvic bones may show delayed or incomplete fusion of ischium and pubis. Dental development is affected, leading to delayed shedding 

of the primary dentition, delayed or incomplete 

eruption ofthe secondary dentition (Figure 531) 

and formation of dentigerous cysts. Since this 

disturbance does not interfere with survival, the 

adult skeleton may demonstrate changes that are 

fairly diagnostic of this anomaly. 

Osteopetrosis 

PATHOLOGY 

Osteopetrosis is a congenital disorder of the 

skeleton characterized by severe inhibition of osteoclastic activity. The disease often is familial, 

occurring in several generations and in multiple 

siblings. There is no sex predilection. Parental 

consanguinity is common. The disease occurs in 

an infantile severe form leading to death in infancy or early childhood, and a mild form, starting in later childhood or adolescence and compatible with adult survival. 

INFANTILE OSTEOPETROSIS.—This condition begins in fetal life. The basic defect is severe inhibition of osteoclastic activity without suppression 

of osteoblastic activity. This leads to preservation 

of primary trabeculae of enchondral growth containing cores of calcified cartilage. Continued 

deposition of bone on such trabeculae results in 

FIGURE 533.—Osteopetrosis of both femora with pathological 

fracture of one. Notice the complete bony filling of the 

medullary canal and the lack of metaphysial remodeling. 

(15-month-old male, MG H autopsy 34143.) 

a jumbled, solid mass of bone and calcified cartilage, filling the bone marrow spaces and ultimately causing fatal anemia. All remodeling has 

to be initiated by osteoclastic resorption, but it is 

generally inhibited in this disease. This condition 

first becomes noticeable on the metaphysial side 

of the fast growing plates, such as the distal femur 

and proximal tibia; however, ultimately all bones 

show abnormal density. Since there is some fluctuation in the degree of osteoclastic suppression, 

parallel banding of denser and more lucent areas 

occur in the metaphyses. Corresponding to this 

are concentric layers of alternating degrees of 

density in ossification centers (Figures 533, 534). 

Ultimately, the whole medullary space is filled 

with the abnormal bone containing calcified cartilage (Figure 535). On the long bones the physi-
NUMBER 28 341 

FIGURE 534.—Osteopetrosis. X-ray of vertebral bodies. Notice the great density and concentrical arrangement of bone. 

(15-month-old male, MGH autopsy 34143.) 

©logical remodeling of the metaphysis is inhibited, resulting in marked widening of this area 

instead of the usual flare. In spite of the excessive 

amount of bone present, its quality is inferior and 

a stress-oriented trajectorial trabecular system is 

not developed. Therefore, pathological, usually 

transverse, fractures commonly occur (Figure 

533), 

The skull shows thickening of the base and of 

the vault. In cases with severe anemia there may 

be expansion of the medullary space beneath the 

outer periosteum, giving a striated pattern on Xray (Schinz, Baensch, Friedl, and Uehlinger, 

1951-1952, (1):699). The suppressed osteoclastic 

activity prevents the normal endocranial resorption and the necessary widening of the foramina 

for the passage of the various cranial nerves. The 

FIGURE 535.—Osteopetrosis. X-ray of femur. Notice the great 

density of the secondary ossification centers and the alternating bands of density and lucency in the unremodeled 

metaphyses. (15-month-old male, MGH autopsy 34143.) 

facial bones also become dense. The normally 

cancellous bones (vertebrae, ribs, sternum, pelvis) 

show marble-like density on X-ray without distinct trabecular pattern. The bones are heavy. 

OSTEOPETROSIS TARDA.—In this milder form, 

the fetal encroachment on the bone marrow space 

does not occur and the remodeling defects on the 

long bones and the skull are slight or absent. 

However, the density and heaviness of many 

bones is apparent (Figures 536, 537), the inferior 

architecture of the bones remains, and repeated 

pathological fractures in adults are common. The 

delayed remodeling of the diaphysial cortex microscopically shows small osteons separated by 

residual periosteal and enchondral bone (Laubmann, 1935). 
FIGURES 536, 537.—Generalized osteosclerosis, probably osteopetrosis: 536, Massive ivory-like osteosclerosis with occlusion of medullary cavity of distal right humerus. 537, Lower 

thoracic vertebrae with sclerotic obliteration of cancellous 

pattern. (45-year-old male with fractures and progressive 

anemia, WM S66.2 and S66.3 from 1932.) 

SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

Pyknodysostosis 

PATHOLOGY 

This hereditary congenital condition has some 

similarity to osteopetrosis, because the bones are 

unusually dense and easily fracture on minor 

trauma. However, the medullary cavities are not 

obliterated. The skull shows increased density, 

but the sutures remain widely separated and the 

fontanels open. The intervening portions of the 

cranial vault ultimately fill in with Wormian 

bones. An additional feature of this condition is 

tapering of the terminal phalanges with absence 

of the usual tufts. The individuals are frequently 

dwarfed, in part as the result of multiple fractures. 

Metaphysial Dysplasia (Pyle's Disease) 

PATHOLOGY 

This is a familial hereditary disorder characterized by delayed remodeling of metaphysial 

cortical bone. The straight or even convex contour of the metaphysis is most marked on the 

distal femur and proximal tibia. Similar remodeling defects may be observed on the cranial base 

and facial skeleton, revealing thickened bones of 

increased density resembling so-called leontiasis 

ossea. 

PALEOPATHOLOGY 

Urteaga and Moseley (1967) provide an excellent report of a case of metaphysial dysplasia in 

a partial skeleton from a Mochica period (A.D. 

200-800) burial from Peru. Unfortunately, except 

for the right humerus, the upper portion of the 

skeleton was destroyed by grave diggers. This 

humerus has an enlarged metaphysis, which extends toward the midshaft. The shaft itself is 

bowed laterally. The major abnormality is seen 

adjacent to both knees. In this region there is a 

pronounced failure of remodeling during the 

growth phase, which has created the classic Erlenmeyer-flask deformity of the metaphyses associated with metaphysial dysplasia. Both tibiae 
NUMBER 28 343 

FIGURES 538, 539.—Melorheostosis: 538, Left leg, lateral view, showing nodular and plaque-like 

periosteal hyperostosis. 539, Distal left femur, longitudinally cut section, showing medullary 

endosteal sclerosis and spotty epiphysial spongiosclerosis. (24-year-oId male, IPAZ MB 6672 

from 1964.) 
344 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

are deformed with lateral S-shaped bowing. A 

longitudinal section through one femur and tibia 

reveals extensive cancellous bone development in 

the abnormal areas adjacent to the knee. The 

failure of cortical and cancellous bone remodeling 

in the metaphysial areas leaves no doubt about 

the diagnosis of metaphysial dysplasia. 

Diaphysial Sclerosis 

(Camurati-Engelmann's Disease) 

PATHOLOGY 

This familial hereditary disorder is characterized by continued periosteal bone deposition over 

the diaphyses of tubular bones, sparing the metaphyses and epiphyses. This results in columnar 

or even fusiform shape of the long bones. The 

periosteal cortical thickening is most marked at 

middiaphysis and tapers towards both metaphyses. The cancellous bones and the skull are 

not involved. The disease usually manifests itself 

in childhood, but mild cases may not be discovered until adult age. 

Melorheostosis (Leri's Disease) 

PATHOLOGY 

This is probably a developmental disorder usually only involving several bones of one extremity. 

The disease manifests itself usually in childhood 

and adolescence. The changes consist of streamlike deposition of dense bone on the periosteal 

and endosteal surfaces, resembling the distribution of wax running down on a candle (Figures 

538-541). Usually a whole row of bones are involved in continuity, representing a ray of the 

extremity; for instance, humerus, radius, radial 

carpal, thumb, and index finger. Trunk and cranium are spared. 

FIGURES 540, 541.—Melorheostosis: 540, Middiaphysial 

cross-section of left femur, showing periosteal, endosteal, and 

medullary bone deposition (24-year-old male, IPAZ MB 

6672 from 1964). 541, Schematic drawing of the involvement 

of the left pelvis and leg in this case (courtesy Prof E. 

Uehlinger). 

541 
NUMBER 28 345 

PALEOPATHOLOGY 

Lester (1967) provides a brief report of a skeleton found in an Ipiutak cemetery at Point Hope, 

Alaska. The specimen was dated by carbon-14 

analysis to the fifth century A.D. The skeleton is 

male and reported to be in excess of 50 years. It 

is well preserved with most bones represented. 

The only bone affected by the disease process is 

the right fibula. The abnormality is characterized 

by a lumpy deposition of dense bone on the 

periosteal surface of the diaphysis. The metaphysis and joint surfaces appear to be spared. The 

medial aspect of the diaphysial cortex is normal. 

The external appearance of the abnormal bone 

and the dense roentgen-film appearance are compatible with a diagnosis of melorheostosis, although periostitis or a local osteomyelitis should 

be considered as well. 

Osteopoikilosis 

PATHOLOGY 

This is a familial hereditary anomaly of the 

skeleton, which may manifest itself in several 

siblings. It has been found in the newborn. Since 

the anomaly is not visible on external inspection 

and is asymptomatic, only a chance X-ray will 

reveal its presence. The anomaly consists of multiple spotty condensations of dense lamellar bone 

in the spongiosa (Schmorl, 1931). The individual 

foci are one or several millimeters in diameter, 

round or oblong, and, in some areas, confluent. 

They appear on X-ray as foci of cortical density. 

They are most commonly found in the epiphyses 

and metaphyses of the long bones, the carpal and 

tarsal bones, and small tubular bones of hands 

and feet. There is, not uncommonly, symmetrical 

involvement. With the exception of the areas 

adjacent to the glenoid fossa and to the acetabulum, the bones of the trunk and, as a rule, of the 

skull are usually uninvolved. 

This lesion is so characteristic that it should be 

readily identifiable on X-ray of dry bone provided 

that postburial sand infiltration, which could 

mimic the picture, can be excluded. 

Osteopathia Striata 

PATHOLOGY 

This anomaly is similar to osteopoikilosis and 

likewise is not visible by external inspection ofthe 

bones. The lesion consists of parallel, streak-like 

condensations of cancellous bone, involving 

epiphyses and metaphyses of long bones. The 

skeletal distribution is similar to that in osteopoikilosis and mixtures of both anomalies have 

been observed. 
Skeletal Malformations 

Malformations ofthe entire skeleton are mostly 

related to incomplete twinning and usually are 

not compatible with prolonged postfetal life (Figure 542). The various forms of these malformations will not be discussed here. Less serious malformations ofthe skeleton are often due to failure 

of closure of fetal clefts or suppression of a portion 

of the skeletogenic mesenchyme. Many of these 

are compatible with life and maturity. Of these 

the most frequent and characteristic will be discussed here in their regional occurrence. 

Skull 

PATHOLOGY 

The most frequent fatal malformation of the 

skull is anencephaly, a condition in which the 

cranial vault never developed and the rudimentary brain is directly exposed. This condition is 

not infrequently combined with partial or complete failure of closure of the neural canal (craniorachischisis). The skull base shows marked deformities of its constituent bones. The skull vault 

is absent and the orbits may be rudimentary. 

A common malformation compatible with life 

is the uni- or bilateral lack of fusion of the globular and maxillary processes resulting in various 

degrees of hare-lip and cleft palate. The defect is 

located between the lateral incisor and the canine 

tooth. 

Congenital herniations of meninges and brain 

will present on the skull bones as round, midline 

defects above the bridge of the nose or in the 

occipital area (Figures 543, 544). 

Premature synostoses of one or several cranial 

sutures result in various characteristic skull deformities distinctly different from cultural, artificial deformations (Figure 545). The increasing 

pressure of the growing brain leads to separation 

of open sutures (Figure 546) and deep cerebral 

impressions on the inner table (Figure 547), 

PALEOPATHOLOGY 

CLEFT LIP AND CLEFT PALATE.—These abnormalities are uncommon in archeological skeletons. However, this does not mean that cleft lip 

and palate were rare in antiquity. Tretsven (1965: 

229) found the incidence of cleft abnormalities 

among living American Indians in Montana to 

be higher than non-Indian people. He further 

notes (p. 236) that many American Indian groups 

have descriptive terms for cleft abnormalities in 

their native language. Mortality of infants with 

cleft lip and/or palate would have been high in 

antiquity. The defect inhibits effective nursing 

which would have contributed to early death. 

Also many infants with grossly observable deformities would have been killed. 

Berndorfer (1962) has described a female skull 

about 25-30 years of age excavated in southern 

Hungary and dated to the fifteenth century A.D. 

The only abnormality of the skull is a poorly 

developed premaxilla and a small defect of the 

inferior aspect ofthe right pyriform aperture. The 

anterior alveolar region ofthe maxilla has a slight 

indentation suggestive of a cleft lip. The incisors 

are missing antemortem and the sockets for their 

roots are not present. Berndorfer rules out gingival atrophy following antemortem loss of the 

incisors, because the remaining teeth are normal. 

He does not consider cultural artificial extraction 

of the teeth as a possible cause of the slight defect 

in the alveolar bone. However, the abnormality 

of the pyriform aperture and subnormal development of the premaxilla would support a diagnosis of slight cleft lip. 

Brooks and Hohenthal (1963) report the presence of cleft abnormalities in three indigenous 

skulls from two archeological cemeteries in California, USA. Two of the skulls are from the 

Newark site on the southeastern shore of San 

Francisco Bay. The skulls come from the Late 

Middle Horizon level dated by carbon-14 to 2340 

346 
FIGURE 542.—Dicephalic infant with duplication of the 

spine. (Newborn, FPAM 1576.) 

years B.P. The skulls are stored in the Museum of 

Anthropology at the University of California, 

Berkeley, USA (Nos. 8474 and 9859). The third 

skull (No. 22,117) is from a site in Sacramento 

County in California and is dated between 2000 

and 4000 years B.P. 

Skull No. 8474 is from a male about 30 to 40 

years of age. Both the maxilla and palate have 

cleft defects. The upper right incisors were missing antemortem. The mandible is reported to be 

normal. Skull No. 9859 is also male with an 

estimated age between 22 and 25 years. The nasal 

bones are abnormal but the picture is obscured 

by postmorteiji damage. Both the maxilla and 

palate have cleft-type defects. The extensive nature of the facial abnormality added to the general porosity of the bones of the forehead and face 

are atypical of cleft palate and lip. The authors 

suggest the possibility of injury, although they 

conclude that cleft abnormality is the best interpretation ofthe defect. Cranium No. 22,117 is a 

FIGURES 543, 544.—Anterior midline encephalocele: 543, 

Anterior view; notice flattened protruding nasal bones above 

defect. 544, Endocranial view; notice smooth-edged defect 

of ethmoid area. (5 years old, PMUG 3824, autopsy 17395 

from 1890.) 
348 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

FIGURE 547.—Premature synostosis of the sagittal and midportion of the coronal suture, showing pressure atrophy with 

deep cerebral impressions and midline perforations of the 

cranial vault; endocranial view. (2-year-old male, FPAM 

2118 from 1844.) 

FIGURES 545, 546.—Premature synostosis of sagittal suture 

with midline bony ridge and lateral defects along suture 

lines, secondary to intracranial pressure: 545, Top view. 546, 

Lateral view of skull. (9-week-old infant, FPAM 3576 from 

1877.) 

FIGURE 548.—Cleft palate of the central and posterior area. 

(Nubian skull, BMNH 210 72/291.) 
NUMBER 28 349 

FIGURES 549, 550.—Cleft lip and palate in a skull from an 

indigenous South Pacific islander: 549, Facial view. 550, 

View of palate. (WM A 1.3.) 

female skull between 25 and 28 years of age. The 

skull has a marked unilateral loss of bone of the 

alveolar portion of the right maxilla. There are 

also extensive inferior bony projections on the 

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FIGURES 551, 552.—Cleft palate and possible cleft lip in a 

young adult, female skull from an archeological site in 

Colorado, USA: 551, Facial view. 552, View of palate. 

(NMNH 316482.) 

maxilla near the suture with the zygomatic bone. 

The authors conclude that this is a case of unilateral hare-lip. On this specimen there is also evidence of porosity, which in my opinion is suggestive of a reactive response to injury and/or infection. Such a possibility should be kept in mind in 

studying paleopathological specimens with abnormalities of the maxilla and palate. 

Derry (1938a) reports two examples of agenesis 

of the premaxillary region of the maxilla. The 

first example is a skull from a Twenty-fifth Dynasty Egyptian site on the east bank of the Nile. 
350 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

FIGURES 553, 554.—Cleft lip and palate in the skull of an 8-

to 10-year-old child from the Nasca region in Peru (right) 

compared with a normal skull (left) of about the same age 

from an archeological site in Kentucky, USA: 553, Facial 

view. 554, View of palate. (NMNH 293252, right; NMN H 

243198, left.) 

The skull is female, past middle age and normal 

except for the absence of the premaxilla. The 

hard palate is reduced in size and the maxillary 

incisors are absent antemortem. The provenience 

ofthe second skull is unknown. The skull appears 

to be from an adult female. As in the first skull 

the premaxilla is absent. The mandibles associated with the skulls project beyond the anterior 

border of the maxilla (mandibular prognathism) 

supporting the observation of subnormal development of the maxilla. 

In the Nubian pathology collection of the British Museum (Natural History) there is a complete 

cranium of an adult female which exhibits cleft 

palate (BMNH 210 72/291). Most ofthe teeth 

have been lost postmortem, but judging from the 

intact dental alveoli the teeth were normal. The 

cleft defect is bilateral and involves only the 

FIGURES 555, 556.—Cleft lip and palate in the incomplete 

adult skull from an archeological site in Kentucky, USA: 

555, Facial view. 556, View of palate. (NMNH 243208.) 

central and posterior portions of the palate (Figure 548). 

An example of both cleft lip and palate is seen 

in a skull from the Wellcome Museum of the 

Royal College of Surgeons of England in London 

(Figures 549, 550). The specimen (WM A 1.3) is 

from an indigenous South Pacific islander. The 

right side ofthe alveolar arch is relatively normal, 

although there is a complete cleft through the left 

portion of the anterior maxilla, which is contin-
NUMBER 28 351 

uous with the cleft of the left hard palate. The 

maxillary defect is continuous with the pyriform 

aperture. 

Three specimens from the National Museum 

of Natural History collections at the Smithsonian 

Institution, Washington, D.C, USA, provide additional evidence for the presence of cleft abnormalities in New World indigenous populations. 

The first of these two specimens is a complete 

cranium of a young adult female about 18 to 20 

years of age from southwestern Colorado, USA 

(NMNH 316482). The archeological age of the 

skull is unknown. The skull exhibits some occipital flattening, which is unrelated to the abnormality of the maxilla. Both maxillary central 

incisors and the right lateral incisor are absent 

antemortem. The sockets are absent and the alveolar bone is thin. Dental alveolei are present for 

the remaining teeth although the socket for the 

upper right canine is poorly formed with the 

anterior portion missing. There is a small cleft in 

the central portion of the intermaxillary suture 

(Figure 551). The nasal bones are depressed about 

15 millimeters below nasion, as if the result of a 

healed blow in childhood. The palate is cleft 

primarily to the right of the midline with slight 

abnormality to the left (Figure 552). Both the 

palatine process of the maxilla and the palatine 

bone are involved although the defect is less 

severe in the posterior portion of the palate. The 

mandible is normal. 

The second specimen is from an 8- to 10-yearold child from the Nasca region in Peru (NMNH 

293252). The archeological age is not known. 

Only the anterior portion of the skull is present 

including the frontal, sphenoid, zygomatic, nasal, 

palatine bones, and the maxilla. The cleft defect 

is primarily on the left side (Figure 553, 554) and 

involves the alveolar and palatine process of the 

maxilla, as well as the palatine bone and the 

internal bones ofthe nasal cavity. The cleft ofthe 

alveolus and palate are continuous with each 

other and with the nasal cavity. There has been 

a lateral deviation of the intermaxillary suture 

toward the right side of the face. 

The final example of cleft palate is from an 

archeological site in Kentucky, USA (NMNH 

243208). The archeological age is unknown. The 

alveolar portion ofthe left maxilla may have been 

affected as is suggested by the antemortem loss of 

the central and lateral incisors (Figures 555, 556). 

However the major defect is a large oval opening 

in the palate. The vomer and conchae are missing 

as well. 

The above-published and original examples 

serve to document the presence of the cleft lip 

and palate in both New and Old World indigenous ancient populations. They also serve to illustrate the point that other conditions such as 

trauma and infection need to be considered in 

differential diagnosis. 

CONGENITAL HERNIATION.—Stewart (1975) has 

called attention to the misinterpretation of congenital herniations (dysraphism) ofthe skull. The 

defects in the bone produced by such herniations 

have been attributed to the practice of trephination (Powell, 1965; Sublett and Wray, 1970). 

Both examples, published by Stewart (1975), exhibit herniation very close to bregma. They have 

a sharply defined anterior border but a more 

gradual slope to the depression posteriorly. 

Another example of this abnormality was 

brought to my attention by T. D. Stewart. The 

skull is from the skeletal collections of the Field 

Museum of Natural History (FM 40208) and is 

from a child 6 to 8 years of age from Ancon, Peru. 

The archeological age is thought to be between 

A.D. 1000 and 1200. The large abnormality is 

located on the frontal bone anterior to bregma 

(Figures 557, 558). The defect extends completely 

through both tables of the frontal bone. The 

margin is most sharply defined on the posterior 

edge with a gradual elongated depression extending anteriorly about midway toward nasion. Lateral to the defect are two areas of porous reactive 

bone. The defect itself is well circumscribed, exhibiting smooth compact bone throughout. 

The nature of the soft tissue lesion, of course, 

is not known. Stewart (1975:437) notes that the 

prognosis in a living patient depends on the type 

of herniated tissue and the amount of herniation. 

The prognosis for survival to adulthood would be 

poor in a case where the herniation was as extensive as evidenced by the size of the skull defect. 
352 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

FIGURES 557, 558.—Congenital herniation ofthe skull vault 

in a 6- to 8-year-old child from an archeological site in 

Ancon, Peru: 557, Facial view. 558, Top view; note the 

porous, reactive bone surrounding the herniation. (FM 

40208.) 

Thus, it appears that this abnormality may have 

led to the premature death of the child. 

BIPARIETAL PERFORATIONS.—Broca (1875) has 

described another congenital defect of the skull 

vault in which there are unusually large perforations of the parietal bones often occurring as an 

enlargement of the parietal foramina. An example of this condition is seen in a skull from California, USA (NMNH 276981). The skull is that 

of an adult male with bilateral perforations ofthe 

parietals exceeding one centimeter in diameter 

(Figure 559). The perforations are located on the 

posterior portion of both parietals near the sagittal suture. 

PREMATURE FUSION OF SUTURES OF THE SKULL 

(Craniostenosis).—This abnormality can change 

the normal shape of the skull. The changes in 

shape will depend on which sutures are involved 

and the age of onset of the fusion. For example, 

fusion of the sagittal suture in early childhood 

produces an elongated skull with a prominent 

forehead. Fusion of the coronal suture in early 

childhood results in a shorter skull but prominent 

development of the frontal region with a very 

high forehead. Several reports on craniostenosis 

in archeological skeletons have been published 

(e.g., Davis, 1865; Eiseley and Asling, 1944; Hohenthal and Brooks, 1960; Comas, 1965; Bennett, 

1967; Stewart, 1972). 

Of the many examples of craniostenosis in the 

collections of the National Museum of Natural 

History, Washington, D.C, USA, I have chosen 

^^H^ 

:§f^^'«7ai. ; ^ • 

^^I^R^ 

^ -

^ 

S3li«ilfc.-*' 

^m^^H 

•*-^v' "^5^B 

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'^.i^^^MSi 

4^^H 

FIGURE 559.—Biparietal perforations in an adult skull from 

an archeological site in California, USA. (NMNH 276981.) 
NUMBER 28 353 

FIGURES 560, 561.—Premature fusion ofthe sagittal suture 

in the skull of a 3- to 4-year-old child from the Twentieth to 

Twenty-fifth Dynasty site of Karga in Egypt: 560, Left 

lateral view; note the somewhat abnormal length of the 

skull. 561, Top view, showing the fused sagittal suture. 

(NMNH 258504.) 

three cases to illustrate the relevant features associated with this abnormality. A child's skull 

(NMNH 258504) from the Twentieth to Twentyfifth Dynasty site of Karga in Egypt illustrates 

premature closure of the sagittal suture (Figures 

560, 561). This child was 3 to 4 years of age at 

FIGURES 562, 563.—Premature fusion of the coronal and 

sphenoparietal suture in a young adult skull from Wales, 

Alaska, USA: 562, Left lateral view, showing the complete 

fusion of the sphenoparietal suture and the slight saddledepression near bregma. 563, Top view. (NMNH 333470.) 

the time of death. Except for the anterior 2 

centimeters, the entire sagittal suture was fused. 

All other sutures, which are normally open at 3 

to 4 years of age, are open. Even at this early age, 

the skull is slightly elongated with a slight axial 
354 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

FIGURES 564-566.—Early premature fusion of the sagittal 

suture in an adult male skull from an archeological site in 

the region of Cinco Cerros, Peru: 564, Facial view, showing 

the keel-like vault of the skull. 565, Left lateral view. 566, 

Top view. (NMNH 293841.) 

deviation of the skull suggestive of excessive 

growth on the right side ofthe skull vault. 

Premature fusion of the coronal suture is seen 

in a female Eskimo skull from Wales, Alaska, 

USA (NMNH 333470). The skull is from an 

individual about 25 to 30 years of age at the time 

of death. Endocranially the coronal, sagittal, and 

lambdoid sutures are fused. Ectocranially both 

the sagittal and lambdoid have begun to fuse. 

Except for 2 centimeters on either side of the 

midline, the coronal suture is completely fused 

ectocranially with obliteration of the sutural lines 

(Figures 562, 563). The sphenoparietal suture is 

also fused and obliterated. In profile the skull 

vault exhibits a saddle-like depression just posterior to bregma. Otherwise, the shape of the skull 
NUMBER 28 355 

is normal indicating that the premature fusion of 

the coronal and sphenoparietal suture occurred 

after significant growth ofthe brain and skull had 

ceased. 

Another example of craniostenosis in an adult 

skull illustrates the morphological features that 

occur when premature fusion occurs early in 

childhood or infancy. The skull is from Cinco 

Cerros, Peru, and is from an adult male (NMNH 

293841). The archeological age is not known with 

certainty but is thought to be pre-Columbian. 

The skull is long and very narrow (markedly 

dolichocephalic) with the elongation primarily in 

the posterior portion of the skull (Figures 564-

566). The sagittal suture is completely fused both 

endo- and ectocranially. The coronal and lambdoid sutures are completely fused endocranially 

and partially fused ectocranially. 

HYDROCEPHALUS.—Although this condition is 

rarely a congenital abnormality, it does produce 

malformation of the skull that could be observed 

in archeological specimens; for this reason brief 

mention of this condition is included below. Derry 

(1913) provides a detailed report on an abnormally large skull and postcranial bones from the 

Roman period in Egypt. The bones are those of 

a fully adult male. Derry reports that the cranial 

capacity is at least 2900 cubic centimeters, which 

exceeds the normal range of cranial capacity by 

several hundred cubic centimeters. The lateral 

drawing of the skull exhibits relatively normal 

proportions for the face so that the skull abnormality is limited to the brain case. The postcranial bones exhibit abnormalities that Derry attributes to partial paralysis of the left side. Grim 

and Plathner (1952) describe a hydrocephalic 

skull from central Europe dated to the Stone Age. 

Armelagos (1969) reports the presence of a hydrocephalic skull of a child in Nubian skeletal material dated between A.D. 350 and 550. 

Spine 

PATHOLOGY 

Complete lack of closure of the neural canal 

shows the two halves of the spinous processes and 

neural arches pointing laterally (complete spina 

bifida). Incomplete bony fusion of one or several 

spinous processes (spina bifida occulta) is common, especially in the sacral area (Figure 567). 

Lateral or dorsal hemivertebrae occur, causing 

abnormal curvature of the spine (congenital scoliosis and kyphosis) (Figures 568, 569). Segmental 

disarrangement of vertebral ossification centers 

may result in fusion of vertebral segments, particularly in the cervical area (Klippel-Feil syndrome). Symmetrical or asymmetrical sacralization of the fifth lumbar vertebra is common. 

Lumbarization of the first sacral vertebra is more 

rare. The sacrum and coccyx may completely fail 

to develop, resulting in close approximation of 

the posterior iliac spines. 

FIGURE 567.—Spina bifida of sacrum. (Young adult female, 

FPAM 2381.) 
356 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

FIGURES 568, 569.—Supernumerary wedge vertebra between first and second lumbar with 

secondary scoliosis and right sacralization of fifth lumbar vertebra: 568, Anterior view. 569, 

Lateral view. (60-year-old male, FPAM autopsy 61729.) 

PALEOPATHOLOGY 

Spina bifida is a commonly mentioned abnormality in reports of archeological specimens. Indeed, references to this condition are so common 

that a review of all would be beyond the objectives of this book. Post (1966) has reviewed the 

existence of population differences in the frequency of spina bifida occulta in modern human 

groups. These differences suggest a genetic substrate in the expression of spina bifida. Ferembach 

(1963) reports an unusually high frequency of 

this abnormality in the sacra of a skeletal sample 

from a cave at Taforalt in northeastern Morocco. 

The site is dated to 10,500 to 12,070 years B.P. 

Ferembach calls attention to the problem of deciding what constitutes an abnormal condition in 

sacra since many sacra have some evidence of 

incomplete development of a neural arch. Until 

this problem is resolved, comparisons of the frequency of spina bifida as reported by different 

authors will be impossible. 

I excavated an unambiguous example of sacral 

spina bifida from the Early Bronze Age site of 

Bab edh-Dhra in Jordan. The specimen is dated 

between 3150 and 3000 B.C. and is from the 

skeleton of a young male (Tomb AlOOE). In life 

the individual had probably suffered from tuberculosis, which resulted in destruction ofthe fourth 

lumbar vertebral body. This infectious condition 

is unrelated to the spina bifida occulta of the 

sacrum. The neural arch of the first sacral segment is divided at the midline ofthe spine (Figure 

570). The arches of segment two through five 

never formed, leaving the canal exposed. 

Other types of vertebral malformations are less 
NUMBER 28 357 

FIGURE 570.—Sacral spina bifida in a young adult skeleton 

from the Early Bronze Age site of Bab edh-Dhra, Jordan. 

(NMNH uncataloged, from tomb AlOOE.) 

commonly reported than spina bifida. BarclaySmith (1911) has provided a detailed report of 

multiple anomalies in the vertebral column of a 

young female skeleton from excavations at Sakkara in Egypt. The site probably dates to a period 

between 600 and 500 B.C. In this specimen there 

are eight cervical vertebrae. The first or atlas 

vertebra is fused to the base of the skull, the 

second or axis vertebra and the third cervical are 

fused together. The neural arch of C7 is divided 

through the spinous process and an extra cervical 

vertebra (C8) has an associated cervical rib on 

the right side. Damage to the left side precludes 

evaluation of the presence of a cervical rib on 

that side. The thoracic vertebrae are normal except for the diarthrodial joints between Til and 

T12. The left joint has the morphology of a 

lumbar vertebra, while the right is a typical 

thoracic joint. The lumbar vertebrae exhibit a 

slight lateral curvature. The neural arches of L3 

through L5 are divided at the lateral portion of 

the right lamina. L5 has an additional division of 

the spine creating a separate arch segment. The 

sacrum also has a separate neural arch segment 

including a portion of the left lamina of the first 

sacral vertebra (SI). Barclay-Smith (1911:170) 

suggests that the multiple anomalies were the 

result of early training and activity as a contortionist. A developmental malformation would appear to be more likely. 

Jarcho (1965) has reviewed a vertebral abnormality, first described by MacCurdy (1923), 

which Jarcho thinks is an example of Klippel-Feil 

syndrome. The specimen is from Poricarcancha, 

Peru, and apparently is from an adult male. The 

sixth and seventh cervical and first thoracic vertebrae are fused. There are two hemivertebrae on 

the right side, the first between T3 and T4, the 

second between T4 and T5. These wedge vertebrae have resulted in a sharply angled scoliosis 

with T4 at the apex of the angle. 

On the right side of the thoracic vertebrae 

there are 13 rib facets with the extra rib on the 

hemivertebra between the third and fourth vertebrae. On the left side there are the normal 12 

facets. The first four ribs are fused near their 

proximal ends. The abnormalities of this case 

certainly suggest the congenital Klippel-Feil syndrome. 

Another case of vertebral malformation is seen 

in a young adult female skeleton from the preColumbian site of Puye in New Mexico, USA 

(NMNH 262939). The skeleton is well preserved 

and normal except for the abnormal segmentation and fusion of the third through the fifth 

thoracic vertebrae. The spines, the diarthrodial 

joints, and the vertebral bodies of these vertebrae 

are fused (Figure 571). The left segment of T4 is 

fused to T3. Likewise, the left segment of T5 is 

fused to the right segment of T4. The right segment of T5 is also fused to T4, but the line of the 

early division between T5 and T4 is still apparent. 

Because there are no extra ossification centers 

and an abnormal segment is on each side, there 

is no scoliosis. 

Another defect of the spine involves the separation of a major portion of the neural arch 

(spondylolysis) from one or more vertebrae. The 

defect separates the main part of the vertebra 

from the inferior facets and may permit the vertebral body to slide forward (spondylolisthesis). 
358 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

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^^^^^^^^^^HMb^^B^^^'^ ^^^^HHRVPHHU^BH^^^^^HJ^^^I 

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FIGURE 571.—Malformation of the third, fourth and fifth 

thoracic vertebrae from the prehistoric site of Puye, New 

Mexico, USA. (NMNH 262939.) 

Stewart (1931) has reported on the frequency of 

this condition among Eskimo skeletal remains 

and found an unusually high frequency (27.4 

percent) in this human group. Within the Eskimos he found that skeletons from the northern 

part of Alaska had a greater frequency than those 

from the southern part. Since the condition was 

thought to be congenital, Stewart attributed the 

differences to inbreeding of an isolated group for 

the northern skeletal sample or perhaps differences in origins for the two groups. Stewart (1956) 

later found an age-related association in which 

the incidence of spondylolysis increased with age 

and concluded that stress rather than genetics 

was the significant factor in the expression of 

separate neural arches. He did not rule out a 

genetic substrate but expressed the opinion that 

any genetic predisposition was related to erect 

posture rather than any specific genetic defect of 

the bone. 

Lester and Shapiro (1968) in a study of another 

Eskimo skeletal sample also found a high incidence (40 percent) of spondylolysis and that the 

frequency of the defect increased with age. Curiously, in spite of the latter finding, the authors 

suggest that a hereditary weakness is an important factor in the expression of the abnormality. 

Spondylolysis is not limited to the New World 

although comparative data are not available for 

Old World groups. I have found two examples 

out of 92 burials in the Early Bronze I (3150 to 

3000 B.C.) shaft tombs excavated at Bab edhDhra, Jordan, in 1977. Both examples are from 

adult males. One of these specimens is from the 

east chamber of tomb A100 (Figure 572). The 

age of the skeleton is in excess of 50 years. The 

arch defect is on the fifth lumbar vertebra. The 

arch is completely free of the vertebra, with the 

break occurring at the pars interarticularis. The 

broken edges of the bone exhibit considerable 

remodeling indicating that the break was long 

standing. The anterior surface of the vertebral 

body has considerable periosteal reactive bone, 

perhaps the result of periosteal activation due to 

anterior slippage of the vertebra. The inferior 

edge of the vertebral body has slight arthritic 

lipping as do the corresponding areas of the first 

sacral vertebra. The second and third thoracic 

FIGURE 572.—Separate neural arch of the fifth lumbar vertebra in an adult male skeleton from the Early Bronze Age 

site of Bab edh-Dhra, Jordan. (NMNH uncataloged, from 

tomb AlOOE.) 
NUMBER 28 359 

vertebrae of this skeleton are fused. Fusion occurred at the spines, diarthrodial joints, and the 

lateral portions of the vertebral bodies. The disc 

space is preserved and the cause of the fusion is 

not apparent. 

Ribs 

PATHOLOGY 

Rudimentary unilateral or bilateral supernumerary cervical ribs attached to the seventh cervical vertebra are not uncommon. A supernumerary thoracic rib is often attached to a lateral 

supernumerary hemivertebra. Segmental disarrangement may result in a forked rib with one 

cartilage. This abnormal rib is usually broader 

than normal. 

Pelvis 

PATHOLOGY 

Failure of proper development of the anterior 

abdominal wall may leave the urinary bladder 

open (extrophy of bladder). In this situation, 

which is compatible with adult life, the symphysis 

pubis is absent and, although the pubic and 

ischial rami are properly fused, there is a gap of 

several centimeters between the two halves of the 

pelvis anteriorly (cleft pelvis) (Figure 573). Failure of development of the massa lateralis of the 

first sacral vertebra results in marked pelvic asymmetry (Figure 574). 

FIGURE 573.—Cleft pelvis of a patient with extrophy of the 

bladder and sacrum with 6 segments. (20-year-old male, 

FPAM 3545 from 1877.) 

FIGURE 574.—Asymmetrical pelvis due to absence of right 

massa lateralis of first sacral vertebra. (About 30- to 40-yearold male, FPAM 4071.) 

A hypoplastic shallow acetabulum on one or 

both sides leads to congenital dislocation of the 

femur upwards without disruption ofthe capsule 

or the round ligament. This is compatible with 

adult life and will result in formation of a bony 

reaction on the lateral cortex of the ilium, resembling a new acetabulum (Figure 575). Subsequent 

degenerative arthritis in this abnormal 'joint" 

even will reveal eburnation of the bony surface. 

The femoral head is flattened and shows a vertical 

groove for the flattened round ligament. There is 

often a large marginal exostosis present, which 

points downward (Figure 576). The acetabulum 

is small, flat, and triangular, indicating that it 

never articulated with a mature femoral head. 
360 

FIGURE 575.—Congenital dislocation of left hip showing 

rudimentary acetabulum and iliac neo-acetabulum with 

shelf-like roof (Adult, VM 1694.) 

FIGURE 576.—Congenital dislocation of right hip with severe 

degenerative arthritis. Notice the rudimentary acetabulum, 

the neo-acetabulum on the iliac wing and the characteristic 

downward exostosis on the femoral head. (VM autopsy 224 

from 1920, Roessle Collection.) 

SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

PALEOPATHOLOGY 

In addition to the formation of a secondary 

acetabulum some abnormalities of the hip may 

result in only chronic slippage of the femoral 

head within the shallow actabulum, with no permanent dislocation and no formation of a new 

joint. It will not always be possible to distinguish 

between dislocation induced by trauma and congenital dislocation. 

Baudouin (1906) found that the incidence of 

congenital dislocation in prehistoric European 

skeletal samples was rare. Moodie (1923) reported 

an example of hip dislocation in an ancient Peruvian skeleton in which a new joint was formed. 

Pales (1930, pi. 2: figs. 1, 2) published a photograph and a roentgen film of a pathological femur 

from the Neolithic period, which he attributed to 

congenital dislocation. However, the morphology 

is more compatible with slipped epiphysis. Brothwell (1967b) reviews several reports and cases of 

congenital hip dislocation. Morse (1969:33, 92, 

pi. 6B) includes a brief description of congenital 

hip dislocation in a specimen (Burial 10) from the 

Morse site in Illinois, USA. The abnormal bones 

include the left innominate and both femora. The 

acetabulum is abnormally shallow and distorted 

and the femoral heads irregular and small. A 

diagnosis of congenital hip dislocation would appear correct, although the reported age of 10 

years appears too young. 

An adult male skeleton from tomb AlOOE at 

the Early Bronze Age cemetery of Bab edh-Dhra 

in Jordan has an abnormally shallow acetabulum 

of the right hip. This is the same skeleton that 

had a separate neural arch. The acetabulum is 

also much larger in diameter than the corresponding acetabulum of the left innominate (Figure 

577). There is a moderate amount of arthritic 

lipping on the margin of the abnormal acetabulum, but there is no secondary joint. The clearest 

evidence of dislocation is seen on the head of the 

right femur (Figure 578). The head itself is enlarged with two obvious defects on the inferior 

surface. The most anterior of these defects is a 

shallow curved depression about 1 centimeter 

wide by 2 centimeters long. The margins are 
NUMBER 28 361 

sharply defined and the base of the lesion is 

porous but well remodeled. The posterior defect 

is a narrow deep groove beginning with the pit 

for the ligamentum teres and continuing posteriorly through the boundary of the joint surface. 

FIGURES 577, 578.—Chronic subluxation of the right hip, 

perhaps of congenital origin, in a skeleton from the Early 

Bronze Age site of Bab edh-Dhra, Jordan: 577, Comparative 

views of the right (left portion of photograph) and lefi 

acetabula showing the shallow and enlarged diameter ofthe 

right. 578, Bony components of the right hip; note the 

grooves from pressure erosion on the femoral head. (NMNH 

uncataloged, from tomb AlOOE.) 

The curvature of the anterior defect corresponds 

to the curvature of the anterior margin of the 

acetabulum. There is little doubt that chronic 

and abnormal abrasion of the femoral head during repeated episodes of partial, anterosuperior 

subluxation produced this defect. The posterior 

defect is due to abnormal pressure on the joint 

surface by the ligamentum teres perhaps during 

dislocation. Another possibility is that part of an 

abnormally elongated ligamentum teres might 

have lain across the joint surface when the head 

was in the normal anatomical position. In view 

ofthe lack of a secondary joint and any evidence 

of fracture, congenital dislocation would appear 

to be the most appropriate diagnosis. 

An example of hip dislocation with secondary 

joint formation is seen in an adult female from 

the ancient Pueblo site of Kwasteyerkiva in New 

Mexico, USA (NMNH 271828). The specimen 

consists of the right innominate and femur, although only the innominate was available for 

study. The most noticeable feature is the presence 

of a large secondary joint projecting well above 

the acetabular rim (Figure 579). The articular 

FIGURE 579.—Hip dislocation with secondary joint formation in the right innominate of an adult female from an 

ancient Pueblo site in New Mexico, USA. Note the bony 

remodeling in the original acetabulum and the porosity of 

the new joint. (NMNH 271828.) 
362 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

surface is rough with many pores penetrating the 

surface. Considerable remodeling has taken place 

in the acetabulum. The original surface is very 

coarse and is almost completely covered over by 

a concave layer of bone, which may have been a 

temporary shallow joint before the femur slipped 

again and stimulated the formation of the final 

joint. Trauma cannot be ruled out, in part due to 

postmortem damage. The acetabulum appears to 

be abnormally shallow, which would support a 

diagnosis of congenital hip malformation leading 

to dislocation and secondary development of another joint. 

Extremities 

PATHOLOGY 

Complete failure of development of one or 

several limb buds results in amelia; partial suppression results in peromelia. At times, only the 

proximal portions of the limb are rudimentary, 

while hands or feet are developed (phocomelia). 

As far as individual simple long bone defects are 

concerned, the radius and the tibia (Figure 580) 

are more often missing than the ulna or the fibula. 

Congenital bony ankylosis between the proximal 

radius and ulna (Figure 581) and between the 

distal tibia and fibula are typical anomalies, preventing, in the former, pronation of the forearm 

but not affecting the function of the ankle significantly in the latter. There are many, frequently hereditary and familial, syndromes concerning the number, length, and position of digits 

of fingers and toes (polydactyly, brachydactyly, 

clinodactyly). The number may be more or less 

than normal (Figure 582). Single rays may be 

fused through their entire length or only distally 

(various forms of syndactyly). Clubfoot deformity 

(pes equino-varus), often bilateral, can also occur 

FIGURE 580.—Congenital absence of left tibia with hypertrophic fibula and equinovarus deformity of foot. (18-yearold female, WM S 16.2 from 1892.) 

FIGURE 581.—Proximal congenital radioulnar synostosis 

(left) in pronation, radial head hypoplastic. (Adult WM S 

8.1.) 
NUMBER 28 363 

FIGURE 582.—Polydactyly of right hand and right foot. The 

supernumerary finger branches off from the fifth metacarpal 

and has only two phalanges; the supernumerary toe articulates with the fifth metatarsal and has three phalanges. 

(FPAM 2866b) 

on a congenital basis with or without malformation ofthe spine (Figure 583, 584). 

PALEOPATHOLOGY 

Identification of congenital absence of one or 

more limbs in archeological specimens is difficult, 

due to the many postmortem conditions that 

affect the recovery of skeletons. A case has been 

reported by Hawkes and Wells (1976) in which 

such a diagnosis appears appropriate. The specimen was excavated from an archeological site in 

Hampshire, England, probably dated to the late 

sixth or early seventh century A.D. The skeleton 

(burial 38) is that of a man about 28 to 30 years 

of age. The preservation was good and the excavation was carefully done. The entire left extremity, scapula and clavicle were missing at the time 

of excavation. The authors conclude that this 

absence of the limb is a congenital condition. 

They point to the presence of other abnormalities 

FIGURES 583, 584.—Congenital clubfoot deformity, bilateral 

(maximal pes equinovarus): 583, Dorsal view. 584, Plantar 

view. (About 16 years of age, FPAM 152.6 and 147.6.) 

and compensatory development of other bones in 

support of the conclusion that the abnormality 

was a long-standing antemortem condition. 

Congenital fusion of the proximal radius and 

ulna has been noted in archeological specimens. 

Morse (1969:33, fig. 4) reports two cases of this 

abnormality from the Crable site in Illinois, USA. 

Both cases involve the left arm. Vyhnanek, Hanakova, Stloukal and Kolai^ (1965:2190) report the 

presence of congenital radioulnar synostosis in 

ancient Slavic skeletal material. The congenital 

nature of radioulnar synostosis is demonstrated in 

two specimens from archeological sites in North 

America. The first of these specimens (NMNH 

384347) is the fused right radius and ulna from 

the skeleton of a near-term fetus or young infant 

(Figure 585). The specimen is from Ossuary II, 

Juhle site in Nanjemoy, Maryland, USA. No 

European trade goods were found, although the 
364 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

FIGURES 585, 586.—Synostosis of the proximal right radius and ulna: 585, Near-term fetus or 

young infant from the late prehistoric Juhle site at Nanjemoy, Maryland, USA (NMNH 

384347). 586, Adolescent skeleton from the historic period, Mobridge site in South Dakota, 

USA (NMNH 382993). 

date is Late Woodland and thus could be postColumbian. Even at the young age of this specimen, the radioulnar fusion is well established. 

The second example of radioulnar synostosis is 

from an adolescent skeleton from the Mobridge 

site in South Dakota, USA (NMNH 382993). 

This site contained trade goods and is thought to 

date around A.D. 1750. The right ulna and radius 

are fused in a slightly pronated position (Figure 

586). The fusion has taken place in the radial 

tuberosity and the supinator fossa of the ulna. 

The radial head is not involved. There is no 

evidence of trauma and the young age of the 

specimen, as well as the nature of the fusion, 

make congenital radioulnar synostosis the appropriate diagnosis. 

Deformities attributed to clubfoot have been 

described in the literature on paleopathology. 

Pales (1930:36-38) reviews some of the earlier 

reports on this condition. His discussion highlights the problems in distinguishing between 

congenital clubfoot and postparalytic deformities, 

such as those produced by poliomyelitis. Brothwell (1967b:424) has reviewed one reported case 

of clubfoot in a Twelfth Dynasty Egyptian 

mummy and finds the evidence inadequate to 

support this diagnosis. Brothwell (1967b:425-

428) describes a fragmentary Neolithic skeleton 

from Gloustershire, England, with foot deformities attributable to clubfoot. Johnson and Kerley 

(1974) found evidence of clubfoot deformity in 

four skeletons from the pre-European site at 

Mokapu in Hawaii, USA. They also note the 

problem in distinguishing between congenital 

and postparalytic deformities. Johnson and Kerley make the useful conceptual distinction between malformation, which could be associated 

with congenital abnormalities, and deformation, 

which would be more likely in postparalytic 

changes. 
Tumors 

General Discussion 

PATHOLOGY 

Tumors and tumor-like cysts arising primarily 

in the skeleton are uncommon. They are the 

result of uncontrolled proliferation of any one of 

the tissue components of the osteogenic mesenchyme (bone, cartilage, fibrous tissue, or blood 

vessels). If the growth consists of well-differentiated (mature) tissue and remains localized, the 

tumor is called benign. If the tumor consists of 

poorly differentiated (immature) tissue, and continues to grow unchecked and can spread to other 

parts of the body through blood vessels and/or 

lymphatics, the neoplasm is designated as malignant. In contrast to those in other parts of the 

body, primary benign and malignant tumors of 

the skeleton mostly arise in young, actively growing individuals. 

Malignant tumors arising in various organs 

and tissues of the body (carcinomas and sarcomas) may spread, mainly through the bloodstream, to bones, resulting in metastatic tumors. 

In contrast to the primary tumors ofthe skeleton, 

metastatic tumors are usually multiple and 

predilect the older age group. In present populations, metastatic tumors in bone are much more 

common than primary ones. 

The identification of specific tumor types in 

dry bone is not always possible; however, location 

and age as well as alteration of the surrounding 

bone offer helpful clues. Obviously, tumors producing benign or malignant neoplastic bone offer 

the best chance of identification. 

The following discussions concentrate on those 

lesions and features that offer some chance of 

recognition in archeological material. (For a review of all the aspects of skeletal neoplasms consuh Jaffe, 1958.) 

PALEOPATHOLOGY 

With respect to the paleopathology of human 

tumors one needs to keep in mind the fundamental difference between modern medical experience and conditions associated with ancient populations. Most important are differences in average age at death. People in populations on which 

much of modern medical experience with tumors 

is based, live about twice as long as people in 

populations studied by paleopathologists. Since 

primary malignant tumors usually occur or arise 

FIGURE 587.—Unicameral bone cyst of proximal left humerus; bisected wet preparation. Notice the thin expanded 

new cortex and the contact ofthe cyst with the growth plate. 

(7-year-old male, WM S 61a 44 from 1905.) 

365 
366 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

during the growth period, their frequency in ancient skeletons might be expected to be similar to 

modern skeletal samples. However, secondary tumors of bone are associated with the older age 

categories and are thus less likely to be found in 

archeological skeletons. Individuals who lived in 

antiquity usually died of other causes before secondary tumors could become a serious factor in 

morbidity and mortality. 

Another factor is the well known environmental effect on the type and incidence of cancer. 

Carcinoma of the lung, for example, is associated 

with smoking and air pollution. Metastases to the 

skeleton from this type of cancer may be minimal 

where such environmental problems did not exist. 

It is important to emphasize, however, that exposure to other conditions, such as smoke from a 

wood fire, may be carcinogenic. Wells (1964b: 

1611) has noted the relatively high incidence of 

nasopharyngeal tumors of bone in paleopathological specimens. Today, this condition is rare in 

the Western world but rather common in Africa. 

The condition is also rather common among the 

Chinese. 

Primary Benign Tumors 

PATHOLOGY 

Cysts 

A cyst, in the anatomical sense, is a lesion 

characterized by a fluid-filled cavity surrounded 

by a distinct wall. Several types of lesions fulfilling 

these criteria occur in bone in different characteristic locations. 

UNICAMERAL BONE CYST.—This tumor-like lesion occurs about as frequently as giant cell tumor. It consists, in the fully developed state, of a 

round or oval fluid-filled single cavity of several 

centimeters in diameter that is lined by a thin 

membrane of poorly vascularized osteogenic mesenchyme. The lesion occurs most often in young 

children or adolescents but may be carried into 

adult age. It is most common in long bones and 

starts in the metaphysis in close proximity to the 

growth plate (Figure 587). Its location is central 

in regard to the axis of the involved bone. It 

always spares the epiphysis. In the course of 

longitudinal growth of the individual, it usually 

seems to move away, towards the diaphysis, by 

interposition of newly grown bone between it and 

the growth plate. The most frequent locations are 

proximal humerus, proximal and distal femur, 

proximal and distal tibia, and proximal fibula. 

All other locations are unusual, especially in small 

tubular and in flat bones. In Jaffe's (1958:63) 

material of 75 cases, the male-female sex ratio 

was 2:1. 

The enlargement of the cyst leads to smooth, 

tapering resorption of the overlying cortex, due 

to increasing fluid pressure. Ultimately the cortex 

may be replaced with a newly formed shell of 

cortical bone, which may show reinforcing ridges 

on the inner surface. Usually the actively enlarging cyst shows osteoclastic resorption on the inside 

and osteoblastic bone deposition on the outside 

of the shell. Pathological fractures, crushing the 

thin wall, are common and often heal readily. 

ANEURYSMAL BONE CYST.—This is a much less 

common lesion of older children and adolescents. 

It is always eccentric in location as regards the 

axis of the involved bone. It shows a distinct 

bulge, consisting of a thin newly formed shell 

over the eroded cortex, which accounts for its 

name (Figures 588, 589). The contralateral cortex 

of the involved bone and the adjacent cancellous 

bone are usually spared. The lesion occurs with 

equal frequency in long bones and in the spine. 

In long bones, the location is usually the metaphysis, seldom the diaphysis. The epiphysis is 

spared. In the spine, vertebral bodies, transverse 

processes and neural arches may be involved. If 

the lesion is large, pressure defects on adjacent 

vertebrae can occur. In 35 cases studied by Jaffe 

(1958:56), the lesion was more common in females. 

The aneurysmal bone cyst is usually multilocular, but the different compartments are separated only by soft tissue septa, which are devoid 

of bone. The wall consists of highly vascular 

connective tissue with numerous giant cells. The 
NUMBER 28 367 

multilocular character of the lesion is reflected in 

the bosselated outline, especially of the wall fac-

ing the axis of the bone. 

TRAUMATIC EPIDERMAL INCLUSION CYST.— 

Crushing trauma to the terminal phalanx, more 

often of fingers than toes, may displace some 

squamous epithelium of the nail bed into the 

fractured bone. This displaced epithelium contin-

ues to grow, forming a cystic space in the bone 

which fills with keratin material. In the dry bone 

this would present as a central cavity, usually not 

more than one centimeter in diameter, with or 

without evidence of a healed fracture. It would 

be difficult or impossible to distinguish the lesion 

from the much more common enchondroma. 

CONGENITAL EPIDERMAL INCLUSION CYST.— 

This lesion is fairly rare and occurs only in the 

bones of the calvarium. In the course of the 

closure of the cranial cavity during embryonic 

development, ectodermal skin epithelium may 

become trapped in the developing bone of the 

cranial vault. The cyst resulting from the proliferation of such epithelium may be located in any 

part of the vault but occurs most frequently in 

the parietal bone. Usually the lesion is single. The 

cyst is lined by squamous epithelium and filled 

with keratin. Mostly the cyst is small, confined to 

the diploe, appearing as a round or anteroposte-

riorly elongated radiolucent area on X-ray. Oc-

casionally such cysts can become rather large, 10 

centimeters or more in diameter. In these cases 

the overlying tables bulge, the inner one more 

than the outer. Occasionally the cyst lining may 

show various skin appendages (hair follicles, se-

baceous glands and sweat glands) representing all 

skin elements (dermoid cyst). These occur partic-

ularly in the vicinity of the orbit (Figure 590). 

The small round inclusion cysts may not be dis-

tinguishable from the more common eosinophilic 

granulomas of the skull in children. 

FIGURES 588, 589.—Aneurysmal bone cyst of left distal fem-

oral metaphysis: 588, Showing a big cystic mass with thin 

reticulated bony shell. 589, X-ray of specimen, showing the 

slight mineralization of the shell and some sclerosis at the 

deep border. (12-year-old male, PMES 1 TF 14(2) from 

before 1842.) 
368 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

FIGURE 590.—Cranial defect from dermoid cyst. Notice the 

smooth destruction ofthe left frontal bone and supraorbital 

ridge with inward sloping, slightly sclerotic edges. (61-yearold male, DPUS 7878 from 1905.) 

Osteoblastic Tumors 

OSTEOMA.—This condition is a benign borderline-neoplastic lesion consisting of mostly dense 

lamellar bone with vascular channels but practically without marrow spaces. In several typical 

locations and appearances, it occurs almost exclusively in the skull. The mineral density of the 

lesion permits excellent preservation in archeological material. 

The most common lesion is the so-called button 

osteoma of the cranial vault, usually located on 

the outer table and consisting of an ivory-hard 

smooth lump of not more than 2 centimeters in 

maximal diameter. Sometimes it shows a peripheral circular constriction at the junction with the 

outer table. The lesion is found in at least one 

percent of all autopsies. Usually the lesion is 

single, but multiple lesions occur. The most frequent locations are the frontal and parietal bones. 

Similar lesions on the internal table ofthe cranial 

vault are much rarer. 

The second most common osteoma is a horseshoe-shaped or circular overgrowth of cortical 

bone on the inner aspect of the bony auditory 

canal. The maximal thickness usually does not 

exceed 5 millimeters but narrows the canal considerably. Both of these lesions are well documented in various races and in archeological 

material. 

The third type of osteoma is a more formidable 

lesion, most commonly consisting of a tumorous 

bony proliferation projecting into the frontal or 

other paranasal sinuses (Figures 591, 592). This 

lesion begins with a fibro-osseous proliferation 

made up of fibrous tissue and woven bone trabeculae. As the lesion matures it becomes more 

solidly bony with lamellar bone predominating. 

These tumors may occasionally reach large sizes, 

disfiguring the facial bony contours, projecting 

into the orbit, and/or the nasal cavity. Occasionally a sizeable nodular projection into the anterior 

cranial fossa with compression of the frontal lobe 

of the brain occurs. This lesion is much less 

common than the two other cranial osteomas 

described above. Osteomas should be easily identifiable even on archeological specimens. 

OSTEOID OSTEOMA.—This type of osteoma is a 

not infrequent, small, tumor-like lesion consisting 

of poorly mineralized woven bone developing in 

the cortex or in the spongiosa of a bone. The 

lesion rarely exceeds one centimeter in diameter. 

It occurs most commonly in older children and 

young adults. The location is most often on a 

long bone of an extremity. The localization in 

150 cases of Jaffe's (1958:94) series was 25 percent 

in the femur, 25 percent in the tibia, 35 percent 

in the fibula, humerus, vertebrae (transverse process and arch), and tarsal bones (talus and calcaneus) combined. Most other bones may be 

affected occasionally, but the cranium seems to 

be largely spared. 

The lesion produces a small radiolucent focus, 

with or without central calcification, which, if the 

lesion involves the cortex, elicits an osteosclerotic 

response of the surrounding bone, out of propor-
NUMBER 28 369 

FIGURES 591, 592.—Osteoma of frontal sinus: 591, Cut surface view from below. Notice the ivory-like tumor masses 

bulging and penetrating the sinus wall externally and 

endocranially. 592, Frontal view, showing multiple tumor 

perforations through outer table. (Adult, H M P809 from 

before 1799.) 

tion to the size ofthe lesion. This reactive buildup 

of dense lamellar bone may appear as an external 

or internal cortical thickening of several centimeters axial length, reaching its maximum over 

the small lesion (Figure 593). If located in the 

spongiosa, the reactive perifocal bone formation 

is usually much less marked. The density of the 

reactive bone should preserve the appearance of 

the lesion in dry bone, although the osteoid portion would disintegrate. The differentiation from 

a small intracortical abscess may not be possible. 

FIGURE 593.—X-ray of osteoid osteoma of femur. Notice the 

lytic corticomeduUary lesion with a central nidus of increased 

density and pronounced cortical hyperostosis. (Adult, AFIP 

116267.) 

OSTEOBLASTOMA.—This is a rare benign tumor 

of bone consisting of various components of osteogenic mesenchyme producing poorly mineralized 

woven bone trabeculae. To a great extent, the 

histologic pattern resembles that of osteoid osteoma. However, this tumor may reach considerable size. The lesion appears most often in the 

spine (vertebral bodies and/or arches) and small 

tubular bones of hands and feet (Jaffe, 1958:108). 

The tumor occurs mostly in adolescents and 

young adults with no predilection to sex. 

In long bones, the tumor is usually in the 

metaphysis and is seen as a moderately radiolucent lesion with occasional perifocal osteosclerosis. 

Identification in dry bone cannot be made with 

assurance. 
370 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

Chondroblastic Tumors 

CHONDROMA.—This is a benign tumor consisting of hyaline cartilage. It is one of the more 

common bone tumors, usually arising within the 

bone (enchondroma), much less often in the periosteum (juxtacortical chondroma). The lesion is 

most frequently found from later childhood 

through middle age. There is no sex predilection. 

It occurs usually in the metaphysial area of a 

tubular bone of the extremities with special 

predilection of the small tubular bones of hands 

and feet. The localization in Jaffe's (1958:169) 

material, arranged in order of decreasing frequency, was as follows: finger phalanges, metacarpals, humerus, femur, toe phalanges, metatarsals, tibia, fibula, and ulna. The tumor does not 

occur in bones developing through intramembranous ossification. At least in part, enchondromas develop from residual portions of growth 

cartilage that have become detached from the 

growth plate. This used to be common in the 

healing of rickets. Scherer (1928) found metaphysial cartilage rests in 1.7 percent of over 1000 

right femora of individuals over 25 years of age 

examined at autopsy. This explains that chondromas are located in the proximity of the area of 

the growth plate: in either metaphysis of long 

bones, in the distal metaphysis of metacarpals 

and metatarsals, and in the proximal metaphysis 

of phalanges. The tumor partly destroys the cancellous bone and, if large, scallops the inner cortex 

of long bones. The outer contour of large long 

bones may not be altered. In the small bones of 

hands and feet the outer contour may be distorted 

and expanded, revealing a thin, new cortical shell, 

which may be perforated. The joint surfaces are 

always spared. The center ofthe tumor is usually, 

and often heavily, calcified and sometimes ossified. 

The juxtacortical chondroma is rare. It usually 

is located over the metadiaphysial area of a large 

long bone of an extremity. In its development it 

causes a cup-shaped depression of the underlying 

cortex with an elevated cortical lip surrounding 

the defect. However, it usually remains separated 

from the interior ofthe bone by a distinct sclerotic 

border. The central portion of the tumor may 

calcify and/or ossify. 

CHONDROMATOSIS (Ollier's Disease).—This is a 

rare condition in which multiple and often numerous chondromas manifest in early childhood 

in various parts of the enchondrally ossified skeleton. Again, the most frequent manifestations 

concern the bones of the extremities, including 

hands and feet. In the small bones these cartilage 

tumors cause ballooning deformities bordered by 

a thin cortical shell (Figure 594). The cranial base 

and facial skeleton, although enchondrally ossified, is usually spared Qaffe, 1958:185). There is 

a high incidence of development of a malignant 

cartilage tumor (chondrosarcoma) in later life. 

Ollier's disease produces changes which are, in 

several ways, different from those of solitary enchondroma. Speiser (1925) has shown that, in 

addition to the large metaphysial enchondromas 

FIGURE 594.—Multiple enchondromas of right fifth metacarpal and basal phalanx. Notice the ballooning projections 

on both bones covered by a thin shell of new cortex. (Adolescent, PMES ITD 120(1).) 
NUMBER 28 371 

derived from the growth plate, numerous smaller 

chondromas are formed by faulty differentiation 

ofthe inner layer ofthe periosteum. In the process 

of growth some of these assume an elongated, 

streak-like, radiolucent appearance. The presence 

of large cartilage masses during the growing period results in alteration of the normal process 

consisting of diminished growth, bowing deformities due to uneven growth, and widening of the 

metaphyses of involved bones due to delayed and 

incomplete remodeling. 

CARTILAGINOUS EXOSTOSIS (Osteochondroma).—Cartilaginous exostosis, appearing as a solitary lesion, is one of the most common benign 

bone tumors. Its initiation is limited to the growing period of the skeleton beginning most often 

in childhood. There is no sex predilection. The 

lesion may occur on any bone that develops by 

enchondral ossification, but the cranial base and 

the facial bones are rarely involved. The tumor 

most commonly occurs in proximity to the growth 

plate on the metaphysial surface of long bones. 

The distal metaphysis of the femur and the proximal metaphysis of the tibia are the site of the 

majority of the lesions. Other long bones of the 

extremities, including small tubular bones of 

hands and feet, ribs, pelvis, and scapula are less 

commonly involved. The spine and sternum are 

usually spared. 

The lesion begins close to the growth cartilage 

with a faulty differentiation of the inner layer of 

the periosteum into cartilage. This cartilage undergoes enchondral ossification from the underlying osteogenic mesenchyme, mimicking to a 

great extent the enchondral growth of the growth 

plate. Since, in the involved area, the periosteum 

produces cartilage instead of bone, there is never 

a cortex separating the medullary spaces of the 

exostosis from those of the affected bone. Thus, 

the exostosis enlarges continuously due to the 

growth of the basal layer of the cartilage cap. 

Usually the growth of the exostosis stops when 

the nearby growth plate terminates its growth. 

The lesion begins as a rounded outgrowth on 

the periosteal surface. The final shape is greatly 

modified by mechanical stresses (muscle pull and 

tendon insertions) in the affected area. Thus, the 

common exostoses around the knee area become 

elongated polypoid structures with bulbous tips 

pointed away from the joint; upward on the 

femur and downward on the tibia. This is an 

effect of secondary remodeling. Fractures of slender, elongated exostosis in this area are not uncommon. The flaring remodeling of the metaphysis is often inhibited on the side of the bone 

bearing the osteochondroma. On the proximal 

humerus, osteochondromas tend to remain broadbased and rather bulky without pedunculation. 

Osteochondromas of the pelvis appear as cauliflower-like osteochondrous masses projecting outward or toward the pelvic canal (Figure 595). 

In dry bone and on X-ray, the tumor shows 

easily recognized diagnostic characteristics. If 

transsected, the continuity ofthe cancellous marrow spaces of the lesion and of the involved bone 

are readily apparent as is the reflection of the 

cortex onto the lesion. The inner structure consists 

of more or less regular cancellous bony trabeculae 

FIGURE 595.—Osteochondroma of left ilium. (59-year-old 

female, IPAZ autopsy 1776 from 1962.) 
372 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

FIGURES 596, 597.—Multiple cartilaginous exostoses: 596, Right femur; notice lack of metaphysial remodeling in area of exostoses. 597, Left tibia and fibula with multiple exostoses. (54-

year-old male, IPAZ S.1201 from 1965.) 
NUMBER 28 373 

mingled with areas of densely calcified cartilage 

or sclerotic bone. 

HEREDITARY MULTIPLE EXOSTOSES (Diaphysial 

Aclasia).—This dominant hereditary condition, 

which affects multiple bones of the skeleton, is 

rare. It usually manifests itself in several siblings 

and several generations of one family. There is a 

marked predominance in the male sex. Basically, 

the individual lesion is identical with that of 

solitary cartilaginous exostosis. The predominant 

location is again the knee area, often involved 

symmetrically (Figures 596, 597). In addition, the 

proximal humeral metaphysis, the distal tibial 

metaphysis, and the small tubular bones of the 

hands are frequently involved. Other locations in 

decreasing order of frequency are: proximal fibula, iliac bone, metatarsals and toes, radius, ulna, 

ribs, and scapula. The spine is rarely affected; 

neither are the facial bones. The skull base occaFIGURE 598.—Secondary chondrosarcoma on cartilaginous 

exostosis of proximal right femur (center); the distal right 

femur (left), and the proximal right fibula and tibia (right) 

show smaller benign exostoses. (43-year-old male, GHPM 

4041 from 1841.) 

sionally shows a lesion on the endocranial aspect. 

The number of lesions may vary from a few to 

several hundred in different cases. 

If numerous lesions are present in a metaphysial area, remodeling of the metaphysis is lacking, 

leaving a broad metaphysis without flare (Figure 

596). Growth is retarded and, at times, irregular, 

leading to shortening and axial deviation of the 

affected bone. If the distal ulnar metaphysis is 

severely involved, the ulna is shortened and the 

radius, due to its intimate attachment to the ulna, 

is abnormally curved, giving the appearance of a 

Madelung's deformity of the forearm. In a moderate number of cases in the older age group, a 

chondrosarcoma develops from the residual cartilage cap in one or several of the lesions (Figure 

598). 

CHONDROBLASTOMA.—This fairly rare benign 

tumor is made up of primitive chondroblasts and 

giant cells. It occurs mainly in adolescents and 

young adults, with a marked preponderance of 

males over females. The tumor occurs most commonly in the epiphyses of long bones (Figure 

599). In fact, this is the only bone tumor that 

FIGURE 599.—X-ray of chondroblastoma of proximal left 

humeral epiphysis. Notice the eccentric lucency with a thin 

bony shell and slight sclerotic reaction. (Adolescent, courtesy 

Dr. S. Werthammer, Huntington, West Virginia, USA, 

1952.) 
374 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

always arises and often is confined to an epiphysis 

or apophysis. This is helpful in identification in 

dry bone. The location in 30 cases of Jaffe's (1958: 

44) material, in decreasing order of frequency, 

was in the following epiphyses: distal femur, proximal tibia, proximal humerus, distal tibia, proximal femur, calcaneus, talus, ilium, and ischium. 

The tumor usually produces a purely lytic 

lesion of several centimeters in diameter. After 

closure of the adjacent growth plate the lesion 

may extend into the adjacent metaphysis. There 

is often some degree of calcification in the center, 

which, however, probably would be lost in dry 

bone. Occasionally, bony sclerosis is found adjacent to the lesion. In the humerus and femur the 

separate apophyses for the greater tubercle and 

for the greater trochanter are favored locations 

(Jaffe, 1958:45). 

CHONDROMYXOID FIBROMA.—This rare benign 

bone tumor occurs in adolescents and young 

adults. The lesion is most commonly found in the 

metaphysial area of long and short tubular bones, 

mainly ofthe lower extremity. The most common 

bone involved is the tibia. The lesion is located 

eccentrically but starts within the cancellous 

bone. It consists of neoplastic proliferation of 

fibroblastic cells producing large amounts of mucoid matrix. There are also giant cells scattered 

through the lesion. The radiologic picture is similar to that of nonossifying fibroma, but the lesion 

tends to be more rounded and there is often 

marked bony sclerosis in the wider vicinity of the 

lesion. In small tubular bones, after closure ofthe 

growth plate, the lesion may extend into the 

epiphysis. 

Fibroblastic Tumors 

FIBROUS CORTICAL DEFECT.—This is a very 

common lesion of the skeleton, present in about 

one-third of all children with a male-female ratio 

of 2:1 (Jaffe, 1958:78). It seldom appears before 

2 years of age. The location is always on the 

metaphysial cortex of the long bones. The lesion 

begins in the periosteum, close to the growth plate 

but may be moved away from it in the process of 

FIGURE 600.—X-ray of fibrous cortical defect of distal right 

tibia. Notice the eccentric lobulated lesion with slightly 

bulging cortex and pronounced deep sclerotic margin. (Adolescent, MG H surgical specimen 14645 from 1969.) 

subsequent growth. It is always longer than wide 

and may be multiloculated. The adjacent portion 

of the cortex may be sclerotic, and there is always 

a layer of dense bone separating it from the 

medullary space (Figure 600). This is the area 

where, in the normal process of growth, remodeling resorption of the metaphysial cortex occurs. 

The lesions are often multiple and symmetrical. 

The most commonly involved area is the distal 

metaphysis ofthe femur. Other locations, in order 

of decreasing frequency, are: proximal tibia, proximal and distal fibula, proximal femur, distal 

tibia, humerus, radius, and ulna (Jaffe, 1958:80). 

The lesion consists of spindle-shaped mesenchymal cells and giant cells, probably representing a faulty development of the remodeling inner 

layer of the metaphysial periosteum. On the dry 
NUMBER 28 375 

bone the lesion would present as a streak-like or 

multiloculated defect beneath the cortex, bordered by smooth surfaced sclerotic bone in the 

depth. These lesions may reach several centimeters in length but usually not more than one 

centimeter in diameter. They may fill in spontaneously or remain stationary. In few instances 

they behave agressively and become truly neoplastic (nonossifying fibroma). 

In Caffey's (1955) series of 1000 healthy children examined radiologically, the most common 

location of the defect was found on the distal 

femur and with equal frequency as a unilateral 

or bilateral symmetrical lesion. The solitary unilateral lesions were, in both sexes, twice as often 

located in the right than in the left femur. Of 254 

femoral defects, 224 were present on the medial 

cortex of the metaphysis and only 30 on the 

lateral cortex. The anterior cortex was involved 

only once. Multiple defects within a single femur 

were found only 19 times. No defects were demonstrated in the first two years of life, but in the 

third, almost 8 percent of the children showed 

defects. In the fourth year, the number of affected 

children rose sharply to 15 percent, maintaining 

a frequency of 14 to 17 percent through the 

twelfth year. In the thirteenth year, the frequency 

of cortical defects dropped sharply to 10 percent 

and reached 8 percent in the fourteenth year. The 

defects in the distal femoral metaphysis were 25 

times more frequently encountered than those in 

the proximal tibial metaphysis and 60 times more 

common than those in the proximal fibular metaphysis. Cortical defects in the proximal femoral 

metaphysis were rare. 

NONOSSIFYING FIBROMA.—As already indicated 

(p. 374), this neoplastic lesion derives from a 

fibrous cortical defect that behaves aggressively 

and continues to grow. The location is the same 

as that of the latter. The age of the individuals 

affected is older (later childhood and adolescence). The occurrence is much less common than 

the fibrous cortical defect and is usually unifocal. 

The lesion always starts eccentrically in the metaphysis of long bones and, even after penetration 

into the medullary portion of the bone, is separated by a distinct, frequently scalloped, bony 

shell from the medullary tissue. Only in a thin 

long bone, like the fibula, may the tumor ultimately transect the entire diameter, but even 

then the contralateral cortex is usually less involved. However, since large portions of cancellous bone and cortex are progressively destroyed, 

pathological, usually diagonal, fracture occurs 

commonly, especially in weight-bearing bones. 

The tumors may reach up to 10 centimeters in 

length. 

CORTICAL DESMOID.—A lesion, similar to fibrous cortical defect, is occasionally seen on long 

and short tubular bones in which a similarly 

scalloped cortical defect is filled with tough mature collagen. There is also a separating cortical 

shell at the deep margin of the lesion. The individuals affected are often adult. On the dry bone, 

the defect would appear very similar to that of a 

fibrous cortical defect. 

Giant Cell Tumor 

One ofthe most common primary bone tumors 

is the giant cell tumor (osteoclastoma), a borderline-benign neoplasm made up of stromal cells 

and multinucleated giant cells similar to osteoclasts. The lesion most commonly occurs in adolescents and young adults, mostly less than 40 

years of age. The tumor is eccentric, epimetaphysial in location, and most often found in long 

bones. The predilected areas are distal femur, 

proximal tibia, distal radius, and proximal humerus. All other locations are rare, but it can 

occur in vertebrae, pelvis, cranial vault, or small 

bones of the extremities. 

The most characteristic lesion, and the only 

one that could be identified with a reasonable 

degree of certainty in dry bone, is the epimetaphysial lesion of long bones. The tumor usually 

completely destroys the preexisting spongiosa and 

the original cortex, allowing the formation of a 

thin, new, periosteal cortical shell in an expanded 

position, which often has small rounded perforations and reinforcing ridges on the inner surface 

(Figures 601, 602). This accounts for the radiolog-
376 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

ical "soap bubble" appearance of the cortical 

shell. The lesion often excavates the epiphysis and 

closely approaches the articular surface, without 

penetrating into the joint. The zone of transition 

FIGURES 601, 602.—Giant cell tumor of distal femur: 601, 

Outside view, showing expanded cortical shell with small 

perforations. 602, Cut surface, showing lytic center and 

ridged cortical shell. (HM P837.) 

into the intact cortex on the diaphysial end ofthe 

lesion is usually sharp and narrow. Pathological 

fractures through advanced lesions, especially in 

weight-bearing bones, are not uncommon. The 

normal consistency and appearance of the rest of 

the bone and of other bones of the same skeleton 

should permit differentiation from reactive giant 

cell tumors (brown tumors) in severe hyperparathyroidism. 

Hemangioma 

True hemangioma is a neoplasm formed by 

proliferating blood vessels. This type of lesion is 

very rare in any part of the skeleton. However, 

lesions showing marked dilatation of preexisting 

bone marrow sinusoids that are not true neoplasms are commonly found in the vertebrae 

(Putschar, 1929). These vascular lesions are often 

combined with proliferation of fatty marrow (angiolipoma). 

This vertebral lesion is rather common in older 

individuals. Schmorl and Junghanns (1971:325-

327) report an incidence of 12.2 percent in males 

and 15.9 percent in females over 60 years of age 

in their series of close to 4000 complete spinal 

columns studied at autopsy. Of these, two-thirds 

were solitary and one-third multiple lesions affecting different vertebrae. In their large series, 

close to 70 percent of the lesions were found in 

the thoracic vertebrae, especially the three lowest 

ones, 20 percent in the lumbar vertebrae, and the 

rest were evenly divided between lower cervical 

and upper sacral vertebrae. 

This lesion does not alter the contour of the 

vertebral body. The hemopoietic marrow is replaced by dilated blood vessels with a varying 

admixture of fat cells. Characteristically, the vertical trabeculae are reduced in number and increased in diameter, giving the picture of coarse, 

vertical striation on X-ray (Figure 603). Small 

lesions may not show any reduction or alteration 

of trabeculae. 

There are rare instances of true vascular neoplasms of the spine. They mostly occur in the 

younger age group and destroy the bone, ballooning the outer configuration of the vertebra and 
NUMBER 28 377 

FIGURE 603.—X-ray of angiolipoma of two vertebrae. Notice 

reduced number of thickened trabeculae in top and center 

vertebra; bottom vertebra normal. (Adult, studied by Putschar.) 

encroaching upon the lumen of the spinal canal. 

Pathological fractures occur in these tumors but 

are absent in the common older age vascular 

ectasias. 

True hemangiomas occur in the cranial vault 

FIGURE 604.—Hemangioma of cranial vault. Transverse cut 

showing radiant bone trabeculae between distended marrow 

spaces, protruding bluntly outward and sharply inward. (35-

year-old female, IPAZ surgical specimen 16132 from 1966.) 

FIGURES 605, 606.—Hemangioma of frontal bone: 605, Wet 

specimen, endocranial view, showing spongy bone with large 

vascular channels. 606, X-ray, showing the typical wheelspoke pattern of cranial hemangioma. (47-year-old female, 

2 years duration, PMSG 9/1.741a, surgical specimen 2369 

from 1955.) 

showing a characteristic radial arrangement of 

coarse diploic trabeculae around large vascular 

channels, giving a "sunburst" effect on X-ray 

(Figures 604-606). These lesions are usually 

round, several centimeters in diameter, and destroy the inner and outer table. The tumor expands mostly outward and shows a circular lytic 

margin in the periphery. Hemangiomas in long 
378 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

FIGURES 607, 608.—Meningioma of cranial vault of 6 years 

duration: 607, External view; notice the massive bone formation outward. 608, Cut surface; notice the radiant arrangement of the new bone, sclerosis of diploe, destruction 

of both tables and only slight endocranial build-up. (20-

year-old Sinhalese male, WM N9.2 from 1884.) 

FIGURE 609.—Unusually deep niches for pacchionian granulations of frontal bone. Notice the bilateral deep (dark) 

defects ofthe inner table. (63-year-old female, MGH surgical 

specimen 8045 from 1970.) 

bones are extremely rare. They produce loculated 

lytic and sometimes sclerotic lesions, which are 

not characteristic enough for identification in dry 

bone. 

Meningioma 

Meningioma is not primarily a bone tumor. It 

arises from the mesothelial lining cells ofthe dura 

mater of the brain and spinal cord. Not uncommonly the cranial meningiomas invade the cranium through the internal table often eliciting a 

massive response of reactive bone in form of 

radiant spicules, which may project outward from 

the destroyed outer table (Figures 607, 608). This 

finding may be indistinguishable from osteosarcoma in dry bone, but a destructive defect of the 

inner table without internal spiculation favors the 

diagnosis of meningioma. Meningioma invading 

the cranial base tends to be more osteosclerotic 

with less tendency of spicule formation. Unusually large arachnoid granulation may occasionally create deep, smooth-walled defects in the 

cranial vault. However, they are usually lined by 

a thin internal table (Figure 609). 

PALEOPATHOLOGY 

Osteoblastic Tumors 

Of the several primary benign tumors of bone 

known in modern medical practice few have been 

identified in archeological specimens. This may 

be due partly to the lack of knowledge by paleopathologists of the gross morphological features 

associated with these tumors but also may be due 

to the problems in identifying a tumor in a dry 

bone specimen. Osteomas are fairly common in 

archeological specimens and have been described 

by several authors. Small button osteomas occur 

primarily on the outer table of the skull vault. 

Typically this osteoma is no larger than one 

centimeter in diameter. It is solitary, dense, with 

little relief but with a slight degree of undercutting at the boundary with normal bone (Figure 

610). Large osteomas also occur as seen on a skull 

from near Lima, Peru (NMNH 242462). This 

tumor measures 2.0 centimeters in diameter and 
NUMBER 28 379 

FIGURE 610.—Button osteoma ofthe frontal bone in an adult 

female skull from Pachacamac, Peru. (NMNH 267377.) 

^ < "3 

FIGURE 611.—Large osteoma ofthe right parietal in an adult 

skull from a site near Lima, Peru. (NMNH 242462.) 

almost 4 millimeters above the plane of normal 

bone at the center ofthe lesion (Figure 611). 

Another common type of tumor seen in archeological specimens is the small bony growth, 

which may partially to completely fill the external 

auditory meatus. Hrdlicka (1935) was unable to 

reach any firm conclusion regarding the cause of 

these ear exostoses. He did not feel that they were 

the result of infectious or malignant diseases and 

suggested chemical or mechanical irritation as a 

possibility. Hrdlicka (1935:80) observed that 

males are far more subject to the disease. His 

report of racial variation suggests a genetic component but environmental or cultural conditions 

cannot be ruled out. Hrdlicka (1935:80) did find 

that the incidence increased with the age of the 

individual. Other scholars, including Adis-Castro 

and Neumann (1948) and Gregg and McGrew 

(1970), have described cases in archeological populations. Stewart (1979b: 268) has called attention 

to lytic lesions of the bony external auditory 

canal, which he suggests may be the bony response to a soft-tissue tumor (ear cholesteatoma). 

The circumscribed enlargement of the canal does 

FIGURE 612.—Bony tumor ofthe left external auditory meatus of an adolescent skull from Chicama, Peru. (NMNH 

264344.) 

FIGURE 613.—Large bony tumor ofthe left external auditory 

meatus of an adult male from an archeological site in Illinois, 

USA. (NMNH 243180.) 
380 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

not exceed the size of an acorn. The condition 

appears to be fairly common among the Eskimos 

and Aleuts of Alaska, USA. 

There are numerous examples of ear exostoses 

in the collections of the National Museum of 

Natural History, USA. Only two will be described 

here. The first of these is an adolescent skull from 

Chicama, Peru (NMNH 264344) illustrating 

what appears to be the incipient stage of this 

condition (Figure 612). All secondary teeth have 

erupted. The basioccipital synchondrosis is not 

fused indicating an age of around 18 years at the 

time of death. Sex is thought to be female. Both 

auditory canals exhibit narrowing; the right auditory meatus has a slight, hypertrophic ridge 

that may represent the early stage of tumor development. 

The second skull is from Illinois, USA (NMNH 

243180). It is from a fully adult male. The mandible is missing and the maxilla has a slight 

development of bony tumors in the buccal region 

of both sides. Like the previous specimen the 

auditory canals are abnormally narrow. In addition there are large bony tumors in both external 

meatus with the most pronounced development 

on the left side (Figure 613). Both tumors arise 

from the posterior portion of the canal. 

Beraud, Morel and Boyer (1961) describe an 

osteoma of the ethmofrontal region in a skull 

from France. The specimen is from the medieval 

cemetery of St. Hermentaire and is dated to the 

11th century A.D. The authors estimate the age at 

death to be 22-25. The tumor encroaches on the 

endocranium. 

Chondroblastic Tumors 

CARTILAGINOUS EXOSTOSIS.—A probable example of cartilaginous exostoses is seen in a right 

innominate in a Twelfth Dynasty Rock Tomb at 

Lisht in Upper Egypt (NMNH 256474). There 

are no other bones associated with this specimen. 

The morphology ofthe innominate indicates that 

it is from an adult female skeleton. The tumor 

occurs at the junction between the fused pubic 

and iliac bones (Figures 614, 615). The lesion 

measures 25 by 33 millimeters and extends 18 

millimeters above the plane of the normal adjacent surface. The surface ofthe tumor is irregular 

and has a rounded, lumpy appearance. The joint 

surface of the acetabulum is normal; however, 

FIGURES 614, 615.—Cartilaginous exostosis in the area of 

fusion between the pubic and iliac bones of a right innominate bone: 614, Anterolateral view, showing the irregular 

surface ofthe tumor. 615, Superior view, showing projection 

of the tumor from the bone surface. (Adult female from the 

Rock Tombs, Lisht, Egypt, Twelfth Dynasty, NMNH 

256474.) 
FIGURE 616.—Hereditary multiple exostoses in a child's skeleton from a Saxon cemetery, 

Winchester, England. Arrows indicate the location of some of the exostoses; scale in cm. 

(BMNH G932, CG69, TR XL 1085.) 
382 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

the tumor bone has extended the anterosuperior 

margin of the acetabulum. The X-ray film of the 

tumor reveals that the medullary space of the 

exostosis is continuous with the innominate. 

HEREDITARY MULTIPLE EXOSTOSES (Diaphysial 

Aclasia).—Singer (1962) describes a case of diaphysial aclasia in a young adult female skeleton 

from a cave in South Africa. The archeological 

age is reported to be post-European. There are 

multiple exostoses on all the major long bones. 

Gladykowska-Rzeczycka and Urbanowicz (1970) 

report a case of this condition in a skeleton of an 

adolescent from a cemetery in Pruszcy Gdanski, 

Poland. The site is dated to between the first 

century B.C. and the fourth century A.D. There 

are multiple bony projections primarily of the 

metaphysial areas of the major long bones. Sj0vold, Swedborg, and Diener (1974) describe a most 

FIGURE 617.—A probable case of hereditary multiple exostoses in an isolated right femur of an adult from an archeological site in Chicama, Peru. Medial view of the distal 

femur, arrows indicate the location of some ofthe exostoses. 

(NMNH, uncataloged.) 

interesting burial from a cemetery on the island 

of Gotland off the southeastern coast ofthe Swedish mainland. The burial is dated to about A.D. 

1250 and includes the skeleton of a young female 

between 17 and 20 years of age and a near-term 

fetus. Both skeletons exhibit multiple exostoses. 

The authors suggest that exostoses protruding 

from the pelvis prevented the birth of the infant 

and led to the death of both the mother and fetus. 

Another archeological example of multiple cartilaginous exostoses is located in the Winchester 

Saxon skeletal-pathology collections of the British 

Museum (Natural History) in London. This specimen (BMNH G932, CG69, TR XL 1085) includes most of the major postcranial bones. The 

age estimate based on femur length is around 4 

years, sex is unknown. Prominent bony projections can be seen on the distal metaphyses of the 

left humerus and of both femora (Figure 616). 

The left scapula and both iliac bones are affected 

as well. Other bones, including the ribs, vertebrae, 

and tarsals, are normal. Since this tumor is usually benign, it is unlikely to have been the cause 

of death. 

A New World example of multiple cartilaginous exostoses is seen in a right femur of an adult 

from Chicama, Peru (NMNH, uncataloged). 

There are no other bones associated with the 

specimen and the archeological age is unknown. 

There is a large bony exostosis, which developed 

between the greater trochanter and the superior 

surface ofthe femoral neck. The remaining lesions 

are in the distal metaphysial region (Figure 617) 

and consist of multiple bony projections. 

Meningioma 

Abbot and Courville (1939) attribute a parosteal osteoblastic lesion seen in two skulls located 

in the Museum of Man, San Diego, California, 

USA, to periosteal reactions to underlying tumors 

of the dura (meningiomas). One skull was from 

Peru and had a large lesion of the skull vault 

consisting of fused spicules of bone, which radiate 

out perpendicular to the skull surface. The abnormal bone is attached to the underlying outer 

table, which is largely intact. The second skull is 
NUMBER 28 383 

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FIGURES 618, 619.—Multiple lytic lesions ofthe skull possibly due to meningioma. Specimen an 

adult male from an archeological site on St. Lawrence Island, Alaska, USA: 618, Posterolateral 

view, showing large lesion on the left parietal. 619, Detailed view of large, parietal lesion; note 

the partial bony fill-in ofthe exposed diploe in the larger lesion. (NMNH 280091.) 

from San Nicolas Island off the coast of southern 

California. The lesion is similar to the Peruvian 

specimen. Meningiomas are known to produce 

lytic lesions in early stages of the tumor development (Schinz, Baensch, Friedl, and Uehlinger, 

1951-1952:1628), but blastic lesions are common 

(Gushing, 1922:150). 

Rogers (1949) briefly describes two skulls from 

Egypt having lesions, which he attributes to meningiomas. The first of these is from the First 

Dynasty and shows a hyperostotic lesion of the 

right parietal involving both the inner and outer 

table. The second specimen is from the Twentieth 

Dynasty and exhibits a large honeycomb lesion 

with a focus in the right parietal but involving 

the left parietal and the frontal bone. The lesion 

is large including most of the right parietal. It is 

not clear whether the inner table was involved. 

The first of these two cases differs from the two 

cases of Abbot and Courville (1939) in involving 

both tables of the skull. 

MacCurdy (1923:264, pi. 39) describes an adult 

male skull from Paucarcancha, Peru, with a large 

tumor of the left parietal and frontal bones (probably the same Peruvian skull described later by 

Abbot and Courville (1939)). The coalescing osteophytes extend outward from the skull about 

4.5 centimeters. The tables ofthe skull have been 

destroyed beneath the tumor. MacCurdy attributes this tumor to osteosarcoma, but a meningioma would seem to be more likely. 

An Eskimo skull from St. Lawrence Island, 

Alaska, USA (NMNH 280091) exhibits lesions 

that can be attributed to meningioma ofthe lytic 

type. The archeological provenience is obscure. 

The skull is male and fully adult, probably in the 

45 to 65 year age range. The mandible is missing 

as are all the postcranial bones. On the external 

table of the vault, there is a diffuse porosity, 

which is also seen to a more limited degree on the 

nasal bones and maxilla. There has been some 

postmortem erosion that obscures the surface texture somewhat, but the remaining surface has a 

pumice-like quality. On the posterior portion of 

the left parietal the most dramatic feature is a 

large lytic lesion, which is confluent with a 

smaller lytic lesion encroaching on the right parietal (Figures 618, 619). The larger of the two 
384 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

lytic lesions has a maximal diameter of 4 centimeters and a slightly scalloped but well-circumscribed appearance, with the inner table somewhat more affected than the outer. The smaller 

lytic lesion is similar in appearance but less well 

circumscribed, suggesting lytic activity at the 

time of death. Other smaller lesions occur primarily on the left side of the skull with only one 

moderately large lesion, which measures 1.5 centimeters in diameter in the right temporal bone, 

and which also involves the sphenoid. The skull 

is somewhat thicker than normal, measuring 13 

millimeters near the edge ofthe major lytic focus. 

There are several conditions that could give 

rise to the pattern seen in the skull. Eosinophilic 

granuloma produces lesions similar to that seen 

in this skull. Metastatic carcinoma and angiosarcoma are also possibilities. 

Primary Malignant Bone Tumors 

PATHOLOGY 

Primary malignant bone tumors are comparatively rare lesions that, in contrast to other malignant lesions, most frequently occur during the 

growing period. These sarcomas arise from osteogenic mesenchyme and are classified according to 

their matrix production as osteosarcomas, chondrosarcomas, fibrosarcomas, reticulum cell sarcomas, and angiosarcomas. The most common 

primary malignant bone tumor is the osteosarcoma followed by chondrosarcoma and Ewing's 

sarcoma in decreasing frequency. All other types 

are rare. 

Osteosarcoma 

This tumor occurs most often in adolescents 

and young adults. Males are about twice as often 

affected as females. The appearance of this tumor 

is closely related to the areas and periods of 

greatest enchondral growth. The most active 

growth plates in the skeleton are those of the 

distal femur, the proximal tibia, and the proximal 

humerus. The most common location of this tumor is in the distal femoral metaphysis, followed 

in frequency by the proximal tibial metaphysis 

and proximal humeral metaphysis. The epiphyses 

are practically never the primary site and often 

remain uninvolved, being protected by the open 

growth plate. The tumor predilects the long bones 

ofthe extremities, rarely involving the cancellous 

bones, the small tubular bones of the extremities, 

or the skull. Of the skull bones, the mandible is 

most often involved. Osteosarcomas arising past 

middle age may develop in abnormal bone, particularly in Paget's disease of bone. 

Osteosarcoma arises within the bone at or near 

the metaphysial side of the growth plate. The 

tumor destroys varying amounts of the normal 

bone and extends through the cortex into the 

surrounding soft tissue. The appearance of the 

tumor, especially in dry bone, depends on the 

amount of mineralized bone formation. This 

ranges from almost purely lytic forms (Figure 

620) to those with massive production of sclerotic 

tumor bone (Figures 621, 622). The bone produced by the tumor is woven bone, occurring in 

sheets and masses without architectural arrangement of trabeculae. The extracortical portion of 

the tumor may exhibit a radiant alignment of 

tumor bone, so-called sunburst (Figure 623). The 

elevation of the periosteum at the margin of the 

cortical breakthrough leads to some reactive, nonneoplastic bone formation decreasing in thickness 

away from the tumor. In profile, this area appears 

triangular on X-ray (Codman's triangle) (Figures 

624, 625). The epiphysis adjacent to the tumor 

may ultimately become involved, but the joint 

surface usually remains intact. The tumor extends 

through the medullary cavity but practically 

never involves the epiphysis on the end remote 

from the tumor. Occasionally osteosarcoma metastasizes to other bones (Figures 626, 627). 

Parosteal osteosarcoma arises on the outside of 

the bone in or near the periosteum. This tumor is 

less frequent than endosteal osteosarcoma and 

shows no particular sex predilection. Its occurrence is more evenly spread throughout adult age. 

It, too, occurs most commonly on the distal metaphysis of the femur (Figure 628). This tumor is 

slow growing and may produce large extraosseous 

masses of dense bone (Figure 629). Penetration 
NUMBER 28 385 

FIGURE 620.—Osteolytic osteosarcoma of distal right femur, 

anterior view. Notice cortical destruction and hypervascularity. The epiphysis is spared. (13 year-old female, CGH 

surgical specimen 2229 from 1957.) 

into the marrow cavity is late or absent (Figure 

630). The differentiation from parosteal traumatic myositis ossificans is not always possible on 

dry bone. 

Chondrosarcoma 

This tumor produces malignant cartilage of 

varying degrees of maturity. It also arises most 

commonly in the metaphysis of long bones ofthe 

extremities, either directly or on the basis of a 

previously benign cartilage tumor or developmental cartilage rest. The age distribution is more 

FIGURES 621, 622.—Sclerosing osteosarcoma of distal femur: 

621, Outside view, showing extraosseous portion of tumor 

extending to knee joint. 622, Cut surface, showing sclerotic 

tumor bone filling the medullary cavity. (Young adult male, 

died with pulmonary metastases, HM P826 from 1786.) 
386 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

FIGURE 623.—Osteosarcoma of left frontoparietal area. The 

irregular tumor bone projecting outward is similarly projected endocranially. Specimen recovered from a grave. 

(Adult, ANM 2042.) 

widely spread from late adolescence through 

adult age. There is no marked sex predilection. 

The most common locations are the proximal 

and distal metaphysis of the femur, the proximal 

metaphysis of the humerus and the pelvis. Although the small tubular bones of hands and feet 

are frequently the site of single or multiple enchondromas, chondrosarcomas are uncommon in 

these bones. The tumor masses tend to be nodular, destroying the cancellous bone and causing 

endosteal scalloping of the cortex by pressure 

erosion (Figures 631, 632). The more mature 

forms of chondrosarcoma tend to undergo spotty 

calcification and, in part, enchondral ossification. 

Only such calcified or ossified chondrosarcomas 

would show characteristic features in dry bone. 

Although the enchondral ossification of a chondrosarcoma tends to be more mature and orderly 

than the tumor bone of an osteosarcoma, the 

FIGURES 624, 625.—Sclerosing osteosarcoma of distal left femur: 624, Surface. 625, Cut surface. 

Notice extensions of tumor bone through the cortex into soft tissue and shelf of reactive bone 

at proximal tumor margin (Codman's triangle). (12-year-old male, MG H surgical specimen 

11078 from 1972.) 
NUMBER 28 387 

FIGURE 628.—Parosteal osteosarcoma of distal left femur. 

(Young adult, FPAM 2102 from before 1848.) 

differentiation between the two may be dubious 

in dry bone. 

Ewing's Sarcoma 

This is the third most frequent primary malignant tumor of bone. It occurs most frequently in 

childhood and adolescence, rarely in adults. The 

tumor is formed by very primitive mesenchymal 

round cells, which do not produce matrix of any 

kind. The most common location for this tumor 

FIGURES 626, 627.—Metastatic sclerosing osteosarcoma of 

ninth thoracic vertebra: 626, Lateral view, showing tumor 

bone replacing the vertebral body. 627, Cut surface, showing 

ivory-like tumor bone. There was a smaller second focus in 

the twelth thoracic vertebra. (20-year-old male, FPAM 3171, 

autopsy 56719 from 1870-71; scales in cm.) 
388 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

FIGURES 629, 630.—Parosteal osteosarcoma of proximal right tibial metaphysis: 629, External 

view, showing layer of reactive bone at junction of cortex and tumor. 630, Cut surface, showing 

dense radiating tumor bone. Notice slight involvement of underlying cortex. (Young adult, 

FPAM 3639 from 1878; scales in cm.) 

is a long bone of an extremity or a pelvic bone. 

The structure of the tumor, consisting of loose 

round cells not held together by matrix, is responsible for the permeative pattern of this lesion. The 

tumor cells can easily push through intertrabecular marrow spaces and invade Haversian 

canals of the cortex. The result of this is that a 

large segment of the bone, including the diaphysis, is involved. The destruction of trabecular 

bone may be less marked, but resorption along 

Haversian canals leads to lamination of the cortex. The tumor spreads into and through the 

periosteum, eliciting some reactive bone formation of surface parallel ("onion skin") or radiant 

("sunburst") type. Of all the bone tumors, this is 

the one most often metastasizing to other bones. 

The presence of reactive bone may make the 

differentiation between Ewing's and osteosarcoma impossible on dry bone. The absence of 

massive destruction and the long axial involvement, together with permeative intracortical resorption, would arouse suspicion that the lesion 

may have been a Ewing's sarcoma or a reticulum 

cell sarcoma, which usually affects adults, especially past 50 years of age. 

Chordoma 

Chordoma is a rare tumor arising from notochordal rests. The tumor mostly affects individuals above 40 years of age and somewhat predilects males. During embryonic development the 

notochord extends from the skull base to the tip 

of the coccyx, through the entire spine. In the 
NUMBER 28 389 

FIGURES 631, 632.—Parosteal chondrosarcoma of distal right femur: 631, Outside view; notice 

the nodular character of the mineralized portion of the tumor. 632, Cut surface; notice the 

mature trabecular pattern of the bone replacing the core of the tumor. (31-year-old male, 10 

years duration, WM S.72a.2 from 1894.) 

process of vertebral development the notochordal 

tissue is extruded into the nucleus pulposus of the 

intervertebral disc. In the movable part of the 

spine, it is mostly destroyed by mechanical attrition. Only in mechanically sheltered areas of the 

axis do notochordal remnants survive into later 

life. These areas are the skull base, the sacrum, 

and the second cervical vertebra, where the odontoid process is united with the body of C2 by 

fusion of an intervening disc. These facts explain 

the localizations of chordomas: 55 percent sacral, 

35 percent skull base, and only 10 percent vertebral, especially cervical. 

Small notochordal rests are common in the 

clivus of the skull base and may show a small, 

pitted defect in dry bone in this area. The tumor 

is purely destructive producing large, lytic defects 

in the spheno-occipital portion of the skull base 

or the sacrococcygeal area centered on the midline. Since no mineralized matrix is formed, nothing ofthe tumor itself could remain in dry bone. 

PALEOPATHOLOGY 

Primary malignant tumors of bone are rare in 

modern medical practice and are equally rare in 

archeological specimens. Ruffer and Willmore 

(1914) report a tumor of the pelvis from Egypt 

dated about A.D. 250. The tumor affects the right 

innominate, particularly the ischium and inferior 

ilium. It appears to have started in the cancellous 

tissue of the pelvis and is slightly expansive in 

nature, producing a deformation ofthe obdurator 

foramen and encroaching on the acetabulum. 

The authors rule out carcinoma and infection 

and suggest osteosarcoma adding that they can-
M Iff: 1 

m J 

FIGURES 633-635.—Osteosarcoma or chondrosarcoma ofthe 

proximal left humerus of a Celtic warrior (approximately 

800-600 B.C.) found near Muensingen, Canton Bern, Switzerland: 633, Medial view; note that the articular surface is 

spared. 634, Lateral view. 635, X-ray. (NHMB A95; scales 

in cm.) 
NUMBER 28 391 

not determine if the tumor was primary or secondary. The illustration of the lesion is of little 

value but does not show the active irregular 

growth of bone usually seen in osteoblastic osteosarcoma. The lesion appears to be chronic rather 

than acute, which would tend to rule out osteosarcoma. However, a tumor of some type is possible as is infection. 

Dastugue (1965) describes a tumor ofthe right 

maxilla and zygomatic bone on a skull from a 

Middle Age site associated with the town of Caen 

in France. The tumor measures 60 millimeters 

wide by 40 millimeters high and encroaches both 

on the nasal passage and the right orbit. The 

surface of the tumor is very irregular with relatively large coalescing spicules. There are three 

inferior projections. Curiously, there is antemortem damage to the right zygomatic bone adjacent 

to the tumor and Dastugue suggests the possibility of surgical intervention to explain this defect. 

The tumor appeared malignant to Dastugue and 

he expresses the opinion that it caused the death 

of the individual. The morphology of the lesion 

is compatible with a primary malignant tumor of 

bone. However, other possibilities, such as callus 

following trauma to the face, seem more probable. In my opinion, particularly in view of the 

injury to the zygomatic bone, trauma rather than 

surgical intervention is more probable. 

A tumor of the mandible was found in an 

American Indian skeleton excavated in the state 

of West Virginia (Kelln, McMichael, and Zimmermann, 1967). The authors date the specimen 

to the mid-seventeenth century. The lesion is 

rather large, measuring about 24 millimeters in 

diameter and 19 millimeters in depth. The mandible is probably from a female of about 20 years 

of age. The authors suggest several possible neoplastic conditions including osteoma and osteosarcoma as the cause of the lesion. The position 

of the tumor near the symphysis and the young 

age of the individual are compatible with a diagnosis of primary malignant tumor. However, 

the chin is prone to trauma and infection and 

bony reaction to these morbid conditions is more 

likely. 

An unambiguous example of a primary malignant tumor of bone is found in the skeletal collections of the Natural History Museum in Bern, 

Switzerland. This specimen (NHMB A95) is the 

left humerus from a Celtic warrior tomb dated to 

approximately 800-600 B.C. and found near the 

town of Muensingen in Canton Bern. Brothwell 

(1967a:331) provides a brief description of the 

specimen. Although damaged by postmortem 

erosion, the humerus is complete except for the 

distal epiphysis, which was lost postmortem. The 

lesion extends completely around the proximal 

humerus but is least developed on the medial 

aspect. The bone associated with the lesion is 

approximately 7 centimeters in maximum diameter and abnormal tissue extends slightly more 

than one-third the length ofthe humerus (Figures 

633, 634). Tumor bone overlies the insertion of 

the joint capsule but does not involve the joint 

surface itself. The gross morphology of the tumor 

consists of large coalescing bony projections, 

which have a coarse coral-like appearance. While 

the age at death of the individual cannot be 

determined, the humeral head appears to be fused 

indicating an age in excess of 15 years. 

X-ray films of this specimen were provided 

through the courtesy of Dr. Walter Huber, the 

Director ofthe Natural History Museum in Bern. 

The films reveal a lytic process extending 2 to 3 

centimeters into the externally normal cortex distal to the lesion (Figure 635). The location ofthe 

tumor, as well as its gross and X-ray film appearance, is compatible with the diagnosis of primary 

osteosarcoma or chondrosarcoma. 

Metastatic Tumors 

PATHOLOGY 

Tumors metastatic to the skeleton are a common occurrence in carcinoma but rare in sarcoma. The tumor cells reach the skeleton, usually 

the bone marrow, by the blood stream. The frequency of skeletal metastases of different tumors 

depends, to a considerable extent, on the location 

of the primary tumor. Larger tumor particles 
392 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

FIGURE 636.—Osteolytic metastatic carcinoma of spine and 

pelvis. Notice disseminated round lytic lesions exposing spongiosa and the involvement of the neural arches and spinous 

processes. (32-year-old female with breast cancer, FPAM 

5697, autopsy 182394 from 1929.) 

(tumor emboli) are usually retained in the primary filter, but individual tumor cells, as in 

round cell tumors especially, pass readily through 

a capillary filter. The primary filter for tumors 

drained by the caval system is the lung, for those 

in the portal drainage area the liver, while tumors 

arising in the lung have direct access to the 

systemic circulation through the pulmonary 

veins. 

The frequency of skeletal metastases varies 

with different observers. The largest autopsy statistics based on two decades of cases ofthe Zurich 

Pathological Institute preceding 1948, are as follows: Of over 3000 malignant tumors, 12 percent 

metastasized to the skeleton (Walther, 1948:256). 

Jaffe (1958:599-600) feels that this figure is abFiGURE 637.—Massive osteoblastic metastatic carcinoma of 

pelvis and spine. Notice the diffuse nodular hyperostosis. 

(66-year-old male with cancer of the prostate, IPAZ autopsy 

497 from 1946.) 

normally low due to early postoperative deaths 

in previous decades. He states that presently at 

least 76 percent of tumor cases with metastases 

that come to autopsy show involvement of the 

skeleton. In anthropological material, in the absence of radical surgery, with the malignancy 

having taken its natural course, a high figure for 

skeletal metastases should be expected. 

.Everybody agrees that the carcinomas most 

commonly metastasizing to the skeleton are those 

of the female breast and of the male prostate. 

The figures in Walther's (1948:277) series are as 

follows: breast 47.2 percent, prostate 42.4 percent, 

thyroid 30.8 percent, lung 29.8 percent. 

The bones most commonly involved in metastatic carcinoma are the spine (including the 

sacrum), the proximal metaphysis and epiphysis 

of the femur, ribs, sternum, skull, pelvis, and 

proximal humerus, in decreasing order of frequency. This coincides with the location of 

hemopoietic marrow in the older adult. The figures of Walther (1948:279) concerning only autopsy cases with skeletal metastases are as follows: 

spine 80 percent, femur 40 percent, ribs and 

sternum 25 percent, skull and pelvis 25 percent, 

humerus and shoulder girdle 7 percent, other 

extremity bones 1 to 2 percent. Skeletal metastases distal to the elbow and knee area are distinctly uncommon. 
NUMBER 28 393 

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FIGURES 638-640.—Osteoblastic metastases of adrenal neuroblastoma: 638, External view of frontal bone, showing 

radiating reactive bone spicules in supraorbital area. 639, 

Endocranial view, showing radiating trabeculae replacing 

the inner table. 640, Basal external view of sphenoid, showing involvement of both wings. (14-month-old male, PMES 

1VUH(1 and la) from before 1929.) 

The tumor cells reaching the bone marrow 

grow and first replace the marrow without change 

of the bone architecture. The majority of metastatic deposits discovered at autopsy are not demonstrated by external inspection or radiography. 

In the Zurich series, only 36 percent ofthe skeletal 

metastases were discovered during life (Walther, 

1948:189). Continued growth ofthe tumor cells 

usually leads to destruction and osteoclastic resorption of cancellous bone and internal scalloping or complete destruction of cortical bone (osteolytic metastases). At least microscopically, 

however, some reactive bone formation is often 

seen in some ofthe lesions and/or in their vicinity. 

In other cases, a strong osteoblastic response to 

the presence of the tumor cells is observed, consisting of new bone deposits replacing old trabeculae or coating remaining old trabeculae. This 

results in blotchy or diffuse densities on X-ray. It 

IS not entirely clear what causes this difference. 

In general, however, fast growing tumors are 

mainly osteolytic, while slow growing ones elicit 

an osteoblastic response. 

Carcinoma of the breast mostly shows osteolytic metastases, while carcinoma of the prostate 

usually shows osteoblastic deposits. The great 

majority of metastatic bone tumors are multiple 

and involve more than one bone. Solitary and 

relatively slow growing metastases are most often 

caused by renal cortical or thyroid carcinomas. 

These solitary lesions occur with predilection in 

the shaft of femur or humerus, less commonly in 

the cranial vault. They may appear on X-ray as 

a cystic lesion, with an expanded shell of new 

cortex showing soap bubble appearance. They 

may mimic benign lesions, except for the fact that 

diaphysial benign lesions are very uncommon. 

Lytic metastases progressively destroy cancellous bone and erode the cortex of long bones from 

within. Disseminated lytic metastases may be 

indistinguishable from multiple myeloma in dry 

bone. In the spine, the most frequently involved 
394 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

FIGURE 641.—Probable carcinoma of the ethmoid with destruction of ethmoid, medial orbital wall, and adjacent 

frontal bone. Notice the almost complete absence of bony 

reactivity. (Elderly individual, ANM 2490.) 

FIGURE 642.—Carcinoma ofthe nasal cavity with destruction 

of palate and interior portion of maxilla. Notice the complete 

absence of reactive bone. (Adult, ANM 2051.) 

vertebrae are the lower thoracic, followed in decreasing frequency by the lumbar, sacral, and 

cervical vertebrae. The metastases are prevailingly located in the vertebral bodies, but neural 

arches and spinous processes may also be affected 

(Figure 636). Compression fractures are common, 

secondary to lytic metastases. In the cranial vault, 

the most marked destruction is in the diploe, 

while the outer and inner tables are long spared. 

Metastases in the long bones predilect the intertrochanteric area of the femur or proximal portion of the humerus. Pathological fractures secondary to lytic deposits in long bones are common. The frequency in Copeland's (1931) radiological series is as follows: renal cortical carcinoma 45 percent, thyroid carcinoma 33 percent, 

malignant melanoma 33 percent, carcinoma of 

the colon 33 percent, carcinoma of the lung 25 

percent, carcinoma of the breast 15 percent, carcinoma ofthe stomach 14 percent, carcinoma of 

the prostate 0.2 percent and no pathological fractures in cancers of other primary sites. 

Subperiosteal metastases are uncommon. If 

present they are usually lytic, causing deep scalloping of the underlying cortex. This is seen most 

commonly in renal cortical carcinoma (Schinz, 

Baensch, Friedl, and Uehlinger, 1951-1952(2): 

1008). Osteoblastic metastases are most commonly observed in carcinoma ofthe prostate. The 

distinct lesions may become confluent and extremely sclerotic. There is usually little if any 

bone destruction, and the outer contours of the 

involved bones are not significantly altered except 

for those advanced cases where massive subperiosteal bone is deposited in the form of mossy 

osteophytes (Figure 637). The distribution of metastatic prostate carcinoma is different from that 

of the usual hematogenous metastases. The ear-
NUMBER 28 395 

liest and most massive involvement is in the 

pelvis, sacrum, and lumbar vertebrae. This is 

probably due to the fact that the pelvis and 

vertebral venous plexuses freely communicate 

and thus permit direct colonization of the adjacent bones without passage through the pulmonary filter (Batson, 1940). In most instances blastic or lytic pelvic metastases begin in the floor of 

the acetabulum, spread into the pubic rami, and 

lastly involve the iliac wings (Schinz, Baensch, 

Friedl, and Uehlinger, 1951-1952(2): 1007). The 

differentiation from Paget's disease can be difficult on gross inspection or X-ray. However, microscopic sections should reveal the typical mosaic 

structure if the lesion is Paget's. 

Special mention should be made of the appearance of skeletal metastasis in neuroblastoma, 

a malignant tumor of the adrenal or of the sympathetic chain in infants and children, usually 

under 3 years of age. This tumor, a round cell 

lesion, freely seeds to the bone marrow in wide 

distribution, including trunk, skull, and extremities. The lesions often elicit osteoblastic reaction 

leading to "hair-on-end" appearance in areas of 

the cranial vault and periosteal layered-bone formation of varying thickness on the long bone 

shafts of the actively growing childhood skeleton 

(Figures 638-640). The periosteal deposis differentiate it from similar skull lesions in severe anemias. 

Craniofacial involvement may occur by direct 

extension of paranasal carcinomas. Craniopharyngeal carcinoma may erode the cranial base 

from without. Carcinoma of the ethmoid may 

destroy the adjacent frontal bone and the orbital 

wall (Figure 641). Carcinoma ofthe nasal cavity 

may destroy part of the maxilla and of the hard 

palate (Figure 642). In these cases the absence of 

reactive bone and the strictly localized area of 

destruction usually permits, in dry bone, differentiation from lesions of tertiary syphilis, leprosy, 

and lupus vulgaris. 

PALEOPATHOLOGY 

Secondary tumors of bone are by definition 

malignant. These types of tumors are presently 

much more common then primary malignant 

tumors of bone. Thus, even though they are 

associated with the older age categories, they 

might be more common in archeological skeletons. However, like primary malignant tumors, 

they pose problems in differential diagnosis in 

dry bone specimens, particularly from infectious 

diseases. 

A skeletal specimen from a cemetery near Dubendorf. Canton Zurich, Switzerland, dated between the eleventh and fifteenth centuries exhibits a diffuse osteoblastic reaction. The specimen is an adult male probably in excess of 50 

years of age at death and is currently stored in 

the Anthropological Institute ofthe University of 

Zurich, Switzerland (AIUZ 7757). The right innominate contains a lesion largely limited to the 

periosteal surfaces ofthe ilium (Figure 643). The 

lesion consists of extensive fine porous bony 

buildup. There is no obvious destruction of underlying bone nor evidence of abscess or cloacas. 

There is a similar bony reaction on the right 

anterior proximal femur. Two of the ribs in this 

specimen also show periosteal lesions (Figure 

644). The disseminated nature ofthe disease and 

the morphology ofthe lesions are compatible with 

metastatic tumor. The extensive involvement of 

the innominate and the sex of the case suggest 

prostate cancer. 

Osteolytic metastatic cancer of the skeleton is 

probably the most common type of malignant 

lesion seen in archeological specimens. The major 

problem in diagnosis is to distinguish between 

metastatic carcinoma and multiple myeloma. In 

the skeleton these two types of cancer reflect a 

morphological gradient making differential diagnosis impossible in many cases. A presentation 

of three problem cases is provided in the discussion on reticuloendothelial and hemopoietic disorders (pp. 267-269). 

Bony responses to neoplasms may produce 

mixed blastic and lytic lesions. An archeological 

example of this condition is seen in a skeleton 

from Kachemak Bay, Alaska, USA (FM SEL30 

AMU3 Burial 11). The skeleton was excavated in 

1974 and dated circa A.D. 350 by carbon-14 analysis. The skeleton was shown to me through the 
396 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

courtesy of John Lobdell, currently with the Department of Anthropology at the University of 

Alaska, Anchorage, Alaska, USA. The specimen 

consists of the skull and the incomplete portions 

ofthe postcranial skeleton. The sex is female and 

the pitting on the posterior portion of the pubic 

symphysis suggests multiple pregnancies. Skeletal 

age is in the 50-year-plus range. 

The disease process is multifocal with lesions 

on the skull, ribs, vertebrae, left humerus, both 

innominates, the right femur and both tibiae. 

The skull lesions are circular and fairly large 

(Figures 645-647), the smallest is about 25 millimeters in diameter and the largest about 45 

millimeters in diameter. One lesion is on the 

frontal, two are entirely on the left parietal, and 

a third is partially on the left parietal but crosses 

the sagittal suture into the right parietal. The 

lesions show an active lytic front at the boundary 

with normal bone. The lytic process results in the 

bone having the appearance of a fine sponge. 

There is no osteoblastic circumscription of the 

lytic process. The residual porous, spongy bone 

provides the scaffolding for the formation of 

FIGURES 643, 644.—Osteoblastic lesions of the right innominate possibly due to metastatic carcinoma of the prostate. 

Specimen from an adult male skeleton from a cemetery near 

Dubendorf, Switzerland, dated between the 11th and 15th 

centuries AD. 643, Right innominate. 644, Right rib from 

lower chest region. (AIUZ 7757.) 

coarse fiber bone in the more central portions of 

the lesion. The central osteoblastic activity produces bone that rises above the plane of the 

normal bone. The lesions in this skull are similar 

to lesions occurring in the skull of a modern case 

of metastasis from lung carcinoma. The latter 

case is from the Institute of Pathological Anatomy 

at the University of Zurich, Switzerland (IPAZ 

autopsy 1850/67). In the skull lesions there is a 

lytic front adjacent to normal bone with fiber 

bone formation in the more central portion ofthe 

lesion (Figure 648). 

The postcranial lesions in the Alaskan specimen appear to be more variable morphologically 

than those of the skull, although the picture is 

complicated by considerable postmortem breakage. The cervical vertebrae are missing postmortem. The upper thoracic vertebrae are somewhat 

osteoporotic but are normal, except for slight 

degenerative-arthritic changes. However, TIO 

and T12 both have lytic lesions of the lamina. 

Similar destructive lesions occur on the laminae 

of the first two lumbar vertebrae. The vertebral 

bodies of Ll, L2, L3, and L5 show evidence of 
NUMBER 28 397 

FIGURES 645-648.—Mixed blastic and lytic lesions ofthe skull: 645, Left lateral view of a skull 

showing two large porous lesions on the parietal bone. Specimen from an archeological site 

dated about A.D 350 located near Kachemak Bay, Alaska, USA. 646, Detailed view of parietal 

lesion adjacent to the sagittal suture. 647, Frontal view, showing lesion of right portion of 

frontal bone. (FM SEL 30 AMU3 Burial 11.) 648, Metastatic skull lesions from lung carcinoma 

in a modern case. (IPAZ autopsy 1850/67.) 
398 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

FIGURES 649-651.—Postcranial lesions in archeological skeleton from Kachemak Bay, Alaska: 649, Superior surface of 

the first lumbar vertebrae; note the lytic lesion ofthe posterior portion of the vertebral body. 650, Blastic and lytic 

lesions ofthe diaphysis ofthe right femur. 651, Lytic lesion 

ofthe proximal tibia. (FM SEL30 AMU 3 Burial 11.) 

erosion and disk herniation (Figure 649). The first 

through the third vertebral bodies are wedged 

due to partial collapse. The wedging defect ofthe 

vertebrae is well consolidated, suggesting a longstanding condition that does not appear to be 

related to the active lytic process in the vertebrae. 

The few rib fragments show active lytic involvement. 

On both innominates there is a large lytic area 

in the region of the acetabulum in which the 

bone is entirely destroyed. Both these lesions appear active. The left femur appears to be normal, 

although the distal end is missing postmortem. 

Only the diaphysis ofthe right femur is preserved. 

It shows multiple lesions, all of which combine 

lytic and blastic processes (Figure 650). The proximal ends of both tibiae have large, purely lytic 

defects in the metaphysial cortex (Figure 651). 

Both lesions are oblong, the left measuring about 

40 by 20 millimeters on the X-ray film. Postmortem damage has destroyed part of the lesion on 

the right tibia. What remains suggests a lytic 

lesion that is even larger than the one seen on the 

left. 

The morphological similarity of the skull lesions to those seen in known metastatic carcinoma 

of bone make carcinoma a probable cause of the 

lesions. The lesions of the long bones would be 

compatible with this diagnosis. Another possible 

consideration is a mycotic infection. 
Lesions of the Joints 

In order to avoid duplication, the joint manifestation of the specific infections have been discussed in connection with the respective bone 

lesions in the discussion on infectious disease (pp. 

141, 198). 

Septic Arthritis 

PATHOLOGY 

Septic arthritis is caused by bacteria entering 

the synovium and the joint cavity by the blood 

FIGURE 652.—Septic arthritis of right knee with bony ankylosis following violent trauma to the knee; anterior view. 

Notice reactive bone formation and hypervascularity around 

the joint and on the patella. (45-year-old male, WM HS 84.7 

from 1842.) 

Stream, extension of infection from the bone (osteomyelitis) or soft tissue, or by direct introduction through a wound. Occasionally any joint 

may be involved, but about one-third ofthe cases 

involve the knee and one-third the hip joint, 

leaving one-third for all other locations. About 10 

percent show osteomyelitis. The causative organisms identified are staphylococci in about onethird and streptococci in about one-fourth of the 

cases (Heberling, 1941). Other organisms causing 

septic arthritis are gonococci, pneumococci, meningococci, and various Gram-negative rods from 

enteric infections {Salmonella, Shigella). Gonococcal arthritis is more often multiarticular than 

other septic joint infections. Harkness (1942) observed multiarticular involvement in over 80 percent of instances of gonococcal arthritis. 

The acute phase of septic arthritis is limited to 

the synovial membrane and the articular cartilage and will not be recognizable in dry bone 

FIGURE 653.—Chronic osteomyelitis of left ilium with left 

sacroiliac ankylosis'and septic arthritis of congenitally dislocated left hip. (Underdeveloped 24-year-old male, PMUG 

3477, autopsy 9928 from 1879.) 

399 
400 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

FIGURES 654-656.—Chronic sclerosing osteomyelitis of left 

tibia with involvement of the proximal epiphysis and joint 

surface: 654, External view, showing periosteal hyperostosis. 

655, The bisected specimen shows sclerotic obliteration of 

the medullary cavity and a recent surgical defect in the 

distal metaphysis. 656, The proximal articular surface of 

tibia shows multiple perforations. (ANM 2997.) 

unless the subchondral bone has become involved 

and eroded. Unrelieved septic arthritis will often 

terminate in bony ankylosis (Figure 652). The 

acute and final stages are very similar to tuberculous arthritis in dry bone, although there is 

usually less bone destruction and concomitant 

shortening in septic arthritis than in tuberculosis. 

In infants, before separation of the blood supply of the femoral head from that of the proximal 

metaphysis, direct extension of osteomyelitis to 

the hip joint is common. In such cases, destruction 

of the femoral head and of the growth cartilage 
NUMBER 28 401 

FIGURE 657.—Septic arthritis of left elbow secondary to 

partly healed comminuted fracture. Notice destruction of 

joint constituents, massive reactive bone formation and ulnarhumeral ankylosis; posterior view. (Adult, WM S 81.1 

from 1851.) 

may result in bony ankylosis between the femoral 

metaphysis and the acetabulum, followed by 

marked growth deficit of the proximal femur. 

The most marked destructive changes in dry 

bone are seen in arthritis complicating chronic 

osteomyelitis (Figures 653-656) or infected fractures (Figure 657). 

PALEOPATHOLOGY 

References to arthritic change resulting from 

infection of one or more joints are uncommon in 

the literature on paleopathology. Wells (1962b) 

has attributed the degeneration of the left humeral head in a young female skeleton to septic 

arthritis. This case is from an Early Saxon cemetery at Caister-on-Sea, England. Jarcho, Simon, 

and Bick (1963) have described a fused hip from 

a pre-Columbian archeological site at Wupatki 

Pueblo, Arizona, USA. The authors conclude 

that the fusion was the sequela of infection of the 

hip. Brothwell (1965a, pi. 7E) illustrates a pair of 

humeri from a medieval adult skeleton from Scarborough, England. The head of the left humerus 

is abnormal with a flattened, irregular joint surface. Brothwell suggests a septic condition, such 

as osteomyelitis, as the cause for the arthritic 

change. The humerus is unusually short. This 

could be the result of diminished growth due to 

infection during childhood. However, the combination of reduced length and rather robust 

diaphysis also suggests the possibility of a congenital abnormality, such as achondroplasia. 

Moodie (1928) suggested an association between degenerative arthritis and dental disease. 

He based this observation on degenerative arthritis of the right temporomandibular fossa and 

the presence of dental abscess in a female skull 

from an archeological site at Cinco Cerros, Peru. 

The skull (No. 348) is part of the skeletal collection at the San Diego Museum of Man, California, USA. However, it is apparent in Moodie's 

(1928) figure 1 that there is a fracture through 

the temporomandibular fossa with some refill of 

the defect indicating healing. Thus, a more probable diagnosis would be degenerative arthritis 

following trauma. 

Inglemark, M0ller-Christensen, and Brinch 

(1959) report a correlation between arthritic 

change in the spine and the presence of dental 

infection in a cemetery population from Aebelholt Monastery in Northern Zealand, Denmark, 

dating from approximately A.D. 1185 to 1559. 

The authors controlled for one variable, age, 

which would be a major factor in this correlation. 

However, this does not mean that a causal relationship between the two pathological conditions 

can be assumed, because there may be other 

underlying factors to which the pathological conditions may be related. Morse (1969, pi. HE) 

briefly describes an arthritic right hip joint from 

an adult male skeleton. The acetabulum is shallow and enlarged. The head of the femur is 
402 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

FIGURES 658, 659.—Septic arthritis of the knee resulting in fusion of the left femur and tibia: 

658, Medial view; note the periosteal reactive bone on the distal femur. 659, X-ray of 

mediolateral view. (Adult, surface find from Chancay, Peru, NMN H uncataloged.) 

deformed. Two isolated pieces of bone appear to 

be sequestra from the head of the femur. The 

specimen is from the Klunk site in Illinois, USA, 

and is probably pre-Columbian (Hopewell Culture). Morse attributes the arthritic changes to 

infection. 

Clear evidence of septic arthritis is seen in the 

fused left femur and tibia from an isolated surface 

find near Chancay, Peru (Figures 658-661). 

There are no data on cultural association or date. 

The specimen is part of the skeletal collections of 

the National Museum of Natural History, Washington, D.C, USA (NMNH, uncataloged). Although the bones are somewhat short, they are 

robust. Arthritic change is limited to the knee. 

The X-ray film indicates normal cortical bone 

thickness and density indicating that the limb 

was used throughout the life of the individual 

(Figure 659, 661). The knee has fused in the 

extended position with some rotation of the axis 

of the tibia relative to the femoral condyles. Because of this rotation the medial condyle of the 

tibia projects posteriorly. There is extensive periosteal bone reaction on the distal diaphysis and 

metaphysis of the femur. Periosteal reactive bone 

on the tibia is minimal and limited to the bone 

adjacent to the proximal articular surface. There 

is a cloaca in the posterior cortex of the distal 

femur just superior to the lateral condyle (Figure 

660). The X-ray film reveals considerable sclerosis 

in the distal femur. The periosteal reactive bone, 

sclerosis, and cloaca are indicative of infection 

and inflammation, making a diagnosis of septic 

arthritis highly probable. 
NUMBER 28 403 

FIGURES 660, 661.—Septic arthritis ofthe knee resulting in fusion ofthe left femur and tibia: 

660, Posterior view; note the cloaca (arrow) in the femur. 661, X-ray of anteroposterior view. 

(Adult, surface find from Chancay, Peru, NMNH uncataloged.) 

Rheumatoid Arthritis 

PATHOLOGY 

Rheumatoid arthritis is a generalized connective tissue disease of unknown etiology with most 

significant involvement of joints. Genetic factors 

and climatic conditions are thought to be important. Generally, the disease is thought to be more 

common in cold than in hot climates. However, 

a statistical study carried out on the Blackfoot 

Indians of northern Montana and the Pima Indians of southern Arizona confirmed neither of 

these viewpoints (Bunim, Burch, and O'Brien, 

1964). The disease manifests itself in the adult 

and in the juvenile forms. Although the pathology 

in both conditions is essentially the same, the 

areas of involvement are sufficiently different to 

necessitate a separate discussion. In either situation I am here only concerned with the late stages 

exhibiting significant bone changes. 

Adult Rheumatoid Arthritis 

This disease usually commences in the fourth 

and fifth decades and continues through the lifetime of the patient. There is a great predilection 

of females over males with a ratio of about 3:1. 

The disease is not rare. In northern Europe, about 

4 percent of the males and 16 percent of the 

females over 65 years of age showed some presumptive or definite evidence of this disease (Lawrence, Laine, and de Graaff, 1961). 

Rheumatoid arthritis usually involves multiple 

joints and is frequently symmetrical. Joints ofthe 

hands are most frequently, most characteristically, and often first involved. In the hands, the 
404 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

predilected locations are the metacarpophalangeal joints and the proximal interphalangeal 

joints. The second interphalangeal joints are usually spared. The knee is the most frequently 

involved large joint. The temporomandibular 

joint is affected in about 25 percent of the cases 

(Garrod, 1890:250). Other commonly involved 

joints are wrist, carpal joints, shoulder, and elbow. 

Tarsal, tarsometatarsal, metatarsophalangeal 

joints, and toe joints are less often involved than 

the corresponding joints of the hands. The hip 

joint is the least often affected ofthe large joints. 

The joints of the trunk are much less commonly 

involved. If the spine is affected, the changes are 

usually most marked in the diarthrodial joints of 

the cervical spine, including the joint between 

axis and atlas. 

The disease process consists of an inflammatory 

infiltration and proliferation of the synovium, 

which is slowly progressive over many years and 

ultimately destroys and disfigures the joint. The 

process in untreated cases often terminates in 

either loosening of the joint with subluxation or 

ankylosis (Figure 662) with bony continuity. In 

the active phase the joint changes are accompanied by marked osteoporosis in the adjacent 

bones. If joint mobility is maintained, degenerative arthritis is superimposed on the rheumatoid 

lesion. However, in contrast to primary degenerative arthritis, osteoporosis still prevails and marginal lipping is less prominent. 

The bone changes on large joints consist of 

osteoporosis of the articular ends, thinning and 

resorption of the subchondral bone plate, subchondral bone resorption, and lytic foci due to 

subchondral cysts (Figure 663). The contour of 

the articular surface is deformed and irregular. 

Subluxation is most commonly observed on 

metacarpophalangeal joints with axial deviation 

towards the ulnar side. On dry bone, evidence of 

subluxation would consist of extension of the 

convex articular surface on the side of deviation. 

Corresponding unilateral marginal lipping may 

be present on the concave articular facet. 

Ankylosis may fuse carpals and tarsals into 

solid blocks of extremely porotic bone showing 

sparse trabeculae. Carpometacarpal and tarsometatarsal joints may also be found ankylosed. 

FIGURE 662.—Rheumatoid arthritis of hip with cartilaginous 

ankylosis. Notice minimal separation between acetabulum 

and femur and severe osteoporosis, especially of the unburdened portion ofthe femoral head. (73-year-old male, MG H 

autopsy 34283.) 

FIGURE 663.—Rheumatoid arthritis of shoulder. Bisected 

proximal humerus shows large cyst and severe osteoporosis; 

24 years duration, most joints involved. (59-year-old male, 

IPAZ autopsy 303 from 1960.) 
NUMBER 28 405 

The large joints and interphalangeal joints may 

undergo bony ankylosis, usually in flexed position, secondary to contracture and muscular imbalance. 

Excessive bone resorption (mutilating arthritis), probably on a basis of neurovascular disturbance, is occasionally observed. It occurs most 

frequently on hands or feet, resulting in concentric atrophy of metacarpals, metatarsals, and 

phalanages. These extreme cases of bone resorption in themselves may be indistinguishable from 

those seen in leprosy. 

Juvenile Rheumatoid Arthritis (Still's Disease) 

Juvenile rheumatoid arthritis (Still's disease) 

usually begins in early childhood with a second 

peak before puberty. The predilection of the females over males for getting the juvenile form is 

less marked than in the adult form. The pathology is identical with that of the adult form, but 

there are some differences in location and type of 

involvement. The disease often begins in a knee 

or other large joint and occasionally may be 

mono-articular. In contrast to the adult form, the 

cervical spine is involved in about two-thirds of 

the cases (Ansell and Bywaters, 1963). Intervertebral diarthrodial joints and vertebral bodies 

may become fused. The atlantoaxial joint occasionally may become subluxed or fused. 

Although wrists and ankles, carpal and tarsal 

joints are frequently involved, the other joints of 

hands and feet are more often free. If the interphalangeal joints are involved, the distal interphalangeal joints also participate in about 15 

percent ofthe cases (Ansell and Bywaters, 1963). 

In contrast to adult rheumatoid arthritis, the hips 

are frequently diseased and the temporomandibular joint is usually spared. Subluxation of metacarpophalangeal joints is towards the radial side, 

but usually less marked than in the adult form. 

Ankylosis occurs more often in the carpal and 

tarsal joints than in large joints (Figure 664). 

Only the advanced and severe cases will show 

significant bone changes. 

FIGURE 664.—^Juvenile rheumatoid arthritis of lower right 

leg, with ankylosis of ankle, tarsal, and tarsometatarsal joints 

and extreme osteoporosis of disuse. Notice the translucency 

ofthe tibial cortex. Eight years duration, most joints affected. 

(18-year-oId male, PMES 1SUT16(1) from 1838.) 

Psoriatic Arthritis 

In psoriasis, a chronic disease of unknown etiology, arthritis similar to rheumatoid arthritis occurs. The disease involves and sometimes is limited to the distal interphalangeal joints of fingers 

and toes. In this condition osteoporosis is often 

absent, but mutilating arthritis of hands and feet 

is observed (Avila, Pugh, Slocumb, and Winkelmann, 1960). 

PALEOPATHOLOGY 

Because ofthe problems in differentiating rheumatoid arthritis from other types of arthritic con-
406 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

FIGURES 665-667.—Rheumatoid arthritis of the feet: 665, 

Superior view; note the porosity apparent in the tarsal bones. 

666, Detail of the fusion between the tarsal and metatarsal 

bones of the left foot. 667, Detail of the bony fusion of the 

right great toe. (Adult specimen from the medieval cemetery 

at Winchester, England, BMN H XXIII, Burial 2.) 
FIGURES 668, 669.—Probable rheumatoid arthritis: 668, Anterior view ofthe spine with fused ribs. 669, Detail of cervical 

and first two thoracic vertebrae; note the fusion of the first 

rib and the fusion of the seventh cervical and first thoracic 

vertebral bodies (arrows). (Adult male skeleton from Golovnin Bay, Alaska, USA, NMN H 346117.) 

FIGURES 670, 671.—Probable rheumatoid arthritis: 670, Inferior aspect of third (right) and fourth (left) lumbar vertebrae; note the severe arthritic change of the diarthrodial 

joints.671,Detail of rib fusion to thoracic vertebrae. (Adult 

male skeleton from Golovnin Bay, Alaska, USA, NMNH 

346117.) 
408 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

FIGURES 672, 673.—Probable rheumatoid arthritis: 672, Posterior view of spine. 673, Detail of 

joint fusion of ribs and thoracic vertebrae. (Adult male skeleton from Golovnin Bay, Alaska, 

USA, NMN H 346117.) 

ditions in dry bone specimens, there are very few 

case descriptions of this type of arthritis in the 

literature on paleopathology. Indeed the evidence 

for rheumatoid arthritis in antiquity is so limited 

that Short (1974) suggests that this disease did 

not occur until fairly recent times with no convincing evidence before A.D. 1676. 

May (1897) describes a skeleton excavated by 

Sir Flinders Petrie from a tomb at Deshasheb, 

Egypt, dated to the Fifth Dynasty. The skeleton 

is from a male probably 50 to 60 years of age. 

There is considerable arthritic degeneration of 

the spine. The arthritic change affects with decreasing severity the cervical, thoracic, and lumbar vertebrae. The vertebral bodies are flattened, 

but the anterior margins bulge out with irregular 

lip-like projections. The plate published as part 

of May's report shows a deformity of the hands 

and feet compatible with a diagnosis of rheumatoid arthritis. 

Hormell (1940) attributes arthritic changes in 

a skeleton from Lower Egypt, dated about 1300 

B.C., to rheumatoid arthritis. Morse (1969:15, pis. 

6E, 11 A) reports a case of possible rheumatoid 

arthritis from the Dickson Mound in Illinois, 

USA. The skeleton is from an old male whose 

knees were buried in a partly flexed position. 

Although evidence of arthritic change in the skeleton is minimal, Morse argues that the flexed 

knee is the only example of this burial position at 

the site and that this may be evidence of rheumatoid deformity without marked bone changes. 

A possible case of rheumatoid arthritis is found 

in the skeletal material excavated in Cathedral 

Green at Winchester, England (BMNH XXIII, 

Burial 2). This specimen is medieval in date and 
NUMBER 28 409 

FIGURES 674-677.—Probable rheumatoid arthritis: 674, Anterior view of pelvis; note the 

marginal osteophyte development and erosion in the region of the pubic symphysis. 675, 

Erosion and porosity of the distal joint of the femur. 676, Erosion and porosity of the distal 

joint of the second and third, right metacarpal bones. 677, X-ray of first, second, and third 

right metacarpals; note the subchondral joint sclerosis of the distal, second and third metacarpals (arrows). (Adult male skeleton from Golovnin Bay, Alaska, USA, NMN H 346117.) 

consists of most of the bones of both feet. There 

is bilateral ankylosis of most tarsometatarsal 

joints accompanied by marked osteoporosis (Figures 665-666). The porosity associated with the 

joints is indicative of a chronic inflammatory 

condition. The interphalangeal joint of the right 

great toe is fused as well (Figure 667). 

Another possible case of rheumatoid arthritis is 

a male Eskimo skeleton about 34 years of age 

(Figures 668-677) from Golovnin Bay, Alaska, 

USA (NMNH 346117). The specimen consists of 

most of the bones from the postcranial skeleton. 

The skull and mandible were not recovered. The 

archeological age is not known. The articular 

surfaces of the shoulder joints are intact. However, there has been some arthritic lipping and 

marginal erosion and porosity. There is some 

degenerative change on the articular surfaces of 
410 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

FIGURE 678.—X-ray of rheumatoid arthritis ofthe arm in an 

Indian skeleton from Puye, New Mexico, USA; skeleton is 

that of an adult male and is from the historic period. Note 

the flexion contracture of the hand and the lytic, expansive 

nature of the metaphyseal areas of the humerus. (X-ray 

courtesy Dr. Christy Turner,. Arizona State University, G Q 

391.) 

both elbows. This includes some porosity on the 

left side and considerable disruption of the articular surface of the right ulna. Marginal porosity 

is minimal. The radioulnar joint surfaces of the 

wrist exhibit some marginal lipping but are otherwise normal. The carpal bones are missing except 

the right and left capitate, left scaphoid and 

lunate, and the right triquetrum. Joint surfaces 

appear normal, but there is periarticular erosion 

on the left scaphoid. The first, second, third, and 

fifth metacarpals ofthe right hand were recovered 

as was the fifth metacarpal ofthe left hand. Only 

the distal joints of the second and third metacarpals show arthritic change with both having joint 

surface degeneration with porosity and development of marked peripheral osteoarthritis (Figures 

676, 677). The clavicles are normal except for 

erosion of the right acromioclavicular joint surface. The normal complement of vertebrae are 

present, and all exhibit arthritic change of both 

the amphiarthrodial and diarthrodial joints. Arthritis is minimal on the cervicals and very 

marked on the thoracic and lumbar vertebrae 

(Figures 668-673). This pattern is atypical for 

rheumatoid arthritis. Many of the diarthrodial 

joints ofthe vertebrae and between the vertebrae 

and ribs are fused (Figures 669, 671). The vertebral bodies have remained intact although there 

is considerable development of marginal osteophytes and evidence of periosteal reactive bone 

particularly on the anterior surface of the body 

(Figure 670). In some vertebrae, adjacent osteophytes have fused. In those diarthrodial joints 

that can be inspected, there is considerable erosion and degeneration of the joint surface with 

extensive marginal lipping. 

The bones of the pelvis are not fused. The 

sacroiliac joint surface has sparsely distributed 

pores about 1 millimeter in diameter. There is 

periarticular reactive bone, particularly at the 

superior margins of the joint. The pubic symphysis is normal, but there is evidence of some 

erosion and extensive osteophyte development on 

the anterior margin (Figure 674). 

The joint surfaces of the hip show minimal 

arthritic change primarily in the right acetabulum where there is porosity on the anterosuperior 

surface. There is very little marginal lipping. 

Arthritic degeneration of the knee joint surfaces 

is limited to the femur and patella, although all 

joint components exhibit slight marginal lipping. 

The joint surface degeneration on the femur is 

largely restricted to the areas of articulation with 

the patella (Figure 675). Both surfaces show erosion and porosity with isolated areas of hypertrophic bone development. The joints of the ankles and feet are incomplete, but those which are 

present do not exhibit any evidence of articular 

surface degeneration and there is minimal marginal lipping. 

Differential diagnosis of this case involves, in 
NUMBER 28 411 

addition to rheumatoid arthritis, ankylosing 

spondylitis and degenerative arthritis. The fusion 

of the diarthrodial joints of the spine would be 

very unlikely for degenerative arthritis. Differentiation from ankylosing spondylitis is much less 

certain. Favoring a diagnosis of rheumatoid arthritis would be peripheral joint involvement, 

lack of fusion of the sacroiliac joint, and the 

absence of any squaring off of the vertebral bodies. The distribution of arthritic change in the 

spine with minimal arthritis of the cervical vertebrae is more typical of ankylosing spondylitis. 

However, the overall pattern of arthritic change 

favors a diagnosis of rheumatoid arthritis. 

From a Pueblo Indian site dated around A.D. 

1559-1672 Steinbock (1976:305-309) describes a 

skeleton, which has partial ankylosis of the spine 

and many other joints, including some bones of 

the hands and fingers (Figure 678). Steinbock 

attributes this condition to ankylosing spondylitis, and this is certainly a possible diagnosis. 

However, the involvement of peripheral joints, 

including severe flexion contractures ofthe hands, 

is more typical of rheumatoid arthritis. 

Ankylosing Spondylitis 

(Marie-Striimpell's Disease) 

PATHOLOGY 

Ankylosing spondylitis is a progressive inflammatory disease of unknown etiology primarily 

affecting the diarthrodial joints of the spine, the 

costovertebral joints, and the sacroiliac joints. 

The pathologic changes in the active phase are 

practically identical with those of rheumatoid 

arthritis. The question of the relationship of the 

two diseases is still open but does not concern us 

here. The manifestations are sufficiently different 

to justify a separate discussion. 

Ankylosing spondylitis prevailingly involves 

males, in contrast to rheumatoid arthritis. The 

male to female ratio is about 9:1. The disease 

usually begins in the second or third decade of 

life. In about half of the cases other joints, particularly hips or shoulders, are affected (Policy and 

Slocumb, 1947). Involvement of peripheral joints, 

if present, is indistinguishable from rheumatoid 

arthritis anatomically. The disease usually begins 

in the lumbar spine and in the sacroiliac joints 

and progressively ascends until the entire spine 

and all costovertebral joints are affected (Figure 

679). 

The disease develops as an inflammatory arthritis of the diarthrodial joints of the spine, 

which leads to early bony ankylosis, either limited 

to the periphery of the joints or across the entire 

facet. In the same type of process, the joints 

between the necks of the ribs and the transverse 

processes and those between the heads of the ribs 

and the vertebral bodies become ankylosed. In 

addition, the peripheral portion of the annulus 

fibrosus becomes ossified, bridging the inner portions of the intervertebral discs, which at first are 

not affected, but later bony replacement of the 

nucleus pulposus does occur. The vertebral bodies 

lose their concave flare on the outer circumference, resulting in the so-called squaring of their 

contour in lateral view. This process of fusion of 

the spinal segments is accompanied by pronounced osteoporosis ofthe vertebral bodies (Figure 680). The result of this ankylosing process is 

the rigid, so-called bamboo spine with loss of its 

physiological curvatures. In late stages, also, the 

various ligaments attached to the spine ossify. 

The changes at the sacroiliac joints are usually 

bilateral and are never absent if the lumbar spine 

is involved. They commence with irregular erosion of the articular surfaces accompanied by 

sclerotic condensation of the subchondral bone 

on both the sacral and the iliac sides of the joint. 

This process ultimately establishes trabecular 

continuity between ilium and sacrum and completely effaces the joint. After establishment of 

complete ankylosis the subchondral sclerosis disappears (Schinz, Baensch, Friedl, and Uehlinger, 

1951-1952(2): 1514). Erosive changes also occur 

on the symphysial facet ofthe pubis, but ankylosis 

of the symphysis pubis is uncommon. If peripheral joints are involved in this disease, early bony 

ankylosis without marked bone destruction commonly occurs (Rutishauser and Jacqueline, 1959: 

10-11). The atlantoaxial, the atlantooccipital, 

and occasionally the temporomandibular joint 

can also be ankylosed. 
412 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

FIGURES 679, 680.—Ankylosing spondylitis: 679, Frontal view, showing smooth ankylosis of left 

sacroiliac joint and "bamboo spine.'' 680, Cut surface, showing ankylosis ofth e diarthrodial 

joints, ossification of interspinal ligaments and the anulus fibrosus, and severe osteoporosis of 

vertebral bodies. (67-year-old male, IPAZ autopsy 572 from 1963.) 

PALEOPATHOLOGY 

Ruffer and Rietti (1912) and Ruffer (1918b) 

describe a case of "spondylitis deformans" in an 

adult male from the Third Dynasty in Egypt. In 

this case the vertebrae are fused from the fourth 

cervical through the coccyx. Both the anterior 

and posterior longitudinal figments were ossified. 

Wood-Jones (1910b: 278) reports many cases of 

fusion of several vertebrae in ancient Nubian 

skeletons. Elliot-Smith (in Wood-Jones, 1908a:59) 

comments on an adult male from Nubia that 

showed complete bony ankylosis of the entire 

vertebral column. Pales (1930:117, pi. 24: figs. 1, 

2) describes from the Neolithic period two isolated, fused thoracic vertebrae, which he feels 

were due to ankylosing spondylitis. Shore (1936) 

reviews several specimens from the pre-Dynastic 

site of Hierakonpolis, Egypt. All the specimens 

had at least partial ankylosis of the vertebral 

column. He attributes the abnormality to infection. Bourke (1967:357-360) describes three possible cases of ankylosing spondylitis from Egypt. 

Two of these are from the cemetery at Hou. One 

specimen from the B cemetery included the second cervical through the lumbar vertebrae. The 

diarthrodial joints and the spinal ligaments were 

ossified with smoothing of the anterior vertebral 

bodies. The second specimen is from cemetery Y 

and dated to the Twelfth Dynasty. It consists of 

six fused thoracic vertebrae. Ossification had occurred in the diarthrodial joints as well as spinal 

ligaments. The third case included all lumbar 

vertebrae and is from the cemetery at Nagada 
NUMBER 28 413 

FIGURES 681, 682.—Ankylosing spondylitis of spine: 681, Anterior view of spine. 682, X-ray of 

anteroposterior view of fused vertebrae and ribs. (Adult male skeleton from Kuskokwim River, 

Alaska, USA, NMN H 351296.) 

but currently stored at the British Museum (Natural History). Both the diarthrodial joints and 

amphiarthrodial joints were fused. Kidd (1954) 

reports the presence of ankylosing spondylitis in 

two skeletons from a post-Columbian, Huron 

cemetery in Ontario, Canada. Morse (1969, pi. 2 

B, C) briefly describes two possible cases of ankylosing spondylitis from archeological sites in 

Illinois, USA. Bass, Gregg, and Provost (1974) 

report one case of ankylosing spondylitis in 2600 

skeletons of Plains Indians from North and South 

Dakota, USA. Steinbock (1976:304-309) attributed the fusion of the spine in a Zuni skeleton 

from New Mexico, USA (NMNH 239208) to 

ankylosing spondylitis. 

A probable example of ankylosing spondylitis 

is seen in the postcranial skeleton of an adult 

male Eskimo from Alaska, USA (NMNH 

351296). On the skull there is some arthritic 

degeneration of the occipital condyles with marginal lipping and porosity of the left surface. The 

temporomandibular joints are normal. The sixth 

cervical vertebra is missing. The diarthrodial 

joints of the second and third cervical are fused. 

There is some erosive degeneration of the atlantooccipital joint surface and some marginal lipping of all the cervical diarthrodial joint surfaces, 

but this is minimal. The first thoracic vertebra 

(TI) is unfused. T2 through T4 are fused and 

may have been fused to T5 although postmortem 

damage makes this uncertain. T5 through the 

fourth lumbar vertebrae were fused during life. 

Interlocking osteophytes between L4 and L5 

would have limited the movement of L5. The 
683 

k'JI^^^^^^I 

s^ipv 

^ 4 /-^ 

^^H^ 

^^^1 

^^^H 

684 ^ HJ^HJHl^^'' '^H^^ifllil 

^ : V ~' ^ 

l^^ t ^^ 

•i^}!^^VB 

FIGURES 683, 684.—Ankylosing spondylitis of spine: 683, Posterior view of spine. 684, Detail of 

diarthrodial joint fusion of thoracic vertebrae and ribs. (Adult male skeleton from Kuskokwim 

River, Alaska, USA, NMN H 351296.) 

FIGURES 685, 686.—Ankylosing spondylitis of spine and pelvis: 685, Right lateral view of spine; note smooth anterior 

surface of fused vertebral bodies. 686, Anterior view of pelvis; 

note the fusion and osteophyte development ofthe sacroiliac 

joint. (Adult male skeleton from Kuskokwim River, Alaska, 

USA, NMN H 351296.) 
NUMBER 28 415 

FIGURES 687, 688.—Anklylosing spondylitis of spine: 687, Detail of rib and vertebral body 

fusion; note smooth anterior surface of vertebral bodies. 688, X-ray of lateral view of fused 

vertebrae; note the "squaring off" ofthe vertebral bodies. (Adult male skeleton from Kuskokwim 

River, Alaska, USA, NMNH 351296.) 

fifth through twelfth ribs appear to have been 

fused to the vertebrae during life, although postmortem damage makes this uncertain in some 

vertebral joints. Generally the diarthrodial and 

amphiarthrodial joints were fused (Figures 681-

684). There has been remodeling ofthe thoracic 

vertebral bodies producing the square profile 

characteristic of ankylosing spondylitis (Figures 

685, 687, 688). The sacroiliac joints are fused 

across the joint surfaces (Figure 686); there is also 

marginal lipping which, on the left anterosuperior 

margin, has fused. In this specimen the characteristics ofthe fusion ofthe pelvis, spinal column, 

and ribs and the lack of peripheral joint involvement make the diagnosis of ankylosing spondylitis 

highly probable. 

Metabolic Arthritis 

PATHOLOGY 

Gouty Arthritis 

Gout is a disease due to a disturbance of the 

purine metabolism characterized by accumulation of its end product—sodium urate—in the 

body. Gout seldom manifests itself before 40 years 

of age and shows such a strong sex predilection 

that 9 out of 10 patients are male. Gout is rare in 

African Negroes, which may be due to a dietary 

rather than racial difference (Shepherd-Wilson 

and Gelfand, 1962). Of the many manifestations 

of this disease, I am here only concerned with 
416 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

FIGURE 689.—Gout. X-ray of right foot showing severe involvement ofthe first metatarsophalangeal and interphalangeal joint. The scooped-out subperiosteal defects on both 

sides of the joint are characteristic. (Studied by Putschar; no 

data.) 

FIGURE 690.—Gout. Longitudinal cut of first toe, showing 

para-articular deposits of urates (white) extending into meta 

tarsal and phalanges. (83-year-old male, MGH autopsy 

33972 from 1970.) 

chronic gouty arthritis in its advanced stages, 

mostly affecting old individuals. 

In the course of chronic gout, sodium urate 

crystals are deposited in various tissues, particularly cartilage, para-articular connective tissues, 

and bone marrow. These gross deposits elicit an 

inflammatory foreign body reaction, resulting in 

the formation of circumscribed nodules filled with 

the crystals (tophi). The crystal deposition in the 

cartilage leads to early degeneration and ushers 

in secondary degenerative arthritis. Gouty arthritis affects mostly joints of the extremities rather 

than those of the trunk. The most common location is the metatarsophalangeal joint ofthe great 

toe. Generally, small joints are more often involved than big ones and the lower extremities 

more often than the upper. With the loss of soft 

tissue, the crystal deposits are also lost so that 

only bone changes of advanced gouty arthritis in 

typical skeletal locations could suggest the diagnosis in dry bone material. The most characteristic change is the pressure erosion due to paraarticular tophi on metatarsophalangeal, metacarpophalangeal, and interphalangeal joints of toes 

and fingers. These scooped-out defects are located 

near the margin ofthe articular surface and often 

involve both bones forming the joint (Figure 689). 

They bulge into the bone but usually remain 

separated from the marrow cavity by a thin layer 

of bone (Figure 690). Intraosseous tophi may 

manifest as lytic lesions, expanding the small 

bones of hands and feet. These lesions are usually 

multiple and may simulate, in dry bone, the 

findings of enchondromatosis, predilecting the 

same skeletal areas. The main difference would 

be that, over large intraosseous tophi, the subchondral plate would be at least partly destroyed, 

while over an enchondroma it would be intact. 

Ochronosis (Alkaptonuria) 

Ochronosis is due to an inborn gene defect 

resulting in absence or deficiency of the enzyme 

homogentisic acid oxidase. Homogentisic acid is 

an intermediate product in the metabolism ofthe 

amino acids phenylalanine and tyrosine. In members of affected families homogentisic acid, form-
NUMBER 28 417 

FIGURE 691.—Ochronosis of vertebral column. The affected 

intervertebral discs are narrowed and discolored black. 

There is marked osteosclerosis and bony bridging of some 

segments. (MGH autopsy 29047 from 1965.) 

ing a black melanin-like pigment, accumulates in 

various tissues ofthe body, especially in cartilage. 

The lifelong accumulation of homogentisic acid 

damages the cartilage of the intervertebral discs 

and of the diarthrodial joints. The cartilage becomes brittle and undergoes mechanical attrition 

and degeneration. In the spine, the intervertebral 

disc spaces are narrowed and peripheral osteophytic bridging is common (Figure 691). Not 

unusually, ossification of the nucleus pulposus 

with bony union of the two adjacent vertebrae 

occurs. Complete ankylosis across the destroyed 

intervertebral disc is sometimes also seen. In the 

affected cases, all intervertebral discs are involved, resulting, finally, in a straight or kyphotic 

rigid spine, as in the late phase of ankylosing 

spondylitis. The radiologic finding of focally increased density is mainly due to ossification. In 

the large diarthrodial joints (knee, hip, and shoulder) ochronosis leads to earlier and more severe 

degenerative arthritis. On dry skeletal material, 

the diagnosis of ochronosis could only be suspected. The main reason for discussing this entity 

here is that purported cases of ochronosis have 

been observed in Egyptian mummies where cartilage tissue was, at least in part, preserved. 

Hemophilic Arthropathy 

Hemophilia is a heritable sex-linked disorder 

of the blood-clotting mechanism, which is transmitted as a recessive Mendelian trait and manifests itself only in males. Until recently, in the 

great majority of cases, repeated intra-articular 

hemorrhages, precipitated by minor trauma, led 

ultimately to severe joint disease. Although intraarticular hemorrhages begin in childhood, demonstrable bone changes do not develop until 

adolescence or adult life and increase with the 

age of the individual. 

Thomas (1936) reported that in a series of 98 

hemophiliac males 61 percent showed permanent 

joint deformity. The most commonly affected 

joint was the knee (68 percent) followed by the 

ankle (56 percent), elbow (53 percent) and hip 

(16 percent), with less frequency of other and 

especially of small joints. The changes often involve more than one joint and, especially in the 

knee, may be bilateral. 

Repeated articular hematomas and their subsequent resorption and organization lead to 

marked synovial proliferation and hemosiderotic 

fibrosis and to damage of the cartilage. The underlying bone is particularly eroded at the margins of the articular cartilage by undermining 

ingrowth of fibrous tissue. In this manner erosion 

and widening of the intercondylar notch of the 

distal femur occurs, which is fairly characteristic 

for this condition (Schinz, Baensch, Friedl and 

Uehlinger 1951-1952(2): 1427). In the elbow, the 

trochlea ofthe ulna is first and often most severely 

affected. In advanced cases extensive destruction 

of subchondral bone with alternating porotic and 

sclerotic areas ensues. Multiple and large sub-
418 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

chondral cysts are often present, especially in the 

distal femur and proximal tibia. Femoral condyles and corresponding portions of the tibial 

plateau can be extensively destroyed. Large pressure erosions through the cortex can occur near 

the capsular attachment. Severe grooving and 

eburnation of secondary osteoarthritis is often 

absent due to limited motion in the severely 

altered joint. For the same reason the irregularities in the level of the joint surface are more 

marked than in ordinary degenerative arthritis. 

In some cases limited mobility leads to bony 

ankylosis, especially between patella and femur 

and between femur and tibia. Early changes may 

be indistinguishable from tuberculous arthritis in 

dry bone because of the undermining marginal 

erosion common to both. 

Hemophilic Pseudotumor 

In some cases of hemophilia, massive subperiosteal or medullary hemorrhages occur. These 

subperiosteal or intraosseous hematomas may create large pressure defects and reactive bony shells 

simulating neoplasm. Such pseudotumors may be 

found on the diaphysis or near the joint. Pathological fractures through such lesions do occur 

(Ghormley and Clegg, 1948). Medullary hematomas may also result in formation of large 

metaphysial and diaphysial cysts (Stiris, 1958). 

PALEOPATHOLOGY 

Gouty Arthritis 

A possible case of gout has been reported by 

Elliot-Smith and Dawson (1924:157-158) in an 

old male mummy from a Christian cemetery near 

the temple of Philae, Egypt. Many of the joints 

of the extremities have white concretions. The 

most noticeable of these is seen on the metatarsal 

bones of the great toe. One of these concretions 

measured 23 by 10 by 5 millimeters. The upper 

extremity was less affected than the lower. Analysis ofthe concretion produced a reaction typical 

of uric acid. Rowling (1961:414) has reconfirmed 

this analysis. 

More recently Wells (1973) has described a 

male skeleton from a Roman cemetery (A.D. 150) 

at Gloucester, England. There were lytic lesions 

in the bone adjacent to the joints of the ankles 

and feet, suggestive of the type of bone reaction 

that could occur in long-standing chronic gout. 

Ochronosis (Alkaptonuria) 

Simon and Zorab (1961) examined one young 

female Egyptian mummy from the Roman Period before 30 B.C. The X-ray films ofthe mummy 

show radiodensities ofthe intervertebral discs and 

end-plate cartilage between all vertebrae. Corresponding X-ray films of other mummies did not 

show this feature. On the basis of similar radiologic findings in known cases of ochronosis, the 

authors suggest that the mummy may have had 

ochronosis during life. 

Wells and Maxwell (1962) describe a possible 

case of ochronosis in another female Egyptian 

mummy. This specimen is dated to the Twentysixth Dynasty and exhibits dense shadows in the 

region of the lumbar discs with narrow, translucent zones adjacent to the dense zones. These 

roentgen features are seen in modern clinical cases 

of ochronosis, and the authors conclude that this 

disease was present in the mummy specimen. 

They also prepared histological sections of affected tissue but found no satisfactory microscopic support for their conclusion. 

The major unresolved problem in these reports 

is that shrinkage of cartilage occurs during desiccation of the mummy, and as -cartilage discs 

shrink they become more radiodense. The variation in radiodensity between mummies reported 

by Simon and Zorab (1961) may reflect different 

conditions of desiccation and preservation. 

Stenn, Milgram, Lee, Weigand, and Veis 

(1977) report another possible case of ochronosis 

in Egyptian mummy material. The radiologic 

appearance of the spine suggests mineralization 

of the intervertebral discs. Furthermore, samples 

ofthe discs had zones of black pigment suggestive 

of local concentrations of homogentisic acid. 

Chemical analysis of this dark substance supports 

this suggestion. 
NUMBER 28 419 

Cartilage in naturally desiccated human mummies is typically very dark or black. This indicates 

that chemical changes in cartilage through time 

naturally produce dark-pigmented substances. 

Whether such cartilage would produce an analytical pattern similar to cartilage containing 

homogentisic acid has not been demonstrated. 

Until this type of experiment has been conducted 

and the effect of other variables on mummy tissue 

considered, it would appear prudent to defer final 

judgment on the presence of ochronosis in antiquity. 

Degenerative Arthritis 

PATHOLOGY 

Degenerative arthritis is the most common of 

all articular diseases. As the term "degenerative" 

indicates, it is not an inflammatory disease but 

develops on the basis of aging changes and degeneration of articular cartilage. There is no 

sharp borderline between aging phenomena and 

incipient degenerative arthritis. The condition is 

slowly progressive, and demonstrable bone 

changes are preceded by many years of alterations 

ofthe articular cartilage alone. In addition to this 

primary degenerative arthritis, intimately associated with aging and physiological wear and tear, 

secondary degenerative arthritis develops early in 

structurally or functionally abnormal joints. 

Thus, degenerative arthritis becomes, in part, the 

end-stage of various inflammatory, traumatic, 

metabolic, and congenital or acquired joint diseases, provided that joint function continues under altered conditions for a long time. 

The Appendicular Skeleton 

The joint earliest and ultimately most often 

involved is the knee, followed in decreasing order 

of frequency by the first metatarsophalangeal 

joint, the hip, the shoulder, the elbow, the acromioclavicular joint, and the sternoclavicular 

joint. These statistical data, presented in Table 

12, are taken from a study of Heine (1926), in 

which the above-listed joints were examined in 

1000 autopsies of individuals above the age of 15 

years. This does not mean that other joints not 

accessible at autopsy or not included in this study 

do not also considerably contribute to the total 

picture of degenerative arthritis. Heine's data 

indicate that a significant degree of degenerative 

arthritis, which may be accompanied by bone 

changes, does not appear before the fourth decade 

and increases with age after that time. Since, for 

our purpose here, only the advanced lesions showing significant bone changes are of interest, the 

life span of an archeological population will 

greatly influence the recognition and frequency 

of this condition in skeletal material. 

TABLE 12.—Incidence of moderate to severe degenerative 

arthritis, stated in percentage of incidence (sample: 1000 

autopsies of individuals above 15 years of age; modified after 

Heine, 1926) 

Age by 

decade 

4th 

5th 

6th 

7th 

8th 

9th 

Knee 

1.0 

0.8 

2.6 

12.0 

33.3 

39.4 

Great 

toe 

0 

0 

7.9 

13.7 

18.2 

24.6 

Hip 

0 

0.8 

0.7 

2.7 

12.2 

16.7 

Shoulder 

0 

0 

0.7 

2.6 

9.7 

15.7 

Elbow 

0 

0 

1.3 

5.2 

10.5 

15.5 

Acromioclavicular 

0 

0.8 

1.3 

9.6 

12.3 

11.4 

Sternoclavicular 

0 

0 

0 

1.1 

1.5 

7.0 

In the knee joint, the articular changes begin 

in the patellar cartilage followed by lesions on the 

patellar facet of the femur, then on the tibial 

condyles not protected by the menisci, on the 

anterior portion ofthe medial condyle and, lastly, 

on the anterior portion of the lateral condyle of 

the femur. The posterior portions of the condyles 

are usually spared (Bennett, Waine, and Bauer, 

1942). This pattern follows the locations of maximal pressure and friction, stressing the mechanical factors in the causation of degenerative arthritis. 

Significant bone changes usually develop many 

years after the initiation of degenerative and 

proliferative cartilage changes. These usually begin at the margin of the articular cartilage and 

manifest themselves as marginal lipping and ex-
420 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

ostoses. It is realized that marginal lipping can 

represent a feature of joint remodeling without 

degenerative cartilage changes. However, for our 

purpose in the study of dry bone, it has to be 

included in the manifestations of degenerative 

joint disease. Admittedly there is no sharp line of 

separation between aging changes and degenerative joint disease, but severe and irregular marginal lipping definitely represents a manifestation 

of the latter. 

Focal or complete attrition of articular cartilage leads to a sclerotic osteoblastic response in 

the subchondral bone and to mechanical attrition 

and polishing of the exposed bony articular surface (eburnation). These polished areas are absolutely diagnostic of severe degenerative arthritis. Within and around eburnated areas smaller 

and larger pits occur on the joint surface leading 

into subchondral bone. In part, such defects connect with smaller and larger cystic spaces, which 

may be sizeable in the articulating bone ends. In 

ball and socket joints, such as the hip and shoulder, these processes lead to enlargement, altered 

curvature, and deformation, especially ofthe convex joint surface. The eburnation in these joints 

has a smoothly polished appearance resembling 

porcelain. In joints with a hinge-like action, such 

as the knee and elbow, eburnated areas may 

exhibit deep parallel grooves. In joints with little 

mobility, such as the diarthrodial joints of the 

spine, eburnation may be minimal or absent, 

while marginal lipping dominates the picture. 

In addition to changes on and around the 

articular surface, subsynovial osteophytes, as on 

the neck of the femur or humerus, and osteophytes at the insertion of capsule and ligaments 

occur in advanced cases. Regardless of the severity of changes, ankylosis does not occur in degenerative arthritis. A brief discussion of the local 

pecularities of degenerative arthritis in different 

joints follows. 

HIP.—The most severe changes are found on 

the femoral head. Eburnation and erosion are 

most marked on the upper surface. Marginal 

exostoses may completely overhang the femoral 

neck (mushroom deformity). Osteophytes occur 

on the intracapsular portion of the neck. Large 

lytic cavities are not uncommon in the head. 

Acetabular changes mostly consist of marginal 

lipping and deepening, leading occasionally to 

protrusion into the pelvis. The acetabular roof is 

often sclerosed and may also contain cystic cavities. Degenerative arthritis of the hip often is 

preceded by other disease processes in this joint, 

particularly Perthes' disease and slipped epiphysis. 

SHOULDER.—The changes are similar to those 

in the hip but usually less severe because of lack 

of weight-bearing. 

KNEE.—The dominant feature is marginal lipping, often most pronounced on the patella. Eburnation is usually less extensive than in the hip. 

Exaggerated medial condylar lipping is seen in 

genu varum deformity and on the lateral condyle 

in genu valgum. The tibial surface is usually less 

affected because of the protective effect of the 

menisci. 

ELBOW.—Eburnation occurs on all joint surfaces. Excavation is observed on the trochlea of 

the ulna. The radial head shows more overhanging lipping. 

BIG TOE.—Th e frequent severe involvement of 

the first metatarsophalangeal joint in Heine's 

(1926) series may, in part, reflect the effect of 

heeled shoes, particularly in women. However, 

even in a barefoot population the pressure transmission through the first metatarsal is great, resulting in eburnation and sclerosis, especially of 

the metatarsal head. Lateral deviation of the big 

toe (hallux valgus) leads to formation of a new 

joint facet of the lateral slope of the metatarsal 

head. 

FINGERS.—Degenerative arthritis usually involves the distal interphalangeal joints, characterized by marked marginal osteophytes (Heberden's nodes). This condition is usually multiarticular and bilateral. It is much more common in 

females than in males. 

Spondylitis Deformans (Spinal Osteophytosis) 

Degenerative changes leading to bony spur 

formations in the vicinity of intervertebral discs 

are exceedingly common in skeletal material past 
NUMBER 28 421 

middle age. Although these changes around synchondroses are not arthritic in the strict sense, 

they represent an equivalent to the changes on 

the diarthrodial joints and are best discussed in 

this connection. In the study of Schmorl and 

Junghanns (1971:186-187) on more than 4000 

autopsied spines, some degree of spinal osteophytosis was present in 60 percent of females and 80 

percent of males at the end of the fifth decade, 

increasing to almost 100 percent in the ninth 

decade. Any segment ofthe spine may be affected 

and the lesions usually involve several or many 

vertebrae. Minimal lesions begin to appear as 

early as the third decade. 

The lesion typically consists of shelf-like bony 

protrusions on the cortex of the vertebral body. 

Arising at the junction ofthe body and the fused 

marginal epiphysis, the lesion points toward the 

adjacent intervertebral space. The pathogenesis 

of this lesion is not entirely clear. Schmorl (in 

Schmorl and Junghans, 1971:188-189) thinks 

that disruption of annulus fibrosus bundles inserting on the marginal epiphysis, followed by 

protrusion of disc material, are the causative factors. We need not concern ourselves here with the 

various other theories. Suffice it to say that degeneration of the intervertebral disc is not necessarily a precursor of osteophytic formation. These 

shelf-like osteophytes of two adjacent vertebrae 

approach each other and pinch off a peripheral 

portion of annulus fibrosus. Complete fusion of 

the osteophytes is not uncommon. On dry bone 

it becomes obvious that the shelf of newly formed 

bone is buttressed by ossification within the anterior spinal ligament and extends over the entire 

height of the vertebral body in severe cases (Figure 692). These osteophytes are quite characteristic and easily recognized on skeletal material. If 

the fusion of osteophytes is complete and of long 

standing, remodeling may give these bony bridges 

a smooth surface, resembling the changes observed in ankylosing spondylitis. However, the 

diarthrodial vertebral joints and the costovertebral joints are not fused in spondylitis deformans. 

Degenerative and traumatic changes of the 

intervertebral disc may lead to herniation of disc 

cartilage through the annulus fibrosus anteriorly. 

FIGURE 692.—Deforming spondylitis with massive bony 

bridges across intervertebral discs. (71-year-old male, IPAZ 

autopsy 1485 from 1957.) 

laterally, or posteriorly or through the vertebral 

end-plate into the subchondral spaces of the vertebral body. Of these the latter are the most 

common and are the only ones that can be identified on dry bone. 

Such extruded disc cartilage can proliferate to 

a limited extent, forming round or lobulated 

nodules up to one centimeter in diameter. Such 

disc protrusions are present in the great majority 

of spines of individuals past 40 years of age and 

increase in size and frequency with age. They do 

not occur in children and adolescents. These cartilage nodules are more frequently seen in the 

lower thoracic and lumbar vertebrae and occur 

most often in the center of the end-plate where 

the closure of the notochord canal leaves a weak 

spot (Schmorl, 1927; Putschar, 1927a, 1927b). In 
422 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

dry bone they appear as round or oval defects in 

the bony end-plate bordered by a basket-like 

arrangement of reactive bone within the vertebral 

body. Corresponding lesions in two adjacent vertebrae bordering the same disc are common. 

PA LEOPATHO LOGY 

The expression of degenerative arthritis in archeological material affects both joint surfaces 

and the articular margins of bone. Degenerative 

arthritis of joint surfaces may result in bone destruction and/or bony hypertrophy. Arthritic destruction is expressed as porosity, often with eburnation (polishing) of the disturbed bone surface. 

Arthritic hypertrophy is less common and is seen 

as an irregular thickening of the joint surface, 

which may be somewhat porous. Marginal degenerative arthritis is also expressed as a destructive 

and/or hypertrophic process although the latter, 

in contrast with joint-surface degenerative arthritis, is more common. In diarthrodial joints, hypertrophic, marginal, degenerative arthritis is 

usually seen as a fairly smooth extension of the 

joint surface. In amphiarthrodial joints of the 

vertebral bodies, hypertrophic arthritic change 

gives rise to osteophytes or finger-like projections 

from the bony periphery of the joint. 

While several factors may contribute to the 

development of degenerative arthritis, stress undoubtedly is the most significant of these factors. 

Thus, as Ortner (1968:146) suggested, the distribution and severity of degenerative arthritis in 

the skeleton are likely to vary between societies 

and with different roles (e.g., male-female) within 

a society. Hrdlicka's data (1914:62-69) indicates 

that the elbow joint was the most frequent site 

for degenerative arthritis in ancient Peruvian 

skeletal remains. The knee was next in severity 

(Table 13). This finding differs from modern 

populations where the knee is most frequently 

affected. 

In a study comparing modern American 

Whites, Blacks, pre-Columbian Indians from 

New Mexico, and protohistoric Eskimos, Jurmain 

(1977) found the Eskimos to be most severely 

TABLE 13.—Frequency of degenerative arthritis in major 

long bones of adult archeological skeletons from the Chicama 

Valley, Peru (from Hrdlicka, 1914:62-69) 

Bones 

Humeri 

Proximal 

Distal 

Ulnae 

Proximal 

Distal 

Radii 

Proximal 

Distal 

Femora 

Proximal 

Distal 

Tibiae 

Proximal 

Distal 

Fibulae 

Proximal 

Distal 

No. examined 

593 

301 

255 

1210 

781 

266 

No. arthritic 

1 

12 

16 

0 

6 

1 

16 

36 

12 

0 

1 

2 

% of total 

0.2 

2.0 

5.3 

0 

2.4 

0.4 

1.3 

3.0 

1.5 

0 

0.4 

0.8 

affected by degenerative arthritis. He concludes 

that their vigorous life style is the major causative 

factor in this difference. In an earlier study, Stewart (1947) found differences in the degree and 

location of vertebral degenerative arthritis between Eskimo, Pueblo Indian, and modern White 

skeletons. He suggested that cultural differences 

were important, but he also noted that racial 

variation in the structure ofthe vertebral column 

may affect patterns of movement ofthe vertebrae 

and thus affect the expression of spinal degenerative arthritis. 

Although stress is a major factor in degenerative arthritis, it is likely that different types of 

stress will affect the development of arthritis in 

different ways. It is here that the paleopathologist 

with access to the entire skeleton and joint surfaces, could contribute to the understanding of 

degenerative arthritis. For example, what is the 

effect of relatively continuous but moderate stress 

on a joint, as contrasted with intermittant but 

high stress? In such a problem comparisons of 

degenerative arthritis in joints of the left and 

right side and male versus female joints or skele-
FIGURES 693, 694.—Degenerative arthritis of the shoulder 

and hip: 693, Lateral view of the left scapula showing 

porosity of the glenoid cavity. 694, Porous degeneration of 

the right hip joint. (Adult female Eskimo skeleton from 

Hooper Bay, Alaska, USA, NMNH 339115.) 

tons from different cultures where characteristics 

of body use are known or can be inferred might 

be used to clarify this and other problems. 

Perhaps the biggest problem in the study of 

degenerative arthritis is the methodology for 

qualifying and, ideally, quantifying the observations. The degenerative conditions of bone destruction and hypertrophy need to be described 

in terms of location in the skeleton and in the 

joint and also with respect to the extent of involvement (Jurmain, 1975, 1977). In this context 

an important methodological consideration is the 

percentage of the total joint surface area affected 

by degenerative change. 

The Appendicular Skeleton 

Severe degenerative arthritis is seen in both the 

shoulder and hip joints (Figures 693, 694); however, its occurrence in the shoulder joint is uncommon in archeological skeletons. An example of 

what, in my experience, is moderate degenerative 

change is seen in the scapulae of an adult female 

Eskimo from Hooper Bay, Alaska, USA (NMNH 

339115). The right scapula has a small area of 

porosity on the posterior margin of the glenoid 

fossa with a slight amount of marginal lipping. 

r.ti.UimMitii'. 

gairvfi£i!lj^< 

FIGURES 695, 696.—Subchondral bone in a section through the capitulum: 695, Normal joint 

surface and subchondral trabeculae. 696, Sclerosis of trabeculae underlying porous degenerative 

change of the capitular joint surface. (NMNH, unidentified humeri from the Huntington 

collection.) 
424 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

The left scapula has considerable porosity on the 

anteroinferior surface of the glenoid fossa with a 

small area of porosity on the posterior margin 

(Figure 693). Marginal lipping is minimal. 

In archeological skeletal remains the elbow is 

a common site of degenerative arthritis. Ortner 

(1968) discussed the anatomical and functional 

aspects of arthritic change in the elbow. Briefly, 

of the three related but distinct changes that 

occur, the first is a degenerative change of the 

joint surface, which is most common between the 

head of the radius and the capitulum. This is 

probably related to the fact that both flexionextension and rotation are movements associated 

FIGURES 697-700.—Degenerative arthritis of the elbow and wrist: 697, Anterior view of the 

distal humerus; note the porosity of the capitular surface and the bone hypertrophy of the 

capitular and trochlear fossae. 698, Marginal lipping adjacent to the trochlear joint surface. 

699, Hypertrophic bone filling in the olecranon fossa. 700, Degenerative arthritis of the distal 

joints of the radius and ulna. (Adult male Eskimo skeleton from Golovnin Bay, Alaska, USA, 

NMN H 279209.) 
NUMBER 28 425 

with this joint surface. Porous degeneration ofthe 

joint stimulates sclerosis of subchondral trabeculae (Figures 695, 696). Second, there is marginal 

Upping primarily adjacent to the trochlear joint 

surface. Third, there is bony fill-in of the three 

fossae of the humeral component of the elbow. 

An adult male Eskimo from a site on Golovnin 

Bay, Alaska, USA (NMNH 279209) exhibits the 

major features associated with degenerative arthritis ofthe humerus. Nearly the entire capitular 

joint surface is porous with slight traces of eburnation (Figure 697). Marginal lipping is most 

pronounced on the margins of the trochlear surface (Figure 698). There is considerable fill-in of 

both the capitular and trochlear fossae (Figure 

697). This condition is more severe on the right 

side. Similarly the olecranon fossa has a large bar 

of hypertrophic bone filling in most of the depression (Figure 699). The hypertrophic bone in 

the fossae would have limited the amount of 

flexion and extension of the elbow. 

The distal joint of the radius and ulna of the 

same specimen also shows marked degenerative 

arthritis (Figure 700). The joint between the ulna 

and radius exhibits marked marginal lipping as 

does the joint surface ofthe wrist. There is coarse 

porous degeneration, particularly on the ulnar 

surface, with some evidence of eburnation. It is 

possible that fracture may have stimulated some 

of the arthritic degeneration in the wrist. The 

bones of the hands are often lost in archeological 

skeletons. However, a common site for arthritic 

change in Eskimo skeletal specimens is the joint 

between the trapezium and the first metacarpal 

bone. 

Arthritic degeneration of the hip is a fairly 

common condition in archeological specimens. 

Wells (1963a) and Pitt-Rivers (1965) are among 

many who have described typical cases. An example of moderate arthritic change is seen in the 

Eskimo skeleton also discussed below in the context of spinal degenerative arthritis (NMNH 

339115). The right hip joint of this specimen 

exhibits marked porosity on the superior joint 

surface ofthe acetabulum with a trace of porosity 

on the peripheral margin of the remaining joint 

FIGURE 701.—Severe degenerative arthritis of the left hip. 

Note the abnormal contour of the femoral head. (HMCS 

GR 1248.) 

FIGURE 702.—Marginal lipping, porosity, and eburnation of 

the proximal joint of a right tibia. (Specimen from an 

archeological site in Paragonah, Utah, USA, NMNH 

292012.) 
426 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

FIGURES 703-705.—Degenerative arthritis of the spine and 

knee: 703, Anterior view of fused tenth thoracic through 

fifth lumbar vertebrae. Note the extreme development of 

hypertrophic bone on the right side. The diarthrodial joints 

are not fused. Both features are not associated with ankylosing spondylitis. The absence of hypertrophic bone on the left 

side is due to the overlying, descending aorta. 704, Right 

lateral view of fused vertebrae. 705, Bone surfaces of the 

right knee joint. Note erosion ofthe medial surface and the 

marginal lipping. Not apparent in the figure is extensive 

eburnation of the worn surfaces. (Specimen from an archeological site in Jersey County, Illinois, USA, NMNH 

380071.) 
NUMBER 28 427 

FIGURES 706, 707.—Porous, hypertrophic degenerative arthritis of the left knee: 706, Joint surfaces of the femur and 

tibia; note particularly the hypertrophic build-up of irregular bone on the lateral surface of the tibia (arrow). 707, 

Posterior view of femur, showing porous hypertrophic bone 

on the medial condyle. (Adult male Eskimo skeleton from 

an archeological site in Wales, Alaska, USA, NMN H 

333467.) 

surface. There is a slight amount of marginal 

lipping. The posteroinferior surface of the right 

femoral head has an area of porosity about 1 by 

{V2 centimeters (Figure 694). A much more severe 

case of degenerative arthritis of the hip is seen in 

archeological specimen from the Historical Museum in Chur, Switzerland (HMCS GR 1248). 

The specimen is from the ancient cemetery at 

Bonaduz. The severe arthritic degeneration is 

associated with the left hip (Figure 701). The 

acetabulum shows severe porosity and eburnation 

with enlargement of the joint. There is marked 

marginal lipping superiorly and posteriorly. The 

left femur shows marked degeneration of the joint 

surface with eburnation and marginal lipping. 

The appearance of this case is very similar to a 

Peruvian specimen described by Hrdlicka (1914: 

60-61). He used the term "caput penis" to describe the rather distinctive morphology of this 

severe type of degenerative change of the femoral 

head. 

The incidence of degenerative arthritis of the 

knee is only slightly less than that of the elbow in 

archeological material. The condition is well 

known in the literature on paleopathology (e.g.. 

Wells, 1965a). Three specimens serve to illustrate 

the significant features of degenerative change of 

the knee. The first of these is an isolated right 

tibia from Paragonah, Utah, USA (NMNH 

292012). The posterior joint surfaces of both tibial 

condyles are eroded, porous, and eburnated (Figure 702). The degenerated surface is also grooved, 

which is indicative of long-standing bone-to-bone 

contact. There is well-developed marginal lipping, which has extended the joint surfaces particularly on the medial and posterior margins. 

The second case is the right knee of a specimen 

from Jersey County, Illinois, USA. This skeleton 

(NMNH 380071) has a fused spine (p. 433). The 

medial condylar surface of the knee is eroded, 

porous, and eburnated with slight grooving (Figure 705). The lateral condyles are intact. There 

is very marked marginal lipping. The left knee is 

similarly affected by degenerative change. 

The third specimen is from an adult male 

Eskimo from an archeological site in Wales, 
428 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

FIGURES 708-711.—Degenerative arthritis ofthe third through fifth lumbar vertebrae and left 

and right first metatarsals: 708, Osteophyte development of vertebral bodies. 709, Superior 

aspect of the fourth (left) and fifth (right) lumbar vertebrae; note the erosive lesion suggestive 

of the presence of Schmorl's node in the fifth vertebral body (arrow). 710, Inferior view ofthe 

fifth lumbar vertebra; note the marked porosity ofthe vertebral body surface. 711, The distal 

articular surface of the right and left first metatarsal bones; note the porosity and eburnation 

associated with the central ridge of the joint surface. (Adult male Eskimo skeleton from an 

archeological site in Pastolik, Alaska, USA, NMN H 332556.) 
NUMBER 28 429 

Alaska, USA (NMNH 333467). Both knees are 

affected. The right knee exhibits erosion, porosity, 

and eburnation of the lateral condylar surfaces. 

The medial posterior portion of the femoral portion of the knee has a lytic porous focus with a 

small area of hypertrophic bone adjacent to the 

porosity. There is some marginal lipping. The left 

knee exhibits degenerative changes, which are 

somewhat different from those described earlier 

(p. 427). On the medial condyle ofthe femur, the 

arthritic change is characterized by a large area 

of irregular hypertrophic bone on the posterior 

portion (Figures 706, 707). There is some porosity, 

eburnation, and marginal lipping. The lateral 

condyle has a small area of irregular hypertrophic 

bone on the posterior portion. Marginal lipping 

is minimal. There is a defect between the condylar 

surfaces suggestive of an old well-healed fracture. 

On the tibia the medial condyle is eroded, porous, 

and eburnated with slight marginal lipping. On 

the lateral condyle, arthritic change is primarily 

a focus of irregular hypertrophic bone rising 

above the joint surface. On both condyles there 

is slight marginal lipping. The tibial portions of 

the ankle joints of this specimen also exhibit 

slight, porous degeneration of the joint surface. 

There is minimal marginal lipping. Arthritic degeneration of the ankle is uncommon in archeological specimens, even when there is marked 

degenerative change in other joints. 

Bones of the feet commonly exhibit degenerative arthritis. The bones most often affected are 

those of the great toe. An example of this condition is seen on the distal joint surface of the right 

and left first metatarsal (Figure 711) from an 

Eskimo burial from Pastolik, Alaska, USA 

(NMNH 332556). The left metatarsal exhibits 

considerable porous erosion on the central ridge 

of the joint surface. There is minimal marginal 

lipping, although there is an erosive depression 

on the medial margin of the joint extending onto 

the adjacent cortex. On the right first metatarsal 

there is some porosity, but the major degenerative 

change is eburnation of the central ridge. There 

is also an erosive depression on the medial margin. 

The other metatarsals are normal. 

The Axial Skeleton 

SKULL AND MANDIBLE.—In the adult the skull 

has only two joints—the temporomandibular and 

atlantooccipital. The latter is most appropriately 

considered with the vertebral column. Degenerative arthritis of the temporomandibular joint 

has received little attention in the literature on 

paleopathology (see reviews of by Pales, 1930: 

165-173, and Alexandersen, 1967:586-590). 

Given the hard use of the jaw often thought to be 

associated with archeological skeletal populations 

it is surprising that the frequency of arthritic 

change in the temporomandibular joint is not 

greater. As with other joints, degenerative change 

in this joint may involve porosity, eburnation, 

and hypertrophy of the joint surface. Marginal 

lipping is not common. 

A fairly typical expression of temporomandibular degenerative arthritis is seen in an adult 

female skull from the Nushagak Region in Alaska, 

USA (NMNH 363530). Both the glenoid fossa 

and the mandibular condyles are involved (Figure 712) but the most severe change is on the 

glenoid fossa. There the porous lesions are restricted to the anterior edge of the fossa and are 

FIGURE 712.—Degenerative arthritis of the left temporomandibular joint. (Adult female Eskimo skull from an archeological site in the Nushagak Region, Alaska, USA, NMNH 

363530.) 
430 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

characterized by erosion and porosity of the surface. 

VERTEBRAL COLUMN.—Wood-Jones (1910b: 

277) observed that virtually all adult ancient 

Nubian skeletons showed some evidence of degenerative arthritis of the spine. A similar generalization would apply to virtually any archeological 

skeletal sample. However, the frequency, age of 

onset, severity, and distribution within the spine 

varies in different populations (Snorrason, 1942; 

Stewart, 1947; Zorab, 1961; Chapman, 1965). 

All vertebrae have diarthrodial joints, which 

permit movement of adjacent joint surfaces. 

These joints are between the facets ofthe articular 

processes of adjacent vertebrae. In addition the 

vertebral bodies are connected by cartilage discs 

in which gliding does not occur. All movement is 

due to the compression and expansion of the disc. 

The thoracic vertebrae have additional joints for 

the articulation of the ribs on the bodies and 

transverse processes. Porosity, eburnation, and 

marginal lipping are associated with degenerative 

arthritis of the diarthrodial joints. Erosion and 

marginal osteophyte development are associated 

with degenerative change ofthe vertebral bodies; 

porosity and eburnation occur rarely. The joints 

between ribs and vertebrae (costovertebral joints) 

exhibit marginal lipping and porosity but rarely 

eburnation. 

Two cases serve to illustrate degenerative arthritis of diarthrodial joints ofthe vertebrae. The 

first of these is an adult female skeleton from 

Hooper Bay, Alaska, USA (NMNH 339115). The 

archeological age is uncertain. The diarthrodial 

joints between the vertebrae all exhibit arthritic 

degeneration (Figures 713, 714). However, the 

cervicals have the most extensive involvement 

including porosity, eburnation, and marginal lipping (Figure 713). The lumbar vertebrae are 

somewhat less affected and the thoracic vertebrae 

least affected. The vertebral bodies of the lower 

thoracic and lumbar vertebrae exhibit the greatest osteophyte development. The inferior surface 

of the tenth vertebral body shows the typical 

bony erosion associated with Schmorl's nodes 

(Figure 715). 

The second example is from an archeological 

site on the Seward Peninsula, Alaska, USA 

(NMNH 342482). The specimen is from an adult 

male Eskimo of uncertain archeological age. Diarthrodial joints between the vertebrae exhibit minimal evidence of abnormality except for the fusion 

of C2 and C3 and degenerative arthritis of the 

joints from the seventh cervical through the sixth 

thoracic (Figures 717-719). The spine of TI was 

broken off (Figure 716) and the degenerative 

change ofthe diarthrodial joints may be a sequela 

of the trauma. This conclusion is supported by 

the relative lack of degeneration in the remaining 

vertebrae. 

Degenerative arthritis of the amphiarthrodial 

vertebral joints is more easily noticed and has 

received greater attention in the literature on 

paleopathology. Two degenerative conditions are 

associated with these joints. In the first of these, 

degeneration of the disc may result in herniation 

of the disc and pressure erosion of one or more 

foci on the bony articular surface (Schmorl's 

nodes) of the vertebral body. With disc degeneration there may also be a generalized porosity of 

virtually the entire surface of the vertebral body. 

The second type of degenerative arthritis involves 

marginal development of osteophytes. In some 

cases the antecedent cause of osteophyte development appears to be anterior herniation of the 

disc. This condition is suggested in a specimen 

from an Eskimo skeleton from Pastolik, Alaska, 

USA (NMNH 332553). The specimen is from a 

young adult male of uncertain archeological age. 

The vertebral column is incomplete but the degenerative change is limited to the joint between 

the fourth and fifth vertebral bodies (Figures 720, 

721). The lesion consists of anterior periarticular 

lipping with adjacent periosteal reactive bone on 

the anterior cortex of the bodies with rather 

marked erosion ofthe anterior joint surfaces particularly on the fifth vertebral body. The lesions 

of the two bodies are suggestive of an anterior 

herniation of the disc resulting in focal pressure 

erosion and peripheral periosteal reactive bone. 

Another example of degenerative arthritis of 

the vertebral bodies is seen in the spinal column 
NUMBER 28 431 

FIGURES 713-715.—Degenerative arthritis of vertebrae: 713, 

Diarthrodial joint eburnation and porosity ofthe third and 

fourth cervical vertebrae. 714, Porous degeneration of the 

diathrodial joint between the tenth and eleventh thoracic 

vertebrae. 715, Depression in the inferior vertebral body due 

to Schmorl's node (arrow). (Adult female Eskimo skeleton 

from an archeological site in the Hooper Bay area of Alaska, 

USA, NMNH 339115.) 

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B^4 ^B ailr .^ 

Hk^^Pyfe^'^* -^H ^^^HB^^RM^^,.' . J^ H 

wSj^BSj^ $• ^siikijiii^^flB 

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(B^ 

of another specimen from Pastolik, Alaska, USA 

(NMNH 332556). The skeleton is an adult male 

of uncertain archeological age. The vertebral column is complete, although there is some postmortem damage. All of the vertebral joints, both 

diarthrodial and amphiarthrodial, show evidence 

of degenerative arthritis. However, the most severe changes are seen in association with the 

amphiarthrodial joints of the lumbar vertebrae 

(Figures 708-710). The superior joint surfaces of 

Ll, L2, and L5 exhibit slight to moderate lytic 

activity suggestive of pressure erosion from a 

Schmorl's node. The inferior surface of L5 (Figure 

710) and the corresponding surface of the first 

sacral body are porous. There is extensive development of marginal osteophytes, some of which 

were in contact with osteophytes of adjacent vertebral bodies. Within the periarticular lipping 
432 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

FIGURES 716-719.—Localized degenerative arthritis ofthe spine probably initiated by trauma: 

716, Left lateral view of sixth cervical through third thoracic vertebrae; note truncated spine of 

first thoracic vertebra (arrow). 717, Superior aspect of the sixth (left) and seventh (right) 

cervical vertebrae, showing porous degeneration of the vertebral body. There is some hypertrophic bone formation on the body surfaces. 718, Porosity and eburnation of the left 

diarthrodial joint between the seventh cervical (left) and the first thoracic (right) vertebrae. 

719, Bilateral diarthrodial joint porosity between the second (left) and third (right) thoracic 

vertebrae. (Adult male Eskimo skeleton from an archeological site on the Seward Peninsula, 

Alaska, USA, NMN H 342482.) 

there is a concave depression, often with cyst-like 

cavities, between the outer edge of the original 

body and the outer edge of the degenerative 

lipping (Figure 709). The severity ofthe periarticular lipping increases toward the fifth lumbar 

body. These vertebrae exhibit a typical, although 

rather severe, pattern of degenerative arthritis of 

the spine. 
NUMBER 28 433 

FIGURES 720, 721.—Erosion and osteophyte development of 

the fourth and fifth lumbar vertebral bodies: 720, Left lateral 

view; note the anterior erosion of the adjacent edges of the 

vertebral bodies with evidence of bony reaction. 721, Anterior view; the appearance of the lesion is suggestive of the 

bony reaction to an anterior herniation of the disk. (Adult 

male Eskimo skeleton from an archeological site in Pastolik, 

Alaska, USA, NMN H 332553.) 

Very extensive development of hypertrophic 

bone from the vertebral bodies may result in bony 

ankylosis. A possible example of this condition is 

seen in an archeological skeleton from Jersey 

County, Illinois, USA (NMNH 380071). The burial appears to be associated with the pre-Columbian period (Hopewellian). The skeleton is incomplete, but all the major long bones, pelvis, 

and the fused tenth thoracic through fifth lumbar 

vertebrae are present. The joints ofthe long bones 

all exhibit degenerative arthritis, particularly of 

the knee in which there is joint surface degeneration as well as extensive periarticular lipping. 

The most obvious arthritic changes are seen on 

the fused lower vertebrae. The extensive bony 

hypertrophy is largely limited to the right side 

and cons'sts of massive bony overgrowths of marginal bone (Figures 703, 704). The disc spaces are 

normal and fusion does not appear to have occurred between the diarthrodial joints. The massive bone hypertrophy and lack of diarthrodial 

joint involvement contrasts with conditions seen 

in either rheumatoid arthritis or ankylosing spondylitis. 

Other Lesions of the Joints 

PATHOLOGY 

Neuropathic Arthropathy (Charcot's Joint) 

Neuropathic arthropathy develops secondary 

to disturbance of the sensory and neurovascular 

innervation. The most common causes of Charcot's joint are (1) tabes dorsalis, a late manifestation of neurosyphilis, (2) syringomyelia, which 

is an intrinsic disturbance of the spinal cord, (3) 

diabetic neuropathy, and (4) traumatic nerve 

damage. 

About 5 to 10 percent of tabetic patients develop a Charcot's joint. Tabetic arthropathy 

mostly affects large joints and localizes in the 

lower extremity in 75 percent of these cases (Figures 722, 723). The most commonly involved 

joint is the knee (about 50 percent), followed in 

descending order by the hip, shoulder, ankle, 

tarsus, and elbow. Only occasionally the dorsolumbar region of the spine, the temporomandibular, sternoclavicular, and finger or toe joints are 

involved. The affection is frequently bilateral. 

Charcot's joint is the result of uncontrolled 

mechanical abuse in the absence of normal pain 

and position sensations, combined with abnormal 

neurovascular control of circulation. 

In syringomyelia, a rare disease mainly located 

in the cervicodorsal portion of the spinal cord, 
FIGURES 724, 725.—Charcot's joint of right knee: 724, Anterior view, showing large bone fragments between tibia and 

patella. 725, Posterosuperior view, showing deep excavation 

and eburnation of tibial articular surface and polished bone 

fragments. (PMUG 4942/60.) 

FIGURES 722, 723.—Charcot's joints of hip and knee in a 

patient with tabes doralis: 722, Left hip, showing joint 

destruction and massive periarticular bony build-up. 723, 

Left knee, showing massive osteocartilaginous loose bodies 

and subluxation. (73-year-old female, IPAZ 6650, autopsy 

1817 from 1961.) 
NUMBER 28 435 

destructive joint disease develops in about 25 

percent of the patients. About 80 percent of these 

cases involve joints of the upper extremity, particularly the shoulder, and often are unilateral. 

In diabetic neuropathy, mostly concerning elderly patients with long-standing diabetes, mostly 

the joints of the feet and, less commonly, of the 

ankle are affected (all statistical data from Jaffe, 

1972:847-874). A similar distribution of neuropathic arthropathy occurs in late stages of neural 

leprosy. The end result is severe destruction, attrition, and fragmentation of the joint ends ofthe 

bones and formation of many loose bodies containing bone fragments. In addition, focal osteoporosis or osteosclerosis and transmetatarsal 

pathological fracture may be observed. Severe 

eburnation and articular grooving, as well as 

reactive exostoses of superimposed degenerative 

arthritis, are found (Figures 724, 725). In archeological material the fragments may not be recovered but the irregular destruction of the convex and the deep excavation ofthe concave joint 

end, as, for instance, the femoral condyles and 

the tibial plateau, should be recognizable. 

Pigmented Villonodular Synovitis 

Pigmented villonodular synovitis is a rare condition characterized by tumor-like proliferation 

of the synovial stroma with accumulation of 

blood pigment. Usually the disease is limited to 

the soft tissues of the joint. The reason to discuss 

it here is that the joint ends of the articulating 

bones occasionally become involved. The most 

common location is the knee joint, but any other 

diarthrodial joint may be involved. The disease 

is usually monoarticular and affects young adults. 

In joints with a tight synovial compartment, as 

interphalangeal joints, undermining erosion of 

the bone next to the cartilaginous articular surface can occur on both sides of the joint. This can 

look about the same on dry bone as the corresponding lesion in gouty arthritis, although in the 

latter the lesion is rarely limited to only one joint. 

In exceptional cases extensive involvement of 

epiphyses occurs, producing large lytic lesions in 

the affected bone ends. A solitary lesion of this 

type could, in the dry bone, be indistinguishable 

from an epiphysial tumor (chondroblastoma or 

enchondroma). 

Synovial Osteochondromatosis 

Synovial osteochondromatosis is a rare condition characterized by formation of multiple foci 

of metaplastic cartilage in the synovium. These 

cartilaginous foci frequently undergo enchondral 

ossification. Some of them separate from the synovium and become loose bodies in the Joint cavity. The condition occurs more commonly in 

young adult males than in females. Only large 

joints are affected and the knee is more frequently 

involved than the hip or the shoulder. Usually 

only one joint is involved. The osteocartilaginous 

nodules, which can be very numerous, usually 

appear rounded and are of about equal size. Since 

the nodules arise from the synovium, the articular 

bone ends appear normal. This fact and the 

smooth contour, even size, and large number of 

these ossified nodules would permit differentiation from loose bodies of Charcot's joint and of 

osteochondritis dissecans in dry bone material. Of 

course, if the condition did not proceed beyond 

the cartilage stage, nothing recognizable would 

be present in the dry bone material. 
Lesions of Jaws and Teeth 

The Jaws 

PATHOLOGY 

The jaws participate in a great variety of lesions, which also may affect other parts of the 

skeleton. Here I will discuss only the lesions that 

are found exclusively in the jaws, because of their 

intimate relationship to' the teeth and to the 

complicated development of the facial skeleton. 

These lesions fall into two groups: odontogenic 

and nonodontogenic. 

Odontogenic Cysts 

The complicated dental development resulting 

from the coordinated interplay of the ectodermal 

enamel epithelium and of the mesodermal tooth 

bud lends itself to a variety of malformations. 

Since the third molar is regressing in the human 

and may be not developed, or at least not erupted, 

anomalies affecting its development are not too 

uncommon. 

PRIMORDIAL CYST.—This cyst is the result of an 

abortive development of a dental follicle without 

formation of a tooth. The cyst has a fibrous wall 

and is lined by odontogenic epithelium. It predilects the area of the third molar, more often in 

the mandible than in the maxilla. As the cyst 

enlarges it may occupy part of the ascending 

mandibular ramus. In dry bone it would appear 

as a cystic cavity that may bulge the overlying 

cortex but is not intimately associated with a 

dental root and does not contain a tooth. 

DENTIGEROUS CYST.—This type of cyst is the 

product of a later stage of deranged dental development. After the crown of a tooth is already 

developed the enamel epithelium fails to involute 

but remains, forming a cyst into the base of which 

the incomplete tooth projects. Again it is the area 

of the third molar that is predilected. This type 

of cyst usually develops from a tooth bud of the 

second dentition or from a supernumerary dental 

follicle. In dry bone it would be similar to the 

primordial cyst except for the presence of an 

incomplete tooth projecting into the cavity if it 

were preserved intact. 

RADICULAR CYST.—This third type of odontogenic cyst is the most common of all. It is not the 

result of maldevelopment but of infection of the 

pulp cavity and the root canal of an erupted 

tooth. It starts as an apical abscess or granuloma 

and secondarily acquires an epithelial lining from 

remnants of the epithelial sheath of the dental 

root. It may be located on any erupted tooth of 

the mandible or maxilla and is always intimately 

associated to the root of an erupted tooth. This 

tooth may have fallen out but its alveolus would 

still connect with the cyst cavity. In contrast to 

the dentigerous cyst, where the tooth is below the 

cyst, in the radicular cyst the tooth is above. 

Odontogenic Tumors 

A variety of tumors can arise from epithelial or 

mesenchymal components ofthe dental bud. The 

most important of these is the ameloblastoma 

arising from enamel epithelium. This lesion is 

more common in the mandible than in the maxilla, predilecting the area of the third molar. 

Males are more often affected than females. The 

lesion is unusually frequent in certain populations 

of African Negroes, but it can occur in all races. 

The lesion begins in childhood or adolescence 

and slowly progresses. It is basically a benign 

436 
NUMBER 28 437 

lesion. The fully developed tumor presents as a 

cystic mass, often multiloculated, which expands 

the bone but maintains a thin, ridged, bony shell. 

Enamel is not formed by the tumor tissue and a 

tooth is not included in the lesion. 

All the other odontogenic tumors are of mesenchymal origin. The odontoma is a tumor prevailingly consisting of dentin, but cementum and 

enamel can be intermixed. This tumor may be a 

shapeless mass of tissue of increased radiodensity, 

but in its most mature form it may show a 

conglomeration of fairly well-developed teeth. 

Thin, polished, undecalcified sections should 

readily reveal the finely tubular structure of dentin microscopically. The cementoma is usually a 

tumor of moderate size, intimately attached to 

one or several adjacent erupted teeth. Cementum 

is a mineralized tissue resembling bone, which 

covers the dental root in a thin layer and serves 

as attachment of the alveolar ligament. Tumorlike proliferations of cementum are not uncommon in the jaws of persons with Paget's disease. 

The myxoid mesenchyme normally forming 

the tooth pulp may give rise to an odontogenic 

fibroma. This would appear in the dry bone 

merely as a smooth-walled, more or less expanded, lytic defect without any identifiable 

characteristics. 

Nonodontogenic Cysts 

These cysts are related to the closure of various 

fissures in the development of the facial skeleton 

or remnants of the nasopalatine duct. Most of 

them are located in the maxilla, and all but the 

unicameral bone cyst arise on the basis of minor 

developmental disturbances. 

The median cysts occur between the central 

incisors of the maxilla or of the mandible, due to 

trapping of epithelium between the two halves of 

the maxilla or mandible. This is the only nonodontogenic epithelial cyst found in the mandible. 

The globomaxillary cyst results from epithelial 

inclusions between the maxillary and globular 

processes of the maxilla. It is always located 

between the lateral upper incisor and the canine 

tooth in the alveolar process. 

The nasoalveolar cyst is due to epithelial remnants between the lateral nasal and the maxillary 

process. It is not located between the teeth and 

tends to bulge into the nasal cavity when it 

enlarges. 

The nasopalatine cyst is based on persistence 

and continued secretion ofthe epithelial lining of 

the vestigial nasopalatine duct. It may form unilaterally or bilaterally in the incisive canal and 

destroy or partly destroy the anterior portion of 

the hard palate. 

Unicameral bone cysts occur in the jaws as in 

other bones. In the mandible they tend to be 

located below the nerve canal rather than primarily in the alveolar process. In the maxilla they 

tend to bulge the cortex forward and towards the 

antrum. 

Nonodontogenic Tumors 

Various fibro-osseous tumors occur in the jaws, 

more often in the maxilla than in the mandible. 

They are characterized by production of finely or 

coarsely trabecular, mostly woven, bone. The 

relationship of such lesions to fibrous dysplasia is 

open to question. Bilateral disfiguring fibro-osseous maxillary tumors are seen in young individuals (cherubism). Recognition of such lesions in 

dry bone would depend on perfect preservation 

of frail trabecular bone. 

A variety of lytic lesions, such as eosinophilic 

granuloma, "brown tumor" of hyperparathyroidism, giant cell reparative granuloma or metastatic 

carcinoma, occur with some frequency in the 

jaws. In dry bone such lesions are devoid of 

identifying characteristics in themselves but may 

be interpretable in the context of findings elsewhere in the skeleton. 

Carcinoma of the oral or nasal cavity, the 

paranasal sinuses, and even the facial skin may 

cause extensive destruction of a jaw or other facial 

bone by direct invasion. As a rule the lesion would 

show a frayed margination in dry bone with little, 

if any, osteosclerotic reaction. 
438 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

The Teeth 

There are many parallels between the diseases 

that affect bone and those that affect teeth. 

Trauma, infection, metabolic abnormalities, congenital malformations, and tumor are among 

morbid conditions that affect both. However, 

there are fundamental differences in the biology 

of teeth that affect the expression of disease. 

Dental enamel lacks cells, vascular and nerve 

supply. For this reason enamel can be affected by 

morbid conditions only during the development 

of the dental crown and by extrinsic lytic processes (primarily dental caries) after eruption of 

the teeth. Dentin also has a very limited potential 

response to morbid conditions. Cells (odontoblasts) line the inner surface of dentin and cellular 

extensions pass through the dentin. Blood and 

nerve supply, as the major components of the 

pulp cavity, are in close proximity to the dentin. 

Odontoblasts have limited potential to form secondary dentin and this is often seen in worn teeth. 

Dentin may be affected by morbid conditions 

present during development, and like enamel, 

may be affected by lytic processes after eruption. 

There is a vast literature on dental pathology. 

Pindborg (1970) and Gorlin and Goldman (1970) 

are the major sources for the discussion of dental 

disease. Much has been published on dental paleopathology as well. However, this aspect of 

paleopathology has not received the same attention as skeletal paleopathology. Much of the following discussion of dental paleopathology is the 

result of my own experience and the observations 

made on specimens from the human skeletal collections of the National Museum of Natural History, Washington, D.C, USA. 

Dental Caries 

PATHOLOGY 

Pindborg (1970:256) defines dental caries as an 

infectious and transmissible disease in which progressive destruction of tooth structure is initiated 

by microbial activity on the tooth surface. Unlike 

destructive processes of bone, destruction of dental hard tissue is the direct result of lytic activity 

by bacteria. Bacterial organisms associated with 

dental caries include lactobacilli and streptococci, 

although the causative mechanisms by which 

organisms produce caries is still not clear (Darling, 1970:273). 

Dental surfaces exposed to potential caries include: (1) the cutting or chewing (occlusal) surfaces, (2) the smooth surfaces ofthe crown including the mesiodistal surfaces (interproximal) in 

contact with other teeth and buccolingual surfaces, and (3) the root, which may be directly 

affected by caries after the recession of the gingiva. Each of these surfaces has varying cariogenic 

potentials. These potentials, in combination with 

varying mouth bacteria and diet, appear to produce different patterns of dental caries (Keyes, 

1968). Thus, the characteristic location of dental 

caries in an archeological skeletal sample may 

provide insight regarding the diet of the people. 

It is important to emphasize that all cavity-like 

defects in teeth are not the result of caries. Pits 

and fissures are naturally occurring features of a 

normal tooth. They may, of course, become a site 

for caries. The distinction between a natural pit 

and a cavity induced by dental caries may not be 

apparent externally. However, when dental caries 

passes through the enamel and reaches the dentin, 

the destructive process spreads rapidly in the 

dentin, adjacent to the boundry between enamel 

and dentin, creating a funnel-shaped lytic lesion 

(Figure 726). Evidence of such a lesion would be 

indicative of caries and would be apparent in an 

X-ray film or could be demonstrated with a 

dental explorer or bent needle. 

Pindborg (1970:256-258) notes the existence of 

acute and chronic dental caries. The former tends 

to be associated with young individuals and appears as a white chalky spot in early stages. 

Chronic caries is often seen on interproximal 

surfaces of teeth often opposed to a carious lesion 

on an adjacent tooth. Lesions in chronic caries 

tend to be darker in color varying from yellow to 

brown. 
NUMBER 28 439 

FIGURE 726.—Dental caries of the right mandibular first 

molar. Interproximal caries (white arrow) and occlusial surface caries (central lesion). On the central lesion note the 

spread ofthe decay process below the enamel (black arrows). 

(Mesiodistal section, NMN H unidentified anatomical specimen.) 

While bacterial activity appears to be a necessary condition for the development of caries, factors intrinsic to the tooth structure may affect the 

development and location of caries. Aside from 

the anatomical features mentioned above, developmental defects in the quality of the enamel 

create conditions favorable to cariogenic activity. 

Untreated caries may result in destruction of 

the entire crown and/or significant portions of 

the root. Exposure of the pulp chamber creates a 

high risk of infection with the almost inevitable 

sequela of abscess and destruction of the supporting tissues. Abscess of a tooth frequently leads to 

its exfoliation followed by alveolar repair involving bone resorption and partial refill ofthe alveolus. Hematogenous dissemination ofthe infection 

may also occur and results in serious complications including meningitis and hematogenous osteomyelitis (see p. 123 and Figures 165-168). 

PALEOPATHOLOGY 

Two basic approaches characterize the literature on the paleopathology of dental caries. The 

first of these is largely descriptive, in which an 

important focus is the history and antiquity of 

dental caries (e.g., Baudouin, 1923). In the more 

recent literature the major emphasis has been on 

the difference in caries frequency between populations (e.g.. Angel, 1974b), with emphasis on 

caries as an indicator of varying food resources as 

in the nutritional differences between huntergatherers and agriculturists (e.g., Cassidy, 1974; 

Sciulli, 1977; Turner, 1979; Cook and Buikstra, 

1979). Caries frequency is low among huntergatherers (approximately two to three lesions per 

mouth) and more than twice as high among 

agriculturists. Both malnutrition affecting tooth 

development and higher carbohydrates in the 

diet have been invoked to explain the higher 

caries frequency in agricultural populations. 

With the recent addition of refined sugar and 

flour to the diet, caries frequency has become 

even greater (Brothwell, 1963:274). 

There are two major problems in studying 

dental caries in archeological skeletons. First, 

teeth are frequently lost or damaged postmortem. 

Postmortem tooth loss is most common with the 

anterior teeth, which are usually less affected by 

caries. Antemortem tooth loss also creates problems in evaluating caries incidence. This condition is often but not always the result of caries 

complicated by abscess. The second problem is 

that most archeological skeletons exhibit considerable dental attrition due to coarse particles in 

the food. The effect of this wear is to grind away 

occlusal surfaces before dental caries can develop. 

Occasionally this wear is so severe that the pulp 

cavity is exposed with the tooth root and supporting tissues often becoming infected. If wear is 

extreme the abscess is more likely to be due to 

attrition rather than caries, although it may not 

always be possible to make this distinction. 

OCCLUSAL SURFACE CARIES.—This type of caries is primarily associated with the molars and 

premolars and begins in the crevices of the occlusal surface. In early stages there may be only a 

small penetrating hole through the enamel surface (Figure 727) as seen in a young adult mandible from an archeological site in Arizona 
440 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

FIGURE 727.—Occlusal surface caries, early to moderate 

stages in the lower jaw. The lower right first molar exhibits 

moderate wear and a fairly large cavity in the mesial-buccal 

quadrant. Other molars exhibit early development of dental 

caries (white arrows) with only small holes apparent externally. Probing with a dental explorer reveals much greater 

destruction below the enamel. There is a pit on the lower 

left second molar (black arrow), which is not carious. (Young 

adult female mandible from an archeological site in Arizona, 

NMNH 239202.) 

(NMNH 239202). A much more severe example 

of probable occlusal surface caries is seen in the 

upper left second molar (Figure 728) of an adult 

FIGURE 728.—Severe occlusal surface caries ofthe upper left 

second molar. Virtually the entire crown has been destroyed. 

The other teeth are worn but not carious (Adult male from 

Early Bronze Age site of Bab edh-Dhra, Jordan, NMNH 

A lOON Burial 1.) 

male from the Early Bronze Age site of Bab edhDhra in Jordan (NMNH AlOON Burial 1). This 

is the only evidence of caries in the dentition. 

There is some alveolar resorption at the base of 

the carious tooth that is suggestive of infection. 

FIGURE 729.—Interproximal caries of the upper left second 

premolar. Adjacent first molar is missing antemortem, probably due to caries and abscess. (Adult female from Moorehead Cave, Texas, NMNH 372528.) 

FIGURE 730.—Interproximal caries ofthe maxillary incisors. 

(Adult male from a Late Woodland site in Virginia, USA, 

NMN H 382419.) 
NUMBER 28 441 

FIGURE 731.—Root caries ofth e mesial, interproximal surface of the lower left first molar. Note the evidence of 

moderate alveolar resorption indicated by the distance between the cemento-enamel junction and the alveolar bone. 

The soft tissue would have receded with the bone, exposing 

the tooth root to caries; anterolateral view. (Adult female 

from archeological site of Puye, New Mexico, USA, NMNH 

262944.) 

NONOCCLUSAL SuRFACE CARIE S ON THE 

CROWN.—An example of interproximal caries is 

seen in a skull of an adult female from Moorehead 

Cave, Texas, USA (NMNH 372528). The upper 

left second premolar is carious on the distal surface. The first molar appears to have been lost 

antemortem (Figure 729). The molar socket 

shows considerable resorption and evidence of 

abscess. The carious lesion on the premolar continues past the cemento-enamel junction into the 

root. The lesion did not penetrate to the pulp 

cavity. 

Interproximal caries can also affect the incisors. 

An example of this condition is seen in an adult 

male skull from the Shannon site in Virginia, 

USA (NMNH 382419). This site is Late Woodland in date with no European trade goods. All 

of the interproximal surfaces between the maxillary incisors are carious (Figure 730). 

ROOT CARIES.—An example of root caries is 

seen on the mesial interproximal surface of the 

lower first molar of an adult female skull from 

the pre-Columbian archeological site of Puye, 

FIGURES 732, 733.—Dental caries with destructive lesions 

penetrating the pulp cavity of both first molars: 732, Occlusal view; left central incisor missing postmortem. Right 

second premolar and third molar sockets show evidence of 

alveolar remodeling suggestive of antemortem tooth loss. 

There is an abscess associated with the premolar. 733, Anterior view of maxilla, showing lytic bony response to abscessed first molars and right second premolar. (Adult male 

from archeological site of Puye, New Mexico, USA, NMNH 

262948.) 

New Mexico, USA (NMNH 262944). On the 

buccal side of this tooth the upper margin of the 

alveolar bone is almost 4 millimeters below the 

cemento-enamel junction (Figure 731). On the 

lingual side this dimension is almost 5 millimeters. 
442 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

These distances are more than twice the normal 

distance between alveolar bone and the cementoenamel junction and are indicative of considerable alveolar resorption, which exposed the root 

to caries. 

SECONDARY EFFECTS OF DENTAL CARIES.—If 

tooth destruction from dental caries penetrates 

the pulp cavity, infection of the support tissues is 

an almost inevitable result. Bone tissue reaction 

to infection initially involves bone destruction 

providing a drain for pus. Chronic infection leads 

to at least partial bony circumscription around 

the infectious focus. Tooth exfoliation and hematogenous dissemination of the infection are additional potential secondary effects. 

Most of these morbid processes, secondary to 

dental caries, are demonstrated in the maxillary 

dentition of an adult male skull from the preColumbian site of Puye, New Mexico, USA 

(NMNH 262948). The left central incisor is missing postmortem. The right second premolar and 

right third molar are missing antemortem. In the 

case of the premolar there is evidence of abscess 

at the base of alveolus. The alveolus of the third 

molar is shallow with evidence of remodeling 

suggestive of infection. However, there is no evidence of a draining sinus through the alveolar 

bone. The major periapical lesions are associated 

with the first molars. Both teeth have large cavities in the crown, which have penetrated the pulp 

cavity (Figure 732). The resulting infection has 

resulted in lytic lesions of the maxilla, which 

penetrate the external cortex of the maxilla on 

both sides and the inner cortex on the left (Figure 

733). Whether this condition led to disseminated 

infection elsewhere in the body cannot be determined. Indeed evidence for such a complication 

would be rare in dry skeletal material. 

Periodontal Disease 

PATHOLOGY 

Ruben, Goldman, and Schulman (1970:394) 

note that several morbid conditions result in periodontal disease. Identification of many of these 

conditions depends on good medical histories, soft 

tissue pathology, and bacteriology. It is thus unlikely that all the specific factors that induce 

periodontal disease will be identifiable in dry 

bone specimens. For this reason I shall limit my 

discussion to the more common causative factors 

and those which may be identifiable in archeological specimens. 

As a general principle, periodontal disease involves an inflammatory response to one or more 

irritants. This inflammation often results in resorption of alveolar bone creating an abnormally 

large distance between bone and the cementoenamel junction. A common irritant is calculus 

and its precursor, bacterial plaque, which consists 

of a sticky coating including protein, food particles, living and dead microorganisms. When 

plaque mineralizes, it becomes calculus and in 

this form can be found on archeological skeletal 

specimens as relatively hard additions to the tooth 

surface. The role of calculus in periodontal disease 

is not clear. Ruben, Goldman, and Schulman 

(1970:397) express the opinion that mechanical 

irritation from calculus is secondary to inflammation directly induced by bacterial activity. In 

any case the presence of calculus on dental tissues 

is an important consideration in evaluating the 

cause of periodontal disease in archeological skeletal material. 

Metabolic problems may result in inflammatory conditions that affect the periodontal tissues. 

In scurvy, for example, the quality of the connective tissue associated with teeth is weakened. 

Bleeding results from weakened blood vessel walls 

being traumatized by chewing. The inflammatory response in scurvy may lead to exfoliation of 

teeth, particularly those with single roots. Similarly, protein deficiency may lead to diminished 

quality of supporting tissue and periodontal disease. 

Peridontal abscess may result in relatively localized periodontal disease. The effect on supporting tissue may be similar to that produced by 

periapical abscess. However, the focus of infection 

in periodontal abscess is outside the pulp cavity 

and often between the roots of multirooted teeth 
NUMBER 28 443 

(Ruben, Goldman, and Schulman, 1970:423). 

Abscess of alveolar bone without evidence of caries involvement of the pulp cavity would be 

suggestive of periodontal abscess. 

PALEOPATHOLOGY 

In archeological skulls the major manifestation 

of periodontal disease will be local or general 

FIGURES 734, 735.—Alveolar resorption indicative of periodontal disease: 734, Anterior view of lower jaw showing 

marked exposure ofthe roots ofthe anterior teeth; note the 

dental calculus adjacent to the exposed roots. 735, Left 

lateral view, showing root exposure of the premolars and 

molars. There is considerable dental attrition but no evidence of caries or exposure of the pulp chambers of any 

teeth. (Adult male from Horr's Island, Florida, USA, 

NMNH 352156.) 

alveolar resorption. The distinction will need to 

be made between alveolar resorption from periodontal disease and resorption associated with 

periapical abscess and tooth loss. Clearly if there 

is alveolar resorption but little or no evidence of 

caries or tooth loss, a diagnosis of periodontal 

disease is appropriate. An example of this condition is seen in the mandible of a skeleton from an 

archeological site on Horr's Island, Florida, USA 

(NMNH 352156). The maxilla was broken postmortem and only fragments recovered. On the 

mandibular teeth there is considerable root exposure, which is indicative of alveolar resorption 

(Figures 734, 735). Dental calculus is adherent on 

the exposed buccal root surfaces of the incisors 

and canines. Alveolar resorption is particularly 

noticeable in the bone supporting the first molars. 

Although there is considerable wear, there is no 

evidence of pulp-cavity exposure or caries. The 

presence of calculus in association with alveolar 

resorption and lack of dental caries supports a 

diagnosis of periodontal disease. 

Another example of marked tooth root exposure with no evidence of dental caries is found in 

the mandible of a skeleton from an archeological 

FIGURE 736.—Molar root exposure and reactive alveolar 

bone suggestive of periodontal disease. Note calculus on the 

distolingual portion ofthe third molar (arrow). Left medial 

view of mandible. (Adult male from Canaveral, Florida, 

USA, NMNH 377439.) 
444 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

site at Canaveral, Florida, USA (NMNH 

377439). The maxilla was broken postmortem 

and only fragmentary portions were recovered. 

These fragments exhibit considerable root exposure of the right incisors, canine, and first premolar. These teeth were extensively worn with 

evidence of secondary dentin formation in the 

incisors. The mandibular incisors appear to have 

been lost antemortem as was the left first premolar. The right canine, premolars, left second 

premolar and first molar were probably lost postmortem. However, in the case of the left first 

molar, alveolar resorption had resulted in very 

poor support for the tooth roots. There is considerable root exposure of the second and third 

molars and marked build up of calculus on the 

crown and exposed root (Figure 736). Rough 

porosity characterizes the bone associated with 

the left molar roots. This is indicative of an 

inflammatory condition, probably including the 

overlying soft tissues. The pattern of alveolar 

exposure and lack of caries supports a diagnosis 

of periodontal disease. 

Disturbances in Dental Development 

PATHOLOGY 

Abnormal (Quality of Teeth 

Several morbid conditions may result in an 

abnormal quality of teeth. Some conditions affect 

dentin (see above), some affect enamel, and others 

affect both. The most common condition is a 

hypoplastic defect in the enamel. Pindborg (1970: 

75-210) provides an extensive review ofthe various conditions that produce this defect, many of 

which are rare or caused by modern problems. 

The reader is referred to this source for a more 

comprehensive treatment of this subject. I shall 

limit my comments to those pathological conditions that are fairly common in paleopathological 

specimens. 

Infectious diseases, primarily congenital syphilis and tuberculosis, as well as metabolic and 

endocrine disorders, are known to adversely affect 

the formation of dental tissue. Fairly typical multiple hypoplastic lines are seen in the dentition of 

a 26-year-old male from the Pathology Museum 

of the University of Graz in Austria (PMUG 

3421, autopsy 9497 from 1879). Autopsy records 

state that the individual was a syphilitic. Transverse hypoplastic lines are most pronounced on 

the maxillary dentition, particularly the central 

incisors (Figure 737). In addition to the defective 

lines, there are numerous fine pores in the enamel. 

Congenital syphilis may result in defective first 

molars (mulberry molars). The crown size is 

smaller than normal, tending to be smaller than 

that of the second molar; normally the crown of 

the first molar is the larger. The occlusal surface 

is very irregular. A skull from a modern female 

about 30 years of age exhibits dental defects fairly 

typical of congenital syphilis (NMNH 219398). 

The upper right central, lower right central, and 

lower left lateral incisor crowns have hypoplastic 

defects ofthe incisal edge (Figure 738). The first 

molars are smaller than the second and have a 

pitted, poorly formed, occlusal surface (Figure 

739). 

Dental hypoplasia is also thought to be associated with rickets. Figures 424 and 426 show hyFiGURE 737.—Dental hypoplasia associated with syphilis. 

Note multiple transverse, hypoplastic lines and pitting of 

enamel between the lines. (26-year-old male, PMU G 3421, 

autopsy 9497 from 1879.) 
NUMBER 28 445 

FIGURES 738, 739.—Dental hypoplasia associated with probable syphilis: 738, Anterior view; note defect of incisal edges 

of incisors. 739, Occlusal view of mandibular molars. The 

first molar is smaller than the second and has an abnormal 

pitted occlusal surface typical of congenital syphilis. (Female 

about 30 years of age, NMNH 219398, dissecting-room 

specimen from before 1903. 

poplastic defects of the teeth. A rachitic skull 

(FPAM 2694) from the Federal Pathologic-Anatomy Museum in Vienna, Austria, exhibits 

marked hypoplastic defects of the teeth (Figures 

740, 741). The skull is from a child about 6 years 

of age. The most severe changes are seen in the 

crowns ofthe upper second deciduous molars, the 

right upper first permanent molar, and the first 

FIGURES 740, 741.—Dental hypoplasia associated with rickets: 740, Occlusal view of maxillary dentition; note defective 

crowns of second deciduous molars and right first permanent 

molar. 741, Occlusal view of mandibular dentition. The 

crowns of both first permanent molars are defective. (Child 

about 6 years of age, FPAM 2694 from before 1858.) 

permanent molars of the mandible. Both the 

enamel and dentin appear to be affected. 

Tuberculosis is most commonly a disease of 

childhood, so it is not surprising to find hypoplastic dental lesions associated with tuberculosis. 

A skull of a child, between 3 and 6 years of age, 

reported to have had tuberculosis, is part of the 

collections of the National Museum of Anthropology in Prague, Czechoslovakia (ANM 2028). 

All of the deciduous teeth have erupted and 
446 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

i 

FIGURE 742.—Dental hypoplasia associated with a case of 

tuberculosis. Hypoplastic lines or spots are visable in the 

crowns of all the deciduous teeth. (Child between 3 and 6 

years of age, ANM 2028 from before 1895.) 

FIGURE 743.—Dental hypoplasia associated with tuberculosis. Note multiple hypoplastic lines in the teeth. (17-yearold-male, FPAM 2016, autopsy 16648 from 1842.) 

exhibit hypoplastic lines and spots (Figures 742). 

There are no autopsy data available for this case, 

so that the diagnosis of tuberculosis cannot be 

evaluated. The lytic lesion on the mandible is not 

typical of tuberculosis. The disease processes 

would have had to begun in late fetal life or early 

infancy to have produced these effects on the 

incisors. 

An undoubted case of tuberculosis with multiple hypoplastic lines is associated with the skull 

of a 17-year-old boy, which is part of the Federal 

Pathologic-Anatomy Museum in Vienna, Austria 

(FPAM 2016, autopsy 16648 and 1842). There 

are multiple lytic lesions ofthe skull. The incisors, 

canines, and premolars that remain in the jaws 

show hypoplastic lines (Figure 743). 

Abnormal (^antity of Teeth 

Rather commonly, there is an increase in the 

normal number of teeth (hyperodontia). This 

typically affects the permanent dentition and 

most often results in more than the normal 32 

teeth (hyperodontia). The extra teeth may be 

heterotopic, meaning that they develop outside of 

the alveolar region, or they may be normotopic, 

meaning that they develop in the alveolar region 

and erupt in the normal orientation. Supernumerary teeth may be the result of the retention of 

deciduous teeth or the development of extra permanent teeth. 

Fewer than normal teeth (hypodontia) occurs 

when one or more teeth fail to develop. The 

frequency of agenesis varies with the tooth. In 

descending order of frequency the commonly affected teeth are: third molars, maxillary lateral 

incisors, second premolars, mandibular central 

incisors, and maxillary first premolars (Salzmann, 

1957:256). Occasionally, often because there is 

insufficient room, one or more teeth will become 

impacted and fail to erupt. This is not a true case 

of hypodontia, since the dental element did develop. However, the external appearance of the 

dentition and jaw may be very similar and an Xray film would be needed to differentiate dental 

agenesis from impaction. 
NUMBER 28 447 

Abnormal Size and Shape of Teeth 

Teeth may be larger than normal (macrodontia). This condition may affect the entire dentition or just one tooth. It may be symmetrical or 

unilateral. In the latter case macrodontia is easily 

confused with the fusion of two teeth and differentiation may not be possible (Pindborg, 1970: 

35). Teeth smaller than normal (microdontia) are 

more common. This condition is associated with 

a number of congenital morbid conditions, including heart disease, Down's syndrome, and cleft 

palate (Pindborg, 1970:36). Often the shape in 

microdontia will be abnormal as well. 

Dental Anomalies 

There is considerable normal, genetically based 

variation in the shape of the teeth. Variants 

include the shovel-shaped incisors of Asian populations and many variations in molar cusp pattern. Fairly common dental anomalies include 

fused teeth and enamel pearls. Teeth may be 

fused at the crowns, the roots or both. The factors 

contributing to fusion include both genetic abnormalities and inflammation. Pindborg (1970: 

47-57) distinguishes between concrescence, in 

which tooth roots are joined only by hyperplastic 

cementum, and fusion, which occurs during the 

development of the teeth. Fusion affects the deciduous dentition more commonly than the permanent teeth. Incisors and canines are the most 

frequently affected teeth. 

Enamel pearls are thought to be the result of 

abnormalities in embryological development. 

They may project from the surface of the tooth 

(extradental) or may be included within the dentin (intradental). The former are the ones encountered fairly commonly in archeological specimens. They occur only on multirooted teeth and 

vary in size from barely visible to about 2 millimeters in diameter. They are most frequent on 

the maxillary teeth where they tend to be on the 

interproximal surfaces. On the mandibular teeth 

they tend to be on the buccal or lingual surfaces 

(Pindborg, 1970:45-47). 

Dental Crowding 

The development of teeth appears to be primarily under the control of genetic fields and 

environmental conditions, which are relatively 

independent of those factors that affect the development of jaws. Because of this independence, 

the size of the two types of structure may not be 

congruent. Most often the incongruence is expressed as an inadequate size of the jaw relative 

to the size ofthe teeth. This is particularly true of 

the mandible. Inadequate space for the teeth 

results in tooth crowding. This problem may be 

particularly severe in conditions such as pituitary 

dwarfism, where the lack of growth hormone 

severely limits bone development but has minimal effect on tooth size. 

PALEOPATHOLOGY 

Abnormal (Quality of Teeth 

I have previously described (p. 207) a possible 

case of congenital syphilis in which the deciduous 

dentition had marked hypoplastic enamel defects 

(Figures 320, 322). Most ofthe examples of dental 

hypoplasia in archeological skeletons are not as 

noticeable. Two examples of hypoplasia in archeological specimens illustrate more subtle manifestations. The first of these is a specimen from the 

protohistoric archeological site of Mobridge in 

South Dakota, USA (NMNH 325416). The skuU 

is from an adult female skeleton. The teeth are 

worn, with development of secondary dentin on 

the incisors and upper canines. The wear may 

have obliterated some of the hypoplastic lines. 

The third molars did not develop. All the teeth 

except the molars have at least one hypoplastic 

transverse line (Figure 744). 

Multiple hypoplastic transverse lines are present on the canines (Figure 745) in an adult male 

skull from an archeological site in Fort Concho, 

Texas, USA (NMNH 243490). The upper incisors 

are missing and the lower incisors have been 

damaged postmortem. The lower lateral incisor, 

however, appears to have at least one hypoplastic 

line, suggesting that the incisors may have been 

defective. The premolars and molars are normal. 
448 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

FIGURE 744.—Enamel hypoplasia expressed as hypoplastic 

transverse lines of the buccal crown surface of all teeth 

except the molars. Anterior tooth wear is marked with 

secondary dentin apparent on the occlusal surfaces. (Adult 

female from Mobridge site. South Dakota, USA, NMN H 

325416. 

Abnormal Quantity of Teeth 

Supernumerary teeth (hyperodontia) are 

rather common in archeological specimens (e.g., 

Brothwell, 1965a: 114, 115). Two cases serve to 

illustrate the development of supernumerary 

teeth outside the alveolar region of the jaws (hetFIGURE 745.—Multiple hypoplastic transverse defects of the 

canine teeth. (Adult male from Fort Concho, Texas, USA, 

NMN H 243490.) 

erotopic). The first of these is the facial portion of 

a child's skull from Chicama, Peru (NMNH 

293595). The mandible was not recovered. The 

archeological age is unknown. Both second permanent molars have erupted, although the third 

permanent molar is still deep in the maxilla. Most 

of the teeth have been lost postmortem. The 

alveoli indicate that the normal number of teeth 

FIGURE 746.—Heterotopic supernumerary canine projecting 

through the left maxilla. (Child's skull about 12 years of age 

from Chicama, Peru, NMN H 293595.) 

FIGURE 747.—Heterotopic supernumerary canine projecting 

through the left palate (Adult skull from Pachacamac, Peru, 

NMN H 267104.) 
NUMBER 28 449 

were present. However, the alveolus of the left 

canine indicates that this tooth was much smaller 

than normal. Projecting through the maxilla in 

the region over the first premolar is the crown of 

a normal sized canine (Figure 746). An X-ray 

film reveals the relatively normal size and shape 

of the canine root. 

The second example of heterotopic hyperodontia is an adult skull from Pachacamac, Peru 

(NMNH 267104). The mandible was not recovered. Only the first and second molars are 

present, the remaining teeth were lost postmortem. The alveoli are intact and indicate a normal 

number and root morphology for the missing 

teeth. A dental element with the crown and root 

morphology of a canine projects partially through 

the left palate (Figure 747). 

It should be emphasized that not all heterotopic teeth are supernumerary. Another adult 

skull from Pachacamac, Peru (NMNH 266005) 

illustrates this point. Except for a heterotopic 

central incisor, all the teeth are missing. Some 

alveoli are present indicating postmortem loss. 

However, there is also alveolar bone resorption, 

indicative of antemortem tooth loss as well. There 

is a dental element with the morphology of an 

upper central incisor embedded in the maxilla in 

the region above where the central incisor should 

have been. The crown of the tooth projects buccally (Figure 748). The tooth root is shortened 

but may project posteriorly. This is a case where 

the tooth erupted in the wrong direction, but 

there is no evidence that the tooth was supernumerary. 

An example of a supernumerary tooth erupting 

in the normal orientation and in the alveolar 

region (normotopic) is seen in the mandible of an 

adult female skull from the Virgin Islands 

(NMNH 385695). The specimen is from the historic period. There is some antemortem tooth 

loss, but the only evidence of supernumerary teeth 

is a fourth molar of the left mandible (Figure 

749). This condition is not present on the right 

side. 

Retention of deciduous teeth may lead to extra 

teeth in the tooth row. This condition can be 

FIGURE 748.—Heterotopic maxillary central incisor, probably not supernumerary. Crown of tooth is in contact with 

anterior nasal spine. (Adult skull from Pachacamac, Peru, 

NMNH 266005.) 

FIGURE 749.—Supernumerary molar on the left side of a 

mandible. (Adult female skeleton from an archeological site 

in the Virgin Islands, NMNH 385695.) 

observed in the mandible of a young adult specimen from Chicama, Peru (NMNH 264521). 

There is no skull associated with the mandible. 

Age cannot be determined precisely, although the 

third permanent molars have erupted indicating 

a minimal age of 18 years. The entire primary 

dentition has been retained on the left side (Figure 750). The permanent incisors have erupted. 

The central incisor is in a relatively normal posi-
450 SMITHSONIAN CONTRIBUTIONS TO ANTHKOPOLOG Y 

tion. The lateral incisor is displaced lingually. 

The tip of the impacted permanent canine is 

projecting through alveolar bone. The premolars 

are completely impacted beneath the primary 

molars (Figure 751). On the right side, the permanent dentition has erupted. However, remnants of some of the deciduous roots still project 

through alveolar bone. The left permanent incisors and canine are missing postmortem. 

FIGURES 750, 751.—Retention of primary dentition into 

adulthood on the left side of the mandible. Although the 

permanent teeth have erupted in the right side, a few 

fragments ofthe deciduous roots remain embedded in alveolar bone: 750, Occlusal view. 751, X-ray of left side; note 

impacted permanent canine (arrow) and premolars. (Adult 

mandible from Chicama, Peru, NMN H 264521.) 

FIGURE 752.—Dental agenesis of the mandibular lateral 

incisors, occlusal view. (Adult female from Mobridge, South 

Dakota, USA, NMN H 325417.) 

Dental agenesis (hypodontia) is rather common 

in archeological specimens. It is most commonly 

seen in the failure of the third permanent molar 

to develop (Brothwell, Carbonell, and Goose, in 

Brothwell, 1963:182). An example of dental agenesis of the lower lateral incisors is found in an 

adult female skull from Mobridge, South Dakota, 

USA (NMNH 325417). The maxillary dentition 

is normal. On the mandible, the canines are 

adjacent to the central incisors (Figure 752). An 

X-ray film ofthe anterior teeth shows no evidence 

FIGURE 753.—Abnormally small maxillary lateral incisors in 

an adult skull from Chicama, Peru (NMNH 264518.) 
NUMBER 28 451 

of impacted teeth, indicating that the lateral 

incisors did not develop. 

Abnormal Size and Shape of Teeth 

Abnormal variations in size and shape of teeth 

should be readily recognizable to people familiar 

with skeletal specimens. One example is sufficient 

to illustrate this condition. This specimen is an 

adult skull, lacking the mandible, from Chicama, 

Peru (NMNH 264518). Many teeth are missing 

postmortem, although the alveoli indicate a normal number of teeth. The upper lateral incisors 

are smaller than normal (Figure 753). 

Dental Anomalies 

Three cases of dental fusion illustrate the basic 

features of this dental anomaly. The first of these 

is seen in the mandible of a young child about 

\^h. years of age. The specimen is from the historic 

period in Nebraska, USA (NMNH 243355). Fusion occurred between the central and lateral 

right incisors (Figure 754). The second case is 

from an archeological site in New Mexico, USA 

(NMNH 269221) and involves the deciduous 

mandibular right lateral incisor and canine (Figure 755). The child was about 8 years of age. An 

X-ray film indicates that the roots were fused. 

The third case is from an adult dentition in the 

mandible of a skeleton from an archeological site 

in New Jersey, USA (NMNH 285307). Fusion 

has taken place between the right lateral incisor 

and canine and has created a very large tooth, 

which might, on superficial inspection, be confused with macrodontia (Figure 756). The roots 

of the two teeth are fused. 

I; Another dental anomaly involves the development of "enamel pearls" on the surface of the 

E0Ots. An example of multiple enamel pearls is 

seen in the mandible of an adult female skeleton 

from South Dakota, USA (NMNH 325367). An 

enamel pearl developed on the distal surface of 

the roots of the left second and third molars 

(Figures 757, 758). The growth encroached on the 

alveolar bone creating a marked cavity adjacent 

to the second molar but only a slight depression 

adjacent to the third molar. 

FIGURE 754.—Fusion of the mandibular right incisors. 

(American Indian child about 1V2 years of age from a historic 

period site in Nebraska, USA, NMNH 243355.) 

FIGURE 755.—Fusion of the mandibular deciduous right 

lateral incisor and canine. (Child, about 8 years of age, from 

an archeological site in New Mexico, USA, NMNH 269221.) 

FIGURE 756.—Fusion of the permanent mandibular, right 

lateral incisor and canine (arrow). An X-ray reveals that the 

roots are fused. This fusion should be distinguished from 

abnormally large teeth (macrodontia). (Specimen is from an 

archeological site in New Jersey, USA, NMNH 285307.) 
452 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOG Y 

FIGURES 757, 758.—Enamel pearls on the distal root surface 

of the mandibular, left permanent second and third molars: 

757, Molars, in situ; note that the enamel pearl encroaches 

on alveolar bone. 758, Detail of enamel pearl on second 

molar. (Specimen from archeological site in South Dakota, 

USA, NMNH 325367.) 

FIGURE 759.—Severe crowding of the maxillary dentition in 

a child's skull about 10 years of age. Note the displacement 

ofthe anterior teeth. (Specimen is from an archeological site 

in Canaveral, Florida, USA, NMN H 377496.) 

to the retention of the second deciduous molars; 

however, the estimated age would be about 10 

years. The fragmentary long bones are small and 

gracile. The estimated age, based on femur 

length, is about 8 years suggesting subnormal 

growth. The skull is small with a maximum 

length of 149 millimeters and a maximum 

breadth of 131 millimeters. The right lateral incisor is displaced lingually due to inadequate 

space in the maxilla. Although the skeleton is 

small, there is no evidence of pituitary dysfunction. The probable pituitary dwarf described in 

the chapter on endocrine disorders did not exhibit 

serious crowding in the dentition, in part due to 

the prognathous jaws (see Figures 468, 469). 

Dental Crowding 

A small skull, lacking the mandible, of a child 

from an archeological site in Canaveral, Florida, 

USA (NMNH 377496) illustrates the problems 

that develop when normal or large permanent 

teeth erupt in a small jaw (Figure 759). The 

dental eruption stage is somewhat anomalous due 

Dental Trauma 

PATHOLOGY 

In modern populations the major causes of 

dental fracture are automobile accidents and injury during participation in sports or the rough 

and tumble play of children. Pindborg (1970:277) 
NUMBER 28 453 

reports that the central maxillary incisors are 

most frequently fractured, and males fracture 

teeth twice as often as females. Enamel, dentin, 

pulp, and cementum may be involved in fracture. 

The crown is involved in about 98 percent of the 

cases of dental fracture, the root in about 2 

percent (Pindborg, 1970:279). Crown fractures 

most frequently involve both the enamel and 

dentin, less commonly the enamel only. Exposure 

of the dentinal tubules may permit infection of 

the pulp and this may lead to periapical abscess. 

PALEOPATHOLOGY 

Antemortem dental fracture in dry bone specimens may be very difficult to differentiate from 

postmortem damage in the ground or in museum 

storage. Most often postmortem damage involves 

the enamel, which chips off easily. However, major portions of the tooth may split involving the 

dentin and pulp cavity. One possible criterion for 

making the distinction between ante- and postmortem fracture is the smoothing ofthe fractured 

edges of the tooth, which would occur in antemortem fracture if sufficient time had elapsed 

between the fracture and death. 

FIGURE 760.—Possible antemortem fracture of the dental 

crowns (arrows), occlusal view of mandible. Note the 

rounded edges of the remaining crowns suggesting wear of 

the teeth after the fracture. (Adult female from archeological 

site on Perico Island, Florida, USA, NMNH 373547.) 

FIGURE 761.—Dental mutilation of the maxillary left incisors. (Adult female, probably a Negro burial, from Saint 

Croix, Virgin Islands, NMNH 382048.) 

A possible example of antemortem tooth fracture is in the mandibular teeth of an archeological 

skeleton from Perico Island, Florida, USA 

(NMNH 373547). Fairly substantial portions of 

the crowns ofthe left and right second premolars, 

first molars, and right second molar have been 

chipped off primarily on the buccal side (Figure 

760). The fractured edges ofthe affected crowns 

have been smoothed, suggesting attrition of the 

broken surface after the fracture. All the teeth are 

worn, indicating a fairly abrasive diet, so attrition 

of broken edges could be expected if antemortem. 

Fracture of teeth may be induced intentionally 

as an expression of a cultural practice. Two basic 

cultural practices occur. The first of these is ritual 

ablation or removal of teeth (Baudouin, 1923). 

Typically this involves the incisors, which may be 

extracted or broken off leaving the roots. The 

second practice is mutilation of the teeth. This 

practice also, typically, involves the incisors. The 

teeth may be ground, filed, or broken to create a 

special shape or they may be inlayed with metals 

or mineral materials. This practice is primarily 

associated with the continents of Africa and 

South America with some evidence for its presence in the indigenous cultures of North America 

(e.g., Jhering, 1882; Starr, 1909; Stewart, 1944; 
454 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

Romero, 1958, 1970). Tooth filing, associated 

with blackening with burnt oil, is common in 

Sumatra and probably throughout much of the 

Pacific. 

The variation in the practice of dental mutilation is remarkable, although beyond the objectives of this book. One previously unpublished 

case will serve to illustrate this type of dental 

trauma. The specimen is from Saint Croix in the 

Virgin Islands and was discovered when it was 

washed out by a storm (NMNH 382048). The 

morphology ofthe skull is distinctively Negro and 

may have been the remains of one ofthe slaves in 

the slave camps located on the island. The archeological age is not known but is certainly in the 

historic period. The skull appears to be that of an 

adult female. The maxillary right incisors and 

third molar are missing postmortem, as is the 

mandibular left central and right incisors and the 

right third molar. The maxillary left incisors have 

been mutilated, creating a point with its apex 

between the two teeth (Figure 761). 

Dental Attrition 

PATHOLOGY 

Pindborg (1970:294) makes the distinction between attrition resulting from natural mastication 

(physiologic attrition) and attrition, often localized, caused by abnormal use or position of teeth 

(pathologic attrition). The factors contributing to 

attrition are varied and include the occlusion of 

the opposing teeth, the quality of the teeth, abrasives in the diet, and the use of abrading instruments, such as a pipe or the use of teeth to hold 

objects. 

Attrition of the occlusal surfaces may destroy 

the enamel, exposing the underlying dentin. Attrition continued beyond this point may threaten 

exposure of the pulp cavity. In response to attrition, the odontoblasts begin forming secondary 

dentin in the threatened areas of the pulp cavity, 

and attrition may expose the secondary dentin. If 

attrition occurs at a rate faster than the formation 

of secondary dentin, the pulp cavity will be exposed creating the potential for infection of the 

pulp and supporting alveolar bone. 

Attrition also takes place on the opposing surfaces of adjacent teeth (interproximal attrition). 

This type of wear is due to the contact between 

teeth and the slight movement of the teeth that 

accompanies chewing. This type of attrition is 

relatively slight, rarely if ever exposing the dentin. 

PALEOPATHOLOGY 

Dental attrition is a well-known phenomenon 

in archeological skeletons. Because of its association with biological aging, the degree of wear has 

been used as a method for estimating the age of 

the skeleton (e.g., Brothwell 1965a:69). Brothwell 

notes (1965a:68) that methods of aging based on 

attrition and developed for one population cannot be applied to a population where the conditions contributing to wear are different. 

The severity of attrition is much greater in 

archeological skeletons than most modern skeletons (Pindborg, 1970:296). Mehta and Evans 

(1966:254) studied attrition in archeological skeletons from Arkansas, USA. A majority of teeth 

had dentin exposure (62 percent). This finding is 

similar to attrition among modern primitive 

groups, such as the Australian Aborigines. 

Three archeological cases illustrate the essential 

features of dental attrition. The first case illustrates extensive attrition with secondary dentin 

formation but no pulp cavity exposure (Figure 

762). The specimen is the mandible of an adult 

male from an archeological site in South Dakota, 

USA (NMNH 325360). The third molars apparently did not develop. The left central incisor and 

second premolar are missing postmortem. 

A rather unusual pattern of attrition occurs on 

the mandibular central incisors of an adult female 

skull from an archeological site in New Mexico, 

USA (NMNH 262915). While attrition has exposed secondary dentin in the maxillary and 

mandibular incisors, the lower central incisors are 

beveled anteriorly (Figure 763). This type of wear 
NUMBER 28 455 

FIGURE 762.—Marked dental attrition and secondary dentin 

formation (arrows). Note large darkened area of secondary 

dentin in the center of the crowns of the first molars. 

(Specimen from an archeological site in South Dakota, USA, 

NMNH 325360.) 

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FIGURE 763.—Angular attrition of the mandibular central 

incisors, probably due to wear from causes other than chewing food. (Adult female, Pueblo Indian, New Mexico, USA, 

NMNH 262915.) 

is suggestive of attrition due to the use of teeth 

for purposes other than chewing food. 

Marked antemortem tooth loss, severe attrition 

complicated by pulp cavity exposure and periapical abscesses are seen in the dentition of an 

adult male skull from the pre-Columbian site at 

Puye, New Mexico (NMNH 262957). On the 

maxilla the incisors and canines are present but 

badly worn. The incisors have exposed secondary 

dentin and the canines have wear exposing the 

pulp cavity on the left. There is carious destruction of the crown of the right canine. There is a 

periapical abscess associated with the left canine. 

The remaining teeth are missing antemortem 

with considerable alveolar resorption. On the 

mandible the central incisors are missing antemortem as apparently are the third molars. The 

remaining incisor crowns are worn away with 

exposure of secondary dentin. The canine crowns 

are almost worn away. There is pulp exposure of 

the left lateral incisor and left canine with a 

periapical abscess associated with both teeth (Figure 764). The crown ofthe left first premolar has 

been destroyed by caries. 

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FIGURE 764.—Severe attrition of the mandibular incisors 

and canines with exposure of secondary dentin. The pulp 

cavities of the left lateral incisor and left canine are exposed; 

both teeth have a periapical abscess. (Adult male from the 

archeological site of Puye, New Mexico, NMNH 262957.) 
456 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOG Y 

Dental Discoloration 

PATHOLOGY 

Discoloration may occur in dental tissue during 

formation of the teeth or after the teeth have 

erupted. It may affect otherwise normal teeth or 

teeth with defective enamel and/or dentin. Some 

of the conditions that result in discoloration in 

modern cases are the effect of dental or medical 

intervention and are of no significance in archeological skeletons. Conditions that can result in 

color changes of teeth and that might be seen in 

archeological specimens include: fluorosis, congenital heart disease, erythroblastosis fetalis, neonatal hepatitis, congenital defects ofthe bile duct, 

porphyria, hemorrhage or necrosis of the pulp, 

the use of tobacco, and betel (Pindborg, 1970: 

212, 221). A summary of pattern and color 

changes is presented in Table 14. 

TABLE 14.—Abnormal conditions resulting in discoloration 

of the teeth, with typical pattern and color change (based 

primarily on Pindborg, 1970:211-224) 

Cause of 

discoloration 

Fluorosis 

Congenital heart 

disease 

Erythroblastosis 

fetalis 

Neonatal hepatitis 

Congenital defect 

of bile duct 

Porphyria 

Hemorrhage or 

necrosis of pulp 

Tobacco 

Betel 

Pattern 

Mottled 

Diffuse 

Diffuse 

Diffuse 

Diffuse 

Striated 

Diffuse 

Diffuse 

Diffuse 

Color 

Yellow to brown 

Bluish white 

Green to yellow, brown 

or gray 

Yellowish brown 

Green (particularly 

the roots) 

Pinkish brown (roots 

indigo) 

Light brown to gray 

Brown 

Dark brown (occlusal 

surface and roots tend 

not to be affected) 

PALEOPATHOLOGY 

Discolorations of teeth and their pathological 

implications have received little attention in the 

literature on paleopathology. With the exception 

of staining from betel chewing, I am unable to 

provide examples of paleopathological specimens 

FIGURE 765.—Dental discoloration ofthe crowns from chewing betel nut; roots and occlusal surfaces tend not to be 

affected. (Adult male from Malay Archipelago, NMN H 

225052.) 

that illustrate these conditions. Hopefully the 

brief review above will call attention to the potential of observing teeth for color changes as a 

supplemental diagnostic feature. 

The example of discoloration from chewing 

betel nut or intentional staining with blackened 

coconut oil is seen in a skull and mandible of an 

adult male from the Malay Archipelago (NMNH 

225052). The specimen was collected in the late 

nineteenth century and little is known about the 

cultural association. Accession records indicate 

the tribal association is the Buginese (Boeginees). 

Some of the teeth are missing postmortem. Those 

that remain show little evidence of wear or caries. 

There has been some alveolar resorption suggestive of periodontal disease. The maxillary right 

central incisor has an unusual wear pattern on 

the buccal side suggestive of intentional filing. 

Staining has resulted in a dark brown color of all 

crown surfaces (Figure 765) except most of the 

occlusal surfaces. An exception to this is the maxillary right third molar. However, the opposing 

molar on the mandible had not erupted indicating that the lack of staining on the occlusal 

surface was due to chewing. This conclusion is 

supported by the presence of slight staining deep 

in the crevices of the premolars and molars. 
Literature Cited 

Abbot, K. H., and C. B. Courville 

1939. Historical Notes on the Meningiomas, I: A Study 

of Hyperostoses in Prehistoric Skulls. Bulletin ofthe 

Los Angeles Neurological Society, 4:101-113. 

Acsadi, Gy., and J. Nemeskeri 

1970. History of Human Life Span and Mortality. Budapest: 

Akademiai Kiado. 

Adelstein, L. J., and C. B. Courville 

1933. Traumatic Osteomyelitis of the Cranial Vault 

(with Particular Reference to Pathogenesis and 

Treatment). Archives of Surgery, 26:539-569. 

Adis-Castro, E., and G. Neumann 

1948. The Incidence of Ear Exostosis in the Hopewell 

People of Illinois Valley. The Proceedings of Indiana 

Academy of Science, 57:33-36. 

Aegerter, E., and J. A. Kirkpatrick, Jr. 

1968. Orthopedic Diseases. Third edition. Philadelphia: 

W. B. Saunders Company. 

1975. Orthopedic Diseases. Fourth edition. Philadelphia: 

W. B. Saunders Company. 

Ahern, R. T. 

1958. Tuberculosis of the Femoral Neck and Greater 

Trochanter. yoMTTaa/ of Bone and Joint Surgery, 40B: 

406-419. 

Ahlquist, J., and O. Damsten 

1969. A Modification of Kerley's Method for the Microscopic Determination of Age in Human Bone. 

Journal of Forensic Sciences, 14:205-212. 

Aksoy, M., N. Qamli, and S. Erdem 

1966. Roentgenographic Bone Changes in Chronic Iron 

Deficiency Anemia. Blood, 27:677-685. 

Albright, F., A. M. Butler, A. O. Hampton, and P. Smith 

1937. Syndrome Characterized by Osteitis Fibrosa Disseminata, Areas of Pigmentation and Endocrine 

Dysfunction, with Precocious Puberty in Females. 

New England Journal of Medicine, 216:727-746. 

Aldred,C. 

1964. A Possible Case of Amputation. Man, 64:56. 

Alexandersen, V. 

1967. The Pathology of the Jaws and the Temporomandibular Joint. In D. R. Brothwell and A. T. Sandison, editors, Diseases in Antiquity: A Survey of the 

Diseases, Injuries and Surgery of Early Populations, 

pages 551-595. Springfield, Illinois: Charles C. 

Thomas. 

Alfer, C. L. 

1892. Die Haiufigkeit der Knochen und Gelenktuberkulose in Beziehung auf Alter, Geschlecht, Stand 

und Erblichkeit. Beitraege zur Klinischen Chirurgie, 

8:277-290. 

Allison, M. J., E. Gerszten, R. Sotil, and A. Pezzia 

1976. Primary Generalized Hyperostosis in Ancient 

Peru. Medical College of Virginia (^arterly, 12:49-51. 

Allison, M. ]., D. Mendoza, and A. Pezzia 

1973. Documentation of a Case of Tuberculosis in PreColumbian America. American Review of Respiratory 

Disease, 107:985-991. 

Altner, P. C , and R. R. Turner 

1970. Sporotrichosis of Bones and Joints: Review of the 

Literature and Report of Six Cases. Clinical Orthopedics, 68:138-148. 

Alvik, J. 

1949. Tuberculosis of the Greater Trochanter. Acta Orthopedica Scandinavica, 19:247-262. 

Amprino, R., and A. Bairati 

1936. Processi di Ricostruzione e di Reassorbimento 

nella Sostanza Compatta delle Ossa dell'Uomo. 

Zeitschrift fiir Zellforschung und Mikroskopische Anatomie, 24:439-511. 

Amprino, R., and A. Engstrom 

1952. Studies on X-ray Absorption and Diffraction of 

Bone Tissue. Acta Anatomica, 15:1-22. 

Andersen, J. G. 

1969. Studies in the Mediaeval Diagnosis of Leprosy in Denmark. Copenhagen: Costers Bogtrykkeri. 

Angel, J. L. 

1964. Osteoporosis: Thalassemia? American Journal of 

Physical Antrhopology, 22:369-374. 

1966. Porotic Hypertostosis, Anemias, Malarias and 

Marshes in the Prehistoric Eastern Mediterranean. 

Science, 153:760-763. 

1969a. The Bases of Paleodemography. American Journal of 

Physical Anthropology, 30:427-437. 

1969b. Paleodemography and Evolution. American Journal 

of Physical Anthropology, 31:343-353. 

1971. The People of Lerna: Analysis of a Prehistoric Aegean 

Population. Princeton and Washington: American 

School of Classical Studies at Athens and Smithsonian Institution Press. 

1974a. Patterns of Fracture from Neolithic to Modern 

Times. Anthropologiai KHzlemenyek, 18:9-18. 

1974b. The Cultural Ecology of General Versus Dental 

Health. In W. Bernhard and A. Kandler, editors, 

Bevolkerungsbiologie: Beitrdge zur Strucktur und Dynamik 

Menschlicher Populationen in Anthropologischer Sichl, 

pages 382-392. Stuttgart: G. Fischer. 

Angulo, A., and L. Pollak 

1971. Paracoccidioidomycosis. In R. D. Baker, editor, 

Human Infection with Fungi, Actinomycetes and Algae, 

pages 507-576. New York: Springer-Verlag. 

457 
458 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

Ansell, B. M., and E. G. L. Bywaters 

1963. Rheumatoid Arthritis (Still's Disease). Pediatric 

Climes of North America, 10:921-940. 

Arkin, A. M., and A. J. Schein 

1948. Aseptic Necrosis in Gaucher's Disease. Journal of 

Bone and Joint Surgery, 30A:631-641. 

Armelagos, G. J. 

1969. Disease in Ancient Nubia. Science, 163:255-259. 

Ascenzi, A., and V. Marinozzi 

1958. Sur le Crane en Bosse au Cours des Polyglobulie 

Secondaires a I'Hypoxemie Chronique. Acta Haematologica, 19:253-262. 

Aschoff, L., and W. Koch 

1919. Skorbul: Eine Pathologisch-Analomische Studie. Jena: 

G. Fischer. 

Askanazy, M., and E. Rutishauser 

1933. Die Knochen der Basedow-Kranken: Beitrag zur 

latenten Osteodystrophia Fibrosa. Virchows Archiv 

fiir Pathologische Anatomic, 291:653-681. 

Asling, C. W., and H. M. Evans 

1956. Anterior Pituitary Regulation of Skeletal Development. In C. Bourne, editor, The Biochemistry and 

Physiology of Bone, pages 671-701. New York: Academic Press. 

Avila, R., D. G. Pugh, C. H. Slocumb, and R. K. Winkelmann 

1960. Psoriatic Arthritis: A Roentgenologic Study. Radiology, 75:691-702. 

Axhausen, G. 

1913. Beitrage zur Knochen- und Gelenksyphilis. Klinische Wochenschrift, 50:2361-2369. 

Bailleul, L. 

1911. Des Oste'ites Tuberculeuses des Petils Os Longs de la 

Main et du Pied (Spina-Ventosa). Faculte De Medicine de Paris: These pour le Doctorat en Medecine. 

Paris: G. Steinheil. 

Baker, D. H. 

1964. Roentgen Manifestations of Cooley's Anemia. Annals of the New York Academy of Sciences, 119:641-

661. 

Baker, R. D. 

1971. Mucormycosis. In R. D. Baker, editor. Human Infections with Fungi, Actinomycetes and Algae, pages 

832-918. New York: Springer-Verlag. 

Baracz, R. V. 

1902. Ueber die Aktinomykose des Menschen auf Grund 

eigener Beobachtungen. Archiv fiir Klinische Chirurgie, 68:1050-1133. 

Baranoff, A. F. 

1934. Incidence of Osteomyelitis of Jaw Bones among 

Chinese. Chinese Medical Journal, 48:638. 

Barclay-Smith, E. 

1911. Multiple Anomaly in a Vertebral Co\umn. Journal 

of Anatomy and Physiology, 45:144-171. 

Barlow, T. 

1883. On Cases Described as "Acute Rickets" Which 

Are Probably a Combination of Scurvy and Rickets, the Scurvy Being an Essential, and the Rickets 

a Variable, Element. Medico-Chirurgical Transactions, 66:159-219. 

Bartels, P. 

1907. Tuberkulose in der Jvingeren Steinzeit. Archiv fir 

Anthropologic, 6:243-255. 

Bass, W. M., J. B. Gregg, and P. E. Provost 

1974. Ankylosing Spondylitis (Marie-Striimpell Disease) 

in Historic and Prehistoric Northern Plains Indians. Plains Anthropologist, 19:303-305. 

Batson, O. V. 

1940. The Function of the Vertebral Veins and Their 

Role in the Spread of Metastases. Annals of Surgery, 

112:138-149. 

Baudouin, M. 

1906. La Prehistoire de la Luxation Congenitale de la 

Hanche. Homme Prehistorique, 7:129-139. 

1923. L'Extraction Dentaire Prehistorique de Nature 

Cultuelle. Se'maine Dentaire, 5:154. 

Behn, F. 

1938. Echinokokken, Statistik des Pathologischen Instituts der Universitaet Concepcion (Chile) mit besonderer Beriicksichtigung eines Falles von todlicher Piablutung durch Echinococcus hydatidosus (VIII: Beitrag zur geographischen Pathologie 

Chiles). Frankfurter Zeitschrift fur Pathologie, 51:535-

538. 

Beitzke, H. 

1934a. Erworbene Syphilis der Knochen. In O. Lubarsch, 

F. Henke, and R. Rossle, editors, Handbuch der 

Speziellen Pathologischen Anatomic und Histologic, 9(2): 

468-538. Berlin: J. Springer. 

1934b. Aktinomykose der Knochen und Gelenke. In O. 

Lubarsch, F. Henke, and R. Rossle, editors, Handbuch der Speziellen Pathologischen Anatomie und Histologic, 9(2):539-567. Berlin: J. Springer. 

1934c. Rotz der Knochen und Gelenke. In O. Lubarsch, 

F. Henke, and R. Rossle, editors, Handbuch der 

Speziellen Pathologischen Anatomie und Histologic, 9(2): 

589 593. Berlin: J. Springer. 

1934d. Erkrankungen der Knochen und Gelenke bei Lepra. In O. Lubarsch, F. Henke, and R. Rossle, 

editors, Handbuch der Speziellen Pathologischen Anatomic und Histologic, 9(2):594-611. Berlin: J. Springer. 

1934e. Seltene Mykosen der Knochen und Gelenke. In O. 

Lubarsch, F. Henke, and R. Rossle, editors, Handbuch der Speziellen Pathologischen Anatomie und Histologic, 9(2):pages 612-634. Berlin: J. Springer. 

Beninde 

1920. Die Verbreitung der durch die Hungerblockade 

hervorgerufenen Knochenerkrankungen unter der 
NUMBER 28 459 

Bevdikerung Preussens (Rachitis, Spatrachitis, Osteomalacic). Veroffentlichungen aus dem Gebiete der 

Medizin- Verwaltung, 10:121-131. 

Bennett, G. A., H. Waine, and W. Bauer 

1942. Changes in the Knee Joint at Various Ages. New York: 

Commonwealth Fund. 

Bennett, K. A. 

1967. Craniostenosis: A Review of the Etiology and a 

Report of New Cases. American Journal of Physical 

Anthropology, 27:1-9. 

Beraud, C , P. Morel, and A. Boyer 

1961. Osteome Geant Fronto-Ethmoidal Decouvert sur 

un Crane Medieval du Var. Journal de Radiologic 

d'Electrologie et de Medecine Nucleaire, 42:45-47. 

Berndorfer, A. 

1962. A 500-Year-Old Skull with Cleft Lip. British Journal of Plastic Surgery, 15:123-128. 

Binford, Chapman 

1965. Response to Lecture by V. M0ller-Christensen. 

International Journal of Leprosy, 33:611. 

Birsner, J. W., and S. Smart 

1956. Osseous Coccidioidomycosis: A Chronic Form of 

Dissemination. American Journal of Roentgenology, Radium Therapy, and Nuclear Medicine, 76:1052-1060. 

Blankoff, B. 

1927. Osteite Tuberculeuse Primitive de la Tuberosite 

d'Ischion. Archive Franco-Beige de Chirurgie, 30:895-

896. 

Bleyer, A. 

1940. The Antiquity of Achondroplasia. Annals of Medical 

History, 2:306-307. 

Bloch, I. 

1901. Der Ursprung der Syphilis. Volume 1. Jena: G. 

Fischer. 

1908. The History of Syphilis. In D. Power and J. K. 

Murphy, editors, A System of Syphilis, 1:1-40. London: Oxford University Press. 

1911. Der Ursprung der Syphilis. Volume 2, pages 317-364. 

Jena: G. Fischer. 

Blum T. 

1924. Osteomyelitis ofthe Mandible and Maxilla, yowrnal of the American Dental Association, 2:802-805. 

Blumberg, J. M., and E. R. Kerley 

1966. A Critical Consideration of Roentgenology and 

Microscopy in Paleopathology. In S. Jarcho, editor. Human Palaeopathology, pages 150-170. New 

Haven: Yale University Press. 

Boecker, A. 

1868. Zur Statistik der Echinococcen. Inaugural dissertation. 

University of Berlin. 

Bogue, D. 

1969. Principles of Demography. New York: J. C. Wiley and 

Sons, Inc. 

Bohler, L. 

1935. The Treatment of Fractures. Fourth English edition. 

translated by E. W. H. Groves. Bristol, England: 

J. Wright and Sons Ltd. 

Boswell, W. L. 

1959. Roentgen Aspects of Blastomycosis. American Journal of Roentgenology, Radium Therapy, and Nuclear 

Medicine, 81:224-230. 

Bourke, J. B. 

1967. A Review of the Palaeopathology of the Arthritic 

Diseases. In D. R. Brothwell and A. T. Sandison, 

editors. Diseases in Antiquity: A Survey of the Diseases, 

Injuries and Surgery of Early Populations, pages 352-

370. Springfield, Illinois: Charles C. Thomas. 

Bouvier, M., and D. H. Ubelaker 

1977. A Comparison of Two Methods for the Microscopic Determination of Age at Death. American 

Journal of Physical Anthropology, 46:391-394. 

Brenner, G., and R. P. Allen 

1963. Skeletal Changes in Erythroblastosis Foetalis. Radiology, 80:427-429. 

Breus, C , and A. Kolisko 

1900-1911. Die Pathologischen Beckenformen. 3 volumes. 

Leipzig and Wien: F. Deuticke. 

Broca, P. 

1875. Sur les Trous Parietaux et sur la Perforation Congenitale Double et Symetrique des Parietaux. Bulletins de la Socie'te d'Anthropologic de Paris, 10:326-

336. 

1876. Sur I'Age des Sujets a la Trepanation Chirurgicale 

Neolithique. Bulletins de la Socie'te d'Anthropologie de 

Pans, 11:572. 

Brooks, S. T., and W. D. Hohenthal 

1963. Archaeological Defective Palate Crania from California. American Journal of Physical Anthropology, 21: 

25-32. 

Brooks, S. T., and J. Melbye 

1967. Skeletal Lesions Suggestive of Pre-Columbian 

Multiple Myeloma in a Burial from the Kane 

Mounds, Near St. Louis, Missouri. In W. D. Wade, 

editor. Miscellaneous Papers in Paleopathology, I, pages 

23-29. Flagstaff Museum of Northern Arizona. 

Brothwell, D. R. 

1958. Evidence of Leprosy in British Archaeological Material. Medical History, 2:287-291. 

1961. The Paleopathology of Early British Man: An 

Essay on the Problem of Diagnosis and Analysis. 

Journal of the Royal Anthropological Institute, 91:318-

344. 

1963. The Macroscopic Dental Pathology of Some Earlier Human Populations. In D. R. Brothwell, editor. Dental Anthropology, pages 271-288. Oxford: 

Pergamon Press. 

1965a. Digging Up Bones. London: Trustees ofthe British 

Museum (Natural History). 

1965b. The Palaeopathology ofthe E.B.-M.B. and Middle Bronze Age Remains from Jericho (1957-1958 
460 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

Excavations). In K. M. Kenyon, editor, Excavations 

at Jericho, 2:685-693. London: British School of 

Archeology in Jerusalem. 

1967a. The Evidence for Neoplasms. In D. R. Brothwell 

and A. T. Sandison, editors. Diseases in Antiquity: A 

Survey of the Diseases, Injuries and Surgery of Early 

Populations, pages 320-345. Springfield, Illinois: 

Charles C. Thomas. 

1967b. Major Congenital Anomalies ofthe Skeleton: Evidence from Earlier Populations. In D. R. Brothwell and A. T. Sandison, editors. Diseases in Antiquity: A Survey of the Diseases, Injuries and Surgery of 

Early Populations, pages 423-446. Springfield, Illinois: Charles C. Thomas. 

Brothwell, D. R., and M0ller-Christensen 

1963a. Medico-Historical Aspects of a Very Early Case of 

Mutilation. Danish Medical Bulletin, 10:21-25. 

1963b. A Possible Case of Amputation, Dated to Circa 

2000 B.C. Afan, 63:192-194. 

Brothwell, D. R., and .A. T. Sandison, editors. 

1967. Diseases in Antiquity: A Survey of the Diseases, Injuries 

and Surgery of Early Populations. Springfield, Illinois: 

Charles C. Thomas. 

Brown, J. S., and J. H. Middlemiss 

1956. Bone Changes in Tropical Ulcer. British Journal of 

Radiology, 29:213-217. 

Browne, S. G. 

1970. How Old Is Leprosy? British Medical Journal, 3: 

640-641. 

Briihl, G. 

1880. On the Pre-Columbian Existence of Syphilis. Cincinnati Lancet Clinic, 43:487-493. 

Brutzer, C. 

1898. Sectionsbefunde aus dem Leprosorium zu Riga. 

St. Petersburger Medicinsche Wochenschrift, 15:363-

367. 

Buhr, A. J., and A. M. Cooke 

1959. Fracture Patterns. The Lancet, 1:531-536. 

Buikstra, J. E. 

1976. The Caribou Eskimo: General and Specific Disease. American Journal of Physical Anthropology, 45: 

351-368. 

Bunim, J. J., T. A. Burch, and W. M. O'Brien 

1964. Influence of Genetic and Environmental Factors 

on the Occurrence of Rheumatoid Arthritis and 

Rheumatoid Factor in American Indians. Bulletin 

on Rheumatic Diseases, 15:349-350. 

Burkhardt, L. 

1970. Pathologische Anatomie des Schadels. In O. Lubarsch, F. Henke, R. Rossle and E. Uehlinger, 

editors, Handbuch der Speziellen Pathologischen Anatomie und Histologic, 9(7): 1-352. Berlin: J. Springer. 

Burko, H., H. Z. Millins, and J. Watson 

1961. Skull Changes in Iron Deficiency Anemia Simulating Congenital Hemolytic Anemia. American 

Journal of Roentgenology, Radium Therapy, and Nuclear 

Medicine, 86:447-452. 

Caffey, J. 

1937. The Skeletal Changes in the Chronic Hemolytic 

Anemias (Erythroblastic Anemia, Sickle Cell Anemia and Chronic Hemolytic Icterus). American Journal of Roentgenology and Radium Therapy, 37:293-324. 

1939. Changes in the Growing Skeleton after the Administration of Bismuth. Syphilis of the Skeleton 

in Early Infancy: The Non-Specificity of Many of 

the Roentgenographic Changes. American Journal of 

Roentgenology and Radium Therapy, 42:637-655. 

1951. Gargoylism (Hunter-Hurler Disease, Dysostosis 

Multiplex, Lipochondrodystrophy): Prenatal and 

Neonatal Bone Lesions and Their Early Postnatal 

Evolution. Bulletin of the Hospital of Joint Diseases, 

12:38-66. 

1952. Gargoylism (Hunter-Hurler Disease, Dysostosis 

Multiplex, Lipochondrodystrophy): Prenatal and 

Neonatal Lesions and Their Early Postnatal Evolution. American Journal of Roentgenology, Radium 

Therapy, and Nuclear Medicine, 67:715-731. 

1955. On Fibrous Defects in Cortical Walls of Growing 

Tubular Bones. Advances in Pediatrics, 7:13-51. 

1957a. Cooley's Anemia: A Review of the Roentgenographic Findings in the Skeleton. American Journal 

of Roentgenology, Radium Therapy, and Nuclear Medicine, 78:381-391. 

1957b. Infantile Cortical Hyperostosis: A Review of the 

Clinical and Radiographic Features. Proceedings of 

the Royal Society of Medicine, 50:347-354. 

1972. Pediatric X-ray Diagnosis. Sixth edition, volumes 1 

and 2. Chicago: The Year Books Publishers. 

Caffey, J., and W. A. Silverman 

1945. Infantile Cortical Hyperostosis: Preliminary Report on a New Syndrome. American Journal of Roentgenology and Radium Therapy, 54:1-16. 

Camp, J. D., and L. A. Nash 

1944. Developmental Thinness of the Parietal Bones. 

Radiology, 42:42-47. 

Carter, R. A. 

1934. Infectious Granulomas of Bones and Joints, with 

Special Reference to Coccidioidal Granuloma. Radiology, 23:1-16. 

Cassidy, C. M. 

1974. Determination of Nutritional and Health Status 

in Skeletal Populations, the Use of MuKiple Techniques for Data Analysis (abstract). American Journal of Physical Anthropology, 41:472. 

Catlin, G. 

1844. Letters and Notes on the Manners, Customs, and Condition 

ofthe North American Indians. Fourth edition, volume 

1. London: D. Bogue. 
NUMBER 28 461 

Chalmers, J., and K. C. Ho 

1970. Geographical Variations in Senile Osteoporosis: 

The Association with Physical Activity. Journal of 

Bone and Joint Surgery, 52B:667-675. 

Chapman, F. H. 

1965. Comparison of Osteoarthritis in Three Aboriginal 

Populations. Proceedings of the Indiana Academy of 

Science for 1964, 74:84-86. 

Chester, W. 

1930-1931. Uber Lipogranulomatose. Virchow's Archiv fiir 

Pathologische Anatomie und Physiologie, 279:561-602. 

Cheyne, W. W. 

1911. Tuberculous Diseases of Bone and Joints: Their Pathology, 

Symptoms and Treatment. (Oxford Medical Publications.) London: H. Frowde, Oxford University 

Press. 

Chiari, H. 

1931. Die generalisierte Xanthomatose vom Typus 

Schiiller-Christian. Ergebnisse der allgemeinen Pathologie und Pathologischen Anatomie, 24:396-450. 

Chick, E. W. 

1971. North American Blastomycosis. In R. D. Baker, 

editor. Human Infections with Fungi, Actinomycetes and 

Algae, pages 465-506. New York: Springer-Verlag. 

Chung, S. M. K., and E. L. Ralston 

1969. Necrosis of the Femoral Head Associated with 

Sickle Cell Anemia and Its Genetic Variants: A 

Review of the Literature and Study of Thirteen 

Cases. Journal of Bone and Joint Surgery, 51 A: 33-58. 

Claffey, T. J. 

1960. Avascular Necrosis ofthe Femoral Head: An Anatomical Study. Journal of Bone and Joint Surgery, 

428:802-809. 

Cochrane, R. G. 

1964. The History of Leprosy and Its Spread throughout 

the World. In R. G. Cochrane and T. F. Davey, 

editors. Leprosy in Theory and Practice. Second edition, pages 1-12. Bristol, England: J. Wright and 

Sons Ltd. 

Cockburn, T. A. 

1961. The Origin of the Treponematoses. Bulletin of the 

World Health Organization, 24:221-228. 

Cockshott, P., and M. MacGregor 

1958. Osteomyelitis Variolosa. Quarterly Journal of Medicine, 27:369-387. 

1959. The Natural History of Osteomyelitis Variolosa. 

The Journal of the Faculty of Radiologists, London, 10: 

57-63. 

Cockshott, W. P. 

1958. Haemoglobin SC Disease. Journal of the Faculty of 

Radiologists, London, 9:211-216. 

Cockshott, W. P., and A. O. Lucas 

1964. Radiological Findings in Histoplasma Duboisii 

Infections. British Journal of Radiology, 37:653-660. 

Collins, D. H. 

1966. Pathology of Bone. London: Butterworths. 

Collins, V. P. 

1950. Bone Involvement in Cryptococcosis (Torulosis). 

American Journal of Roentgenology and Radium Therapy, 

63:102-112. 

Comas, J. 

1965. Cranes Mexicaines Scaphocephales. L'Anthropologie, 69:213-301. 

Cook, D. C , and J. E. Buikstra 

1979. Health and Differential Survival in Prehistoric 

Populations: Pre-Natal Dental Defects (abstract). 

American Journal of Physical Anthropology, 50:429-430. 

Cook, S. F. 

1960. Dating Prehistoric Bone by Chemical Analysis. In 

R. F. Heizer and S. F. Cook, editors. The Application of Quantitative Methods in Archaeology. 

Viking Fund Publications in Anthropology, 28:223-239. 

Cooney, J. P., and E. H. Crosby 

1944. Absorptive Bone Changes in Leprosy. Radiology, 

42:14-19. 

Copeland, M. M. 

1931. Bone Metastasis: A Study of 334 Cases. Radiology, 

16:198-210. 

Courville, C. B. 

1967. Cranial Injuries in Prehistoric Man. In D. R. 

Brothwell and A. T. Sandison, editors, Diseases in 

Antiquity: A Survey ofthe Diseases, Injuries and Surgery 

of Early Populations, pages 606-622. Springfield, 

Illinois: Charles C. Thomas. 

Cressman, L. S., and O. Larsell 

1945. A Case of Probable Osteomylitis in an Indian 

Skeleton. Western Journal of Surgery, Obstetrics and 

Gynecology, 53:332-335. 

Crocker, A. C , and S. Farber 

1958. Niemann-Pick Disease: A Review of Eighteen Patients. Medicine, 37:1-95. 

Crosby, A. W. 

1969. The Early History of Syphilis: A Reappraisal. 

American Anthropologist, 71:218-227. 

Cruess, R. L., and J. Dumont 

1975. Healing of Bone, Tendon, and Ligament. In C. A. 

Rockwood and D. P. Green, editors, Fractures, 

pages 97-118. Philadelphia: J. B. Lippincott Company. 

Cule, J., and I. L. Evans. 

1968. Porotic Hyperostosis and the Gelligaer Skull./ournal of Clinical Pathology, 21:753-758. 

Currarino, G., and M. E. Erlandson 

1964. Premature Fusion of Epiphyses in Cooley's Anemia. Radiology, 83:656-664. 

Currarino, G., E.B.D. Neuhauser, G. C. Reyersbach, and 

E. H. Sobel 

1957. Hypophosphatasia. American Journal of Roentgerwl-
462 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOG Y 

Darling 

1970. 

ogy, Radium Therapy, and Nuclear Medicine, 78:392-

419. 

Gushing, H. 

1922. The Cranial Hyperostoses Produced by Meningeal 

Endotheliomas. Archives of Neurology and Psychiatry, 

8:139-152. 

Cuvier, G. 

1820. Recherches sur les Ossements Fossiles. Volume 4. Paris: 

G. Dufour and E. d'Ocagne. 

Daland, J. 

1935. Depressed Fracture and Trephining of the Skull 

by the Incas of Peru. Annals of Medical History, 7: 

550-558. 

Dalyell, E. J., and H. Chick 

1921. Hunger-Osteomalacia in Vienna, 1920, I: Its Relation to Diet. Lancet, 2:842-849. 

A.I. 

Dental Caries. In R.J. Gorlin and H. M. Goldman, 

editors, Thoma's Oral Pathology, pages 239-307. St. 

Louis: The C. V. Mosby Company. 

Dastugue, J. 

1965. Tumeur Maxillaire sur un Crane du Moyen-Age. 

Bulletin de L'Association Franqaise pour L'Etude du 

Cancer, 52:69-72. 

David, V. C. 

1924. Tuberculosis of the Os Coccygis. Journal of the 

American Medical Association, 82:21-24. 

Davidson, J. C , and P. E. S. Palmer 

1963. Osteomyelitis Variolosa, yourna/ of Bone and Joint 

Surgery, 45B:687-693. 

Davis, J. B. 

1865. On Synostotic Crania among Aboriginal Races of 

Man. Natuurkundige Verhandelingen van de Hollandsche 

Maatschappij der Wetenschappen te Haarlem, 22:1-39. 

DeBeurmann, L., and H. Gougerot 

1912. Les Sporotrichoses. Paris: Felix Alcan. 

de La Camp 

1900. Periostitis bei Lepra. Fortschritte auf dem Gebiete der 

Roentgenstrahlen, 4:36-40. 

Dennie, C. D. 

1962. A History of Syphilis. Springfield, Illinois:Charles C. 

Thomas. 

Denninger, H. S. 

1931. Osteitis Fibrosa in Skeleton of Prehistoric American Indian. Archives of Pathology, 11:939-947. 

1933. Paleopathological Evidence of Paget's Disease. Annals of Medical History, 5:73-81. 

de Quervain, F., and C. Wegelin 

1936. Der Endemische Kretinismus. Berlin: J. Springer. 

Derry, D. E. 

1913. A Case of Hydrocephalus in an Egyptian of the 

Roman Period. Journal of Anatomy and Physiology, 

47:436-458. 

1938a. Two Skulls with Absence of Pre-Maxilla.yowrna/ of 

Anatomy and Physiology, 72:295-299. 

1938b. Pott's Disease in Ancient Egypt. Medical Press and 

Circular, 197:196-199. 

Derry, D. E., and G. Elliot-Smith 

1909. Anatomical Report, Dealing with the Work from 

November 1 to December 31, 1909. Archaeological 

Survey of Nubia Bulletin (Cairo), 5. 

DeSouza, L. J. 

1973. An Analysis of Fracture Patterns at Uganda's 

Largest Hospital. East African Medical Journal, 50: 

594-604. 

Dewey, J., G. Armelagos, and M. Bartley 

1969. Femoral Cortical Involution in Three Nubian Archaeological Populations. Human Biology, 4:1:13-28. 

Diggs, L. W. 

1967. Bone and Joint Lesions in Sickle-Cell Disease. 

Clinical Orthopedics, 52:119-143. 

Diggs, L. W., H. N. Pullian, and J. C. King 

1937. The Bone Changes in Sickle Cell Anemia. Southern 

Medical Journal, 30:249-259. 

Dingwall, E. J. 

1931. Artificial Cranial Deformation: A Contribution to the 

Study of Ethnic Mutilations. London: Bale and Danielsson. 

Doberenz, A. R., and P. Matter III. 

1965. Nitrogen Analysis of Fossil Bones. Comparative Biochemistry and Physiology, 16:253-258. 

Doebbelin 

1898. Uber Knochenechinokokken des Beckens. Deutsche 

Zeitschrift fiir Chirurgie, 48:38-40. 

Donati, M. 

1906. Uber die Acute und Subacute "Osteomyelitis Purulenta" der Wirbelsaiile. Archiv fiir Klinische Chirurgie, 79:1116-1163. 

Dubois, E. L., and L. Cozen 

1960. Avascular (Aseptic) Bone Necrosis Associated with 

Systemic Lupus Erythematosus.youma/o/'<A^ American Medical Association, 174:966-971. 

Duckworth, W.L.H. 

1912. On the Natural Repair of Fractures, as Seen in the 

Skeletons of Anthropoid Apes. Journal of Aruitomy 

and Physiology, 46:81-85. 

Dykes, J., J. K. Segesman, and J. W. Birsner 

1953. Coccidioidomycosis of Bone in Children. American 

Journal of Diseases of Children, 85:34-42. 

Dykstra, O. H., and J. Halbertsma 

1940. Polycythemia Vera in Childhood: Report of a 

Case with Changes in the Skull. American Journal of 

Diseases of Children, 60:907-916. 

Eastman Kodak Company 

1969. Radiography in Modem Industry. Third edition. Rochester: Eastman Kodak Company. 

Eastoe, J. E., P. Martens, and N. R. Thomas 

1973. The Amino-Acid Composition of Huma n Hard 

Tissue Collagens in Osteogenesis Imperfecta and 

Dentinogenesis Imperfecta. Calcified Tissue Research, 12:91-100. 
NUMBER 28 463 

Edelmann, A. 

1919. Uber Gehauftes Auftreten von Osteomalazie und 

eines Osteomalazieahnlichen Symptomenkomplexes. Wiener Klinische Wochenschrift, 32:82. 

Edington, G. M. 

1971. African Histoplasmosis. In R. D. Baker, editor. 

Human Infection with Fungi, Actinomycetes and Algae, 

pages 131-138. New York: Springer-Verlag. 

Eiseley, L. C , and C. W. Asling 

1944. An Extreme Case of Scaphocephaly from a 

Mound Burial near Troy, Kansas. Transactions of 

the Kansas Academy of Science, 47:241-255. 

Elliot-Smith, G. 

1908. The Most Ancient Splints. British Medical Journal, 

1:732-734. 

1912. The Royal Mummies. Catalogue General des Antiquites Egyptiennes du Musee du Caire, 59 (61051-

61100). 

Elliot-Smith, G., and W. R. Dawson 

1924. Egyptian Mummies. New York: The Dial Press Incorporated. 

Elliot-Smith, G., and M. A. Ruffer 

1910. Pottsche Krankheit an einer Agyptischen Mumie 

aus der Zeit der 21. Dynastie (um 1000 v. Chr.). 

In Zur Historischen Biologic der Krankheitserreger, 2:9-

16. 

Elliot-Smith, G., and F. Wood-Jones 

1910. The Archaeological Survey of Nubia Report for 1907-

1908, Volume II: Report on the Human Remains. Cairo: 

National Printing Department. 

El-Najjar, M. Y., B. Lozoff, and D. J. Ryan 

1975. The Paleoepidemiology of Porotic Hyperostosis in 

the American Southwest: Radiological and Ecological Considerations. The American Journal of 

Roentgenology, Radium Therapy, and Nuclear Medicine, 

125:918-924. 

Emmons, C. W., C. H. Binford, and J. P. Utz 

1970. Medical Mycology. Second edition. Philadelphia: 

Lea and Febiger. 

Eng, L. L. 

1958. Chronic Iron Deficiency Anemia with Bone 

Changes Resembling Cooley's Anemia. Acta Haematologica, 19:263-268. 

Enlow, D. H. 

1963. Principles of Bone Remodeling. Springfield, Illinois: 

Charles C. Thomas. 

Epstein, B. S. 

1953. The Concurrence of Parietal Thinness with Postmenopausal, Senile or Idiopathic Osteoporosis. 

Radiology, 60:29-35. 

Epstein, H. C. 

1973. Traumatic Dislocations of the Hip. Clinical Orthopaedics, 92:\\6-\\2. 

Erdheim, J. 

1916. Nanosomia Pituitaria. Beitrdge zur Pathologischen 

Anatomie und zur Allgemeinen Pathologie, 62:302-377. 

1931a. Uber Wirbelsaulenveranderungen bei Akromegalie. Virchow's Archiv fiir Pathologische Anatomie und 

Klinische Medizin, 281:197-296. 

1931b. Die Lebensvorgdnge im Normalen Knorpel und Seine 

Wucherung bei Akromegalie, Pathologie und Klinik in 

Einzeldarstellungen. Wien: J. Springer. 

1932. Uber Tuberkulose des Knochens im Allgemeinen 

und die des Schaedeldaches im Besonderen. Virchow 's Archiv fiir Pathologische Anatomie und Physiologie 

und fur Klinische Medizin, 283:354-412. 

1935. Uber die Genese der Paget' schen Knochenerkrankung. Beitrdge zur Pathologischen Anatomie und Allgemeinen Pathologie, 96:1-60. 

Ericksen, M. F. 

1976. Cortical Bone Lost with Age in Three Native 

American Populations. American Journal of Physical 

Anthropology, 45:443-452. 

Escherich, T. 

1899. Rickets. In Comptes Rendus du XII. Congress Internationale de Medicine, Moscow, 1899, 3 (6). [Cited on 

page 48 in A. F. Hess, Rickets Including Osteomalacia 

and Tetany. Philadelphia: Lea and Febiger, 1929.] 

Esguerra-Gomez, G., and E. Acosta 

1948. Bone and Joint Lesions in Leprosy. Radiology, 50: 

619-631. 

Esper, J. F. 

1774. Ausfiihrliche Nachricht von Neuentdeckten Zoolithen, Unbekannter Vierfussiger Thiere, und denen sie Enthaltenden, 

so wie Verschiedenen Andern Denkwiirdigen Griiften der 

Obergebiirgischen Lande des Marggrafthums Bayreuth. 

Niirnberg. 

Faget, G. H., and A. Mayoral 

1944. Bone Changes in Leprosy: A Clinical and Roentgenologic Study of 505 Cases. Radiology, 42:1-13. 

Fares, G., and A. Pagani 

1966. La Osteite Tubercolare del Pube. Minerva Ortopedica, 17:459-469. 

Ferembach, D. 

1963. Frequency of Spina Bifida Occulta in Prehistoric 

Human Skeletons. Nature, 199:100-101. 

Fisher, A. K. 

1935. Additional Paleopathological Evidence of Paget's 

Disease. Annals of Medical History, 1:197-198. 

Flemming M0ller, P., and Sk. V. Gudjonsson 

1932. Massive Fluorosis of Bones and Ligaments. Acta 

Radiologica, 13:269-294. 

Follis, Jr., R. H. 

1943. Effect of Mechanical Force on the Skeletal Lesions 

in Acute Scurvy in Guinea Pigs. Archives of Pathology, 35:579-582. 

1948. The Pathology of Nutritional Disease. Springfield, Illinois: Charles C. Thomas. 

Follis, Jr., R. H., D. Jackson, and W. H. Carnes 

1942. Skeletal Changes Associated with Erythroblastosis 

Fetalis. yo!/rna/ of Pediatrics, 21:80-92. 
464 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

Follis, Jr., R. H., D. A. Jackson, and E. A. Park 

1940. The Problem of the Association of Rickets and 

Scurvy. American Journal of Diseases of Children, 60: 

745-747. 

Fournier, A. 

1886. La Syphilis Hereditaire Tardive. Paris: G. Masson. 

1906. Traitede la Syphilis. Paris: F. Rueff et Cie. 

Fowke, G. 

1902. Archaeological History of Ohio. Columbus: Ohio State 

Archeological and Historical Society. 

Fraenkel, E. 

1929. Infantiler Skorbut (Moller-Barlowsche Krankheit). In O. Lubarsch and F. Henke, editors, 

Handbuch der Speziellen Pathologischen Anatomie und 

Histologic, 9(1):222-239. Berlin: J. Springer. 

Eraser, J. S., and J. P. Stewart 

1936. Tuberculous, Syphilitic and Malignant Disease of 

the Ear. In A. L. Turner, editor, Diseases ofthe Nose, 

Throat and Ear, pages 402-410. Baltimore: William 

Wood and Company. 

Freeman, L. 

1918. Primitive Surgery of the Western Hemisphere. 

Journal of the American Medical Association, 70:443-

448. 

Freund, E. 

1933. Uber Syphilis der Gelenke. Virchow's Archiv fiir 

Pathologische Anatomie und Physiologie und fur Klinische 

Medizin, 289:575-623. 

Frost, H. M. 

1958. Preparation of Thin Undecalcified Bone Sections 

by Rapid Manual Method. Stain Technology, 33: 

273-277. 

Fuste, M. 

1955. Antropologia de las Poblaciones Pirenaicas Durante el Periodo Neo-eneolitico. Instituto de Bernardino de Sahagun de Antropologia y Etnologia: Trabajos, 

14:109-135. 

Gaal, A. 

1933. Das Rontgenbild der Knochenveranderungen bei 

Essentieller Xanthomatose (Diathesis Xanthomatosa). Fortschritte auf dem Gebiete der Rontgenstrahlen 

48:292-299. 

Ganado, W., and A. J. Craig 

1958. Brucellosis Myelopathy, yourna/ of Bone and Joint 

Surgery, 40A: 1380-1387. 

Gangolphe, M. 

1894. Maladies Infeclieuses et Parasitaires des Os. Paris: G. 

Masson. 

Garn, S. M. 

1970. The Earlier Gain and the Later Loss of Cortical Bone. 

Springfield, Illinois: Charles C. Thomas. 

Garre, C. 

1893. Uber Besondere Formen und Folgezustande der 

Akuten Infektiosen Osteomyelitis. Bruns Beitrdge 

zur Klinischen Chirurgie, 10:241-298. 

Garrod, A. E. 

1890. A Treatise on Rheumatism and Rheumatoid Arthritis. 

Philadelphia: P. Balkiston. 

Ghormley, R. K., and R. S. Clegg 

1948. Bone and Joint Changes in Hemophilia, with 

Report of Cases of So-Called Hemophilic Pseudotumor, yowrwa/ of Bone and Joint Surgery, 30A:589-

630. 

Gilbert, B. M., and T. W. McKern 

1973. A Method for Aging the Female Os Pubis. American 

Journal of Physical Anthropology, 38:31-38. 

Gildenhorn, H. L., and G. D. Amromin 

1961. Report of a Case of Niemann-Pick Disease: Correlation of Roentgenographic and Autopsy Findings. American Journal of Roentgenology, Radium Therapy, and Nuclear Medicine, 85:680-684. 

Giles, E., and O. Elliot 

1962. Race Identification from Cranial Measurements. 

Journal of Forensic Sciences, 7:147-157. 

Girdlestone, G. R. 

1965. Tuberculosis of Bone and Joint. Third edition, revised 

by E. W. Somerville and M. C. Wilkinson. London: Oxford University Press. 

Gjestland, T. 

1955. The Oslo Study of Untreated Syphilis. Oslo: Akademisk 

Forlag. [See especially, pages 162-182.] 

Gladykowska-Rzeczycka, J. 

1976. A Case of Leprosy from a Medieval Burial 

Ground. Folia Morphologica, 35:253-264. 

Gladykowska-Rzeczycka, J., and M. Urbanowicz 

1970. Multiple Osseous Exostoses of the Skeleton from 

a Prehistoric Cemetery of a Former Population of 

Pruszez Gdanski. Folia Morphologica, 29:284-296. 

Glasgow, M. M. 

1976. Brucellosis of the Spine. The British Journal of Surgery, 63:283-288. 

Goldberg, A. 

1963. The Anaemia of Scurvy. Quarterly Journal of Medicine, 32:51-64. 

Golding, J. S. R , J. E. Maclver, and L. N. Went 

1959. The Bone Changes in Sickle Cell Anaemia and Its 

Genetic Variants. yoMJTza/ of Bone and Joint Surgery, 

41B:711-718. 

Goldmann, C. H., and S. J. Smith 

1943. X-ray Appearances of Bones in Yaws. Journal of 

Bone and Joint Surgery, 266:672-681. 

Goldsmith, W. M. 

1922. The Catlin Mark, the Inheritance of an Unusual 

Opening in the Parietal Bones. Journal of Heredity, 

13:69-71. 

1945. Trepanation and the "Catlin Mark." American 

Journal of Antiquity, 10:348-352. 

Gorlin, R. J., and H. M. Goldman, editors. 

1970. Thoma's Oral Pathology. St. Louis: The C. V. Mosby 

Company. 
NUMBER 28 465 

Gosse, L. A. 

1855. Essai sur les deformations artificielles du crane. 

Annates de Hygiene Publique et Medecine Legale, series 

2, 3:317-393; series 2,4:1-83. 

Gray, P. H. K. 

1968. Bone Infarction in Antiquity. Clinical Radiology, 19: 

436-437. 

1970. A Case of Osteogenesis Imperfecta Associated with 

Dentinogenesis Imperfecta Dating from Antiquity. 

Clinical Radiology, 21:106-108. 

Green, W. T., and J. G. Shannon 

1936. Osteomyelitis of Infants: A Disease Different from 

Osteomyelitis of Older Children. Archives of Surgery, 

32:462-493. 

Greenfield, G. B. 

1970. Bone Changes in Chronic Adult Gaucher's Disease. American Journal of Roentgenology, 110:800-807. 

1975. Radiology of Bone Diseases. Second edition. Philadelphia: J. B. Lippincott. 

Gregg, J. B., and R. N. McGrew 

1970. Hrdlicka Revisited (External Auditory Canal Exostosis). American Journal of Physical Anthropology, 33: 

37-40. 

Grimm, H., and C. H. Plathner 

1952. Uber einen Jungsteinzeitlichen Hydrocephalus 

von Seeburg in Mansfelder Seekreis und sein Gebiet. Deutsche Zahnaerzteblatt, Mund, und Kieferheilkunde, 15:1-7. 

Grin, E. I. 

1935. Endemic Syphilis in Bosnia and Herzegovina. Urologic and Cutaneous Review, 39:482-487. 

Guiard, E. 

1930. La Trepanation Crdnienne chez les Neolithiques et chez 

les Primilifs Modemes. Paris: Masson et Cie. 

Hackett, C. J. 

1936. Boomerang Leg and Yaws in Autralian Aborigines. Monograph 1. London: Royal Society of Tropical 

Medicine and Hygiene. 

1957. An International Nomenclature of Yaws Lesions. Geneva: World Health Organization. 

1963. On the Origin of the Human Treponematoses. 

Bulletin of the World Health Organization, 29:7-41. 

1976. Diagnostic Criteria of Syphilis, Yaws and Treponarid (Treponaematoses) and of Some Other Diseases in Dry Bones. Sitzungsberichte der Heidelberger 

Akademie der Wissenschaften Mathematisch-naturwissenschaftliche Klasse, Abhandlung 4. Berlin: SpringerVerlag. 

1978. Treponematoses (Yaws and Treponarid) in Exhumed Australian Aboriginal Bones. Records of the 

South Australian Museum, 17:387-405. 

Ham, A. W. 

1930. A Histological Study of the Early Phases of Bone 

Repair, yowrna/ of Bone and Joint Surgery, 12:827-844. 

1974. Histology. Seventh edition. Philadelphia: J. B. Lippincott Company. 

Hamilton, F. H. 

1853. Fracture Tables. Buffalo: Jewett, Thomas and Company. 

Hamilton, W. J., and H. W. Mossman 

1972. Human Embryology. Fourth edition. Cambridge, 

England: W. Heffer and Sons Limited. 

Hamperl, H. 

1966. Discussion (of Problems in the Pathology and 

Paleopathology of Bone). In S. Jarcho, editor. 

Human Palaeopathology, pages 81-83. New Haven: 

Yale University Press. 

Hamperl, H., and W. S. Laughlin 

1959. Osteological Consequences of Scalping. Human Biology, 31:80-89. 

Hancox, H. M. 

1972. Biology of Bone. Cambridge, England: The University Press. 

Hare, P. E. 

1974. Amino Acid Dating—A History and an Evaluation. University of Pennsylvania Museum of Archeology 

News, 10:4-8. 

Harkness, A. H. 

1942. Gonococcal Arthritis. Medical Press, 207:60-64. 

Haslhofer, L. 

1958. Zur Kentniss des Schwangerschafts-Osteophyts 

am Schadeldach. Wiener Klinische Wochenschrift, 

pages 297-299. 

Hassan, A. A., and D. J. Ortner 

1977. Inclusions in Bone Material as a Source of Error 

in Radiocarbon Dating. Archaeometry, 19:131-135. 

Hawkes, S. C , and C. Wells. 

1975. An Anglo-Saxon Obstetri c Calamity from 

Kingsworthy, Hampshire. Medical and Biological 

Illustration, 25:47-51. 

1976. Absence of the Left Upper Limb and Pectoral 

Girdle in a Unique Anglo-Saxon Burial. Bulletin of 

the New York Academy of Medicine, 52:1229-1235. 

Heberling, J. A. 

1941. A Review of Two Hundred and One Cases of 

Suppurative Arthritis, yowrna/ of Bone and Joint Surgery, 23:917-921. 

Heine, J. 

1926. Uber die Arthritis Deformans. Virchow's Archiv fiir 

Pathologische Anatomie und Physiologie und fur Klinische 

Medizin, 260:b2\-663. 

Henschen, F. 

1949. Morgagni's Syndrome. Edinburgh: Oliver and Boyd. 

1961. Cribra Cranii, a Skull Condition Said To Be of 

Racial or Geographical Nature. Pathologia et Microbiologia, 24:724-729. 

Hess, A. F. 

1921. Newer Aspects of Some Nutritional Disorders. 

Journal of the American Medical Association, 76:693-

700. 

1929. Rickets Including Osteomalacia and Tetany. Philadelphia: Lea and Febiger. 
466 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

Highman, J. H. 

1967. Congenital Osseous Rubella. Clinical Radiology, 18: 

445-449. 

Hoffman, J. M. 

1976. An Achondroplastic Dwarf from the Augustine 

Site (CA-Sac-127). Contributions of the University of 

California Archaeological Research Facility, 30:65-119. 

Hohenthal, W. D., and S. T. Brooks 

1960. An Archeological Scaphocephalic from California. 

American Journal of Physical Anthropology, 18:59-67. 

Holcomb, R. C. 

1940. Syphilis ofthe Skull among Aleuts and the Asian 

and North American Eskimo about Bering and 

Arctic Seas. United States Naval Medical Bulletin, 38: 

177-192. 

1941. The Antiquity of Congenital Syphilis. Bulletin of 

the History of Medicine, 10:148-177. 

Holt, J. F., and W. I. Owens 

1949. The Osseous Lesions in Sarcoidosis. Radiology, 53: 

11-30. 

Hook, E. W., C. G. Campbell, H. S. Weens, and G. R. 

Cooper 

1957. Salmonella Osteomyelitis in Patients with SickleCell Anemia. New England Journal of Medicine, 257: 

403-407. 

Hooton, E. A. 

1930. The Indians of Pecos Pueblo: A Study of their Skeletal 

Remains. New Haven: Yale University Press. 

Hopkins, R. 

1928. Bone Changes in Leprosy. Radiology, 11:470-473. 

Hormell, R. S. 

1940. Notes on the History of Rheumatism and Gout. 

The New England Journal of Medicine, 223:754-760. 

Howells, W. W. 

1973. Cranial Variation in Man. Papers of the Peabody 

Museum of Archaeology and Ethnology, 67. Cambridge: 

Harvard University. 

Hrdlicka, A. 

1907. Health and Disease. In F. W. Hodges, editor, 

Handbook of American Indians North of Mexico. 

Bureau of American Ethnology Bulletin, 30:540-541. 

1909. Tuberculosis among Certain Indian Tribes ofthe 

United States. Bureau of American Ethnology Bulletin, 

42. 

1914. Special Notes on Some of the Pathological Conditions Shown by the Skeletal Material of the 

Ancient Peruvians. Smithsonian Miscellaneous Collections, 61:57-69. 

1935. Ear Exostoses. Smithsonian Miscellaneous Collections, 

93:1-100. 

1939. Trepanation among Prehistoric People, Especially 

in America. Ciba Symposia, 1:170-177. 

1943. Skull of a Midget from Peru. American Journal of 

Physical Anthropology, 1:77-82. 

Hudson, E. H. 

1958. Treponematoses or Treponematosis? The British 

Journal of Venereal Diseases, 34:22-23. 

1965. Treponematosis and Man's Social Evolution. 

American Anthropologist, 67:885-901. 

1968. Christopher Columbus and the History of Syphilis. Acta Tropica, 25:1-16. 

Huntington, Jr., R. W. 

1959. Morphology and Racial Distribution of Fatal Coccidioidomycosis: Report of a Ten-Year Autopsy 

Series in an Endemic Area. Journal of the American 

Medical Association, 169:115-118. 

1971. Coccidioidomycosis. In R. D. Baker, editor. Human 

Infections with Fungi, Actinomycetes and Algae, pages 

147-210. New York: Springer-Verlag. 

Hutchinson, J. 

1909. Syphilis. New and enlarged edition. London: Cossell. 

Hyde, J. B. 

1891. A Contribution to the Study of Pre-Columbian 

Syphilis in America. American Journal of Medical 

Science, 102:117-131. 

Ingelmark, B. E., V. M0ller-Christensen, and O. Brinch 

1959. Spinal Joint Changes and Dental Infections. Acta 

Anatomica, supplement 36 of volume 38. 

International Union Against Tuberculosis 

1964. Some Statistical Data Concerning Tuberculosis in Europe 

and North America. Limoges, France: Imprimerie 

Bontemps. 

Iqbal, Q. M. 

1974. Long Bone Fractures among Children in Malaysia. International Surgery, 59:410-415. 

Ivanissevich, O. 

1934. Hidatidosis Osea. Buenos Aires: Imprenta Amorrortu. 

Jaffe, H. L. 

1958. Tumors and Tumorous Conditions of Bones and Joints. 

Philadelphia: Lea and Febiger. 

1972. Metabolic, Degenerative, and Inflammatory Diseases of 

Bones and Joints. Philadelphia: Lea and Febiger. 

Jaffe, H. L., and M. M. Pomeranz 

1934. Changes in the Bones of Extremities Amputated 

Because of Arteriovascular Disease. Archives of Surgery, 29:566-588. 

Jande , S. S. 

1972. Effects of Parathormone on Osteocytes and Their 

Surrounding Bone Matrix. Zeitschrift fur Zellforschung und Mikroskopische Anatomie, 130:463-470. 

Jarcho, S. 

1965. Anomaly of the Vertebral Column (Klippel-Feil 

Syndrome) in American Aborigines. Journal of the 

American Medical Association, 193:843-844. 

Jarcho, S., editor 

1966. Human Paleopathology. New Haven: Yale University 

Press. 
NUMBER 28 467 

Jarcho, S., N. Simon, and E. M. Bick 

1963. A Fused Hip from Wupatki. Plateau, the Quarterly 

ofthe Museum of Northern Arizona, 35:69-74. 

Jarcho, S., N. Simon, and H. L. Jaffe 

1965. Symmetrical Osteoporosis in a Prehistoric Skull 

from New Mexico. El Palacio, a Quarterly Journal of 

the Museum of New Mexico, 72:26-30. 

Jhering, H. von 

1882. Die Kiinstliche Deformirung der Zahne. Zeitschrift 

fiir Ethnologic, 14:220-240. 

Job, C. K., A. B. Karat, and S. Karat 

1966. The Histopathological Appearance of Leprous 

Rhinitis and Pathogenesis of Septal Perforation in 

Leprosy. Journal of Laryngology and Otology, 80:718-

732. 

Johannsson, S. 

1926. Uber die Knochen- und Gelenk- Tuberkulose im Kindesalter. Jena: G. Fischer. 

Johnson, L. C. 

1964. Morphologic Analysis in Pathology. In H. M. 

Frost, editor, Bone Biodynamics, pages 543-654. Boston: Little, Brown and Company. 

1965. Histogenesis and Mechanisms of Osteofluorosis. In 

J. H. Simons, editor. Fluorine Chemistry, 4:424-441. 

New York: Academic Press. 

1966. The Kinetics of Skeletal Remodeling. Birth Defects 

Original Article Series, 2:66-142. 

Johnson, L. C , and E. R. Kerley 

1974. Report on Pathological Specimens from Mokapu. 

In C. E. Snow, Early Hawaiians, appendix B. Lexington: The University Press of Kentucky. 

Jones, J. 

1876. Explorations of the Aboriginal Remains of Tennessee. Smithsonian Contributions to Knowledge, number 259. 

Jowsey, J. 

1955. The Use of the Milling Machine for Preparing 

Bone Sections for Microradiography and Microautoradiography. Journal of Scientific Instrumentation, 32:159. 

1960. Age Changes in Human Bone. Clinical Orthopaedics, 

17:210-218. 

Junghanns, H. 

1939. Die Pathologie der Wirbelsaule. In O. Lubarsch., 

F. Henke, and R. Rossle, editors, Handbuch der 

Speziellen Pathologie und Histologie, 9(4): 216-429. 

Berlin: J. Springer. 

Jurmain, R. D. 

1975. Distribution of Degenerative Joint Disease in Skeletal Populations. Doctoral dissertation. Harvard 

University, Cambridge, Massachusetts. 

1977. Stress and the Etiology of Osteoarthritis. American 

Jourruil of Physical Anthropology, 46:353-366. 

Kasabach, H. H., and A. B. Gutman 

1937. Osteoporosis Circumscripta of the Skull and Paget's Disease. The American Journal of Roentgenology 

and Radium Therapy, 37:577-602. 

Kastert, J., and E. Uehlinger 

1964. Skelettuberkulose: Mit einen Beitrag iiber AUgemeine Pathologie und Pathologische Anatomie 

der Skelettuberkulose. In J. Hein, H. Kleinschmidt, and E. Uehlinger, editors, Handbuch der Tuberkulose, 4:443-532. Stuttgart: G. Thieme. 

Keenan, J. D., and C. W. Metz 

1972. Brucella Spondylitis. Clinical Orthopaedics, 82:89-

91. 

Keith, A. 

1913. Abnormal Crania—Achondroplastic and Acrocephalic. Jourruil of Anatomy and Physiology, 47:189-

206. 

Kelln, E. E., E. V. McMichael, and B. Zimmermann 

1967. A Seventeenth Century Mandibular Tumor in a 

North American Indian. Oral Surgery, Oral Medicine 

and Oral Pathology, 23:78-81. 

Kelly, P, J., W. J. Martin, A. Schinger, and L. A. Weed 

1960. Brucellosis of the Bones and Joints: Experience 

with Thirty-six Patients. Journal of the American 

Medical Association, 174:347-353. 

Kelsey, J. L., K. J. Keggi, and W. O. Southwick 

1970. The Incidence and Distribution of Slipped Capital 

Femoral Epiphysis in Connecticut and Southwestern United States. Journal of Bone and Joint Surgery, 

52A: 1203-1216. 

Kerley, E. R. 

1965. The Microscopic Determination of Age in Human 

Bone. American Journal of Physical Anthropology, 22: 

149-163. 

Keriey, E. R., and D. H. Ubelaker 

1978. Revisions in the Microscopic Method of Estimating Age at Death in Human Cortical Bone. American Journal of Physical Anthropology, 49:545-546. 

Keyes, P. H. 

1968. Research on Dental Cartes. Journal of the American 

Dental Association, 76:1357-1373. 

Kidd, K. E. 

1954. A Note on the Paleopathology of Ontario. American 

Journal of Physical Anthropology, 12:610-615. 

Klages, F. 

1930. Der Alveolare Echinokokkus in Genf, Insbesondere 

Sein Auftreten im Knochen. Virchow's Archiv fur 

Pathologische Anatomie und Physiologie und fir Klinische 

Medizin, 278:125-148. 

Kline, A. H., and G. H. Holman 

1957. Hereditary Spherocytosis in the Negro. American 

Journal of Diseases of Children, 94:609-615. 

Knaggs, R. L. 

1923-1924. Leontiasis Ossea. The British Journal of Surgery, 

11:347-379. 

K6hler, A. 

1923. Typical Disease of the Second Metatarsopha-
468 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

langeal Joint. American Journal of Roentgenology, 10: 

705-710. 

Konig, F. 

1906. Die Tuberculose der Menschlichen Gelenke Sowie der 

Brustwand und des Schadels. Berlin: A. Hirschwald. 

Konschegg, J. 

1934. Die Tuberkulose der Knochen. In O. Lubarsch 

and F. Henke, editors, Handbuch der Speziellen Pathologischen Anatomie und Histologie, 9(2):377-437. Berlin: J. Springer. 

Kranz, P. 

1927. Zahndeformitaten bei Angeborener Syphilis. In 

J. Jadassohn, editor, Handbuch der Haul- und Geschlechtskrankheiten, 19:240-270. Berlin: J. Springer. 

Krause, F. 

1899. Die Tuberkulose der Knochen und Gelenke. 

Deutsche Chirurgie, 28A: 19-95. 

Kremer, W., and O. Wiese 

1930. Die Tuberkulose der Knochen und Gelenke. Ihre 

Pathologie, Diagnostik, Therapie und Ihre Soziale 

Bedeutung. In L. Brauer and H. Ulrici, editors. 

Die Tuberkulose und Ihre Grenzgebiele in Einzeldarstellungen, volume 8. Berlin: J. Springer. 

Krogman, W. M. 

1962. The Human Skeleton in Forensic Medicine. Springfield, 

Illinois: Charles C. Thomas. 

Krumbhaar, E. B. 

1936. Pre-Columbian Peruvian Tibia Exhibiting Syphilitic (?) Periostitis with Recognizable Varieties of 

Bone Marrow Cells. Annals of Medical History, 8: 

232-235. 

Kulowski, J. 

1936. Pyogenic Osteomyelitis ofthe Spine: An Analysis 

and Discussion of 102 Cases. Journal of Bone and 

Joint Surgery, 18:343-364. 

Lamb, D. S. 

1898. Pre-Columbian Syphilis. In Proceedings of the Tenth 

Annual Session ofthe Association of American Anatomists, 

10:63-69. 

Lanzkowsky, P. 

1968. Radiological Features of Iron Deficiency Anemia. 

American Journal of Diseases of Children, 116:16-29. 

Laubmann, W. 

1935. Uber die Knochenstruktur bei Marmorknochenkrankheit. Virchow's Archiv fur Pathologische Anatomie 

und Physiologie, 296:343-357. 

Lauche, A. 

1939. Die Unspezifischen Entziindungen der Knochen. 

In O. Lubarsch and F. Henke, editors, Handbuch 

der Speziellen Pathologischen Anatomie und Histologie, 

9(4): 1-80. Berlin: J. Springer. 

Lawrence, J. S., V. A. J. Laine, and R. de Graaff 

1961. The Epidemiology of Rheumatoid Arthritis in 

Northern Europe. Proceedings of the Royal Society of 

Medicine, 54:454-462. 

League of Nations 

1922. Annual Epidemiological Report No. 6: Corrected Statistics 

for the Year 1921. Geneva: League of Nations 

Health Organization. 

Lees, Sidney 

1979. A Model for the Distribution of HAP Crystallites 

in Bone—An Hypothesis. Calcified Tissue International, 27:53-56. 

Lester, C. W. 

1967. Melorheostosis in a Prehistoric Alaskan Skeleton. 

Journal of Bone and Joint Surgery, 49:142. 

Lester, C. W., and H. L. Shapiro 

1968. Vertebral Arch Defects in the Lumba r Vertebrae 

of Pre-Historic American Eskimos: A Study of 

Skeletons in the American Museum of Natural 

History, Chiefly from Point Hope, Alaska. American Journal of Physical Anthropology, 28:43-47. 

Lewis, J. H. 

1942. The Biology of the Negro. Chicago: The University 

of Chicago Press. 

Lichtenstein, L. 

1953. Histiocytosis X: Integration of Eosinophilic Granuloma of Bone, "Letterer-Siwe Disease," and 

"Schiiller-Christian Disease" as Related Manifestations of a Single Nosologic Entity. Archives of 

Pathology, 56:84-102. 

Lichtenstein, L., and H. L. Jaffe 

1942. Fibrous Dysplasia of Bone. Archives of Pathology, 33: 

777-816. 

Lichtor, J., and A. Lichtor 

1957. Paleopathological Evidence Suggesting Pre-Columbian Tuberculosis ofthe Spine, yot/rna/ of Bone 

and Joint Surgery, 39A: 1398-1399. 

Lodge, T. 

1967. Thinning ofthe Parietal Bones in Early Egyptian 

Populations and Its Aetiology in the Light of 

Modern Observations. In D. R. Brothwell and A. 

T. Sandison, editors, Diseases in Antiquity: A Survey 

ofthe Diseases, Injuries and Surgery of Early Populations, 

pages 405-412. Springfield, Illinois: Charles C. 

Thomas. 

Looser, E. 

1920. Uber Pathologische Formen von Infraktionen und 

Callusbildungen bei Rachitis und Osteomalacic 

und Anderen Knochenerkrankungen. Zentralblatt 

fur Chirurgie, 47:1470-1479. 

1929. Uber die Ossifikationsstorungen bei Kretinismus. 

Verhandlungen der Deulschen Pathologischen Gesellschafl, 

24:352-360. 

Lowbeer, L. 

1948. Brucellotic Osteomyelitis ofthe Spinal Column in 

Man. American Journal of Pathology, 24:723-724. 

1949. Brucellotic Osteomyelitis of Ma n and Animal. 

Proceedings of Staff Meeting of Hillcrest Memorial Hospital, 6:1-36. 
NUMBER 28 469 

Lurie, H. I. 

1971. Sporotrichosis. In R. D. Baker, editor, Human Infections with Fungi, Actinomycetes and Algae, pages 614-

675. New York: Springer-Verlag. 

MacArthur, W. 

1953. Medieval "Leprosy" in the British Isles. Leprosy 

Review, 24:8-19. 

MacCurdy, G. G. 

1905. Prehistoric Surgery—A Neolithic Survival. American Anthropologist, 7:7-23. 

1923. Human Skeletal Remains from Highlands of Peru. 

American Journal of Physical Anthropology, 6:217-330. 

Mallin, R., and T. A. Rathbun 

1976. A Trephined Skull from Iran. Bulletin of the New 

York Academy of Medicine, 52:782-787. 

Manouvrier, L. 

1895. Le T-Sincipital. - Curieuse Mutilation Cranienne 

Neolithique. Bulletins de la Socie'te D'Anthropologie de 

Paris, series 4, 6:357-360. 

Marat ka, Z. 

1946. Contribution a I'Etude Clinique et Histopathologique des Osteopathies de Carence. Archives Maladies Appareil Digestive, 35:318-335. 

Marchiafava, V., E. Bunocci, and A. Ascenzi 

1974. Fungal Osteoclasia: A Model of Dead Bone Resorption. Calcified Tissue Research, 14:195-210. 

May, W. P. 

1897. Rheumatoid Arthritis (Osteitis Deformans) Affecting Bones 5,500 Years Old. British Medical Journal, 2:\63\-\632. 

Mayock, R. L., R. Bertrand, C. E. Morrison, and J. H. Scott 

1963. Manifestations of Sarcoidosis: Analysis of 145 Patients, with a Review of Nine Series Selected from 

the Literature. American Journal of Medicine, 35:67-

89. 

McElligott, G. L. M. 

1960. Venereal Disease and the Public Health. British 

Journal of Venereal Diseases, 36:207-215. 

McGibbon, H. 

1912. Artificially Deformed Skulls with Special Reference to the Temporal Bone and Its Tympanic 

Portion. Laryngoscope, 22:1165-1184. 

McKern, T. W., and T. D. Stewart 

1957. Skeletal Age Changes in Young American Males, Technical Report EP-45. Natick, Massachusetts: Headquarters, Quartermaster Research and Development Command. 

McKusick, V. A. 

1972. Heritable Disorders of Connective Tissue. Fourth edition. St. Louis: C. V. Mosby. 

McLean, F. C , and M. R. Urist 

1968. Bone. Third edition. Chicago: The University of 

Chicago Press. 

McNeur, J. C , and A. E. Pritchard 

1955. Tuberculosis of the Greater Trochanter. Journal of 

Bone and Joint Surgery, 37B:246-251. 

Mehta, J. D., and C. C. Evans 

1966. A Study of Attrition of Teeth in the Arkansas 

Indian Skulls. The Angle Orthodontist, 36:248-257. 

Menard, V. 

1900. Etude Pratique sur le Mai de Pott. Paris: Masson et 

Cie. 

Mensforth, R. P., C. O. Lovejoy, J. W. Lallo, and G. J. 

Armelagos 

1978. The Role of Constitutional Factors, Diet, and 

Infectious Disease in the Etiology of Porotic Hyperostosis and Periosteal Reactions in Prehistoric 

Infants and Children. Medical Anthropology, volume 

2, issue 1 (Winter), part 2. 

Merchant, V. L., and D. H. Ubelaker 

1977. Skeletal Growth ofthe Protohistoric Arikara. American Journal of Physical Anthropology, 46:61-72. 

Merrill, A. S. 

1920. Case of Xanthoma Showing Multiple Bone Lesions. American Journal of Roentgenology, 7:480-484. 

Meschan, I. 

1975. An Atlas of Anatomy Basic to Radiology. Philadelphia: 

W. B. Saunders Company. 

Meyerding, H. W., and R. J. Mroz 

1933. Tuberculosis of the Greater Trochanter, yowrna/ of 

the American Medical Association, 101:1308-1313. 

Michels, J. W. 

1973. Dating Methods in Archaeology. New York: Seminar 

Press. 

Middlemiss, H. 

1962. Tropical Radiology. London: W. Heinemann Medical Books Ltd. 

Middlemiss, J. H., and A. B. Raper 

1966. Skeletal Changes in the Haemoglobinopathies. 

Journal of Bone and Joint Surgery, 48B:693-702. 

Milkman, L. A. 

1930. Pseudofracture (Hunger Osteopathy, Late Rickets, Osteomalacia): Report of a Case. American 

Journal of Roentgenology and Radium Therapy, 24:29-

37. 

Miller, D., and J. W. Birsner 

1949. Coccidioidal Granuloma of Bone. American Journal 

of Roentgenology and Radium Therapy, 62:229-236. 

Mitchell, J. K. 

1900. Study of a Mummy Affected with Anterior Poliomyelitis. Transactions of the Association of American 

Physicians, 15:134-136. 

Moller 

1862. Zwei Falle von Acuter Rachitis. Konigsberger Medicinische Jahrbucher, 3:136-149. 

M0ller-Christensen, V. 

1952. Case of Leprosy from the Middle Ages of Denmark. Acta Medica Scandinavica, supplement 266: 

101-108. 

1953. Ten Lepers from Naestved in Denmark: A Study of 

Skeletons from a Medieval Danish Leper Hospital. Copenhagen: Danish Science Press Ltd. 
470 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

1961. Bone Changes in Leprosy. Copenhagen: Munksgaard. 

1965. New Knowledge of Leprosy Through Paleopathology. International J ournal of Leprosy, 33:603-610. 

1967. Evidence of Leprosy in Earlier Peoples. In D. R. 

Brothwell and A. T. Sandison, editors, Diseases in 

Antiquity: A Survey of the Diseases, Injuries and Surgery 

of Early Populations, pages 295-306. Springfield, 

Illinois: Charles C. Thomas. 

1978. Leprosy Changes of the Skull. Odense, Denmark: 

Odense University Press. 

M0ller-Christensen, V., and D. R. Hughes 

1966. An Early Case of Leprosy from Nubia. Man, 1: 

242-243. 

M0ller-Christensen, V., and R. G. Inkster 

1965. Cases of Leprosy and Syphilis in the Osteological 

Collection of the Department of Anatomy at the 

University of Edinburgh, with a Note on the Skull 

of King Robert The Bruce. Danish Medical Bulletin, 

12:11-18. 

M0ller-Christensen, V., and A. T. Sandison 

1963. Usura Orbitae (Cribra Orbitalia) in the Collection 

of Crania in the Anatomy Department of the 

University of Glasgow. Pathologia et Microbiologia, 

26:175-180. 

Moodie, R. L. 

1919. Ancient Skull Lesions and the Practice of Trephining in Prehistoric Times. Surgical Clinic of Chicago, 3:481-496. 

1920. Amputation of the Finger by Neolithic and Modern Primitive Races, and Other Voluntary Mutilations Indicating Some Knowledge of Surgery. 

Surgical Clinic of Chicago, 4:1299-1306. 

1921. A Variant ofthe Sincipital T from Peru. American 

Journal of Physical Anthropology, 4:219-222. 

1922. Disease and Injury in Fossil Men and the Beginnings of Surgery. Scientific Monthly, 14:391-394. 

1923. Paleopathology: An Introduction to the Study of Ancient 

Evidences of Disease. Urbana: University of Illinois 

Press. 

1928. Studies in Paleo-Odontology, IX: Definite Association of Rheumatic Lesions with Disease of the 

Teeth in an Ancient Peruvian. Pacific Dental Gazette, 36:757-759. 

Moore, C. B. 

1910. Antiquities of the St. Francis, White, and Black 

Rivers, Arkansas. The Journal of the Academy of Natural Science of Philadelphia, 14:254-364. 

Moore, S. 

1929. The Bone Change in Sickle Cell Anemia with 

Similar Changes Observed in the Skull of Ancient 

Mayan Indians. yoMrwa/ of the Missouri Medical Association, 26:561-564. 

1955. Hyperostosis Cranii. Springfield, Illinois: Charles C. 

Thomas. 

M0rch, E. T. 

1941. Chondrodystrophic Dwarfs in Denmark, Inheritance of 

Chondrodystrophy. Copenhagen: E. Munksgaard. 

Moreland, G. 

1968. Preparation of Polished Thin Sections. American 

Mineralogist, 53:2070-2074. 

Morgan, E. L. 

1894. Pre-Columbian Syphilis. Virginia Medical SemiMonthly, 21:1042-1054. 

Morse, D. 

1961. Prehistoric Tuberculosis in America. American Review of Respiratory Diseases, 83:489-503. 

1967. Tuberculosis. In D. R. Brothwell and A. T. Sandison, editors, Diseases in Antiquity: A Survey of the 

Diseases, Injuries and Surgery of Early Populations, 

pages 249-271. Springfield, Illinois: Charles C. 

Thomas. 

1969. Ancient Disease in the Midwest. Illinois State Museum Reports of Investigations, number 15. 

Morse, D., D. R. Brothwell, and P. J. Ucko 

1964. Tuberculosis in Ancient Egypt. American Review of 

Respiratory Diseases, 90:524. 

Morse, D., R. C. Dailey, and J. Bunn 

1974. Prehistoric Multiple Myeloma. Bulletin ofthe New 

York Academy of Medicine, 50:447-458. 

Moseley, J. E. 

1961. Skull Changes in Chronic Iron Deficiency Anemia. 

American Jourruil of Roentgenology, Radium Therapy, and 

Nuclear Medicine, 85:649-652. 

1963. Bone Changes in Hematologic Disorders (Roentgen Aspects). New York: Grune and Stratton. 

1965. The Paleopathologic Riddle of "Symmetrical Osteoporosis." American Journal of Roentgenology, Radium 

Therapy, and Nuclear Medicine, 95:35-142. 

1966. Radiographic Studies in Hematologic Bone Disease: Implications for Paleopathology. In S. Jarcho, editor. Human Paleopathology, pages 121-130. 

New Haven: Yale University Press. 

Moss, M. L. 

1958. The Pathogenesis of Artificial Cranial Deformation. American Journal of Physical Anthropology, 16; 

269-286. 

Miiller, W. 

1926. Uber das Verhalten des Knochengewebes bei Herabgesetzter Zirkulation und das Bild von Nekrose 

der Zwischenlamellen. Bruns' Beitrdge zur Klinischen 

Chirurgie, 138:614-624. 

Murphy, J. B. 

1916. Bone and Joint Disease in Relation to Typhoid 

Fever. Surgery, Gynecology and Obstetrics, 23: 119-

143. 

Murray, J. F., A. M. Merriweather, and M. L. Freedman 

1956. Endemic Syphilis in the Bakwena Reserve of the 

Bechuanaland Protectorate. Bulletin of the World 

Health Organization, 15:975-1039. 
NUMBER 28 471 

Nadean, G. 

1941. Indian Scalping Technique in Different Tribes. 

Bulletin ofthe History of Medicine, 10:178-194. 

Nathan, M. H., W. P. Radman, and H. L. Barton 

1962. Osseous Actinomycosis of the Head and Neck. 

American J ournal of Roentgenology, Radium Therapy, and 

Nuclear Medicine, 87:1048-1053. 

Nemeskeri, J., and L. Harsanyi 

1959. Die Bedeutung Palaopathologischer Untersuchungen fiir die Historische Anthropologie. Homo, 10: 

203-226. 

Neuman, W. F., and M. W. Neuman 

1958. The Chemical Dynamics of Bone Mineral. Chicago: 

The University of Chicago Press. 

Neumann, G. K. 

1940. Evidence for the Antiquity of Scalping from Central Illinois. American Antiquity, 5:287-289. 

Nowakowski, H. 

1955. Die Wirkungen der Sexualhormone auf das Skelett 

und den Skelettstoffwechsel: In Stoffwechselwirkungen der Steroidhormone: Zweiles Symposion der Deulschen 

Gesellschafl fiir Endokrino logic, pages 93-110. Berlin: 

Springer-Verlag. 

Oakley, K. P. 

1950. Relative Dating ofthe Piltdown Skull. Advancement 

of Science, 6:343-344. 

1963a. Dating Skeletal Material. Science, 140:488. 

1963b. Analytical Methods of Dating Bones. In D. R. 

Brothwell and E. Higgs, editors. Science in Archeology, pages 24-34. New York: Basic Books. 

Oakley, K. P., M. A. Brooke, A. R. Akester, and D. R. 

Brothwell 

1959. Contributions on Trepanning or Trepanation in 

Ancient and Modern Times. Man, 59:92-96. 

Oehlecker, F. 

1924. Tuberkulose der Knochen und Gelenke. Berlin: Urban 

und Schwarzenberg. 

Ortner, D. J. 

1968. Description and Classification of Degenerative 

Bone Changes in the Distal Joint Surfaces of the 

Humerus. American Journal of Physical Anthropology, 

28:139-156. 

1970. The Effects of Aging and Disease on the Micromorphology of Human Compact Bone. Doctoral 

dissertation. University of Kansas, Lawrence. 

1975. Aging Effects on Osteon Remodeling. Calcified 

Tissue Research, 18:27-36. 

1976. The Paleopathology Program at the Smithsonian 

Institution: Purposes and Present Status. Bulletin 

of the New York Academy of Medicine, 52:1197-1206. 

Ortner, D. J., and R. S. Corruccini 

1976. The Skeletal Biology ofthe Virginia Indians. American Jourruil of Physical Anthropology, 45:717-722. 

Ortner, D. J., and D. W. Von Endt 

1971. Microscopic and Electron Microprobe Characterization of the Sclerotic Lamellae in Human Osteons. Israel Journal of Medical Sciences, 7:480-482. 

Ortner, D. J., D. W. Von Endt, and M. S. Robinson 

1972. The Effect of Temperature on Protein Decay in 

Bone: Its Significance in Nitrogen Dating of Archaeological Specimens. American Antiquity, 37: 

514-520. 

Ortner, D. J., and D. Yong 

1975. A Precision Microdissection Procedure for Undecalcified Bone Thin Sections. Calcified Tissue Research, 17:169-172. 

Owsley, D. W., H. E. Berryman, and W. M. Bass 

1977. Demographic and Osteological Evidence for Warfare at the Larson Site, South Dakota. Plains Anthropologist Memoir, 13 (2): 119-131. 

Oyston, J. K. 

1961. Madura Foot: A Study of Twenty Cases. Journal of 

Bone and Joint Surgery, 43B: 259-267. 

Paget, J. 

1877. On a Form of Chronic Inflammation of Bones 

(Osteitis Deformans). Transactions of the MedicalChirurgical Society, 60:37-64. 

Pales, L. 

1929. Maladie de Paget Prehistorique, avec Note Additionelle du Professeur R. Verneau. L'Anthropologic, 

39:263-270. 

1930. Paleopathologic et Pathologie Comparative. Paris: Masson et Cie. 

Panders, A. K., and H. N. Hadders 

1970. Chronic Sclerosing Inflammations of the Jaw: Osteomyelitis Sicca (Garre), Chronic Sclerosing Osteomyelitis with Fine-meshed Trabecular Structure, and Very Dense Sclerosing Osteomyelitis. 

Oral Surgery, 30:396-412. 

Park, E. A. 

1954. Bone Growth in Health and Disease. Archives of 

Disease in Childhood, 29:269-281. 

Park, E. A., H. G. Guild, D. Jackson, and M. Bond 

1935. The Recognition of Scurvy with Especial Reference to the Early X-ray Changes. Archives of Disease 

in Childhood, 10:265-294. 

Parry, T. W. 

1931. Neolithic Man and Penetration of Living Human 

Skull. Lancet, 2:1388-1390. 

1936. Three Skulls from Palestine Showing Two Types 

of Primitive Surgical Holing, Being the First Skulls 

Exhibiting This Phenomenon That Have Been 

Discovered on the Mainland of Asia. Man, 36:170-

171. 

Partsch, F. 

1919. Uber Gehauftes Aufreten von Osteomalazie. 

Deutsche Medizinische Wochenschrift, 45:1130-1133. 

Pasquali, E. 

1930. Sulla Localizzazione Ossea dell'Echinococco. Chirurgia Degli Organi di Movimento, 15:355-380. 
472 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

Paterson, D. E., and C. K. Job 

1964. Bone Changes and Absorption in Leprosy: A Radiological, Pathological and Clinical Study. In 

R. G. Cochrane and T. F. Davey, editors. Leprosy 

in Theory and Practice, second edition, pages 425-

446. Bristol, England: J. Wright and Sons, Ltd. 

Pena, C. E. 

1971. Aspergillosis. In R. D. Baker, editor. Human Infections with Fungi, Actinomycetes and Algae, pages 762-

831. New York: Springer-Verlag. 

Pendergrass, E. P., R. L. Gilman, and K. B. Castleton 

1930. Bone Lesions in Tardive Heredosyphilis. American 

Journal of Roentgenology and Radium Therapy, 24:234-

257. 

Pepper, O. H. P., and E. P. Pendergrass 

1936. Hereditary Occurrence of Enlarged Parietal Foramina. American Journal of Roentgenology and Radium 

Therapy 35:1-8. 

Phenice, T. W. 

1969. A Newly Developed Visual Method of Sexing the 

Os Pubis. American Journal of Physical Anthropology, 

30:297-302. 

Pick, L. 

1927. Die Skelettform (Ossudre Form) des Morbus Gaucher. 

Jena: G. Fischer. 

Piggot, S. 

1940. A Trepanned Skull of the Beaker Period from 

Dorset and the Practice of Trepanning in Prehistoric Europe. Proceedings of the Prehistoric Society of 

EaslAnglia, 6:112-132. 

Pindborg, J. J. 

1970. Pathology of the Dental Hard Tissues. Philadelphia: 

W. B. Saunders Company. 

Pitt-Rivers, G. H. 

1965. Osteoarthritis of a Bronze-Age Pelvic Skeleton. 

Journal of the College of General Practitioners, 9:266-

269. 

Pizzolato, P. 

1971. Nocardiosis. In R. D. Baker, editor. Human Infections 

with Fungi, Actinomycetes and Algae, pages 1059-

1080. New York: Springer-Verlag. 

Plehn, A. 

1928. Madurafuss (Mycetoma Pedis). In W. Kolle and 

A. von Wassermann, editors, Handbuch der Palhogenen Mikroorganismen, third edition, pages 113-132. 

Jena: G. Fischer. 

Policy, H. G., and C. H. Slocumb 

1947. Rheumatoid Spondylitis: A Study of 1035 Cases. 

In American Rheumatism Association Proceedings 

of the Reunion Meeting. Annals of the Rheumatic 

Diseases, 6:95-98. 

Pommer, G. 

1885. Untersuchungen uber Osteomalacie und Rachitis. Leipzig: 

F. C. W. Vogel. 

Posner, A. S. 

1969. Crystal Chemistry of Bone Mineral. Physiological 

Reviews, 49:160-192. 

Posselt, A. 

1900. iJberblick iiber das Herstammen der Alveolarechinokokkenfalle. Die Geographische Verbreitung des Echinococcus Hydatidosus. In Die Geographische Verbreitung des Blasewurmleidens, pages 232-

315. Stuttgart: F. Enke. 

Post, R. H. 

1966. Pilot Study: Population Differences in the Frequency of Spina Bifida Occulta. Eugenics Quarterly, 

13:341-352. 

Poswall, B. D. 

1976. Coccidioidomycosis and North American Blastomycosis: Differential Diagnosis of Bone Lesions in 

Pre-Columbian American Indians. American J ournal 

of Physical Anthropology, 44:199-200. 

Powell, B. W. 

1965, Spruce Swamp: A Partially Drowned Coastal 

Midden in Connecticut. American Antiquity, 30:460-

469. 

Prader, A., and A. P. Maassen 

1953. Die Wirkung der Androgenen Hormone auf das 

Skelett: Knochen und Zahnenwicklung, Calcium, 

Phosphor und Phosphatasen im Serum beims 

Kongenitalen Adrenogenitalen Syndrom. Helvetica 

Paediatrica Acta, 8:136-151. 

Priesel, A. 

1920. Ein Beitrag zur Kenntnis des Hypophysaren 

Zwergwuchses. Beitrdge zur Pathologischen Anatomie 

und zur Allgemeinen Pathologie, 67:220-274. 

Putschar, W. G. J. 

1927a. Uber Knorpelinsein in den Wirbelkorpern. Verhandlungen der Deulschen Pathologischen Gesellschafl, 

22:262-266. 

1927b. Zur Kenntnis der Knorpelinsein in den Wirbelkorpen. Beitrdge zur Pathologischen Anatomie und zur Allgemeinen Pathologie, 79:150-165. 

1929. Uber Gefassgeschwiilste in der Wirbelsaule. Zeitschrift fur Kreislaufforschung, 21:495-500. 

1931. Entwicklung, Wachstum und Pathologie der Beckenverbindungen des Menschen, mit besonderer Beriicksichtigung 

von Schwangerschaft, Geburl und ihren Folgen. Jena: G. 

Fischer. 

1937. Der Funktionelle Skeletumbau und die Sogenannten Belastungsdeformitaten. In O. Lubarsch., 

F. Henke, and R. Rossle, editors, Handbuch der 

Speziellen Pathologischen Anatomie und Histologie, 9(3): 

617-787. BeHin: J. Springer. 

1939. Spezielle Pathologie des Beckens. In O. Lubarsch., 

F. Henke, and R. Rossle, editors, Handbuch der 

Speziellen Pathologischen Anatomie und Histologie, 9(4): 

430-579. Berlin: J. Springer. 
NUMBER 28 473 

1960. General Pathology of the Musculo-Skeletal System. In F. Biichner., E. Letterer, and F. Roulet, 

editors, Handbuch der Allgemeinen Pathologic, 3(2): 

363-488. Beriin: J. Springer. 

1966. Problems in the Pathology and Palaeopathology 

of Bone. In S. Jarcho, editor. Human Paleopathology, 

pages 57-65. New Haven: Yale University Press. 

1976a. Osteomyelitis including Fungal. In L. V. Ackerman, H. J. Spjut, and M. R. Abel, editors, Bones 

and Joints. International Academy of Pathology Monograph, 17:39-60. Baltimore, Maryland: The Williams and Wilkins Company. 

1976b. The Structure of the Human Symphysis Pubis 

with Special Consideration of Parturition and Its 

Sequelae. American Journal of Physical Anthropology, 

45:589-594. 

Racic, J. 

1935. Uber Knochenechinokokkose. Beitrdge zur Klinischen Chirurgie, 161:411-422. 

Rathbun, J. C. 

1948. "Hypophosphatasia," New Developmental Anomaly. American Journal of Diseases of Children, 75:822-

831. 

Recklinghausen, F. von 

1891. Die Fibrose oder Deformirende Ostitis, die Osteomalacie und die Osteoplastische Carcinose in ihren 

Gegenseitigen Beziehungen. In Festschrift Rudolf 

Virchow (zu seinem 71. Geburstage), pages 1-89. 

Berlin: G. Reimer. 

1910. Rachitis urul Osteomalacie. 2 volumes. Jena: G. 

Fischer. 

Reese, H. H. 

1940. The History of Scalping and Its Clinical Aspects. 

The 1940 Yearbook of Neurology, Psychiatry and Endocrinology, pages 3-16. Chicago: The Year Book 

Publishers. 

Reinhart, M. 

1932. Die Falle von Spondylitis Tuberculosa in der Aargauischen Heilstatte Barmelweid aus den Jahren 

1912-1930. Beitraege zur Klimk der Tuberkulose, 79: 

745-749. 

Richman, E. A., and D. J. Ortner 

1976. Intracortical Bone Remodeling in Three Aboriginal American Populations: Possible Dietary Factors in Differences (abstract). American Journal of 

Physical Anthropology, 48:429. 

Richman, E. A., D. J. Ortner, and F. P. Schulter-Ellis 

1979. Differences in Intracortical Bone Remodeling in 

Three Aboriginal American Populations: Possible 

Dietary Factors. Calcified Tissue International, 28: 

209-214. 

Riordan, D. C. 

1960. The Hand in Leprosy. Jourruil of Bone and Joint 

Surgery, 42A:661-690. 

Ritchie, W. A. 

1952. Paleopathological Evidence Suggesting Pre-Columbian Tuberculosis in New York State. American 

Journal of Physical Anthropology, 10:305-317. 

Ritchie, W. A., and S. L. Warren 

1932. The Occurrence of Multiple Bony Lesions Suggesting Myeloma in the Skeleton of a Pre-Columbian Indian. American Journal of Roentgenology and 

Radium Therapy, 28:622-628. 

Rockwood, Jr., C. A. 

1975. Dislocations About the Shoulder. In C. A. Rockwood, Jr. and D. P. Green, editors, Fractures, pages 

624-787. Philadelphia: J. B. Lippincott Company. 

Rogers, L. 

1949. Meningiomas in Pharaoh's People: Hyperostosis 

in Ancient Egyptian Skulls. British Journal of Surgery, 36:423-424. 

Rokitansky, C. 

1844. Handbuch der Pathologischen Anatomy. Volume 2. 

Vienna: Braumiiller und Seidel. 

Romero, J. 

1958. Mutilaciones Dentarias, Prehispanicas de Mexicoy America en General. Mexico: Instituto Nacional de Anthropologia e Historia. 

1970. Dental Mutilation, Trephination and Cranial Deformation. In T. D. Stewart, editor. Handbook of 

Middle American Indians: Physical Anthropology, 9:50-

67. Austin: University of Texas Press. 

Roney, Jr., J. G. 

1966. Palaeoepidemiology: An Example from California. In S. Jarcho, editor. Human Palaeopathology, 

pages 99-107. New Haven: Yale University Press. 

Roper, M. K. 

1969. A Survey ofthe Evidence for Intrahuman Killing 

in the Pleistocene. Current Anthropology, 10:427-459. 

Rost, G. S. 

1942. Roentgen Manifestations of Bejel ("Endemic 

Syphilis") as Observed in the Euphrates River 

Valley. Radiology, 38:320-325. 

Rourke, J. A., and D. J. Heslin 

1965. Gaucher's Disease: Roentgenologic Bone Changes 

over 20 Year Interval. American Journal of Roentgenology, Radium Therapy, and Nuclear Medicine, 94:621-

630. 

Rowland, R. E. 

1966. Exchangeable Bone Calcium. Clinical Orthopaedics, 

49:233-248. 

Rowling, J. T. 

1961. Pathological Changes in Mummies. Proceedings of 

the Royal Society of Medicine, 54:409-415. 

1967. Paraplegia. In D. R. Brothwell and A. T. Sandison, 

editors, Diseases in Antiquity: A Survey ofthe Diseases, 

Injuries and Surgery of Early Populations, pages 272-

278. Springfield, Illinois: Charles C. Thomas. 
474 SMITHSONIAN CONTRIBIJTIONS TO ANTHROPOLOGY 

Ruben, M. P., H. M. Goldman, and S. M. Schulman 

1970. Diseases ofthe Periodontium. In R. J. Gorlin and 

H. M. Goldman, editors, Thoma's Oral Pathology, 

pages 394-444. St. Louis: The C. V. Mosby Company. 

Rucknagel, D. L. 

1966. On the Geographical Distribution and Ethnic Origin of Thalassaemia. New Zealand Medical Journal, 

65:826-832. 

Ruffer, M. A. 

1910. Remarks on the Histology and Pathological Anatomy of Egyptian Mummies. Cairo Scientific Journal, 

4:1-5. 

1918a. Studies in Palaeopathology: Some Recent Researches on Prehistoric Trephining. Journal of Pathology and Bacteriology, 22:90-104. 

1918b. Arthritis Deformans and Spondylitis in Ancient 

Egypt. Journal of Pathology and Bacteriology, 22:152-

196. 

Ruffer, M. A., and A. Rietti 

1912. On Osseous Lesions in Ancient Egyptians. yoMrna/ 

of Pathology and Bacteriology, 16:439-465. 

Ruffer, M. A., and J. G. Willmore 

1914. Note on a Tumor of the Pelvis Dating from Roman Times (250 A. D.) and Found in Egypt. 

Journal of Pathology and Bacteriology, 18:480-484. 

Rutishauser, E., and F. Jacqueline 

1959. Die Rheumatischen Koxitiden. Documenta Rheumatologica, 16:1-124. 

Salfelder, K. 

1971. Cryptococcosis. In R. D. Baker, editor. Human 

Infections with Fungi, Actinomycetes and Algae, pages 

383-464. New York: Springer-Verlag. 

Salzmann, J. A. 

1957. Orthodontics: Principles and Prevention. Philadelphia: 

Lippincott and Company. 

Sankaran, B., and N. Gadekar 

1964. Skeletal Fluorosis. In Proceedings ofthe First European 

Bone and Tooth Symposium, Oxford, 1963. Oxford: 

Pergamon Press. 

Sarjeant, G. R. 

1974. 772^ Clinical Features of Sickle Cell Disease. New York: 

American Elsevier Publishing Company. 

Saul, F. P. 

1972. The Human Skeletal Remains of Altar de Sacrificios. Papers ofthe Peabody Museum of Archaeology and 

Ethnology, 63(2). 

Scarpelli, D. G. 

1956. Fat Necrosis of Bone Marrow in Acute Pancreatitis. American Journal of Pathology, 32:1077-1085. 

Schenk, R. K. 

1973. Fracture Repair—Overview. In H. Czitober and J. 

Eschberger, editors. Calcified Tissue Proceedings Ninth 

European Symposium on Calcified Tissues, pages xiiixxii. Vienna: Facta-Publication. 

Scherer, E. 

1928. Exostosen, Enchondrome und ihre Beziehung zum 

Periost. Frankfurter Zeitschrift fiir Pathologie, 36:587-

605. 

Scheuermann, H. 

1921. Kyphosis Dorsalis Juvenilis. Zeitschrift fiir Orthopddische Chirurgie, 41:305-317. 

Schinz, H. R., W. E. Baensch, E. Friedl, and E. Uehlinger 

1951-1952. Roentgen Diagnostics: Skeleton. Volumes 1 and 

2, English translation by J. T. Case. New York: 

Grune and Stratton. 

Schlumberger, H. G. 

1946a. Fibrous Dysplasia of Single Bones (Monostotic 

Fibrous Dysplasia). Military Surgeon, 99:504-527. 

1946b. Fibrous Dysplasia (Ossifying Fibroma) ofthe Maxilla and Mandible. American Jourruil of Orthodontics, 

32:579-587. 

Schmidt, M. B. 

1929. Rachitis und Osteomalacie. In O. Lubarsch and 

F. Henke, editors, Handbuch der Speziellen Pathologischen Anatomie und Histologie, 9(1): 1-165. Berlin: 

J. Springer. 

Schmorl, G. 

1901. Zur Pathologischen Anatomie der Barlow'schen 

Krankheit. Beitrdge zur Pathologischen Anatomie und 

zur Allgemeinen Pathologie, 30:215-266. 

1909. Die Pathologische Anatomie der Rachitischen 

Knochenerkrankung mit Besonder Beriicksichtingung ihre Histologie und Pathogenese. Ergebnisse 

der Inneren Medizin und Kinderheilkunde, 4:403-454. 

1927. Uber die an den Wirbelbandscheiben vorkommenden Ausdehnungs und Zerreissungsvorgange 

und die dadurch an ihnen und der Wirbelspongiosa hervorgerufenen Veranderungen. Verhandlungen der Deulschen Pathologischen Gesellschafl, 22:250-

262. 

1930. Die Pathogenese der Juvenilen Kyphose. Fortschritte auf dem Gebiete der Rontgenstrahlen, 41:359-

393. 

1931. Anatomische Befunde bei einem Falle von Osteopoikilie. Fortschritte aud dem Gebiete der Rontgenstrahlen, 44:1-8. 

1932. Uber Ostitis Deformans Paget. Virchow's Archiv fur 

Pathologische Anatomie und Physiologie und fiir Klinische 

Medizin, 283:694-751. 

Schmorl, G., and H. Junghanns 

1971. The Human Spine in Health and Disease. Second 

American edition, translated and edited by E. F. 

Besemann. New York: Grune and Stratton. 

Schneider, P. 

1923-1924. Anatomie, Rontgenologic und Bakteriologie 

der Angeborenen Friihsyphilis des Knochensystems. Engebnisse der Allgemeinen Pathologie, 20:185-

212. 

Schoeninger, M. J. 

1979. Dietary Reconstruction at Chalcatzingo, A Form-
NUMBER 28 475 

ative Period Site in Morelos, Mexico. University of 

Michigan, Museum of Anthropology, Technical Report, 9. 

Schultz, A. H. 

1939. Notes on Diseases and Healed Fractures of Wild 

Apes and Their Bearing on the Antiquity of 

Pathological Conditions in Man. Bulletin of the 

History of Medicine, 7:571-582. 

1956. The Occurrence and Frequency of Pathological 

and Teratological Conditions and of Twinning 

Among Non-human Primates. Primatologia, 1:965-

1014. 

Schwarz, J. 

1971. Histoplasmosis. In R. D. Baker, editor. Infections 

with Fungi, Actinomycetes and Algae, pages 67-130. 

New York: Springer-Verlag. 

Sciulli, P. W. 

1977. A Descriptive and Comparative Study ofthe Deciduous Dentition of Prehistoric Ohio Valley 

Amerindians. American Journal of Physical Anthropology, 41:1 \-S0. 

Seligmann, C. G. 

1912. A Cretinous Skull ofthe Eighteenth Dynasty. Man, 

12:17-18. 

Seltzer, C. C. 

1944. Racial Prehistory in the Southwest and the Hawikuh Zunis. Papers ofthe Peabody Museum, number 

23. 

Senn,N. 

1886. Periostitis. The Philadelphia Medical Times, July 24. 

, Shahidi, N. J., and L. K. Diamond 

1960. Skull Changes in Infants with Chronic Iron-Deficiency Anemia. New England Journal of Medicine, 

262:137-139. 

Shepherd-Wilson, W., and M. Gelfand 

1962. Gout in the African: Report of a Case. Central 

African Journal of Medicine, 8:181-183. 

Sherman, M. S., and W. G. Selakovich 

1957. Bone Changes in Chronic Circulatory Insufficiency: A Histopathological Study. Journal of Bone 

and Joint Surgery, 39A:892-901. 

Shore, L. R. 

1936. Some Examples of Disease of the Vertebral Column Found in Skeletons of Ancient Egypt: A 

Contribution to Palaeopathology. British Journal of 

Surgery, 24:256-211. 

Short, C. L. 

1974. The Antiquity of Rheumatoid Arthritis. Arthritis 

and Rheumatism, 17:193-205. 

Sicher, H., and S. N. Bhaskar, editors 

1972. Orban's Oral Histology and Embryology. Saint Louis: 

The C. V. Mosby Company. 

Simon, G., and P. A. Zorab 

1961. The Radiographic Changes in Alkaptonuric Arthritis; A Report on Three Cases (One an Egyptian Mummy). British Journal of Radiology, 34:384-

386. 

Singer, R. 

1962. A Skeleton with Diaphyseal Aclasis. South African 

Archeological Bulletin, 17:14. 

Singleton, E. B., A. J. Rudolph, H. S. Rosenberg, and D. B. 

Singer 

1966. The Roentgenographic Manifestations ofthe Rubella Syndrome in Newborn Infants. American Journal of Roentgenology, Radium Therapy, and Nuclear 

Medicine, 91:82-91. 

Sissons, H. A. 

1956. The Osteoporosis of Cushing's Syndrome, yownza/ 

of Bone and Joint Surgery, 38B:418-433. 

Sissons, H. A., J. Jowsey, and L. Stewart 

1960. The Microradiographic Appearance of Normal 

Bone Tissue at Various Ages. In A. Engstrom, V. 

Cosslett, and H. Pattee, editors. X-ray Microscopy 

and X-ray Microanalysis, pages 206-215. Amsterdam: Elsevier Publishing Company. 

Sj0vold, T., I. Swedborg, and L. Diener 

1974. A Pregnant Woman from the Middle Ages with 

Exostosis Multiplex. Ossa, 1:3-23. 

Smith, Jr., F. R. 

1933. Late Congenital Syphilis (A Study ofthe Results 

of Treatment in 267 Cases). yo/i«j Hopkins Hospital 

Bulletin, 53:231-245. 

Smith, W., R. B. Woodbury, and N. F. S. Woodbury 

1966. The Excavation of Hawikuh by Frederick Webb 

Hodge. Contributions from the Museum ofthe American 

Indian Heye Foundation, volume 20. 

Snorrason, E. S. 

1942. Rheumatism, Past and Present, in the Light of 

Palaeopathology and Social Prehistory. Canadian 

Medical Association Journal, 46:589-594. 

1946. Cranial Deformation in the Reign of Akhnaton. 

Bulletin ofthe History of Medicine, 20:601-610. 

Snow, C. E. 

1943. Two Prehistoric Indian Dwarf Skeletons from 

Moundville. Alabama Museum of Natural History Paper, 21:1-90. 

1948. Indian Knoll Skeletons. University of Kentucky Reports in Anthropology, 4:371-545. 

Sorrel, E., and Mme. Sorrel-Dejerine 

1932. Tuberculose Osseuse et Osteo-Articulaire. Paris: Masson 

et Cie. 

Speiser, F. 

1925. Ein Fall von Systematisierter Enchondromatose 

des Skeletts. Virchow's Archiv fur Pathologische Anatomie und Physiologic, 258:126-160. 

Spink, W. W. 

1956. The Nature of Brucellosis. Minneapolis: University of 

Minnesota Press. 

Star, F. 

1909. Ethnographic Notes from the Congo Free State: 

An African Miscellany. Proceedings of the Davenport 

Academy of Sciences, 12:115-124. 
476 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

Steele, D. G. 

1970. Estimation of Stature from Fragments of Long 

Bones. In T. D. Stewart, editor, Personal Identification in Mass Disasters, pages 85-97. Washington, 

D. C : National Museum of Natural History, 

Smithsonian Institution. 

Steinbach, H. L., and W. G. Obat a 

1957. The Significance of Thinning of the Parietal 

Bones. American Journal of Roentgenology, Radium 

Therapy, and Nuclear Medicine, 78:39-45. 

Steinbock, R. T. 

1976. Paleopathological Diagnosis and Interpretation. Springfield, Illinois: Charles C. Thomas. 

Stenn, F. F., J. W. Milgram, S. L. Lee, R. J. Weigand, and 

A. Veis 

1977. Biochemical Identification of Homogentisic Acid 

Pigment in an Ochronotic Egyptian Mummy. 

Science, 197:566-568. 

Stewart, T. D. 

1931. Incidence of Separate Neural Arch in the Lumbar 

Vertebrae of Eskimos. American Journal of Physical 

Anthropology, 16:51-62. 

1941. The Circular Type of Cranial Deformity in the 

United States. American Journal of Physical Anthropology, 28:343-351. 

1944. Filed Indian Teeth from Illinois. Journal of the 

Washington Academy of Sciences, 34:317. 

1947. Racial Patterns in Vertebral Osteoarthritis. American Journal of Physical Anthropology, 5:230-231. 

1948. The True Form of the Cranial Deformity Originally Described under the Name "Tete Trilobee." 

Journal of the Washington Academy of Sciences, 38:66-

72. 

1950. Deformity, Trephining, and Mutilation in South 

American Indian Skeletal Remains. In}. H. Steward, editor. Handbook of South American Indians. 

Bureau of American Ethnology Bulletin, 143(6): 43-48. 

1956. Examination ofthe Possibility that Certain Skeletal Characters Predispose to Defects in the Lumbar Neural Arches. Clinical Orthopaedics, 8:44-59. 

1958a. The Rate of Development of Vertebral Osteoarthritis in American Whites and Its Significance in 

Skeletal Age Identification. The Leech, 28:144-151. 

1958b. Stone Age Skull Surgery: A General Review with 

Emphasis on the New World. Annual Report of the 

Smithsonian Institution, 1957, pages 469-491. 

1962. Anterior Femoral Curvature, Its Utility for Racial 

Identification. Human Biology, 34:49-62. 

1966. Some Problems in Human Palaeopathology. In S. 

Jarcho, editor, Human Palaeopathology, pages 43-55. 

New Haven: Yale University Press. 

1968. Identification by the Skeletal Structures. In F. E. 

Camps, editor, Gradwohl's Legal Medicine, pages 

123-154. Bristol, England: J. Wright and Sons, 

Ltd. 

1970. Identification of the Scars of Parturition in the 

Skeletal Remains of Females. In T. D. Stewart, 

editor. Personal Identification in Mass Disasters, pages 

127-135. Washington, D. C : National Museum 

of Natural History, Smithsonian Institution. 

1972. Racial Differences in the Manifestation of Scaphocephaly. American Journal of Physical Anthropology, 

37:451. 

1974. Nonunion of Fractures in Antiquity, with Description of Five Cases from the New World Involving 

the Forearm. Bulletin of the New York Academy of 

Medicine, 50:^15-891. 

1975. Cranial Dysraphism Mistaken for Trephination. 

American J ournal of Physical Anthropology, 42:435-438. 

1979a. Essentials of Forensic Anthropology. Springfield, Illinois: Charles C. Thomas. 

1979b. Patterning of Skeletal Pathologies and Epidemiology. In W. S. Laughlin and A. B. Harper, 

editors. The First Americans: Origins, Affinities and 

Adaptations, pages 257-274. New York: Gustav 

Fischer. 

Stewart, T. D., and A. Spoehr 

1952. Evidence on the Paleopathology of Yaws. Bulletin 

ofthe History of Medicine, 26:538-553. 

Stiris, G. 

1958. Bone and Joint Changes in Haemophiliacs. Ada 

Radiologica, 49:269-275. 

Stougaard, J. 

1964. Familial Occurrence of Osteochondritis Dissecans. 

Journal of Bone and Joint Surgery, 46:542-543. 

Stout, S., and D. J. Simmons 

1979. Use of Histology in Ancient Bone Research. Yearbook of Physical Anthropology, 22:228-249. 

Straatsma, B. R., L. E. Zimmerman, and J. D. M. Gass 

1962. Phycomycosis: A Clinicopathologic Study of FiftyOne Cases. Laboratory Investigation, 11:963-985. 

Straus, D. C. 

1933. Tuberculosis of the Flat Bones of the Vault of the 

Skull. Surgery, Gynecology and Obstetrics, 57:384-398. 

Sublett, A. J., and C. F. Wray 

1970. Some Examples of Accidental and Deliberate Human Skeletal Modification in the Northeast. Bulletin of the New York State Archaeological Association, 

50:14-26. 

Swedlund, A. C , and G. J. Armelagos 

1976. Demographic Anthropology. Dubuque, Iowa: Wm. C. 

Brown Company. 

Thomas, H. B. 

1936. Some Orthopedic Findings in Ninety-eight Cases 

of Hemophilia, yowrna/ of Bone and Joint Surgery, 18: 

140-147. 

Thorndike, L. 

1942. A Possible Reference to Syphilis before the Discovery of America. Bulletin ofthe History of Medicine, 

11:474. 

Todd, T. W. 

1920. Age Changes in the Pubic Bone, I: The Male 
NUMBER 28 477 

White Pubis. American Journal of Physical Anthropology, 3:285-334. 

1921. Age Changes in the Pubic Bone. American Journal 

of Physical Anthropology, 4:1-70. 

Tomes, J., and C. de Morgan 

1853. Observations on the Structure and Development 

of Bone. Philosophical Transactions ofthe British Royal 

Society, 143:109-139. 

Tomlinson, W. J. 

1945. The Incidence of Sickle Cell Anemia in 3000 

Canal Zone Examinations upon Natives of Central America. American Journal of Medical Science, 

209:181-186. 

Toole, H. 

1964. Fractures of the Skull: Diagnosis and Treatment 

in Ancient Greece. Journal ofthe International College 

of Surgeons, 42:89-94. 

Tregubow, S. 

1929. Die Reelle Verlangerung der Extremitaten bei der 

Knochen und Gelenktuberkulose. Zeitschrift fiir Orthopddische Chirurgie, 51:282-295. 

Tretsven, V. E. 

1965. Impressions Concerning Clefts in Montana Indians ofthe Past. Cleft Palate Journal, 2:229-236. 

Trotter, M., and G. C. Gleser 

1952. Estimation of Stature from Long Bones of American Whites and Negroes. American Journal of Physical Anthropology, 10:463-514. 

1958. A Re-evaluation of Estimation of Stature Based 

on Long Bones After Death. American Journal of 

Physical Anthropology, 16:79-123. 

Trueta, J. 

1957. The Normal Vascular Anatomy of the Human 

Femoral Head during Growth. Journal of Bone and 

Joint Surgery, 39B:358-394. 

1959. The Three Types of Acute Hematogenous Osteomyelitis, a Clinical and Vascular Study, yowrna/ of 

Bone and Joint Surgery, 41B:671-680. 

Trueta J., and M. H. M. Harrison 

1953. The Normal Vascular Anatomy of the Femoral 

Head in Adult Man. Journal of Bone and Joint Surgery, 

356:442-461. 

Turner, C. G. 

1979. Dental Anthropological Indications of Agriculture 

Among the Jomon People of Central Japan. American Journal of Physical Anthropology, 51:619-635. 

Turner, C. G., and N. T. Morris 

1970. A Massacre at Hopi. American Antiquity, 35:320-

331. 

Ubelaker, D. H. 

1974. Reconstruction of Demographic Profiles from Ossuary Skeletal Samples. Smithsonian Contributions to 

Anthropology, number 18. 

1978. Human Skeletal Remains. Chicago: Aldine Publishing Company. 

Uehlinger, E. 

1936. Myositis Ossificans Progressiva. Ergebnisse der Strahlenforschung, 7:175-220. 

1941. Hyperostosis Generalisata mit Pachydermie (Idiopathische Familiare Generalisierte Osteophytose 

Friedreich-Erb-Arnold). Virchow's Archiv fiir Pathologische Anatomie, 308:396-444. 

1957. Thyreogene Osteodystrophie bei Inkretorisch 

Aktivem Metastasierendem, Kleinfollikularem 

Schilddriisenadenom. Schweizer Medizinische Wochenschrift, 87:683-688. 

1960. Osteofibrosis Deformans Juvenilis (Polyostotische 

Fibrose Dysplasie Jaffe-Lichtenstein). Virchow's 

Archiv fiir Pathologische Anatomie, 306:255-299. 

Urteaga, B. O., and J. E. Moseley 

1967. Craniometaphyseal Dysplasia in an Ancient Skeleton from the Mochica Culture of Peru. American 

Journal of Roentgenology, Radium Therapy and Nuclear 

Medicine, 99:712-716. 

Van Wersch, H. J. 

1954. Scurvy as a Skeletal Disease. Utrecht: Dekherand 

Van De Vigt. 

Virchow, R. 

1848. Uber die Puerperalen Krankheiten. Verhandlungen 

der Gesellschafl fiir Geburtshulfe in Berlin, 3:151-196. 

1856. Die Multiloculare, Ulcerirende Echinokokkengeschwulst der Leber. Verhandlungen Physikalisch 

Medicinische Gesellschafl Wurzburg, 6:84-95. 

1858. Uber die Natur der Constitutionell-syphilitischen 

Affectionen. Virchow's Archiv fiir Pathologische Anatomic und Physiologic, 15:217-236, 243-253. 

1874. Altpatagonische, Altchilenische und Moderne 

Pampas Schadel. Verhandlungen der Berliner Gesellschafl fiir Anthropologic, Ethnologic und Urgeschichte, 6: 

51-64. 

1896. Beitrage zur Geschichte der Lues. Dermatologische 

Zeitschrift, 3:1-9. 

1898. Knochen aus Alten Grabern von Tennessee. Verhandlungen der Berliner Gesellschafl fiir Anthropologie, 

30:342-344. 

Volkmann, J. 

1915. Uber die Primaere Akute und Subakute Osteomyelitis Purulenta der Wirbel. Deutsche Zeitschrift 

fiir Chirurgie, 132:445-510. 

Von Endt, D. W. 

1979. Techniques of Amino Acid Dating. In R. Humphrey and D. Stanford, editors, Pre-Llano Cultures 

of the Americas: Paradoxes and Possibilities, pages 71-

100. Washington, D. C : Anthropological Society 

of Washington. 

Von Endt, D. W., and D.J. Ortner 

1977. Amino Acid Analysis of Bone in a Suspected Case 

of Iron Deficiency Anemia (abstract). American 

Journal of Physical Anthropology, 47:165. 

1981. Amino Acid Analysis of Bone from a Suspected 

Case of Prehistoric Iron Deficiency Anemia. Amer-
478 SMITHSONIAN CONTRIBUTIONS TO ANTHROPOLOGY 

ican Journal of Physical Anthropology, in press. 

Vyhnanek, L., H. Hanakova, M. Stloukal, and J. Kola? 

1965. Congenital Synostoses in Old Slavic Bone Material. Zentralblatt fur Chirurgie, 90:2188-2191. 

Vyhnanek, L., J. Kolai^, and M. Stloukal 

1963. "Hair-Brush" Skulls in Early Medieval Finds of 

Mikulcice. Anthrpoplogic, 1:81-82. 

Walther, H. E. 

1948. Krebsmetastasen. Basel: B. Schwabe. 

Warren, J. C. 

1822. A Comparative View ofthe Sensorial and Nervous Systems 

in Man and Animals. Boston: J. W. Ingraham. 

Wassersug, J. D. 

1940. Tuberculosis of the Greater Trochanter and Trochanteric Bxirsae. Journal of Bone and Joint Surgery, 

22:1075-1079. 

Weidenreich, F. 

1939. The Duration of Life of Fossil Man in China and 

the Pathological Lesions Found in His Skeleton. 

Chinese Medical Journal, 55:34-44. 

Weiss, P. 

1955. Casos Peruanos Prehistoricos de Cauterizaciones. 

T-sincipital de Manouvrier. Museo Nacional de Antropologia y Arqueologia Revista, 2:3-23. 

Wells, C. 

1961. A Case of Lumbar Osteochondritis from the 

Bronze Age. Journal of Bone and Joint Surgery, 436: 

575. 

1962a. A Possible Case of Leprosy from a Saxon Cemetery 

at Beckford. Medical History, 6:383. 

1962b. Joint Pathology in Ancient Anglo-Saxons, yourna/ 

of Bone and Joint Surgery, 446:948-949. 

1963a. Hip Disease in Ancient Man: Report of Three 

Cases. Journal of Bone and Joint Surgery, 456:790-

791. 

1963b. Polyostotic Fibrous Dysplasia in a Seventh Century 

Anglo-Saxon. British Journal of Radiology, 36:925. 

1964a. Bones, Bodies and Disease. London: Thames and 

Hudson. 

1964b. Two Mediaeval Cases of Malignant Disease. British Medical Journal, 1:1611-1612. 

1965a. Diseases of the Knee in Anglo-Saxons. Medical and 

Biological Illustration, 15:100-107. 

1965b. Osteogenesis Imperfecta from an Anglo-Saxon 

6urial Ground at 6yrgh Castle, Suffolk. Medical 

History, 9:88-89. 

1968. Osgood-Schlatter's Disease in the Ninth Century? 

British Medical Journal, 2:623-624. 

1973. A Paleopathological Rarity in a Skeleton of Roman Date. Medical History, 17:399-400. 

1974a. The Results of "Bone Setting" in Anglo-Saxon 

Times. Medical and Biological Illustration, 24:215-

220. 

1974b. Osteochondritis Dissecans in Ancient British Skeletal Material. Medical History, 18:365-369. 

1975. Ancient Obstetric Hazards and Female Mortality. 

Bulletin of the New York Academy of Medicine, 51: 

1235-1249. 

1976. The Huma n Burials. East Anglian Archaeology, 3: 

103-120. 

Wells, C , and C. Dallas 

1976. Romano-British Pathology. Antiquity, 50:53-55. 

Wells, C , and 6. M. Maxwell 

1962. Alkaptonuria in an Egyptian Mummy. British 

Journal of Radiology, 35:679-682. 

Wells, C , and N. Woodhouse 

1975. Paget's Disease in an Anglo-Saxon. Medical History, 

19:396-400. 

Wells, J. R. 

1942. A Diminutive Skull from Peru. American Journal of 

Physical Anthropology, 29:425-427. 

Wheeler, R. E. M. 

1923. A New 6eaker from Wales. Antiquaries Journal, 3: 

21-23. 

Whitney, J. L., and W. I. 6aldwin 

1915. Syphilis ofthe Spine. Journal of the American Medical 

Association, 65:1989-1994. 

Wilensky, A. O. 

1932. Osteomyelitis of the Jaws. Archives of Surgery, 25: 

183-237. 

1934. Osteomyelitis: Its Pathogenesis, Symptomatology, and 

Treatment. New York: Macmillan Company. 

Wilkins, L. 

1941. Epiphysial Dysgenesis Associated with Hypothyroidism. American Jourruil of Diseases of Children, 61: 

13-34. 

1950. The Diagnosis and Treatment of Endocrine Disorders in 

Childhood and Adolescence. Springfield, Illinois: 

Charles C. Thomas. 

Williams, G. D., W. A. Ritchie, and P. F. Titterington 

1941. Multiple 6ony Lesions Suggesting Myeloma in 

Pre-Columbian Indian Aged Ten Years. American 

Journal of Roentgenology and Radium Therapy, 46:351-

355. 

Williams, H. U. 

1929. Huma n Paleopathology, with Some Original Observations on Symmetrical Osteoporosis of the 

Skull. Archives of Pathology, 7:839-902. 

1932. The Origin and Antiquity of Syphilis: The Evidence from Diseased 6ones, a Review with Some 

New Material from America. Archives of Pathology, 

13:779-814,931-983. 

1935. Pathology of Yaws. Archives of Pathology, 20:596-

630. 

Willson, J. R., C. T. 6eecham, and E. R. Carrington 

1971. Obstetrics and Geography. Saint Louis: Th e C. V. 

Mosby Company. 

Wilson, J. V. K. 

1967. Organic Diseases of Ancient Mesopotamia. In D. 

R. 6rothwell and A. T. Sandison, editors, Diseases 
NUMBER 28 479 

in Antiquity: A Survey of the Diseases, Injuries and 

Surgery of Early Populations, pages 191-208. Springfield, Illinois: Charles C. Thomas. 

Wilson, P. W., and M. S. Mathis 

1930. Epidemiology and Pathology of Yaws, Based on 

Study of 1423 Consecutive Cases in Haiti. Journal 

ofthe American Medical Association, 94:1289-1292. 

Wimberger, H. 

1925. V. Klinisch-Radiologische Diagnostik von Rachitis, Skorbut und Lues Congenita im Kindesalter. 

Ergebnisse der Inneren Medizin urul Kinderheilkunde, 28: 

264-370. 

Winslow, J. D. 

1971. Mycetoma. In R. D. Baker, editor. Human Infections 

with Fungi, Actinomycetes and Algae, pages 589-613. 

New York: J. Springer. 

Withington, E. T., translator 

1927. Hippocrates. London: W. Heinemann. 

Witorsch, P., and J. P. Utz 

1968. North American Blastomycosis: A Study of 40 

Patients. Medicine, 47:169-200. 

Wong, K. C , and L. T. Wu 

1936. History of Chinese Medicine. Shanghai: National 

Quarantine Service. 

Wood-Jones, F. 

1908a. The Pathological Report. Archaeological Survey of 

Nubia Bulletin, 2:55-69. 

1908b. The Examination ofthe Bodies of 100 Men Excavated in Nubia in Roman Times. The British Medical Journal, 1:736-737. 

1910a. Anatomical Variations, and the Determination of 

the Age and Sex of Skeletons. In G. Elliot-Smith 

and F. Wood-Jones, editors, The Archaeological Survey of Nubia Report for 1907-1908, Volume II: Report 

on the Human Remains, pages 221-262. Cairo: National Printing Department. 

1910b. General Pathology (Including Diseases of the 

Teeth). In G. Elliot-Smith and F. Wood-Jones, 

editors. The Archaeological Survey of Nubia Report for 

1907-1908, Volume II: Report on the Human Remains, 

pages 263-292. Cairo: National Printing Department. 

1910c. Fractured Bones and Dislocations. In G. ElliotSmith and F. Wood-Jones, editors, The Archaeological Survey of Nubia Report for 1907-1908, Volume II: 

Report on the Human Remains, pages 293-342. Cairo: 

National Printing Department. 

World Health Organization 

1976. World Health Statistics Annual 1973-1976. Geneva: 

World Health Organization. 

Yoeli, M. 

1955. A "Facies Leontina" of Leprosy on an Ancient 

Canaanite Jar. Journal ofthe History of Medicine, 10: 

331-333. 

Young, W. 6. 

1960. Actinomycosis with Involvement of the Vertebral 

Column: Case Report and Review ofthe Literature. Clinical Radiology, 11:175-182. 

Zaborowski, M. 

1897. Le T Sincipital.—Mutilation des Cranes Neolithiques, Observee en Asie Centrale. Bulletins de la 

Societe d'Anthropologie de Paris, series 4, 8:501-503. 

Zaino, E. 

1964. Paleontologic Thalassemia. Annals of the New York 

Academy of Sciences, 119:402-412. 

Zandy, C. 

1896. Uber die Tuberculose der Alveolarfortsatze. Archiv 

fdr Klinische Chirurgie, 52:178-189. 

Zeiliger, V. 

1911. Les Fractures Sponlanees dans la Sportrichose. These de 

Faculte de Medicine de Paris, 466. Paris: Jouve et 

Cie. 

Zeuner, F. E. 

1958. Dating the Past. Fourth edition. London: Methuen 

and Company, Ltd. 

Zorab, P. A. 

1961. The Historical and Prehistorical 6ackground of 

Ankylosing Spondylitis. Proceedings of the Royal Society of Medicine, 54:415-420.