Bone Health and Osteoporosis

A Report of the Surgeon General

Department of Health and Human Services
2004

U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES

Public Health Service

Office of the Surgeon General

Rockville, MD

Bone Health and Osteoporosis

A Report of the Surgeon General
National Library of Medicine Cataloging in Publication

Bone health and osteoporosis : a report of the Surgeon

General. - Rockville, Md. : U.S. Dept. of Health and

Human Services, Public Health Service, Office of

the Surgeon General ; Washington, D.C. : For sale

by the Supt. of Docs., U.S. G.P.O., 2004.

 p.436

 Includes index.

1. Bone Diseases - prevention & control. 2. Bone

Diseases - etiology. 3. Osteoporosis - prevention &

control. 4. Bone and Bones - physiology. 5. Health

Promotion - methods. 6. United States. I. United

States. Public Health Service. Office of the Surgeon

General.

WE 225 B71259 2004

This publication is available on the

World Wide Web at

http://www.surgeongeneral.gov/library

For sale by the Superintendent of Documents, U.S.

Government Printing Office, Washington, D.C. 20402.

Use of trade names is for identification only and does

not constitute endorsement by the U.S. Department of

Health and Human Services.

U.S. Department of Health and Human Services. Bone

Health and Osteoporosis: A Report of the Surgeon

General. Rockville, MD: U.S. Department of Health

and Human Services, Office of the Surgeon General, 2004.

 Suggested Citation
iii

Secretary of the U.S. Department of Health and Human Services

This first-ever Surgeon General’s Report on bone health and osteoporosis illustrates

the large burden that bone disease places on our Nation and its citizens. Like other

chronic diseases that disproportionately affect the elderly, the prevalence of bone

disease and fractures is projected to increase markedly as the population ages. If these

predictions come true, bone disease and fractures will have a tremendous negative

impact on the future well-being of Americans. But as this report makes clear, they

need not come true: by working together we can change the picture of aging in

America. Osteoporosis, fractures, and other chronic diseases no longer should be

thought of as an inevitable part of growing old. By focusing on prevention and lifestyle

changes, including physical activity and nutrition, as well as early diagnosis and

appropriate treatment, Americans can avoid much of the damaging impact of bone

disease and other chronic diseases.

In recognition of the importance of promoting bone health and preventing

fractures, President George W. Bush has declared 2002–2011 as the Decade of the

Bone and Joint. With this designation, the United States has joined with other nations

throughout the world in committing resources to accelerate progress in a variety of

areas related to the musculoskeletal system, including bone disease and arthritis.

As a part of its Healthy People 2010 initiative, the U.S. Department of Health

and Human Services (HHS) has developed an important goal for Americans—to

increase the quality and years of healthy life. Our hope is that Americans can live

long and live well. Unfortunately, fractures—the most common and devastating

consequence of bone disease—frequently make it difficult and sometimes impossible

for people to realize this goal.

HHS is committed to developing a wide array of creative and innovative

approaches that can help make the goal of living long and living well a reality for

Americans. Several programs of particular relevance to bone health include:

• The National Institutes of Health’s Osteoporosis and Related Bone Diseases

~ National Resource Center. The National Resource Center provides timely

information for health professionals, patients, and the public on osteoporosis,

Paget’s disease of bone, osteogenesis imperfecta, and other metabolic bone

diseases.

• The National Bone Health Campaign. Targeted at 9- to 12-year-old girls and

their parents, this campaign uses Web sites and other activities to promote

nutritional choices and physical activities that benefit bone health.

Message From Tommy G. Thompson
iv

• Steps to a HealthierUS Initiative. HHS launched this initiative in 2003 to

advance the President’s goal of helping Americans live longer, better, and

healthier lives. At the heart of this program lies both personal responsibility

for the choices Americans make and social responsibility to ensure that

policymakers support programs that foster healthy behaviors and prevent

disease.

• VERBTM. It’s what you do. This national, multicultural, social marketing

campaign encourages young people ages 9–13 to be physically active every

day as a means of promoting overall health, including bone health.

This Surgeon General’s Report brings together for the first time the scientific

evidence related to the prevention, assessment, diagnosis, and treatment of bone

disease. More importantly, it provides a framework for moving forward. The

report will be another effective tool in educating Americans about how they can

promote bone health throughout their lives. I appreciate the efforts of Surgeon

General Richard H. Carmona and the many scientists and researchers who

contributed to the development of this report.
Preface

 From the Surgeon General,

U.S. Department of Health and Human Services

As Surgeon General, my primary role is to provide the American people with the

best scientific information available on how to improve health and reduce the risk of

illness and injury. This first-ever Surgeon General’s Report on bone health and

osteoporosis provides much needed information on bone health, an often overlooked

aspect of physical health. This report follows in the tradition of previous Surgeon

Generals’ reports by identifying the relevant scientific data, rigorously evaluating

and summarizing the evidence, and determining conclusions.

A healthy skeletal system with strong bones is essential to overall health and quality

of life. Yet, today, far too many Americans suffer from bone disease and fractures,

much of which could be prevented. An estimated 10 million Americans over age 50

have osteoporosis (the most common bone disease), while another 34 million are at

risk. Each year an estimated 1.5 million people suffer an osteoporotic-related fracture,

an event that often leads to a downward spiral in physical and mental health. In fact,

20 percent of senior citizens who suffer a hip fracture die within 1 year. One out of

every two women over 50 will have an osteoporosis-related fracture in their lifetime,

with risk of fracture increasing with age. Due primarily to the aging of the population

and the previous lack of focus on bone health, the number of hip fractures in the

United States could double or even triple by the year 2020.

However, the evidence in this report is clear: Hope is not lost. Over the past

several decades, scientists have learned a significant amount about the prevention,

diagnosis, and treatment of bone disease. Our next and most critical step is to transfer

this knowledge from the research laboratories to the general population.

One of my priorities is to promote disease prevention by helping Americans take

actions to make themselves and their families healthier. The good news is that regarding

bone health, these steps are clear—with appropriate nutrition and physical activity

throughout life, individuals can significantly reduce the risk of bone disease and

fractures. Health professionals can also make significant improvements in our Nation’s

bone health by proactively assessing, diagnosing, and treating at-risk patients and

then helping them apply this scientific knowledge in their everyday lives.

v
However, individuals and health professionals acting alone will not

make a long-term difference. This brings us to the primary message of this

report: A coordinated public health approach that brings together a variety

of public and private sector stakeholders in a collaborative effort is the

most promising strategy for improving the bone health of Americans. This

report calls for the development of a national action plan to achieve

improved bone health, and it highlights the unique and valuable perspectives

that key stakeholders can bring to this effort. While government ought to

be a part of the plan’s development, leadership must be shared among the

many public, private, nonprofit, academic, and scientific stakeholders.

Over the past 2 years, I have worked to improve the health literacy of

Americans; that is, to ensure that individuals can access, understand, and

use health-related information and services to make appropriate health

decisions. To that end, a short, easy-to-read companion piece to this report

has been developed. Available in English and Spanish, this People’s Piece

takes the best scientific information available in this report and provides

Americans with important, practical information on how they can improve

their own bone health.

I am encouraged by the participation of so many people and

organizations in developing this report, and I would like to thank them for

their willingness and eagerness to assist us in gathering the best scientific

information available. I am confident that their passion will be a catalyst

for action. Working together, we can take real steps to improve the bone

health status of Americans. Our reward for this effort will be to prove the

forecasters wrong—instead of seeing ever-increasing numbers of individuals

suffering from the agony of bone disease and fractures, we will see the day

when fewer and fewer Americans bear this burden.

Richard H. Carmona, M.D., M.P.H., FACS

Surgeon General

vi
Blank
Blank
Acknowledgments ix

Acknowledgments

This report was prepared by the U. S.

Department of Health and Human Services

under the general direction of the Office of the

Surgeon General.

Richard H. Carmona, M.D., M.P.H., F.A.C.S.,

Surgeon General, U.S. Public Health Service,

Office of the Surgeon General, Office of the

Secretary, Washington, D.C.

Christina Beato, M.D., Acting Assistant

Secretary for Health, Office of the Secretary,

Washington, D.C.

Arthur Lawrence, Ph.D., R.Ph., Assistant

Surgeon General, U.S. Public Health Service,

Deputy Assistant Secretary for Health

(Operations), Office of Public Health and

Science, Office of the Secretary, Washington,

D.C.

Kenneth Moritsugu, M.D., M.P.H., Deputy

Surgeon General, U.S. Public Health Service,

Office of the Surgeon General, Office of the

Secretary, Washington, D.C.

Allan S. Noonan, M.D., M.P.H., CAPT, U.S.

Public Health Service, Scientific Editor, Surgeon

General’s Report, Office of the Surgeon General,

Office of the Secretary, Washington, D.C.

Stephen I. Katz, M.D., Ph. D., Director,

National Institute of Arthritis and

Musculoskeletal and Skin Diseases, National

Institutes of Health, Bethesda, Maryland.

The editors of the report were

Joan A. McGowan, Ph.D., Senior Scientific

Editor, Surgeon General’s Report, Director,

Musculoskeletal Diseases Branch, Extramural

Program, National Institute of Arthritis and

Musculoskeletal and Skin Diseases, National

Institutes of Health, Bethesda, Maryland.

Lawrence G. Raisz, M.D., Scientific Editor,

Surgeon General’s Report, Board of Trustees

Distinguished Professor of Medicine, Interim

Director, Musculoskeletal Institute, Division of

Endocrinology and Metabolism, University of

Connecticut Health Center, Farmington,

Connecticut.

Allan S. Noonan, M.D., M.P.H., CAPT, U.S.

Public Health Service, Scientific Editor, Surgeon

General’s Report, Office of the Surgeon General,

Office of the Secretary, Washington, D.C.

Ann L. Elderkin, P.A., Managing Editor and

Project Director, Surgeon General’s Report,

Health Systems Research, Inc., Washington, D.C.

The scientific writer was

Larry S. Stepnick, M.B.A., Scientific Writer,

The Severyn Group, Inc., Ashburn, Virginia.

Coordinating authors were

Deborah T. Gold, Ph.D., Associate Professor,

Departments of Psychiatry and Behavioral Sci-
x Acknowledgments

ences, Sociology and Psychology: Social and

Health Sciences, Duke University Medical Center, Durham, North Carolina.

Susan L. Greenspan, M.D., Professor of

Medicine, University of Pittsburgh, Pittsburgh,

Pennsylvania.

Anne Looker, Ph.D., Senior Research

Epidemiologist, Health Examination Statistics,

National Center for Health Statistics, Centers

for Disease control and Prevention, Hyattsville,

Maryland.

L. Joseph Melton, III, M.D., Eisenberg

Professor, Department of Health Sciences

Research, Mayo Clinic and Foundation,

Rochester, Minnesota.

Lynne Wilcox, M.D., M.P.H., CAPT, U.S.

Public Health Service, Editor-in-Chief,

Preventing Chronic Disease, National Center for

Chronic Disease Prevention and Health

Promotion, Centers for Disease Control and

Prevention, Atlanta, Georgia.

Deborah E. Sellmeyer, M.D., Assistant

Professor of Medicine, Director, University of

Calfornia San Francisco / Mt. Zion Osteoporosis

Center, San Francisco, California.

David Reuben, M.D., Professor of Medicine,

Division of Geriatrics, David Geffen School of

Medicine, University of California at Los

Angeles, Los Angeles, California.

Contributing authors were

Laura Bachrach, M.D., Pediatrics Department,

Stanford University Medical Center, Stanford,

Connecticut.

Douglas Bauer, M.D., Associate Professor of

Clinical Medicine, University of California, San

Francisco, San Francisco, California.

John P. Bilezikian, M.D., Professor of Medicine

and Pharmacology, College of Physicians and

Surgeons, New York, New York.

Dennis Black, Ph.D., Professor, Department of

Epidemiology and Biostatistics, University of

California, San Francisco, San Francisco,

California.

Jane Cauley, Dr.P.H., Associate Professor,

Department of Epidemiology, University of

Pittsburgh, Pittsburgh, Pennsylvania.

Jan A. Christensen, M.S.W., J.D., Manager,

Diabetes, Kidney and other Chronic Diseases,

Chronic Disease and Injury Control, Michigan

Department of Community Health, Lansing,

Michigan.

Carolyn Crandall, M.D., F.A.C.P., Associate

Professor of Medicine, Iris Cantor-UCLA

Women’s Health Center, University of

California at Los Angeles, David Geffen School

of Medicine, Los Angeles, California.

Steven R. Cummings, M.D. University of

California, San Francisco, San Francisco,

California.

Denise Cyzman, M.S., R.D., Senior Project

Coordinator, Health Promotion and Disease

Prevention, Osteoporosis, and Other Chronic

Conditions, Michigan Public Health Institute,

Okemos, Michigan.

Susan Davidson, M.S., R.D., Consultant,

Germantown, Maryland.
Acknowledgments xi

Bess Dawson-Hughes, M.D., Professor of

Medicine, Metabolism Lab, Tufts University,

U.S.D.A. Human Research Center on Aging,

Boston, Massachusetts.

Deborah A. Galuska, Ph.D., M.P.H.,

Epidemiologist, Division of Nutrition and

Physical Activity, Centers for Disease Control

and Prevention, Atlanta, Georgia.

Gail Greendale, M.D., Professor of Medicine

and Opbstetrics-Gynecology, University of

California at Los Angeles, David Geffen School

of Medicine, Los Angeles, California.

Robert P. Heaney, M.D., F.A.C. P., F.A.C.N.,

John A. Creighton University Professor,

Professor of Medicine, Department of

Medicine, Creighton University, Omaha,

Nebraska.

Gregory Heath, D.H.Sc., M.P.H., Division of

Nutrition and Physical Activity, National

Center for Chronic Disease Prevention and

Health Promotion, Centers for Disease Control

and Prevention, Atlanta, Georgia.

Ann Hewitt, Ph.D., C.H.E.S., Assistant

Director, Master in Healthcare Administration

Program, Seton Hall University, Center for

Public Service, Mendham, New Jersey.

David P. Hopkins, M.D., M.P.H., Staff

Scientist, Health Promotion and Chronic

Disease Program, Oregon Department of

Human Services, Portland, Oregon.

Anne M. Kenny, M.D., Assistant Professor,

University of Connecticut Center on Aging,

Farmington, Connecticut.

Sundeep Khosla, M.D., Professor of Medicine,

Department of Endocrinology, Mayo Clinic and

Foundation, Rochester, Minnesota.

Douglas P. Kiel, M.D., M.P.H., Director of

Medical Research, Research and Training

Institute, Hebrew Rehabilitation Center for the

Aged, Boston, Massachusetts.

Anne Klibanski, M.D., Chief, Neuroendocrine

Unit, Massachusetts General Hospital,

Neuroendocrine Unit, Boston, Massachusetts.

Nancy E. Lane, M.D., Associate Professor,

Division of Rheumatology, University of

California at San Francisco, San Francisco,

California.

Craig B. Langman, M.D., Isaac A. Abt, MD

Professor of Kidney Diseases, Feinberg School

of Medicine, Northwestern University, Chicago,

IL. Head, Division of Kidney Diseases, Children’s

Memorial Medical Center, Chicago, Illinois.

Peggy Lassanske, President, Elder Floridians

Foundation, Tallahassee, Florida.

Meryl LeBoff, M.D., Director, EndocrineHypertension Division, Skeletal Health and

Osteoporosis, Brigham and Women’s Health,

Boston, Massachusetts.

Karen Lim, Acting Executive Director, National

Asian Women’s Health Organization, San

Francisco, California.

Geraldine Mackenzie, Supervisor, New Jersey

Department of Health and Senior Services,

Older Adult Health and Wellness, Trenton,

New Jersey.
xii Acknowledgments

Catherine MacLean, M.D., Ph.D., Assistant

Professor of Medicine, Division of Rheumatology,

University of California at Los Angeles School of

Medicine, Los Angeles, California.

John McGrath, Ph.D., Chief, Public Information

and Communications Branch, National Institute

of Child Health and Human Development,

National Institutes of Health, Bethesda,

Maryland.

Heather McKay, Ph.D., Associate Professor,

School of Human Kinetics, University of British

Columbia, Vancouver, British Columbia, Canada.

Paul Miller, M.D., F.A.C.P., Clinical Professor of

Medicine, University of Colorado Health Sciences

Center, Denver, Colorado. Medical Director,

Colorado Center for Bone Research, Lakewood,

Colorado.

Heidi D. Nelson, M.D., M.P.H., Investigator and

Associate Director, Clinical Prevention Center,

Oregon Health Sciences University, Portland,

Oregon.

Eric S. Orwoll, M.D., Professor of Medicine,

Program Director, General Clinical Research

Center, Associate Dean for Clinical Research,

Assistant Vice President for Research, Oregon

Health and Science University, Portland, Oregon.

Rebecca Payne, M.P.H., Public Health Analyst,

Nutrition and Physical Activity Communication

Team, Centers for Disease Control and

Prevention, Atlanta, Georgia.

Munro Peacock, M.D., Professor of Medicine,

General Clinical Research Center, Indiana

University Medical Center, Indianapolis, Indiana.

B. Lawrence Riggs, M.D., Distinguished

Investigator, May Foundation, Purvis and

Roberta Tabor Professor of Medical Research,

Mayo Medical School, Division of

Endocrinology, Mayo Clinic and Foundation,

Rochester, Minnesota.

G. David Roodman, M.D., Ph.D., Professor of

Medicine, Division of Hematology/Oncology,

School of Medicine, University of Pittsburgh,

Pittsburgh, Pennsylvania.

Clifford Rosen, M.D., Chief of Medicine, Maine

Center for Osteoporosis Research, St. Joseph

Hospital, Bangor, Maine.

Elizabeth Shane, M.D., Professor of Clinical

Medicine, College of Physicians and Surgeons,

Department of Medicine, Columbia University,

New York, New York.

Kathy Shipp, P.T., Ph.D., Assistant Research

Professor, Physical Therapy, Community and

Family Medicine, Duke University Medical

Center, Durham, North Carolina.

Ethel S. Siris, M.D., Madeline C. Stabile

Professor of Clinical Medicine, Endocrinology

Division, Columbia University and Columbia

Presbyterian Medical Center, Harkness Pavilion,

New York, New York.

MaryFran Sowers, Ph.D., Professor,

Department of Epidemiology, University of

Michigan, Ann Arbor, Michigan.

Anna N. Tosteson, Sc.D., Professor,

Departments of Medicine and Community and

Family Medicine, Dartmouth Medical School,

Lebanon, New Hampshire.
Acknowledgments xiii

Nelson Watts, M.D., Director, Bone Health and

Osteoporosis Center, University of Cincinnati,

Cincinnati, Ohio.

Connie M. Weaver, Ph.D., Distinguished

Professor, Department Head, Foods and

Nutrition, Purdue University, West Lafayette,

Indiana.

Michael F. White, Consultant, Michael F. White

and Associates, Women’s Health Council,

Association of State and Territorial Directors of

Chronic Disease Programs, Alexandria, Virginia.

Michael P. Whyte, M.D., Professor of Medicine,

Pediatrics, and Genetics, Bone and Mineral

Diseases, Department of Medicine, BarnesJewish Hospital at Washington University

School of Medicine, St. Louis, Missouri.

Joseph D. Zuckerman, M.D., Chairman,

Department of Orthopedic Surgery, Hospital for

Joint Diseases, New York, New York.

Reviewers were

Steven A. Abrams, M.D., Professor, Pediatric/

Children’s Nutrition Research Center, Baylor

College of Medicine, Houston, Texas.

Amy Allina, Program and Policy Director,

National Women’s Health Network,

Washington, D.C.

Nell Armstrong, Ph.D., R.N., Program Director,

Division of Extramural Activities, National

Institute of Nursing Research, National

Institutes of Health, Bethesda, Maryland.

David Atkins, M.D., M.P.H., Senior Health

Policy Analyst, Center for Practice and

Technology Assessment, Agency for Healthcare

Research and Quality, U.S. Department of

Health and Human Services, Rockville,

Maryland.

John Baron, M.D., M.S., M.Sci., Professor of

Medicine and of Community and Family

Medicine, Biostatistics and Epidemiology,

Dartmouth Medical School, Lebanon, New

Hampshire.

Douglas Bauer, M.D., Associate Professor of

Clinical Medicine, University of California, San

Francisco, San Francisco, California.

L. Tony Beck, Ph.D., Program Officer, Division

of Clinical Research, National Center for

Research Resources, National Institutes of

Health, Bethesda, Maryland.

Michele F. Bellantoni, M.D., Associate Professor

of Medicine, Division of Geriatric Medicine and

Gerontology, Johns Hopkins University School

of Medicine (representing American Geriatrics

Society), Baltimore, Maryland.

Francis J. Bonner, Jr., M.D., Physiatrist,

Department of Physical Medicine,

Rehabilitation Hospital of South Jersey,

Vineland, New Jersey.

Kathryn Brewer, P.T., G.C.S., M.Ed., Health

Educator and Consultant, Arizona Osteoporosis

Coalition, Phoenix, Arizona

David Brown, Ph.D., Senior Behavioral

Scientist, Division of Nutrition and Physical

Activity, Physical Activity and Health Branch,

National Center on Chronic Disease Prevention

and Health Promotion, Centers for Disease

Control and Prevention, Atlanta, Georgia.
xiv Acknowledgments

Lenore Buckley, M.D., M.P.H., Professor, Division

of Rheumatology, Medical College of Virginia,

Richmond, Virginia.

Mona S. Calvo, Ph.D., Expert Regulatory

Review Scientist, Office of Applied Research

and Safety Assessment, Center for Food Safety

and Applied Nutrition, Food and Drug

Administration, Laurel, Maryland.

Thomas G. Carskadon, Ph.D., Professor of

Psychology, Mississippi State University,

Mississippi State, Mississippi.

Mary Concannon, M.A., Osteoporosis Prevention

Coordinator, Maryland Department of Health and

Mental Hygiene, Baltimore, Maryland.

Cyrus Cooper, M.A., D.M., F.R.C.P., Professor,

MRC Environmental Epidemiology Unit,

Southampton General Hospital, Shirley,

Southampton, United Kingdom.

Judith A. Cranford, Executive Director, National

Osteoporosis Foundation, Washington, D.C.

Ann Cranney, M.D., M.Sc.,Assistant Professor,

Division of Rheumatology, Queen’s University,

Kingston, Ontario, Canada.

William H. Dietz, M.D., Ph.D., Director,

Division of Nutrition and Physical Activity,

Division of Nutrition and Physical Activity,

Centers for Disease Control and Prevention,

U.S. Department of Health and Human

Services, Atlanta, Georgia.

Marc K. Drezner, M.D., Professor of Medicine,

Endocrinology Section, University of Wisconsin,

Madison, Wisconsin.

Michael Econs, M.D., Professor of Medicine,

School of Medicine, Indiana University Medical

Center, Indianapolis, Indiana.

Kristine Ensrud, M.D., M.P.H., Associate

Professor, Division of Epidemiology, University

of Minnesota, School of Public Health,

Minneapolis, Minnesota.

Martin Erlichman, M.S., Senior Health Science

Analyst, Center for Practice and Technology

Assessment, Agency for Healthcare Research

and Quality, U.S. Department of Health and

Human Services, Rockville, Maryland.

Bruce Ettinger, M.D., Senior Investigator,

Research Division, Kaiser Permanente, San

Francisco, California.

Caswell A. Evans, D.M.D., National Institute

of Dental and Craniofacial Research, Bethesda,

Maryland.

Murray J. Favus, M.D., University of Chicago,

Chicago, Illinois.

Nancy Libby Fisher, Coordinator, Disease

Prevention and Control, Office of Women’s

Health, Rhode Island Department of Health,

Providence, Rhode Island.

Judith E. Fradkin, M.D., Director, Division of

Diabetes Endocrinology and Metabolism,

National Institute of Diabetes and Digestive and

Kidney Diseases, Bethesda, Maryland.

Harry K. Genant, M.D., Professor Emeritus of

Radiology, Orthopaedic Surgery, Medicine, and

Epidemiology, University of California San

Francisco, San Francisco, California.
Acknowledgments xv

Lou Glasse, M.S.W., President Emeritus,

Older Women’s League, Poughkeepsie, New

York.

Joan Goldberg, Executive Director, American

Society for Bone and Mineral Research,

Washington, D.C.

Frank R. Greer, M.D., Professor, Pediatrics/

Nutritional Sciences, American Academy of

Pediatrics, Meriter Hospital, Perinatal Center,

Madison, Wisconsin.

Jack Guralnik, M.D., Ph.D., Chief,

Epidemiology and Demography Office,

National Institute on Aging, National Institutes

of Health, Gateway Boulevard, Bethesda,

Maryland.

Ralph Hale, M.D., Executive Vice President,

American College of Obstetricians and

Gynecologists, Washington, D.C.

R. Scott Hanson, M.D., M.P.H., Past

President, Rhode Island Public Health

Association, Narragansett, Rhode Island.

Olof Johnell, M.D., Professor, Department of

Orthopaedics, University General Hospital,

Malmo, Sweden.

Clifford Johnson, M.S.P.H., Director, National

Health and Nutrition Examination Survey,

National Center for Health Statistics, Centers

for Disease Control and Prevention, Hyattsville,

Maryland.

C. Conrad Johnston, Jr., M.D., Distinguished

Professor, School of Medicine, Indiana

University, Indianapolis, Indiana.

John Kanis, M.D., Professor, Centre for

Metabolic Bone Diseases, University of Sheffield

Medical School, Sheffield, S. Yorkshire, United

Kingdom.

Theresa Kehoe, M.D., Medical Officer, Food

and Drug Administration, Parklawn Building,

Rockville, Maryland.

Jennifer Kelsey, Ph.D., Professor, University of

Massachusetts Medical School, Clinton,

Connecticut.

Jane E. Kerstetter, Ph.D., R.D., Associate Professor, School of Allied Health, University of

Connecticut, Stafford Springs, Connecticut.

Patricia A. Kipperman, Omaha, Nebraska.

John H. Klippel, M.D., Medical Director,

Arthritis Foundation, Atlanta, Georgia.

Joan M. Lappe, Ph.D., R.N., Associate

Professor, Creighton Osteoporosis Research

Center, Creighton University, Omaha,

Nebraska.

Angelo Licata, M.D., Ph.D., Director of

Research, Center for Osteoporosis and Metabolic

Bone Disease, Cleveland Clinic Foundation,

Cleveland, Ohio.

Robert Lindsay, M.D., Ph.D., Chief of Internal

Medicine, Regional Bone Center, Helen Hayes

Hospital, West Haverstraw, New York.

Jean L. Lloyd, M.S., R.D., Nutritionist, Office

of Community Based Services, U.S.

Administration on Aging, U.S. Department of

Health and Human Services, Washington, D.C.
xvi Acknowledgments

Jay Magaziner, Ph.D., M.S., Professor and

Director, Division of Gerontology,

Epidemiology and Preventive Medicine,

University of Maryland, Baltimore, Maryland.

Deborah R. Maiese, Director, Maternal and

Child Health Bureau, Office of Women’s Health,

Health Resources and Services Administration,

Rockville, Maryland.

Robert Marcus, M.D., Professor Emeritus,

Stanford University, Stanford, California.

Medical Advisor, USMD Endocrinology, Eli

Lilly, Indianapolis, Indiana.

Ronald Margolis, Ph.D., Senior Advisor for

Molecular Endocrinology, Division of Diabetes,

Endocrinology and Metabolism, National

Institute of Diabetes and Digestive and Kidney

Diseases, Bethesda, Maryland.

Joan C. Marini, M.D., Ph.D., Chief, Heritable

Disorders Branch, National Institute of Child

Health and Human Development, Bethesda,

Maryland.

Betsy McClung, R.N., Associate Director,

Oregon Osteoporosis Center, Portland, Oregon.

Michael McClung, M.D., F.A.C.E., Director,

Oregon Osteoporosis Center, Portland, Oregon.

Daniel McDonald, M.D., Scientific Review

Administrator, Center for Scientific Review,

National Institutes of Health, Bethesda,

Maryland.

Barbara Miller, Ph.D., Category Manager,

Professional and Scientific Relations, Procter and

Gamble Pharmaceuticals, Mason, Ohio.

Gregory Miller, Ph.D., M.A.C.N., Senior Vice

President of Nutrition and Scientific Affairs,

National Dairy Council, Rosemont, Illinois.

Ron Nelson, P.A.-C., President/CEO, Health

Services Associates, Inc., Fremont, Michigan.

Eric S. Orwoll, M.D., Professor of Medicine,

Program Director, General Clinical Research

Center, Associate Dean for Clinical Research,

Assistant Vice President for Research, Oregon

Health and Science University, Portland,

Oregon.

Susan Ott, M.D., Associate Professor,

Department of Medicine, University of

Washington Medical Center, Seattle,

Washington.

Susana Perry, M.S., Health Programs

Coordinator, Office of Women’s Health, Food

and Drug Administration, Rockville, Maryland.

Steven Petak, M.D., J.D., F.A.C.E., representing

American Association of Clinical

Endocrinologists, Houston, Texas.

Sandra C. Raymond, Executive Director,

Lupus Foundation of America, Inc.,

Washington, D.C.

Robert R. Recker, M.D., Director, Osteoporosis

Research Center, Creighton University, Omaha,

Nebraska.

Trish Reynolds, R.N., M.S., Education

Manager/Assistant Project Director, National

Institutes of Health Osteoporosis and Related

Bone Diseases ~ National Resource Center,

Washington, D.C.
Acknowledgments xvii

Elena Rios, M.D., President, National Hispanic

Medical Association, Washington, D.C.

Helena W. Rodbard, M.D., Past President,

American Association of Clinical

Endocrinologists, Rockville, Maryland.

William Sacks, M.D., Ph.D., Medical Officer,

Center for Devices and Radiological Health,

Office of Device Evaluation, Food and Drug

Administration, Rockville, Maryland.

Paul Scherr, Ph.D., D.Sc., Epidemiologist,

Division of Adult and Community Health,

Emerging Investigations and Analytic Methods

Branch, National Center for Chronic Disease

Prevention and Health Promotion, Centers for

Disease Control and Prevention, Atlanta,

Georgia.

Mary Jean Schumann, Director, Practice and

Policy, American Nurses Association,

Washington, D.C.

Heller An Shapiro, Executive Director,

Osteogenesis Imperfecta Foundation,

Gaithersburg, Maryland.

Harriet R. Shapiro, R.N., M.A., Director,

Patient and Professional Education, National

Osteoporosis Foundation, Washington, D.C.

Frederick R. Singer, M.D., Chairman, Paget

Foundation Board of Directors, John Wayne

Cancer Institute, Santa Monica, California.

Christine Snow, Ph.D., F.A.C.S.M., Director,

Bone Research Laboratory, Professor, Exercise

and Sport Science, College of Health and

Human Sciences, Oregon State University,

Corvallis, Oregon.

Christine Spain, M.A., Director, Research,

Planning, and Special Projects, President’s

Council on Physical Fitness and Sports,

Washington, D.C.

Barry Stein, M.D., Surgeon-in-Chief, Urology,

Rhode Island Hospital, Providence, Rhode Island.

Susan S. Swift, D.P.A., President, Susan S.

Swift, Ltd., New York, New York.

J. Scott Toder, M.D., Physician, Johnston,

Rhode Island.

Mehrdad Tondravi, Ph.D., Program Director,

Division of Diabetes, Endocrinology and

Metabolic Diseases, National Institute of

Diabetes and Digestive and Kidney Diseases,

Bethesda, Maryland.

Charlene Waldman, Executive Director, The

Paget Foundation, New York, New York.

Michael F. White, Principal, Michael F. White

and Associates, Women’s Health Council,

Association of State and Territorial Directors of

Chronic Disease Programs, Alexandria, Virginia.

Paul J. Wiesner, M.D., District Health Director,

Dekalb County Board of Health, Decatur, Georgia.

T. Franklin Williams, M.D., Professor of

Medicine Emeritus, General Medicine and

Geriatrics Unit, University of Rochester School

of Medicine and Dentistry, Rochester, New York.

Karen Winer, M.D., Fellow, Center for Research

for Mothers and Children, Endocrinology,

Nutrition, and Growth Branch, National Institute

of Child Health and Human Development,

Bethesda, Maryland.
xviii Acknowledgments

Betty H. Wiser, Ed.D., M.S., Director of Older

Adult Health Branch, Division of Public Health,

North Carolina Department of Health and

Human Services, Raleigh, North Carolina.

Susan Wood, Director, Office of Women’s

Health, Food and Drug Administration,

Rockville, Maryland.

Adeline M. Yerkes, R.N., M.P.H., Chief,

Chronic Disease, Oklahoma State Department

of Health, Oklahoma City, Oklahoma.

Surgeon General Workshop participants were

Amy Allina, Program and Policy Director,

National Women’s Health Network,

Washington, D.C.

Nell Armstrong, Ph.D., R.N., Program Director,

Division of Extramural Activities, National

Institute of Nursing Research, National

Institutes of Health, Bethesda, Maryland.

David Atkins, M.D., M.P.H., Senior Health Policy

Analyst, Center for Practice and Technology

Assessment, Agency for Healthcare Research and

Quality, U.S. Department of Health and Human

Services, Rockville, Maryland.

Roberta Biegel, Director of Government

Relations, Society for Women’s Health

Research, Washington, D.C.

Dennis Black, Ph.D., Professor, Department of

Epidemiology and Biostatistics, University of

California San Francisco, San Francisco,

California.

Henry G. Bone, III, M.D., Director, Michigan

Bone and Mineral Clinic, Detroit, Michigan.

Joyce M. Briscoe, Cavarocchi Ruscio Dennis

Associates, LLC, Washington, D.C.

David Buchner, M.D., M.P.H., Chief, Physical

Activity and Health Branch, Division of

Nutrition and Physical Activity, Centers for

Disease Control and Prevention, Department of

Health and Human Services, Atlanta, Georgia.

Mona S. Calvo, Ph.D., Expert Regulatory

Review Scientist, Office of Applied Research

and Safety Assessment, Center for Food Safety

and Applied Nutrition, Food and Drug

Administration, Laurel, Maryland.

Thomas G. Carskadon, Ph.D., Professor of

Psychology, Mississippi State University,

Mississippi State, Mississippi.

Jane Cauley, Dr.P.H., Associate Professor,

Department of Epidemiology, University of

Pittsburgh, Pittsburgh, Pennsylvania.

Nicholas G. Cavarocchi, Cavorocchi Ruscio

Dennis Associates, LLC, Washington, D.C.

David A. Chambers, Ph.D., M.Sc., Program

Officer, Dissemination and Implementation

Research Program, Services Research and

Clinical Epidemiology Branch, National Institute

of Mental Health, National Institutes of Health,

Bethesda, Maryland.

Katherine Moy Chin, R.D., L.D., Commissioner,

State of Maryland Governor’s Commission on

Asian Pacific American Affairs, Baltimore,

Maryland.

Wojtek Chodzko-Zajko, Ph.D., Professor and

Department Chair, Department of Kinesiology,

University of Illinois, Urbana, Illinois.
Acknowledgments xix

Kathleen Cody, Executive Director, Foundation

for Osteoporosis Research, and Education,

Oakland, California.

Rosaly Correa-de-Araujo, M.D., Health

Scientist Administrator, Agency for Healthcare

Research and Quality, Rockville, Maryland.

Judith Cranford, Executive Director, National

Osteoporosis Foundation, Washington, D.C.

Denise Cyzman, Senior Project Coordinator,

Health Promotion and Disease Prevention,

Osteoporosis and Other Chronic Conditions,

Michigan Public Health Institute, Okemos,

Michigan.

Susan Davidson, M.S., R.D., Consultant,

Germantown, Maryland.

Bess Dawson-Hughes, M.D., Professor of

Medicine, Metabolism Lab, Tufts University,

U.S. Department of Agriculture, Human

Research Center on Aging, Boston,

Massachusetts.

Susan Dentzer, Health Correspondent,

NewsHour with Jim Lehrer, Arlington, Virginia.

Barbara DeVinney, Ph.D., AAAS Science Policy

Fellow, Office of Behavioral and Social Sciences

Research, Office of the Director, National

Institutes of Health, Bethesda, Maryland.

Ann L. Elderkin, P.A., Managing Editor and

Project Director, Surgeon General’s Report,

Health Systems Research, Inc., Washington, D.C.

Martin Erlichman, M.S., Senior Health Science

Analyst, Center for Practice and Technology

Assessment, Agency for Healthcare Research

and Quality, U.S. Department of Health and

Human Services, Rockville, Maryland.

Christine M. Everett, M.P.H., Special Assistant

to the Acting Director, Food and Drug

Administration, Rockville, Maryland.

Suzanne Feetham, Ph.D., R.N., F.A.A.N.,

Senior Advisor, Office of Director, Bureau of

Primary Health Care, Health Resources and

Services Administration, Bethesda, Maryland.

Lawrence Fields, M.D., Senior Executive

Advisor to the Assistant Secretary for Health,

Department of Health and Human Services,

Washington, D.C.

Michael Fleischman, Intern, President’s Council

on Physical Fitness and Sports, Washington, D.C.

Susan M. Friedman, Deputy Director,

Government Relations, American Osteopathic

Association, Washington, D.C.

Deborah A. Galuska, Ph.D., M.P.H.,

Epidemiologist, Division of Nutrition and

Physical Activity, Centers for Disease Control

and Prevention, U.S. Department of Health and

Human Services, Atlanta, Georgia.

Jean Gearing, Ph.D., M.P.H., Acting

Osteoporosis Program Manager, Chronic

Disease Prevention and Health Promotion

Branch, Georgia Division of Public Health,

Atlanta, Georgia.

Deborah T. Gold, Ph.D., Associate Professor,

Departments of Psychiatry and Behavioral

Sciences, Sociology, and Psychology: Social and

Health Sciences, Duke University Medical

Center, Durham, North Carolina.
xx Acknowledgments

Joan Goldberg, Executive Director, American

Society for Bone and Mineral Research,

Washington, D.C.

Jean Gonzalez, Lovettsville, Viginia.

Julie Gonzalez, Lovettsville, Viginia.

Christine W. Gould, Director of Health, YWCA

of the USA, Washington, D.C.

Amy Greene, Director, Prevention Policy,

Adolescent Health, Association of State and

Territorial, Health Officials, Washington,

D.C.

Susan L. Greenspan, M.D., Professor of

Medicine, University of Pittsburgh, Kaufmann

Medical Building, Pittsburgh, Pennsylvania.

Betty Lee Hawks, Special Assistant to the

Director, Office of Minority Health, Office of

Public Health and Science, U.S. Department of

Health and Human Services, Rockwall II,

Rockville, Maryland.

Leanne Jerome, Writer, Office of the Surgeon

General, Department of Health and Human

Services, Rockville, Maryland.

Sara Johnson, Ph.D., Director, Health Behavior

Change Programs, Pro-Change Behavior

Systems, Inc., West Kingston, Rhode Island.

Linda Johnson, Brentwood, Maryland.

Wanda K. Jones, Dr.P.H., Deputy Assistant

Secretary and Director of the Office of Women’s

Health, Office of the Secretary, Office of Public

Health and Science, Department of Health and

Human Services, Washington, D.C.

Jason Jurkowski, Fellow, Office of the Surgeon

General, Department of Health and Human

Services, Rockville, Maryland.

Stephen I. Katz, M.D., Ph.D., Director,

National Institute of Arthritis and

Musculoskeletal and Skin Diseases, National

Institutes of Health, Bethesda, Maryland.

Douglas P. Kiel, M.D., M.P.H., Director of

Medical Research, Research and Training

Institute, Hebrew Rehabilitation Center for the

Aged, Boston, Massachusetts.

Raynard S. Kington, M.D., Ph.D., Associate

Director, Office of the Director, Office of

Behavioral and Social Sciences Research, National

Institutes of Health, Department of Health and

Human Services, Bethesda, Maryland.

Richard L. Kravitz, M.D., M.S.P.H., Professor

of Medicine, Center for Health Services Research

in Primary Care, University of California, Davis

Medical Center, Sacramento, California.

Peggy Lassanske, President, Elder Floridians

Foundation, Tallahassee, Florida.

Marie-Michele Leger, M.P.H., P.A.-C., Director,

Professional Education, American Academy of

Physician Assistants, Alexandria, Viginia.

Jewel F. Lewis, Retired Chief Judge and Chair,

Board of Contract Appeals, Department of

Agriculture, Associate General Counsel and

General Counsel of Service Corps of Retired

Executives, Washington, D.C.

Karen Lim, Acting Executive Director, National

Asian Women’s Health Organization, San

Francisco, California.
Acknowledgments xxi

Anita M. Linde, Senior Program Analyst, Office

of the Director, National Institute of Arthritis

and Musculoskeletal and Skin Diseases, Bethesda,

Maryland.

Jean Lloyd, M.S., R.D., National Nutritionist,

Office of Community Based Services, U.S.

Administration on Aging, U.S. Department of

Health and Human Services, Washington, D.C.

Anne Looker, Ph.D., Senior Research

Epidemiologist, Health Examination Statistics,

National Center for Health Statistics, Centers

for Disease Control and Prevention, Hyattsville,

Maryland.

Robert Lorigan, Orient, Maine.

Annie Lorigan, Orient, Maine.

Kathryn R. Mahaffey, Ph.D., Director, Office

of Science Coordination and Policy, Division of

Exposure Assessment, Environmental

Protection Agency, Washington, D.C.

Edward W. Maibach, M.P.H., Ph.D.,

Worldwide Director of Social Marketing, Porter

Novelli, Washington, D.C.

Deborah Maiese, former Director, Maternal and

Child Health Bureau, Office of Women’s Health,

Health Resources and Services Administration,

Rockville, Maryland.

Jean Mandeville, Hopkins, Minnesota.

Ronald Margolis, Ph.D., Senior Advisor for

Molecular Endocrinology, Division of Diabetes,

Endocrinology and Metabolism, National

Institute of Diabetes and Digestive and Kidney

Diseases, Bethesda, Maryland.

Joan C. Marini, M.D., Ph.D., Chief, Heritable

Disorders Branch, National Institute of Child

Health and Human Development, Bethesda,

Maryland.

Saralyn Mark, M.D., Senior Medical Advisor,

Office on Women’s Health, Office of Public

Health and Science, National Aeronautics and

Space Administration, Department and Health

and Human Services, Washington, D.C.

Jeff Martin, Office of the Surgeon General,

Department of Health and Human Services,

Rockville, Maryland.

Joan A. McGowan, Ph.D., Senior Scientific

Editor, Surgeon General’s Report, Director,

Musculoskeletal Diseases Branch, Extramural

Program, National Institute of Arthritis and

Musculoskeletal and Skin Diseases, National

Institutes of Health, Bethesda, Maryland.

John McGrath, Ph.D., Chief, Public Information

and Communications Branch, National Institute

of Child Health and Human Development,

National Institutes of Health, Bethesda, Maryland.

Taya McMillan, Intern, Office on Women’s

Health, Office of Public Health and Science,

Department of Health and Human Services,

Washington, D.C.

L. Joseph Melton, III, M.D., Eisenberg

Professor, Department of Health Sciences

Research, Mayo Clinic and Foundation,

Rochester, Minnesota.

Kenneth P. Moritsugu, M.D., M.P.H., Deputy

Surgeon General of the United States, Office of

the Surgeon General, Department of Health and

Human Services, Rockville, Maryland.
xxii Acknowledgments

Miriam Nelson, Ph.D., Director, Friedman

School of Nutrition Science and Policy, Center

for Physical Activity and Nutrition, Tufts

University, Boston, Massachusetts.

Debra Nichols, M.D., Public Health Advisor,

Office of Disease Prevention and Health

Promotion, Office of Public Health and Science,

Department of Health and Human Resources,

Washington, D.C.

Allan S. Noonan, M.D., M.P.H., CAPT, U.S.

Public Health Service, Scientific Editor, Surgeon

General’s Report, Office of the Surgeon General,

Office of the Secretary, Washington, D.C.

Eric S. Orwoll, M.D., Professor of Medicine,

Program Director, General Clinical Research

Center, Associate Dean for Clinical Research,

Assistant Vice President for Research, Oregon

Health and Science University, Portland,

Oregon.

Lucille Norville Perez, M.D., Past President,

National Medical Association, Bethesda, Maryland.

Diana Pethtel, Washington, D.C.

Robert A. Phillips, Ph.D., Chief, Radiological

Devices Branch, Center for Devices and

Radiological Health, Office of Device

Evaluation, Food and Drug Administration,

Rockville, Maryland.

Vivian W. Pinn, M.D., Associate Director for

Research on Women’s Health, Office of the

Director, National Institutes of Health, Bethesda,

Maryland.

Geraldine B. Pollen, M.A., Research Activities

Coordinator, National Institute of Arthritis and

Musculoskeletal and Skin Diseases, Extramural

Program, National Institutes of Health, One

Democracy Plaza, Bethesda, Maryland.

Lawrence G. Raisz, M.D., Scientific Editor,

Board of Trustees Distinguished Professor of

Medicine, Interim Director, Musculoskeletal

Institute, Division of Endocrinology and

Metabolism, University of Connecticut Health

Center, Farmington, Connecticut.

Claudia Reid Ravin, C.N.M., M.S.N., Associate

Director, Women’s Health Programs,

Association of Women’s Health, Obstetric, and

Neonatal Nurses, Washington, D.C.

B. Lawrence Riggs, M.D., Distinguished

Investigator, Mayo Foundation, Purvis and

Roberta Tabor Professor of Medical Research,

Mayo Medical School, Division of

Endocrinology, Mayo Clinic and Foundation,

Rochester, Minnesota.

Edward J. Roccella, Ph.D., M.P.H.,

Coordinator, National High Blood Pressure

Education Program, Office of Prevention,

Education and Control, National Heart, Lung

and Blood Institute, National Institutes of

Health, Bethesda, Maryland.

Clifford Rosen, M.D., Chief of Medicine, Maine

Center for Osteoporosis Research, St. Joseph

Hospital, Bangor, Maine.

Bruce S. Schneider, M.D., Medical Officer,

Division of Metabolic and Endocrine Drug

Products, Center for Drug Evaluation and

Research, Food and Drug Administration,

Rockville, Maryland.

Jean Scott, Dr.P.H., R.N., Senior

Epidemiologist, Quality Measurement & Health
Acknowledgments xxiii

Assessment Group, Centers for Medicare and

Medicaid Services, Department of Health and

Human Services, Baltimore, Maryland.

Jay R. Shapiro, M.D., Director, Osteogenesis

Imperfecta Clinic, Kennedy Krieger Institute,

Baltimore, Maryland.

Heller An Shapiro, Executive Director,

Osteogenesis Imperfecta Foundation,

Gaithersburg, Maryland.

Sherry Sherman, Ph.D., Director, Clinical

Endocrinology and Osteoporosis Research,

National Institute on Aging, National Institutes

of Health, Bethesda, Maryland.

Kathy Shipp, P.T., Ph.D., Assistant Research

Professor, Physical Therapy, Community and

Family Medicine, Duke University Medical

Center, Durham, North Carolina.

Ethel S. Siris, M.D., Madeline C. Stabile Professor

of Clinical Medicine, Endocrinology Division,

Columbia University and Columbia Presbyterian

Medical Center, New York, New York.

Eve Slater, M.D., Assistant Secretary for Health,

Department of Health and Human Services,

Washington, D.C.

Christine Snow, Ph.D., F.A.C.S.M., Director,

Bone Research Laboratory, Professor, Exercise

and Sport Science, College of Health and

Human Sciences, Oregon State University,

Corvallis, Oregon.

Christine Spain, M.A., Director, Research,

Planning, and Special Projects, President’s

Council on Physical Fitness and Sports,

Washington, D.C.

Larry Stepnick, M.B.A., Consultant, The

Severyn Group, Inc., Ashburn, Virginia.

Jeannie Suarez-Reyes, M.P.H., Project Director,

Center for Consumers, National Alliance for

Hispanic Health, Washington, D.C.

William W. Tipton, Jr., M.D., Executive Vice

President, American Academy of Orthopaedic

Surgeons, Rosemount, Illinois.

Mehrdad Tondravi, M.D., Program Director,

Division of Diabetes, Endocrinology and

Metabolic Diseases, National Institute of

Diabetes and Digestive and Kidney Diseases,

Bethesda, Maryland.

Laura Tosi, M.D., Division Chief, Orthopaedic

Surgery and Sports Medicine, Children’s

National Medical Center, Washington, D.C.

Anna N. Tosteson, Sc.D., Professor,

Departments of Medicine and Community and

Family Medicine, Dartmouth Medical School,

Lebanon, New Hampshire.

Wulf H. Utian, M.D., Ph.D., Executive

Director, North American Menopause Society,

Mayfield Heights, Ohio.

Charlene Waldman, Executive Director, The

Paget Foundation, New York, New York.

Nelson Watts, M.D., Director, Bone Health and

Osteoporosis Center, University of Cincinnati,

Cincinnati, Ohio.

Connie M. Weaver, Ph.D., Distinguished

Professor, Department Head, Foods and

Nutrition, Purdue University, West Lafayette,

Indiana.
xxiv Acknowledgments

Michael F. White, Consultant, Michael F. White

and Associates, Women’s Health Council,

Association of State and Territorial Directors of

Chronic Disease Programs, Alexandria, Virginia.

Susan Whittier, M.H.A., Director, National

Institutes for Health Osteoporosis and Related

Bone Diseases ~ National Resource Center,

Washington, D.C.

Michael P. Whyte, M.D., Professor of Medicine,

Pediatrics, and Genetics, Bone and Mineral

Diseases, Department of Medicine, BarnesJewish Hospital at Washington University

School of Medicine, St. Louis, Missouri.

Lynne Wilcox, M.D., M.P.H., CAPT, U.S.

Public Health Service, Editor-in-Chief,

Preventing Chronic Disease, National Center for

Chronic Disease Prevention and Health

Promotion, Centers for Disease Control and

Prevention, Atlanta, Georgia.

Betty H. Wiser, Ed.D., Director of Older Adult

Health Branch, Division of Public Health, North

Carolina Department of Health and Human

Services, Raleigh, North Carolina.

Susan Wood, Director, Office of Women’s

Health, Food and Drug Administration,

Rockville, Maryland.

Surgeon General’s Interagency Work Group

on Osteoporosis and Bone Health

Nell Armstrong, Ph.D., R.N., Program Director,

Division of Extramural Activities, National

Institute of Nursing Research, National

Institutes of Health, Bethesda, Maryland.

William H. Dietz, M.D., Ph.D., Director,

Division of Nutrition and Physical Activity,

Division of Nutrition and Physical Activity,

Centers for Disease Control and Prevention,

U.S. Department of Health and Human

Services, Atlanta, Georgia.

Sherri A. Clark, Aging Services Program

Specialist, Administration on Aging,

Washington, D.C.

Agnes Donahue, Advisor to Director, Office of

Intergovernmental Affairs, Department of

Health & Human Services, Washington, D.C.

Ann L. Elderkin, P.A., Managing Editor and

Project Director, Surgeon General’s Report,

Health Systems Research, Inc., Washington,

D.C.

Martin N. Erlichman, M.S., Senior Health

Science Analyst, Vice-Chair International

Network of Agencies for Health Technology

Assessment, Center for Practice and Technology

Assessment, Agency for Healthcare Research

and Quality, Rockville, Maryland.

MAJ Rachel Evans, Ph.D., R.P.T, Director,

Bone Health Research Program, U.S. Army

Research Institute of Environmental Medicine,

Military Performance Division, Natick,

Massachusetts.

Christine M. Everett, M.P.H., Special Assistant

to the Acting Director, Food and Drug

Administration, Rockville, Maryland.

Deborah A. Galuska, Ph.D., M.P.H,

Epidemiologist, Division of Nutrition and
Acknowledgments xxv

Physical Activity Centers for Disease Control

and Prevention, Atlanta, Georgia.

Melissa Johnson, M.S., Executive Director,

President’s Council on Physical Fitness and

Sports, Washington, D.C.

Annette Kirshner, PhD, Health Science

Administrator, National Institute of

Environmental Health Sciences, Division of

Extramural Research and Training, Research

Triangle Park, North Carolina.

Anita Linde, Senior Program Analyst, Office of

the Director, National Institute of Arthritis and

Musculoskeletal and Skin Diseases, Bethesda,

Maryland.

Jean Lloyd, M.S., R.D., Nutritionist, Center for

Community Based Services, U.S.

Administration on Aging, Washington, D.C.

Anne Looker, Ph.D., Senior Research

Epidemiologist, National Center for Health

Statistics, Centers for Disease Control and

Prevention, Hyattsville Maryland.

Sabrina Matoff, Acting Director, Office of

Women’s Health, Maternal and Child Health

Bureau, Health Resources and Services

Administration, Rockville, Maryland.

Ronald Margolis, Ph.D., Senior Advisor for

Molecular Endocrinology, Division of Diabetes,

Endocrinology, and Metabolism, National

Institute of Diabetes and Digestive and Kidney

Diseases, Bethesda, Maryland.

Saralyn Mark, M.D., Senior Medical Advisor,

NASA & Office of Women’s Health,

Department of Health & Human Services,

Washington, D.C.

Joan A. McGowan, Ph.D., Senior Scientific

Editor, Surgeon General’s Report, Director,

Musculoskeletal Diseases Branch, Extramural

Program, National Institute of Arthritis and

Musculoskeletal and Skin Diseases, National

Institutes of Health, Bethesda, Maryland.

Debra Nichols, M.D., Office of Disease

Prevention and Health Promotion, Department

of Health and Human Services, Washington,

D.C.

Allan S. Noonan, M.D., M.P.H., CAPT, U.S.

Public Health Service, Scientific Editor, Surgeon

General’s Report, Office of the Surgeon General,

Office of the Secretary, Washington, D.C.

Susana Perry, M.S., Health Programs

Coordinator, Office of Women’s Health, Food

and Drug Administration, Rockville,

Maryland.

Jean Scott, Dr.P.H., R.N., Senior

Epidemiologist, Quality Measurement & Health

Assessment Group, Centers for Medicare and

Medicaid Services, Department of Health and

Human Services, Baltimore, Maryland.

Sherry Sherman, Ph.D., Director, Clinical

Endocrinology and Osteoporosis Research,

National Institute on Aging, National Institutes

of Health, Bethesda, Maryland.

Christine Spain, M.A., Director, Research,

Planning, and Special Projects, President’s

Council on Physical Fitness and Sports,

Washington, D.C.
xxvi Acknowledgments

Maxine E. Turnipseed, M.B.A., Insurance

Analyst, Partnership Development, Centers for

Medicare and Medicaid Services, Baltimore,

Maryland.

Valerie A. Welsh, Senior Health Policy Analyst

and Evaluation Officer, Office of Minority

Health, OS/DHHS, Rockville, Maryland.

Judith Wilson, M.P.H., R.D., Director, Nutrition

Services, U.S. Department of Agriculture,

Washington, D.C.

Susan Wood, Director, Office of Women’s

Health, Food and Drug Administration,

Rockville, Maryland.

Elizabeth Yetley, Ph.D., Lead Scientist for

Nutrition, Food and Drug Administration,

College Park, Maryland.
Table of Contents xxvii

PART ONE: WHAT IS BONE HEALTH?.......................................................................... 1

Chapter 1: A Public Health Approach To Promote Bone Health .......................................... 2

Key Messages ......................................................................................................................... 2

The Magnitude of the Problem ............................................................................................ 5

The Challenge ........................................................................................................................ 6

The Opportunity ................................................................................................................... 8

The Charge............................................................................................................................. 9

Evidence Base for the Report................................................................................................ 11

Organization of the Report ................................................................................................... 11

References............................................................................................................................... 14

Chapter 2: The Basics of Bone in Health and Disease .............................................................. 16

Key Messages ......................................................................................................................... 16

Why Do We Have Bones? .................................................................................................... 17

How Bones Work .................................................................................................................. 18

How Bones Change Throughout Life ................................................................................. 20

What Keeps Bones Healthy? ................................................................................................ 25

What Causes Diseases of Bone? ............................................................................................ 29

What Is Osteoporosis? ........................................................................................................... 30

The Future: Where a Better Understanding of Bone Biology Can Take Us.................... 32

Key Questions for Future Research ..................................................................................... 35

References............................................................................................................................... 36

Chapter 3: Diseases of Bone ........................................................................................................ 40

Key Messages ......................................................................................................................... 40

Osteoporosis ........................................................................................................................... 41

Rickets and Osteomalacia ...................................................................................................... 53

Renal Osteodystrophy........................................................................................................... 54

Paget’s Disease of Bone ......................................................................................................... 54

Developmental Skeletal Disorders ....................................................................................... 55

Malignancy and the Skeleton ............................................................................................... 57

Bone Health and Osteoporosis

A Surgeon General’s Report
xxviii Table of Contents

Oral Health and Bone Disease .............................................................................................. 59

Key Questions for Future Research ..................................................................................... 60

References............................................................................................................................... 61

PART TWO: WHAT IS THE STATUS OF BONE HEALTH IN AMERICA? .......... 67

Chapter 4: The Frequency of Bone Disease .............................................................................. 68

Key Messages ......................................................................................................................... 68

Fractures Caused by Bone Disease ...................................................................................... 69

Osteoporosis ........................................................................................................................... 75

Other Metabolic Bone Diseases ............................................................................................ 81

Developmental Skeletal Disorders ....................................................................................... 81

Acquired Skeletal Disorders ................................................................................................. 81

Prospects for the Future ....................................................................................................... 82

Key Questions for Future Research ..................................................................................... 83

References............................................................................................................................... 84

Chapter 5: The Burden of Bone Disease .................................................................................... 88

Key Messages ......................................................................................................................... 88

Impact on Society .................................................................................................................. 89

Impact on the Individual ....................................................................................................... 95

The Burden of Other Bone Diseases .................................................................................... 102

Key Questions for Future Research ..................................................................................... 103

References............................................................................................................................... 105

PART THREE: WHAT CAN INDIVIDUALS DO TO

 IMPROVE THEIR BONE HEALTH?..................................................... 109

Chapter 6: Determinants of Bone Health .................................................................................. 110

Key Messages ......................................................................................................................... 110

Nutrition’s Impact on Bone Health: A Review of the Evidence ....................................... 115

Physical Activity .................................................................................................................... 122

Weight .................................................................................................................................... 130

Falls and Fall Prevention ....................................................................................................... 132

Reproductive Factors............................................................................................................. 135

Medical Conditions and Drugs ............................................................................................. 137

Smoking, Alcohol, and Environmental Threats to Bone ................................................... 139

Key Questions for Future Research ..................................................................................... 141

References............................................................................................................................... 142
Table of Contents xxix

Chapter 7: Lifestyle Approaches To Promote Bone Health .................................................... 158

Key Messages ......................................................................................................................... 158

Nutrition................................................................................................................................. 159

Physical Activity .................................................................................................................... 171

Fall Prevention ....................................................................................................................... 177

Other Aspects of a Bone-Healthy Lifestyle ......................................................................... 179

Summary ................................................................................................................................ 180

Key Questions for Future Research ..................................................................................... 180

References............................................................................................................................... 181

PART FOUR: WHAT CAN HEALTH CARE PROFESSIONALS

 DO TO PROMOTE BONE HEALTH? ..................................................... 185

Chapter 8: Assessing the Risk of Bone Disease and Fracture................................................... 186

Key Messages ......................................................................................................................... 186

Step 1: Identify At-Risk Individuals Who Require Further Evaluation ........................... 188

Step 2: Measuring Bone Mineral Density (BMD)

 for Individuals at Risk of Osteoporosis .......................................................................... 198

Looking to the Future: Potential Complements to BMD ................................................... 208

Key Questions for Future Research ..................................................................................... 212

References............................................................................................................................... 213

Chapter 9: Prevention and Treatment for Those Who Have Bone Diseases ......................... 218

Key Messages ......................................................................................................................... 218

A Pyramid Approach ............................................................................................................ 221

 The Base of the Pyramid: Maintaining Bone Health and Preventing Fractures ......... 222

 The Second Level of the Pyramid: Assessing and Treating Secondary Causes ......... 224

 The Third Level of the Pyramid: Treatment ................................................................. 226

Key Questions for Future Research ..................................................................................... 244

References............................................................................................................................... 245

Chapter 10: Putting It All Together for the Busy Health Care Professional .......................... 254

Key Messages ......................................................................................................................... 254

Children and Adolescents ..................................................................................................... 256

Adults...................................................................................................................................... 261

Older Adults........................................................................................................................... 268

Key Questions for Future Research ..................................................................................... 275

References............................................................................................................................... 276
xxx Table of Contents

PART FIVE: WHAT CAN HEALTH SYSTEMS AND POPULATION

 BASED APPROACHES DO TO PROMOTE BONE HEALTH? ........... 279

Chapter 11: Systems-Based Approaches to Bone Health ......................................................... 280

Key Messages ......................................................................................................................... 280

Overview ................................................................................................................................ 281

Systems-Based Approaches for Various Stakeholders ....................................................... 284

Special Populations................................................................................................................ 300

Conclusions ............................................................................................................................ 303

Key Questions for Future Research ..................................................................................... 303

References............................................................................................................................... 305

Chapter 12: Population-Based Approaches To Promote Bone Health ................................... 310

Key Messages ......................................................................................................................... 310

Definition of Population-Based Interventions ..................................................................... 311

Evidence of the Effectiveness of Population-Based Interventions ..................................... 313

Communication Tools for Population-Based Interventions ............................................... 317

Population-Based Interventions: Conclusions ..................................................................... 321

Program Examples................................................................................................................. 320

Building on Success ............................................................................................................... 334

Key Questions for Future Research ..................................................................................... 338

References............................................................................................................................... 340

PART SIX: CHALLENGES AND OPPORTUNITIES:

 A VISION FOR THE FUTURE ....................................................................... 345

Chapter 13: A Vision for the Future:

A Framework for Action To Promote Bone Health ........................................................... 347

A Framework for Action ....................................................................................................... 347

The Role of Key Stakeholders .............................................................................................. 350

Key Action Steps ................................................................................................................... 348

The Importance of Partnerships Among Stakeholders ...................................................... 354

Conclusion .............................................................................................................................. 354

APPENDICES............................................................................................................................ 357

Appendix A: Congressional Language Calling for Surgeon General’s Report ....................... 357

Appendix B: How Do We Know What We Know: The Evidence Behind the Evidence .... 359

Appendix C: Resources and Related Links................................................................................ 365

ABBREVIATIONS AND ACRONYMS .......................................................................................... 373

LIST OF TABLES AND FIGURES .................................................................................................. 377

INDEX ......................................................................................................................................... 381
Table of Contents xxxi
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Bone Health and Osteoporosis

 PART ONE: What Is Bone Health? 1

This introductory part of the report explores the answer to this question, defining bone health as a public health issue with an emphasis on

prevention and early intervention to promote strong bones and prevent

fractures and their consequences. The first chapter describes this public

health approach along with the rationale for the report and the charge

from Congress and from the Surgeon General.

Chapter 2 provides a brief overview of the fundamentals of bone biology, helping the reader to understand why humans have bones, how bones

work, how bones change during life, what keeps bones healthy, what causes

bone disease, and what is in store in the future. It begins to outline the role

of genetic and environmental factors such as nutrition and physical activity in keeping bones healthy, an issue that is addressed in more detail later

in the report.

Chapter 3 offers a summary review of the more common diseases, disorders, and conditions that both directly and indirectly affect bone. While

much of Chapter 3 focuses on osteoporosis (including other diseases and

medications that can cause it), it also covers other related bone diseases,

including rickets and osteomalacia, renal osteodystrophy, Paget’s disease

of bone, developmental skeletal disorders, and acquired skeletal disorders.

Both Chapters 2 and 3 should be considered as important scientific

background for the remainder of the report.

One

WHAT IS BONE HEALTH?

Part One
2 Chapter

A Report of the Surgeon General

1

• Bone health is critically important to the

overall health and quality of life of Americans. Healthy bones provide the body

with a frame that allows for mobility and

for protection against injury. Bones serve

as a storehouse for minerals that are vital

to the functioning of many other life-sustaining systems in the body. Unhealthy

bones, however, perform poorly in executing these functions and can lead to

debilitating fractures.

• The bone health status of Americans appears to be in jeopardy, and left unchecked it is only going to get worse as

the population ages. Each year an estimated 1.5 million individuals suffer an

osteoporotic-related fracture.

• Great improvements in the bone health

status of Americans can be made “simply” by applying in a timely manner that

which is already known about prevention, assessment, detection, diagnosis, and

treatment.

• There is a large gap between what has

been learned and what is applied by

American consumers and health care proChapter 1: Key Messages

viders. The biggest problem is a lack of

awareness of bone disease among both

the public and health care professionals.

• An area of particular concern relates to

serving ethnic and racial minorities and

other underserved populations, including the uninsured, underinsured, and

those living in rural areas. Closing this

gap will not be possible without specific

strategies and programs geared toward

bringing improvements in bone health to

all currently underserved populations.

• The area of bone health is ideally suited

to a public health approach to health

promotion. This Surgeon General’s report is calling for Federal, State, and local governments (including State and

local public health departments) to join

forces with the private sector and community organizations in a coordinated,

collaborative effort to promote bone

health. This type of approach can serve

as the primary vehicle for improving the

bone health status of Americans. Some

of the work has already begun, but

much more work remains.
Bone Health and Osteoporosis

3

This first report of the Surgeon General on

bone health and osteoporosis, which was requested by Congress, comes at a critical time.

Tremendous progress has been made in bone

health in the last several decades, particularly in

the past 15 years. Research has accelerated markedly, enabling the medical community to develop

a much more detailed understanding of the factors that promote bone health and cause bone

disease and fractures. This enhanced level of

knowledge has led to significant advances in the

ability to prevent, assess risk factors for, diagnose, and treat bone disease.

Physical activity and calcium and vitamin D

intake are now known to be major contributors

to bone health for individuals of all ages. Even

though bone disease often strikes late in life, the

importance of beginning prevention at a very

young age and continuing it throughout life is

now well understood. Advances in knowledge

about risk factors have allowed work to begin

on tools that assess the potential for bone disease in an individual. These risk-factor assessment tools help to identify high-risk individuals

in need of further evaluation. With respect to

diagnosis, the development of noninvasive tools

to measure bone density and bone mass has been

one of the most significant advances in the last

quarter century. As a result, it is now possible to

detect bone disease early and to identify those

at highest risk of fracture. Therapeutic advances

in bone disease have equaled if not surpassed

advances in the areas of prevention and diagnosis. Within the last 10–15 years, new classes of

drugs have been developed that, for the first time,

have been shown in large-scale trials to significantly reduce the risk of fractures in individuals

with bone disease. Large-scale trials have also

confirmed the value of vitamin D and calcium

supplementation in reducing bone loss and the

risk of fractures in some populations.

Research has also led to a much better understanding of the role of secondary factors in the

development of bone disease, including use of certain medications and the presence of certain diseases. For example, glucocorticoids are now known

to be a significant contributor to osteoporosis. As

a result, interventions are available that help minimize the risk of bone disease in those who need

these drugs. Similarly, much more is now understood about a leading cause of fractures in the elderly—falls in those who have weakened bones.

Enhanced knowledge about why people fall has

led to interventions that target the risk factors for

falls, such as avoiding or minimizing use of medications that cause dizziness, making environmental modifications in the home, and training to improve strength and balance.

A PUBLIC HEALTH APPROACH TO

PROMOTE BONE HEALTH

A Public Health Approach To Promote Bone Health

Chapter 1
4 Chapter

A Report of the Surgeon General

In short, the last several decades represent

an era of great excitement and progress in the

field of bone health. Thirty years ago, relatively

little was known or could be done about osteoporosis; both the disease and the fractures that

go along with it were thought of as an inevitable

part of old age. Today, however, advances in

scientific knowledge have ushered in a new era

in bone health, one in which bone diseases can

be prevented in the vast majority of individuals

and identified early and treated effectively in

those who do get them.

However, the tremendous potential offered

by this new era of bone health has yet to become a reality. Bone diseases, including osteoporosis, Paget’s disease of the bone, osteogenesis imperfecta, rickets, osteomalacia, renal osteodystrophy, and hyperparathyroidism, remain

a major public health problem in this country.

They affect more than 10 million individuals

today, a figure that will rise significantly in the

decades ahead unless action is taken now. They

cause approximately 1.5 million fractures each

year, fractures that impose tremendous physical and emotional costs on those who suffer them

and their family members. They represent a significant financial burden to both individuals and

society at large. Many of these costs are avoidable, since much is already known about how to

effectively prevent, diagnose, and treat bone disease throughout the life span. However, much

of what could be done to reduce this burden is

not being done today, largely due to a lack of

awareness of the problem and the failure to apply current knowledge. In fact, many in the public and even the medical community believe that

osteoporosis is a natural consequence of aging

and that nothing can be done about it. This view

must be changed. The intent of this first-ever

report of the Surgeon General on bone health

and osteoporosis is to serve as a catalyst for the

development of a public health approach to promoting bone health. The central focus of this

effort is to alert individuals and the medical community to the meaning and importance of bone

health, including its impact on overall health and

well-being, and of the need to take action to ensure the timely prevention, assessment, diagnosis, and treatment of bone disease and fractures

throughout life.

This report comes at a very critical time. Like

many nations, the United States faces the prospect of an aging population and with it the expectation that the burden of chronic diseases,

including osteoporosis, will increase. In fact, without concerted action to address this issue, it is

estimated that in 2020 one in two Americans over

age of 50 will have, or be at high risk of developing, osteoporosis. If these predictions come true,

they will have a devastating impact on the wellbeing of Americans as they age. In fact, a major

theme of this report is that bone health is critically important to the overall health and quality

of life of Americans. Healthy bones provide the

body with a frame that allows for mobility and

for protection against injury. Bones also serve as

a storehouse for minerals that are vital to the

functioning of many other life-sustaining systems in the body. Unhealthy bones, however,

perform poorly in executing these functions.

They also lead to fractures, which are by far

the most important consequence of poor bone

health since they can result in disability, diminished function, loss of independence, and

premature death.

In recognition of the importance of promoting bone health and preventing fractures, the

President has declared 2002–2011 as the Decade

of the Bone and Joint. With this designation, the

United States has joined with other nations

throughout the world in committing resources

to accelerate progress in a variety of areas related

1
Bone Health and Osteoporosis

5

to the musculoskeletal system, including bone

disease and arthritis. As a part of its Healthy

People 2010 initiative, the U.S. Department of

Health and Human Services (HHS) has developed two overarching goals that are highly relevant to bone health and osteoporosis. The first

goal is increased quality and years of healthy life.

In other words, the hope is that Americans can

live long and live well. As life expectancy has

increased, attention has turned to living

healthfully throughout life. Fractures, the most

common and devastating consequence of bone

disease, frequently make it difficult, if not impossible, for elderly individuals to continue to

live well. The second goal is to eliminate health

disparities across different segments of the population. In addition, the President has launched

the HealthierUS initiative and, as a part of this

effort, HHS has implemented Steps to a

HealthierUS, both of which emphasize the importance of physical activity and a nutritious diet.

This Surgeon General’s Report fits into these

larger efforts to highlight the importance of the

musculoskeletal system to the health status of

Americans and to provide individuals, clinicians,

public health officials, policymakers, and other

stakeholders with the information and tools they

need to improve bone health in all Americans.

The Magnitude of the Problem

Realizing the vision of a “bone-healthy”

America will be challenging, given the magnitude of the problem. The bone health status of

Americans appears to be in jeopardy, a fact that

represents another key theme of this report. Fractures due to bone disease are common, costly,

and often become a chronic burden on individuals and society. An estimated 1.5 million individuals suffer a bone disease-related fracture

each year (Riggs and Melton 1995, Chrischilles

et al. 1991). However, this figure significantly

understates the true impact of bone disease, because it captures the problem at a point in time.

The impact of bone disease is more appropriately

evaluated over a lifetime. Four out of every 10

White women age 50 or older in the United States

will experience a hip, spine, or wrist fracture

sometime during the remainder of their lives; 13

percent of White men in this country will suffer

a similar fate (Cummings and Melton 2002).

While the lifetime risk for men and non-White

women is less across all fracture types, it is nonetheless substantial, and may be rising in certain

populations, such as Hispanic women

(Zingmond et al. 2004).

Fractures can have devastating consequences

for both the individuals who suffer them and

their family members. For example, hip fractures

are associated with increased risk of mortality.

The risk of mortality is 2.8–4 times greater among

hip fracture patients during the first 3 months

after the fracture, as compared to the comparable

risk among individuals of similar age who live in

the community and do not suffer a fracture.

Those who are in poor health or living in a nursing home at the time of fracture are particularly

vulnerable (Leibson et al. 2002, Richmond et al.

2003). For those who do survive, these fractures

often precipitate a downward spiral in physical

and mental health that dramatically impairs quality of life. Nearly one in five hip fracture patients, for example, ends up in a nursing home,

a situation that a majority of participants in one

study compared unfavorably to death (Salkeld

et al. 2000). Many fracture victims become isolated and depressed, as the fear of falls and additional fractures paralyzes them. Spine fractures,

which are not as easily diagnosed and treated as

are fractures at other sites, can become a source

of chronic pain as well as disfigurement.

Osteoporosis is the most important underlying cause of fractures in the elderly. Although

A Public Health Approach To Promote Bone Health
6 Chapter

A Report of the Surgeon General

osteoporosis can be defined as low bone mass

leading to structural fragility, it is difficult to

determine the extent of the condition described

in these qualitative terms. Using the World

Health Organization’s quantitative definition

based on bone density measurement, there are

roughly 10 million Americans over age 50 with

osteoporosis and an additional 34 million with

low bone mass or “osteopenia” of the hip,

which puts them at risk for osteoporosis, fractures, and their potential complications later

in life (NOF 2002).

Left unchecked, the bone health status of

Americans is only going to get worse, due primarily to the aging of the population. In fact,

the prevalence of osteoporosis and osteoporoticrelated fractures will increase significantly unless the underlying bone health status of Americans is significantly improved. By 2010, roughly

12 million individuals over age 50 are expected

to have osteoporosis and another 40 million to

have low bone mass. By 2020, those figures are

expected to jump to 14 million cases of osteoporosis and over 47 million cases of low bone mass

(NOF 2002). These demographic changes could

cause the number of hip fractures in the United

States to double or triple by 2040 (Schneider

and Guralnik 1990).

While much less is known about the prevalence

and treatment of other bone diseases, they too can

have a severe impact on the health and well-being

of those who suffer from them, especially if they

are not diagnosed and treated in a timely manner.

Many of the drugs that are used for osteoporosis

are also effective as treatments for other bone diseases. While these diseases cannot be prevented,

treatment can reduce levels of deformity and suffering. Further research on osteoporosis is likely to

yield additional improvements in the treatment of

these diseases, and may even yield insights into

how they can be prevented.

Not surprisingly, bone disease takes a significant financial toll on society and individuals

who suffer from it. The direct care expenditures

for osteoporotic fractures alone range from $12.2–

$17.9 billion each year, measured in 2002 dollars (Tosteson and Hammond 2002). Adding in

the direct costs of caring for other bone diseases

as well as the indirect costs (e.g., lost productivity for patients and family members) would

likely add billions of additional dollars to this tab.

The Challenge

Much of this considerable burden can be prevented. There is no question that significant gaps

in knowledge (and hence research needs) remain.

However, another important theme of this report

is that great improvements in the bone health status of Americans can be made by applying what

is already known about early prevention, assessment, diagnosis, and treatment. In fact, the evidence clearly suggests that individuals can do a

great deal to promote their own bone health. Prevention of bone disease begins at birth and is a

lifelong challenge. By choosing to engage in regular physical activity, to follow a bone-healthy diet,

and to avoid behaviors such as smoking that can

damage bone, individuals can improve their bone

health throughout life. Health care professionals

can play a critical role in supporting individuals

in making these choices and in identifying and

treating high-risk individuals and those who have

bone disease.

As noted earlier, the importance of achieving adequate levels of physical activity and calcium and vitamin D intake is now known, as is

the need to begin prevention at a very young

age and continue it throughout life. It is never

too late for prevention, as even older individuals

with poor bone health can improve their bone

health status through appropriate exercise and

calcium and vitamin D intake. Much is also

1
Bone Health and Osteoporosis

A Public Health Approach To Promote Bone Health 7

known about how to ensure timely diagnosis of

bone disease. Thanks to the development of bone

mineral density (BMD) testing, fractures need

not be the first sign of poor bone health. It is

now possible to detect osteoporosis early and to

intervene before a fracture occurs. Promising

new approaches to assessment and screening will

likely provide an even better understanding of

the early warning signs of bone disease in the

future. On the treatment front, a variety of drugs

have been developed that improve bone health

and reduce the incidence of fractures. New and

potentially more effective drugs are currently

under development. There are effective treatments not only for osteoporosis, but also for other

bone diseases such as Paget’s disease, hyperparathyroidism, rickets, and osteomalacia. There are

also promising new directions for the treatment

of osteogenesis imperfecta.

However, too little of what has been learned

thus far about bone health has been applied in

practice. As a result, the bone health status of

Americans is poorer than it should be. Perhaps

the biggest problem is a lack of awareness of bone

disease among both the public and health care

professionals, many of whom do not understand

the magnitude of the problem, let alone the ways

in which bone disease can be prevented and

treated.

Relatively few individuals follow the recommendations related to the amounts of physical

activity, calcium, and vitamin D that are needed

to maintain bone health. National surveys suggest that the average calcium intake of individuals is far below the levels recommended for optimal bone health (Wright et al. 2003.). Measurements of vitamin D in nursing home residents,

hospitalized patients, and adults with hip fractures suggest a high prevalence of insufficiency

(Webb et al.1990, LeBoff et al. 1999, Thomas et

al. 1998). Many Americans do not engage regularly in leisure-time physical activity. As shown

in Chapter 6, the participation by both adult men

and women declines with age, with women being consistently less active than men (Schiller et

al. 2004). In addition, only half those 12–21 years

old exercise vigorously on a regular basis and 25

percent report no exercise at all (Gordon-Larsen

et al. 1999).

Health care professionals can do a better job

as well. Studies show that physicians frequently

fail to diagnose and treat osteoporosis, even in

elderly patients who have suffered a fracture

(Solomon et al. 2003, Andrade et al. 2003,

Kiebzak et al. 2002, Kamel et al. 2000, Feldstein

et al. 2003). For example, in a recent study of

four well-established Midwestern health systems,

only one-eighth to a quarter of patients who had

a hip fracture were tested for their bone density;

fewer than a quarter were given calcium and vitamin D supplements; and fewer than one-tenth

were treated with effective antiresorptive drugs

(Harrington et al. 2002). Other studies have found

low usage rates for testing and treatment among

the high-risk population, including BMD testing

(which ranged from 3–23 percent), calcium and

vitamin D supplementation (11–44 percent), and

antiresorptive therapy (12–16 percent) (Morris

et al. 2004, Smith et al. 2001). In fact, most physicians do not even discuss osteoporosis with their

patients, even after a fracture (Pal 1999). Finally,

even when physicians do suggest therapy it often does not conform with recommended practice; for example, many patients with low BMD

are not treated while others with high BMD are

(Solomon et al. 2000).

Managed care organizations and other insurers that provide coverage to individuals under

age 65 may not see the full impact of bone disease in their enrollees, since most will have moved

on to Medicare by the time they suffer a fracture. Therefore, the commercial providers may
8 Chapter

A Report of the Surgeon General

not pay sufficient attention to bone health and

to the preventive strategies available to and suitable for younger people.

In short, therefore, the gap between clinical

knowledge and its application in the community

remains large and needs to be closed, a fact that

represents another key theme of this report. Of

particular concern is the fact that some populations suffer additional barriers in trying to achieve

optimal bone health. Overcoming these barriers

will not be possible without specific strategies and

programs geared towards bringing improvements

in bone health to these populations.

Some of the most important barriers relate

to men and racial and ethnic minorities. Osteoporosis and fragility fractures are often mistakenly viewed by both the public and health

care practitioners as only being a problem for

older White women. This commonly held but

incorrect view may delay prevention and even

treatment in men and minority women who are

not seen as being at risk for osteoporosis. While

a relatively small percentage of the total number

of people affected, these populations still represent millions of Americans who are suffering the

debilitating effects of bone disease.

For the poor (especially the low-income elderly population), individuals with disabilities,

individuals living in rural areas, and other

underserved populations, timely access to care

represents an additional important barrier. Poor

access to care may be caused by any number of

factors, such as limited knowledge about bone

health; a lack of available providers; inadequate

income or insurance coverage; the high costs of

diagnosis and treatment; a lack of transportation;

or the inability to take time off from work to attend to personal or family care needs. Whatever

the causes, the goal of better bone health for all

Americans cannot be reached without greater

efforts to educate underserved populations about

bone health and without significant improvements in their access to appropriate preventive

services and counseling, screening, diagnosis,

and treatment. Today these underserved populations rely on an unorganized patchwork of providers (e.g., emergency rooms) that are illequipped to provide or even facilitate the coordinated, ongoing preventive and treatment services that are needed to maintain bone health

and overall health and well-being.

Underserved populations not only have difficulty in accessing care, but there are also concerns about the quality of those services they do

receive. A recent study by the Institute of Medicine concluded that racial and ethnic minorities

tend to receive lower-quality health care than

does the majority population, even after accounting for access-related factors (Smedley et al.

2003). These disparities are consistent across a

wide range of services, including those critical

to bone health. Moreover, in a large study of

older adults who had suffered a hip or wrist fracture, certain groups of patients—including men,

older persons, non-Whites, and those with comorbid conditions—were less likely than White

women to receive treatment for their bone disease after their fractures (Solomon et al. 2003).

The Opportunity

This Surgeon General’s Report looks upon

the Nation’s at-risk bone status as an opportunity to do better rather than as an intractable

problem. A variety of factors make bone health

an ideal candidate for a public health approach.

These factors include: a) the prospects of declining bone health status due to an aging population; b) the significant gap between what we

know and what we apply; c) the need for early

prevention of an often “silent” disease; d) the fact

that most bone disease does not strike until

people are on Medicare; and e) the lack of sys1
Bone Health and Osteoporosis

A Public Health Approach To Promote Bone Health 9

tematic evaluation of the prevalence and impact

of bone disease. This Surgeon General’s Report

is calling for Federal, State, and local governments (including State and local public health

departments) to join forces with the private sector and community organizations in a coordinated effort to promote bone health and prevent

disease. This type of approach can serve as the

primary vehicle for improving the bone health

status of Americans. To be successful it must

involve all stakeholders—individual citizens;

volunteer health organizations; health care professionals; community organizations; private industry; and government—and must emphasize

policies and programs that promote the dissemination of best practices for prevention, screening, and treatment for all Americans.

Some of the work on this public health approach has already begun. The aforementioned

Healthy People 2010 initiative lays out 467 specific objectives in 28 different areas of health to

be achieved during the first decade of the 21st

century. Included in these objectives are targets

for reducing the number of individuals with osteoporosis and the number of hip fractures, along

with increasing levels of calcium intake and

physical activity. (See Table 1-1 for more information on those Healthy People 2010 goals that

relate to osteoporosis and bone health.)

One of the purposes of this Surgeon

General’s Report is to build support at many levels to include current Healthy People 2010 objectives in health agendas and activities at the

Federal, State, and local levels. Developing data

systems to track progress on these objectives will

be critical to achieving improvements in bone

health status. Going forward, it is anticipated

that the number of objectives related to osteoporosis and bone health will increase when

Healthy People 2020 objectives are developed,

and that existing measures will be refined as our

understanding of the science and our data collection and measurement systems improve.

The Charge

Recognizing that bone health can have a significant impact on the overall health and wellbeing of Americans, Congress instructed that this

report cover a range of important issues related

to improving bone health, including: challenges

in the diagnosis and treatment of osteoporosis and

related bone diseases; the impact of these diseases

on minority populations; promising prevention

strategies; how to improve health provider education and promote public awareness; and ways

to enhance access to key health services. (See

Appendix A for more details.)

To initiate the development of the report, an

interagency work group was convened by the

Surgeon General with staff representatives from

the National Institutes of Health (NIH), the

Centers for Disease Control and Prevention

(CDC), the Food and Drug Administration

(FDA), the Health Resources and Services Administration (HRSA), the Agency for

Healthcare Research and Quality (AHRQ), the

Administration on Aging, the Centers for Medicare and Medicaid Services (CMS), the Office

of Disease Prevention and Health Promotion,

the Office on Women’s Health, the Office on

Minority Health, the President’s Council on

Physical Fitness and Sports, the Regional Health

Administrators, and the U.S. Department of

Agriculture.

As a second step, a Surgeon General’s Workshop was convened in December 2002 that

brought together a wide range of researchers,

public health experts, and patient representatives

to discuss key areas that should be addressed in

the report. Prior to the workshop, public comments on what the priorities for the report should

be were solicited through the Surgeon General’s
10 Chapter

A Report of the Surgeon General

1
Bone Health and Osteoporosis

A Public Health Approach To Promote Bone Health 11

Web site. Following the workshop, a summary

of its key findings was released by the Surgeon

General (Report 2003).

This report includes contributions from more

than 50 authors across the country, while over

100 experts provided valuable guidance and insights in their reviews of initial drafts.

This report is intended to be a catalyst

for the advancement of research in bone

health, and for accelerating the translation of

existing evidence on how to improve bone

health status into everyday practice. The net

result should be an improvement in the bone

health status of Americans.

Evidence Base for the Report

This report is based on a review of the

published scientific literature. The scope of

the review encompassed studies written in

English from throughout the world. The

quality of the evidence, based on study design and its rigor, was considered as a part of

this review. All studies used in the report are

referenced in the text, with full citations at

the conclusion of each chapter.

This report does not offer any new standards

or guidelines for the prevention, diagnosis, or

treatment of bone disease. Rather, it summarizes

knowledge that is already known and can be

acted upon.

The clinical literature in bone disease includes

the full range of studies, from randomized controlled trials to case studies. Comprehensive reviews of the literature have been used for Chapters 2 through 9, and Chapter 11. Chapter 10,

which is an attempt to summarize key, actionable findings for busy health care professionals,

contains few references, as it largely draws on findings cited elsewhere in the report. Chapter 12

draws on both published studies and case studies

of population-based initiatives in bone health,

which were selected in order to highlight particular lessons about such approaches. Additional information on the various kinds of evidence and

studies that were used in preparing this report

can be found in Appendix B, entitled, “How We

Know What We Know: The Evidence Behind

the Evidence.”

Experts in their respective fields of bone

health contributed to this report. Each chapter was

prepared under the guidance of a coordinating

author for that chapter. Independent, expert peer

review was conducted for all chapters. The full

manuscript was reviewed by a number of senior

reviewers as well as the relevant Federal agencies.

All who contributed are listed in the Acknowledgments section of the report.

Organization of the Report

This report attempts to answer five major

questions for a wide variety of stakeholders, including policymakers; national, State, and local

public health officials; health system leaders;

health care professionals; community advocates;

and individuals. The report is organized around

each of these five questions. The first section

strives to define bone health and bone disease in

terms that the public can understand. The second section reviews today’s less-than-optimal

bone health status and documents the magnitude

of the problem facing the Nation. The third,

fourth, and fifth sections of the report tackle the

issue of what can be done to improve bone

health—first from the perspective of the individual, then from the perspective of the health

care professional, and finally from the perspective of the larger health system. The final section

lays out a vision for the future.

Part One: What Is Bone Health?

This introductory part of the report defines

bone health as a public health issue with an emphasis on prevention and early intervention to
12 Chapter

A Report of the Surgeon General

promote strong bones and prevent fractures and

their consequences. This first chapter describes

this public health approach along with the rationale for the report and the charge from Congress

and from the Surgeon General. Chapter 2 provides a brief overview of the fundamentals of

bone biology, helping the reader to understand

why humans have bones; how bones work; how

bones change during life; what keeps bones

healthy; what causes bone disease; and what is

in store in the future. Chapter 3 offers a summary review of the more common diseases, disorders, and conditions that both directly and indirectly affect bone. While much of Chapter 3

focuses on osteoporosis (including other diseases

and medications that can cause it), it also covers

other bone diseases, including rickets and osteomalacia, renal osteodystrophy, Paget’s disease of

bone, developmental skeletal disorders, and acquired skeletal disorders. Both Chapters 2 and 3

should be considered as important scientific background for the remainder of the report.

Part Two: What Is the Status of Bone Health

in America?

This part of the report describes the magnitude and scope of the problem from two perspectives. The first is the prevalence of bone disease within the population at large, and the second is the burden that bone diseases impose on

society and those who suffer from them. Chapter 4 provides detailed information on the incidence and prevalence of osteoporosis, fractures,

and other bone diseases. Where available, it also

provides data on bone disease in men and minorities and offers projections for the future.

Chapter 5 examines the costs of bone diseases

and their effects on well-being and quality of life,

both from the point of view of the individual

patient and society at large. It includes some reallife vignettes that highlight the impact that osteoporosis, Paget’s disease, osteogenesis

imperfecta, and other related bone diseases can

have on those who suffer from them and their

family members.

Part Three: What Can Individuals Do To

Improve Their Bone Health?

This part of the report examines factors that

determine bone health and describes lifestyle

approaches that individuals can take to improve

their personal bone health. Chapter 6 provides a

thorough review of the evidence on how nutrition, physical activity, and other factors influence bone health, including those behaviors that

promote it (e.g., physical activity, adequate calcium intake) and those that can impair it (e.g.,

smoking). Chapter 7 provides practical, realworld guidance on lifestyle approaches that individuals can take to improve their own bone

health, including the following: what foods are

the best sources of calcium and vitamin D; how

to calculate daily calcium intake; when calcium

and/or vitamin D supplementation should be

considered; and what types of physical activity

can contribute to bone health and overall health.

Part Four: What Can Health Care

Professionals Do To Promote Bone Health?

This part of the report describes what health

care professionals can do with their patients to

promote bone health. Chapter 8 examines the

potential risk factors for bone disease; highlights

red flags that signal the need for further assessment; reviews the use of formal assessment tools

to determine who should get a bone density test;

and provides detailed information on how to use

BMD for both assessment and monitoring purposes. The chapter also provides a glimpse into

the future of bone disease assessment and diagnosis. It includes real-life vignettes that highlight

the need for the medical profession to become

1
Bone Health and Osteoporosis

13

aware of the potential for severe osteoporosis to

develop in younger men and women. Chapter 9

focuses on preventive and therapeutic measures

for those who have or are at risk for bone disease.

It reviews a “pyramid approach” to treating bone

diseases and to preventing falls and fractures, with

maintenance of bone health through calcium, vitamin D, physical activity, and fall prevention

representing the base of the pyramid for all individuals, including those with bone disease. The

second level of the pyramid relates to addressing

and treating secondary causes of osteoporosis.

The third level of the pyramid is pharmacotherapy. The chapter describes currently available anti-resorptive, anabolic therapies and hormone therapies and offers a glimpse into future

directions for pharmacologic treatment of osteoporosis. The chapter also reviews the treatment

and rehabilitation of osteoporotic fractures and

highlights treatment options for other bone diseases. Chapter 10 “puts it all together” for health

care professionals by translating the research into

practical advice for preventing, diagnosing, and

treating bone disease in patients of all ages. Key

symptoms of major metabolic bone diseases are

identified, as are red flags that signal a need for

further intervention.

Part Five: What Can Health Systems and

Population-Based Approaches Do To Promote

Bone Health?

This part of the report examines how health

systems and population-based approaches can

promote bone health. Chapter 11 looks at the

key systems-level issues and decisions that affect

bone health care, including evidence-based

medicine; clinical practice guidelines; training

and education of health care professionals; quality

assurance; coverage policies; and disparities in

prevention and treatment. It also evaluates the

key roles of various stakeholders in promoting a

more systems-based approach to bone health

care, including individual clinicians; medical

groups; health plans and other insurers; public

health departments; and other stakeholders.

Chapter 12 describes the various potential

components of population-based approaches at

the local, State, and Federal levels to promote

bone health and reviews the evidence supporting

their use. This chapter also includes several

detailed profiles of innovative and/or effective

population-based programs, each of which was

selected to illustrate an important concept in

population-based health. Chapter 12 also draws

lessons for bone health from population-based

approaches that have been used in other areas

of health, such as the National Cholesterol

Education Program, to reduce cholesterol levels

in Americans.

Part Six: Challenges and Opportunities:

A Vision for the Future

The final part summarizes the key themes of

the report, highlights those opportunities that

have been identified for promoting bone health,

and lays out a vision for how these opportunities

can be realized so that bone health can be improved today and far into the future. The key to

success will be for public and private stakeholders—including individual consumers; voluntary

health organizations and professional associations; health care professionals; health systems;

academic medical centers; researchers; health

plans and insurers; public health departments;

and all levels of government—to join forces in

developing a collaborative approach to promoting timely prevention, assessment, diagnosis, and

treatment of bone disease throughout life.

A Public Health Approach To Promote Bone Health
14 Chapter

A Report of the Surgeon General

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Cummings SR, Melton LJ 3rd. Epidemiology

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CG, Siff SJ, Heggeness MH. Undertreatment

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LeBoff MS, Kohlmeier L, Hurwitz S, Franklin

J, Wright J, Glowacki J. Occult vitamin D

deficiency in postmenopausal US women

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Leibson CL, Tosteson AN, Gabriel SE, Ransom

JE, Melton LJ. Mortality, disability, and

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Morris CA, Cheng H, Cabral D, Solomon DH.

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Low Bone Mass in Our Nation. Washington,

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Richmond J, Aharonoff GB, Zuckerman JD, Koval

KJ. Mortality Risk After Hip Fracture. J

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Schiller JS, Coriaty-Nelson Z, Barnes P. Early

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Alan R. editors. Unequal treatment:

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Smith MD, Ross W, Ahern MJ. Missing a

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Solomon DH, Levin E, Helfgott SM. Patterns

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Solomon DH, Finkelstein JS, Katz JN, Mogun

H, Avorn J. Underuse of osteoporosis

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of exposure to sunlight and of diet to the

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2004 Mar 4 [Epub ahead of print].
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2

• The bony skeleton is a remarkable organ

that serves both a structural function, providing mobility, support, and protection for

the body, and a reservoir function, as the

storehouse for essential minerals.

• During childhood and adolescence

bones are sculpted by a process called

modeling, which allows for the formation of new bone at one site and the removal of old bone from another site

within the same bone. This process allows individual bones to grow in size

and to shift in space.

• Much of the cellular activity in a bone consists of removal and replacement at the

same site, a process called remodeling. The

remodeling process occurs throughout life

and becomes dominant by the time that

bone reaches its peak mass (typically by

the early 20s). Remodeling continues

throughout life so that most of the adult

skeleton is replaced about every 10 years.

• Both genes and the environment contribute to bone health. Some elements

of bone health are determined largely

by genes, and errors in signaling by

these genes can result in birth defects.

External factors, such as diet and physical activity, are critically important to

bone health throughout life, and these

factors can be modified.

Chapter 2: Key Messages

• The growth of the skeleton, its response

to mechanical forces, and its role as a mineral storehouse are all dependent on the

proper functioning of a number of systemic or circulating hormones that respond to changes in blood calcium and

phosphorus. If calcium or phosphorus

are in short supply, the regulating hormones take them out of the bone to serve

vital functions in other systems of the

body. Too many withdrawals can

weaken the bone.

• Many things can interfere with the development of a strong and healthy skeleton. Genetic abnormalities can produce

weak, thin bones, or bones that are too

dense. Nutritional deficiencies can result

in the formation of weak, poorly mineralized bone. Many hormonal disorders

can also affect the skeleton. Lack of exercise, immobilization, and smoking can

also have negative effects on bone mass

and strength.

• Osteoporosis, the most common bone

disease, typically does not manifest until late in life, when bone loss begins due

to bone breakdown and decreased levels of bone formation. Loss of bone mass

leads to the development of structural

abnormalities that make the skeleton

more fragile.
Bone Health and Osteoporosis

The Basics of Bone in Health and Disease 17

The purpose of this chapter is to provide an

overview of bone biology that will help the reader

to understand:

• why humans have bones;

• how bones work;

• how bones change during life;

• what keeps bones healthy;

• what causes bone disease, including the

most common form, osteoporosis; and

• the future of bone biology and what it

means for preventing and treating

bone disease.

While dealing with a subject that is highly

technical in nature, this chapter attempts to explain bone biology in terms that a lay person can

generally understand. It is intended to provide

the reader with the background needed to understand the basis for some of the preventive, diagnostic, and treatment approaches related to

bone disease that are discussed in detail later in

this report. Those interested in a more detailed

review of bone biology and bone disease can consult any of a number of recent texts (Bilezikian et

al. 2001, Marcus et al. 2001, Favus 2003).

Why Do We Have Bones?

The bony skeleton is a remarkable organ that

serves both a structural function—providing

mobility, support, and protection for the body—

and a reservoir function, as the storehouse for

Chapter 2

THE BASICS OF BONE IN

HEALTH AND DISEASE

essential minerals. It is not a static organ, but is

constantly changing to better carry out its functions. The development of the bony skeleton

likely began many eons ago, when animals left

the calcium-rich ocean, first to live in fresh water where calcium was in short supply, and then

on dry land where weight bearing put much

greater stress on the skeleton. The architecture

of the skeleton is remarkably adapted to provide

adequate strength and mobility so that bones do

not break when subjected to substantial impact,

even the loads placed on bone during vigorous

physical activity. The shape or structure of bone

is at least as important as its mass in providing

this strength.

The skeleton is also a storehouse for two minerals, calcium and phosphorus, that are essential

for the functioning of other body systems, and

this storehouse must be called upon in times of

need. The maintenance of a constant level of

calcium in the blood as well as an adequate supply of calcium and phosphorus in cells is critical

for the function of all body organs, but particularly for the nerves and muscle. Therefore, a

complex system of regulatory hormones has developed that helps to maintain adequate supplies

of these minerals in a variety of situations. These

hormones act not only on bone but on other tissues, such as the intestine and the kidney, to
18 Chapter

A Report of the Surgeon General

regulate the supply of these elements. Thus one

reason that bone health is difficult to maintain is

that the skeleton is simultaneously serving two

different functions that are in competition with

each other. First, bone must be responsive to

changes in mechanical loading or weight bearing,

both of which require strong bones that have

ample supplies of calcium and phosphorus. When

these elements are in short supply the regulating

hormones take them out of the bone to serve vital

functions in other systems of the body. Thus the

skeleton can be likened to a bank where we can

deposit calcium or phosphorus and then withdraw

them later in times of need. However, too many

withdrawals weaken the bone and can lead to the

most common bone disorder, fractures.

Both the amount of bone and its architecture

or shape are determined by the mechanical forces

that act on the skeleton. Much of this is determined genetically so that each species, including

humans, has a skeleton that is adapted to its functions. However, there can be great variation within

a species, so that some individuals will have strong

bones and others will have weak bones, largely

because of differences in their genes (Huang et

al. 2003). Moreover, bone mass and architecture

are further modified throughout life as these functions and the mechanical forces required to fulfill

them change. In other words, bones will weaken

if they are not subjected to adequate amounts of

loading and weight bearing for sufficient periods

of time. If they are not (such as in the weightless

condition of space travel), rapid bone loss can occur. In other words, as with muscle, it is “use it or

lose it” with bone as well. Conversely, the amount

and architecture of the bones can be improved

by mechanical loading. However, as described in

Chapter 6, some types of exercise may be better

than others in strengthening the skeleton.

To respond to its dual roles of support and

regulation of calcium and phosphorus, as well

as to repair any damage to the skeleton, bone is

constantly changing. Old bone breaks down and

new bone is formed on a continuous basis. In

fact, the tissue of the skeleton is replaced many

times during life. This requires an exquisitely

controlled regulatory system that involves specialized cells that communicate with each other.

These cells must respond to many different signals, both internal and external, mechanical and

hormonal, and systemic (affecting the whole skeleton) and local (affecting only a small region of

the skeleton). It is not surprising that with so

many different tasks to perform and so many

different factors regulating how the skeleton

grows, adapts, and responds to changing demands, there are many ways that these processes

can go astray.

How Bones Work

Bone is a composite material, consisting of

crystals of mineral bound to protein. This provides both strength and resilience so that the

skeleton can absorb impact without breaking. A

structure made only of mineral would be more

brittle and break more easily, while a structure

made only of protein would be soft and bend

too easily. The mineral phase of bone consists of

small crystals containing calcium and phosphate,

called hydroxyapatite. This mineral is bound in

an orderly manner to a matrix that is made up

largely of a single protein, collagen. Collagen is

made by bone cells and assembled as long thin

rods containing three intertwined protein chains,

which are then assembled into larger fibers that

are strengthened by chemical connections between them. Other proteins in bone can help to

strengthen the collagen matrix even further and

to regulate its ability to bind mineral. Very small

2
Bone Health and Osteoporosis

19

changes in the shape of the bone can act on the

cells inside bone (the osteocytes), which produce

chemical signals that allow the skeleton to respond to changes in mechanical loading. Abnormalities in the collagen scaffold can occur as a

result of a genetic disorder called osteogenesis

imperfecta, while the failure of mineral deposition can be the result of rickets and osteomalacia, conditions that result in marked weakening

of the skeleton (see below and Chapter 3).

To provide the body with a frame that is

both light and strong, bones are hollow. The

outer dense shell is called cortical bone, which

makes up roughly three-quarters of the total skeletal mass. Inside the cortical shell is a fine network of connecting plates and rods called trabecular bone that makes up the remaining 25 percent (Figure 2-1). Most bones are hollow structures in which the outer cortical bone shell defines the shape of the bone. This cortical shell is

essential because it provides strength, sites for

firm attachment of the tendons, and muscles and

protection without excessive weight. The inner

trabecular network has two important functions.

It provides a large bone surface for mineral exchange. In addition, trabecular bone helps to

maintain skeletal strength and integrity, as it is

particularly abundant in the spine and at the ends

of the long bones, sites that are under continuous stress from motion and weight-bearing. Fractures are common at these sites when the bone

is weakened (Kontulainen, Sievanen et al. 2003).

The rods and plates of trabecular bone are

aligned in a pattern that provides maximal

strength without too much bulk, much in the

way that architects and engineers design buildings and bridges. The shape and size of both

cortical and trabecular bone can respond to different kinds of stress produced by physical activity. For example, in most people the cortex of

their dominant arm is larger than that of their

non-dominant arm. The difference in cortex size

is even larger for tennis players and other athletes who routinely use a dominant arm in their

sporting activities. Bones do not work in isolation, but rather are part of the musculoskeletal

system, providing the “lever” that allows muscles

to move (by pulling on the lever). Thus muscle

activity is important for the normal function of

the bone. When the mechanical force produced

by muscle is lost—for example, in patients with

muscular dystrophy or paralysis—bone mass

and strength are also rapidly lost. Many bones

in the skeleton also have connecting joints that

provide greater flexibility of movement. These

joints are sites of great mechanical stress and are

subject to injury and to degeneration with aging. The most common type of joint degeneration is osteoarthritis, a painful, degenerative condition that affects the hip, knees, neck, lower

back, and/or small joints of the hand. These joint

diseases result from very different causes and

require very different management than do bone

diseases, and consequently they are not covered

in this report. However it is important to recognize that the bones, joints, and muscles are

the key parts of an integrated “musculoskeletal

system.” Problems with any one component of

this system can affect the other components.

Thus, weakness of the muscles can lead to loss

of bone and joint damage, while degeneration

of the joints leads to changes in the underlying

bone, such as the bony spurs or protuberances

that occur in osteoarthritis.

The Basics of Bone in Health and Disease
20 Chapter

A Report of the Surgeon General

How Bones Change

Throughout Life

Throughout life, bones change in size, shape,

and position. Two processes guide these

changes—modeling and remodeling. When a

bone is formed at one site and broken down in a

different site its shape and position is changed.

This is called modeling (Figure 2-2). However,

much of the cellular activity in a bone consists

of removal and replacement at the same site, a

process called remodeling. The remainder of this

section explains why and how these processes

occur.

Why We Need Modeling and Remodeling

During childhood and adolescence bones are

sculpted by modeling, which allows for the formation of new bone at one site and the removal

of old bone from another site within the same

bone (Seeman 2003) (Figure 2-2). This process

allows individual bones to grow in size and to

shift in space. During childhood bones grow

because resorption occurs inside the bone while

formation of new bone occurs on its outer (periosteal) surface. At puberty the bones get thicker

because formation can occur on both the outer

and inner (endosteal) surfaces. As people get

older, resorption occurs on inner surfaces while

formation occurs on outer surfaces, which can

partially compensate for the loss of strength due

to the thinning of the cortex. The size and shape

of the skeleton follows a genetic program, but

can be greatly affected by the loading or impact that occurs with physical activity. Ultimately bones achieve a shape and size that fits

2
Bone Health and Osteoporosis

The Basics of Bone in Health and Disease 21

best to their function. In other words, “form

follows function.”

The remodeling process occurs throughout

life and becomes the dominant process by the

time that bone reaches its peak mass (typically

by the early 20s). In remodeling, a small amount

of bone on the surface of trabeculae or in the

interior of the cortex is removed and then replaced at the same site (Figure 2-2). The remodeling process does not change the shape of the

bone, but it is nevertheless vital for bone health,

for a variety of reasons. First, remodeling repairs

the damage to the skeleton that can result from

repeated stresses by replacing small cracks or

deformities in areas of cell damage. Remodeling

also prevents the accumulation of too much old

bone, which can lose its resilience and become

brittle. Remodeling is also important for the

function of the skeleton as the bank for calcium

and phosphorus. Resorption (the process of

breaking down bone), particularly on the surface of trabecular bone, can supply needed calcium and phosphorus when there is a deficiency

in the diet or for the needs of the fetus during

pregnancy or an infant during lactation. When

calcium and phosphorus supplies are ample the

formation phase of remodeling can take up these

minerals and replenish the bank.

Modeling and remodeling continue throughout life so that most of the adult skeleton is replaced about every 10 years. While remodeling

predominates by early adulthood, modeling can

still occur particularly in response to weakening

of the bone. Thus with aging, if excessive

amounts of bone are removed from the inside,

some new bone can be laid down on the outside, thus preserving the mechanical strength of

the bone despite the loss of bone mass.

How Modeling and Remodeling Occur

The process of building the skeleton and

continuously reshaping it to respond to internal and external signals is carried out by specialized cells that can be activated to form or

break down bone. Both modeling and remodeling involve the cells that form bone called

osteoblasts and the cells that break down bone,

called osteoclasts (Figure 2-3). In remodeling

there is an important local interaction between

osteoblasts or their precursors (the cells that will

develop into osteoblasts by acquiring more specialized functions—a process called differentiation) and osteoclasts or their precursors. Since

remodeling is the main way that bone changes

in adults and abnormalities in remodeling are the

primary cause of bone disease, it is critically important to understand this process. In addition,

recent research has provided exciting information about these cell interactions.

Osteoblasts are derived from precursor cells

that can also be stimulated to become muscle,

fat or cartilage; however, under the right conditions these cells change (or differentiate) to form

new bone, producing the collagen that forms the

scaffolding or bone matrix. This calcium- and

phosphate-rich mineral is added to the matrix to

form the hard, yet resilient, tissue that is healthy

bone. Osteoblasts lay down bone in orderly layers that add strength to the matrix. Some of

the osteoblasts are buried in the matrix as it is

being produced and these are now called osteocytes. Others remain as thin cells that cover

the surface and are called lining cells. Osteocytes are the most numerous cells in bone and

are extensively connected to each other and to

the surface of osteoblasts by a network of small

thin extensions. This network is critical for the
22 Chapter

A Report of the Surgeon General

2
Bone Health and Osteoporosis

The Basics of Bone in Health and Disease 23

ability of bone to respond to mechanical forces

and injury. When the skeleton is subjected to

impact there is fluid movement around the osteocytes and the long-cell extensions that provides signals to the bone cells on the surface to

alter their activity, either in terms of changes in

bone resorption or formation. Failure of the osteoblasts to make a normal matrix occurs in a

congenital disorder of the collagen molecule

called osteogenesis imperfecta. Inadequate bone

matrix formation also occurs in osteoporosis,

particularly in the form of osteoporosis produced
24 Chapter

A Report of the Surgeon General

2

by an excess of the adrenal hormones called glucocorticoid-induced osteoporosis. This form of osteoporosis differs from primary osteoporosis and

most other forms of secondary osteoporosis because with glucocorticoid-induced osteoporosis

inhibition of bone formation is the dominant

mechanism for weakening of the skeleton.

The osteoclasts remove bone by dissolving

the mineral and breaking down the matrix in a

process that is called bone resorption. The osteoclasts come from the same precursor cells in the

bone marrow that produce white blood cells.

These precursor cells can also circulate in the

blood and be available at different sites in need of

bone breakdown. Osteoclasts are formed by fusion of small precursor cells into large, highly active cells with many nuclei. These large cells can

fasten onto the bone, seal off an area on the surface, and develop a region of intense activity in

which the cell surface is highly irregular, called a

ruffled border. This ruffled border contains transport molecules that transfer hydrogen ions from

the cells to the bone surface where they can dissolve the mineral. In addition, packets of enzymes

are secreted from the ruffled border that can break

down the matrix. Excessive bone breakdown by

osteoclasts is an important cause of bone fragility

not only in osteoporosis, but also in other bone

diseases such as hyperparathyroidism,

Paget’s disease, and fibrous dysplasia (see

Chapter 3). Inhibitors of osteoclastic bone

breakdown have been developed to treat

these disorders (see Chapter 9).

Removal and replacement of bone in the remodeling cycle occurs in a carefully orchestrated

sequence that involves communication between

cells of the osteoblast and osteoclast lineages

(Hauge, Qvesel et al. 2001; Parfitt 2001). It is

controlled by local and systemic factors that regulate bone remodeling to fulfill both its structural

and metabolic functions. The activation of this

process involves an interaction between cells of

the osteoblastic lineage and the precursors that

will become osteoclasts. What stops this process

is not known, but the osteoclasts machinery

clearly slows down and the osteoclasts die by a

process that is called programmed cell death.

Thus the amount of bone removed can be controlled by altering the rate of production of new

osteoclasts, blocking their activity, or altering

their life span. Most current treatments for osteoporosis work by slowing down osteoclastic

bone breakdown through use of antiresorptive

agents.

The activation and resorption phases are followed by a brief reversal phase (Everts, Delaisse

et al. 2002). During the reversal phase the resorbed

surface is prepared for the subsequent formation

phase, in part by producing a thin layer of protein, rich in sugars, which is called the cement

line and helps form a strong bond between the

old bone and the newly formed bone.

These three phases are relatively rapid, probably lasting only 2 to 3 weeks in humans. The

final phase of bone formation takes much longer,

lasting up to 3 or 4 months. Thus active remodeling at many sites can weaken the bone for a

considerable period of time (even if formation

catches up eventually), as many defects form in

the bony structure that have not yet been filled.

Formation is carried out by large active osteoblasts that lay down successive layers of matrix

in an orderly manner that provides added

strength. The addition of minerals to the collagenous matrix completes the process of making

strong bone. Any error in this complex process

can lead to bone disease.

Since remodeling serves both the structural

and metabolic functions of the skeleton, it can

be stimulated both by the hormones that regulate mineral metabolism and by mechanical loads

and local damage acting through local factors.
Bone Health and Osteoporosis

The Basics of Bone in Health and Disease 25

Repair of local damage is an important function

of remodeling. Over time repeated small stresses

on the skeleton can produce areas of defective

bone, termed micro-damage. Replacement of

that damaged bone by remodeling restores bone

strength. Signals for these responses are probably developed by the network of osteocytes and

osteoblasts, which, through their multiple connections, can detect changes in the stress placed

upon bone and in the health of the small areas of

micro-damage. Factors that affect the formation,

activity, and life span of osteoclasts and osteoblasts as they develop from precursor cells can

affect the remodeling cycle. Drugs have been

developed that act in these ways, with the goal

of reducing bone loss or increasing bone formation and maintaining skeletal health.

What Keeps Bones Healthy?

Both genes and the environment contribute

to bone health. Some elements of bone health

(e.g., the size and shape of the skeleton) are determined largely by genes, and errors in signaling by these genes can result in birth defects.

External factors, such as diet and physical activity, are critically important to bone health

throughout life and can be modified. As noted

above, the mechanical loading of the skeleton is

essential for maintenance of normal bone mass

and architecture. In addition, the skeleton needs

certain nutritional elements to build tissue. Not

only does the skeleton require the same nutritional elements as the rest of the body, but it

also has a special requirement for large amounts

of calcium and phosphorus. While adequate levels of these minerals can be obtained from the

mother during pregnancy and nursing, they

must come from the diet thereafter.

The growth of the skeleton, its response to

mechanical forces, and its role as a mineral storehouse are all dependent on the proper functioning of a number of systemic or circulating hormones produced outside the skeleton that work

in concert with local regulatory factors. The systemic hormones that affect the supply of calcium

and phosphorus and the formation and breakdown of bone are listed in Table 2-1. This complex system of regulatory hormones responds to

changes in blood calcium and phosphorus, acting not only on bone but also on other tissues

such as the intestine and the kidney. The system

is illustrated for calcium regulation in Figure 2-4.

Under normal conditions only part of the dietary

calcium is absorbed and some calcium is secreted

into the intestinal tract so that the net amount of

calcium entering the body normally is only a small

proportion of dietary calcium. In healthy young

adults there is calcium balance, where the amount

taken in is equal to the amount excreted. The bones

are constantly remodeling, but breakdown and

formation are equal. The kidney filters the blood,

including a large amount of calcium, but most of

this is taken back into the body by the kidney cells.

When calcium and/or phosphorus are in short supply, the regulating hormones take them out of the

bone to serve vital functions in other systems of

the body. Too many withdrawals can weaken the

bone. The regulatory hormones also play critical

roles in determining how much bone is formed at

different phases of skeletal growth and how well

bone strength and mass is maintained throughout

life. For example, sex hormones and the growth

hormone system described below are increased

during puberty, a time of rapidly increased skeletal growth. Finally, it is important to remember

that the effects of hormones and mechanical forces

on the skeleton are closely linked. For example,

the ability of bone to respond to mechanical loading is impaired in animals lacking the receptor for

estrogen (Lee et al. 2003).

Genes, hormones, local factors, and lifestyle

all play a role in determining one’s peak bone
26 Chapter

A Report of the Surgeon General

mass, a level that is typically achieved by the

time an individual reaches his or her late teens

or early 20s. The stronger the bones are at this

time, the better able they are to deal with any

withdrawals of calcium and phosphorus that are

needed and with any other changes to bone that

occur with aging.

What follows is a brief description of the most

important regulating hormones with respect to

bone health.

Calcium-Regulating Hormones

Three calcium-regulating hormones play an

important role in producing healthy bone: 1) parathyroid hormone or PTH, which maintains the

level of calcium and stimulates both resorption

and formation of bone; 2) calcitriol, the hormone

derived from vitamin D, which stimulates the

intestines to absorb enough calcium and phosphorus and also affects bone directly; and 3) calcitonin, which inhibits bone breakdown and may

protect against excessively high levels of calcium

in the blood.

Parathyroid hormone or PTH

PTH is produced by four small glands adjacent to the thyroid gland. These glands precisely

control the level of calcium in the blood. They

are sensitive to small changes in calcium concentration so that when calcium concentration decreases even slightly the secretion of PTH increases. PTH acts on the kidney to conserve calcium and to stimulate calcitriol production,

which increases intestinal absorption of calcium.

PTH also acts on the bone to increase movement of calcium from bone to blood. Excessive

production of PTH, usually due to a small tumor of the parathyroid glands, is called hyperparathyroidism and can lead to bone loss. PTH

stimulates bone formation as well as resorption.

When small amounts are injected intermittently,

bone formation predominates and the bones get

stronger (Rubin, Cosman et al. 2002). This is the

basis for a new treatment for osteoporosis (see

Chapter 9).

In recent years a second hormone related to

PTH was identified called parathyroid hormonerelated protein (PTHrP). This hormone normally

regulates cartilage and bone development in the

fetus, but it can be over-produced by individuals

who have certain types of cancer. PTHrP then

acts like PTH, causing excessive bone breakdown

and abnormally high blood calcium levels, called

hypercalcemia of malignancy (Stewart 2002).

2
Bone Health and Osteoporosis

The Basics of Bone in Health and Disease 27
28 Chapter

A Report of the Surgeon General

Calcitriol

Calcitriol is the hormone produced from vitamin D (Norman, Okamura et al. 2002).

Calcitriol, also called 1,25 dihydroxy vitamin

D, is formed from vitamin D by enzymes in

the liver and kidney. Calcitriol acts on many

different tissues, but its most important action

is to increase intestinal absorption of calcium

and phosphorus, thus supplying minerals for

the skeleton. Vitamin D should not technically

be called a vitamin, since it is not an essential

food element and can be made in the skin

through the action of ultra violet light from

the sun on cholesterol. Many people need vitamin D in their diet because they do not derive adequate levels from exposure to the sun.

This need occurred as people began to live

indoors, wear clothes, and move further north.

In northern latitudes the sun’s rays are filtered

in the winter and thus are not strong enough

to make sufficient vitamin D in the skin. Vitamin D deficiency leads to a disease of defective mineralization, called rickets in children

and osteomalacia in adults. These conditions

can result in bone pain, bowing and deformities of the legs, and fractures. Treatment with

vitamin D can restore calcium supplies and reduce bone loss.

Calcitonin

Calcitonin is a third calcium-regulating hormone produced by cells of the thyroid gland,

although by different cells than those that produce thyroid hormones (Sexton, Findlay et al.

1999). Calcitonin can block bone breakdown by

inactivating osteoclasts, but this effect may be

relatively transient in adult humans. Calcitonin

may be more important for maintaining bone

development and normal blood calcium levels

in early life. Excesses or deficiencies of calcitonin in adults do not cause problems in maintaining blood calcium concentration or the strength

of the bone. However, calcitonin can be used as

a drug for treating bone disease.

Sex Hormones

Along with calcium-regulating hormones, sex

hormones are also extremely important in regulating the growth of the skeleton and maintaining the mass and strength of bone. The female

hormone estrogen and the male hormone testosterone both have effects on bone in men and

women (Falahati-Nini, Riggs et al. 2000). The

estrogen produced in children and early in puberty can increase bone growth. The high concentration that occurs at the end of puberty has

a special effect—that is, to stop further growth in

height by closing the cartilage plates at the ends of

long bone that previously had allowed the bones

to grow in length.

Estrogen acts on both osteoclasts and osteoblasts to inhibit bone breakdown at all stages in

life. Estrogen may also stimulate bone formation.

The marked decrease in estrogen at menopause

is associated with rapid bone loss. Hormone

therapy was widely used to prevent this, but this

practice is now controversial because of the risks

of increased breast cancer, strokes, blood clots,

and cardiovascular disease with hormone therapy

(see Chapter 9).

Testosterone is important for skeletal growth

both because of its direct effects on bone and its

ability to stimulate muscle growth, which puts

greater stress on the bone and thus increases

bone formation. Testosterone is also a source of

estrogen in the body; it is converted into estrogen in fat cells. This estrogen is important for

the bones of men as well as women. In fact, older

men have higher levels of circulating estrogen

than do postmenopausal women.

2
Bone Health and Osteoporosis

The Basics of Bone in Health and Disease 29

Other Important Hormones

Growth hormone from the pituitary gland is

also an important regulator of skeletal growth. It

acts by stimulating the production of another hormone called insulin-like growth factor-1 (IGF-1),

which is produced in large amounts in the liver

and released into circulation. IGF-1 is also produced locally in other tissues, particularly in bone,

also under the control of growth hormone. The

growth hormone may also directly affect the

bone—that is, not through IGF-1 (Wang et al.

2004). Growth hormone is essential for growth

and it accelerates skeletal growth at puberty. Decreased production of growth hormone and IGF1 with age may be responsible for the inability of

older individuals to form bone rapidly or to replace bone lost by resorption (Yakar and Rosen

2003). The growth hormone/IGF-1 system stimulates both the bone-resorbing and bone-forming

cells, but the dominant effect is on bone formation, thus resulting in an increase in bone mass.

 Thyroid hormones increase the energy production of all body cells, including bone cells.

They increase the rates of both bone formation

and resorption. Deficiency of thyroid hormone

can impair growth in children, while excessive

amounts of thyroid hormone can cause too much

bone breakdown and weaken the skeleton

(Vestergaard and Mosekilde 2002). The pituitary

hormone that controls the thyroid gland, thyrotropin or TSH, may also have direct effects

on bone (Abe et al. 2003).

Cortisol, the major hormone of the adrenal gland,

is a critical regulator of metabolism and is important

to the body’s ability to respond to stress and injury.

It has complex effects on the skeleton (Canalis and

Delany 2002). Small amounts are necessary for normal bone development, but large amounts block bone

growth. Synthetic forms of cortisol, called glucocorticoids, are used to treat many diseases such as asthma

and arthritis. They can cause bone loss due both to

decreased bone formation and to increased bone

breakdown, both of which lead to a high risk of fracture (Kanis et al. 2004).

There are other circulating hormones that affect the skeleton as well. Insulin is important for

bone growth, and the response to other factors that

stimulate bone growth is impaired in individuals

with insulin deficiency (Lu et al. 2003, Suzuki et

al. 2003). A recently discovered hormone from fat

cells, leptin, has also been shown to have effects on

bone (Elefteriou et al. 2004, Cornish et al. 2002).

What Causes Diseases of Bone?

Maintaining a strong and healthy skeleton

is a complicated process that requires having the

right amount of bone with the right structure

and composition in the right place. There are

many things that can go wrong along the way.

Genetic abnormalities can produce weak,

thin bones, or bones that are too dense. The disease osteogenesis imperfecta is caused by abnormalities in the collagen molecule that make the

matrix weak and can lead to multiple fractures.

In another congenital disorder, osteopetrosis, the

bones are too dense because of failure of osteoclast formation or function. This failure of the

remodeling process results in persistence of trabecular bone in the marrow space so that the

marrow cavity may not be large enough to form

red and white blood cells normally. These dense

bones cannot remodel well in response to mechanical forces or micro damage and hence may

be weaker and subject to fracture even though

bone mass is increased. There are also other abnormalities of the genes that affect the size and

shape of the skeleton and can cause deformities

or abnormal growth.

Nutritional deficiencies, particularly of vitamin D, calcium, and phosphorus, can result
30 Chapter

A Report of the Surgeon General

2

in the formation of weak, poorly mineralized

bone. In children, vitamin D deficiency produces rickets in which there is not only a

marked weakness of bone and fractures but also

bowing of the long bones and a characteristic

deformity due to overgrowth of cartilage at the

ends of the bones. In adults, vitamin D deficiency leads to a softening of the bone (a condition known as osteomalacia) that can also lead

to fractures and deformities.

Many hormonal disorders can also affect the

skeleton. Overactive parathyroid glands or hyperparathyroidism can cause excessive bone

breakdown and increase the risk of fractures. In

severe cases, large holes or cystic lesions appear

in the bone, which makes them particularly fragile. A deficiency of the growth hormone/IGF-1

system can inhibit growth, leading to short stature. Loss of gonadal function or hypogonadism

in children and young adults can cause severe

osteoporosis due to loss of the effects of testosterone and estrogen. In addition, too much cortisol

production by the adrenal gland can occur in

Cushing’s syndrome.

Use of glucocorticoids as medication is a

common cause of bone disease. Excess glucocorticoids will stop bone growth in children and

cause marked thinning of the bone in adults,

often leading to fracture.

Many bone disorders are local, affecting

only a small region of the skeleton. Inflammation can lead to bone loss, probably through

the production of local resorbing factors by

the inflammatory white cells. This process can

occur around the affected joints in patients

with arthritis. Bacterial infections, such as severe gum inflammation or periodontal disease,

can produce loss of the bones around the teeth,

and osteomyelitis can produce a loss of bone

at the site of infection. This type of bone loss

is due to the direct damaging effect of bacterial

products as well as the production of resorbing

factors by white cells. Paget’s disease is a multifaceted condition in which the first change is

the formation of large, highly active, and unregulated osteoclasts that produce abnormal

bone resorption. The precise cause of Paget’s

disease is not known, but it appears to be the

consequence of both genetic factors and environmental factors, possibly a viral infection.

The osteoblasts try to repair this damage by

increasing bone formation. However, the normal bone architecture has been disrupted, leading to weak bones and the potential for fractures and deformities (even though the bones

may appear dense on an x-ray). One reason for

this is that the new bone formed is disorderly,

“woven” bone, which does not have the

proper alignment of mineral crystals and collagen matrix. In addition, the new bone may

not be in the right place to provide strength.

What Is Osteoporosis?

Osteoporosis is by far the most common bone

disease. Osteoporosis is “a skeletal disorder characterized by compromised bone strength, predisposing to an increased risk of fracture” (Osteoporosis 2000). The composition of the mineral and matrix, the fine structure of the trabecular bone, the porosity of the cortical bone, and

the presence of micro-fractures and other forms

of damage in bone are all important in determining bone strength. Changes in the fine structure

or micro-architecture of trabecular bone are particularly important since the most common fractures in osteoporosis occur at the spine, wrist, and

hip, sites where trabecular bone predominates.

As shown in Figure 2-5, the structure of normal

trabecular bone consists of well-connected plates

or broad bands that provide great strength. In

individuals with osteoporosis these bands are disrupted and often become thin, weakened rods.
Bone Health and Osteoporosis

The Basics of Bone in Health and Disease 31

Some of these rods are no longer connected to

another piece of bone, meaning that they no

longer contribute to bone strength.

Unfortunately, however, it is not possible to

measure bone strength directly, or to detect

changes in the micro-architecture of bone in living patients. The mass of bone, its density, and

its general shape can be determined by radiographs and absorptiometry (see Chapter 8). These

measures are used as “proxies” for bone strength

in assessing the risk of osteoporosis today.

There are a number of different ways in

which osteoporosis can develop, with the skeleton becoming more fragile and the risk of fracture increasing (Raisz and Rodan 2003). Some

of the most important mechanisms that lead to

skeletal fragility and fractures are listed in Table

2-2. Many people have relatively weak bones

even as young adults because of their genes or

because of suboptimal nutrition and lifestyle.

However, fractures due to bone fragility rather

than severe injury are uncommon in young

adults. It is typically not until later in life that bone

loss begins due to bone breakdown, a process that

accelerates around the time of menopause in

women. At the same time, bone formation tends
32 Chapter

A Report of the Surgeon General

2

to decrease with age in both men and women,

typically failing to keep up with the rate of bone

resorption. An imbalance between bone resorption and bone formation results in loss of bone

mass, leading to the development of structural

abnormalities that make the skeleton more fragile. There are a number of different combinations

of increased resorption and decreased formation

that can result in a weakened skeletal structure

(see Figure 2-5). Each of these pathways can be

involved in producing skeletal fragility at different times or sites within an individual patient.

Since bone breakdown is the first step in this process, blocking bone resorption is one way to decrease bone loss and prevent fractures. It is currently the most widely used therapeutic approach in osteoporosis. Stimulation of bone formation can also reverse skeletal fragility; new

therapies based on this approach have recently

been developed (Chapter 9).

The Future: Where a Better

Understanding of Bone Biology

Can Take Us

This brief overview of the basics of bone

health and disease provides a framework for the

discussion of what is known about the causes,

prevention, and treatment of skeletal disorders

today. Many knowledge gaps remain, and it is

still unclear precisely why so many people suffer fractures. Fortunately there have recently

been a number of exciting new discoveries

about skeletal regulation, and there are undoubtedly many more to come. These discoveries will further increase our understanding

of bone health and disease.

For example, recent discoveries have shown

how osteoblastic and osteoclastic cells communicate and provide signals to begin the process

of resorption (Figure 2-6). The osteoblastic cells

produce macrophage colony stimulating factor
Bone Health and Osteoporosis

The Basics of Bone in Health and Disease 33

(M-CSF) and receptor activator of nuclear factor kappa B ligand (RANKL) (Khosla 2001), proteins that bind to receptors on the osteoclast precursors, stimulate their proliferation and differentiation, and increase osteoclast activity. Osteoblastic cells also produce a protein called

osteoprotegerin that can bind RANKL and prevent it from interacting with osteoclastic cells.

The hormones and local factors that stimulate

bone resorption act on this system. The balance

between RANKL and osteoprotegerin (OPG)

production is probably critical in determining

how fast bone breaks down. RANKL in bone is

increased in individuals with estrogen deficiency

(Eghbali-Fatourechi et al. 2003). While RANKL

excess or osteoprotegerin deficiency would be

expected to cause bone loss, measurements of

the amounts of these proteins in circulating blood

do not support this theory. OPG levels are

higher and RANKL levels are lower in patients

with fractures or low bone mass (Schett et al.

2004, Jorgensen et al. 2004). On the other hand,

OPG or drugs that act like it by interfering with

the binding of RANKL could be useful in the

treatment of osteoporosis.

Recently another signaling system was discovered in bone involving a receptor called lipoprotein receptor-related protein 5. Patients with

over-activity in this receptor have strong bones

that typically do not fracture (Boyden, Mao et

al. 2002; Little, Carulli et al. 2002). Patients in

whom this receptor does not function form severe osteoporosis (Gong, Slee et al. 2001). Smaller

variations in the gene for this receptor may have

an important influence on bone size and strength

(Ferrari et al. 2004). Many other genes have also

recently been identified as influencing bone mass

and strength. A gene for an enzyme called

lipoxygenase was recently found to affect bone

mass in mice (Klein et al. 2004). Genetics studies

in Iceland have shown that variants in one of the

genes for bone morphogenetic proteins are associated with osteoporosis (Styrkarsdottir et al.

2003). There are also unidentified genes on specific sites on chromosomes that appear to control

bone mass and architecture.

All of these new findings could ultimately

lead to much better ways of determining

whether or not an individual will develop a

disorder of the skeleton. Enough information

exists today about the causes, prevention, diagnosis, and treatment of bone diseases to increase the bone health and decrease the risk of

fracture among Americans today. The goal of

this report is to describe how this can be accomplished and how both personal and public

health measures can promote bone health in

our population.
34 Chapter

A Report of the Surgeon General

2
Bone Health and Osteoporosis

The Basics of Bone in Health and Disease 35

Key Questions for Future

Research

Remarkable progress in furthering our understanding of the cellular, molecular biology,

and genetics of skeletal tissues in the last quarter

century has provided answers to many key questions. As expected, these answers have given rise

to additional research questions, as outlined below. The answers to these new questions should,

in turn, lead to new approaches to diagnosis,

prevention, and treatment. Thus it is important

to maintain strong support for basic research,

even as existing research findings are applied to

the everyday practice of medicine.

• How does the normal skeleton respond

to mechanical forces and maintain the

best structure?

• How is this response lost in those

individuals who develop bone disease?

Local factors that contribute to this

process have been identified but their

specific roles are not known. In addition,

there is a general understanding of bone

remodeling, but there are many specific

steps—in particular the reversal phase—

about which little is known.

• How precisely does estrogen maintain

bone mass and strength?

• What is the relative importance of other

circulating hormones in maintaining bone

health? These include not only the

calcium and growth-regulating hormones, but also recently identified

hormones such as leptin.

• How do newly identified genes and

proteins (e.g., the Wnt signaling pathway)

that affect bone cells work?
36 Chapter

A Report of the Surgeon General

2

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Aug;45(8 Pt 2):1347-52.

Norman AW, Okamura WH, Bishop JE, Henry

HL. Update on biological actions of

1alpha,25(OH)(2)-vitamin D(3) (rapid

effects) and 24R,25(OH)(2)-vitamin D(3).

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Parfitt AM. The bone remodeling compartment:

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J Bone Miner Res. 2001 Sep;16(9):1583-5.

Raisz LG, Rodan GA. Pathogenesis of

osteoporosis. Endocrinol Metab Clin North

Am. 2003 Mar;32(1):15-24.

Rauch F and Glorieux FH. Osteogenesis

imperfecta. Lancet. 2004 Apr

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Rubin MR, Cosman F, Lindsay R, Bilezikian JP.

The anabolic effects of parathyroid hormone.

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Schett G, Kiechl S, Redlich K, Oberhollenzer

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Q, Pietschmann P, et al. Soluble RANKL

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Seeman E. Periosteal bone formation—a

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parathyroid hormone-related protein on the

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40 Chapter 3

A Report of the Surgeon General

• Osteoporosis affects millions of Americans.

Individuals with osteoporosis are at high

risk of suffering one or more fractures,

which are often physically debilitating and

can potentially lead to a downward spiral

in physical and mental health.

• The most common form of osteoporosis

is known as “primary osteoporosis.” It is

the result of the cumulative impact of

bone loss and deterioration of bone

structure as people age. This bone loss

can be minimized and osteoporosis

prevented through adequate nutrition,

physical activity, and, if necessary,

appropriate treatment.

• There are a wide variety of diseases and

certain medications and toxic agents that

can cause or contribute to the

development of osteoporosis. If

recognized as a potential threat, this form

of the disease—known as secondary

osteoporosis—can often be prevented

through proper nutrition and physical

activity, along with appropriate therapy

if needed.

• A number of childhood diseases cause

rickets, a condition that results from a

delay in depositing calcium phosphate

mineral in growing bones. This delay

leads to skeletal deformities, especially

bowed legs. In adults, the equivalent

disease is called osteomalacia. Both

diseases can generally be prevented by

Chapter 3: Key Messages

ensuring adequate levels of vitamin D,

but they can have devastating

consequences for affected individuals.

• Patients with chronic renal disease are at

risk for developing a complex bone

disease known as renal osteodystrophy.

While dialysis and transplantation have

extended the life-expectancy of these

patients, it may not prevent further

progression of bone disease.

• Paget’s disease of bone is a progressive,

often crippling disorder of bone

remodeling that commonly involves the

spine, pelvis, legs, or skull (although any

bone can be affected). If diagnosed early,

its impact can be minimized.

• A large number of genetic and

developmental disorders affect the

skeleton. Among the more common of

these is osteogenesis imperfecta (OI).

Patients with this condition have bones

that break easily.

• Some skeletal disorders tend to develop

later in life. One of the most common of

these acquired skeletal disorders is a

malignancy of the bone. These

malignancies can originate in the bone

(primary tumors) or, much more

commonly, result from the seeding of

bone by tumors outside of the skeleton

(metastatic tumors). Primary bone cancer

also occurs in children. Both types of

tumors can destroy bone.
Bone Health and Osteoporosis

Diseases of Bone 41

The body systems that control the growth

and maintenance of the skeleton, which are

described in Chapter 2, can be disrupted in

different ways that result in a variety of bone

diseases and disorders. These include problems

that can occur at or before birth, such as genetic

abnormalities and developmental defects, as well

as diseases such as osteoporosis and Paget’s

disease of bone that damage the skeleton later in

life. In addition to conditions that affect bone

directly, there are many other disorders that

indirectly affect bone by interfering with

mineral metabolism. This chapter reviews some

of the more common diseases, disorders, and

conditions that both directly and indirectly

affect bone.

Osteoporosis

As pointed out in Chapter 2, osteoporosis is

a disease characterized by low bone mass and

deterioration of bone structure that causes bone

fragility and increases the risk of fracture. For

practical purposes, the World Health

Organization has defined osteoporosis as a bone

mineral density (BMD) value more than 2.5

standard deviations below the mean for normal

young White women. Osteoporosis is a common

disease affecting millions of Americans. As

described in Chapters 4 and 5, it can have

devastating consequences. Individuals with

osteoporosis are at high risk of suffering one or

more fractures, injuries that can often be

DISEASES OF BONE

Chapter 3

Classical Case

“A classical case of osteoporosis may start

in a woman about 55 years of age with a wrist

fracture. Ten years later she may present

with back pain, with or without minor

trauma, and thoracolumbar spine x-rays may

show a vertebral fracture. She might have

one of several risk factors: low body weight,

premature menopause, a family history of

fractures, smoking, heavy alcohol

consumption, inactivity, calcium or vitamin

D deficiency, or corticosteroid use. The back

pain may remit and relapse with subsequent

vertebral fractures. Approximately 10–15

years later, at the age of 75–80 years, the

patient may fall and sustain a hip fracture,

resulting in hospitalization, a 20 percent

excess risk of death, considerable functional

impairment and possibly a loss of

independence if she survives. Although this

scenario is instantly recognizable,

osteoporosis may present with any of a wide

range of fractures and at a variety of ages; it

is also increasingly recognized among men”

(WHO 2003). Recognition that the first

fracture was a sentinel event may have

triggered a detailed assessment that could

potentially have prevented additional

fractures. See Chapter 8 for more

information on such assessments.
42 Chapter 3

A Report of the Surgeon General

physically debilitating and potentially lead to a

downward spiral in physical and mental health

(Figure 3-1). Generalized osteoporosis is the most

common form of the disease, affecting most of the

skeleton. Osteoporosis can also occur in localized

parts of the skeleton as a result of injury or

conditions that reduce muscle forces on the bone,

such as limb paralysis. There are a variety of

different types of osteoporosis. The most common

form of osteoporosis is known as “primary

osteoporosis”—that is, osteoporosis that is not

caused by some other specific disorder. Bone loss

caused by specific diseases or medications (see

below) is referred to as “secondary osteoporosis.”

Each of these major categories of osteoporosis is

discussed in more detail on the following pages.
Bone Health and Osteoporosis

Diseases of Bone 43

Primary Osteoporosis

Primary osteoporosis is mainly a disease of

the elderly, the result of the cumulative impact

of bone loss and deterioration of bone structure

that occurs as people age (Seeman 2003). This

form of osteoporosis is sometimes referred to as

age-related osteoporosis. Since postmenopausal

women are at greater risk, the term

“postmenopausal” osteoporosis is also used.

Younger individuals (including children and

young adults) rarely get primary osteoporosis,

although it can occur on occasion. This rare form

of the disease is sometimes referred to as

“idiopathic” osteoporosis, since in many cases

the exact causes of the disease are not known, or

idiopathic. Since the exact mechanisms by which

aging produces bone loss are not all understood

(that is, it is not always clear why some

postmenopausal women develop osteoporosis

while others do not), age-related osteoporosis is

also partially idiopathic. A brief review of

“idiopathic” primary osteoporosis and a more

detailed review of the more common condition

of age-related osteoporosis follows.

Idiopathic Primary Osteoporosis

There are several different forms of

idiopathic osteoporosis that can affect both

children and adolescents, although these

conditions are quite rare (Norman 2003).

Juvenile osteoporosis affects previously healthy

children between the ages of 8 and 14. Over a

period of several years, bone growth is impaired.

The condition may be relatively mild, causing

only one or two collapsed bones in the spine

(vertebrae), or it may be severe, affecting

virtually the entire spine. The disease almost

always goes into remission (spontaneously)

around the time of puberty with a resumption

of normal bone growth at that time. Patients with

mild or moderate forms of the disease may be

left with a curvature of the spine (kyphosis) and

short stature, but those with a more severe form

of the disease may be incapacitated for life.

Primary osteoporosis is quite rare in young

adults. In this age-group, the disease is usually

caused by some other condition or factor, such as

anorexia nervosa or glucocorticoid use (Khosla et

al. 1994). When idiopathic forms of primary

osteoporosis do occur in young adults, they appear

in men as often as they do in women (this is in

contrast to age-related primary osteoporosis,

which occurs more often in women). The

characteristics of the disease can vary broadly and

may involve more than one disorder. Some young

adults with idiopathic primary osteoporosis may

have a primary defect in the regulation of bone

cell function, resulting in depressed bone

formation, increased bone resorption, or both (see

Chapter 2). Others with a mild form of the disease

may simply have failed to achieve an adequate

amount of skeletal mass during growth. In some

patients, the disease runs a mild course, even

without treatment, and the clinical manifestations

are limited to asymptomatic spinal compression

fractures. More typically, however, multiple spine

fractures occur over a 5–10 year period leading to

a height loss of up to 6 inches.

Age-Related Osteoporosis

Age-related osteoporosis is by far the most

common form of the disease (Figure 3-2). There

are many different causes of the ailment, but the

bone loss that leads to the disease typically begins

relatively early in life, at a time when corrective

action (such as changes in diet and physical

activity) could potentially slow down its course.

While it occurs in both sexes, the disease is two

to three times more common in women (see

Chapter 4). This is partly due to the fact that

women have two phases of age-related bone

loss—a rapid phase that begins at menopause and
44 Chapter 3

A Report of the Surgeon General

lasts 4–8 years, followed by a slower continuous

phase that lasts throughout the rest of life (Riggs

et al. 2002). By contrast, men go through only

the slow, continuous phase. As a result, women

typically lose more bone than do men. The rapid

phase of bone loss alone in women results in

losses of 5–10 percent of cortical bone (which

makes up the hard outer shell of the skeleton)

and 20–30 percent of trabecular bone (which fills

the ends of the limb bones and the vertebral

bodies in the spine, the sites of most osteoporotic

fractures). The slow phase of bone loss results

in losses of 20–25 percent of cortical and

trabecular bone in both men and women, but

over a longer period of time (Riggs et al. 2002).

Although other factors such as genetics and

nutrition contribute, both the rapid phase of bone

loss in postmenopausal women and the slow phase

of bone loss in aging women and men appear to

be largely the result of estrogen deficiency. (This

is demonstrated by the fact that correction of

estrogen deficiency can prevent these changes.)

For women, the rapid phase of bone loss is

initiated by a dramatic decline in estrogen

production by the ovaries at menopause. The loss

of estrogen action on estrogen receptors in bone

results in large increases in bone resorption (see

Chapter 2), combined with reduced bone

formation. The end result is thinning of the

cortical outer shell of bone and damage to the

trabecular bone structure (see Figure 2-5, Chapter

2). There may be some countervailing forces on

this process, as the outside diameter of the bone

can increase with age, thus helping to maintain

bone strength (Ahlborg et al. 2003).

By contrast, the slower phase of bone loss is

thought to be caused by a combination of factors

including age-related impairment of bone

formation, decreased calcium and vitamin D

intake, decreased physical activity, and the loss

of estrogen’s positive effects on calcium balance

in the intestine and kidney as well as its effects

on bone (Riggs et al. 2002). This leads to further

impairment of absorption of calcium by the

intestine and reduced ability of the kidney to

conserve calcium. If the amount of calcium

absorbed from the diet is insufficient to make

up for the obligatory calcium losses in the stool

and urine, serum calcium begins to fall.

Parathyroid hormone levels will then increase,

removing calcium from bone to make up for the

loss, as illustrated in Figure 3-3. The net result

of this process is an increase in bone resorption.

It is important to realize that these mineral losses

need not be great to result in osteoporosis. A

negative balance of only 50–100 mg of calcium

per day (far less than the 300 mg of calcium in a

single glass of milk) over a long period of time is

sufficient to produce the disease.

For aging men, sex steroid deficiency also

appears to be a major factor in age-related

osteoporosis. Although testosterone is the major

sex steroid in men, some of it is converted by the

aromatase enzyme into estrogen. In men,

however, the deficiency is mainly due to an

increase in sex hormone binding globulin, a

substance that holds both testosterone and

estrogen in a form that is not available for use by

the body. Between 30–50 percent of elderly men

are deficient in biologically active sex steroids

(Khosla et al. 1998). In fact, except for the lack of

the early postmenopausal phase, the process of

bone loss in older men is similar to that for older

women. As with women, the loss of sex steroid

activity in men has an effect on calcium absorption

and conservation, leading to progressive

secondary increases in parathyroid hormone

levels. As in older women, the resulting imbalance

between bone resorption and formation results

in slow bone loss that continues over life. Since

testosterone may stimulate bone formation more

than estrogen does, however, decreased bone
Bone Health and Osteoporosis

Diseases of Bone 45
46 Chapter 3

A Report of the Surgeon General

formation plays a relatively greater role in the

bone loss experienced by elderly men.

Secondary Osteoporosis

Young adults and even older individuals who

get osteoporosis often do so as a byproduct of

another condition or medication use. In fact,

there are a wide variety of diseases (Table 3-1)

along with certain medications and toxic agents

(Table 3-2) that can cause or contribute to the

development of osteoporosis (Stein and Shane

2003). Individuals who get the disease due to

these “outside” causes are said to have

“secondary” osteoporosis. They typically

experience greater levels of bone loss than would

be expected for a normal individual of the same

age, gender, and race. Secondary causes of the

disease are common in many premenopausal

women and men with osteoporosis (Khosla et

al. 1994); in fact, by some estimates the majority

of men with osteoporosis exhibit secondary
Bone Health and Osteoporosis

Diseases of Bone 47
48 Chapter 3

A Report of the Surgeon General

causes of the disease (Orwoll 1998). In addition,

up to a third of postmenopausal women with

osteoporosis also have other conditions that may

contribute to their bone loss (Tannenbaum et

al. 2002). This section briefly describes some of

the more common diseases, disorders, and

medications that can cause or contribute to the

development of osteoporosis.

Diseases and Disorders That Can Cause

Osteoporosis

Several genetic diseases have been linked to

secondary osteoporosis. Idiopathic hypercalciuria and cystic fibrosis are the most

common. Patients with cystic fibrosis have

markedly decreased bone density and increased

fracture rates (Ott and Aitken 1998) due to a

variety of factors, including calcium and vitamin

D malabsorption, reduced sex steroid production

and delayed puberty, and increased

inflammatory cytokines (see Chapter 2). Some

patients with idiopathic hypercalciuria have a

renal defect in the ability of the kidney to

conserve calcium. This condition may be

aggravated if they are advised to lower their

dietary calcium intake to prevent kidney stones.

Several studies have documented low bone

density in these individuals, and they may

respond to drugs that decrease calcium excretion

in the urine. Other genetic disorders (listed in

Table 3-1), although rare, should be considered

in patients with osteoporosis after more common

causes have been excluded.

Estrogen or testosterone deficiency during

adolescence (due to Turner’s, Kallman’s, or

Klinefelter’s syndrome, anorexia nervosa,

athletic amenorrhea, cancer, or any chronic

illness that interferes with the onset of puberty)

leads to low peak bone mass (Riggs et al. 2002).

Estrogen deficiency that develops after peak

bone mass is achieved but before normal

menopause (due to premature ovarian failure for

example) is associated with rapid bone loss. Low

sex steroid levels may also be responsible for

reduced bone density in patients with androgen

insensitivity or acromegaly. By contrast, excess

thyroid hormone (thyrotoxicosis), whether

spontaneous or caused by overtreatment with

thyroid hormone, may be associated with

substantial bone loss (Ross 1994); while bone

turnover is increased in these patients, bone

resorption is increased more than bone

formation. Likewise, excess production of

glucocorticoids caused by tumors of the pituitary

or adrenal glands (Cushing’s syndrome) can lead

to rapidly progressive and severe osteoporosis,

as can treatment with glucocorticoids (see

below). The relationship between diabetes and

osteoporosis is more controversial (Stein and

Shane 2003). For example, hip fractures are

increased in some studies of diabetic patients,

but not in others. In general, patients with type

1 (insulin-dependent) diabetes, particularly those

with poor control of their blood sugar (Heap et

al. 2004), are at greater risk of osteoporosis than

are those with type 2 (non-insulin dependent)

diabetes (Piepkorn et al. 1997).

Primary hyperparathyroidism is a relatively

common condition in older individuals,

especially postmenopausal women, that is caused

by excessive secretion of parathyroid hormone.

Most often, the cause is a benign tumor

(adenoma) in one or more parathyroid glands;

very rarely (less than 0.5 percent of the time)

the cause is parathyroid cancer (Wynne et al.

1992). Since most patients now come to clinical

attention when they are unexpectedly found on

routine examination to have an abnormally high

calcium level in the blood (Wermers et al. 1997),

the clinical presentation has changed over the

past 30 years from an uncommon but highly

symptomatic disorder involving renal stones and

bone disease (osteitis fibrosa cystica) to a
Bone Health and Osteoporosis

Diseases of Bone 49

common but relatively asymptomatic condition

(Silverberg and Bilezikian 2001). Typically,

cortical bone (for example, in the distal forearm)

is affected to a greater extent than trabecular

bone (for example, in the spine) in primary

hyperparathyroidism (Silverberg et al. 1989). It

is presumed that the reduction in bone mass is

associated with the increased risk of fracture seen

in these patients (Khosla and Melton 2002).

Diseases that reduce intestinal absorption of

calcium and phosphorus, or impair the

availability of vitamin D, can also cause bone

disease. Moderate malabsorption results in

osteoporosis, but severe malabsorption may

cause osteomalacia (see below). Celiac disease,

due to inflammation of the small intestine by

ingestion of gluten, is an important and

commonly overlooked cause of secondary

osteoporosis (Bianchi and Bianchi 2002).

Likewise, osteoporosis and fractures have been

found in patients following surgery to remove

part of the stomach (gastrectomy), especially in

women. Bone loss is seen after gastric bypass

surgery even in morbidly obese women who do

not have low bone mass initially (Coates et al.

2004). Increased osteoporosis and fractures are

also seen in patients with Crohn’s disease and

ulcerative colitis (Bernstein et al. 2000).

Glucocorticoids, commonly used to treat both

disorders, probably contribute to the bone loss.

Similarly, diseases that impair liver function

(primary biliary cirrhosis, chronic active

hepatitis, cirrhosis due to hepatitis B and C, and

alcoholic cirrhosis) may result in disturbances

in vitamin D metabolism and may also cause

bone loss by other mechanisms. Primary biliary

cirrhosis is associated with particularly severe

osteoporosis. Fractures are more frequent in

patients with alcoholic cirrhosis than any other

types of liver disease, although this may be

related to the increased risk of falling among

heavy drinkers (Crawford et al. 2003). Human

immunodeficiency virus (HIV) infected patients

also have a higher prevalence of osteopenia or

osteoporosis (Brown et al. 2004). This may

involve multiple endocrine, nutritional, and

metabolic factors and may also be affected by

the antiviral therapy that HIV patients receive

(Thomas and Doherty 2003).

Autoimmune and allergic disorders are

associated with bone loss and increased fracture

risk. This is due not only to the effect of

immobilization and the damage to bone by the

products of inflammation from the disorders

themselves, but also from the glucocorticoids

that are used to treat these conditions (Lien et

al. 2003, Orstavik et al. 2004). Rheumatic diseases

like lupus and rheumatoid arthritis have both

been associated with lower bone mass and an

increased risk of fractures. A study found that

12 percent of women with systemic lupus

erythematosus reported at least one fracture

since the onset of disease, a 4.7-fold higher risk

of fracture than for the typical woman. Fractures

in these women were found to be associated with

the following: older age at diagnosis, longer

disease duration, longer duration of steroid use,

and post-menopausal status (Ramsey-Goldman

et al. 1999, Haugeberg et al. 2003).

Many neurologic disorders are associated

with impaired bone health and an increased risk

of fracture (Whooley, Kip et al. 1999; Lloyd,

Spector et al. 2000). This may be due in part to

the effects of these disorders on mobility and

balance or to the effects of drugs used in treating these disorders on bone and mineral metabolism. Unfortunately, however, health care providers often fail to assess the bone health of patients who have these disorders or to provide

appropriate preventive and therapeutic measures.

For example, patients with stroke, spinal cord injury, or neurologic disorders show rapid bone loss
50 Chapter 3

A Report of the Surgeon General

in the affected areas (Dauty, Perrouin Verbe et

al. 2000; Poole, Reeve et al. 2002; Tuzun, Altintas

et al. 2003). There are many disabling conditions

that can lead to bone loss, and thus it is important

to pay attention to bone health in patients with

developmental disabilities, such as cerebral palsy,

as well as diseases affecting nerve and muscle, such

as poliomyelitis and multiple sclerosis. Children

and adolescents with these disorders are unlikely

to achieve optimal peak bone mass, due both to

an increase in bone resorption and a decrease in

bone formation. In some cases very rapid bone

loss can produce a large enough increase in blood

calcium levels to produce symptoms (Carey and

Raisz 1985; Go 2001). Fractures are common in

these individuals not only because of bone loss,

but also because of muscular weakness and neurologic impairment that increases the likelihood

of falls. Bone loss can be slowed—but not completely prevented—by antiresorptive therapy

(Sato, Asoh et al. 2000). Epilepsy is another neurologic disorder that increases the risk of bone

disease, primarily because of the adverse effects

of anti-epileptic drugs. Many of the drugs used

in epilepsy can impair vitamin D metabolism,

probably by acting on the liver enzyme which

converts vitamin D to 25 hydroxy vitamin D

(Farhat, Yamout et al. 2000, Sheth 2002). In addition, there may be a direct effect of these agents

on bone cells. Due to the negative bone-health

effects of drugs, most epilepsy patients are at risk

of developing osteoporosis. In those who have low

vitamin D intakes, intestinal malabsorption, or

low sun exposure, the additional effect of antiepileptic drugs can lead to osteomalacia. Supplemental vitamin D may be effective in slowing

bone loss, although patients who develop osteoporosis may require additional therapy such

as bisphosphonates.

Psychiatric disorders can also have a negative

impact on bone health. While anorexia nervosa

is the psychiatric disorder that is most regularly

associated with osteoporosis, major depression,

a much more common disorder, is also associated

with low bone mass and an increased risk of

fracture (Coelho, Silva et al. 1999; Cizza, Ravn

et al. 2001; Robbins, Hirsch et al. 2001). Many

studies show lower BMD in depressed patients

(Michelson et al. 1996). In addition, one large

study found an increased incidence of falls and

fractures among depressed women, even though

there was no difference between their BMD and

that of non-depressed women included in the

study (Whooley, Kip et al. 1999). Higher scores

for depressive symptoms have also been reported

in women with osteoporosis. Yet what these

studies do not make clear is whether major

depression causes low BMD and increased

fracture risk, or whether the depression is a

consequence of the diminished quality of life and

disability that occurs in many osteoporotic

patients. One factor that may cause bone loss in

severely depressed individuals is increased

production of cortisol, the adrenal stress

hormone. Whatever the cause of low BMD and

increased fracture risk, measurement of BMD is

appropriate in both men and women with major

depression. While the response of individuals

with major depression to calcium, vitamin D, or

antiresorptive therapy has not been specifically

documented, it would seem reasonable to

provide these preventive measures to patients at

high risk.

Finally, several diseases that are associated

with osteoporosis are not easily categorized.

Aseptic necrosis (also called osteonecrosis or

avascular necrosis) is a well-known skeletal

disorder that may be a complication of injury,

treatment with glucocorticoids, or alcohol abuse

(Pavelka 2000). This condition commonly affects

the ends of the femur and the humerus. The

precise cause is unknown, but at least two theories
Bone Health and Osteoporosis

Diseases of Bone 51

have been suggested. One is that blood supply to

the bone is blocked by collapsing bone. The other

is that microscopic fat particles block blood flow

and result in bone cell death. Chronic obstructive

pulmonary disease (emphysema and chronic

bronchitis) is also now recognized as being

associated with osteoporosis and fractures even

in the absence of glucocorticoid therapy.

Immobilization is clearly associated with rapid

bone loss; patients with spinal cord lesions are at

particularly high risk for fragility fractures (Kiratli

2001). However, even modest reductions in

physical activity can lead to bone loss (see Chapter

6). Hematological disorders, particularly

malignancies, are commonly associated with

osteoporosis and fractures as well. These are

discussed in more detail later in the chapter.

Medications and Therapies That Can Cause

Osteoporosis

Osteoporosis can also be a side effect of

particular medical therapies (Table 3-2).

Glucocorticoid-Induced Osteoporosis

(GIO). GIO is by far the most common form

of osteoporosis produced by drug treatment.

While it has been known for many years that

excessive production of the adrenal hormone

cortisol can cause thinning of the bone and

fractures, this condition, a form of Cushing’s

syndrome, remains uncommon. With the

increased use of prednisone and other drugs

that act like cortisol for the treatment of many

inflammatory and autoimmune diseases, this

form of bone loss has become a major clinical

concern. The concern is greatest for those

diseases in which the inflammation itself and/

or the immobilization caused by the illness also

caused increased bone loss and fracture risk.

Glucocorticoids, which are used to treat a wide

variety of inflammatory conditions (e.g.,

rheumatoid arthritis, asthma, emphysema,

chronic lung disease), can cause profound

reductions in bone formation and may, to a lesser

extent, increase bone resorption (Saag 2002),

leading to loss of trabecular bone at the spine

and hip, especially in postmenopausal women

and older men. The most rapid bone loss occurs

early in the course of treatment, and even small

doses (equivalent to 2.5–7.5 mg prednisone per

day) are associated with an increase in fractures

(van Staa et al. 2002). As shown in Figure 3-4,

the risk of fractures increases rapidly in patients

treated with glucocortocoids, even before much

bone has been lost. This rapid increase in fracture

risk is attributed to damage to the bone cells,

which results in less healthy bone tissue. To

avoid this problem, health care providers are

urged to use the lowest possible dose of

glucocorticoids for as short a time as possible.

For some diseases, providers should also consider

giving glucocorticoids locally (e.g., asthma

patients can inhale them), which results in much

less damage to the bone.
52 Chapter 3

A Report of the Surgeon General

Other Medications That Can Cause

Osteoporosis. Cyclosporine A and tacrolimus are

widely used in conjunction with glucocorticoids

to prevent rejection after organ transplantation,

and high doses of these drugs are associated with

a particularly severe form of osteoporosis (Cohen

and Shane 2003). Bone disease has also been

reported with several frequently prescribed

anticonvulsants, including diphenylhydantoin,

phenobarbital, sodium valproate, and

carbamazepine (Stein and Shane 2003). Patients

who are most at risk of developing this type of

bone disease include those on long-term therapy,

high medication doses, multiple anticonvulsants,

and/or simultaneous therapy with medications

that raise liver enzyme levels. Low vitamin D

intake, restricted sun exposure, and the presence

of other chronic illnesses increase the risk,

particularly among elderly and institutionalized

individuals. In contrast, high intakes of vitamin

A (retinal) may increase fracture risk

(Michaelsson et al 2003). Methotrexate, a folate

antagonist used to treat malignancies and (in

lower doses) inflammatory diseases such as
Bone Health and Osteoporosis

Diseases of Bone 53

rheumatoid arthritis, may also cause bone loss,

although research findings are not consistent. In

addition, gonadotropin-releasing hormone

(GnRH) agonists, which are used to treat

endometriosis in women and prostate cancer in

men, reduce both estrogen and testosterone

levels, which may cause significant bone loss and

fragility fractures (Smith 2003).

Rickets and Osteomalacia

Rickets (which affects children) and

osteomalacia (which affects adults) are

relatively uncommon diseases in the United

States, since they can generally be prevented

by ensuring adequate levels of vitamin D.

These diseases can have devastating

consequences to those who get them (Chesney

2001, Pettifor 2002 and 2003).

A number of childhood diseases cause

rickets, a condition that results from a delay in

depositing calcium phosphate mineral in

growing bones, thus leading to skeletal

deformities, especially bowed legs. In adults,

the equivalent disease is called osteomalacia.

Since longitudinal growth has stopped in

adults, deficient bone mineralization does not

cause skeletal deformity but can lead to

fractures, particularly of weight-bearing bones

such as the pelvis, hip, and feet. Even when

there is no fracture, many patients with rickets

and osteomalacia suffer from bone pain and can

experience severe muscle weakness.

Rickets and osteomalacia are typically caused

by any of a variety of environmental

abnormalities. While rare, the disorder can also

be inherited (Drezner 2003) as a result of

mutations in the gene producing the enzyme that

converts 25-hydroxy vitamin D to the active

form, 1,25-dihydroxy vitamin D, or in the gene

responsible for the vitamin D receptor.

Osteomalacia can also be caused by disorders

that cause marked loss of phosphorus from the

body. This can concur as a congenital disorder

or can be acquired in patients who have tumors

that produce a protein that affects phosphorus

transport in the kidney.

Since vitamin D is formed in the skin by

sunlight, the most common cause is reduced sun

exposure. This is particularly important in

northern latitudes where the winter sun does not

have the power to form vitamin D in the skin.

Thus the disease is often seen in individuals

living at northern latitudes, particularly

immigrants who have pigmented skin that

decreases the formation of vitamin D or who

habitually cover themselves. This problem can

also occur in children who are confined indoors

and in individuals who are house-bound (e.g.,

due to chronic ill health or frailty). Patients with

diseases of the gastrointestinal tract, such as

gastrectomy, malabsorption syndromes, and

small bowel resection, are also at higher risk,

since these conditions reduce vitamin D

absorption from the diet.

There is also a second form of rickets and

osteomalacia that is caused by phosphate

deficiency. This condition can be inherited (this

is known as X-linked hypophosphatemic

rickets), but it is more commonly the result of

other factors. Individuals with diseases affecting

the kidney’s ability to retain phosphate rapidly

are at risk of this condition, as are those with

diseases of the renal tubule that affect the site of

phosphate reabsorption. While most foods are

rich in phosphate, phosphate deficiency may also

result from consumption of very large amounts

of antacids containing aluminum hydroxide,

which prevents the absorption of dietary

phosphate. Finally, rickets due to phosphate

deficiency may occur in individuals with

acquired or inherited defects in acid secretion

by the kidney tubule and those who take certain
54 Chapter 3

A Report of the Surgeon General

drugs (Table 3-3) that interfere with phosphate

absorption or the bone mineralization process.

Renal Osteodystrophy

Patients with chronic renal disease are not

only at risk of developing rickets and

osteomalacia (Elder 2002), but they are also at

risk of a complex bone disease known as renal

osteodystrophy (Cunningham et al. 2004). This

condition is characterized by a stimulation of

bone metabolism caused by an increase in

parathyroid hormone and by a delay in bone

mineralization that is caused by decreased

kidney production of 1,25-dihydroxyvitamin

D. In addition, some patients show a failure of

bone formation, called adynamic bone disease.

As a result of this complexity, bone biopsies

are often needed to make a correct diagnosis

(Martin et al. 2004). By the time the patient

progresses to end-stage renal failure, clinical

manifestations of the disease appear, including

bone cysts that result from stimulation of

osteoclasts by the excess parathyroid hormone.

While dialysis can significantly extend the lifeexpectancy of patients with chronic renal

failure, it does nothing to prevent further

progression of the osteodystrophy. In fact, the

managing of the patient through dialysis may lead

to further bone abnormalities that become

superimposed on the underlying osteodystrophy,

thus increasing the risk of fractures (Alem et al.

2000). While a renal transplant (offered to a

growing number of patients on dialysis) may

reverse many features of renal osteodystrophy,

the use of antirejection medication in transplant

patients may cause bone loss and fractures.

Paget’s Disease of Bone

Paget’s disease of bone (Siris and Roodman

2003) is a progressive, often crippling disorder

of bone remodeling (see Chapter 2) that

commonly involves the spine, pelvis, legs, or

skull (although any bone can be affected). If

diagnosed early, its impact can be minimized.

 There are also patients who develop tumors

that secrete a factor that causes loss of phosphate

from the body. This condition is called tumorinduced or oncogenic osteomalacia.
Bone Health and Osteoporosis

Diseases of Bone 55

Individuals with this condition experience an

increase in bone loss at the affected site due to

excess numbers of overactive osteoclasts. While

bone formation increases to compensate for the

loss, the rapid production of new bone leads to

a disorganized structure. The resulting bone is

expanded in size and associated with increased

formation of blood vessels and connective tissue

in the bone marrow. Such bone becomes more

susceptible to deformity or fracture (Figure 3-

5). Depending on the location, the condition

may produce no clinical signs or symptoms, or

it may be associated with bone pain, deformity,

fracture, or osteoarthritis of the joints adjacent

to the abnormal bone. Paget’s disease of bone

can also cause a variety of neurological

complications as a result of compression of

nerve tissue by pagetic bone. In very rare cases

(probably less than 1 percent of the time) the

disease is complicated by the development of

an osteosarcoma.

Although Paget’s disease is the second most

common bone disease after osteoporosis (see

Chapter 4), many questions remain regarding

its pathogenesis. There is a strong familial

predisposition for Paget’s disease, but no single

genetic abnormality has been identified that can

explain all cases. Paget’s disease can be

transmitted (or inherited) across generations in

an affected family; 15–40 percent of patients

have a relative with the disorder (Morales-Piga

et al. 1995). Studies in the United States (Siris

et al. 1991) suggest that a close relative of a

pagetic patient is seven times more likely to

develop Paget’s disease than is someone who

does not have an affected relative. However,

environmental factors are likely play a role in

the majority of cases. For example, some studies

have suggested that Paget’s disease may result

from a ”slow virus” infection with measles

(Friedrichs et al. 2002).

Paget’s Disease of Bone

Paget’s disease may present in many

different ways since it can affect bones

throughout the body. A typical case might

be a man in his 60s who complains to his

doctor of pain in the hip. The doctor might

tell him he has arthritis and suggest that he

take ibuprofen or acetaminophen (Tylenol).

Then, several years later, a routine screening

may show a high alkaline phosphatase level.

This test would then prompt use of a bone

scan and radiographs, which would finally

show Paget’s disease of his femur and pelvic

bone. Unfortunately, by this time the man

likely has developed some bowing of the leg

and suffered damage to the joints, neither of

which can be reversed by treatment.

However, treatment with a bisphosphonate

can stop the progression of the disease. As a

result, the man lives the rest of his life with

some pain and he walks with a limp. Not

surprisingly, the man, his family, and his

doctor all wish that the diagnosis had been

made earlier. Since Paget’s disease runs in

families, they decide to test the man’s

relatives. These tests show that the man’s

younger brother has a similar problem. He

is treated immediately and no deformities

ever develop.

Developmental Skeletal Disorders

A large number of genetic and developmental

disorders affect the skeleton. Among the more

common and more important of these is a group

of inherited disorders referred to as osteogenesis

imperfecta or OI (Whyte 2003, Rauch and

Glorieux 2004). Patients with this condition have

bones that break easily (therefore, the condition

is also known as brittle bone disease). There are
56 Chapter 3

A Report of the Surgeon General

a number of forms of OI (see Table 3-4) that

result from different types of genetic defects or

mutations. These defects interfere with the

body’s production of type I collagen, the

underlying protein structure of bone. As

illustrated in Table 3-4, most, but not all, forms

of OI are inherited. The disease manifests

through a variety of clinical signs and symptoms,

ranging from severe manifestations that are

incompatible with life (that is, causing a

stillbirth) to a relatively asymptomatic disease.

However, most OI patients have low bone mass

(osteopenia) and as a result suffer from recurrent

fractures and resulting skeletal deformities.

There are four main types of OI, which vary

according to the severity and duration of the

symptoms. The most common form (Type I) is

also the mildest version; and patients may have

relatively few fractures. The second mildest form

of the disease (which is called Type IV, because

it was the fourth type of OI to be discovered)

results in mild to moderate bone deformity, and

sometimes in dental problems and hearing loss.

These patients also sometimes have a blue,
Bone Health and Osteoporosis

Diseases of Bone 57

purple, or gray discoloration in the whites of

their eyes, a condition known as blue sclera. A

more severe form of the disease (Type III) results

in relatively frequent fractures, and often in short

stature, hearing loss, and dental problems.

Finally, patients with the most severe form of

the disease (Type II) typically suffer numerous

fractures and severe bone deformity, generally

leading to early death.

OI is not the only group of developmental

skeletal disorders. An even larger group of rare

diseases (sclerosing bone disorders) causes an

increase in bone mass (Whyte 2003). One of these,

osteopetrosis (marble bone disease), is more or

less the opposite of osteoporosis. Instead of

overactive osteoclasts, osteopetrosis results from

a variety of genetic defects that impair the ability

of osteoclasts to resorb bone. This interferes with

the normal development of the skeleton and leads

to excessive bone accumulation. Although such

bone is very dense, it is also brittle and thus

fractures often result. In addition, by compressing

various nerves, the excess bone in patients with

osteopetrosis may cause neurological symptoms,

such as deafness or blindness. These patients may

also suffer anemia, as blood-forming cells in the

bone marrow are “crowded out” by the excess

bone. Similar symptoms can result from overactivity of these bone cells, as in fibrous dysplasia

where bone-forming cells produce too much

connective tissue.

Malignancy and the Skeleton

Some other skeletal disorders are not inherited but rather develop only later in life. One of

the most common of these acquired skeletal disorders is a tumor of the bone. Bone tumors can

originate in the bone (these are known as primary tumors) or, much more commonly, result

from the seeding of bone by tumors outside of

the skeleton (these are known as metastatic tuOsteogenesis Imperfecta (OI)

There is an enormous range of severity

in OI cases, from children who are stillborn

due to multiple fractures in the womb and

the inability to breathe, to children who

suffer a few fractures, to mild cases where

fractures do not occur until later in life, much

like in patients with osteoporosis.

One scenario that causes tremendous

hardship for the patient and the family is the

occurrence of multiple fractures in the first

few years of life in a child without the telltale

sign of OI—a blue color in the “whites” of

their eyes. Often the parents of these children

are accused of child abuse. While it may be

possible to make a diagnosis by analyzing the

child’s tissues, this expensive, difficult-toperform test is not widely available.

Typically, the frequency of fractures

decreases over time and may even stop

entirely at puberty. As an adult, an OI patient

may be left with considerable deformity and

short stature, but he or she can generally

function well with the right environment and

support. When females with OI reach

menopause they sometimes start to fracture

again. Since treatment is now available, it is

important to identify OI patients at all stages

of life, and to alert family members of the

possibility that they may also be affected.

Pediatricians, orthopedists, emergency room

physicians, and others who see children with

fractures need to consider OI as a possible

cause, particularly in cases involving multiple

fractures or a family history of fractures.

These points are covered in detail in a recent

book (Chiasson et al. 2004).
58 Chapter 3

A Report of the Surgeon General
Bone Health and Osteoporosis

Diseases of Bone 59

mors, since they have spread from elsewhere).

Both types of tumors can destroy bone, although

some metastatic tumors can actually increase

bone formation. Primary bone tumors can be

either benign (noncancerous) or malignant (cancerous). The most common benign bone tumor

is osteochondroma, while the most common

malignant ones are osteosarcoma and Ewing’s

sarcoma. Metastatic tumors are often the result

of breast or prostate cancer that has spread to

the bone (Coleman 2001). These may destroy

bone (osteolytic lesion) or cause new bone formation (osteoblastic lesion). Breast cancer metastases are usually osteolytic, while most prostate cancer metastases are osteoblastic, though

they still destroy bone structure (Berruti et al.

2001). Many tumor cells produce parathyroid

hormone related peptide, which increases bone

resorption (Bryden et al. 2002). This process of

tumor-induced bone resorption leads to the release of growth factors stored in bone, which in

turn increases tumor growth still further.

Bone destruction also occurs in the vast majority (over 80 percent) of patients with another

type of cancer, multiple myeloma, which is a

malignancy of the plasma cells that produce antibodies (Berenson 2002). The myeloma cells

secrete cytokines (see Chapter 2), substances that

may stimulate osteoclasts and inhibit osteoblasts

(Roodman 2001, Tian et al. 2003). The bone

destruction can cause severe bone pain, pathologic fractures, spinal cord compression, and lifethreatening increases in blood calcium levels

(Callander and Roodman 2001). A benign form

of overproduction of antibodies, called monoclonal gammopathy, may also be associated with

increased fracture risk (Melton et al. 2004).

Bone-resorbing cytokines are also produced in acute and chronic leukemia, Burkitt’s

lymphoma, and non-Hodgkins’s lymphoma;

patients with these chronic lymphoproliferative disorders often have associated osteoporosis. Both osteoporosis and osteosclerosis (thickening of trabecular bone) have been

reported in association with systemic mastocytosis, a condition of abnormal mast cell proliferation (Schneider and Shane 2001). In addition, there are other infiltrative processes

that affect bone, including infections and marrow fibrosis (myelofibrosis).

Oral Health and Bone Disease

Oral bone, like the rest of the skeleton,

comprises both trabecular and cortical bone

and undergoes formation and resorption

throughout the life span. When oral bone loss

exceeds gain, it can cause a loss of tooth-anchoring support or it can diminish the remaining ridge in those areas where partial or complete tooth loss has occurred.

The prevalence of oral bone loss is significant among adult populations worldwide, and it

increases with age for both sexes. Oral bone loss

and attendant tooth loss are associated with estrogen deficiency and osteoporosis. As a consequence, osteoporosis or osteopenia in postmenopausal women may have an impact on the need

for, and the outcomes from, a variety of periodontal and prosthetic procedures, including

guided tissue regeneration and tooth implantation. Furthermore, it is possible that oral examination and radiographic findings may be useful

signs of extra-oral bone loss (Jeffcoat et al. 2000,

Geurs et al. 2000).
60 Chapter 3

A Report of the Surgeon General

Key Questions for Future

Research

The major diseases of bone have been

broadly characterized, but many questions

remain unanswered, as outlined below:

• Within the spectrum of clinical disorders

that represent “primary osteoporosis,”

are there differences in the mechanisms

that lead to bone loss and bone fragility?

What implications do these differences

have for diagnosis and treatment?

• How do the environmental and genetic

determinants of bone mass and strength

interact in individuals with certain

diseases? For example, are there genetic

differences in the response to estrogen or

calcium deficiency that affect their

relative importance in the pathogenesis

of osteoporosis?

• Are the animal studies on the role of

cytokines relevant to human disease?

• What are the implications of research on the

pathogenetic mechanisms for diseases other

than osteoporosis? For example, further

research on Paget’s disease could uncover

more about the ways in which excessive

osteoclastic bone resorption can occur.

• What is the role of phosphate in bone

mineralization?

• How is bone affected in patients who

have cancer? What implications do

these changes have with respect to both

the spread of the cancer and to other

skeletal disorders?
Bone Health and Osteoporosis

Diseases of Bone 61

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Two

Bone Health and Osteoporosis

 PART TWO: What Is the Status of Bone Health in America? 67

Part Two

WHAT IS THE STATUS OF BONE

HEALTH IN AMERICA?

To provide an answer to this question, this part of the report describes

the magnitude and scope of the problem from two perspectives. The first

is the prevalence of bone disease within the population at large, and the

second is the burden that bone diseases impose on society and those who

suffer from them.

Chapter 4 provides detailed information on the incidence and

prevalence of osteoporosis, fractures, and other bone diseases. Osteoporosis

is by far the most common bone disease, although other related bone

diseases are important as well. Where available, the chapter also provides

data on bone disease in men and minorities. While older White women

are clearly at risk, bone disease can strike anyone, at any age, including

men, premenopausal women, and ethnic minorities. Chapter 4 also offers

some chilling projections for the future prevalence of bone disease, citing

forecasts of significant increases in the prevalence of both osteoporosis

and fractures, and a steep rise in the costs of caring for bone disease.

Chapter 5 examines the costs of bone diseases and their effects on wellbeing and quality of life both from the point of view of the individual

patient and society at large. While bone disease seldom leads directly to

death, it can start a downward spiral in physical and mental health that

has a dramatic impact on an individual’s functional status and quality of

life. All too often this downward spiral concludes with premature death.

To illustrate the burden of bone diseases, the chapter includes real-life

vignettes that describe the terrible impact that osteoporosis, Paget’s disease,

osteogenesis imperfecta, and other related bone diseases can have on those

who suffer from them and their family members.
68 Chapter 4

A Report of the Surgeon General

• The biggest problem created by bone

disease, especially osteoporosis, is

fractures, which may be the first visible

sign of disease in patients. Each year an

estimated 1.5 million individuals suffer

a fracture due to bone disease.

• The risk of a fracture increases with age

and is greatest in women. Roughly 4 in

10 White women age 50 or older in the

United States will experience a hip,

spine, or wrist fracture sometime during

the remainder of their lives. Looking

ahead, the lifetime risk of fractures will

increase for all ethnic groups as people

live longer.

• Osteoporosis is the most common cause

of fractures. Roughly 10 million

individuals over age 50 in the United

States have osteoporosis of the hip. An

additional 33.6 million individuals over

age 50 have low bone mass or

“osteopenia” of the hip and thus are at

risk of osteoporosis and its potential

complications later in life.

• Due primarily to the aging of the

population, the prevalence of

osteoporosis and low bone mass is

expected to increase. By 2020, one in two

Americans over age 50 is expected to have

or be at risk of developing osteoporosis

of the hip; even more will be at risk of

Chapter 4: Key Messages

developing osteoporosis at any site in the

skeleton.

• Osteoporosis does not affect everyone to

the same degree. Women, especially

older women, are more likely to get the

disease than are men. An estimated 35

percent of postmenopausal White

women have osteoporosis of the hip,

spine, or distal forearm. That said, men,

especially elderly men, can and do get

osteoporosis.

• The age-adjusted prevalence of

osteoporosis and the rate of hip fracture

are lower in Black women than in White

women in the United States. The

prevalence of osteoporosis in Hispanic

and Asian women is similar to that found

in White women, and the incidence of

hip fractures among Hispanic women in

California appears to be on the rise.

However, it is important to remember

that osteoporosis is a real risk for any

aging man or woman.

• Much less is known about the frequency

of most other skeletal diseases, due in part

to underdiagnosis and underreporting.

Some data, however, are available. An

estimated one million individuals in the

United States have Paget’s disease, while

roughly 20,000 to 50,000 Americans may

have OI.
Bone Health and Osteoporosis

The Frequency of Bone Disease 69

While they may not get as much attention as

heart disease, cancer, and other major diseases,

bone diseases are common in the United States,

especially among the elderly, and they take a

large toll on the Nation’s overall health status.

Fractures are the biggest problem associated with

bone disease; they are common, costly, and

become a chronic burden on both individuals

and society. Osteoporosis is a leading underlying

cause of fractures, especially among the elderly.

It affects both sexes and all races, although to

varying degrees. The reason for the disease’s

high prevalence is relatively simple—almost

everyone loses bone as they grow older. Other

bone disorders, such as Paget’s disease of bone,

hyperparathyroidism, osteogenesis imperfecta,

rickets, and osteomalacia are much less common.

Like osteoporosis, these diseases also have

adverse effects on bone strength and fracture risk

by affecting bone density, bone turnover, or

bone structure. Although some bone diseases

lead to pain and deformity, most adverse effects

relate to fractures.

This chapter reviews the most recent

evidence related to the occurrence of fractures

and bone diseases in the community. The

following chapter deals with the burden caused

by these fractures and diseases, including the

most common complications that may ensue,

such as physical disability, depression, a reduced

quality of life, and potentially death. The

THE FREQUENCY OF BONE DISEASE

Chapter 4

following chapter also discusses the large costs

associated with fractures and bone disease.

Fractures Caused by Bone

Disease

Fractures are by far the biggest problem

caused by bone disease. They are common and

can be quite debilitating. In many cases they are

the first sign of the disease in patients.

Incidence of Fractures

An estimated 1.5 million individuals suffer a

fracture caused by bone disease annually (Riggs

and Melton 1995, Chrischilles et al. 1991). In fact,

fractures are the most common musculoskeletal

condition requiring hospitalization among

Medicare enrollees (who are age 65 and older).

Approximately one-third (500,000) of fracture

patients are hospitalized (see Table 5-1 in

Chapter 5 for more details), while many more

suffer fractures that do not require or result in

hospitalization.

The risk of fracture increases dramatically

with age in both sexes, both because bones

become more fragile and the risk of falling

increases. Roughly one in four (24 percent)

women age 50 or older fall each year, compared

to nearly half (48 percent) of women age 85 or

older; comparable figures for men are 16 percent

and 35 percent (Winner et al. 1989). These falls

can result in fractures, and when they do the

fracture is almost always caused by low bone
70 Chapter 4

A Report of the Surgeon General

mass or osteoporosis. (See next section for more

on osteoporosis and low bone mass.)

Another way to examine the frequency of

fractures is to consider the chances of

experiencing one or more of them during a

lifetime of average length. What is clear from

this analysis is that a substantial portion of the

population faces a serious risk. As illustrated in

Table 4-1, roughly 4 in 10 White women age 50

or older in the United States will experience a

hip, spine, or wrist fracture sometime during the

remainder of their lives; 13 percent of White men

in this country will suffer a similar fate

(Cummings and Melton 2002). Figures for men

are lower due to their shorter life expectancy and

lower fracture incidence rates. However, these

data do not include other fractures (e.g., of the

upper arm, pelvis, lower leg, ribs); if all fractures

are included, the overall lifetime risk of fracture

is even greater. Hip fractures are the most serious

threat, as 17 percent of White women and 6

percent of White men age 50 and older will suffer

a hip fracture sometime during the remainder

of their life. The lifetime risks of clinically

diagnosed spine fractures in these populations

are 16 percent and 5 percent, respectively, and

16 percent and 2 percent for wrist fractures

(Cummings and Melton 2002). The lifetime risk

for nonwhites is less across all of these fracture

types.

Looking ahead, the lifetime risk of fractures

will increase for all groups as people live longer.

An analysis in Sweden, for example, found that

increasing life expectancy significantly increased

the lifetime risk of hip fracture, from 14 percent

to 23 percent in women and from 5 percent to

11 percent in men (Oden et al. 1998). If incidence

rates were to rise by just 1 percent annually in

Sweden, the lifetime risk of hip fracture could

increase still further, to 35 percent in women and

17 percent in men. Of course, most hip fractures

occur in the elderly and thus affect individuals

only late in life. Other types of fractures are more

likely to strike younger. For example, wrist and

other limb fractures are ten times more common

than are hip fractures among women who have

just gone through menopause (Cooper and

Melton 1992).

Although fractures of the upper arm, pelvis,

and some other sites are more common in the

elderly, the fractures most closely associated

with bone disease are those of the hip (proximal

femur), spine (vertebrae), and wrist (distal

forearm). The annual incidence of hip fractures

increases dramatically with age, from just 2

fractures per 100,000 among White women
Bone Health and Osteoporosis

The Frequency of Bone Disease 71

under age 35 to over 3,000 fractures per 100,000

among White women age 85 and older (Figure 4-

1). Hospital discharge rates for hip fractures per

1,000 Medicare enrollees increased by 9.2 percent

between 1992 and 1999, and then fell by 5.5

percent from 1999 to 2001 (Dartmouth 2004).

Although achieved over a short time interval, this

recent decline in hip fracture incidence is

consistent with falling hip fracture rates that have

been observed among White women in California

(Zingmond et al. 2004). While the reasons for this

decline are not entirely clear, it could potentially

be due to the use of new therapies, e.g.,

pharmaceuticals, as discussed in Chapter 9.

Nevertheless, even with modest reductions in the

incidence rate of fractures (i.e., the number of

fractures per 1,000 Medicare enrollees), the total

number of hip fractures will likely increase

significantly over the next 20–50 years due to the

aging of the population. In other words, a modest

decline in fracture rates per 1,000 Medicare

enrollees will be overwhelmed by the growth in

(and aging of) the overall Medicare population.

The only way to realize meaningful reductions

in the absolute number of hip fractures is to

significantly reduce hip fracture rates, as outlined

in the Healthy People 2010 goals. These goals call

for more than a 50 percent reduction in the hip

fracture rates for females and a 20 percent decrease

for males (see Table 1-1 for more details). Hip

fracture incidence in men is about half that in

women at any given age. Since there are fewer

elderly men than there are women (due to

shorter life expectancy), women account for 80

percent of all hip fractures (Cooper and Melton

2002). The greater risk of hip fractures in elderly

women has been attributed both to their lower

bone density compared to men as well as to their

high risk of falling.

There is no generally accepted definition of

a spine fracture (Genant and Jergas 2003), and

estimates of the overall prevalence of spine

fractures in postmenopausal women vary widely

depending on the definition used (Black et al.

1991). Although experts do not always agree

with the morphometric classification of specific

patients, x-ray readings suggest that an estimated

20–25 percent of postmenopausal White women

have at least one moderately deformed vertebra

(Grados et al. 2004), while about 10 percent have

the more severe spine fractures that are most

likely to produce symptoms (see below). Most

studies also show that the prevalence of spine

fractures is similar in middle-aged women and

men, but some of those in men may not be due

to osteoporosis but rather to job-related injuries

or trauma (O’Neill et al. 1996). It is important

to remember, however, that the incidence of

clinically diagnosed spine fractures (i.e., those

diagnosed by a physician after a patient

complains of symptoms) is much less than the

incidence rates suggested by vertebral

morphometry. In a recent study from Sweden,

only 23 percent of vertebral deformities in

women were diagnosed clinically (Kanis et al.

2004). In other words, there are many “silent”

spine fractures that produce no obvious

symptoms to the patient. These silent fractures

may involve compression (or flattening or

crushing) of the vertebrae, can result in kyphosis

(curvature of the spine) and chronic back pain,

and may be associated with an increase in

morbidity.

Falls account for about one-fourth of the

spine fractures that come to clinical attention

(Cooper et al. 1992a); the majority of clinically

diagnosed spine fractures result from excess

stresses on the spine caused by everyday

activities (Myers and Wilson 1997). The

incidence of clinically recognized spine fractures

increases rapidly with age in both sexes (Figure

4-1). Since rates are higher among women, who
72 Chapter 4

A Report of the Surgeon General

also live longer, three-fourths of all spine

fractures are diagnosed in women (Cooper et al.

1992a).

 Finally, wrist fractures tend to occur

among younger individuals with osteoporosis,

but these patients are at increased risk of a hip

fracture later in life (Klotzbuecher et al. 2000).

The incidence of wrist fracture rises little

with age among men (Figure 4-1), so most

distal forearm fractures are in women.

Variations Across Ethnic Groups and

Geographic Regions

Fracture incidence in the United States is

usually highest for Whites and lower for other

ethnic groups (Melton and Cooper 2001,

Lauderdale et al. 1997). The lower incidence of

fractures among Blacks has generally been

explained by their greater bone mass. But

differences in bone mass fail to explain the lower

hip fracture rates observed in Hispanics and
Bone Health and Osteoporosis

The Frequency of Bone Disease 73
74 Chapter 4

A Report of the Surgeon General

Asians. One hypothesis for these lower fracture

rates is that Asians are less likely to fall (Davis et

al. 1999). Hip fracture hospitalization rates for

male and female non-Hispanic Whites, Blacks,

Hispanics, and Asians over age 50 were tracked

in New York City from 1988 to 2002. Females

were more likely to fracture than males across

all ethnic and racial minorities, and the risk of a

hip fracture in these minority groups was onethird to one-half that of their White counterparts

(Fang et al. 2004). This finding is consistent with

recent data from California, which also shows a

lower risk of fractures in minorities and men (see

Figure 4-2). However, in California, the State

with the largest population of Hispanic residents

in the United States, hip fracture incidence

increased among Hispanic women and men from

1983 to 2000, while it fell among non-Hispanic

White women during the same time period. The

magnitude of the decrease—almost 1 percent per
Bone Health and Osteoporosis

The Frequency of Bone Disease 75

year—is similar to rates observed in White

women in Rochester, MN (Zingmond et al.

2004). As a consequence of these trends,

although the majority of hip fracture patients

continue to be non-Hispanic Whites, ethnic

minorities are an increasing proportion of all

cases encountered in California.

Spine fractures among Asians are about as

frequent as they are in Whites (Ross et al. 1995).

Few data are available for other ethnic groups.

Hospital admissions for spine fractures in the

United States are about four times greater for

elderly Whites than for Blacks (Jacobsen et al.

1992). Hospital admissions, however, may not

be a very accurate marker of spine fractures, as

few patients are actually admitted for spine

fractures. Also, African Americans and other

underserved groups may not have ready access

to hospital care. Likewise, spine fractures are less

frequent among Mexican-Americans as

compared to non-Hispanic White women (Bauer

and Deyo 1987). Forearm fractures are also less

common in Black and Asian populations (Chung

and Spilson 2001). Lower rates for Blacks than

Whites have also been reported for most other

types of fractures. Finally, although limited data

are available on the prevalence of osteoporosis

in the American Indian and Alaska Native

(AIAN) population, one study suggests that

fracture risk in AIAN women is similar to that

in White women (Siris et al. 2001).

Fracture rates tend to vary across countries

and regions within countries (Cummings and

Melton 2002). For example, wrist and hip

fracture rates in the United Kingdom are around

30 percent lower than in the United States.

However, hip fracture rates vary more than

sevenfold from one country to another within

Europe (Melton and Cooper 2001), and similar

variation has been observed for spine fractures

(O’Neill et al. 1996). Differences in the

frequency of falls in different parts of Europe

may explain in part the difference in limb

fractures (Roy et al. 2002). Likewise, hip fracture

incidence differs among various Asian countries

(Lauderdale et al. 1997). Marked variation in

fracture incidence is seen even within specific

countries. As shown in Figure 4-3, hip fractures

in the United States are most prevalent in the

South (where hip bone density is lowest [Looker

et al. 1998]), with two areas of Texas having the

highest rates of fracture (Dartmouth 2004).

However, the incidence of arm fractures is

higher in the East and lower in the West (Karagas

et al. 1996).

Osteoporosis

Osteoporosis and osteopenia (see box) are by

far the most common causes of the fractures

discussed in the previous section (although other

bone diseases can cause fractures as well). In fact,

decreased bone density is an important risk factor

for fractures both in postmenopausal women

(Stone et al. 2003) and older men (Nguyen et al.

1996). A panel of experts judged that skeletal

fragility might be responsible for 80–95 percent

of hip and spine fractures in White women,

depending on age, along with 70–80 percent of

distal forearm fractures and 45–60 percent of

fractures at other skeletal sites (Melton et al.

1997). The comparable figures were less for

women of other races and for men. While the

risk of fracture is highest in those who have

osteoporosis, many more individuals with

osteopenia (low bone mass) are at increased risk

as well. In fact, an analysis of peripheral bone

mineral density (BMD) and fractures in over

200,000 women (The National Osteoporosis

Risk Assessment, or NORA, study) suggests that

at least half of all fragility fractures occur in this

low bone mass group (Siris et al. 2001).
76 Chapter 4

A Report of the Surgeon General

Prevalence

As noted in the previous chapter, the World

Health Organization has defined osteoporosis, for

practical purposes, as a bone mineral

density(BMD) value more than 2.5 standard

deviations below the mean for normal young White

women. Based on this definition, it has been

estimated that roughly 10 million individuals over

age 50 in the United States have osteoporosis of

the hip, as shown in Figure 4-4 (NOF 2002, Looker

1997, Looker 1998). (The precise number suffering

from the disease is difficult to determine, since bone

loss varies in the different parts of the skeleton

where bone mass is measured and definitions of

osteoporosis have not been developed for all

subpopulations.) An additional 33.6 million

individuals over age 50 have low bone mass or

“osteopenia” of the hip and they are at risk of

osteoporosis and its potential complications later

in life (NOF 2002, Looker 1997, Looker 1998).
Bone Health and Osteoporosis

The Frequency of Bone Disease 77

What Is Osteopenia?

The term “osteopenia” is used to define

individuals who have low bone mass and

some increased risk of fracture. Their bone

mass is not so low that they are deemed to

have osteoporosis. This classification is

similar to that used for people with high levels

of LDL (or so-called “bad”) cholesterol,

where individuals with values over 160 mg/

dl are deemed “high risk” and those between

130 and 160 mg/dl are deemed “moderate

risk.” The range defining osteopenia or low

bone mass is quite large, ranging from -1 to -

2.5 T-scores (that is, bone density levels that

are 1 to 2.5 standard deviations below the

average for young adults who have achieved

normal peak bone mass), which translates

into bone mass that is 10–30 percent below

this average level. Thus, osteopenia is not a

disease but rather a way of describing the

results of a measurement. Obviously, given

the wide range in this measurement, not

everyone with osteopenia is at the same risk

of fracture. Since individuals who are told

they have osteopenia may become

excessively concerned, providers should be

sure to frame the bone health issue in terms

of fracture risk. As emphasized elsewhere in

this report (see Chapter 8), BMD T-scores

are only one component of that risk, and

fracture risk may actually be quite low for

many people with osteopenia, particularly

younger individuals. To avoid causing

unnecessary alarm among patients, many

health care professionals prefer to avoid the

term “osteopenia,” instead telling patients

that they have “somewhat low bone mass”

and then explaining what that means in terms

of fracture risk and how the problem can best

be dealt with to minimize that risk.

Due primarily to the aging of the population,

the prevalence of osteoporosis and low bone mass

is expected to increase to 12 million cases of

osteoporosis and 40 million cases of low bone

mass among individuals over the age of 50 by

2010, and to nearly 14 million cases of

osteoporosis and over 47 million cases of low

bone mass in individuals over that age by 2020

(NOF 2002). In other words, by 2020 one in two

Americans over age 50 is expected to have or to

be at risk of developing osteoporosis of the hip;

even more will be at risk of developing

osteoporosis at any site in the skeleton.

One problem in estimating the frequency of

osteoporosis is that many individuals may have

the disease but not know it. The National Health

and Nutrition Examination Survey (NHANES)

revealed that only 1 percent of men and 11

percent of women age 65 and older reported that

they had osteoporosis; testing at the hip showed

that four times as many men (4 percent) and 2.5

times as many women (26 percent) actually had

the disease (Table 4-2). In fact, more men (2

percent) reported a history of hip fracture than

reported a prior diagnosis of osteoporosis (1

percent); for women the figures were reversed,

6.1 percent and 11.1 percent, respectively. These

data for both men and women reveal not only

the underdiagnosis of osteoporosis but also the

failure to recognize that most hip fractures are

due, at least in part, to osteoporosis. The

likelihood of experiencing most other bone

diseases is lower. In fact, only about 1 percent

of the population age 45 and older has evidence

of Paget’s disease of bone and probably less than

1 percent has hyperparathyroidism (see below).

Variations Across Gender, Race, and Ethnicity

 Osteoporosis does not affect everyone to the

same degree. Women, especially older women,

are much more likely to get the disease than are
78 Chapter 4

A Report of the Surgeon General

men. In fact, women over age 50 accounted for

over 75 percent (7.8 million) of the total cases of

osteoporosis at the hip in 2002 (NOF 2002).

Women are more susceptible than men to

osteoporosis because they begin with less bone

mass and lose it at a somewhat faster rate. As

shown in Figure 4-5 (Looker et al. 1998), White

women lose one-third of their hip BMD between

the ages of 20 and 80, while White men lose only

a quarter during this time. These data on hip

BMD are from NHANES III, where a large

representative sample of the U.S. population was

assessed at a single point in time (cross-sectional

data). Bone loss in other parts of the body,

however, does not necessarily follow the same

pattern. For example, while bone loss from the

hip is approximately linear across adult life, bone

loss in other parts of the skeleton begins around

the time of menopause in women and at a

comparable age or later in men (Melton et al. 2000).

Using the World Health Organization’s

definition, an estimated 35 percent of

postmenopausal White women have

osteoporosis of the hip, spine, or distal forearm

(Melton et al. 1998) and are at increased risk of

future fractures. Since bone mass decreases

slowly over time, it is no surprise that the

prevalence of osteoporosis (the proportion of the

population within a certain age range affected at

any given time) increases with age. NHANES

data show that the prevalence of osteoporosis at

the hip increases over tenfold among

postmenopausal White women, from 4 percent

in those between the ages of 50 and 59 to 52
Bone Health and Osteoporosis

The Frequency of Bone Disease 79
80 Chapter 4

A Report of the Surgeon General

percent among those age 80 and older (Looker et

al 1997). The overall prevalence of osteoporosis

of the hip among postmenopausal White women

is 17 percent in NHANES, compared to 21

percent in Sweden (Kanis et al. 2000) and only 8

percent in Canada (Tenenhouse et al. 2000).

These variations may explain the differences in

hip fractures among women in these various

countries, with Swedish women being the most

likely to suffer fractures and Canadian women

the least (Melton and Cooper 2001).

While NHANES did not assess bone

density at the spine or wrist (and consequently

more such data are needed), other studies suggest

that the prevalence of osteoporosis at these sites

follows a somewhat similar pattern. For example,

the prevalence of osteoporosis at the wrist

increases thirteenfold, from 6 percent among

women age 50–59 to 78 percent among those age

80 and older, yielding an overall prevalence of

osteoporosis of the wrist among postmenopausal

White women of 33 percent (Melton et al. 2000).

Due to increasing difficulty in accurately

assessing bone loss from the spine as individuals

age (because of artifacts that mask bone loss; see

Chapter 8 for more details), the diagnosed

prevalence of osteoporosis in White women age

80 and older is only twice that among those

between the ages of 50 and 59 (Melton et al.

2000). Thus, just 8 percent of postmenopausal

women appear to have osteoporosis of the spine.

The comparable figure in Canadian women is

12 percent (Tenenhouse et al. 2000).

There is some lack of agreement about how

osteoporosis should be defined in men and nonWhites. Since aging men of all races also lose

bone from the hip (Figure 4-1), one would expect

the prevalence of osteoporosis to increase with

age in men as it does in women. However, due

to the limited data available at the time, the

World Health Organization did not propose a

specific definition of osteoporosis for men. Based

on the same absolute cut-off value for men as

for women (0.56 g/cm2 for femoral neck BMD),

the prevalence of osteoporosis among White,

Mexican-American, and Black men age 50 and

older is 4 percent, 2 percent, and 3 percent,

respectively, according to NHANES III (Looker

et al. 1997). When the normal values for a young

adult male are used as the cut-off point, the

estimated prevalence of osteoporosis in these

men increases substantially to 7 percent, 3

percent, and 5 percent, respectively. The

comparable figure for Canadian men is about 4

percent (Tenenhouse et al. 2000). The fact that

many fewer men than women develop very low

levels of bone density, where fracture risk is

greatest, helps explain the lower incidence of hip

fractures in men.

With respect to non-White women,

comparisons of BMD to normal values for nonHispanic White women suggest that the ageadjusted prevalence of osteoporosis at the hip

among Black women in the United States is 6

percent, compared to 17 percent for

postmenopausal White women. This is

consistent with the much lower fracture rates

observed in Blacks (Melton and Cooper 2001).

Mexican-American women in the United States

have an estimated prevalence of hip osteoporosis

of 14 percent (Looker et al. 1997), which is

consistent with the somewhat lower risk of hip

fractures in most populations of Spanish

heritage compared to those of Northern

European extraction. It has generally been

presumed that Asians have a prevalence of

osteoporosis similar to that in Whites. Japanese

data indicate that the prevalence of osteoporosis

at the lumbar spine is as high or higher than in

White women while the prevalence of

osteoporosis at the hip (12 percent) is lower (Iki

et al. 2001). This goes along with the fact that
Bone Health and Osteoporosis

The Frequency of Bone Disease 81

spine fractures are almost as common among

Asian women as they are in White women,

while hip fractures are considerably less

common (Melton and Cooper 2001).

Other Metabolic Bone Diseases

Much less is known about the frequency of

most other skeletal diseases. This is because

many of them, such as Paget’s disease of bone

and primary hyperparathyroidism, appear to be

underdiagnosed. Others, such as osteomalacia

and renal osteodystrophy, may in some cases be

complications of some other condition and thus

they are not counted separately. For example,

the U.S. Renal Data System reports that almost

325,000 Americans are being treated for chronic

renal failure by dialysis or renal transplantation

(USRDS 2000). Over a third of those are Black,

and their dialysis rate is five times greater than

that of Whites. Although fracture rates are

increased in these individuals (Alem et al. 2000),

there appear to be no estimates of the actual

prevalence of renal bone disease (see Chapter 3).

By contrast, Black Americans are at a lower risk

of primary hyperparathyroidism than are White

Americans (Melton 2002). The condition is more

common in women than men, and its prevalence

increases with age in both sexes. Although there

are indications that up to 1 percent of the

population may be affected at any given time

(Melton 2002), the annual incidence of diagnosed

primary hyperparathyroidism has been

estimated at only 21 per 100,000 (Wermers et al.

1997). However, the frequency of diagnosis of

primary hyperparathyroidism is affected by how

often blood calcium levels are measured and

acted upon in clinical practice.

Paget’s Disease of Bone

Based on an x-ray survey of the hip, pelvis,

and spine by the first National Health and

Nutritional Examination Survey, the prevalence

of Paget’s disease of bone has been estimated at

1.3 per 100 women and men age 45–74 (Siris

1999). This would represent over one million

affected individuals in this country today.

However, just as for spine fractures, many

Pagetic bone lesions are asymptomatic and

consequently undetected by health care

professionals, meaning that the prevalence of

clinically diagnosed cases of Paget’s disease is

much less. The incidence of the disease rises with

age but is generally less than one per 1,000 per

year, even among elderly individuals. The

incidence is about twice as great in men as it is

in women, and most patients are of Northern

European heritage. Indeed, Paget’s disease is

most common in North America and Western

Europe, except Scandinavia (Siris 1999). There

is some evidence that the incidence of Paget’s

disease may be falling, but this may be the result

of a decrease in the frequency of routine

screening procedures (Tiegs et al. 2000).

Developmental Skeletal Disorders

There are many congenital disorders of the

skeleton, but most are quite rare. Two of the

more common conditions are osteopetrosis and

the various forms of osteogenesis imperfecta (see

Chapter 3). Altogether, 20,000 to 50,000

Americans may have osteogenesis imperfecta

according to the Osteogenesis Imperfecta

Foundation. The Paget’s Foundation estimates

that about 14,000 people in the United States

(equivalent to one out of every 20,000

individuals) have osteopetrosis.

Acquired Skeletal Disorders

There are no estimates of the incidence of

aseptic necrosis, despite its being a not

uncommon complication of hip fracture and

glucocorticoid therapy (see Chapter 3). Primary

bone neoplasms, such as osteosarcoma, are less
82 Chapter 4

A Report of the Surgeon General

common. The most frequent malignancy arising

in bone is multiple myeloma, which was

described in Chapter 3. This malignancy affects

men more than women and Blacks more than

Whites. Altogether, there are about 2,400 new

cases and 1,300 deaths each year in this country

from cancer of the bones and joints, compared

to 14,600 new cases and 10,900 deaths annually

from multiple myeloma (ACS 2001). Of the

more than 560,000 people who die of cancer each

year, most will have had skeletal complications

of their malignancy (bone metastases) at some

point during their illness. Bone metastases most

commonly occur in individuals with breast,

prostate, kidney, lung, pancreatic, colorectal,

stomach, thyroid, and ovarian cancers. People

dying of breast and prostate cancer almost always

experience bone metastases, causing a great deal

of the pain in the last days of life. Bone metastases

most commonly occur in the spine; other

common sites include the pelvis, hip, upper leg

bones, and the skull (ACS 2004).

Prospects for the Future

The prevalence of bone diseases is going to

increase significantly as the population ages. In

the United States, the number of people age 65

and older is expected to rise from 35 to 86 million

between 2000 and 2050, while the number age

85 and older will increase from 4 to 20 million

(US Census Bureau 2004). Much of this increase

will occur in the next 25 years as the “baby

boomers” reach their 70s and 80s. Unless

prevention activities are greatly enhanced, this

demographic change alone will cause a

substantial increase in the number of people with

bone diseases. For example, based on data from

NHANES, it is estimated that 7.8 million

women and 2.3 million men in the United States

already have osteoporosis at the hip. These

figures could rise to 10.5 million women and 3.3

million men (an increase of 35 percent in women

and 43 percent in men, respectively) by 2020

(Figure 4-4) (NOF 2002). These trends make

reaching the Healthy People 2010 goal (which

is to reduce the overall prevalence of osteoporosis

at the hip among adults from 10 percent to 8

percent) all the more difficult (USDHHS 2000).

In fact, these demographic changes could cause

the number of hip fractures in the United States to

double or triple by 2040 (Schneider and Guralnik

1990). Any such increase will also make it very

difficult to achieve another Healthy People 2010

goal of reducing the annual incidence of hip fractures

by 60 percent (from 1,056 to 416 per 100,000) among

women age 65 or older, and by 20 percent (from

593 to 474 per 100,000) among elderly men

(USDHHS 2000). History does not offer much

optimism that these goals will be reached, either. In

fact, Healthy People 2000 called for a nearly 15

percent reduction in the overall incidence of hip

fractures among men and women age 65 and older

(from 714 per 100,000 in 1988 to 607 per 100,000

by 2000) (USDHHS 1991). The annual incidence

among this population actually increased by over

17 percent, to 840 per 100,000, in 2000.

The aging phenomenon and its potential

impact on bone disease are not unique to the United

States. Across the globe, the number of individuals

age 65 and older is expected to increase nearly

fivefold between 1990 and 2050, from 323 million

to 1.55 billion. This trend alone could result in a

3.7-fold increase in the number of hip fractures

worldwide, from an estimated 1.7 million in 1990

to a projected 6.3 million in 2050 (Cooper et al.

1992b). Even this figure may prove conservative,

as it assumes that the incidence of hip fractures

among individuals of a given age remains constant.

If, instead, incidence rates remain constant in

Europe and North America (they have stabilized

in these areas recently) but increase by 3 percent

annually elsewhere (as is occurring in some parts
Bone Health and Osteoporosis

The Frequency of Bone Disease 83

of the world), the total worldwide number of hip

fractures each year could exceed 21 million by

2050 (Gullberg et al. 1997).

Key Questions for Future

Research

Research questions for Chapter 4 have been

merged with those for Chapter 5 because of the

close relationship between frequency and burden

of disease issues. (See Chapter 5, page 103.)
84 Chapter 4

A Report of the Surgeon General

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88 Chapter 5

A Report of the Surgeon General

• Bone diseases have a major impact on the

population as a whole and especially on

affected individuals and their families.

Although some bone diseases lead

directly to pain and deformity, bone

disease often is a “silent” disorder until

it causes fractures.

• The 1.5 million osteoporotic fractures

in the United States each year lead to

more than half a million hospitalizations,

over 800,000 emergency room

encounters, more than 2,600,000

physician office visits, and the

placement of nearly 180,000 individuals

into nursing homes. Hip fractures are

by far the most devastating type of

fracture, accounting for about 300,000

hospitalizations each year.

• Caring for these fractures is expensive.

Studies show that annual direct care

expenditures for osteoporotic fractures

range from $12 to $18 billion per year in

2002 dollars. Indirect costs (e.g., lost

productivity for patients and caregivers)

likely add billions of dollars to this figure.

These costs could double or triple in the

coming decades.

• From an individual’s perspective, bone

disease has a devastating impact on

patients and their families. While few die

directly from bone disease, for many

individuals a fracture can lead to a

Chapter 5: Key Messages

downward spiral in physical and mental

health that for some ultimately results in

death. In fact, hip fractures are associated

with a significantly increased risk of

death, especially during the first year

after the fracture.

• Bone diseases dramatically affect

functional status. Many individuals who

suffer fractures experience significant

pain and height loss, and may lose the

ability to dress themselves, stand up, and

walk. These individuals are also at risk

of complications such as pressure sores,

pneumonia, and urinary tract infections.

Nearly one in five hip fracture patients

ends up in a nursing home, a situation

that a majority of participants in one

study compared unfavorably to death.

• Fractures can also have a negative impact

on self-esteem, body image, and mood,

which may lead to psychological

consequences. Individuals who suffer

fractures may be immobilized by a fear

of falling and suffering additional

fractures. Not surprisingly, they may

begin to feel isolated and helpless.

• Many bone disorders other than

osteoporosis add greatly to the burden

of bone disease in the population,

although the impact varies enormously

and is largely dependent upon the

severity of the disease.
Bone Health and Osteoporosis

The Burden of Bone Disease 89

Bone diseases have a major impact on the

population as a whole and especially on affected

individuals and their families. Osteoporosis, in

particular, is an important public health problem

that affects a large segment of the community.

Although some bone diseases lead directly to

pain and deformity, bone disease more

commonly is a “silent” disorder until it causes

one or more fractures. The many individuals

with bone disease who suffer fractures must deal

with the complications that may ensue, including

ill health (morbidity), disability, a reduced

quality of life, and possibly even death. The care

of patients with these fractures is also very

expensive, and costs will continue to rise as the

frequency of bone disease increases in the future

with the anticipated growth of the elderly

population. These aspects of the problem are

reviewed in the sections that follow, focusing

first on the effects of bone disease on society as a

whole and then on the problems that bone

diseases pose for individuals. What these

statistics make clear is that the burden of bone

disease is enormous.

Most of the statistics that follow relate to

osteoporosis, the most common and perhaps

most “burdensome” bone disease from society’s

perspective. While the burden of osteoporosis

has been well documented, there is relatively

little information on the burden imposed by

other disorders that affect bone health, even

though they can cause marked impairment of

THE BURDEN OF BONE DISEASE

Chapter 5

health and even death in those who are affected.

Recognizing the limits on available information,

this chapter nonetheless provides some general

descriptions on the burden of these other bone

diseases on page 102.

 Impact on Society

Mortality

Despite the large numbers affected, very few

people die as a direct result of bone disease,

although bone disease may be under-appreciated

as an indirect cause of death. Bone diseases

accounted directly for only a tiny fraction of the

2.4 million deaths reported nationally in 1999

(NCHS 1999). Other diseases, such as heart

disease and cancer, are much more likely to

directly cause an individual’s death. Even hip

fractures, which represent one of the most

serious consequences of bone disease, seldom

directly result in death. In fact, in 1999 hip

fractures were listed as the cause of death on only

12,661 death certificates (NCHS 1999),

representing less than 4 percent of the number

of patients who were hospitalized for hip

fractures in that year (Popovic 2001). Bone

disease can indirectly lead to death, as fractures

and their associated complications can in some

cases trigger a downward spiral in health. In one

population sample, the risk of mortality was four

times greater among hip fracture patients during

the first 3 months after the fracture than was the

comparable risk among fracture-free individuals
90 Chapter 5

A Report of the Surgeon General

The Real-Life Burden of Osteoporosis

Osteoporosis has a significant impact on

the everyday lives of those who suffer from

the disease, as the following story clearly

illustrates.

This 73-year-old wife and grandmother

suffered her first fracture 18 years ago and

has had eight additional fractures since that

time. Each caused tremendous pain and

required long hospital stays and extended

periods on medication. Unfortunately,

however, because she does not tolerate

osteoporosis medications well, her primary

treatment has consisted of estrogen, vitamin

D, and calcium supplements. As bad as the

actual fractures have been, it is the fear of

additional fractures that may well have the

largest impact on her life. As a result of this

fear, she limits the time she spends with her

grandchildren, as well as the types of activities

she enjoys with them (three of her fractures

occurred while playing with her

grandchildren). She finds it impossible to lie

down on her back or right side and difficult

to get in and out of bed or a chair. She has

had to give up dancing, one of her favorite

activities, and feels she has become a “drag”

on family members who must slow down to

accommodate her limitations.

A Parent’s Perspective on the Burden of

Bone Disease

This story illustrates the devastating

impact that bone disease can have in those rare

instances when it strikes children.

This mother has two children with bone

disease. Her daughter, now in her mid-20s,

suffers from osteoporosis. Yet it is her son’s

battle with severe OI that is most tragic. Now

in his late 20s, he suffered nearly a dozen bone

fractures at birth. When he was two months old,

the mother endured the horrible sound of

hearing her son’s arm break as she turned him

over in his crib. To date, he has suffered 140

fractures, some caused by acts as simple as

sneezing or being startled. Fractures, however,

are not the only health problems he faces. Like

many OI sufferers, he also must live with

scoliosis, broken teeth, hernias, kidney stones,

and hearing loss. He presently requires full-time

oxygen. Only 3 feet tall, he has never slept

through the night.

Like many OI patients, he is highly

intelligent and engaging, a true joy to be

around. He spoke in complete sentences by the

age of 1 and was reading at the age of 2. He

showed an interest in politics by age 5,

querying his mother on whom she was going

to vote for in the presidential election and why.

His tremendous intellectual abilities and

engaging personality are as much or more a

part of him as are his disabilities. His

personality and story make him an excellent

spokesperson for the disease.

“I had planned to spend these

years enjoying my

grandchildren, but I’ve really

had to curtail my activities

with them. I’ve fractured my

back three times while playing

with them.”

—Long-time osteoporosis

sufferer
Bone Health and Osteoporosis

The Burden of Bone Disease 91

of similar gender and age. Approximately 20

percent of the hip fracture patients died within

a year of the fracture (Leibson et al. 2002).

These overall rates may overstate the increased

risk of death that is attributable to the fracture,

as some of these patients were already in a

nursing home and may have died even in the

absence of the fracture. Another study, which

included only patients who were ambulatory

and not living in nursing homes at the time of

their hip fracture, found that hip fracture

patients had a 2.8-fold increased risk of dying

during the 3 months following the fracture,

although this risk also depended on their prefracture health. Those with poor pre-fracture

health had higher mortality rates (Richmond

et al. 2003). A recent analysis of NHANES I

found that, over a follow-up period of 8–22

years, each standard deviation decrease in

bone density was associated with a 10–40

percent increase in mortality (Mussolino et

al. 2003). A prospective study of women over

65 (which was part of the Study of

Osteoporotic Fractures) showed that each

standard deviation of bone loss at the hip was

associated with a 30 percent increase in total

mortality (Kado et al. 2000). Recent studies

from Sweden have shown increased mortality

after spine fractures as well as hip fractures

(Kanis et al. 2004, Johnell et al. 2004).

Morbidity

Bone diseases are much more likely to lead

to poor health (i.e., morbidity) than they are to

cause death. Most bone diseases disproportionately affect the elderly, who may already

have substantial problems with frailty and

reduced functional capacity. Fractures are the

biggest problem facing most individuals with

bone disease, especially those with osteoporosis.

The cumulative impact of these fractures is quite

devastating. As shown in Table 5-1, osteoporotic

fractures in the United States in 1995 led to more

than half a million hospitalizations, over 800,000

emergency room encounters, more than 2.6

million physician office visits, and the placement

of nearly 180,000 individuals into nursing homes.

Based on a statistical model, it has been estimated

that over a 10-year period White women age 45

and older in the United States could experience

5.2 million fractures of the hip, spine, or forearm,

resulting in 2 million person-years of disability

related to the fractures (Chrischilles et al. 1994).

Unfortunately, comparable estimates are not

available for other diseases of the skeleton.

Hip fractures are by far the most devastating

type of fracture, accounting for about 300,000

hospitalizations each year. Almost all hip fracture

patients are hospitalized, and they represent

nearly half of all hospitalizations for osteoporotic

fractures in the United States (Table5-1). Hip

fractures frequently lead to disability. More than

one in four (26 percent) individuals suffering a

hip fracture becomes disabled in the following

year because of the fracture (i.e., this figure

represents disabilities that are in addition to those

resulting from the functional losses that would

ordinarily occur in frail older persons)

(Magaziner et al. 2003). Due primarily to

dementia and the inability to walk

independently, nearly one out of five requires

long-term nursing home care (Table 5-2). In

aggregate, hip fractures were responsible for

nearly 140,000 nursing home admissions in 1995

(Ray et al. 1997). Spine fractures are less

devastating, with only 1 in 10 patients requiring

hospitalization and less than 2 percent requiring

nursing home care (Chrischilles et al. 1991).

They account for nearly 66,000 physician office

visits and at least 45,000—and perhaps as many

as 70,000—hospital admissions each year (Table

5-1). Half of these patients require some

continuing care in a skilled nursing facility
92 Chapter 5

A Report of the Surgeon General
Bone Health and Osteoporosis

The Burden of Bone Disease 93

 Direct Costs

Studies show that annual direct care

expenditures for osteoporotic fractures range

from $12.2–$17.9 billion per year in 2002

dollars (Tosteson 1999). While women account

for the majority of these costs, White men also

incur substantial overall costs for osteoporotic

fracture care (representing 18 percent of the

total costs of osteoporosis, or $3.2 billion). In

addition, non-White women and men of all ages

account for $1 billion annually in total direct

care expenditures on osteoporotic fractures

(Ray et al. 1997).

Although large, expenditures related to

osteoporosis represent just 7 percent of total

heath care costs among women age 45 and older

(Hoerger et al. 1999). This is more than double

the amount spent for gynecological cancers but

only a fraction of the cost of cardiovascular

disease. However, osteoporosis accounts for

nearly 14 percent of all nursing home days, due

to the late age at which expenses are incurred

for osteoporosis relative to other diseases

(Hoerger et al. 1999).

(Gehlbach et al. 2003). Fractures of the wrist

(also known as the distal forearm) are the least

debilitating. Only about one-fifth of patients

suffering a wrist fracture are hospitalized, and

they rarely require nursing home care (Tables

5-1, 5-2). Yet even this relatively less traumatic

event still accounts for nearly 20,000 hospital

admissions and over 530,000 physician visits

each year (Table 5-1). Surprisingly, these

fractures consume more outpatient physical

therapy services than do hip fractures.

Cost

Bone diseases are expensive, in terms of

direct health care expenditures and indirect

expenditures as well as lost productivity/

workdays for patients and caregivers. While the

figures cited below are large, it is important to

remember that they represent today’s costs.

Given health care inflation and the projections

for significant increases in the number of

fractures (see Chapter 4), it is not unreasonable

to assume that the direct and indirect costs of

bone disease will more than double or triple in

the coming decades (Burge et al. 2003).
94 Chapter 5

A Report of the Surgeon General

Hospital care accounts for more than half of

the total direct costs, with nursing home care

also responsible for a large portion of the total.

As noted, hip fractures are the most devastating

complication of osteoporosis, and therefore it is

no surprise that they account for the largest

proportion (63 percent or $11.3 billion) of

medical care costs (Table 5-3). This is because

hip fractures are very expensive to treat, with

per-fracture costs estimated to range from

$30,100–$43,400 in 2002 dollars (Tosteson 1999).

The costs of caring for hip fractures are not

limited to this initial treatment, however, as those

suffering hip fractures require follow-up care as

a direct result of their injury. A recent study

estimated that hospital and outpatient care

(excluding nursing home care) due to a hip

fracture adds $14,600 to direct medical

expenditures in the year following the fracture

(Gabriel et al. 2002). The overall lifetime cost

attributable to a hip fracture could exceed

$81,000 (Braithwaite et al. 2003).

Although hip fractures account for the

majority of costs, more than $6.5 billion is spent

annually to treat those suffering from other types

of osteoporotic fractures (Ray et al. 1997).

The direct costs of osteoporotic fractures are

typically borne by society, primarily through

Medicare and Medicaid. Among women over

age 45, the government pays for most of the

costs of osteoporotic fractures: Medicaid covers

almost a fourth of the expense and Medicare

pays nearly half (Hoerger et al. 1999). This is

to be expected since nearly three-quarters of
Bone Health and Osteoporosis

The Burden of Bone Disease 95

all hip, spine, and distal forearm fractures

occur among patients 65 years and over.

 Indirect Costs

In addition to imposing direct medical costs

on society, osteoporosis also results in indirect

costs, primarily related to reduced productivity

due to disability and premature death. Indirect

costs are inherently difficult to measure, and much

more needs to be done in this area. One method

judges lost productivity on the basis of reduced

earnings. For bone diseases, which affect a large

number of retired persons, indirect costs are

underestimated by this approach. Nonetheless,

assuming that people are worth what they earn,

one study estimates that the cost of premature

death and of restricted activity resulting from

fractures accounts for 26 percent of total fracture

costs and 12 percent of hip fracture costs (Praemer

et al. 1999). A recent study from California (where

12 percent of the US population resides) found

that the indirect cost to society (based only on

lost earnings from premature deaths) accounted

for 17 percent of the total cost related to

osteoporosis (Max et al. 2002).

Impact on the Individual

While the statistics cited in the previous

section relate to the impact of bone disease on

society, it is important to remember that these

“global” statistics really take on meaning when

examining what they mean for individuals. In

fact, osteoporosis and other bone diseases have

a profound impact on those individuals who

suffer from them and on their families. This

section examines that impact, highlighting the

very real burden that bone disease can place on

the physical health, mental well-being, and

financial stability of those individuals and

family members affected by the disease.

The Chance of Dying From Bone Disease

While the chance of dying varies by fracture

type, the vast majority of individuals suffering

from osteoporosis and osteoporotic-related

fractures do not die directly as a result of their

disease. As noted previously, hip fractures are

among the most devastating type of fracture; it

has been estimated that approximately 20

percent of all patients die within a year (Leibson

et al. 2002). The oldest hip fracture patients are

most likely to die, and survival rates are lower

for men (both White and Black) than for women,

although Black women are more likely to die

from a hip fracture than are White women. These

differences may be due in part to the older age at

which men and Black women are likely to suffer a

hip fracture as well as to differences intheir medical

care (Figure 5-1). It is important to note, however,

that the typical hip fracture patient is about 80 years

old, and thus their risk of death from any cause is

not trivial. Thus, it is more accurate to say that a

hip fracture decreases the chance of survival in the

first year by about 12–20 percent in this already

at-risk population. Another way to look at this

statistic is that 9 out of every 100 women with a

hip fracture will die as a result of the fracture

(Magaziner et al. 1997). The increased risk of death

is especially high (10 times more than the expected

death rate) in the first few weeks following a hip

fracture. While the excess risk of death due to hip

fractures diminishes with time, there may still be

some additional risk for a number of years. For

example, roughly 5 percent of hip fracture patients

experience a severe medical complication, causing

an increase in their risk of death (Lawrence et al.

2002). In addition, as noted previously, most hip

fracture patients have other serious medical

problems (comorbidities that more directly

contribute to death) (Browner et al. 1996). Even

so, with any given amount of preexisting

comorbidity, the occurrence of a hip fracture

substantially increases the likelihood of dying

(Poór et al. 1995).
96 Chapter 5

A Report of the Surgeon General

Other types of fractures are less likely to result

in death. For example, patients suffering a wrist

fracture are no more likely to die than anyone else

(Melton 2003). Other limb fractures have been

linked to an increased risk of death (Browner et

al. 1996), although only a few of these deaths are

related directly to the fracture. Most of the deaths

seem to result from the presence of some other

serious disease. For example, the death rate

following a fracture of the spine is 1.2 to 1.9 times

greater than expected (Melton 2003), but most of

the deaths occur long after the fracture and

appear to be due to serious underlying medical

conditions that not only increase the risk of dying

but also are likely the cause of the bone loss and

associated fractures.

As noted in Chapter 3, inherited bone

diseases have been found to increase the risk of

death; in fact, in some cases these diseases are so

severe that they are incompatible with life.

Likewise, survival is much reduced among

patients with bone cancer and multiple myeloma

(Praemer et al. 1999). It is unclear whether or

not patients with primary hyperparathyroidism

face an increased risk of death, although survival

does appear to be worse for the most severely

affected patients, including those with the

highest blood calcium levels and those with other

serious diseases (Vestergaard et al. 2003).

Impact on Morbidity, Levels of Disability, and

Functional Status

Bone diseases dramatically affect the

functional status of those who get them. Many

individuals who suffer fractures as a result of

osteoporosis suffer significant pain, height loss,

and may lose the ability to dress themselves,

stand up, and walk. These patients are also at

risk of acute complications such as pressure sores,
Bone Health and Osteoporosis

The Burden of Bone Disease 97

pneumonia, and urinary tract infections. Nearly

one in five ends up in a nursing home, a situation

that a majority of participants in one study

compared unfavorably to death (Salkeld et al.

2000). As illustrated in Figure 5-2, different types

of osteoporotic fractures have a different impact

on the patients who suffer them. Wrist fractures

commonly occur in women in their mid-50s and

usually have only a short-term impact, whereas

spine fractures typically occur at a later age and

may give rise to permanent morbidity. By

contrast, hip fractures occur later in life (around

age 80 on average) and usually result in

permanent disability (Kanis and Johnell 1999).

Each of these fracture types will be discussed

in more detail below.

Two-thirds of hip fracture patients do not

return to the level of function they enjoyed

before the fracture (OTA 1994), particularly

those who become depressed (Magaziner et al.

2003). Many lose their ability to walk. In fact,

only 40–79 percent of patients regain their

previous ambulatory function a year after the

fracture, and less than half return to their

prefracture status with respect to the activities

of daily living (Greendale and Barrett-Connor

2001). For example, data from the Established

Populations for Epidemiologic Studies of the

Elderly (EPESE) project show that 86 percent

of patients could dress by themselves before the

fracture, but only 49 percent afterwards.

Similarly, 90 percent could move from chair to
98 Chapter 5

A Report of the Surgeon General

standing before the fracture and only 32 percent

after. Comparable figures for walking across the

room are 75 percent and 15 percent (Marottoli

et al. 1992). Indeed, hip fracture patients are as

likely to have impaired ambulation and other

functional deficits as are those who suffer a stroke

(Lieberman et al. 1999). Even among people who

were previously independent, many activities

cannot be carried out independently following

a hip fracture (Table 5-4). Hip fractures cause

an “extra” 10 percent of women to become

functionally dependent (i.e., 10 percent more

women become dependent than would have in

the absence of the fractures), and 19 percent of

women who suffer hip fractures require longterm nursing home care (Chrischilles et al. 1991).

Other types of fractures, while somewhat

less devastating than hip fracture, nevertheless

take a toll on those who suffer them. For

example, while spine fractures rarely cause

institutionalization (Chrischilles et al. 1991),

their adverse influence on most activities of daily

living is almost as great as that seen for hip

fractures (Greendale et al. 1995).

This loss in functional status is mainly the

result of the pain caused by spine fractures. New

spine fractures may produce severe back pain

that lasts for weeks or months (Ross 1997).

Ettinger and colleagues found that 50 percent of

elderly women had a mild or moderate spine

deformity on x-ray, yet they were only slightly

more likely to have constant or severe back pain,

back disability, or substantial height loss than

those with no evidence of a spine fracture

(Ettinger et al. 1992). Ten percent of the elderly

women in this study had a severe spine

deformity, and this group showed a significantly

increased risk of these problems, especially in

those individuals with fractures in multiple

vertebrae. Not surprisingly, the more severe

fractures are also the most likely to be diagnosed,

and thus they represent the vast majority of spine

fractures that are recognized clinically. However,

even spine fractures that escape diagnosis can

cause an increase in back pain and limited activity

(Nevitt et al. 1998).

Wrist fractures seldom cause long-term

disability, but they nonetheless are painful,

requiring repositioning of the bones to their

normal position and stabilization in a cast for 4–

6 weeks. Recent studies suggest that wrist

fractures may cause a number of short-term

problems, including persistent pain, loss of

function, nerve impairments (such as carpal

tunnel syndrome), bone deformities, and

arthritis (Greendale and Barrett-Connor 2001).

In fact, nearly half of all patients report only fair

or poor functional outcomes 6 months following

a wrist fracture. Women and the elderly are the

most likely to report such outcomes. There is

no question that the overall impact of wrist

fractures on a patient’s functional status is much

less than that of a hip fracture. In fact, less than

1 percent of wrist fracture patients become

completely dependent as a result of the fracture

(Chrischilles et al. 1991). These fractures may

be as disabling as hip fractures with respect to

some specific activities of daily living such as

meal preparation.

Finally, while they are less devastating than

hip fractures, spine, wrist, and the other limb

fractures are more common, and they are the

main contributors to osteoporosis-related

morbidity in middle-aged women and men

(Kanis et al. 2001). In addition, the occurrence

of one of these fractures is a strong risk factor

for additional fractures (see Chapter 8).

Impact on Emotional State

In addition to functional impairments,

fractures from bone disease can have a negative

impact on self-esteem, body image, and mood

(Ross 1997), which may lead to psychological
Bone Health and Osteoporosis

The Burden of Bone Disease 99

consequences (Gold et al. 2001). Individuals who

suffer fractures may be immobilized by a fear of

falling and suffering additional fractures. Not

surprisingly, they may begin to feel isolated and

helpless. In a survey conducted by the National

Osteoporosis Foundation, 89 percent of women

who had already had an osteoporotic fracture

said they feared breaking another bone; 80

percent were afraid that they would be less able

to perform their daily activities; 80 percent feared

losing their independence; 73 percent were

concerned that they would have to reduce

activities with family and friends; and 68 percent

worried that another fracture would result in

their having to enter a nursing home. If not

addressed, fear about the future and a sense of
100 Chapter 5

A Report of the Surgeon General

helplessness can produce significant anxiety and

depression. These problems may be

compounded by an inability to fulfill

occupational, domestic, or social duties (Table

5-5), thus leading to further social isolation.

Impact on Quality of Life

Not surprisingly, the increased levels of

morbidity and disability and the declines in

functional status and mental health that are

typically associated with bone disease and

fractures can have a profound impact on an

individual’s quality of life. Some studies have

begun to address these intangible aspects of

osteoporosis and other bone diseases by having

individuals rate their quality of life in a given

year, using a measure known as quality-adjusted

life years (QALYs). When estimating QALYs,

each year of life is assigned a preference weight

between 1 and 0, where 1 represents perfect

health and 0 represents death. Different

individuals with similar health status may rate

the quality of their life very differently,

depending upon how they personally value that

health status compared to being in perfect health

and to dying. While results vary depending on

the type of fracture being measured, patient age,

and the assessment technique used, individuals

suffering osteoporotic-related fractures

consistently report significant reductions in

QALYs; these reductions range from 0.05–0.55

on the 0 to 1 scale mentioned above (Tosteson

and Hammond 2002). For example, spine
Bone Health and Osteoporosis

The Burden of Bone Disease 101

fractures are associated with a 20 percent

reduction in the quality of life in the first 12

months and a 15 percent reduction after two

years (Tosteson et al. 2001). Even those who

manage to remain independent following a

fracture typically experience a substantially

reduced quality of life. For example, relatively

healthy survivors of a hip fracture report a 52

percent reduction in quality of life in the first 12

months and a 21 percent reduction after two

years (Tosteson et al. 2001). Similar differences

were seen in a recent study comparing function

and quality of life in Belgian women with a hip

fracture compared to age-matched controls

(Boonen et al. 2004). Health-related quality of

life is also decreased in patients with spine

fractures, particularly those who have had

repeated episodes (Cockerill et al. 2004). Quality

of life is also reduced in patients with other bone

diseases. For example, patients with Paget’s

disease report a high frequency of hearing loss

and boney deformities, but many also report

depression (53.4 percent), sleep problems (51.5

percent), and poor quality of life (42.1 percent

report poor or fair QOL). In the only published

study to explore factors related to QOL in

Paget’s disease (Gold et al. 1996), the authors

found that the psychological factors (including

depression and loss of self-esteem) were the

most important contributors to reduced QOL

in these patients; they explained more of the

variance (19 percent) in QOL than did

biomedical (3 percent), social (2 percent), or cost

(1 percent) factors. They also found that QOL

was significantly decreased in patients with

more extensive or symptomatic Paget’s disease.

These data, combined with similar data from

studies of osteoporosis, suggest that the negative

impact of bone disease is substantial.

Impact on Financial Well-Being

In addition to a decline in physical and

mental health, patients with bone disease also

bear significant financial expenses. Although

better information is needed, these patients often

must pay for a variety of expenses out of their

own pockets (Table 5-6), creating a financial

burden for many patients and their families.

Hoerger and colleagues estimated that 17 percent

of the cost of managing osteoporosis is not

covered by insurance (i.e., Medicare, Medicaid,

or private coverage) (Hoerger et al. 1999).

Patients and/or family members may be

responsible for some proportion of the average

$2,000 increase in direct medical expenses that

occur in the year following a fracture (Gabriel

et al. 2002). They may also have to pay a portion

of the cost of any drug therapy to prevent

additional fractures (these costs are not included

in the $2,000 figure cited above) and to bear the

costs associated with disability during the

recovery period and over the long term.

Furthermore, younger family members may

experience reductions in earning power as they

take time away from work to assist older patients

during the convalescence period (Brainsky et al.

1997); few studies to date have accounted for this

type of lost productivity among individuals who

must care for those who sustain fractures. Even if

the hours of care provided by family and friends

(informal care) are valued at the minimum wage,

they represent a substantial proportion of the

overall costs of care in the first 6 months following

a hip fracture (Table 5-6). While the proportion

of total care costs represented by informal care

actually drop following a fracture (due to the high

expenses of treating the fracture), the absolute

dollar value of these costs more than doubles in

the first 6 months after the fracture.
102 Chapter 5

A Report of the Surgeon General

The Burden of Other Bone

Diseases

As indicated in Chapter 4, thousands of

Americans are affected by other bone diseases

such as rickets and osteomalacia, renal

osteodystrophy, primary hyperparathyroidism,

Paget’s disease, osteogenesis imperfecta, bone

cancer, and other developmental and acquired

skeletal disorders. Estimates of the societal burden

of these conditions are not readily available. The

impact of these conditions on individuals,

moreover, varies enormously, and is largely

dependent upon the severity of the disease.

The majority of patients with primary

hyperparathyroidism are asymptomatic, but a

small number suffer from kidney stones,

fractures, or rarely dangerously high blood

calcium levels that can lead to severe impairment

of kidney function, coma, and death. Most

Paget’s disease patients suffer from pain, but

some also develop nerve damage, fractures, or

osteosarcoma (a type of bone cancer). Few

patients with Paget’s disease die from the

condition, although, as discussed earlier, they

often find their QOL to be reduced significantly

because of the disease. Some patients with
Bone Health and Osteoporosis

The Burden of Bone Disease 103

chronic renal disease who are on dialysis develop

a severely debilitating bone disorder that results

in pain and fractures. Others lose bone rapidly

after renal transplantation and, despite the

successful improvement of their kidney function,

have poor health because of fractures.

Among the genetic skeletal disorders, the

dense bones associated with osteopetrosis and

the fragile bones associated with osteogenesis

imperfecta (OI) can both cause severe illness.

While some patients with osteopetrosis can be

treated by bone marrow transplantation and others with stimulators of bone breakdown, success

has been limited and many patients die from

these conditions. OI often causes severe crippling

and in its most severe form is fatal, although

treatment with inhibitors of bone breakdown

appears to be effective and is being explored further. (See box on page 90 for an example of OI’s

impact on an individual patient.) Cancer in bone

often causes severe symptoms and frequently

leads to death. Myeloma causes severe pain and

bone loss with multiple fractures. Other types

of cancer, including breast and prostate, can

spread (metastasize) to bone, although (as discussed in Chapter 9) this can be reduced by treatments that block bone breakdown (Ross et al.

2004, Rosen et al. 2004).

In summary, there are a number of disorders other than osteoporosis that add greatly to

the burden of bone disease in our population.

Fortunately, the ability to diagnosis and treat

many of these disorders has improved in recent

years (see Chapters 8 and 9), thus making it possible to reduce this burden substantially in the

future.

Key Questions for

Future Research

Much more information on the frequency and

burden of osteoporosis and other bone diseases is

needed if plans to prevent the projected “epidemic” are to be successful. Careful collection of

national and local data on all osteoporotic-related

fracture types is needed so that progress in meeting prevention goals can be measured. Specific

research questions that need to be answered include the following:

• How common are fractures in the community? Better data on fractures identified in physician’s offices as well as in

hospitals are needed.

• How common are hip fractures among

the Medicare and non-Medicare population? What are the trends over time and

across geographic regions and racial and

ethnic groups?

• What is the true incidence and burden of

spine fractures, given that many are “silent”?

Surveys using dual x-ray absorptiometry

(DXA) to assess spine deformities may

help to answer this question.

• What is the impact of non-hip fragility

fractures on morbidity, mortality, and

quality of life?

• What is the impact on quality of life of

asymptomatic spine fractures? These

fractures may cause deformity and musculoskeletal symptoms such as low back

pain, and may negatively affect cardiopulmonary and gastrointestinal function.

• What are the economic costs of osteoporosis and fragility fractures? While

some data are presented in this chapter,

more detail is needed, including information on non-Medicare patients, men, and

racial and ethnic minorities.

• What is the prevalence and burden of

osteoporosis and the incidence and burden of fractures in men and racial and

ethnic minorities, including Blacks,

Asians, and Hispanics?
104 Chapter 5

A Report of the Surgeon General

• What environmental factors are responsible

for geographic variations in fracture rates?

• What is the prevalence and burden of bone

diseases and disorders other than osteoporosis, including hyperparathyroidism, osteomalacia, renal osteodystrophy,

osteogenesis imperfecta, and congenital

disorders affecting bone such as osteopetrosis? This examination of other bone

diseases should include a review of their

impact on racial and ethnic minorities.

• What impact do the skeletal implications

of malignancy have on morbidity, mortality, and quality of life?

• What is the projected incidence and burden of bone disease if current practice is

maintained and how much could these

be changed by various levels of improvement in awareness, diagnosis, prevention,

and treatment of bone disease?
Bone Health and Osteoporosis

The Burden of Bone Disease 105

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Bone Health and Osteoporosis

 PART THREE: What Can Individuals Do to Improve Their Bone Health? 109

Part Three Three

Part Three of the report is the first of three sections that address the

question of what can be done to improve the bone health status of

Americans. This part of the report approaches the issue from the

perspective of the individual, examining those factors that determine bone

health and describing lifestyle approaches that individuals can take to

improve their personal bone health.

Chapter 6 highlights the critical role that lifestyle factors such as

nutrition and physical activity play in overall bone health status. It also

provides a thorough review of the evidence on precisely how these factors

influence bone health, including those behaviors that promote it (e.g.,

physical activity, adequate calcium and vitamin D intake) and those that

can impair it (e.g., smoking, excessive alcohol consumption). The chapter

emphasizes the fact that many Americans do not currently get enough

exercise and consume enough calcium and vitamin D to achieve optimal

bone health. The chapter also reviews evidence on the impact of other

factors on bone health, including the presence of other diseases; the use of

certain medications; weight and weight loss; and reproductive issues such

as pregnancy, lactation, amenorrhea, oophorectomy, and contraceptive use.

Chapter 7 provides practical, real-world guidance on lifestyle approaches

that individuals can take to improve their own bone health, including the

following: what foods are the best sources of calcium and vitamin D; how

to calculate daily calcium intake; when calcium and/or vitamin D

supplementation should be considered; and what types of physical activity

can contribute to bone health and overall health. The good-news message

of this chapter is that it is surprisingly easy to meet recommended guidelines

for nutrition and physical activity, and that following these guidelines not

only promotes bone health, but it also enhances overall health and wellbeing and helps to avoid the onset of other chronic diseases.

WHAT CAN INDIVIDUALS

DO TO IMPROVE THEIR

BONE HEALTH?
110 Chapter 6

A Report of the Surgeon General

• While genetic factors play a significant role

in determining bone mass, controllable

lifestyle factors such as diet and physical

activity can mean the difference between

a frail and strong skeleton.

• Calcium has been singled out as a major

public health concern today because it is

critically important to bone health and

the average American consumes levels of

calcium that are far below the amount

recommended for optimal bone health.

• Vitamin D is important for good bone

health because it aids in the absorption

and utilization of calcium. There is a high

prevalence of vitamin D insufficiency in

nursing home residents, hospitalized

patients, and adults with hip fractures.

• Physical activity is important for bone

health throughout life. It helps to increase

or preserve bone mass and to reduce the

risk of falling. All types of physical

activity can contribute to bone health,

albeit in different ways.

• Maintaining a healthy body weight is

important for bone health throughout

life. Being underweight raises the risk of

fracture and bone loss. Weight loss is

associated with bone loss as well,

although adequate diet and physical

activity may reduce this loss.

• Fractures are commonly caused by falls,

and thus fall prevention offers another

Chapter 6: Key Messages

opportunity to protect bones, particularly

in those over age 60. Several specific

approaches have demonstrated benefits,

including muscle strengthening and

balance retraining, professional home

hazard assessment and modification, and

stopping or reducing psychotropic

medications.

• Reproductive issues can affect bone

health. Pregnancy and lactation generally

do not harm the skeleton of healthy adult

women. Amenorrhea (cessation of

menstrual periods) after the onset of

puberty and before menopause is a very

serious threat to bone health and needs

to be attended to by individuals and their

health care providers.

• Several medical conditions and

prescription medications can affect bone

health through various mechanisms, and

health care professionals should treat the

presence of such conditions and the use

of such medications as a potential red flag

that signals the need for further

assessment of bone health and other risk

factors for bone disease.

• Smoking can reduce bone mass and

increase fracture risk and should be

avoided for a variety of health

reasons. Heavy alcohol use has been

associated with reduced bone mass

and increased fracture risk.
Bone Health and Osteoporosis

Determinants of Bone Health 111

As discussed in Chapter 2, bone is a

remarkable tissue with a functional structure (the

skeleton) that is strong enough to withstand

intense physical activity, adaptive enough to

respond to changes in activity, and lightweight

enough to allow efficient movement. Bone is

resilient because of its intrinsic material

characteristics (mass, density, mineral

composition, strength) and its dimensions (size,

shape, and structure). Throughout life, bone

must adapt to the stresses imposed upon it, and

its ability to do so depends on both lifestyle and

genetic factors. A variety of studies indicate that

genetic factors are responsible for determining

50–90 percent of bone mass and other qualitative

aspects of bone (Recker and Deng 2002).

Heredity not only sets limits on how much bone

a person acquires, but also on bone structure,

the rate of bone loss, and the skeleton’s response

to environmental stimuli like nutrients and

physical activity. Normal bone mass and

strength is controlled by many genetic elements

working in concert. The tendency to develop

bone diseases like osteoporosis and Paget’s

disease also appears to be due to genetic factors,

although this tendency may also be influenced

by environmental factors that are not yet

completely understood. Osteogenesis imperfecta

(OI), a condition in which bones break easily,

often for little or no apparent cause, is clearly

determined by the malfunction of specific

DETERMINANTS OF BONE HEALTH

Chapter 6

collagen genes that have been identified. The

search for the particular genes that control bone

mass and affect the tendency to develop bone

diseases is a very active area of research. Finding

these elements may lead to new therapeutic

strategies and prevention tools for osteoporosis.

While genetic factors play an important role

in determining bone mass, it is critical not to

underestimate the important role that individuals

can play in promoting their own bone health

status. In fact, controllable lifestyle factors such

as diet and physical activity are responsible for

10–50 percent of bone mass and structure. These

influences are illustrated in Figure 6-1.

Controlling these factors can literally mean

the difference between a frail and a strong

skeleton. This is because even relatively small

changes in bone mass can have a significant

impact on overall bone health. In fact, it has been

estimated that a 10 percent increase in bone mass

could reduce fracture risk by as much as 50

percent (Cummings et al. 1993). In other words,

paying attention to lifestyle factors such as diet

and physical activity throughout life can yield

bone health benefits that are equal to or greater

than those offered by the most powerful drugs

currently used to treat osteoporosis.

While good nutrition and regular physical

activity are important to bone health throughout

life, the optimal type of nutrition and activity

will vary across the life span, as will the impact
112 Chapter 6

A Report of the Surgeon General

that each will have on bone. As a result, this

chapter will analyze the evidence about the

key determinants of bone health. It uses a life

span approach, considering the following

phases: a) the growth phase that occurs

during childhood and adolescence; b) the

maintenance phase that occurs during young

to middle adulthood; c) the mid-life bone loss

phase that typically occurs in adults between

age 50–70; and d) the frailty phase that

typically occurs in adults over age 70. These

phases are general and do not correspond to

a specific chronological age in an individual.

Additional information on the various kinds

of evidence and studies that are cited in this

chapter can be found in Appendix B, “How We

Know What We Know: The Evidence Behind

the Evidence.”

The goal of this chapter is to discuss the

evidence related to these controllable factors that

affect bone health throughout the different stages

of life. Most of the information in this chapter

focuses on osteoporosis and fracture;

unfortunately, there are no known preventive

regimens to address other bone diseases. Early

recognition and intervention is the optimal

strategy for these other bone diseases at the present

time, as described in Chapters 8, 9, and 10.
Bone Health and Osteoporosis

Determinants of Bone Health 113

A Review of the Critical Life Stages of Bone

As discussed in Chapter 2, bone tissue

continues to renew itself, or remodel,

throughout life by breaking down old bone

(bone resorption) and replacing it with new

bone (bone formation). Figure 6-2 illustrates

how the skeleton changes over the life span.

Because lifestyle changes made during the

acquisition phase affect the achievement of peak

bone mass, these lifestyle changes are critically

important to bone health throughout life.

Adolescence is a particularly critical period

for bone health because the amount of bone

mineral gained during this period typically

equals the amount lost throughout the remainder

of adult life (Bailey et al. 2000). As illustrated in

Figure 6-2, failure to achieve an optimized bone

mass at the end of adolescence leaves an

individual with much less reserve to withstand

the normal losses during later life. Most gains in

bone mass during puberty are due to an increase

in bone length and size rather than bone density

(Katzman et al. 1991). Fracture rates go up

during this period of extremely rapid growth,

possibly because the bone is temporarily weaker

because bone mineralization lags behind growth

in bone length (Khosla et al. 2003).
114 Chapter 6

A Report of the Surgeon General

Review of the Life Stages of Bone, continued

After individuals achieve peak bone mass

in late adolescence, bone health is optimized by

maintaining as much of this bone mass as

possible throughout adulthood. Bone formation

and resorption are generally in balance with

each other during the young to mid-adult years,

so optimally bone mass is maintained at many

skeletal sites. There is bone loss at some skeletal

sites, such as the hip, before age 50, but it does

not normally compromise strength. Bone loss

begins or accelerates at midlife for both men

and women (Riggs et al. 2002), meaning that

the goal during this time of life is to keep bone

loss to a minimum and to recognize and avoid

both bone-specific and non-specific threats to

bone health, such as other illnesses and falls.

After age 40–50, bone loss may progress slowly

in both sexes, with a period of more rapid loss

in women surrounding the menopausal

transition. During this period of age–related

bone loss, both sexes may lose a total of 25

percent of bone. Bone loss continues in both

men and women after age 70 (Riggs et al. 2002).

These later stages in bone life are depicted in

Figure 6-3, which shows three women with

increasingly severe bowing of the spine

(kyphosis) due to osteoporotic fractures of the

spine. But fractures are not a natural consequence

of aging. Rather, they can be avoided, to some

extent, by focusing on controllable factors such

as diet and physical activity.
Bone Health and Osteoporosis

Determinants of Bone Health 115

Nutrition’s Impact on Bone

Health: A Review of the Evidence

The evidence suggests that the composition

of the diet can play an important role in building

and maintaining bone mass throughout life,

primarily by providing bone-building nutrients

and by influencing absorption and retention of

these nutrients. In addition, diet provides calories

(energy input), which together with physical

 Nutrition and Bone Health: What

 the Evidence Tells Us

• Research suggests that a wellbalanced diet is important for bone

health throughout life. Depending on

age, it may help increase or preserve

bone mass.

• Much of the research to date has

focused on calcium and vitamin D.

Calcium and vitamin D play crucial

roles in bone health, although other

nutrients are also important.

• The Institute of Medicine recommends a steady increase in calcium

intake as children age, beginning with

210 mg per day in infants and rising

to 1,300 mg per day in those age 9–18.

Recommended levels drop to 1,000

mg per day in those age 19–50, and

then increase to 1,200 mg per day for

those over age 50. The same agedependent recommendations for

calcium apply to pregnant or nursing

women. Recommended levels of

vitamin D intake are 200 IU per day

for those under age 50, 400 IU per day

for those 50–70, and 600 IU per day

for those over age 70.

activity (energy output), determines body

weight. Maintenance of an adequate body weight

can help promote optimal bone health, as

discussed later in this chapter.

Background: Why Focus on Vitamin D and

Calcium?

As discussed later in this chapter, consuming

adequate levels of calcium and vitamin D

throughout life are critically important to an

individual’s bone health. The Institute of

Medicine conducted a major review of bonerelated nutrients in 1997 (IOM 1997) and

developed a set of evidence-based recommendations for calcium and vitamin D intake. The

goal of this effort was to determine the level of

nutrient intake for normal, healthy individuals

that would prevent the development of a chronic

condition associated with that nutrient. While

many nutrients play a role in bone health,

calcium has been singled out as a major public

health concern today not only because it is a

critical nutrient for bone but also because of

national surveys that suggest that the average

calcium intake of individuals is far below the

levels recommended for optimal bone health

(Figure 6-4). One reason for these low levels of

calcium intake relates to current lifestyle and

food preferences, which have resulted in reduced

intake of dairy products and other naturally

calcium-rich foods. For some individuals lactose

intolerance may play a role in not consuming

adequate levels of calcium. Lactose intolerance

is a condition in which individuals cannot

metabolize lactose, the main sugar found in milk

and other calcium-rich dairy products. An

estimated 30–50 million Americans (about 25

percent of the U.S. population) are affected by

lactose intolerance, although to varying degrees.

While least common among Whites (it affects

about 15 percent of White adults), lactose
116 Chapter 6

A Report of the Surgeon General

intolerance is widespread among other ethnic

groups. Among the adult population, an

estimated 70 percent of African-Americans, 74

percent of Native Americans, 53 percent of

Mexican-Americans, and 90 percent of AsianAmericans are affected (Jackson and Savaiano

2001, National Women’s Health Information

Center 2001).

Lactose intolerance has been shown to be

associated not only with low milk intake, but also

with low bone mass and increased risk of fracture

(Obermayer-Pietsch et al. 2004). Thus, these

individuals may experience a detrimental effect

on their bone health if they avoid consuming

dairy products and do not replace them with

other good sources of calcium. Strategies to cope

with lactose intolerance are described in more

detail in Chapter 7.

While for most individuals the problem is

too little calcium, it is important to remember

that too much calcium does not have any additive

benefit, and can have negative effects in some

individuals. For this reason, the Institute of

Medicine set a tolerable upper limit for calcium

of 2,500 mg per day.

Vitamin D is important for good bone health

because it aids in the absorption and utilization

of calcium. The main source of vitamin D is

sunlight, and most people throughout the world

get their supply of vitamin D by the conversion
Bone Health and Osteoporosis

Determinants of Bone Health 117

of precursors in the skin to active vitamin D, a

process caused by exposure to sunlight. Several

factors can limit the production of vitamin D by

the skin, including where one lives (those who

live in northern latitudes during the winter

months do not get adequate exposure to sunlight

(Webb et al. 1988)), how much body surface is

covered by clothing or sunscreen, the degree of

skin pigmentation (darker skin takes longer to

make active vitamin D), and age (older

individuals are less efficient in making vitamin

D). Strategies for overcoming some of these

limitations are discussed in Chapter 7.

Due to concerns that individuals do not get

enough vitamin D through sunlight,

recommendations for intake are set at a level to

be adequate for individuals having no sun

exposure. The most accurate way to tell if an

individual or population group is getting enough

vitamin D is by measuring levels of serum 25-

hydroxy vitamin D. These levels have been

measured in various populations, and they

indicate a high prevalence of vitamin D

insufficiency in nursing home residents,

hospitalized patients, and adults with hip

fractures (Webb et al.1990, LeBoff et al. 1999,

Thomas et al. 1998). Vitamin D levels commonly

deteriorate in older adults, and thus the

requirement for vitamin D increases with age.

But inadequate vitamin D levels can be a

problem at any age. Exclusively breast-fed

infants, particularly non-Whites or infants with

decreased sunlight exposure, are at greatest risk.

As a result, the American Academy of Pediatrics

(Gartner and Greer 2003) recommends

supplementing breast-fed infants with vitamin

D, since breast milk may be a poor source of

vitamin D. Infant formulas are fortified with

appropriate levels of the vitamin.

Finally, as with calcium, too much vitamin

D can be harmful to the skeleton as well. Vitamin

Absorption of Calcium

To reach the skeleton, calcium eaten in

the diet must first be absorbed into the body.

In fact, much of the calcium consumed in

the diet does not make its way to the skeleton;

studies indicate that in adults only about 30

percent of calcium intake is actually absorbed

by the body (IOM 1997). Moreover, some

calcium is excreted from the body into the

intestine so that the actual net absorption is

even lower (Heaney and Abrams 2004).

Several factors can affect the body’s

ability to absorb dietary calcium, including

vitamin D and estrogen. Deficiencies in

either can reduce calcium absorption. The

problem of reduced calcium absorption is

more acute in older persons, who absorb less

dietary calcium because their intestines are

no longer as responsive to the action of 1,25-

dihydroxy vitamin D (Heaney et al. 1989).

Poor absorption of calcium can be overcome

by increasing overall calcium intake and

maintaining adequate levels of vitamin D.

D is a fat-soluble vitamin, so it can be stored in

the body. Excess vitamin D can be toxic, leading

to hypercalcemia, kidney failure, and calcification

of soft tissue (IOM 1997). As a result, the Institute

of Medicine has established a tolerable upper

limit for dietary vitamin D intake of 2,000 IU

per day. Physicians will often use much higher

levels, however, to correct deficiencies.

The Evidence Supporting the Effect of

Calcium and Vitamin D on Bone

Individuals who consume adequate amounts

of calcium and vitamin D throughout life should

enjoy better overall bone health for two reasons.

First, they are more likely to achieve optimal

skeletal mass early in life, and second, they are
118 Chapter 6

A Report of the Surgeon General

less likely to lose bone later in life. The net result

should be higher bone mass and fewer fractures.

Selected evidence to support the relationship

between these nutrients and bone health during

different stages of life is summarized below.

The Growth Stage (Children and Adolescents)

The role of calcium and other minerals in

achieving peak bone mass begins before birth.

Premature infants tend to have lower bone

mineral content later in life, although this may in

part be due to their tendency to be light and short

for their age (Fewtrell et al. 1999, Bowden et al.

1999). Low birth weight is also associated with

low bone mass later in life (Yarbrough et al. 2000,

Antoniades et al. 2003). As discussed in Chapter

10, providing premature and low birth-weight

infants with supplemental calcium, phosphorus,

and protein may help them to “catch up.”

Many observational studies make it clear that

the role of calcium in achieving optimal peak

bone mass continues into childhood and

adolescence (Heaney et al. 2000). Perhaps the

most often cited study is that of Matkovic et al.,

who compared two regions of Croatia with

different intakes of calcium (Matkovic et al.

1979). Although the high-calcium region had

lower fracture rates, the populations differed in

other variables such as exercise that could

partially explain the different fracture rates. This

study spurred further research into the role of

childhood and lifetime calcium consumption on

the risk of osteoporosis and fracture.

Several randomized clinical trials have

examined the effect of calcium supplements or

calcium-rich foods in children and adolescents

(Lee et al. 1994, Lee et al. 1995, Lloyd et al. 1993,

Nowson et al. 1997, Bonjour et al. 2001, Johnston

et al. 1994, Dibba et al. 2000, Cadogan et al. 1997,

Merrilees et al. 2000, Chan et al. 1995). These

studies have been combined and summarized in

a meta-analysis (Wosje and Specker 2000),

which concluded that higher calcium intake

increases bone mineral density (BMD) in

children and adolescents in certain

circumstances. Increases in BMD were more

likely in cortical bone sites and among

populations with low baseline calcium intakes,

and in most studies the increase did not persist

beyond the calcium supplementation period. A

few studies have examined the impact of higher

calcium intake over time. Results from most of

these studies suggest that the intake must be

maintained for the positive effects on bone to

persist (Bonjour et al. 2001, Slemenda et al. 1997,

Lee et al. 1996).

Adequate levels of calcium intake may also

be important in maximizing the positive effect

of physical activity on bone during the growth

period. Two recent studies found that physical

activity was more beneficial to bone health in

infants or young children consuming higher

amounts of calcium (Specker et al 1999, Specker

and Binkley 2003).

There have been no randomized clinical trials

to measure the impact of vitamin D supplements

alone on bone health in children and adolescents.

However, vitamin D deficiency is known to

cause inadequate mineralization of the growing

skeleton, leading to rickets (Goldring et al. 1995).

In addition, one small observational study found

higher bone density in prepubertal girls who

took vitamin D supplements during infancy

(Zamora 1999).

The Maintenance Stage (Adults)

Eating adequate amounts of nutrients

continues to be important during the young adult

years when bone formation and bone resorption

are balanced. Unfortunately, most studies of diet

and supplement use and bone health have

focused on either younger or older individuals.
Bone Health and Osteoporosis

Determinants of Bone Health 119

A meta-analysis of calcium and bone density in

premenopausal women indicated that calcium

had a positive effect on BMD in this group, as

the supplemented groups lost less bone per year

(Welten et al. 1995). However, only one of the

four intervention studies in this meta-analysis

used a double-blinded, placebo-controlled

design. In addition, these studies focused on

premenopausal women between the age of 30

and 55, not on younger adult women. There have

not been many studies of vitamin D in young

adults. One study did find that even young men

may experience low vitamin D levels in the

winter, and that these low levels were associated

with lower BMD (Valimaki et al. 2004). More

information is needed about the role of calcium,

vitamin D, and other nutrients in maintaining

bone in this age group of women and in men.

The Early Bone Loss and Frailty Stages

(Older Adults)

Most randomized clinical trials examining

the effect of calcium and vitamin D on bone

health have focused on postmenopausal women

and the elderly, so the role of these nutrients in

promoting bone health is more clearly

established for this age group. In fact, a carefully

conducted meta-analysis of randomized clinical

trials on the effects of calcium supplementation

for the prevention of postmenopausal

osteoporosis was recently published (Shea et al.

2002). The investigators performed a thorough

search to identify all trials (including

unpublished ones) examining the effect of

calcium (with minimal vitamin D) on bone

density and fractures in postmenopausal women

since 1966. Of the 66 trials that were identified

and screened, 15 met the inclusion criteria. After

analyzing these trials, the investigators

concluded that calcium supplements reduced

bone loss by approximately 2 percent after two

or more years of use. More importantly, their

results suggested that calcium supplements led

to a significant (roughly 23 percent) reduction

in the risk of spine fractures.

Just as with children, moreover, it appears

that there may be a positive interaction between

the effects of physical activity and calcium on

bone health in older adults. (This relationship is

discussed further in the section on physical

activity.) Calcium may also help enhance the

effect of drugs that reduce bone loss, such as

estrogen and bisphosphonates (e.g., drugs that

restrict the action of cells that resorb bone)

(Heaney 2001).

A carefully conducted meta-analysis of

randomized trials on the effect of vitamin D on

bone density and fracture risk has also been

recently conducted (Papadimitropoulos et al.

2002). All trials, including unpublished studies,

conducted since 1966 were evaluated, with 25

meeting the criteria for inclusion. While the

results from the different trials tended to vary

somewhat, the authors concluded that vitamin

D supplements reduced the risk of spine

fractures by approximately 37 percent. This

decline in fracture risk may be due in part to

vitamin D’s ability to reduce the risk of falls.

Vitamin D may reduce falls by acting directly

on muscle. There are vitamin D receptors in

human muscle that may play a role in increasing

muscle strength and thereby enhancing stability

(Bischoff et al. 2001). While elderly individuals

who are vitamin D deficient face an increased

risk of falls (Flicker et al. 2004), studies have

shown that vitamin D supplementation in these

individuals may negate this effect (Bischoff et

al. 2003, Latham et al. 2003, Dukas et al. 2004).

It is important to note that the design of many

of the randomized, controlled trials examining

the effect of vitamin D supplements on bone loss

or fracture incidence also called for participants
120 Chapter 6

A Report of the Surgeon General

to use a calcium supplement. Thus, it is not

possible to isolate the benefits of calcium and/or

vitamin D alone in these studies. While a few

studies have simultaneously evaluated the effects

of the two nutrients separately, the results are

mixed. For example, one study found that

calcium prevented hip bone loss in most elderly

men and women, but vitamin D only modestly

lowered bone loss (Peacock et al. 2000). In a

different study, annual vitamin D injections did

not prevent hip fractures (Heikenheimo et al.

1992). However, in a third randomized,

controlled trial, 400 IUs of vitamin D per day

prevented hip bone loss over 2 years in elderly

women (Ooms et al. 1995). In a recent study,

vitamin D supplementation was found to have

more beneficial effects when used in

combination with calcium supplementation in

women who had suffered a hip fracture

(Harwood et al. 2004). Thus, the question of the

role of vitamin D alone in promoting bone health

remains unresolved. Vitamin D can probably be

most effective in populations with an underlying

deficiency and in those individuals for whom

other components of bone health, such as

adequate levels of calcium and physical activity,

are optimized.

It may not be realistic, however, to try to

dissect the individual contributions of calcium,

vitamin D, and physical activity on bone health,

since they all need to be optimized. As a result,

some studies have looked at the impact of

combinations of the three on bone health. The

most promising study of a combination of

calcium and vitamin D on bone fractures was

conducted in France in the early 1990s (Chapuy

et al. 1992). Over 3,000 elderly women received

supplements with calcium and vitamin D or

placebo pills. Hip fractures were reduced by 43

percent among the women treated with vitamin

D and calcium compared to those who received

placebo. This is the only large trial to date to

show a reduction in hip fractures due to

supplements. The women in the study were

quite elderly (average age 83) and vitamin D

deficient, so it is possible that correcting the

deficiency led to the dramatic drop in fractures.

In a smaller study of elderly individuals in New

England, Dawson-Hughes and colleagues

showed that supplementation with calcium and

vitamin D moderately reduced bone loss and the

incidence of non-spine fractures (DawsonHughes et al. 1997). Tests of calcium and vitamin

D supplementation to prevent hip fractures are

currently being conducted in a large population

of healthy postmenopausal women in the

Women’s Health Initiative; these results should

be available in late 2005 (Jackson et al. 2003).

Other Nutrients With a Role in Bone Health

Bone health requires more than just attention

to calcium and vitamin D. In fact, data suggest

that many other nutrients can affect bone in

positive or negative ways. (For more

information, see Table 7-5, which lists some of

the other nutrients that can affect bone.) The

roles of many of these nutrients with respect to

bone health have not been as well established as

for calcium and vitamin D. Since the vast

majority of individuals consume an appropriate

amount of these nutrients (i.e., not too much or

too little), they have not become a target for

special attention.

Nevertheless, the Institute of Medicine

recently considered other bone-related nutrients,

including phosphorus, magnesium, and fluoride

(IOM 1997). Phosphates make up more than half

the mass of bone mineral. About 85 percent of

the body’s phosphorus and 60 percent of the

body’s magnesium are found in the skeleton.

Both phosphorus deficiency and excess have

been considered as having adverse effects on

bone health (Heaney 2004), but both can be
Bone Health and Osteoporosis

Determinants of Bone Health 121

avoided with a healthy diet. Magnesium may

enhance bone quality by influencing growth of

crystals of hydroxyapatite, the mineral

compound found in bone. Fluoride is known to

reduce cavities in teeth, a hard tissue that is

similar to bone, but its role in maintaining

skeletal health is less clear (IOM 1997). Other

nutrients/dietary components that appear to play

a positive role in bone health include vitamin K,

vitamin C, copper, manganese, zinc, and iron.

These micronutrients are essential to the

function of enzymes and local regulators and

therefore are important to forming the optimal

bone matrix.

Potassium also appears to play an important

role in bone health. Diets abundant in potassiumrich fruits and vegetables may reduce the need for

calcium to be mobilized from the skeleton.

Epidemiologic and short-term intervention studies

suggest higher intakes of alkaline potassium salts

reduce urine calcium excretion and markers of bone

resorption and have been associated with increased

bone density (Barzel 1995, Sellmeyer et al. 2002,

New et al. 2000, New et al. 2004, Tucket et al.

1999, Sebastian et al. 1994).

It is important to remember that some

dietary components may negatively affect

calcium balance. While their effects tend to be

small, these include caffeine, protein, and excess

phosphorus intake (i.e., more than 3-4 grams per

day) (Fitzpatrick and Heaney 2003; Kerstetter

et al. 2003). Sodium also affects calcium balance

by increasing its excretion, and high-salt diets

are fairly common in the United States. But

unlike with these other nutrients, the effects of

sodium on calcium balance are more

pronounced. Results of two studies in adult

women suggest that each additional gram of

sodium eaten per day increases bone loss by 1

percent per year, unless the extra calcium lost in

the urine is replaced by more calcium in the diet

(Devine et al. 1995, Shortet al. 1988). The

negative effects of sodium and these other dietary

components can be countered by consuming an

adequate amount of calcium in the diet. Diets

high in sodium are associated with hypertension.

Therefore, lowering intake of sodium in concert

with meeting calcium requirements is prudent

(USDA 2000). Finally, although protein causes

some loss of calcium from the body, only very

high protein diets that are not compensated for

by extra calcium are a concern (Dawson-Hughes

2003). In fact, higher protein intakes may be

associated with higher levels of IGF-1, a marker

of bone formation, and lower levels of urinary

n-telopeptide crosslinks, a marker of bone

breakdown (Dawson-Hughes et al. 2004). Far

more serious is the low protein intake of many

older persons (Rizzoli and Bonjour 2004).

Inadequate protein intake negatively affects

bone health in the elderly (Kerstetter et al.

2003) and may diminish the ability to repair

and recover from fractures (Schurch et al. 1998).

Nutritional supplementation has been

recommended as a means of boosting protein

intake in elderly individuals recovering from a

hip fracture (Schurch et al. 1998), although the

evidence to support this approach is limited

(Avenell and Handoll 2004). Finally, excess

dietary vitamin A (as retinol) may also

negatively affect bone health by increasing bone

resorption (Sheven and Hamilton 1990).

Since many nutrients in addition to calcium

and vitamin D play a role in bone health, it is

important to consume a well-balanced diet

containing a variety of food, rather than just

focusing on one or two bone-related nutrients.

This approach can have positive effects on other

aspects of health as well. For example, the

DASH diet (Dietary Approach to Stop

Hypertension), which encourages fruit and

vegetable intake in addition to more calcium and
122 Chapter 6

A Report of the Surgeon General

less sodium intake, has been linked to lower bone

turnover and better cardiovascular status (Lin

et al. 2003). In a recent study of young girls a

high intake of fruits and vegetables was

associated with increased bone mineral content

(Tylavsky et al. 2004). Fruit and vegetables also

provide vitamins, minerals, and fiber, and should

be encouraged for overall good nutrition. As

alluded to above, abundant potassium intake via

increased fruit and vegetable intake may be

particularly beneficial for skeletal health. Specific

suggestions for selecting a well-balanced diet are

provided in Chapter 7.

Physical Activity

Physical activity of all kinds has overall

benefits to health and weight maintenance.

Regular physical activity lowers risk factors for

Physical Activity, Body Weight, and Bone

Health: What the Evidence Tells Us

cardiovascular disease, colon cancer, and type 2

diabetes, and helps to control blood pressure

(USDA 2000). Physical activity plays an

important role in skeletal health because, as

discussed in Chapter 2, bone mass is responsive

to the mechanical loads placed on the skeleton.

Background: Why Focus on Physical Activity?

As discussed in Chapter 2, the body

constantly monitors the strain on bones caused

by muscle action, and any substantial increase

in these forces signals the need to build more

bone. Conversely, reductions in biomechanical

forces from lower activity levels or loss of

muscle mass (sarcopenia) signals less need for

bone, which leads to the elimination of bone.

The latter process may be worsened by

estrogen deficiency, which appears to reduce

the sensing of biomechanical strains by bone

cells (Riggs et al. 2002).

Physical activity has been identified as one

of the Leading Health Indicators in the Healthy

People 2010 health objectives for the Nation

during the next decade. It is one of the most

important controllable lifestyle changes to help

prevent (or reduce the risk of) a number of

chronic conditions, including heart disease,

diabetes, and some cancers. It also helps with

weight control and the lessening of symptoms

related to arthritis (USDHHS 19996).

Many adult Americans do not engage

regularly in leisure-time physical activity. As

shown in Figure 6-5, the participation by both

men and women declines with age, with women

being consistently less active than men (Schiller

et al. 2004). The same problem exists for

children. Many children become far less active

as they pass through adolescence. Only half of

those age 12–21 exercise vigorously on a regular

basis and 25 percent report no exercise at all

(Gordon-Larsen et al. 1999). Children may find

• Physical activity is important for bone

health throughout life.

~ Depending on age, it may help

increase or preserve bone mass.

~ It may also help reduce the risk of

falling.

• All types of physical activity can

contribute to bone health.

~ Activities that are weight bearing or

involve impact are most useful for

increasing or maintaining bone mass.

~ Some activities that are not weight

bearing or are low impact may help

improve balance and coordination

and maintain muscle mass, which can

help prevent falls.

~ Specific recommendations are given

in Chapter 7.
Bone Health and Osteoporosis

Determinants of Bone Health 123
124 Chapter 6

A Report of the Surgeon General

it difficult to get daily physical activity in schools.

While most schools have requirements for

physical activity of some kind, only 8 percent of

elementary schools, 6.4 percent of middle/junior

high school, and 5.8 percent of senior high

schools provide physical education on a daily

basis (SHPPS 2001). At the other extreme, some

girls and young women, especially those training

for elite athletic competition, exercise too much,

eat too little, and as a result develop delayed

puberty or amenorrhea (cessation of menstrual

periods). These girls are at risk for low bone mass

and fractures (Warren 1999). One of the national

health objectives for 2010 is to increase to 30

percent the proportion of adults who perform,

more than 2 days per week, physical activities

that enhance and maintain muscular strength

and endurance (USDHHS 2000). Only 12

percent of people age 65–74 and 10 percent of

those over age 75 meet that objective,

underscoring the need for programs that

encourage older adults to incorporate strength

training and regular physical activity into their

lives (Kruger et al. 2004).

To encourage increased levels of physical

activity among all age groups, “Physical Activity

and Health: A Report of the Surgeon General”

recommends a “minimum of 30 minutes of

physical activity of moderate intensity (such as

brisk walking) on most, if not all, days of the

week” (USDHHS 1996). Children and

adolescents should aim for at least 60 minutes of

physical activity per day (USDA 2000). In

addition to helping achieve healthy weight and

avoid chronic diseases like heart disease and

diabetes, this type of physical activity can benefit

skeletal health by building muscle mass and

promoting balance and coordination, which may

help individuals avoid falls and/or minimize the

impact if a fall does occur. But the skeleton

responds preferentially to strength training and

short bouts of high-load impact activity (such as

skipping or jumping), both of which improve

bone mass and strength, as discussed below. In

light of this, “Physical Activity and Health: A

Report of the Surgeon General” also

recommended that adults supplement their

cardiorespiratory endurance activity with

strength-developing exercise at least two times

per week (USDHHS 1996). Chapter 7 will

address some specific ways to incorporate

strength and loading activities into an overall

habit of physical activity.

Physical Activity and Bone Health: A Review

of the Evidence

This section will discuss the evidence of

the impact of exercise and physical activity

on fractures and on bone mass and other bone

qualities.

Impact of Physical Activity on Fractures

Although no randomized intervention trials

have addressed the issue, data from longitudinal

observational studies have shown a link between

physical activity and reduced fracture risk. In

these studies, subjects are asked about their

physical activity habits and then followed for

some period of time to determine if they fracture.

As suggested earlier, this study design cannot

prove that physical activity causes a reduction

in risk, since there is an inherent bias in the

study—i.e., that healthy people are able to be

more active. A number of risk factors for

osteoporosis and fracture (e.g., health, diet, body

size) may be unequally distributed between

those who choose to be physically active and

those who do not. Nevertheless, recent reviews

of the epidemiologic evidence suggests that

physical activity is associated with reduction in

the risk of hip fracture in both men and women

and that there is a “dose-response” effect, i.e.,

risk goes down as physical activity level goes up

(Gregg et al. 2000, Karlsson 2002). In a large
Bone Health and Osteoporosis

Determinants of Bone Health 125

Challenges in Studying the Impact of

Physical Activity on Bone Health

One of the biggest challenges to

researchers in determining the effect of

physical activity on bone is to have an

accurate and measurable outcome. Fracture

would be the best outcome to study, but

there are no large studies that have

determined the effect of physical activity on

the risk of fracture using a randomized

clinical trial design. Most physical activity

studies have had small sample sizes and have

used BMD, as measured by dual-energy xray absorptiometry (DXA), as the outcome.

As described in Chapter 8, DXA

measurements of bone-mineral content

(measured in grams) and areal bone-mineral

density (g/cm2

 [grams per centimeter

squared]) do not directly measure bone size

or reflect bone geometry, and thus they can

significantly underestimate the effect of

physical activity on overall bone strength

(Jarvinen et al. 1999). Thus, while a

convenient measure, BMD may not be

sensitive to the multiple effects of physical

activity on the musculoskeletal system.

study of older women (Gregg et al. 1998), higher

levels of leisure time physical activity and

household chores were associated with an overall

36 percent reduction in hip fractures. The effect

varied with the level of the activity, with very

active women having greater reductions in risk

compared with inactive women. However, even

walking, the most common leisure time physical

activity for women, can have a positive effect on

bone health. For example, the Nurses Health

Study concluded that walking at least 4 hours

per week was associated with a 41 percent lower

risk of hip fracture compared with walking less

than an hour per week, even among women who

did no other exercise (Feskanich et al. 2002).

Several other longitudinal observational studies

have confirmed a similar reduction in hip

fracture risk in men who exercise regularly

compared to inactive men (Paganini-Hill et al.

1991, Kujala et al. 2000).

Impact on Bone Mass, BMD, and Other

 Bone Qualities

Randomized intervention trials that focused

on the effects of physical activity on bone mass

(either bone mineral density or bone mineral

content) have identified some important points

about physical activity and skeletal health.

• First, these studies show that bone mass

is improved, but only at the skeletal sites

that received the impact. In other words,

lifting weights with arms will not improve

bone density of the hips.

• Second, the effects of physical activity on

bone health will vary by age, and thus

younger individuals should be studied

separately from older individuals.

• Third, the effect of physical activity on

bone does not persist if the activity level

is stopped or reduced (an exception may

be the effect of physical activity on bone

that occurs during childhood and

adolescence). Thus, as with intake of

dietary calcium, physical activity levels

need to be maintained for optimal bone

health to be achieved.

• Fourth, the effect of physical activity on

bone appears to be greater in those who

are less active than in those who are already

active, e.g., bone gains will be greater in a

sedentary person who becomes physically

active than in an active person who

increases his or her level of physical activity.

More specific evidence supporting these

points is presented on the following pages.
126 Chapter 6

A Report of the Surgeon General

Children and Adolescents. As noted earlier,

physical activity appears to increase the positive

effects of calcium. A randomized trial of physical

activity with or without supplemental calcium

in young children (3–5 years old) indicated that

calcium intake can modify the bones’ response

to physical activity (Specker and Binkley 2003).

In this study, bone mineral density was not the

most sensitive indicator of physical activity

effects on bone; rather it was primarily the shape

and size of bone that was being affected. The

combination of both increased activity and 1,000

mg of supplemental calcium increased the width

of the cortical bone and the entire diameter of

the bone in the leg more than did exercise alone.

Both of these changes suggest greater bone

strength, and they are particularly important if

they represent permanent differences. The study

results also suggest that high calcium is necessary

to realize the full potential benefits of physical

activity on the bone of children. A different

study of tennis players found that loading

exercises before puberty increased bone size and

bone’s resistance to bending (Bass et al. 2002).

The pubertal phase of adolescence is a

particularly valuable time to improve bone mass

via physical activity. As noted previously, the

period of puberty represents a 2- to 3-year

window when, on average, 25–30 percent of total

body adult bone mass is gained (Bailey et al.

2000). During this period, bone may be

especially responsive to activity-induced loading

(MacKelvie et al. 2002). Hormone levels may

also influence the amount of bone gained during

this period. In a trial with prepubertal and early

pubertal girls, greater gains in bone mass with

physical activity were seen in the girls in early

puberty, possibly because of their increasing

estrogen levels (MacKelvie et al. 2001).

A study conducted in Finland provided even

more evidence of the benefits of physical activity

during puberty. This study compared the bone

mineral content of the playing arm of adult

woman tennis and squash players with their nondominant arm. In other words, each woman in

the study served as her own control (Kannus et

al. 1995). Most people have about a 3–5 percent

difference in their dominant and non-dominant

arm, which reflects greater use of the dominant

arm in everyday life. In the racquet players, the

difference in bone content between the two arms

was much greater (12–16 percent), due to their

training regimen. But the difference was twofold

greater when the comparison was restricted to

women who began training before puberty

versus those who took up the sport later (Figure

6-6). This observation underscores the

importance of the timing of physical activity and

supports the concept that there is a “window of

opportunity” during childhood and adolescence

for building bone (Khan et al. 2000).

Exercise-intervention studies in girls (Morris

et al. 1997) suggest that relatively short periods

of appropriate exercise can stimulate bone gain

at trabecular bone sites (hip and spine). Jumping

activities appear to be particularly effective, and

the greatest gains occur in early or mid-puberty

(MacKelvie et al. 2003). High-intensity jumping

improves both hip and lumbar spine bone mass

and increases bone area in pre-pubertal children

(Fuchs et al. 2001). Moreover, the bone mass gains

at the hip that accrue from high-impact jumping

are retained for at least a short period of time (an

equivalent period of detraining) (Fuchs and Snow

2002). Thus, jumping from a moderate height

(roughly 20 inches is a safe, effective, and simple

method of improving bone mass and size in

children, and these activities could easily be

incorporated into physical education classes)

(Figure 6-7). What is not clear, however, is

whether or not early gains in bone mass and

geometry confer a long-lasting reduction in
Bone Health and Osteoporosis

Determinants of Bone Health 127

fracture rate. Although some evidence supports

a lasting beneficial effect of early sports training

and exercise on bone (Kontulainen et al. 2001,

Bass et al. 1998), this area remains controversial

and it may be that stopping exercise or reducing

its intensity over time may lessen its benefit in

old age (Seeman 2001). For example, Karlsson et

al. (2000) found little residual protection in soccer

players who had been retired for more than 20

years. So the benefits of physical activity in

reducing fracture risk, even if started in youth

when bone is most malleable, may be attenuated

if an individual becomes sedentary later in life.

Adults. Because adulthood is a time of bone

conservation—not bone building—the primary

impact of physical activity is to maintain bone mass
128 Chapter 6

A Report of the Surgeon General

during this stage. While it is not possible to assign a

specific age range to this period of bone

maintenance, it would optimally last from the end

of puberty until age- or menopause-related bone

loss begins. Very little research has focused on the

impact of physical activity on bone mass in this age

range. However, several reviews and meta-analyses

have included pre-menopausal women (Wolff et

al. 1999, Wallace and Cumming 2000, Kelley

et al 2001) and they have generally found a

modest but consistent positive effect

(approximately 1 percent) from exercise on BMD;

a similar effect was found in postmenopausal

women. The effect is more clear at the spine than

the hip, and no optimal types of exercise could be

discerned from these analyses.
Bone Health and Osteoporosis

Determinants of Bone Health 129

persons, because it delays the onset of functional

limitations and loss of independence that are

common in this population, especially those over

age 75 (Singh 2002). Thus, the substantial

reduction in physical activity that is typically

seen in individuals as they get older (which was

documented earlier in this chapter) represents

another important threat to bone health.

Maintaining, or preferably increasing, customary

physical activity can mitigate some of the

musculoskeletal problems of aging and can also

provide many other health benefits. Although

physical activity must be maintained to preserve

bone mass in this age group, the biomechanical

strains from enhanced physical activity may

promote increases in bone size that can help

preserve bone strength even in the face of bone

loss (Kaptoge et al. 2003). This protective

expansion of bone area is more pronounced in

men, possibly because of their higher

testosterone levels.

One of the biggest bone-related problems

facing the frail elderly relates to the loss of muscle

strength and function (Doherty 2003).

Sarcopenia is the involuntary loss of skeletal

muscle mass and function that occurs as people

age. On average, 5 percent of muscle mass is lost

per decade after age 30 and this loss may

accelerate after age 65. This muscle loss results

in impaired functional performance and

increased risk for falls. It is unclear whether the

age-related decrease in muscle size and strength

is related to the age-related decrease in BMD, or

whether both contribute to increased fracture

risk independently.

The mechanisms that underlie sarcopenia are

just beginning to be understood. As people age,

their ability to synthesize certain proteins

decreases in comparison to their ability to break

down protein. This leads to loss of type II, or

fast-twitch, muscle fibers. Several other ageThe Cochrane Collaboration has reviewed the

trials of exercise for preventing or treating

osteoporosis in postmenopausal women

specifically (Bonaiuti et al, 2002). These analyses

indicated that aerobic, weight-bearing, and

resistance exercises were all effective in increasing

BMD at the spine, while walking (as an exercise

intervention) was effective in increasing BMD at

both the hip and spine.

As alluded to earlier, there is a synergistic

effect between physical activity and calcium

intake. A meta-analysis of 17 randomized and

nonrandomized intervention trials in peri- and

postmenopausal women suggests that physical

activity is more beneficial in increasing BMD in

individuals with high calcium intakes (1,000 mg

per day) than in those with lower calcium intakes

(Specker 1996). Not all of the studies, however,

reported on the calcium intake of participants.

In postmenopausal women, physical activity

programs also serve the all-important role of

maintaining bone mass. Maintaining bone at a

time when bone loss typically increases provides

important benefits for the skeleton. Although

results may vary, studies suggest that high-impact

loading such as jumping, strength-training

exercises, or a combination of these can slightly

increase or conserve spine bone mass in healthy

postmenopausal women and also has a positive

effect at the hip (Bassey and Ramsdale 1994, Kohrt

et al 1995, Going et al 2003).

One of the few studies to date that included

men over age 60 showed significant increases in

bone mass among exercisers after 4–8 months

(Blumenthal et al 1991). These results are consistent

with those found for adult women. In addition,

one meta-analysis found that site-specific exercise

may help to improve and maintain BMD in men

over age 30 (Kelley et al, 2000).

Older Adults (Frailty). Regular physical

activity is particularly important for frail older
130 Chapter 6

A Report of the Surgeon General

related changes are also thought to contribute to

sarcopenia, including declines in: a) enzyme

activity in the muscle cell mitochondria; b)

hormones important in muscle turnover, such

as testosterone and growth hormone; and c)

muscle blood flow and nerve function

(Greenlund and Nair 2003). Sarcopenia occurs

in all individuals to some degree as they age, but

it can be accelerated by a variety of factors,

including chronic illness, inactivity, and poor

nutrition, especially inadequate protein and

caloric intake. Although physical activity cannot

completely reverse the effects of aging, it can

increase mitochondrial enzyme activity. Musclestrengthening exercises and activities appear to

improve strength and performance even in frail

nursing home residents (Morris et al.1999). Thus

it appears that physical activity and muscle

strengthening may be useful for treating or

preventing sarcopenia.

The response of elderly individuals’ muscles

to physical activity may have greater significance

to bone health than does the response of BMD.

Muscle strengthening reduces the risk of fractures

by improving balance, mobility, and speed of

movement, each of which helps to prevent or

reduce the severity of falls. In fact, muscle strength

seems highly adaptable to physical activity in the

elderly, with increases of over 100 percent being

reported in men in their 80s and 90s who exercise

(Fiatarone et al. 1990). This increase is far greater

than the corresponding increase in muscle volume

and BMD. A training program for 21 men over

60 resulted in a 39 percent increase in upper body

and a 38 percent increase in lower body strength,

as well as a 3 percent increase in femoral neck

BMD (Ryan et al. 1994). Generally, strength,

flexibility, balance, and reaction time—the factors

most amenable to modification—can be addressed

in exercise intervention programs to prevent falls

in the elderly (Lord et al. 2002). Several large

studies have reported that exercise leads to 10

percent fewer falls, while balance training leads

to 17 percent fewer falls (Province et al. 1995). In

a series of key studies, lower limb strength and

balance exercises reduced the rate of falls among

women age 80 and older (Robertson et al. 2002).

Weight

Maintaining a healthy body weight is one of

the goals of Healthy People 2010 (USDHHS

2000). Although overweight and obesity are the

focus of most health campaigns that focus on

weight, low body weight can be a problem for

bone health. A higher body weight may

influence BMD through a variety of

mechanisms, including higher mechanical

loading, more muscle mass, higher levels of sex

hormones and their precursors, and lower bone

turnover (Nelson et al. 2002). Body weight may

also be related to the level of fat padding, which

can provide a cushion during a fall on the hip.

Body weight and pubertal development are

the most consistent predictors of bone mass in

adolescents (Bachrach 2001, Heaney et al. 2000).

Fear of fat and obsession with thinness among

pre-teen and teenage girls frequently translates

into diets that fail to meet their caloric, calcium,

and protein needs. Young women who

repeatedly diet to lose weight also have lower

Weight: What the Evidence Tells Us

• Very low body weight in children and

adolescents may limit peak bone mass.

• Low body weight increases the risk of hip

fracture in older women.

• Weight loss of 10 percent or more in older

women also increases the risk of hip

fracture.
Bone Health and Osteoporosis

Determinants of Bone Health 131

bone density, even if they are not underweight

(Van Loan and Keim 2000).

Both low body weight and weight loss have

been associated with reductions in bone mass

and increases in fracture risk in epidemiologic

studies. In a follow-up to the first NHANES,

women who were relatively thin in middle age

(age 50-64) and had lost at least 10 percent of

their body weight had the highest risk of hip

fracture (Langlois et al. 2001). Although body

weight is very strongly associated with BMD

(Reid 2002), the relationship of body weight to

bone mass is confounded by the fact that smaller

people tend to have smaller bones and lower

bone mass. Nevertheless, they can have a

perfectly adequate skeleton.

Low body weight and weight loss are a

particular problem for the elderly, as they may

signal a variety of medical problems. Older

women who are thin have a higher risk of hip

fracture (Farmer et al. 1989, Kiel et al. 1987).

Although “thin” has been defined variably in

different studies and may be open to clinical

interpretation, a large prospective study of older

women found a roughly twofold increased risk

of hip fracture in women who were below 127

pounds (Ensrud et al. 1997). This study also

found no protective effect from increasing

weight in these thin women. The increased risk

was entirely attributable to hip bone density,

which has led to the suggestion that low body

weight be used as a surrogate for increased

fracture risk when bone density measurements

are unavailable. As discussed in Chapters 8 and

10, weight is used in some assessment

instruments as an aid in deciding whether BMD

testing is necessary.

Older women who experience weight loss in

later years have also been found to have a twofold greater risk of subsequent hip fracture, irrespective of current weight or intention to lose

weight. These findings indicate that even voluntary weight loss in overweight elderly women increases hip fracture risk (Ensrud et al. 2003).

Whether being overweight reduces

fracture risk is less clear. Some older studies

have reported a lower risk of fracture in

overweight women (Farmer et al. 1989), but

a more recent study reported that women of

average weight had a risk of hip fracture that

was similar to that of heavier women (Ensrud

et al. 1997). Of course, being overweight

raises the risk of many other health problems,

including heart disease and diabetes. The

epidemic of overweight and obesity in the

United States is well documented (Flegal et

al. 2002). As a result, public health efforts

should continue to focus on weight reduction

in overweight or obese individuals and

maintenance of body weight in normal

weight individuals, especially at older ages.

For overweight individuals, achieving weight

loss while maintaining skeletal integrity is the

goal. The key may be to increase physical

activity in addition to restricting caloric

intake. For example, Salamone (1999) found

that women who lost weight did lose more

bone than weight-stable women, but this

bone loss was lessened among those who

increased their physical activity. Consuming

adequate calcium during weight loss may also

help prevent bone loss, at least in

postmenopausal women (Ricci et al. 1998). If

these results are confirmed in other studies,

weight loss recommendations should include

physical activity, preferably weight bearing,

and adequate calcium to help protect the

skeleton.

Finally, the relationship between weight

and weight loss, bone density, and fracture risk

in men has not been thoroughly addressed.
132 Chapter 6

A Report of the Surgeon General

Falls and Fall Prevention

Background: Why Focus on Falls?

Falls contribute to fractures, and thus fall

prevention offers another opportunity to protect the

bones throughout life, particularly in those over age

60. While low bone mass may put an individual at

high risk of fracture, it is often a fall that precipitates

the injury. Falls are one of the most common

problems that threaten the independence of older

individuals. About 10–15 percent of falls in the

elderly result in fracture (Nevitt et al. 1991), and

some may result in death. The risk of falling increases

with age and varies according to living status. One

study found that between 30–40 percent of those

over age 65 who live in the community fall each

year (Tinetti et al. 1988). The rate of falls is even

greater in long-term care settings, as the general

health of these individuals is more fragile (Thapa et

al. 1996). An elderly individual’s level of social

integration—that is, the degree to which he or she

has developed and maintained networks of family

members and friends, also has an impact on falls.

Those with stronger networks have a lower risk

of falling (Faulkner 2003). A history of falling is

also an important predictor of future falls, as

almost 60 percent of those who fell during the

previous year will fall again (Nevitt et al. 1991).

Falls in older individuals are rarely due to a single

cause. They usually result when a threat to the

normal mechanisms that maintain posture occurs

in someone who already has problems with balance,

mobility, sensory changes and lower extremity

weakness, and/or blood pressure or circulation.

The new threat may involve an acute illness

(e.g., infection, fever, dehydration, arrhythmia),

or an environmental stress (e.g., taking a new

drug or walking on an unsafe surface). Since

they may already have several health problems

as a result of aging or chronic disease, many

elderly people cannot compensate for the

additional burden posed by the new threat.

Falls and Bone Health: What the

Evidence Tells Us

• Falls contribute to most fractures.

• There are a number of identifiable risk

factors for falls in the elderly.

• Interventions targeted at multiple risk

factors can reduce the number of falls and

possible the number of fractures as well.

Risk Factors for Falls

• Age

• Arthritis

• Depression

• Fall in blood pressure upon standing (i.e.,

orthostasis)

• Poor cognition

• Poor vision, gait, or balance

• Need for home health care

• Use of four or more medications

(Tinetti 2003)

Some Facts About the Prevalence of Falls

• One third of people over age 65 fall each

year, with half of those falls being

recurrent (i.e., the individual has fallen

before).

• One in 10 falls results in a serious injury,

such as a hip fracture. In fact, 90 percent of

hip fractures result from falls.

• Falls account for 10 percent of visits to

emergency room visits and 6 percent of

urgent hospitalizations in the elderly.

• The risk of falling varies tremendously

depending upon an individual’s risk

factors. An elderly person with no risk

factors has only a 10 percent chance of

falling each year, compared to an 80

percent likelihood of falling for a person

with four or more risk factors.

(Tinetti 2003)
Bone Health and Osteoporosis

Determinants of Bone Health 133

Falls and Fall Prevention: A Review of the

Evidence

Many well-designed studies of risk factors for

falls have been published over the several decades

(Tinetti et al. 1988, Nevitt et al. 1991). These

studies show that the more risk factors an

individual has, the more likely he or she is to fall

(Tinetti et al. 1988, Nevitt et al. 1991). As noted

previously, one of the most important risk factors

for falls is a previous history of falls. Other risk

factors included age, being female, Alzheimer’s

disease or other types of cognitive impairment,

weakness in the legs and feet, balance problems,

use of drugs for depression and psychosis, and

arthritis. Being hospitalized also increased risk of

falling among those who already had other risk

factors. Age-related declines in vision, balance and

coordination, inner ear function, muscle amount

and responsiveness, blood pressure regulation,

and problems with staying hydrated also can lead

to falls. Finally, those requiring bi- or tri-focal

glasses are also at increased risk of falls and hip

fractures (Lord et al. 2002, Felson et al. 1989).

Medication use is one of the most modifiable

risk factors for falls. Drugs that affect the central

nervous system (CNS) frequently have been

linked to risk of falling. Examples of these drugs

include neuroleptic drugs (used to treat psychotic

behavior), benzodiazepines (used to treat

anxiety), and tricyclic or serotonin reuptake

inhibitors (used to treat depression) (Ensrud et

al. 2002). Drugs to control blood pressure may

also increase the risk of falling (Mukai and Lipsitz

2002). In addition to these specific drug classes,

recent changes in the dose of a medication and

the total number of prescriptions appear to be

associated with an increased risk of falling

(Cumming et al. 1991). Attention by physicians

to the potential effects of medications on falls in

the elderly may lead to some modification of

therapy (e.g., changes in dose or timing of use)

and/or to enhanced fall prevention activities.

Environmental factors, such as poor lighting

or loose rugs, may also increase the risk of falling.

Most well-designed studies on methods to

prevent falls combine efforts to improve the

individual’s health-related risks with efforts to

remove environmental hazards, making it

difficult to separate out the unique contribution

of either set of factors (Tinetti et al. 1994). One

study, for example, investigated the usefulness

of having an experienced occupational therapist

visit the home to assess and help modify potential

environmental hazards (Cumming et al. 1999).

The visits reduced the risk of falling by 36

percent in high-risk patients (e.g., those who fell

one or more times in the previous year).

However, the therapist’s visit may have also

prompted behavior changes in these patients that

lowered their falling risk.

A different study examined the role of hazard

reduction more directly. In that study, people

age 70 and older were randomly assigned either

to a group that received a home hazard

assessment, information on hazard reduction,

and installation of safety devices, or to a control

group that did not receive these things (Stevens

et al. 2001a and b). A research nurse visited the

homes of people in both groups once. At the end

of the study, there were fewer hazards in the

homes of the group that received the information

and safety devices than in the control group, but

the number of falls did not differ between the

two groups (Stevens et al. 2001a and b).

Fall prevention in the hospital and nursing

home settings are also important. In hospital

settings, bed rails do not appear to change the

total number of falls, although they can decrease

the number of serious falls (Hanger et al. 1999).

Several studies to identify effective ways to

reduce falling risk have been conducted over the

past decade. The approaches studied include

programs to improve strength or balance,

educational programs, optimization of

medications, and environmental modifications.
134 Chapter 6

A Report of the Surgeon General

Some approaches have targeted a single risk

factor, while others have focused on modifying

several factors simultaneously. The latter have

been more successful, since falls are generally

caused by more than one risk factor (Gillespie

et al. 2001). Specific approaches that have

demonstrated benefit included: a) muscle

strengthening and balance retraining; b)

professional home hazard assessment and

modification; and c) stopping or reducing

psychotropic medication (Tinetti et al. 1994,

Tinetti 2003). The optimal duration or intensity

of these approaches has not been defined. As

noted earlier in this chapter, vitamin D

deficiency is associated with an increased risk of

falls and hence the use of vitamin D

supplementation to reduce falls may be

promising (Bischoff et al. 2003, Bischoff-Ferrari

et al. 2004, Dukas 2004).

Finally, a complementary approach to

reducing fractures due to falls is to attempt to

minimize the impact of those falls that do occur

through use of a hip protector or hip pad that helps

to “cushion the blow” from a fall, as shown in

Figure 6-8. A recently updated systematic review

of the efficacy of hip protectors concluded that hip

protectors reduce the risk of hip fracture for elderly

individuals who live in nursing homes and

residential care facilities, as well as those in

supported living at home; the generalization of the

results beyond this high risk population is unknown

(Parker 2003). One of the larger studies (Kannus

2000) included in this systematic review found that

41 patients would need to be offered treatment with

a hip protector to prevent one hip fracture over the

course of one year, a finding that suggests that hip

protectors may be a reasonable and cost-effective

option for patients at high risk of falls.
Bone Health and Osteoporosis

Determinants of Bone Health 135

While hip protectors appear to be effective

when used, the biggest problem may relate to

getting people to wear them. A recent

randomized controlled trial among women over

age 70 living in the community found that hip

protectors offered no significant reduction in the

risk of hip fracture (Birks et al. 2004). But

compliance rates were quite low (roughly 30

percent). This study, the Kannus study

described above, and others have documented

low rates of compliance (i.e., those who have hip

protectors do not wear them), suggesting the

need to develop more acceptable, easy-to-use

devices that can protect fragile bones by

absorbing some of the energy of falls. The

policies of nursing homes and other residential

care facilities might also influence usage rates.

While hip protectors may be relatively

inexpensive, the decision to use them for

residents of these facilities may be influenced

by the cost and how much staff time is required

in helping residents to put them on and take them

off. But a recent economic analysis of ambulatory

nursing facility residents demonstrated that hip

protectors save money and are economically

attractive over a wide range of cost and utility

assumptions (Colon-Emeric 2003).

The Bottom Line on Fall Prevention

The approaches summarized above have

modestly reduced the frequency and/or impact

of falling. When combined with strategies to

improve underlying bone strength, they can

likely decrease fracture risk. In fact, based on a

review of the evidence, the USPSTF

recommends counseling elderly patients on

specific measures to prevent falls. The USPSTF

also recommends that more intensive

individualized multi-factorial interventions be

implemented for high-risk elderly patients in

settings where adequate resources to deliver such

services are available (USPSTF 1996).

Reproductive Factors

Reproductive hormones play a central role

in BMD levels among both women and men,

but these hormones have been most widely

evaluated in young to middle-aged women,

particularly with respect to pregnancy, lactation,

and contraception.

Pregnancy and Lactation

Several changes occur during pregnancy and

lactation that can affect bone mass, including

changes in reproductive hormones and in

hormones that affect calcium metabolism. Since

fetal and infant bone growth during pregnancy

and lactation depends on calcium transfer from

the mother, the possibility that pregnancy and

lactation affect risk for osteoporosis later in life

has been investigated. Intestinal calcium

absorption increases during pregnancy to meet

much of the fetal calcium needs, but maternal

bone loss may occur in the last months of

pregnancy (Reed et al. 2003). The mother’s

skeleton also loses bone during breastfeeding,

but this loss is largely restored during weaning,

Reproductive Factors and Bone Health:

What the Evidence Tells Us

• Pregnancy and lactation generally do not

harm the skeleton of healthy adult

women.

• Amenorrhea (cessation of menstrual

periods) is linked to low bone mass.

• Bilateral oophorectomy (removal of both

ovaries) is linked to increased bone loss

and fracture risk.

• The effects of oral contraceptives on bone

health may differ depending on type, and

have not been clearly established.
136 Chapter 6

A Report of the Surgeon General

as ovulation and menses is re-established. This

bone loss and its subsequent restoration appear

to be independent of lifestyle behaviors,

including dietary calcium intake and physical

activity patterns (Kalkwarf and Specker 2002).

Epidemiologic studies indicate that neither

extended lactation nor multiple pregnancies are

associated with subsequent osteoporosis,

whether measured by BMD levels (Karlsson et

al. 2001, Paton et al. 2003) or by assessment of

fracture risk. In fact, the risk of hip fracture in

women has been found to decrease by 5–10

percent with each additional child, and there is

no apparent association between the duration of

lactation and fracture risk (Michaelsson et al.

2001). Thus, in general, pregnancy and lactation

in healthy adult women do not appear to cause

lasting harm to the skeleton. For example, in one

recent study, women with more than 10

pregnancies and extended lactation had BMD

levels similar to those in women who have not

been pregnant (Henderson et al. 2000). Having

more children also does not appear to increase

fracture risk (Cumming and Klineberg 1993).

For pregnant teens who have not yet reached

peak bone mass, the 30 g of calcium required for

the fetal skeleton competes with the demands of

calcium for the teen’s mineral accrual. Whether

peak bone mass is compromised in women who

experience teen pregnancies remains

controversial (Lloyd et al. 2002).

Menstrual Cycling

Regular menstrual cycles are the outward

vital sign of a normally functioning reproductive

system in the premenopausal female. The impact

on bone health of irregular cycles or subtle

hormonal changes during the menstrual cycle

has not been clearly established. However,

amenorrhea, or the cessation of menstrual

periods, should be viewed with concern, and its

cause should be investigated. Primary

amenorrhea may be due to a variety of endocrine

abnormalities, but the cessation of regular

cycling can also be due to an imbalance of energy

intake (nutrition) and energy expenditure

(exercise). Anorexia nervosa is the most serious

cause of secondary amenorrhea and the most

difficult to treat. The onset of anorexia nervosa

frequently occurs during adolescence when

maximal bone mineral accrual takes place,

thereby making adolescent girls with anorexia

nervosa at high risk for reduced peak bone mass

(Soyka et al. 2002).

Female athletes may also experience

amenorrhea, especially those participating in

sports where leanness is an advantage and very

strenuous training is the norm (e.g., cross

country running, ballet). While some athletes

experience amenorrhea due to disordered eating

patterns, others experience it because of

chronically inadequate caloric intake that does

not compensate for the energy expended.

Complications associated with amenorrhea

include compromised bone density, failure to

attain peak bone mass in adolescence, and

increased risk of stress fractures. The most

effective treatment is to decrease the intensity

of the exercise and increase the nutritional intake

(Warren 2003). Adolescent and young adult

women who experience amenorrhea lasting for

more than 3 months (regardless of the cause)

should consult their health care provider.

Contraceptive Practices

Oral contraceptives were first marketed in

the United States in 1960, gaining immediate

and widespread use. It is estimated that 80

percent of American women born since 1945

have used birth control pills at some point in

their lives. About 45 percent of the estimated

24 million women who report using reversible

methods of birth control use oral contraceptives

(Piccinino et al. 1998). Use is highest in women

under age 30, who are also completing bone

mass accrual.
Bone Health and Osteoporosis

Determinants of Bone Health 137

Oral contraceptives contain variable amounts

of the hormones estrogen and progesterone.

Given the known impact of these hormones on

bone, it is natural to ask what effect oral

contraceptives have on bone mass and density.

The factors that determine the effect of an oral

contraceptive on bone health are the dose of

estrogen and the age of the woman. The

formulations of oral contraceptives have changed

dramatically over the years, with older types

having higher estrogen levels than do newer ones.

These different formulations have a different

overall impact on total estrogen exposure and

ultimately on fracture risk. Both the short- and

long-term effects of oral contraceptives on bone

health are unclear at this time (Reed et al. 2003).

There may be may relatively little impact on bone

health from oral contraceptives in women who

have already achieved peak bone mass, but lowdose oral contraceptives could potentially

compromise the acquisition of bone in younger

women (Cromer 2003).

Hysterectomy and Oophorectomy

Roughly 600,000 hysterectomies are

performed annually in the United States, and

55 percent of women undergoing this procedure

also have both ovaries removed (Keshavarz et

al. 2002). Removing the ovaries (oophorectomy)

affects calcium metabolism, fracture risk, and

bone mineral content because it results in

estrogen deficiency.

Bilateral oophorectomy in postmenopausal

women results in a 54 percent increase in

fractures of the hip, spine, and wrist, and a 35

percent increase in fractures at other sites. The

increase in fracture risk among women who

underwent bilateral oophorectomy after natural

menopause is consistent with the hypothesis that

androgens produced by the postmenopausal

ovary may be important for endogenous estrogen

production that protects against fractures

(Melton et al. 2003).

Medical Conditions and Drugs

Many individuals have medical conditions or

take medications that can affect bone health.

Chapter 3 contains two tables with a reasonably

complete list of these drugs and diseases. This

section will discuss the more common

prescription drugs and medical conditions that

affect bone health. These medical situations,

which are known as secondary causes of

osteoporosis (Schneider and Shane 2001), should

act as a “red flag” to individuals and health care

professionals about bone health. A person who

has one of these conditions or takes one of these

drugs should speak to his or her health care

provider about safeguarding bone health.

Children who must take one or more of these

prescription drugs or who have one of these

medical conditions may not accumulate as much

bone as they should during adolescence and thus

may enter adulthood with abnormally low

BMD. Adults who develop one of these diseases

or begin taking one or more of these prescription

drugs may experience even larger or more rapid

bone loss than they would normally have during

menopause and aging. In most cases, therefore,

measurement of bone density will be necessary

to determine whether there has been excessive

bone loss.

Medications that can affect skeletal health

include the following:

Corticosteroids are a class of drugs that

reduce inflammation and suppress the body’s

Medical Conditions and Drugs: What the

Evidence Tells Us

• Several medical conditions and

prescription medications can affect bone

health through various mechanisms. A

detailed list of conditions and

medications is shown in Chapter 3 and

further described below.
138 Chapter 6

A Report of the Surgeon General

immune response. They are called by a number

of different names, including cortisone,

glucocorticoids, prednisone, prednisolone,

steroids, and ACTH. Corticosteroids may be

inhaled, taken by mouth, given through the

veins, or rubbed on the skin. They are used most

commonly to treat lung diseases (emphysema,

asthma, cystic fibrosis, sarcoidosis), diseases of

the joints (lupus, rheumatoid arthritis,

polymyalgia rheumatica), gastrointestinal tract

diseases (ulcerative colitis, Crohn’s disease),

kidney diseases (glomerulonephritis), and certain

skin diseases (psoriasis, eczema). Corticosteroids

are the most common cause of secondary

osteoporosis. They have powerful effects on

bone (Saag 2002). For example, doses of

prednisone (a corticosteroid) above 7.5 mg per

day have been shown to completely shut off

formation of new bone, while the loss of older

bone continues at a faster rate than normal. As a

result, bone is lost very rapidly, particularly

during the first year or so after beginning

corticosteroids. As shown in Figure 3-4 in

Chapter 3, even very small doses may increase

risk of spine fractures (van Staa et al. 2000, Kanis

et al. 2004a). The risk of fracture increases

rapidly after the start of oral corticosteroid

therapy (within 3 to 6 months) and decreases

after stopping therapy. This increase in risk is

independent of underlying disease, age, and

gender (van Staa et al. 2002).

Elevated thyroid hormone is associated with

secondary osteoporosis (Ross 1994). High levels

of thyroid hormone can be the consequence of

endogenous conditions such as Grave’s disease

or thyrotoxicosis (an overly active thyroid gland

that produces too much of this hormone).

However, prolonged, elevated levels are much

more likely to be the result of prescribing thyroid

hormone as a drug to treat an underactive or

enlarged thyroid gland or to control growth of

nodules in the thyroid gland. Too much thyroid

hormone, no matter what the source, increases

both the breakdown of old bone and the

formation of new bone to take its place.

However, more bone is lost than is formed.

People with abnormally high levels of thyroid

hormone are at increased risk for fracture, and

the fractures often occur at younger ages.

Postmenopausal women are probably at greater

risk than premenopausal women or men, but all

patients with a history of an overactive thyroid

gland or those who must take thyroid hormone

for any reason should have bone density testing.

The lowest possible dose of thyroid hormone

that corrects the medical problem being

addressed should be used, since the effects on

bone are related to the dose.

Gonadotrophin-releasing hormone agonists

are drugs that lower the blood levels of male and

female sex hormones (testosterone, estrogen).

They may be referred to as GnRH agonists or

hormone deprivation therapy. In men, these

drugs are used to treat prostate cancer. In

premenopausal women, they may be used to

treat endometriosis or as a form of contraception.

Hormone deprivation therapy causes levels of

bone loss that are similar to that seen in women

after menopause. Both men and premenopausal

women undergoing this therapy have lowerthan-expected BMD, while fracture rates are

higher in men with prostate cancer who have

undergone this treatment (Smith 2003).

Antiseizure or anticonvulsant medications,

particularly diphenylhydantoin, phenobarbital,

carbamazepine, and sodium valproate, can cause

bone loss (Schneider and Shane 2001, Ensrud et

al. 2004). The effect on bone health differs

depending on the specific drug prescribed, and

the mechanisms by which the drug affects bone

are not fully understood. Effects on vitamin D

metabolism and on bone or the parathyroid

glands have been implicated (Fitzpatrick 2004).

Individuals who take these drugs are more likely

to have bone disease if they: a) have been on the

drugs for years; b) require high doses and/or
Bone Health and Osteoporosis

Determinants of Bone Health 139

diseases (celiac disease, intestinal

malabsorption, primary biliary cirrhosis,

Crohn’s disease), blood disorders

(hereditary anemias, multiple myeloma,

leukemia), rheumatoid arthritis, lupus,

and depression. Anyone with these

conditions should consult with a

physician about bone health and

potential preventive measures.

Smoking, Alcohol, and Environmental

Threats to Bone Health

Smoking

Smoking may harm the skeleton both

directly and indirectly (USDHHS 2004). The

nicotine and cadmium found in cigarettes can

have a direct toxic effect on bone cells (Riebel et

al. 1995, Fang et al. 1991). Smoking may also

harm bone indirectly by lowering the amount

of calcium absorbed from the intestine, altering

the body’s handling of vitamin D and various

hormones needed for bone health, or lowering

body weight (Michnovicz et al. 1986, Baron et

al. 1995, Krall and Dawson-Hughes 1999, Brot

more than one anticonvulsant; c) avoid dairy

products and do not take multivitamins and thus

have low dietary intake of vitamin D; d) have

chronic illnesses; and e) are institutionalized and

thus get little sunlight. However, all patients

taking these drugs should be evaluated for

osteoporosis and vitamin D deficiency.

Medical conditions or events that should

prompt a discussion of bone health fall into three

major categories:

1. Warning signs that osteoporosis may

already be present include any fracture

that occurs during adulthood, loss of

height, and the development of

osteoporosis in another family member,

such as a parent, sibling, or child.

2. The development of any disorder that

increases the risk of falling is an important

risk factor to consider. For example, an

individual who has had a stroke that affects

the ability to walk or causes difficulty with

balance might be expected to fall more

often and thus be at increased risk of

fracture. Other diseases that fall into this

category include Parkinson’s disease, spinal

cord injuries, any disorder that causes

muscle weakness, and the onset of frailty

in the elderly. Similarly, it is important for

individuals who are beginning to take

medications that increase the risk of falling

(tranquilizers, sleeping pills, diuretics, and

certain blood pressure pills) to discuss this

risk with their health care providers.

3. Many medical conditions can result in low

bone mass. The most common are genetic

diseases (cystic fibrosis, muscular

dystrophy), diseases that lower estrogen

levels before menopause (eating disorders,

excessive physical activity, ovarian failure

of any cause), endocrine disorders

(diabetes, hyperparathyroidism,

Cushing’s syndrome), gastrointestinal

Smoking, Alcohol, and Environmental

Threats: What the Evidence Tells Us

• Smoking is associated with reduced

bone mass and increased fracture risk.

• Alcohol may have both harmful and

beneficial effects on bone.

~ Heavy alcohol consumption is

associated with reduced bone mass

and increased fracture risk

~ Moderate alcohol use has been

associated with higher bone density

in some studies.

• Lead is among the most significant

environmental threats to bone health in

the United States.
140 Chapter 6

A Report of the Surgeon General

et al. 1999). Smokers may also be less physically

active. Smoking influences estrogen metabolism

and the risk for multiple estrogen-sensitive

outcomes. Smokers are likely to require higher

doses of hormone therapy to achieve clinical

effects on bone density that are comparable to

those observed in nonsmokers (Tansavatdi et al.

2004). All of these factors can lead to lower bone

density and higher risk of fracture (Cummings

et al. 1995, Baron et al. 2001).

Several studies have linked smoking to

higher fracture risk. A meta-analysis of data from

postmenopausal women (Law and Hackshaw

1997) demonstrates that smoking increases the

risk of hip fracture. More recent data on the

association between smoking and fractures at

other skeletal sites, while more limited, also

support a relationship between smoking and

fracture risk (Honkanen et al. 1998, Jacqmin et

al. 1998). A recent meta-analysis, using data from

10 different observational studies from around

the world, found that smoking was associated

with an increased risk of hip and other fractures

in both men and women (Kanis et al. 2004b).

Although the lower BMD and BMI of smokers

were found to contribute to the increased risk of

fracture, these factors did not completely explain

the increased risk. After adjustment for BMD,

BMI, and age, the risk of hip fracture was 55

percent higher in smokers than in non-smokers.

In addition to current smoking, a history of

smoking was also associated with a higher risk

of fracture, although the risk for former smokers

was not as high as for current smokers.

Alcohol

Alcoholism is known to have negative effects

on bone (Scharpira 1990), but moderate alcohol

use in women has been associated with higher

bone density in some studies (Felson et al. 1995,

Sampson 2002). This apparent beneficial effect

of moderate alcohol intake may be seen in

women and not men because of the effect of

alcohol on adrenal androgens or estrogen (Wild

et al. 1987). Alcohol inhibits bone remodeling,

possibly by affecting vitamin D or by reducing

bone formation (Laitinen et al. 1991). It may also

increase calcium and magnesium losses from the

body. Although some studies suggest moderate

alcohol intake increases bone density, it does not

seem to lower fracture risk (Cummings et al.

1995, Hoidrup et al. 1999), and high alcohol

intake may increase likelihood of fracture (Grisso

et al. 1994). It is conceivable that the higher

fracture risk is caused by an increased risk of

falling or other types of trauma.

Environmental Threats to Bone

While a number of heavy metals can be

detrimental to bone health, lead is among the

most significant environmental threats to bone

health in the United States Lead may accumulate

in bone due to environmental or dietary

exposures. Periods of high remodeling

(pregnancy, lactation, postmenopausal period)

are particularly critical since lead can have both

a direct effect on bone and a latent effect on other

organ systems through release from bone long

after the initial exposure (Silbergeld and Flaws

2002, Gulson et al. 2003). High calcium intake

may actually blunt the effect of stored lead

release from bone in pregnant women

(Hernandez-Avila et al. 2003). One potential

dietary source of lead is calcium supplements.

Certain preparations of calcium (e.g., bone meal

and dolomite) can have significant contamination

with lead and other heavy metals. However,

most commercial calcium preparations are tested

to ensure that they do not contain significant

contamination of heavy metals (Optimal 1994).
Bone Health and Osteoporosis

Determinants of Bone Health 141

Key Questions for Future

Research

Much remains to be learned about the

genetic and environmental factors that affect

bone health, and, as discussed in Chapter 7, the

behavior changes that are necessary to promote

bone health throughout life. Some of the most

important research questions for Chapters 6 and

7 are listed below:

• What are the genetic factors involved in

regulating bone mass acquisition, bone loss,

and the response of bone to environmental

factors such as nutrients and loading?

• What are the optimal physical activity

programs to maximize peak bone mass

in children and adolescence and to minimize bone loss in adults?

• What is the potential for changes in the

acid/base balance in blood and extracellular fluid—either through dietary

manipulation or potassium supplementation—to influence bone and muscle

health? Over a long period of time, a

more acidic balance may create an environment in which the breakdown of

existing bone is favored over the formation of new bone.

• What are the optimal muscle loading regimens to prevent sarcopenia and bone loss

in the frail elderly?

• What can be done to imitate the effects of

exercise (i.e., “exercise mimetics”) in individuals who are paralyzed, chronically

immobile, traveling in space, or otherwise

not capable of engaging in loading activities that benefit bone health?

• What mechanisms and interventions can

preserve bone mass during weight loss?

• What is the relationship between weight

and weight loss, bone density, and fracture risk in men?

• What are the best ways to promote the

adoption of bone-healthy practices by

individuals?

• What are the best comprehensive fall prevention programs that can be easily

adopted by communities and individuals?

• What impact do different oral and injectable contraceptives have on bone health?

How does this impact vary by age?

• What interventions optimize bone health

in children and adolescents who need to

take glucocorticoids or other drugs that

can be harmful to bone?
142 Chapter 6

A Report of the Surgeon General

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content in premenopausal women aged 18-

45 y: A cross-sectional study. Am J Clin Nutr

2000 Sep;72(3):837-43.

van Staa T, Leufkens H, Abenhaim L, Zhang

B, Cooper C. Use of oral corticosteroids and

risk of fractures. J Bone Miner Res

2000;15(6): 993-1000.

van Staa TP, Leufkens HG, Cooper C. The

epidemiology of corticosteroid-induced

osteoporosis: A meta-analysis. Osteoporos

Int. 2002 Oct;13(10):777-87.

Wallace BA, Cumming RG. Systematic review

of randomized trials of the effect of exercise

on bone mass in pre- and postmenopausal

women. Calcif Tissue Int. 2000 Jul;67(1):10-8.

Warren MP. Health issues for women athletes:

Exercise-induced amenorrhea. J Clin

Endocrinol Metab 1999 Jun;84(6):1892-6.

Commentary.
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Warren MP, Goodman LR. Exercise-induced

endocrine pathologies. J Endocrinol Invest

2003 Sep;26(9):873-8.

Webb AR, Kline L, Holick MF. Influence of

season and latitude on the cutaneous

synthesis of vitamin D3: Exposure to winter

sunlight in Boston and Edmonton will not

promote vitamin D3 synthesis in human

skin. J Clin Endocrinol Metab. 1988

Aug;67(2):373-8.

Webb AR, Pilbeam C, Hanafin N, Holick MF.

An evaluation of the relative contributions

of exposure to sunlight and of diet to the

circulating concentrations of 25-

hydroxyvitamin D in an elderly nursing

home population in Boston. Am J Clin Nutr

1990;51(6):1075-81.

Welten DC, Kemper HC, Post GB, van

Staveren WA. A meta-analysis of the effect

of calcium intake on bone mass in young and

middle aged females and males. J Nutr 1995

Nov;125(11):2802-13.

Wild RA, Buchanan JR, Myers C, Demers LM.

Declining adrenal androgens: An association

with bone loss in aging women. Proc Soc Exp

Biol Med 1987 Dec;186(3):355–60.

Wolff I, van Croonenborg JJ, Kemper HC,

Kostense PJ, Twisk JW. The effect of

exercise training programs on bone mass: A

meta-analysis of published controlled trials

in pre- and postmenopausal women.

Osteoporos Int. 1999;9(1):1-12.

Wosje KS, Specker BL. Role of calcium in bone

health during childhood. Nutrition Rev 2000

Sep;58(9):253-68.

Wright JD, Wang CY, Kennedy-Stevenson J,

Ervin RB. Dietary intakes of ten key

nutrients for public health, United States:

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Yarbrough DE, Barrett-Connor E, Morton DJ.

Birth weight as a predictor of adult bone mass

in postmenopausal women: The Rancho Bernardo Study. Osteoporos Int 2000;11(7):626-30.

Zamora SA, Rizzoli R, Belli DC, Slosman DO,

Bonjour JP. Vitamin D supplementation

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158 Chapter 7

A Report of the Surgeon General

• There is much that individuals can do

to promote their own bone health,

beginning in childhood and continuing

into old age. These activities contribute

not only to bone health, but to overall

health and vitality.

• Since many nutrients are important for

bone health, it is important to eat a wellbalanced diet containing a variety of

foods, including grains, fruits and

vegetables, nonfat or low-fat dairy

products or other calcium-rich foods,

and meat or beans each day.

• Most Americans do not consume

recommended levels of calcium, but

reaching these levels is a feasible goal.

Approximately three 8-ounce glasses of

low-fat milk each day, combined with

the calcium from the rest of a normal

diet, is enough to meet the recommended

daily requirements for most individuals.

Foods fortified with calcium and calcium

supplements can assist those who do not

Chapter 7: Key Messages

consume an adequate amount of

calcium-rich foods.

• For many, especially elderly individuals,

getting enough vitamin D from

sunshine is not practical. These

individuals should look to boost their

vitamin D levels through diet. Vitamin

D is also available in supplements for

those unable to get enough through

sunshine and diet.

• In addition to meeting recommended

guidelines for physical activity (at least

30 minutes a day for adults and 60

minutes for children), specific strengthand weight-bearing activities are critical

to building and maintaining bone mass

throughout life.

• Individuals should see a health care

provider if they have a medical condition

or use medications that can affect the

skeleton. Women should also see their

health care provider if menstrual periods

stop for 3 months.
Bone Health and Osteoporosis

Lifestyle Approaches To Promote Bone Health 159

As the evidence presented in the previous

chapter makes clear, there is much that individuals can do to promote their own bone health

throughout life. This chapter outlines recommendations for diet, physical activity, and other

lifestyle practices that can help to achieve that

goal. Moreover, the activities and practices suggested in this chapter contribute not only to bone

health, but to overall health and vitality. In fact,

bone-specific recommendations fit well within

an overall program of good nutrition and physical activity that should be followed in order to

prevent the onset of many of the major chronic

diseases affecting Americans.

Nutrition

Since many nutrients are important for bone

health, it is important to eat a well-balanced diet

containing a variety of foods. Following the Dietary Guidelines for Americans (USDA 2000,

USDHHS 2000) can help, although attention

should be paid to serving sizes. These guidelines

urge individuals to eat 6–11 servings of grain

foods, 3–5 servings of vegetables, 2–4 servings

of fruits, 2–3 servings of dairy or other calciumrich foods, and 2–3 servings of meat or beans

each day. The DASH (Dietary Approaches to

Stop Hypertension) Eating Plan (USDHHS

2003), which follows these guidelines, is an exLIFESTYLE APPROACHES TO PROMOTE

BONE HEALTH

Chapter 7

ample of a well-balanced diet that can be good

for bone and heart health, although bone outcomes from DASH have not been specifically

tested. The DASH Eating Plan emphasizes

fruits, vegetables, low-fat or fat-free dairy foods,

whole grains, fish, poultry, and nuts, making it

rich in calcium, magnesium, protein, and potassium while also being low in fat, cholesterol, and

sodium. For more information about the Dietary

Guidelines and the DASH Eating Plan, refer to

Appendix C, Resources and Related Links.

Calcium

The Food and Nutrition Board (FNB) of the

Institute of Medicine updated recommended intakes for several nutrients important to the skeleton in 1997, including calcium (IOM 1997). Recommended amounts of calcium, which are shown

in Table 7-1, differ by age. These recommendations are meant for healthy people. Those with

osteoporosis or other chronic conditions may

need more calcium, but unfortunately the calcium requirements for individuals with this disease have not yet been clearly identified (Heaney

and Weaver 2003). The highest amount (1,300

mg per day) is recommended for children and

adolescents ages 9–18, a period when bones are

growing rapidly. Pregnant or lactating women

are advised to consume an age-appropriate
160 Chapter 7

A Report of the Surgeon General

amount of calcium, as shown in Table 7-1. The

Institute of Medicine also defined a safe upper

limit of 2,500 mg per day for calcium (IOM 1997).

Intakes above 2,500 mg per day may increase the

risk of adverse effects in susceptible individuals.

Americans obtain most of their calcium from

dairy products. In fact, approximately three 8-

ounce glasses of milk each day, combined with

the calcium from the rest of a normal diet, is

enough to meet the recommended daily requirements for most adults. Lowfat or nonfat versions

of dairy products are good choices because they

have the full amount of calcium, but help to avoid

eating too much fat. Foods that have been fortified with calcium are also good sources of the

nutrient. There are many foods that serve as
Bone Health and Osteoporosis

Lifestyle Approaches To Promote Bone Health 161
162 Chapter 7

A Report of the Surgeon General

good sources of calcium, including fortified cereal, nonfat milk, and calcium-fortified orange

juice from frozen concentrate (Keller et al. 2002).

Vegetables also contain calcium, but the amount

of calcium absorbed from these sources varies;

some, like broccoli and kale, contain calcium that

is well absorbed, while others, such as spinach,

do not (Weaver et al. 1999). It would be impractical for most people to eat enough vegetables or

other low-calcium foods to meet recommended

levels if these were the only sources of calcium

in the diet. To assist in planning a diet containing adequate levels of calcium, Table 7-2 provides a list of selected food sources of calcium,

along with the percent daily value that they contain. These percentages indicate whether a serving of the food contains a high (20 percent or more

of the percent daily value) or a low (5 percent or

less) amount of a specific nutrient—in this case,

calcium. Most individuals can design a diet that is

appealing to them (based on their preferences)

while also meeting their nutrient needs.

Many individuals, especially non-Whites,

suffer from lactose intolerance. These individuals may avoid dairy products, which can result

in a low calcium intake unless other good sources

of calcium are consumed. Those with lactose

intolerance may develop the capability to digest

lactose if they slowly build up milk intake over a

period of days or weeks so that they develop an

intestinal flora capable of digesting milk’s lactose

(Suarez et al. 1997). Many lactose-intolerant
Bone Health and Osteoporosis

Lifestyle Approaches To Promote Bone Health 163

A Guide to Calculate Calcium Intake

As shown in Figure 6-4 of Chapter 6,

most Americans above age 9 on average

do not consume recommended levels of

calcium. The following guide allows an

adult to compare a rough estimate of his

or her intake of calcium to the recommended amounts:

• Start by writing down the following

amount:

~ 290 if you are a female, regardless of age, or male age 60 or older

~ 370 if you a male under age 60

This is the average amount of calcium

that most people eat from non-calcium

rich food sources (Cook and Friday 2003,

Wright et al. 2003, Weinberg et al. 2004).

• Add 300 mg for each 8-ounce serving

of milk or the equivalent serving of other

calcium-rich foods (e.g., yogurt, cheese).

• For those taking a calcium supplement or a multi-vitamin containing

calcium, add the amount of calcium

from that source:

~ Check the supplement label for

the amount of calcium per supplement dose.

~ Multiply the amount per supplement dose times the number of

doses taken each day.

~ Add the amount from supplements to the base amount and the

amount from calcium-rich foods.

• Compare this rough estimate of total

calcium intake to the recommended

levels shown in Table 7-1. Individuals should try to meet their recommended level of calcium on most days.

• A useful calcium calculator for children can be found at: http://

www.cdc.gov/powerfulbones/parents/toolbox/calculator.html.
164 Chapter 7

A Report of the Surgeon General

The current recommended intakes of vitamin D are given in Table 7-1. Most individuals

need 200 IU per day, although these recommendations are raised to 400 IU per day in those age

50–70, and to 600 IU per day in those over age

70. There are two sources of vitamin D: sunlight and dietary intake.

As discussed in Chapter 6, vitamin D can be

made in the skin by being exposed to sunlight.

For some individuals, particularly children and

others who get enough exposure during warmer

months, the sun can provide adequate levels of

vitamin D throughout the entire year. For many,

however, it is not practical to get adequate levels

of vitamin D from exposure to sunshine. These

individuals should instead look to boost their

Tips for Those With Lactose Intolerance

• Choose dairy and other calcium-rich

foods with lower amounts of lactose;

a list of the amount of calcium and

lactose in common foods is shown in

Table 7-3:

~ Yogurt with live active cultures

(which provide bacterial lactase

that digests the lactose).

~ Hard cheeses like cheddar,

Colby, Swiss, and Parmesan (the

production process for these

cheeses breaks down the lactose).

~ Lactose-free or lactose-reduced

products, including milk without

lactose.

• Gradually increase the amount of lactose-containing foods consumed.

• Consume non-dairy products that

contain high levels of calcium, such

as fortified soy beverage or fortified

cereal or orange juice.

(Jarvis and Miller 2002)

individuals can tolerate up to one cup of milk

twice a day if it is consumed with food (McBean

and Miller 1998). In addition, some other calcium-rich dairy products such as cheese and

yogurt are usually well tolerated by lactose-intolerant people. Finally, there are a number of

calcium-rich foods that do not contain lactose,

including lactose-free milk, fortified soy beverage, and fortified juice and cereal. Some tips for

those with lactose intolerance are shown in the

box below.

The Institute of Medicine recommends that

nutrients be obtained from food when possible

because they provide a package of nutrients that

are good for other tissues besides bones. However, fortified foods and supplements can assist

those individuals who do not consume an adequate amount of dairy products or other naturally calcium-rich foods to meet recommended

levels of calcium intake. Those who take supplements or consume fortified foods should note

that: a) all major forms of calcium (e.g., carbonate, citrate) are absorbed well when taken with

meals; b) calcium from supplements or fortified

foods is best taken in several small doses (no more

than 500–600 mg at one time) (Heaney 1975)

throughout the day for better absorption; and

c) supplements may differ in their absorbability

due to manufacturing practices (IOM 1997). One

need not choose the most expensive products

on the market, as the cost of supplements of

comparable quality can vary fivefold (Heaney

et al. 2001). In a recent evaluation of calcium

sources, calcium carbonate supplements were

found to be the least expensive supplemental

source of calcium. Since virtually all calcium

sources—food or supplement—reduce the

absorption of iron, calcium and iron supplements should be taken at different times.

Vitamin D
Bone Health and Osteoporosis

Lifestyle Approaches To Promote Bone Health 165

vitamin D levels through diet. This is especially

true for elderly individuals who have higher vitamin D needs and who may have difficulty getting outside everyday. People with dark skin and

those who live in areas with heavy air pollution

may also find it more practical to obtain most or

all of their vitamin D from diet, since they need

longer periods of sun exposure to get adequate

levels of vitamin D. Table 7-4 gives the vitamin

D content of several foods, although the most

common source is fortified milk. One cup of fortified milk contains 100 IU vitamin D, half of

the recommended intake for individuals under

age 50. Since vitamin D-fortified milk is not used

when making cheese, ice cream, or most yogurts,

many other dairy foods are not good sources of

vitamin D. Other good dietary sources of vitamin D include fatty fish and vitamin D-fortified

orange juice. The best way to know whether a

dairy food contains vitamin D is to check the

nutrition label.

Vitamin D is also available in dietary supplements. While few supplements contain vitamin

D alone, many calcium supplements also contain vitamin D. Multivitamin supplements contain up to 400 IU of vitamin D. The amount of

vitamin D in a single dose of many calcium and

multivitamin supplements may not be sufficient

to meet the recommended levels, especially for

people over age 70 who need 600 IU per day.

To make sure that the recommended amount of

vitamin D is consumed as shown in Table 7-1,

check the nutrition label on the supplement for

the amount of vitamin D per dose, and, if necessary, supplement vitamin D intake through other

sources. However, because vitamin D can have

negative effects if taken in very high doses, it is

also important to avoid consuming more vitamin D than the tolerable upper level of 2,000 IU

per day. Larger doses can initially be given to

patients who are deficient as a means of replenishing the stores of vitamin D in the body.

Other Nutrients Important to Bone

As shown in Table 7-1, the Institute of Medicine recently provided recommended intakes for

other bone-related nutrients, including phosphorus and magnesium (IOM 1997). Most Americans consume adequate quantities of phospho-
166 Chapter 7

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168 Chapter 7

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Bone Health and Osteoporosis

Lifestyle Approaches To Promote Bone Health 169
170 Chapter 7

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Bone Health and Osteoporosis

Lifestyle Approaches To Promote Bone Health 171

rus through their regular intake of meats, cereals, milk, and processed foods. While some beverages such as soft drinks also contain phosphorus, they are not a preferred source of phosphorus because they may displace calcium-rich beverages like milk (Whiting et al. 2001).

Magnesium intakes may be suboptimal in

those who do not eat enough green leafy vegetables, whole grains, nuts, and dairy products.

Fortunately, most diets contain adequate levels

of other bone-related micronutrients, such as

vitamins K and C, copper, manganese, zinc, and

iron, to promote bone health.

Some dietary components may potentially

have negative effects on bone health, especially

if calcium intakes are not adequate. For example,

high levels of sodium or caffeine intake can increase calcium excretion in the urine. The effects of these factors can be overcome by increasing the amount of calcium in the diet (Fitzpatrick

and Heaney 2003). Studies have linked excessive amounts of phosphorus to altered calcium

metabolism, but it appears that the typical level

of phosphorus consumed by most individuals

in the United States should not negatively affect bone health (IOM 1997). Excessive amounts

of preformed vitamin A (e.g., retinol) can also

have negative effects on bone, so individuals

should not consume more than the recommended dietary allowance for this vitamin (IOM

2000). The vitamin A precursor (beta carotene)

found in many fruits and vegetables does not

have negative effects on bone, however.

Table 7-5 provides additional information on

other nutrients that affect bone, their recommended dietary allowances, and common dietary sources of these nutrients.

Physical Activity

The foundation of a good physical activity

regimen involves at least 30 minutes (adults) or

60 minutes (children) of moderate physical activity every day. This regimen can and should

involve a variety of activities. Some can be routine activities like walking or gardening. Others

may occur more infrequently and differ from

day to day and week to week, such as dancing,

aerobic classes, biking, swimming, tennis, golf,

or hiking. However, it is clear from the evidence

presented in Chapter 6 that physical activity to

specifically benefit bone health should involve

loading (stressing) the skeleton. As a result,

weight-bearing activities such as walking should

be included in an optimal physical activity regimen to benefit the musculoskeletal system. Moreover, the evidence suggests that the most beneficial physical activity regimens for bone health

include strength-training or resistance-training

activities. These activities place levels of loading

on bone that are beyond those seen in everyday

activities; examples include jumping for the lower

limbs and weight lifting or resistance training for

the lower and upper skeleton. Finally, while a

focus on activities that build or maintain bone

strength is appropriate and necessary, many older

individuals will remain at high risk of fracture.

For these individuals, balance training can provide the added benefit of helping to prevent potentially injurious falls.

As noted in Chapter 6, the evidence does not

lead to a specific set of exercises or practices but

rather a set of principles that can be applied and

varied according to the age and current physical

condition of an individual. Many of these principles have been reviewed by expert panels of

the American College of Sports Medicine

(ACSM) (Kraemer et al. 2002, ACSM 1998a,

ACSM 1998b) and they lead to the following

suggestions for the frequency, intensity, length,

and type of physical activity regimens to benefit

bone health for individuals of all ages:
172 Chapter 7

A Report of the Surgeon General

• Since continued physical activity provides

a positive stimulus for bone, muscle, and

other aspects of health, a lifelong commitment to physical activity and exercise is

critical.

• Ending a physical activity regimen will

result in bone mass returning to the level

that existed before the activity began.

Since repetitive programs of physical activity may be discontinued due to lack of

motivation or interest, variety and creativity are important if physical activity is to

be continued over the long term.

• Physical activity will only affect bone at

the skeletal sites that are stressed (or

loaded) by the activity. In other words,

physical activity programs do not necessarily benefit the whole skeleton, although

any type of activity provides more benefit to bone than does no activity at all.

• For bone gain to occur, the stimulus must

be greater than that which the bone usually experiences. Static loads applied continuously (such as standing) do not promote increased bone mass.

• Complete lack of activity, such as periods of immobility, causes bone loss.

When it is not possible to avoid immobility (e.g., bed rest during sickness), even

brief daily weight-bearing movements

can help to reduce bone loss.

• General physical activity every day and

some weight-bearing, strength-building,

and balance-enhancing activities 2 or more

times a week are generally effective for

promoting bone health for most persons.

• Any activity that imparts impact (such

as jumping or skipping) may increase

bone mass more than will low- and moderate-intensity, endurance-type activities,

such as brisk walking. However, endurance activities may still play an important role in skeletal health by increasing

muscle mass and strength, balance, and

coordination, and they may also help prevent falls in the elderly. Endurance activity is also very important for other aspects of health, such as helping to prevent

obesity, diabetes, or cardiovascular disease.

• Load-bearing physical activities such as

jumping need not be engaged in for long

periods of time to provide benefits to skeletal health. In fact, 5–10 minutes daily

may suffice. Most adults should begin

with weight-bearing exercise and gradually add some skipping and jumping activity. Longer periods (30–45 minutes)

may be needed for weight training or

walking/jogging. Those who have been

inactive should work up to this amount

of time gradually using a progressive program, e.g., start with shorter times and

easier activities (light weights or walking)

and then increase time or intensity slowly

(by no more than 10 percent each week)

in order to avoid injury.

• Physical activities that include a variety

of loading patterns (such as strength

training or aerobic classes) may promote

increased bone mass more than do activities that involve normal or regular loading patterns (such as running).

These fundamental principles can be used

to develop age-specific regimens, as outlined in

the sections that follow.

Physical Activity for Children and Adolescents

For children over age 8 and adolescents, a

bone-healthy program of physical activity could

include the following:

• At least 60 minutes of moderate intensity,

continuous activity on most days, prefer-
Bone Health and Osteoporosis

Lifestyle Approaches To Promote Bone Health 173

ably daily. This level of activity can help

achieve a healthy body weight and lower

the risk of other diseases such as cardiovascular disease and diabetes (USDHHS

1996, USDA 2000, USDHHS 2000,

IOM 2002).

• Inclusion of weight-bearing and short,

intense impact activities such as basketball, gymnastics, and jumping as part of

this regular activity program.

• Performance of weight-bearing activities

that increase muscle strength, such as

running, hopping, or skipping. The best

activities work all muscle groups. Examples include gymnastics, basketball,

volleyball, bicycling, and soccer. Swimming, while highly beneficial to many

aspects of health, is not a weight-bearing

activity and thus does not contribute to

increased bone mass.

Physical Activity for Adults

Adults should strive to get at least 30 minutes of physical activity on most days, preferably daily (USDHHS 1996, USDA 2000,

USDHHS 2000, IOM 2002). As part of that

regular physical activity program, the following

can help enhance bone health:

• For those individuals who can tolerate

impact activities, a simple, 10-minute program of physical activity that incorporates

50 3-inch (8-centimeter) jumps per day.

• A progressive program of weight training that uses all muscle groups, with the

amount of weight lifted increased gradually over time.

• A jogging or stair-climbing program for

those who cannot tolerate higher impact

physical activity.

• Active recreational activities such as tennis, hiking, or basketball.

In addition, it is advisable for adults to try to

find ways to add extra weight-bearing exercise

into everyday activities. For example, consider

parking farther away in the parking lot or taking

the stairs instead of the elevator.

General recommendations for physical activity in adults are shown in the pyramid in Figure 7-2, with the base of the pyramid being 30

minutes or more of moderate physical activity

on most, preferably all, days of the week. It is

also recommended that weight-bearing exercises

and strength and balance training be added as a
174 Chapter 7

A Report of the Surgeon General

part of regular physical activity (Nelson 2002,

Seguin and Nelson 2003). Lifestyle activities

such as walking, gardening, and raking leaves

can also be a valuable part of regular physical

activity (USDHHS 1996).

It is important to begin any physical activity

program slowly and to consider previous activity levels. Those who have been inactive should

begin with 5–10 minutes of activity per day and

a pre-exercise evaluation by a physician may be

advised. Those who are more fit can increase

physical activity levels to 20–30 minutes of moderate activity at a higher heart rate (60–85 percent of maximum heart rate). Generally, it is

advisable to increase activity levels by no

more than 10 percent each week to avoid injury.

For example, those who begin with 15 minutes

per day can progress to 17 minutes the second

week, and so on.

Finally, adults should consult a physician or

physical therapist if orthopedic conditions like

arthritis, functional limitations, or other medical

conditions make these physical activity guidelines difficult or unsafe to follow.

Physical Activity for Older Adults

Most elderly individuals should strongly consider engaging in regular physical activity. Physical activity is the only single therapy that can

simultaneously improve muscle mass, muscle

strength, balance, and bone strength. As a result, it may decrease the risk of fractures, in part

by reducing the risk of falling. In fact, fall-risk

reduction may be the biggest benefit of physical

activity for the elderly.

The following guidelines should be used to

maximize the potential fall prevention benefits

of physical activity in the elderly:
Bone Health and Osteoporosis

Lifestyle Approaches To Promote Bone Health 175

• Physical activity needs to be of sufficient intensity to improve muscle

strength, since poor muscle strength

is a known risk factor for falls.

Strength or resistance training is best

for building muscle, but even aerobic

endurance activity can yield some improvements in muscle strength.

• Improving balance can be an important component of any physical activity program designed to decrease

falls. This program may include balance training exercises or a movement

activity such as Tai Chi. Any activity that requires weight bearing and

challenges the postural system can
176 Chapter 7

A Report of the Surgeon General

improve balance and potentially help

reduce falls.

• Physical activity must be performed on

average 3 times per week for 30–45 minutes per session for at least three months

for strength and balance benefits to be

realized, and it must be continued if benefits are to be maintained.

• Those who suffer a fall that requires a

visit to a health care provider or an

emergency room should ask for a fall

risk assessment that includes a program of physical activity. Physical activity is most effective if delivered as a

part of a comprehensive fall prevention program (see Chapter 6).
Bone Health and Osteoporosis

Lifestyle Approaches To Promote Bone Health 177

Physical Activity for Those With Fragility

Fractures

Individuals who have already experienced

osteoporotic fractures should avoid certain types

of physical activities and exercises. For example,

those who have had vertebral fractures may need

to avoid activities that flex the spine. For more

information about appropriate physical activity

after osteoporotic fracture, see Chapter 9, “Rehabilitation of Osteoporotic Fractures.”

Fall Prevention

It is no surprise that falls are often the “precipitating” event that leads to a fracture in individuals with low bone mineral density (BMD),

and that therefore preventing these falls can reduce the risk of fracture. Falls are a major contributor to hip fractures and are also associated

with a significantly increased risk of many other

fractures, including spine, wrist, pelvis, and upper arm. Since falls are usually caused by multiple factors, successful prevention strategies

should involve multiple components. The benefit of physical activity in reducing the risk of

falls was discussed in the previous section. There

is more that can be done to reduce the chances

of a fall and to minimize the impact of any fall

that does occur. Guidelines issued by the American Geriatrics Society, British Geriatrics Society, and American Academy of Orthopedic Surgeons panel on falls prevention include the following recommendations for older persons

(AGS et al. 2001):

• Inform health care providers about any

fall, even those that do not result in serious injury. Providers should ask their

older patients at least once a year about

falls.

• Those who have fallen one or more times

should ask their health care providers

about the need for a test of their balance

and ability to walk.

• Those who need medical attention after

a fall or who have fallen several times in

the past year should have a fall evaluation. This evaluation should include taking a history related to the circumstances

of the fall and performing an examination of vision, balance, walking, muscle

strength, heart function, and blood pressure. A specialist, such as a geriatrician,

may be needed for this evaluation.

• Health care providers should consider

prescribing a program of physical activity and balance training, with an emphasis on those activities that may help reduce risk of falling. Patients can also seek

these programs on their own.

• Patients should ask their health care providers to review any medications they are

taking (including over-the-counter ones)

at least once per year. This step can help

to avoid various medication-related problems that commonly lead to falls, such as

drug-drug interactions and unnecessarily high doses of certain drugs.

• Vision should be checked annually.

• Individuals should review their homes for

possible hazards that could cause a fall,

such as loose rugs, poor lighting, electrical cords, or lack of handrails in the tub/

shower.

• Individuals should be careful when using step ladders, making sure to use ladders that are stable and have a handrail.

Finally, as discussed in Chapter 6, use of hip

protectors or hip pads may help reduce the risk

of fractures for persons living in institutionalized

care settings.

A good source for tips on how to prevent

falls is “The Tool Kit to Prevent Senior Falls,”

developed by the Injury Center at the Centers

for Disease Control and Prevention (CDC). This
178 Chapter 7

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Bone Health and Osteoporosis

Lifestyle Approaches To Promote Bone Health 179

kit contains “What You Can Do to Prevent Falls,”

an informational brochure, and “Check for

Safety,” a home safety checklist designed to help

older adults and caregivers identify and correct

home hazards. It also contains four fact sheets

and other relevant materials, and is available at

http://www.cdc.gov/injury.

Other Aspects of a Bone-Healthy

Lifestyle

In addition to having a healthy diet, sufficient physical activity, and avoiding falls, there

are some other bone-healthy behaviors that can

help protect the skeleton throughout life:

• Maintain a healthy body weight.

• Avoid smoking.

• If one drinks alcoholic beverages, do so

in moderation (i.e., one drink per day for

women and two drinks per day for men).

• For women, see a health care provider if

menstrual periods stop for three months.

• For those who have a medical condition

or who use medications that can affect

the skeleton (listed in Tables 3-1 and 3-2

in Chapter 3), talk to a health care

provider about ways to safeguard the

skeleton.
180 Chapter 7

A Report of the Surgeon General

Summary

Following the suggestions outlined in this

chapter on diet, physical activity, and other

lifestyle behaviors can help ensure good skeletal

health throughout life. For more specific information on how to adopt a bone-healthy lifestyle,

see the resources listed in Appendix C. It is never

too late for individuals, even frail elders, to start

following a bone-healthy lifestyle.

Key Questions for Future

Research

Research questions related to lifestyle approaches that promote bone health are included

in the questions identified in Chapter 6 on page

141.
Bone Health and Osteoporosis

Lifestyle Approaches To Promote Bone Health 181

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Four

Bone Health and Osteoporosis

 PART FOUR: Health Care Professionals 185

Part Four

WHAT CAN HEALTH CARE

PROFESSIONALS DO TO

PROMOTE BONE HEALTH?

This part of the report describes what health care professionals can do with their

patients to promote bone health. It seeks to dispel the belief among some health

professionals that bone disease and fractures are a natural consequence of aging and

that little can be done about it.

Chapter 8 emphasizes the need for health professionals to evaluate potential risk

factors for bone disease and to promote bone-healthy behaviors in all patients. The

chapter stresses, however, that comprehensive assessments that include diagnostic testing

should be focused on those deemed at high risk of bone disease. To assist in this process,

the chapter examines the potential risk factors for bone disease, highlights red flags that

signal the need for further assessment, and reviews the use of formal assessment tools

to determine who should get a bone density test and who is at risk of fracture. It includes

real-life vignettes that highlight the need for the medical profession to become aware of

the potential for severe osteoporosis to develop in younger men and women.

Chapter 9 focuses on preventive and therapeutic measures for those who have or

are at risk for bone disease. It reviews a “pyramid approach” to treating bone diseases

and to preventing falls and fractures, with maintenance of bone health through calcium,

vitamin D, physical activity, and fall prevention representing the base of the pyramid

for all individuals, including those with bone disease. This chapter also covers the

second and third levels of the pyramid, which relate to addressing and treating

secondary causes of osteoporosis and use of pharmacotherapy in appropriate

individuals. One of the key messages of the chapter is that there are effective treatments

available that can increase bone mass and/or reduce the risk of fractures for most patients

who have or who are at high risk of getting osteoporosis. The chapter reviews the

evidence and provides guidance on currently available anti-resorptive therapies,

anabolic therapies, and hormone therapies, and offers a glimpse into future directions

for treatment of osteoporosis. Finally, the chapter highlights treatment options for

other bone diseases that are related to osteoporosis.

Chapter 10 “puts it all together” for health care professionals by translating the

research into practical advice for preventing, diagnosing, and treating bone disease in

patients of all ages. All health care professionals, especially primary care practitioners,

have the opportunity and responsibility to dedicate themselves to promoting awareness

of factors that influence bone health, identifying patients at risk of bone disease, and

providing lifestyle and pharmacologic interventions where appropriate.
186 Chapter 8

A Report of the Surgeon General

• Much of the burden of bone disease can

potentially be avoided if at-risk

individuals are identified and appropriate

interventions (both preventive and

therapeutic) are made in a timely manner.

The evidence suggests that health care

providers frequently fail to identify and

treat individuals at high risk for future

osteoporosis or other disorders of bone,

even those who have already had a

fracture.

• It is important to evaluate the risks for

poor bone health at all ages. Therefore,

assessment of calcium and vitamin D

intake, physical activity, and adverse

behaviors such as smoking should be a

routine part of health care for all

individuals.

• Those in greatest need should receive a

full assessment of bone health.

Diagnostic methods are available that

can help to identify those in the

population who are at highest risk of

fracture.

• Both the public and health care

professionals need to be aware of a

number of known, easy-to-identify risk

factors for osteoporosis and other bone

diseases.

• Providers should be aware of a number

of red flags that might signal potential

problems with an individual’s bone

Chapter 8: Key Messages

health at different ages. One of the most

important flags is a previous fragilityrelated fracture.

• While osteoporosis is clearly the most

common bone disease, health care providers must also actively look for other

bone diseases. Diseases such as hyperparathyroidism, rickets, osteomalacia,

and Paget’s disease can often be identified by being aware of the warning signs

and/or through simple biochemical measurements. Early identification of such

diseases is critical, since treatment at an

early stage can often be highly effective.

• Bone mineral density or BMD testing

should be performed on any patient for

whom risk factor analysis indicates a

strong potential for osteoporosis. Formal

guidelines have been developed

recommending BMD testing in certain

populations, including postmenopausal

women over age 65, younger women

with multiple risk factors, and men and

women with fragility fractures or who

have other diseases or take medications

that can greatly increase the risk of

fracture.

• Individuals who are diagnosed with

osteoporosis should be further assessed for

secondary, treatable causes of the disease,

particularly men and premenopausal

women who suffer a fragility fracture.
Bone Health and Osteoporosis

Assessing the Risk of Bone Disease and Fracture 187

While individuals undoubtedly can do a great

deal to enhance their bone health through

appropriate lifestyle choices, health care

professionals play an important supporting role

in helping their patients to maintain strong,

healthy bones throughout life. In addition to

providing education about nutrition, physical

activity, and other bone-healthy behaviors,

health care professionals also need to assess the

risks of bone disease and fracture in their patients

and to identify and intervene with those at

greatest risk.

In an optimal health care environment,

expensive diagnostic tools and treatment

interventions should be targeted at those who

are at increased risk of a particular disease or

condition. The challenge is to find simple ways

to identify individuals in greatest need of more

careful assessment. Thus, in contrast to the

public health approaches to bone health in areas

like nutrition and physical activity (which can

be aimed at the entire population), this chapter

discusses the tools available to identify and

intervene with those in the population who are

at highest risk of fracture.

As discussed in previous chapters,

osteoporosis and other bone disorders

represent a large burden for society and for

individuals. Billions of dollars are spent each

year to treat bone-disease-related fractures that

ASSESSING THE RISK OF BONE DISEASE

AND FRACTURE

Chapter 8

often result in reduced function and quality

of life. At worst, fractures start a downward

spiral in health that can ultimately lead to

severe disability or even death. Much of this

burden can potentially be avoided if

individuals who are at risk of bone disease are

identified and appropriate interventions (both

preventive and therapeutic) are made in a

timely manner. Yet there has been relatively

little focus on these strategies in this country.

There are many studies documenting the

failure to identify and treat individuals at high

risk for fractures or other disorders of bone,

even those who have already had a fracture

(Solomon et al. 2003, Andrade et al. 2003,

Kiebzak et al. 2002, Kamel et al. 2000,

Feldstein et al. 2003). In a recent study of four

well-established midwestern health systems,

only one-eighth to a quarter of patients who

had a hip fracture were tested for their bone

density, fewer than a quarter were given

calcium and vitamin D supplements, and fewer

than one-tenth were treated with effective

antiresorptive drugs (Harrington et al. 2002).

The failure to diagnose and treat bone disease in

many high-risk patients has serious implications,

as the risk of future fractures is greatly increased

in patients who have had a previous fragility

fracture, especially in the first year or two after

the fracture (Johnell et al. 2004).
188 Chapter 8

A Report of the Surgeon General

Management of bone disease requires the

appropriate application of current knowledge

concerning the prevention, diagnosis, and

treatment. Those patients who have “healthy”

bones should be advised about appropriate steps

to take with respect to prevention. Those who

are “at risk” for bone disease (e.g., those with

low bone mass and other risk factors) should be

evaluated further, advised about appropriate

prevention, and considered for treatment. Those

with established bone disease should be advised

about secondary prevention (e.g., ways to avoid

first or repeat fractures) and be put on

appropriate treatment. They should also be

evaluated for so-called “secondary causes”—that

is, diseases and drugs that can aggravate or even

cause osteoporosis.

None of these activities can occur without

implementation of strategies for assessing the risk

of bone disease in a given patient. This

assessment process helps to “sort” patients into

different categories of risk, which in turn helps

to determine appropriate next steps with respect

to prevention, further diagnosis, and treatment.

This chapter describes this assessment process,

providing details on the best approaches to

assessing bone health and diagnosing bone

disease. It is important to remember that all of

the many factors that can increase fracture risk

should be considered in evaluation of the

individual patient.

Step 1: Identify At-Risk

Individuals Who Require Further

Evaluation

The first step for health care providers in

assessing individuals is to identify the relatively

small number of younger individuals (out of the

majority of individuals who do not have bone

disease) who require further evaluation. This

initial assessment ensures that more extensive

(and expensive) testing is reserved for those who

likely need it. This multi-pronged process is

described below.

Consider Potential Risk Factors for Bone

Disease

Although there is a great deal more that needs

to be discovered about which risk factors are

most important for deciding to measure bone

mineral density (BMD) in younger men and

women (i.e., those for whom BMD is not

recommended because of age alone), enough

information already exists to dramatically

improve diagnosis, prevention, and treatment of

bone disease. That information needs to be

applied more broadly by health care

professionals.

Both the public and health care professionals

need to be aware of a number of known, easyto-identify risk factors for osteoporosis and

other bone diseases. These factors relate to

either the intrinsic strength of bone or the

propensity to suffer injurious falls. Yet it is

remarkable how often these signals are ignored

in busy practice settings. All individuals, young

and old, should be assessed to determine how

many (if any) of these risk factors they have,

and then those with a sufficient degree of risk

need to undergo further evaluation (often a

BMD test) to determine the appropriate next

course of action (e.g., changes to lifestyle,

pharmacologic treatment). If these steps are

taken, much can be done to decrease the burden

of bone disease in the population, and much

illness and suffering can be avoided. This risk

factor analysis is also critical in ensuring the

efficient use of health care resources, helping

to identify those at-risk individuals in need of

BMD testing and potentially treatments without

the need for expensive, universal screening.

Finally, it is important to remember that bone
Bone Health and Osteoporosis

Assessing the Risk of Bone Disease and Fracture 189

“Twelve thousand people come through our

[health system’s] doors with osteoporosis

and we never notice them.”—Health system

physician

Men Can Get Osteoporosis, Too

This story demonstrates the importance of

not forgetting that men can also get

osteoporosis, even at a relatively young age. It

also highlights the need for the medical

profession to become aware of the potential for

severe osteoporosis to develop in younger men.

This college professor first fractured his

ankle as a young man. The doctor told him he

might have “a little osteoporosis” and

recommended that he take calcium to

strengthen his bones, but did not test for

osteoporosis. It was not until years later, after

many warning signs, that he finally received a

bone density test that showed severe

osteoporosis. At that time he was placed on

bisphosphonates, a treatment that he continues

today. The bisphosphonates have helped him

to regain some bone density. His BMD is

presently stable, albeit at a very low level.

Osteoporosis has had a profound effect on his

life. He is constantly afraid of falling, and as a

result seriously curtails his activities (e.g., he

gave up running).

“Where in the heck were the doctors? I

had a slew of warning signs but no one

picked them up.” —Male with severe

osteoporosis

Not Just a Disease of the Elderly

This woman’s story illustrates the need of

the medical profession to be aware of the

warning signs of bone disease in younger

individuals and to be aware of appropriate

treatments for the disease in this population.

This woman began suffering bone

fractures while still in her 30s. Even as pain

levels increased and her quality of life suffered,

her doctor blamed her problems on clumsiness.

After she turned 40, her internist attributed

her problems to being a natural consequence

of “getting old.” Finally, after breaking her

ankle at age 43, an orthopedist diagnosed

osteoporosis. At this point she had lost bone

mass and was shorter than earlier in life,

probably due to spine fractures. The doctor

told her there was no treatment available for

osteoporosis. He advised her to take calcium

supplements and to exercise, although he

provided no guidance on what types of

exercises would be helpful and safe. While she

had a long list of “don’ts” with respect to her

life, she did find that exercise made her feel

better. Yet she remained paralyzed with fear,

particularly after her physician gave her the

following advice: “above all else, don’t fall.”

Today, at age 55, she has finally turned the

corner on the disease. Thanks to medical

treatment, calcium supplements, and exercise,

her bone mass has improved. She is no longer

considered to have osteoporosis, but rather is

classified as osteopenic (i.e., she has low bone

mass).

“People with osteoporosis do not just die;

they slowly break apart.”

—Long-time osteoporosis sufferer
190 Chapter 8

A Report of the Surgeon General

health can be compromised at any age, and thus

the risks for poor bone health should be evaluated

in individuals of all ages. Assessment of calcium

and vitamin D intake, physical activity, and

adverse behaviors such as smoking should be part

of health care for all.

Be Aware of “Red Flags” That Signal Need

for Further Evaluation

There are a number of “red flags” that might

signal potential problems with an individual’s

bone health at different ages. Specific problems

at different stages of life are discussed in Chapter

10. These “red flags” apply to both men and

women. Indeed they may be particularly

important to keep in mind in men and Black

women, since they are often not considered to

be at high risk for bone disease. One of the most

important flags is a previous fragility-related

fracture, as such a fracture is one of the strongest

indicators that an individual may have

osteoporosis or some other metabolic bone

disease (Ettinger et al. 2003, Haentjens et al.

2003). Any individual with a history of fractures

related to only mild or moderate trauma (e.g., a

fall from standing height or less) should be

assessed further for the potential for bone

disease. Yet most are not adequately evaluated

today. Another important flag relates to family

history of the disease, since there is a component

of heredity not only in osteoporosis, but also in

Paget’s disease and hyperparathyroidism as well

as congenital disorders such as osteogenesis

imperfecta. Thus, both the public and health care

professionals should be alert to looking for other

family members who have bone disease. This

type of family case finding can and should lead

to earlier diagnosis and treatment. The presence

of certain bone diseases (e.g., Paget’s disease)

should be a flag for other family members to be

screened, or for screening for associated disorders

(e.g., a patient with hyperparathyroidism who

has other family members with the disease

should undergo genetic screening for other

associated endocrine disorders, such as multiple

endocrine neoplasia syndromes, familial

conditions in which patients may develop tumors

of several endocrine glands).

Low body weight is another important “red

flag” signaling the potential for osteoporosis; low

body weight is associated with lower BMD and

“Red Flags” That Warrant Further

Assessment for Osteoporosis or Other

Bone Diseases

• History of fractures related to mild or

moderate trauma (e.g., a fall from

standing height or less)

• Family history of bone disease

• Low body weight

• Weight loss of more than 1 percent per

year in the elderly

• Late onset of sexual development

• Unusual cessation of menstrual periods

• Anorexia nervosa (often related to

marked weight reduction)

• Athletic amenorrhea syndrome (related

to intense physical activity)

• Patients being treated with drugs that

affect bone metabolism (e.g.,

glucocorticoids)

• Patients with diseases linked to

secondary osteoporosis (see Chapter 3)

• High levels of serum calcium or

alkaline phosphatase in otherwise

healthy patients

• Hyperparathyroidism, hyperthyroidism, or treatment with high doses

of thyroid hormone

• Height loss or progressive spinal

curvature
Bone Health and Osteoporosis

Assessing the Risk of Bone Disease and Fracture 191

greater bone loss, even in premenopausal women

(Bainbridge et al. 2004). Moreover, weight loss

of more than 1 percent per year in the elderly is

associated with more rapid bone loss and

increased risk of fracture (Hannan et al. 2000,

Knoke et al. 2003, Ensrud et al. 2003).

There are other potential flags as well. While

bone disease is rare in children, the possibility

of congenital disorders should be considered

when children fracture, particularly with little

trauma. In adolescents, health care professionals

should consider abnormalities of sex hormone

function, particularly at puberty, to be a potential

risk factor, along with late onset of sexual

development or loss of sexual function with

cessation of menstrual periods. This is often

related to marked weight reduction, in anorexia

nervosa, or to intense physical activity, in the

athletic amenorrhea syndrome. Individuals of all

ages with calcium and vitamin D deficiency or

prolonged immobilization and paralysis should

also be carefully evaluated, as should those who

have other diseases that increase the risk of bone

loss and fractures, including gastrointestinal and

kidney disorders and arthritis. Those patients

being treated with drugs that affect bone

metabolism (e.g., glucocorticoids) should also be

considered as potentially being at risk. Finally,

patients already diagnosed with osteoporosis

should be screened for secondary, treatable

causes of the disease, especially in men or

premenopausal women who suffer fragility

fractures. Diseases linked to secondary

osteoporosis (see Chapter 3) are relatively

uncommon in the population, but they can have

a devastating effect on the bone health of the

patients with these conditions and consequently

may require specific treatment.

It is important to remember that not all the

“red flags” point to osteoporosis, and that some

may be an indicator of other types of bone

disease. It is important to look for these diseases.

For example, increased levels of serum calcium

and alkaline phosphatase in blood are often found

by routine screening, yet abnormal values are

often ignored (Murff et al. 2003). High serum

calcium concentration in an otherwise healthy

patient most often indicates primary

hyperparathyroidism, although many other

causes of hypercalcemia need to be considered.

Low serum calcium concentrations are less

common but can occur in individuals with

vitamin D deficiency and malabsorption.

Hypocalcemia is also commonly seen in

seriously ill patients and frequently is associated

with increased severity of illness or death.

Apparent hypocalcemia can be due to low serum

protein concentrations, and hypercalcemia can

be masked by such low concentrations. Patients

with Paget’s disease are often identified by the

finding of a high serum alkaline phosphatase

before there is evidence of bone pain or before

the skeletal lesions have actually been detected.

(Elevated serum alkaline phosphatase levels are

often caused by other problems, particularly

liver disease.) Such findings are important

because treatment can be highly effective for

these and other bone disorders if they are

diagnosed early.

Suspicion of vitamin D deficiency (e.g., due

to low intake, little exposure to sunshine) is

another “red flag” that signals the need for further

evaluation. This deficiency is common in the

elderly, particularly individuals living in northern

latitudes. Assessment of vitamin D deficiency can

be accomplished by measuring the most abundant

circulating form, 25-hydroxy vitamin D. This

measurement should be carried out in individuals

who are at high risk of deficiency, including those

with evidence of gastrointestinal disorders that

might result in malabsorption. Measurement of

serum phosphorus is generally not critical in
192 Chapter 8

A Report of the Surgeon General

assessing bone health, but if the levels are low

this may be an indication of hyperparathyroidism or vitamin D deficiency. Finally,

high blood calcium levels can serve as a “red flag”

that potentially indicates primary

hyperparathyroidism, and PTH should be

measured in all such patients. PTH

measurements are also helpful in assessing the

extent of secondary hyperparathyroidism in

patients with calcium and/or vitamin D

deficiency and in those with renal disease.

Consider Use of a Formal Assessment Tool to

Determine the Need for BMD Testing

BMD testing still serves as the “gold

standard” diagnostic test for identifying

osteoporosis and fracture risk. As noted,

population-wide BMD testing is not a costeffective or practical method for assessing the

risk of bone disease. While BMD testing has been

recommended for some populations (women

over age 65), BMD tests are not routinely used

for other individuals, the vast majority of whom

do not have and are not at risk for bone disease.

Widespread BMD testing makes little economic

or medical sense. Rather, as noted, the evidence

supports the assessment of other risk factors first,

in order to identify a subset of at-risk individuals

who are most likely to benefit from the test (e.g.,

younger women with multiple risk factors and

both men and women who have had fragility

fractures or who have diseases that can greatly

increase fracture risk). Some of these risk factors

may act directly or indirectly to affect BMD

levels, but others are independent of bone

density (e.g., risk factors for falling).

Existing clinical recommendations (NOF

2003) already make use of universally accepted

risk factors, such as gender, age, and history of

spine fracture, in determining who should get

BMD testing. Since age is a major determinant

of fracture risk, many groups have

recommended that BMD measurements be

obtained in all White women over age 65 (age is

a risk factor, see Figure 8-1) and for younger

postmenopausal women with additional risk

factors. It is interesting to note that treatment

recommendations are also based on these risk

factors, as treatment is recommended not only

for those with low BMD, but also for those with

an existing (especially recent) low-trauma spine

fracture, regardless of BMD.

There is great interest in developing a

screening tool or “clinical prediction rule” based

on risk factors that can easily be assessed

clinically (e.g., height and weight) or by patient

report (e.g., personal or family history of

fracture). The goal of a risk factor assessment

tool is to produce a more individualized approach

to diagnosis and treatment for all age, gender,

and ethnic groups. Ideally, nurses and other

nonphysician health care professionals should be

able to administer the tool (e.g., by having a

patient fill out a short questionnaire) and

interpret the results, thus allowing someone

other than the busy physician to play a lead role

in identifying at-risk individuals.

A number of risk-factor assessment tools are

in various stages of development. While there

are some problems and limitations with each of

these tools (see text box), progress is being made.

The National Osteoporosis Foundation (NOF)

checklist, for example, may be suitable for

individual self-assessment. Individuals can use

this checklist and discuss any concerns about

their bone health at their next medical encounter.

The Osteoporosis Risk Assessment Instrument

(ORAI) calculates scores based on age, weight,

and current estrogen use; it has a sensitivity of

93 percent—i.e., it identifies 93 percent of the

people with low BMD—and specificity of 39

percent—i.e., 61 percent of the people identified
Bone Health and Osteoporosis

Assessing the Risk of Bone Disease and Fracture 193

do not have low BMD (Cadarette et al. 2000;

Cadarette et al. 2004). The Simple Calculated

Osteoporosis Risk Estimation (SCORE)

considers six risk factors—age, race, weight,

estrogen use, rheumatoid arthritis, and personal

fracture history—and has a sensitivity of 91

percent and specificity of 40 percent (Lydick et

al. 1998), results that are quite similar to the ORAI

tool. The Osteoporosis Self-Assessment Tool

(OST) uses only two risk factors—age and

weight—and also has similar sensitivity (92

percent) and higher specificity (46 percent)

(Geusens et al. 2002, Richy et al. 2004, Cadarette

et al. 2004). A score based on age, body weight,

and fracture history was recently developed from

the Dubbo Osteoporosis Epidemiology Study;

it performed well in predicting low BMD, but

not fractures (Nguyen et al. 2004). Finally, NOF
194 Chapter 8

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practice guidelines consider age, weight, current

cigarette smoking status, family history of

fracture, and personal fracture history, but have

not defined any specific scoring system (Johnston

et al. 1998). Any of these approaches might be

used in clinical practice to determine who would

benefit from BMD testing. Examples of some of

the most simple and useful of these tools appear

in Chapter 10, including those that a busy

clinician or patient could use to assess risk factors

and determine if a BMD test is indicated.

Efforts have also begun to expand clinical

risk assessment tools beyond the question of who

Problems and Limitations With Existing Tools

Some problems and limitations have

slowed the development and widespread

application of risk-factor assessment tools. One

important issue relates to limitations of current

medical knowledge about risk factors for bone

health. While epidemiologic (large population)

studies have established the importance of age,

gender, and ethnic characteristics as important

clinical predictors, there is still considerable

uncertainty about which clinical characteristics to include in a risk-factor assessment tool.

An important problem stems from limitations

in the studies evaluating risk factors; they have

been relatively well studied in older (over age

65) White women, but less well studied in other

groups. It is possible that the importance of

particular factors may differ between women

and men, people of different races, and younger

and older individuals. To date, the generally

accepted risk factors for bone loss account for

only one-third to one-fifth of the differences

in BMD between individuals (Orwoll et al.

1996). Thus, it is clear that important risk

factors remain to be discovered. In fact, one

potential risk factor that has not been included

in any of these instruments is height loss. While

loss of height and curvature of the spine may

not be related to bone health (they can be

caused by poor posture, decreased muscle

strength, or narrowing of the intervertebral

discs (Ettinger et al. 1994, Coles et al. 1994,

Balzini et al. 2003), they could be a sign of

osteoporosis. Substantial height loss (more than

one inch) and new spinal curvature should serve

as a red flag that alerts health care providers to

the possibility of vertebral compression

fractures (Huang et al. 1996, Ensrud et al. 1997,

Vogt et al. 2000). Providers should also consider

tracking changes in height as a means of

monitoring the impact of preventive and

therapeutic measures for osteoporosis. One

problem with this approach is that height loss

is difficult to assess because an individual’s

memory of previous height can often be

inaccurate, as can current height measurements.

To overcome this problem, the use of specific

devices for accurate measurement of height and

spinal curvature (stadiometers and kyphometers) may be appropriate in specialty clinics.

should get a BMD test. Tools are being

developed to assess not just the risk of low BMD,

but also the risk for fractures (which is ultimately

what we are trying to prevent). Individuals

identified as having a high risk of fracture can

be targeted for early intervention. A recently

developed tool allows for a more global

assessment of risk factors. The risk factors used

to develop this tool were derived from the large

“Study of Osteoporotic Fractures” (Cummings

et al. 1995). This study identified numerous risk

factors for hip fracture in elderly White women

that are independent of BMD or personal
Bone Health and Osteoporosis

Assessing the Risk of Bone Disease and Fracture 195

fracture history (see Table 8-1). These risk factors

relate to genetic influences on bone size (e.g.,

maternal fracture history) and bone turnover,

lifestyle issues (e.g., exercise), height loss, weight

changes, and other factors. These risk factors

have been proven to be important in identifying

fracture risk. For example, patients whose BMD

was in the lowest third of the study population

had about 4.6 times the risk of suffering a hip

fracture risk as did women whose BMD was in

the highest third. However, hip fracture risk was

17 times greater among the 15 percent of the

women who had five or more risk factors

(exclusive of bone density) than the 47 percent

of the women with two or fewer risk factors

(Cummings et al. 1995) (Figure 8-2).

Black et al. (2001) turned the most prevalent

risk factors derived from the SOF study into a

questionnaire that can be administered to

patients (see Table 8-2). By assigning a point

value to each of the answers, a summary

FRACTURE score is developed. The

usefulness of this questionnaire was tested in a

large, prospective European study known as

EPIDOS. As shown in Figure 8-3, individuals

with a higher FRACTURE score had a much

higher risk of suffering a hip fracture. It is

important to remember, however, that this and

other approaches to measuring the risk of

fracture may not work as well in certain

populations; some of the predictors of fracture

for nursing home residents are different than

those living in the community. For example,

the risk of falling is especially critical in elderly

nursing home residents, most of whom have

fragile bones (Girman et al. 2002).
196 Chapter 8

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One of the most important needs going

forward with respect to risk assessment tools is

to incorporate the risk of falling into the system,

since so many fragility-related fractures occur

as a direct result of a fall. Risk factors for falling

include visual or cognitive impairment, use of

specific medications, and gait and balance

disorders. Poor vision is a particularly important

risk factor for the elderly (even those with

glasses), since many elderly individuals do not

have their eyes and glasses checked regularly.

Although high-technology testing of gait and

balance are available, these have not been

found to be clinically useful as a way to assess

the risk of falling. Rather, clinicians rely on

patient reports (e.g., prior falls [Nevitt et al.

1991], fear of falling [Tinetti et al. 1994]) and

objective examination (e.g., PerformanceOriented Mobility Assessment [Tinetti 1986],

Functional Reach [Duncan et al. 1992]). It is

important to remember that while any fall

should be investigated carefully, those falls
Bone Health and Osteoporosis

Assessing the Risk of Bone Disease and Fracture 197
198 Chapter 8

A Report of the Surgeon General

that lead to fractures are the biggest concern.

Individuals who have sustained a fracture as a

result of minimal trauma likely do not need

further evaluation by BMD testing to be

considered in the high-risk category for bone

disease and future fractures.

Those individuals who are identified as being

both at risk of bone disease and at high risk of a

fall might become candidates for further

intervention, including exercise programs to

improve strength and balance, modifications to

the home environment, changes in medications

that might make one prone to fall, and use of hip

protectors to “cushion the blow” from a fall. (See

Chapter 9 for more on hip protectors.)

Step 2: Measuring Bone Mineral

Density (BMD) for Individuals at Risk of Osteoporosis

Once a high-risk patient is identified (step

1), further evaluation of that patient is warranted.

This section deals with this evaluation process

for those at risk of osteoporosis—the most

common bone disease.

Why Measure BMD?

BMD testing remains the “gold standard” test

for those at risk of osteoporosis. The reason for

this is relatively straightforward—in the

laboratory, bone strength is strongly related to

BMD. More importantly, BMD remains a strong

independent predictor of fracture risk. In fact,

there is a clear relationship between BMD and

fracture risk in older women. For each standard

deviation decrease in BMD (in the spine, a onestandard deviation drop represents a loss of 10–

12 percent of BMD), the risk of fracture increases

by 1.5–2.5 times. The relationship between

BMD and fracture is stronger than the

relationship between cholesterol and heart

attack, and as strong as the relationship between

blood pressure and stroke (Marshall et al. 1996).

BMD measurement can be used to assess

fracture risk and to establish the diagnosis and

severity of osteoporosis. BMD testing can be

used to assess changes over time (monitoring) in

treated and untreated individuals. (It is important

to note that while standard x-rays are used to

diagnose fractures, they are not useful for

measuring bone mass. It is estimated that one

must lose 30 percent of BMD for bone loss to be

noted on x-ray; furthermore, an improperly

performed x-ray in a normal person may have

the appearance of bone loss.)

Who Should Have a Bone Density Test and

When

As noted earlier, an analysis of risk factors

can be helpful in determining who should or

should not get a BMD. Risk factors for bone

disease and fractures are still not fully

understood, especially for younger individuals,

males, and non-Whites. In an effort to summarize

general conclusions about what is and is not

known, a variety of organizations, including

government agencies and professional societies,

have made attempts to develop guidelines on

who should have a bone density test and when.

This section reviews those recommendations.

Recommendations for Osteoporosis

Screening and for Other Bone Diseases

There is general consensus that all women

age 65 and older should have a BMD test, and

that women at-risk of bone disease who are under

age 65 should also be screened (although there

is not universal agreement on what defines “atrisk” status). At present there are no differences

in these recommendations across racial and

ethnic groups. The U.S. Preventive Services

Task Force (USPSTF) recommends bone

density screening for all women age 65 and older

and for younger postmenopausal women age 60–

64 who are at high risk ( body weight less than
Bone Health and Osteoporosis

Assessing the Risk of Bone Disease and Fracture 199

70 kilograms, no current use of estrogen) (U.S.

Preventive Services Task Force 2002). Risk

factors that should also be considered include

smoking, weight loss, family history, decreased

physical activity, alcohol or caffeine use, or low

calcium and vitamin D intake. The NOF also

recommends testing women age 65 and older,

and emphasizes four common and easily

assessable risk factors that would justify

screening in younger postmenopausal women:

• a family history of osteoporosis;

• a personal history of low-trauma fracture

after age 45;

• current cigarette smoking; and

• low body weight (under 127 pounds)

(NOF 2003).

The NOF also recommends BMD testing

for men who present with fractures or are

receiving treatment with a GNRH agonist for

prostate cancer, as well as for all individuals who

have primary hyperparathyroidism or are on

long-term glucocorticoid treatment (National

Osteoporosis Foundation 2002). The ISCD

agrees with screening all women age 65 and older

and also recommends screening healthy men

starting at age 70, with earlier testing for men

who are at high risk of osteoporosis or fracture

(Binkley et al. 2002).

BMD testing should also be performed on

any individual who has other potential risk

factors for osteoporosis, especially anyone who

has had a low-trauma fracture or who exhibit

another clinical indication of osteoporosis (e.g.,

x-ray evidence of low bone mass), as well as those

who have diseases or conditions known to cause

increased bone loss (e.g., hyperthyroidism

[increased activity of the thyroid gland in the

neck], hyperparathyroidism [increased activity

of the parathyroid gland in the neck], rheumatoid

arthritis, certain diseases of the stomach or

intestines, long-term menstrual irregularities,

 Who Should Have a BMD Test?

• U.S. Preventive Services Task Force

Guidelines

~ All women age 65 and older

~ Women between age 60–64 who

are at high risk (body weight less

than 70 kilograms, no current

hormone therapy)

• National Osteoporosis Foundation

Guidelines

~ All women age 65 and older

~ Postmenopausal women under

age 65 with:

~ Family history of osteoporosis

~ Personal history of low-trauma

fracture after age 45

~ Current cigarette smoking

~ Low body weight (less than 127

pounds)

• Other Clinical Recommendations

~ Low-trauma fractures as an adult

~ Hyperthyroidism

~ Hyperparathyroidism

~ Vitamin D deficiency (osteomalacia)

~ Rheumatoid arthritis

~ Medications that cause bone loss

(glucocorticoids, excessive doses of

thyroid hormone, medications

used to treat seizures, medications

that block sex hormone production)

~ Diseases that cause poor intestinal

absorption

cessation of menstrual bleeding) and those who

are using a medication that may cause increased

bone loss (e.g., glucocorticoids, excessive doses

of thyroid hormone, certain blood thinners,

certain drugs that treat seizures, drugs that block

sex hormone production) (Leib et al. 2004).
200 Chapter 8

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Methods for Measuring BMD

The most widely accepted method for

measuring BMD is dual x-ray absorptiometry

(DXA). DXA is very safe, as it involves levels of

radiation that are lower than that derived from

daily background radiation from the sky when

taking a trans-Atlantic airplane flight, and much

lower than those from undergoing an x-ray of

the back. DXA measures BMD in the spine and

hip, sites that are likely to fracture in patients

who have osteoporosis (see Figures 8-4 and 8-

5). These central skeletal sites are also most

appropriate for monitoring the effectiveness of

therapy, as they are more likely than peripheral

sites to show an increase in BMD in response to

treatment. DXA is precise and permits

monitoring of patients over time. DXA also can

be used to measure bone density in the forearm

and whole body.

Several other techniques are available for

bone mass measurement and are described

briefly below (Genant et al. 1996, Grampp et al.

1997) (Table 8-3). While these methods do assess

bone density and may provide an indication of

fracture risk, it is important to note that the

WHO recommendations and other guidelines

for using BMD and interpreting BMD results

for diagnosis (see next section for more details)
Bone Health and Osteoporosis

Assessing the Risk of Bone Disease and Fracture 201

are based on DXA measurements of the hip or

spine. In the future, these alternative tests may

be further refined and others may be developed,

thus improving the ability to identify individuals

at risk of osteoporosis.

• Peripheral DXA (pDXA) uses scaleddown DXA instrumentation to measure

peripheral sites such as the forearm, heel,

or finger. These tests can help to identify

at-risk individuals who are most likely to

benefit from further BMD testing. Using

the test for this purpose is tricky,

requiring the setting of a proper threshold

for determining who needs further

evaluation. A too-low threshold could

prove ineffective in screening, with the

result being that many healthy

individuals undergo further (expensive)
202 Chapter 8

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evaluation. A too-high threshold could

result in at-risk individuals being

“screened out” and thus failing to receive

further evaluation that could have resulted

in timely diagnosis and treatment of bone

disease. At present there is no scoring

system for peripheral DXA that has been

found to be preferable to using risk factor

analysis as a means of determining who

should and should not undergo DXA of

the spine and hip.

• Peripheral quantitative computed

tomography (pQCT) uses specialized

equipment to measure cortical bone (the

outer, more solid shell of bone) and

cancellous bone (the inner, honeycomblike bone) in the forearm. This technique

is used primarily for research.

• Quantitative computed tomography

(QCT) uses standard computed

tomography equipment, usually with a

phantom that must be scanned with the

patient. It provides a true volumetric

measurement of cancellous bone density

in the spine. Although it involves greater

radiation exposure, it may be used as an

alternative to spine and hip DXA

measurements.

• Quantitative ultrasound (QUS) uses sound

waves to assess bone mass and thus does

not use radiation. It can be used to measure

bone in a variety of peripheral sites, such

as the heel, tibia (leg), radius (wrist), and

finger. Ultrasound devices measure the

speed of sound (SOS), as well as specific

changes in sound waves (i.e., broadband

attenuation or BUA) as the sound waves

pass through bone. Most devices use a

formula to calculate a bone density

equivalent or “T-score equivalent.”

• Radiogrammetry uses measurements

derived from standard x-rays of the hand

to determine an index that compares

cortical thickness with the total bone

width in the mid-shaft of at least two

metacarpal (palm) bones.

• Radiographic absorptiometry (RA), also

called photodensitometry, uses a

standard x-ray of the hand to measure

density in the middle bones of the

second, third, and fourth fingers.

Specialized equipment is used to scan the

film at high resolution, and special

software is used to calculate bone volume

and bone density. The cortical thickness

of the bones also can be measured.

• Single x-ray absorptiometry (SXA) is

used to measure peripheral sites such as

the heel and forearm. The body part

being measured is immersed in a water

bath or water equivalent device. The

SXA picture is similar to that obtained

with DXA technology.

Incorporating these techniques for bone

assessment into future clinical trials and

observational studies will help in better

understanding their appropriate use as a means

of predicting the risk of bone disease and

fracture.

Using and Interpreting BMD Measurements

BMD in young healthy adults is normally

distributed as shown in Figure 8-5. An

individual’s BMD can be compared to the mean

value in a reference population, such as young

healthy adults. The difference between an

individual’s BMD and the mean BMD for the

reference population can be expressed in

standard deviation (SD) units; a score of 0

indicates BMD equal to the mean; a score of +1

indicates one standard deviation above the mean,
Bone Health and Osteoporosis

Assessing the Risk of Bone Disease and Fracture 203
204 Chapter 8

A Report of the Surgeon General

and a score of -1 is one standard deviation below.

When an individual’s BMD is compared to the

mean BMD score in a young healthy population,

this standard deviation measurement is referred

to as a T-score. The T-score is calculated using

the following formula:

In 1994, a working group of the World

Health Organization developed a classification

system for osteoporosis based on BMD using the

known gradient of the risk of fracture in the

population as a whole. They sought to define

osteoporosis using BMD so that the proportion

of individuals identified as having osteoporosis

by this method would be related to the lifetime

risk of fracture in the population. Four general

diagnostic categories were proposed for

assessments done with DXA (Kanis 1994, Kanis

2002b):

• Normal: Hip BMD that is no more than

1 standard deviation below the young

adult female reference mean (T-score

greater than -1).

• Low bone mass (osteopenia): Hip BMD

that is between 1–2.5 standard deviations

below the young adult female mean (Tscore less than -1 and greater than -2.5).

• Osteoporosis: Hip BMD that is 2.5

standard deviations or more below the

young adult female mean (T-score less

than -2.5).

• Severe osteoporosis (established

osteoporosis): Hip BMD that is 2.5

standard deviations or more below the

young adult mean in the presence of one

or more fragility fractures.

In the young healthy population shown in

Figure 8-5, about 15 percent of the women have

a T-score of less than -1 and thus have low bone

mass or osteopenia, while about 0.5 percent of

women fall into the osteoporotic range, with a

T-score of -2.5 or less. The proportion of women

affected by osteoporosis increases with age as

average bone density declines (Figure 8-6) and

risk of fracture increases.

If there were only a single device for

measuring BMD, and only a single skeletal site

that was measured, absolute BMD, in g/cm2,

could be used. However, it is difficult for

clinicians to remember ideal or threshold cut-off

points for absolute BMD levels as measured by

a single type of machine at various locations,

including the spine and hip, let alone remember

the values for different types of machines that

are calibrated (standardized) differently. The Tscore provides a way to use a single set of

numbers for all devices and all skeletal sites.

Another way of expressing BMD is the Zscore, which compares an individual with age-,

gender-, and ethnicity-matched norms. Z-scores

are not used for diagnosis because a person’s Zscore can remain constant throughout life, even

as BMD declines with age. However, the Z-score

is useful in determining how an individual’s

BMD compares with what is expected for a

person of a given age and body size. Although

all patients with osteoporosis deserve at least a

limited evaluation for secondary causes (i.e., not

age-related) of bone loss, patients with a low Zscore (i.e., BMD significantly lower than

expected for age and size) are particularly in need

of an in-depth evaluation for secondary causes

of osteoporosis. Z-scores are also useful in

children to determine how their bone density

compares to that of their peers. Since they have

not reached adult peak bone mass, T-scores

should not be used for children. Figure 8-7 is a

graphical illustration of T-scores and Z-scores.

T-Score

Patient’s BMD – Young Normal Mean

Standard Deviation of Young Normal Mean
Bone Health and Osteoporosis

Assessing the Risk of Bone Disease and Fracture 205
206 Chapter 8

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The WHO classification was derived from

studies of White postmenopausal women and

applies to them, but not for men, premenopausal

women, or non-White postmenopausal women.

In general, men have a higher bone mass than

do women of the same age, and Black men and

women have higher bone mass do White men

and women of the same age (Finkelstein et al.

2002, Looker 2002). Although controversial, the

International Society for Clinical Densitometry

(ISCD) recommends use of a single normative

database (i.e., not adjusted for ethnicity) to

calculate T-scores in non-White as well as White

postmenopausal women, and use of a male

normative database to calculate T-scores for men

(Binkley et al. 2002). There are no official

recommendations for the BMD standard

deviation values that should be used to diagnose

osteoporosis in men, premenopausal women, or

children. The ISCD emphasizes that the

diagnosis of osteoporosis in men, premenopausal

women, and children should not be made on the

basis of BMD alone (Leib et al. 2004). In fact, a

Canadian panel of ISCD has developed

guidelines for the diagnosis of osteoporosis in

premenopausal women, men, and children

(Kahn et al. 2004). This panel recommended that

BMD measurements be used only in patients

with fragility fractures or major secondary causes

of bone loss. The panel also recommended that

Z-scores, not T-scores, be used in children and

pre-menopausal women. Finally, the panel

recommended that the terms osteopenia and

osteoporosis not be used for children, since the

WHO criteria do not apply to them.

Not everyone with low BMD has

osteoporosis; osteomalacia and other bone

disorders should also be considered. In addition,

as noted previously, low bone density is not the

only risk factor for fracture; other factors include

age, risk of falling, risk of injury, previous lowtrauma fracture, family history of osteoporosis,

etc. (see section on Risk Factor Analysis).

The National Osteoporosis Foundation

(NOF) and the ISCD recommend using DXA

to measure BMD in both the hip and spine and

classifying the patient based on the lowest T-score

of these measurements (Hamdy et al. 2002, NOF

2003). ISCD recommends using the mean score

for the L-1 to L-4 vertebrae to calculate spine

BMD and that vertebrae affected by local

structural artifacts be excluded from this

calculation (Leib et al. 2004). The U.S. Preventive

Services Task Force and the Agency for Healthcare

Research and Quality (Nelson et al. 2002) state that

BMD at the femoral neck is the best predictor of

hip fracture and is comparable to spine or forearm

BMD for predicting fractures at other sites. ISCD

recommends using forearm BMD for obese patients

in whom the spine and hip measurements cannot

be obtained (Leib et al. 2004).

Finally, when interpreting scores, it is

important to remember that DXA measures

areal density by calculating grams per square

centimeter (bone mineral content divided by

area), in contrast to “true” measures of density,

which involve volumetric measurement). As a

result, DXA underestimates the density of small

bones and overestimates the density of large

bones. Therefore, the size of the bone should be

taken into account when deciding whether or

not to medicate.

Use of DXA for Monitoring

DXA cannot only be used for making an

initial diagnosis and treatment decision, but

central DXA is also precise enough to be used

for monitoring patients over time, provided the

interval between measurements is tailored to the

specific patient’s situation (Lenchik et al. 2002).

More research is needed on the best regimens

for follow-up testing and for the best way to

interpret changes in BMD in these follow-up
Bone Health and Osteoporosis

Assessing the Risk of Bone Disease and Fracture 207

tests. This section reports on the most

appropriate approaches, given the current state

of scientific evidence.

For individuals who are not currently

receiving treatment, the timing of a repeat test

should be based on the current BMD and the

expected rate of bone loss (e.g., bone loss is faster

during early menopause). For older individuals

with above-average T-scores, repeat testing may

not be necessary at all. For younger individuals

who were initially screened due to risk factors

but who have normal BMD values, repeating a

test every 5–10 years may be helpful. For those

with borderline low BMD and/or who may lose

bone fairly rapidly (e.g., exposure to high doses

of glucocorticoids), repeating the test in 2-3 years

would be appropriate. For monitoring patients

on treatment (which is the main reason for

ongoing monitoring via BMD measurement),

testing annually is inappropriate, and there is

insufficient evidence to determine if testing every

2 years is useful (Nelson et al. 2002).

Nonetheless, many practitioners repeat the test

every 2 years for patients on treatment (Medicare

covers testing every 2 years), while others wait

longer. It is unlikely that repeated BMD
208 Chapter 8

A Report of the Surgeon General

measurements make a difference in patient

compliance with treatment, as many patients

who discontinue treatment do so after less than

a year (before BMD would be repeated). One

exception to the rules related to frequency of

testing applies to patients receiving high-dose

long-term glucocorticoid therapy, for whom

monitoring is recommended every 6 months until

BMD is shown to be stable or improved. When

repeating BMD measurements, it is important

to avoid over-interpretation of small changes as

these can be due to differences in equipment or

changes in positioning. Non-DXA techniques

measuring peripheral sites, QCT, lateral spine

DXA, and Ward’s triangle DXA (the area of the

hip with the lowest density) should not be used

for monitoring osteoporosis.

Limitations of BMD Testing

As noted in various sections of this chapter,

there are still a number of limitations with respect

to BMD testing. Better guidelines are needed on

which individuals should receive the test, how

to interpret the results of initial and follow-up

testing, and how to communicate those results

to patients. Health care providers need clear,

evidence-based approaches that will enable them

to decide who should have BMD testing. They

also need guidance in developing plans for

treatment and prevention based on a combination

of BMD data and other risk factors. More data

on the outcomes of screening, prevention, and

treatment programs should help to close the large

current gap between evidence and practice (Bates

et al. 2002, Cummings et al. 2002).

One important concern about the

interpretation of results is the variability that

exists across different types of BMD machines

(even those made by the same manufacturer),

and across similar types of machines made by

different manufacturers. BMD measured on one

type of machine cannot be accurately compared

to BMD measured on a different type of machine,

nor can BMD performed on the same type of

machine at two different locations. There is also

variability in the ability of technologists to

perform the tests, in the training and ongoing

certification of technologists, and in

interpretations of results by physicians, each of

which can undermine the comparability of results.

As a result of all of these factors, daily equipment

checks and a quality control system related to both

the methodology and reporting of test results is

critical to ensure the validity of DXA analysis.

The ISCD has developed specific, detailed

instructions for quality control as well as reporting

of DXA measurements (Leib et al. 2004).

Depending on the skeletal site assessed, the

prevalence of osteoporosis can be overestimated

(e.g., by use of lateral spine DXA or spinal QCT)

or underestimated (e.g., by heel ultrasound)

compared to DXA of the spine or hip (Faulkner

et al. 1999). There may be differences between

the density of skeletal sites within an individual

patient. For example, a patient may have a normal

spine, but very low bone density at the hip,

examination of multiple sites is more likely to

result in a diagnosis of osteoporosis. It is important

to remember that, despite these limitations, bone

mineral density remains the single best predictor

of fracture risk available today.

Looking to the Future: Potential

Complements to BMD

Researchers in bone disease are developing

new approaches that might one day serve as a

standard complement to BMD tests. These

approaches seek to incorporate additional

information that can prove useful in identifying

at-risk individuals who may be candidates for

further evaluation and treatment, and/or in

monitoring the effectiveness of therapy in
Bone Health and Osteoporosis

Assessing the Risk of Bone Disease and Fracture 209

patients already being treated. This section

reviews these efforts.

Biochemical Markers of Bone Turnover

One major thrust relates to efforts to identify

“markers” that reflect the rates at which bone

breaks down and builds up. As noted in Chapter

2, bone is continuously remodeled in a process

referred to as bone turnover whereby old bone

is removed and replaced by new bone. Thus,

bone resorption (the breaking down of bone) and

formation (the building up of bone) are occurring

throughout the skeleton at different sites and at

different rates. Tests are now available that look

for specific blood and urine markers that reflect

the rate of each of these processes for the whole

skeleton. While BMD measurements provide

valuable information on fracture risk, they

contribute no insight into the rate of bone

turnover in a given patient. To the extent that

the imbalance in the rate of bone resorption and

formation may predict the rate of bone loss or

enhance the ability to predict the risk of fracture,

biochemical markers of bone turnover have the

potential to complement the information

provided by BMD measurements. As reviewed

below, while current bone turnover markers

have clear limitations, they do nonetheless have

some role today in the management of the patient

with osteoporosis, particularly to assess

responses to therapy (Looker et al. 2000). With

further refinement they are likely to play a more

important role in the future.

Table 8-4 lists currently bone turnover

markers that are currently available. These can

be broadly separated into markers of bone

resorption and formation; each of these markers

is discussed briefly below.

Resorption Markers. Resorption markers are

primarily based on measurement of collagen

breakdown products that are released into the circulation as bone is resorbed. In recent years rapid

and relatively inexpensive tests capable of measuring these breakdown products have been developed, representing a major advance in this area.

Most commonly used are the tests for urine and,

more recently, blood (serum) (Looker et al. 2000,

Garnero et al. 1998, Miller et al. 1999). These

markers measure cross-linked (connected) fragments of type I collagen that are released as bone

collagen is broken down (Robins et al. 1994).

While initially a sophisticated technique was re-
210 Chapter 8

A Report of the Surgeon General

quired to measure these molecules, there are

now a number of relatively easy to perform tests

that can measure them in the blood and urine

(Robins et al. 1995).

Formation Markers: Since bone resorption

and formation are coupled processes, bloodbased bone formation markers are also useful in

assessing bone turnover. Osteocalcin and bone

specific alkaline phosphatase (BSAP) can serve

as such markers, as they are proteins that are

made during the process of bone formation

(Deftos et al. 1992, Garnero and Delmas 1993).

In addition, since a major product of osteoblasts

is type I collagen, tests have also been developed

that can measure fragments of the collagen

precursor chain that are removed and released

into the circulation during the processing of the

collagen precursor molecule in bone.

Extensive research studies of bone biochemical

markers have uncovered potential clinical uses for

these markers. These uses, along with current

limitations, are reviewed briefly below.

Estimation of Bone Mass. Bone biochemical

markers cannot and should not be used to diagnose

osteoporosis or to estimate bone mass; direct measurement of BMD is most effective for these tasks.

Estimation of Fracture Risk. There is

evidence to suggest that increased bone turnover

may be an independent predictor of fracture risk.

In a prospective study of elderly (those over age

75) French women, excess excretion of urinary

C–terminal collagen crosslinked peptides (CTx)

and free deoxypyridinoline crosslinks (Dpd), two

of the commonly used biochemical markers of

resorption, was associated with an increased risk

of hip fracture, even after adjusting for femoral

neck BMD (Garnero et al. 1996). Moreover, in a

meta-analysis (combination analysis of multiple

studies) of trials using antiresorptive drugs

(drugs that slow the breakdown of bone),

investigators showed that the change in

resorption markers brought on by these agents

was related to the reduction in non-spine fracture

risk (Hochberg et al. 2002). Specifically, they

found that, on average, a drug that reduced bone

resorption by 70 percent would decrease the risk

of non-spine fractures by 40 percent,

independent of effects on BMD. However, while

estimation of fracture risk independently of

BMD remains an intriguing and potentially

important use of bone turnover markers, their

routine use for this purpose in individual patients

cannot be recommended at this time, largely due

to the variability of the measurements.

Estimation of Rate of Bone Loss. Several

studies indicate that, at least for groups of

individuals, bone biochemical markers can be

used to estimate the rate of bone loss. For example,

a 4-year study by Garnero et al. (Garnero et al.

1999) found that women with normal bone

turnover lost less than 1 percent BMD over 4 years,

while those in the high turnover group lost 3–5

times that amount of bone. Here again, the

variability of measurements is such that markers

may not provide an accurate estimate of bone loss

in an individual patient (Nelson et al. 2002).

Selection of Individuals for Therapy. There

are reports indicating that individuals with the

highest levels of bone turnover appear to have

the best response to antiresorptive therapy. In a

two-year study of estrogen/progestin treatment,

Chesnut and colleagues found that individuals

in the highest quartiles for initial excretion of

urinary NTx (a biochemical marker) had the

greatest gain in BMD in response to hormone

treatment (Chesnut et al. 1997). However, the

review by the Agency for Healthcare Research

and Quality (AHRQ) concluded that studies

relating marker results and bone loss had no

obvious trend and markers were not useful for

patient selection (Nelson et al. 2002). Further

studies are needed to evaluate these issues,
Bone Health and Osteoporosis

Assessing the Risk of Bone Disease and Fracture 211

particularly with respect to more accurate

measurements and better quality control.

Monitoring Effectiveness of Therapy.

Perhaps the most important use for bone

markers today is in monitoring the effectiveness

of ongoing therapy. A number of studies indicate

that a significant reduction in bone resorption

markers occurs within four to 6 weeks after

initiation of antiresorptive therapy, followed by

a decrease in bone formation markers in 2-3

months (Garnero et al. 1994). Thus, bone

turnover markers could theoretically be used to

quickly learn when therapy is not working,

certainly much more quickly than could a followup BMD test 2 years after initiation of therapy.

Markers have been used for this purpose for

many years for monitoring the response to

treatment in Paget’s disease. Failure to show the

expected reduction in resorption markers could

indicate that the patient is not taking the

medication in the prescribed manner or that the

dose or type of therapy needs to be changed.

However, the review by the AHRQ concluded

that no marker could accurately determine if an

individual would respond to therapy as

confirmed by subsequent BMD measurements

(Nelson et al. 2002). Work is ongoing to

determine the clinical usefulness of following

markers in patients being treated with

antiresorptive drugs for osteoporosis.

Summary. To summarize, bone biochemical

markers may have a potential future role in the

identification and management of the patient

with osteoporosis. The remodeling rate itself

may play a central role in bone fragility rather

than just as a marker of bone loss and future

declines in bone mass. When the remodeling rate

is high, many of the material qualities of bone

that contribute to fragility and inability to resist

fracture are sub-optimal (Heaney 2003).

Continued improvements in these markers

may lead to their use as independent estimators

of fracture risk, of rates of bone loss, and perhaps

for optimal selection of patients for specific

therapies as well as for monitoring of response

to these therapies.

Next-Generation Models for Assessment

Advances in understanding of biochemical

markers and genetic factors related to bone

disease are leading to the potential for more

sophisticated tools for assessing the risk of bone

disease in individuals. With that goal in mind,

an effort to develop a system that estimates a

patient’s fracture risk over the next 5–10 years is

now underway as a joint activity of the

International Osteoporosis Foundation and the

National Osteoporosis Foundation of the United

States (Kanis et al. 2002a and 2000c). Data from

most of the world’s epidemiology studies are

being merged in order to identify consistent risk

factors for fracture and to develop a clinical

prediction rule that utilizes this information, plus

BMD measurements if available, to estimate an

individual’s personal fracture risk over the next

decade of his or her life. In this scheme the risk

of all types of osteoporotic-related fractures (not

just hip fractures) would be assessed, so that the

entire burden of the disease can be recognized.

A patient’s personal fracture risk could provide

a much better basis for individualized treatment

decisions. However, it will be important to

validate this approach in the community.

Looking ahead, the evolution of risk factor

analysis will likely involve the expansion of

generally accepted risk factors such as age,

gender, race, and fracture history, all of which

are well-established as validated estimators.

Other potential risk factors are being studied and

may play a larger role in the future. The most

promising include biochemical markers of bone

metabolism and genetic risk factors, which
212 Chapter 8

A Report of the Surgeon General

represents an evolving area of research.

Candidate genes include receptors (proteins in a

cell or on its surface that bind specific substances

such as hormones and are necessary for these

substance to act on the cell) such as the vitamin

D or estrogen receptor genes, and components

of bone itself, such as the collagen gene. In the

future, the characterization of gene subtypes and

further clarification of the roles that these and

many other genes that regulate bone cells play

may allow for the development of assessment

tools that are able to identify at an early age

individuals at high risk of developing

osteoporosis later in life. Additional research on

biochemical markers, genetic factors, and other

clinical risk factors is needed, especially related

to groups other than older White women and

to the prediction of fracture risk over the very

long term.

Key Questions for Future

Research

Assessing the risk of bone disease and

fracture remains a challenge. Not all of the risk

factors have been identified, and the relative

importance of those that are known remains

unclear. The answers to the following research

questions can help in meeting this challenge:

• What strategies would be most effective

in promoting the cost-effective use of

bone densitometry more broadly to the

at-risk population?

• Given the limitations of bone densitometry, what tests and/or tools are most effective in predicting the risk of fracture

and/or deformity in an individual? Which

tools are most practical in different clinical settings? What existing and yet-to-beidentified risk factors are most effective

at predicting this risk?

• What practical methods are most effective

at assessing the other part of the definition

of osteoporosis—“micro-architectural

deterioration” (changes that occur in bone

because of deterioration of its fine

structure)—especially at high-risk sites

such as the vertebral bodies and proximal

femur. New imaging techniques will be

important not only in analyzing skeletal

microarchitecture, but also in detecting

early skeletal lesions (e.g., in those who

have Paget’s disease or cancer).

• How can biochemical markers best be

used in assessing fracture risk? One key

requirement will be the standardization

and quality control of current assays of

bone remodeling.

• Are there new, as yet undiscovered

biochemical markers of bone resorption

and formation that could be useful in

assessing fracture risk? Can these markers

be identified through detailed studies of

proteins produced by bone cells and

deposited in bone matrix?
Bone Health and Osteoporosis

Assessing the Risk of Bone Disease and Fracture 213

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Am Geriatr Soc 1986 Feb;34(2):119-126.

Tinetti ME, Mendes de Leon CF, Doucette JT,

Baker DI. Fear of falling and fall-related

efficacy in relationship to functioning among

community-living elders. J Gerontol 1994

May;49(3):M140-7.

U.S. Preventive Services Task Force. Screening

for osteoporosis in postmenopausal women:

recommendations and rationale. Ann Intern

Med 2002 Sep 17;137(6):526-8.

Vogt TM, Ross PD, Palermo L, Musliner T,

Genant HK, Black D, Thompson DE.

Vertebral fracture prevalence among women

screened for the Fracture Intervention Trial

and a simple clinical tool to screen for

undiagnosed vertebral fractures. Fracture

Intervention Trial Research Group. Mayo

Clin Proc. 2000 Sep;75(9):888-96.
218 Chapter 9

A Report of the Surgeon General

• There have been important advances in

the ability to prevent and treat fractures

in the last 10 years, especially in those

with skeletal fragility. Just as with the use

of diagnostic measures, there has been a

failure in the United States to apply

appropriate preventive and treatment

measures to many persons at risk for

bone disease.

• Everyone should be informed of the basic

elements of maintaining bone health and

preventing bone disease. Paying

attention to the basics—appropriate

physical activity, nutrition, and

smoking—is critical for everyone,

especially those who have, or who are at

risk of developing, osteoporosis.

• Any individual who is diagnosed with

osteoporosis should be evaluated for

potential secondary causes of the disease,

including the presence of other disorders

or the use of medications that can cause

harm to bone. If secondary causes are

present, actions should be taken to

minimize their impact.

• For the most common bone diseases,

drugs that prevent bone breakdown

(antiresorptives) have been shown to be

effective in reducing the risk of future

Chapter 9: Key Messages

fractures. These drugs not only slow any

further deterioration of the skeleton, but

also allow for some repair and restoration

of bone mass and strength.

• When antiresorptive therapy is not

enough, anabolic therapy is available to

help build new bone and further reduce

the risk of fracture. While this approach

has been developed for the prevention and

treatment of osteoporotic fractures, it can

also be applied to other bone diseases.

• For individuals who remain at high risk of

fracture, an extensive fall prevention

program should be developed. This

program should aim to minimize the risk

of falls in the home and community; avoid

the use of drugs that increase the risk of

bone disease or falls; and protect those who

do fall through the use of hip protectors.

• Specific, effective treatments exist for a

number of bone diseases other than osteoporosis, including hyperparathyroidism, rickets, and osteomalacia. Treatment

is also available for some congenital bone

disorders and for bone disease associated

with kidney failure. For all of these conditions, early detection and treatment are

critical to avoiding crippling deformities

and fractures.
Bone Health and Osteoporosis

Prevention and Treatment 219

PREVENTION AND TREATMENT FOR THOSE

WHO HAVE BONE DISEASES

Chapter 9

Just as there have been great advances in the

ability to identify individuals at risk of fracture

(see Chapter 8), there have been equally

important advances in the ability to prevent and

treat fractures in these individuals, especially

those with skeletal fragility. In particular the

introduction of bisphosphonates and selective

estrogen receptor modulators (SERMs) has given

health care providers new approaches to therapy.

Just as for the use of diagnostic measures,

numerous studies indicate that there has been a

failure in the United States to apply preventive

and treatment measures to many persons at risk

for bone disease. As a result, most high-risk individuals (e.g., those who have suffered a fragility fracture) do not get the testing and treatment

that they need. Use of bone mineral density

(BMD) testing in this population ranges from

3–23 percent, while use of calcium and vitamin

D supplementation ranges from 11–44 percent,

and use of antiresorptive therapy ranges from

12–16 percent (Morris et al. 2004, Smith 2001 et

al.). In fact, most physicians fail to discuss osteoporosis with their patients, even after a fracture (Pal 1999). In a large study of older adults,

four out of five hip or wrist fracture patients did

not receive any treatment after the fracture. The

same study also found that certain groups of

patients, including men, older persons, nonWhites, and those with comorbid conditions, were

less likely than White women to receive treatments

(Solomon et al. 2003). Even when physicians do

suggest therapy, it often does not conform with

recommended practice, as many patients with low

BMD are not treated while others with high BMD

are (Solomon et al. 2000). In other words, the gap

between clinical knowledge and its application in

the community remains large.

It is also important to recognize that the ideal

drugs for the treatment of osteoporosis or other

bone disorders have yet to be developed. Inexpensive, effective agents with few side effects are

needed so that they can be used broadly to prevent fractures and deformities in the enormous

number of individuals who will be at risk of bone

disease as the population ages. (See Chapter 4

for more details on the large at-risk population.)

This chapter reviews the latest evidence on

the prevention and treatment of fractures in individuals with or at high risk for bone disease.

As the box below indicates, the use of the terms

“prevention” and “treatment” can be confusing,

since the goal of many treatments is the prevention of disease or fractures. At the same time,

prevention is often considered a treatment for

those with or at risk for bone disease. Nonetheless, it is important to recognize the critical role

of prevention in all individuals, including (and

perhaps especially) in those known to have bone

disease and/or to be at high risk of fracture.
220 Chapter 9

A Report of the Surgeon General

Treatment as Prevention, and Prevention

as Treatment

The concept of prevention within the area

of bone health is complex, and often encompasses measures that may be more commonly

considered as treatments. In fact, in the field

of bone health, the terms treatment and prevention are often used in an interchangeable

manner, since the major goal of treatment is

the prevention of fractures.

Within both bone health and general

health care, prevention can be thought of as

taking anticipatory actions designed to reduce

the possibility that an event or condition will

occur that could lead an individual to a state

of dependency. Within this broad definition

are three different types of preventive activities.

• Primary prevention refers to actions

that prevent a disease or injury (e.g., osteoporosis) that could lead to a state of impairment.

• Secondary prevention refers to activities that block the progression of an existing

impairment (e.g., bone disease) to a disability

(e.g., fracture); interventions within this area

are often also considered to be treatments.

• Tertiary prevention refers to actions

that block or slow the progression of a disability (e.g., fracture) to a state of dependency. In

some cases these actions may also be considered treatments.

Preventive measures within the area of

bone health span all three types. For example,

certain measures to achieve optimal bone mass

can be considered primary prevention, including encouraging adequate intake of calcium

and vitamin D, appropriate physical activity,

and other bone-healthy lifestyle behaviors.

Other measures that are commonly considered

treatments for osteoporosis, such as using

antiresorptive and anabolic agents, should also

be thought of as secondary prevention, since

they are designed to retard the progression of

the disease to prevent disability. Fall prevention in this population may also be seen as secondary prevention, since its purpose is to prevent disability in an individual who already

has bone disease.

Appropriate and comprehensive treatment

of a fracture is considered tertiary prevention,

because such treatment attempts to prevent a

person with a disability from becoming dependent. Drugs prescribed to individuals who

have already sustained a fracture are also a part

of this tertiary prevention effort. From a public health perspective, physical therapy and

other forms of rehabilitation are considered

methods of tertiary prevention in this population.

This paradigm also fits the management of

other bone diseases. For example, early treatment of Paget’s disease can prevent fractures

and hence can be considered as either secondary or tertiary prevention, depending on the

status of the patient when the treatment is

given. The bottom line is that a spectrum of

preventive activities exists within the area of

bone disease, and treatment is a part of that

spectrum. Assuring bone health requires that

preventive measures be implemented in all its

aspects: to optimize peak bone mass;, to block

excessive resorption; to increase bone formation; to decrease skeletal fragility; to decrease

the severity and frequency of falls; and to accelerate recovery from fracture. In fact, this

entire spectrum of prevention is central to promoting bone health in all populations.

Treatment of Osteoporosis = Prevention of Fractures
Bone Health and Osteoporosis

Prevention and Treatment 221

A Pyramid Approach

One of the primary goals in the treatment of

osteoporosis and other bone diseases is to maintain bone health by preventing bone loss and

perhaps even by building new bone. Another

goal is to minimize the risk and/or impact of falls,

since they are typically the precursor to the most

devastating consequence of bone disease: fractures. The best way to realize these goals is to

employ a combination of various prevention and

treatment strategies. In fact, maintaining bone

health and preventing fractures and deformities

requires a “pyramid” approach (Figure 9-1).

The building blocks of physical activity and

good nutrition (particularly with respect to adequate intake of calcium and vitamin D) represent
222 Chapter 9

A Report of the Surgeon General

measures are not enough there are now additional treatments that can be given to build new

bone (anabolics) and further reduce fracture risk.

While this approach has been developed for the

prevention and treatment of osteoporotic fractures, it can also be applied to other bone diseases.

For those individuals who remain at high risk

of fracture even after treatment (e.g., the frail elderly), the base of the pyramid should include an

extensive program to minimize the risk of falls

in the home and community, to avoid the use of

drugs that increase the risk, and to provide hip

protectors that reduce the risk of fracture in those

who do fall.

The Base of the Pyramid: Maintaining Bone

Health and Preventing Fractures

Prevention is, by far, the most effective way

to promote bone health, and thus represents the

base of the pyramid (Figure 9-1a). Everyone

should be informed of the basic elements of maintaining bone health. Everyone should strive for

adequate levels of calcium and vitamin D intake.

Everyone should engage in regular weight-bearing exercise and avoid behaviors that impair

bone health such as smoking. Everyone should

understand the basics about how to avoid falling. These elements serve as the foundation of

prevention of bone disease and fractures. They

may be all that are required in individuals at low

risk of bone disease, but they are critically important for high-risk patients as well.

The remainder of this section provides a very

brief overview of the key elements of prevention that every individual and provider should

know. Much more detail about each of these areas is provided in Chapters 6 and 7.

Calcium: For postmenopausal women, the

recommended total daily calcium intake is 1,200

mg per day in two or more doses. These levels

of intake can be achieved through dietary sources

of calcium, including both dairy and non-dairy

products. A detailed list of these foods and beverages appears in Chapter 7, while another list

ranked by calcium content can be found in

Chapter 10. In addition, calcium supplements

(e.g., calcium carbonate, calcium citrate, other

calcium salts) are available in the form of pills,

chewable tablets, and liquids, as discussed in

Chapter 7. The total daily calcium intake should

not exceed 2,500 mg (IOM 1997).

Vitamin D. Vitamin D is important for absorption of calcium and mineralization (hardening) of bone. As discussed in Chapter 6, vitamin

D is synthesized in the skin through sunlight

exposure, or it may be taken as a supplement.

However, the skin of older individuals does not

synthesize vitamin D as well as the skin of

younger individuals, and in some parts of the

country, the winter sun does not produce vitamin D in the skin of all individuals. In addition,

vitamin D is not available in many foods other

than fortified milk, which contains 100 IU (international units) per cup. Thus, many individuals will need to take a supplement, especially those

who avoid sun exposure, use sun block, or do

not drink milk. The recommended dose of vitamin D is 200 to 600 IU daily, with the dose dependent on age, as shown in Table 7-1 (IOM

1997). However, many experts are recommending more vitamin D for the frail elderly (Heaney

and Weaver 2003). The total daily vitamin D

intake of persons who are not vitamin D deficient should not exceed 2,000 IU (IOM 1997).

Many calcium supplements contain vitamin D.

Most multivitamins contain 400 IU of vitamin

D. Vitamin D supplements can be taken on their

own, or with calcium or food.

Patients who are vitamin D insufficient (low

levels of vitamin D in the blood) or deficient
Bone Health and Osteoporosis

Prevention and Treatment 223

(very low levels of vitamin D in the blood)

require treatment with higher doses of vitamin

D. Vitamin D deficiency can lead to secondary

hyperparathyroidism (see below) with normal

levels of blood calcium. Severe cases lead to

osteomalacia or rickets (see Chapter 3). It should

be noted that the optimal range for 25-

hydroxyvitamin D is higher than the “normal”

ranges reported from clinical laboratories, since

these ranges are obtained from a population that

includes individuals with sub-optimal levels.

Patients can be treated with vitamin D

supplementation of 50,000 IU once a week for

up to 3 months with follow-up blood tests of

vitamin D, calcium, and PTH levels. Some

patients may require longer courses of treatment

(Pettifor 2003).

Physical Activity. Weight-bearing, strength,

and balance-training exercises are also an

important part of any osteoporosis prevention

and treatment program, regardless of age. They

can help increase or preserve bone mass and may

also help reduce the risk of falling. As discussed

in Chapter 6, all types of physical activity can

contribute to bone health. Activities that are

weight bearing or involve impact are most useful

for increasing or maintaining bone mass.

Activities that are not weight bearing or are low

impact may help improve balance and

coordination and maintain muscle mass, which

can help prevent falls. To encourage increased

levels of physical activity among all age groups,

“Physical Activity and Health: A Surgeon

General’s Report” recommends a “minimum of

30 minutes of physical activity of moderate

intensity (such as brisk walking) on most, if not

all, days of the week” (USDHHS 1996). Since

the skeleton responds preferentially to strength

training and short bouts of high-load impact

activity (such as skipping or jumping), the same

report recommends that adults supplement their

cardiorespiratory endurance activity with

strength-developing exercise at least two times

per week. Chapter 7 addresses specific ways to

incorporate strength and loading activities into

an overall habit of physical activity.

For those who cannot engage in regular

physical activity due to disability, mechanical

stimulation of the skeleton might prove

beneficial. Recent, small studies found that use

of vibrating platforms increased BMD and

slowed bone loss (Rubin 2004 et al., Verschueren

et al. 2004, Ward et al. 2004). This may provide

another way to reduce fracture risk both in the

elderly and in younger individuals with

disabling conditions that limit their ability to

exercise. However, the long-term safety and

efficacy of such approaches remain to be

determined, and therefore specific rehabilitation

and exercise programs aimed at increasing

activity and function remain critically important

in the frail elderly and in younger individuals

with neuromuscular disabilities.

Fall Prevention. Falls represent perhaps the

biggest threat to the bone health and the functional independence of older individuals. Falls

are common and frequently are the precipitating event that leads to a fracture or fractures in

an individual. Thus, fall prevention offers another important opportunity to protect the bones

throughout life, but particularly in those over

age 60. Falls occur for a variety of reasons, with

multiple factors often contributing to a single fall.

These factors include problems with balance,

mobility, vision, lower extremity weakness, and/

or blood pressure or circulation. Often these

problems are compounded by an acute illness

(e.g., infection, fever, dehydration, arrhythmia),

a new medication, or an environmental stress

(e.g., standing or walking on an unsafe surface,

poor lighting) that leads to the fall. To reduce

the risk of falls, a variety of fall prevention mea-
224 Chapter 9

A Report of the Surgeon General

sures should be encouraged for frail, elderly individuals. These include regular vision checks;

elimination (where possible) of medications and/

or dosages that may cause dizziness, low blood

pressure, or confusion; and addressing environmental problems or obstacles that can lead to falls,

including removing throw rugs, installing night

lights, installing railings on stairs and grab bars

in showers, encouraging use of rubber-soled

shoes and slippers, and attaching phone cords

and other wires to the baseboard of the wall. Hip

protectors or hip pads might also be useful in

reducing the impact of those falls that do occur.

More information on fall prevention strategies

can be found in Chapter 7.

The Second Level of the Pyramid: Assessing

and Treating Secondary Causes

The first level of the pyramid applies to all

individuals whether or not they have low bone

mass or multiple risk factors for osteoporotic fractures. The second level (Figure 9-1b), which is

important for patients at high risk for fractures,

involves determining whether there are secondary causes or aggravating factors for the osteoporosis and addressing them therapeutically

if they exist.

The vast majority of older postmenopausal

women with osteoporosis will have the primary form

of the disease, with secondary factors likely playing

only a limited role. However, there can be considerable therapeutic benefit from uncovering such factors and dealing with them appropriately if they exist. In men and younger women with osteoporosis,

secondary factors often play a major role, and the

diagnosis and treatment of these factors may be the

most important part of managing their bone disease.

For a complete list of secondary factors that can cause

or contribute to osteoporosis, see Chapter 3.

One important reason for dealing with secondary factors is that the therapeutic response

to specific treatment can be substantial. For example, large increases in BMD have been observed after treatment of hyperparathyroidism

(Silverberg 1995) and epidemiologic studies have

shown that fracture rates decrease substantially

when glucocorticoid therapy is discontinued

(van Staa 2000).

A careful history can suggest possible secondary factors and guide the health care provider in carrying out appropriate tests. At a minimum, serum calcium concentration should be

measured. In populations and geographic areas

where vitamin D deficiency is common, measurement of 25-hydroxy vitamin D is another

useful screening test. Measurement of calcium

and creatinine in fasting, second-voided morning urines or 24-hour urines may be useful in

detecting high or low calcium excretion. High

calcium excretion may be associated with bone

loss while low calcium excretion may be associated with malabsorption and vitamin D deficiency. Patients with gluten-sensitive enteropathy or sprue may present with osteoporosis yet

have few gastrointestinal symptoms. Weight loss

is often a key sign of this disorder or of other

underlying diseases such as malignancy. Many

physicians recommend screening for thyroid

disease, which is relatively inexpensive. Because

screening for Cushing’s syndrome can be difficult and costly, it should be reserved for patients

in whom the history and physical examination

strongly suggest the possibility of this disorder.

Treatment of most secondary causes of bone

loss and fractures is generally well established

and is described later in this chapter. In patients

with severe osteoporosis the treatment of secondary factors should be carried out together with

pharmacotherapy for the bone itself, as this approach helps to improve bone strength and
Bone Health and Osteoporosis

Prevention and Treatment 225

Study Design Issues Related to Treatment

Many studies have focused on the

effectiveness and safety of treatments for

bone disease, and consequently many issues

must be considered in examining and

comparing the results of these studies. First,

therapeutic effectiveness is best examined

with interventions that have been assessed

in randomized (i.e., treatment is randomly

given to patients), double-blinded (i.e.,

patients and physicians are not told what

treatment the patients are on), placebocontrolled (i.e., some participants take an

inactive pill to control for expectations) trials.

Second, a study duration of at least 3 years

is preferable in order to see meaningful

results. In recent years, the FDA has

required organizations that apply for FDA

approval for drugs to treat osteoporosis to

conduct randomized, double-blind, placebocontrolled trials of at least 3 years’ duration

to test the drug’s effectiveness with respect

to fracture reduction. Studies of fracture

reduction can focus on clinical fractures

(fractures that are painful), spine fractures

assessed by standard x-rays (two-thirds of

these fractures are not painful), non-spine

fractures, and hip fractures. Although the

most important study outcome is fracture

risk reduction, changes in BMD or markers

of bone turnover (see Chapter 8) can be used

as supportive evidence of the effectiveness

of treatment. Another study outcome relates

to how quickly the medication will work in

improving BMD or reducing risk of fractures.

In addition, it is important to consider the

duration of therapies (to help in determining

the recommended length of treatment) and to

know what happens when therapies are

discontinued.

Despite the multitude of good studies, it is

not possible to compare the effectiveness of

different therapies by comparing the results

from separate investigations. This is because

the inclusion and exclusion factors for patient

enrollment in the various studies are different;

the duration, intensity of daily physical activity,

outcome measures, and statistical analyses

vary; and the amount or type of calcium/

vitamin D supplements varies. Therapies can

only be compared if they have been given to

patients in the same trial. For this reason, the

differences in effects on fracture reduction and

BMD that are reported for medications from

different studies may not represent true

differences in the efficacy of the drug being

used, but rather differences in the populations

being tested. Because comparative studies

require unrealistically high numbers of

patients, it is unlikely they will be funded.

A meta-analysis is a summary of multiple

studies evaluating the same type of treatment.

Because it incorporates many studies, such

analysis often provides the best available

evidence on the effectiveness of a given

treatment. Several meta-analyses have been

conducted that help to better understand the

value of treatments, including for calcium and

vitamin D. The results of these studies are

reported in Chapter 6.

minimize fracture risk as quickly as possible.

BMD measurements, which are ordinarily done

every 2 yearss during the treatment of primary

osteoporosis, may be done more frequently for

some individuals with secondary osteoporosis,

including those with glucocorticoid-induced osteoporosis, which can cause relatively rapid

changes in BMD.
226 Chapter 9

A Report of the Surgeon General

FDA-approved. Many estrogen preparations are

approved for prevention of bone loss. Nasal and

injectable calcitonin are also approved for treatment of osteoporosis.

Anabolic therapy is now available for those

individuals who continue to fracture or lose bone

on an adequate program of general prevention

and antiresorptive therapy. The only FDA-approved anabolic agent is a synthetic form of parathyroid hormone known as teriparatide.

Teriparatide, which is given as a daily subcutaneous injection, costs substantially more than

does antiresorptive therapy.

 In some situations individuals with osteoporosis have been treated with a combination

of two antiresorptive agents or with an

antiresorptive and an anabolic agent. Sometimes

the two agents are given simultaneously while

other times they are given sequentially. The effectiveness of these types of combination therapies is currently being studied.

The remainder of this section reviews the

evidence to date on the effectiveness of the

different types of antiresorptive and anabolic

agents that are available and of therapies that

combine two antiresorptive agents or an

antiresorptive agent with an anabolic agent.

Antiresorptive Therapy

Bisphosphonates. Bisphosphonates are

phosphate-based, non-hormone compounds that

have been shown to increase BMD and decrease

fractures (Fleisch 2001). At present, there are two

bisphosphonates that are FDA-approved and

readily available for osteoporosis prevention and

treatment: alendronate (Fosamax®) and

risedronate (Actonel®). These medications bind

to the bone surface and then are taken up by

osteoclasts (cells that break down bone) as these

cells attempt to resorb that bone. They block

the pathway that leads to production of certain

The Third Level of the Pyramid: Treatment

Treatment represents the third level of the

pyramid (Figure 9-1c). This section reviews

treatment options for bone disease, with an emphasis on osteoporosis, the disease for which the

most treatment options exist.

Drug Therapy for Osteoporosis

There are two primary types of drug therapy

for osteoporosis. The first is use of antiresorptive

agents, which are drugs that reduce bone loss,

while the second involves use of anabolic agents,

which are drugs that build bone. Antiresorptive

therapies include use of bisphosphonates, estrogen, selective estrogen receptor modulators

(SERMs), and calcitonin. Antiresorptive therapies reduce bone loss, stabilize the

microarchitecture of the bone, and decrease bone

turnover—all leading to fracture reduction. They

increase BMD because the resorption spaces in

bone get refilled with new bone and the amount

of mineral in the bone increases. Antiresorptive

therapies act by decreasing the activity of the

osteoclasts, the cells responsible for bone resorption (breakdown). Antiresorptive therapy

should be considered for all patients with the

diagnosis of osteoporosis as well as for some other

bone disorders. This therapy is effective in reducing the risk of future fractures, although, as

discussed below, different forms of antiresorptive

therapy vary in their safety and efficacy. At

present, the Food and Drug Administration has

approved two bisphosphonates, alendronate and

risedronate, for prevention or treatment of osteoporosis for either daily or weekly oral administration. Another bisphosphonate, ibandronate,

is being considered and additional agents (see

below) are under investigation, including intravenous forms. Only one SERM, raloxifene, is
Bone Health and Osteoporosis

Prevention and Treatment 227

alfacalcidol, an active vitamin D analog, and

found to reduce vertebral fractures by 57 percent

and increase spine BMD by 11.5 percent, as

compared to the alfacalcidol-treated group

(Ringe et al. 2004). Alendronate and calcitriol

were found to slow the rapid bone loss that occurs

after heart transplantation, but calcitriol was

found to cause an excessive increase in urine

calcium excretion in many patients (Shane et al.

2004). Finally, alendronate is approved for the

prevention of steroid-induced osteoporosis (Saag

et al. 1998) and for the treatment of Paget’s

disease (Lyles et al. 2001) and has also been

shown to be helpful for patients with

osteoporosis imperfecta and bone loss due to

hyperparathyroidism (Chow et al. 2003) (see

below and Chapter 3).

Alendronate is currently approved for all

women for prevention of postmenopausal osteoporosis at a dose of 5 mg daily or 35 mg if

taken once a week. It is approved for the treatment of postmenopausal osteoporosis at a dose

as compared to the alfacalcidol-treated group

(Ringe et al. 2004). Alendronate and calcitriol

were found to slow the rapid bone loss that occurs after heart transplantation, but calcitriol

wasof 10 mg daily or 70 mg if taken once a week.

Alendronate is well-tolerated (Liberman et al.

1995, Black et al. 1996, Cranney et al. 2002a);

the most common side effects include pain in

osteoporosis, alendronate was compared to

alfacalcidol, an active vitamin D analog, and

found to reduce vertebral fractures by 57 percent and increase spine BMD by 11.5 percent,

the stomach or esophagus and swallowing difficulties. Esophageal ulcers have occurred in some

patients on these types of daily bisphosphonates.

Alendronate should not be used in patients with

abnormalities of the esophagus that delay esophageal emptying, such as stricture (narrowing) or

achalasia (muscle spasm).

essential lipid compounds inside the osteoclast, thus

leading to earlier cell death and therefore a

diminished ability for osteoclasts to cause bone loss.

The effectiveness of this approach has been

well documented. For example, alendronate has

been shown to increase BMD by 6–8 percent at

the spine and by 3–6 percent at the hip over a

three-year period in postmenopausal women

with osteoporosis (Black et al. 1996, Liberman

et al. 1995). These seemingly modest increases

in BMD are associated with significant reductions in fracture risk—roughly 50 percent, in fact,

for spine, hip, and wrist fractures (Black et al.

1996, Cranney et al. 2002a). These agents show

benefits quickly, as evidence of a reduced risk of

fracture can be seen as early as a year for spinal

fractures and in 18 months for hip fractures

(Black et al. 2000). In addition, approximately

95 percent of postmenopausal women who take

alendronate maintained or increase their bone

mass (Black et al. 2000, Liberman et al. 1995).

Alendronate has been shown to prevent

bone loss in a diverse array of patients, includ

ing younger postmenopausal women without

osteoporosis and elderly, frail residents of longterm care facilities (Fleisch 2001). The drug has

been studied in clinical trials and appears to be

safe and effective for up to 10 years (Bone et al.

2004). Furthermore, the benefits of alendronate

appear to continue after the therapy is stopped;

for example, when older postmenopausal women

discontinue therapy after several years of

treatment, BMD appears to be maintained for 2

yearss (Tonino et al. 2000). Alendronate also

appears to work for men, and it is therefore

approved for the treatment of male osteoporosis.

In one study, BMD of the spine increased

approximately 5 percent at the end of 2 years in

men with osteoporosis (Orwoll et al. 2000). In

another 3-year study of men with primary

osteoporosis, alendronate was compared to
228 Chapter 9

A Report of the Surgeon General

Like alendronate, risedronate has also been

shown to increase BMD and reduce fracture risk

significantly. Studies have found that risedronate

increases spine BMD by approximately 5 percent and hip BMD by 2–3 percent over 3 years

in postmenopausal women with osteoporosis

(Harris et al. 1999). Treatment with risedronate

is associated with a 41 percent reduction in spine

fractures (Harris et al. 1999), a 39 percent reduction in non-spine fractures (Harris et al.

1999), and a 30 percent reduction in hip fractures (McClung et al. 2001). Like alendronate,

the benefits of risedronate can be seen relatively

quickly. For example, reductions in spine fractures can occur after 1 year of therapy (Harris et

al. 1999). Studies have examined the safety and

effectiveness of risedronate for up to 5 years and

have shown persistent reduction in fractures

without adverse effects (Sorensen et al. 2003).

Risedronate also has been shown to prevent bone

loss at the hip and spine in postmenopausal

women with low bone mass who do not have

osteoporosis but have low bone mass (as indicated by BMD). Risedronate is approved for

both the prevention and treatment of steroidinduced osteoporosis in men and pre- and postmenopausal women (Reid et al. 2000), and for

the treatment of Paget’s disease (Lyles et al. 2001)

(see below and Chapter 3). Risedronate is approved at a dose of 5 mg per day or 35 mg once

per week. The most common side effects include

pain in the stomach or esophagus and difficulties in swallowing.

Ibandronate is another bisphosphonate that

is currently FDA-approved for the treatment

and prevention of osteoporosis in postmenopausal women at a dose of 2.5 mg daily; however, it is not readily commercially available.

Over a 3-year period, ibandronate has been

shown to decrease the incidence of new spine

fractures by 52 percent and to increase BMD at

the spine by 5 percent (Delmas et al. 2002), with

no abnormalities found on bone histology

(Recker et al. 2004). Ibandronate has also been

shown to prevent bone loss in early postmenopausal women who are not yet osteoporotic

(McClung et al. 2004).

Etidronate is a bisphosphonate that is not

FDA-approved for the prevention and treatment of osteoporosis in the United States, although it is approved in Canada and other

countries. It is approved in the United States

for the treatment of Paget’s disease (see below).

Several small studies in postmenopausal women

with osteoporosis have shown that etidronate

increases BMD by 4–5 percent at the spine over

2–3 years and decreases spine fractures by approximately 50 percent (Watts et al. 1990,

Hanley et al. 2000). It also has been shown to

prevent bone loss in patients who start or are

on chronic steroid therapy. In contrast to the

other bisphosphonates that are taken daily,

etidronate is taken on an intermittent schedule

of 400 mg per day for 2 weeks every 3 months

which is repeated for 2 years or more. A generally well-tolerated drug (Hanley et al. 2000),

etidronate acts differently than do other

bisphosphonates. When it is removed from the

bone surface by osteoclasts, it forms toxic products inside the cell, thus resulting in early death

of osteoclasts. However, it is not as potent as

the newer bisphosphonates and can also impair

the laying down of mineral during new bone

formation if given in high doses.

All bisphosphonates are poorly absorbed

and therefore should be taken alone first thing

in the morning on an empty stomach with a full

glass of water. Food should not be eaten for at

least 30 minutes after taking the drug. Patients

should not lie down during this period, to
Bone Health and Osteoporosis

Prevention and Treatment 229

prevent irritation of the esophagus. Physicians

should proceed cautiously when prescribing

amino-bisphosphonates (alendronate or

risedronate) to patients with a known history of

narrowing or ulcers of the esophagus or longterm problems with stomach ulcers and

heartburn that require medication.

Bisphosphonates are incorporated into bone

and, therefore, may continue to provide benefits

for a long period of time after treatment is

discontinued (unlike hormone therapy, as

discussed earlier). Bisphosphonates should not

be given to pregnant women or patients with

poor kidney function, since good kidney

function is required to clear this drug from the

blood. Little information is available on the use

of bisphosphonates in children. Bisphosphonates

that need only be administered once a year on

an intravenous basis are currently under

investigation (see Future Agents). This approach

would circumvent the problems of poor

absorption and gastrointestinal irritation and

might also improve compliance.

Hormone Therapy. As noted in earlier

chapters, estrogen is a hormone that is important

throughout life to bone development and

maintenance in both men and women. Unlike

the bisphosphonate drugs discussed earlier in this

chapter, estrogen acts on many reproductive and

non-reproductive tissues in the body. Therefore,

the use of exogenous forms of estrogen as a drug

for the prevention or treatment of osteoporosis

necessarily involves consideration of how the

form and dose of estrogen might affect other

tissues. Of particular importance is whether there

are any risks that might limit its use.

 • Background on Hormone Therapy. Fuller

Albright, a clinical researcher in the 1930s,

observed that most of his patients with

osteoporosis were postmenopausal women.

Given this, Albright proposed that estrogen

triggers a buildup of calcium reserves in bone

during adolescence to provide for later

reproductive needs (pregnancy and lactation),

and that bone is lost after menopause when

estrogen levels decrease (Riggs et al. 2002).

Many subsequent observations have confirmed

the theory that “replacing” estrogen in

postmenopausal women prevents bone loss, and

thus this approach naturally seemed to be an

effective way to stave off the effects of

menopause on bone.

The FDA approved estrogen in 1942 in the

form of conjugated equine estrogens (CEE),

derived from the urine of pregnant horses, for

the relief of menopausal symptoms. The use of

hormone therapy by postmenopausal women

increased dramatically during the 1960s, and, in

1972, the FDA approval was extended to

postmenopausal osteoporosis. This latter

approval was based on evidence from trials that

evaluated the impact of estrogen therapy on bone

mass, not on fracture reduction. However, by

the early 1970s it also became clear that estrogen

alone (without progestin) was associated with an

increased risk of endometrial (uterine) cancer.

Since this time only women who have had their

uterus removed by hysterectomy are prescribed

estrogen alone; others receive estrogen combined

with some form of progesterone, another

hormone, to protect the uterus.

 • The Evidence on Estrogen and Combination

Hormone Therapy. Randomized, placebocontrolled studies have been conducted on the

impact of hormone therapy on BMD, including

the Postmenopausal Estrogen/Progestin

Interventions (PEPI) trial (Writing Group 1996)

and the Women’s Health, Osteoporosis,

Progestin, Estrogen (HOPE) study (Lindsay et

al. 2002). These trials and a recent meta-analysis
230 Chapter 9

A Report of the Surgeon General

(Wells et al. 2002) show that postmenopausal

hormone therapy has a consistent and favorable

effect on BMD at all sites, including increases at

the spine (3.5–7 percent), hip (2–4 percent), and

forearm (3–4.5 percent). These studies also

suggest that increases in BMD become apparent

within the first year of hormone therapy. Both

the PEPI trial and the meta-analysis, which

included different forms of estrogen (CEE as well

as estradiol, the natural form of estrogen in

humans) and combination therapy, found no

significant differences in the effects of different

formulations of estrogen on bone density.

Research evaluating the impact of hormone

therapy on fracture rates, however, is more

limited. Studies comparing women who had

taken postmenopausal hormones over a long

period of time with women who had never taken

hormones indicate that there are fewer fractures

in the hormone users (Kiel et al. 1987, Cauley et

al. 1995). These types of “observational” studies,

which observe what people decide to do or take

on their own, are subject to biases. For example,

women who take hormones are also more likely

to take other measures to enhance their health.

In fact, up until the mid-1990s, there had been

very few randomized clinical trials of estrogen

focusing on fracture as an outcome, and these

trials tended to be quite small.

Nevertheless, Torgerson and Bell-Syer

attempted to fill this evidence gap by

systematically reviewing those randomized trials

of estrogen therapy that did include fractures as

an outcome to be evaluated. Their meta-analyses

suggest that estrogen reduces the risk of nonspine fractures by 27 percent (Torgerson and

Bell-Syer 2001a) and spine fractures by 33

percent (Torgerson and Bell-Syer 2001b).

The WHI Hormone Trials, which were

designed and initiated in the early 1990s to

address the primary question of whether

postmenopausal HT decreased the risk of heart

disease, have provided answers on a range of

chronic disease outcomes in older women,

including fractures. Two separate trials were

conducted. One enrolled women with an intact

uterus and evaluated the effects of an estrogenprogestin combination or E+P (0.625 mg

conjugated equine estrogen, CEE, and 2.5 mg

medroxyprogesterone, MPA, daily) (Rossouw

et al., 2002), while the second evaluated the effect

of estrogen (0.625mg CEE) alone in women who

have had hysterectomies (Anderson et al. 2004).

The WHI trial of combined continuous hormone

therapy confirmed for the first time the effects

of these hormones on osteoporotic fracture

reduction at several sites, including the hip

(Cauley et al., 2003). Hip and spine fractures

were reduced by at least one-third in both of the

trials and total fractures fell by 24–30 percent.

Thus, these two large trials, which included

16,608 women in the E+P study and 10,739

women in the estrogen-only study, confirmed

the anti-fracture efficacy of postmenopausal HT,

and they are consistent with observational studies

of hormone users and the results of trials

evaluating the effect of HT on BMD.

The clear benefits of postmenopausal HT to

the skeleton must be tempered by the other

results from the WHI trials, which were

discontinued early because of the deleterious

effects encountered. Both trials found an

increased risk of stroke, cognitive impairment,

and deep vein thrombosis in the women taking

HT (Rossouw et al. 2002, Anderson et al. 2004,

Shumaker et al. 2003; Shumaker et al. 2004). The

trials also found no clear cardiovascular benefit

to HT. Breast cancer risk was increased in

women taking the combined continuous therapy

(E+P) during the 5.2 years of the study, a
Bone Health and Osteoporosis

Prevention and Treatment 231

finding that is consistent with observational

studies (Collaborative Group 1997, LagroJanssen 2003). This increase in breast cancer was

not observed in the estrogen-only trial after 6.6

years of use. Extended follow-up of all WHI

hormone trial participants is planned, and may

provide further insight into this discrepancy.

 • The Future for Hormone Therapy and Bone

Health. Any decision to use hormone therapy

must take into consideration its impact on the

overall risk of negative health outcomes,

including not only its potential to reduce the risk

of fractures, but also its potential to increase the

risk of other health problems. The Food and

Drug Administration (FDA 2003) has advised

that postmenopausal women who use or are

considering using estrogen or estrogen with

progestin discuss the therapy’s benefits and risks

with their physicians. These products are

approved therapies for relief from moderate to

severe hot flashes and symptoms of vulvar and

vaginal atrophy. Although HT is effective for

the prevention of postmenopausal osteoporosis,

it should only be considered for women at

significant risk of osteoporosis who cannot take

non-estrogen medications. The FDA

recommends that estrogens and progestins

should be used at the lowest possible doses for

the shortest amount of time needed to achieve

treatment goals. It is not yet clear whether

following this advice will lead to long term

benefits for bone health. Lower doses of estrogen

or combination hormones can help to preserve

bone density in the short term in postmenopausal

women. For example, the Women’s HOPE

study, a randomized, placebo-controlled study

that investigated the efficacy of various lower

doses of CEE and CEE/MPA found that doses

as low as 0.3 mg per day of CEE or the

combination significantly increased spine and

hip BMD from baseline within 2 years of

therapy (Lindsay et al. 2002). Prestwood et al.

(2003) showed that low dose estradiol also

preserves bone. Unfortunately, at this point, the

long-term effects of different doses,

formulations (including estrogens or

progesterone), and modes of administration

(e.g., transdermal administration) on bone and

other tissues have simply not been studied.

These results raise the question as to whether

there might be some benefit to using hormone

therapy for a short period of time and then

terminating its use (so as to reduce the likelihood

of negative health outcomes). Two randomized

clinical trials shed some light on this issue, as they

followed women who stopped hormone use at

the end of a clinical trial. These studies indicate

that bone loss begins again when hormones are

withdrawn (Greendale et al. 2002, Greenspan

et al. 2002b). Moreover, the long-term

observational studies (Kiel et al. 1987, Cauley et

al. 1995) suggest that even long-term hormone

therapy users (including those on therapy for

more than 10 years) who terminate therapy do

not enjoy a lower risk of hip fractures many

years later. In fact, a recent study (Yates et al.

2004) found that there was a higher rate of hip

fracture in those who discontinued hormone

therapy than in those who never used it.

Another study, a large prospective trial of 5,200

fractures among 140,000 postmenopausal

women in the United Kingdom, found that

while there was a decrease in fracture risk at all

sites in patients currently on estrogen, there was

no decrease in risk in past users of hormone

therapy, even those who had discontinued use

within the past year (Banks et al. 2004). Thus,

the bottom line is that taking hormone therapy

during early menopause is unlikely to have a

long-term effect on the risk of fractures.
232 Chapter 9

A Report of the Surgeon General

Despite all the negatives that have been

raised recently about HT, it is important to

remember that natural estrogen (i.e., that which

is produced by the body) is still critical to bone

health, even for postmenopausal women (and

older men). The evidence suggests that

postmenopausal women with extremely low

endogenous estrogen levels face an increased

risk of both spine and hip fractures when

compared with postmenopausal women with

average levels of estrogen (Cummings et al.

1998). Very low doses of hormone therapy for

these individuals may be a promising treatment

(Prestwood et al. 2003).

The goal of this type of an approach is to

capture the positive effects of estrogen on bone

without incurring any of the deleterious effects

on other tissues. In fact, this is the principle that

has driven research into the selective estrogen

receptor modulators or SERMS that are

discussed in the next section; these agents

selectively act on the estrogen receptors in bone,

breast, and other tissues.

and DNA. Different SERM medications may

have different actions on cholesterol, breast and

uterine tissue, clotting, BMD, and hot flashes.

They have been shown to provide some of the

benefits of estrogen (improvement of BMD and

cholesterol) without some of the negative side

effects (such as breast tenderness and menstrual

bleeding or spotting) (Ettinger et al. 1999). In

fact, in large-scale clinical trials of

postmenopausal women with osteoporosis,

raloxifene (Evista®), the only FDA-approved

SERM, has been shown to increase spine BMD

by 2–3 percent and hip BMD by approximately

2.5 percent after 3 years (Ettinger et al. 1999).

Spine fractures were reduced by approximately

50 percent, but there was no effect on hip or

other non-spine fractures (Ettinger et al. 1999,

Cranney et al. 2002b). Spine fracture reduction

is evident at 1 year (Maricic et al. 2002) and is

sustained for up to at least 4 years if patients

remain on therapy (Delmas et al. 2002). When

therapy is discontinued, bone turnover

(breakdown) can return to its previous state,

resulting in bone loss. Other potential benefits

include a decrease in total cholesterol and low

density cholesterol; there is no change in high

density cholesterol. Although studies have not

been specifically designed to examine prevention

of breast cancer with raloxifene, investigators

from the study mentioned above found that there

was a decreased incidence of breast cancer in the

women who took raloxifene for 3 years

(Cummings et al. 1999). There are now studies

ongoing to examine raloxifene’s effect on breast

cancer and cardiovascular disease prevention.

Raloxifene is FDA-approved for the

prevention and treatment of postmenopausal

osteoporosis at a dose of 60 mg daily. There are

some side effects, including the potential for a

return of hot flashes, blood clots in the legs, or

blood clots in the lungs. Therapy with SERMs

“In the final analysis very little is known

about anything, and much that seems true

today turns out to be only partly true

tomorrow.”

—Fuller Albright, reflecting on the state of

affairs of medicine in general and of endocrinology in

particular in 1948 (Albright and Reifenstein 1948).

Selective Estrogen Receptor Modulators.

Selective estrogen receptor modulators (SERMs)

interact with estrogen receptors located

throughout the body (McDonnell 2003).

Estrogen receptors are the “switches” that turn

cell activity on and off (see Chapter 2 for more

details). SERMs bind to the estrogen receptors,

altering the way they interact with other proteins
Bone Health and Osteoporosis

Prevention and Treatment 233

must be discontinued for patients who are

immobilized or inactive for long periods of time

(e.g., during hospitalizations).

Another SERM, tamoxifen, is used for the

prevention of breast cancer, but it is not approved

for the prevention and treatment of osteoporosis.

Small clinical trials in premenopausal and

postmenopausal women participating in a breast

cancer prevention study demonstrated that

tamoxifen maintains or improves BMD in

postmenopausal women but causes bone loss in

premenopausal women (Powles et al. 1996).

Information on fracture reduction from clinical

trials is not available.

Newer SERMs under development may be

more beneficial to the bones, heart, and breast

tissue. They may also decrease hot flashes and

improve cholesterol. There are no data to suggest

that SERMs would be beneficial in the treatment

of male osteoporosis, Paget’s disease, or

childhood osteoporosis.

Calcitonin. Calcitonin is a hormone secreted

by the parafollicular (non-thyroid) cells found

within the thyroid gland (Silverman 2003). Its

effect on bone is to inhibit bone resorption by

acting directly on the osteoclasts. Its ability to

inhibit osteoclast activity has been known for

more than four decades. At one time in the 1970s,

calcitonin was the only drug available to treat

hypercalcemia of malignancy and Paget’s disease

of the bone. Calcitonin was also one of the first

drugs available for the treatment of osteoporosis.

In the 1970s and 1980s, calcitonin was

administered as a subcutaneous (under the skin)

injection. More recently, nasal calcitonin

replaced the injection form of this hormone.

Although originally very popular as an

alternative for postmenopausal women who

could not tolerate bisphosphonates, estrogen, or

raloxifene, its use has declined with the advent

of newer treatments for postmenopausal

osteoporosis. Oral and inhaled forms of calcitonin

are currently under development.

There are only a few randomized controlled

trials for nasal calcitonin. The Prevent

Recurrence of Osteoporotic Fractures (PROOF)

trial, the largest RPCT of nasal calcitonin,

reported that spine fractures declined by 33

percent for those individuals taking a 200 IU

dose per day, but there was no significant decline

for those receiving 100 or 400 IU per day.

Furthermore, there were no significant

differences in non-spine fracture rates after 5

years (Chesnut et al. 2000).

The PROOF trial has come under scrutiny

for a number of reasons, including the

somewhat surprising finding that those

individuals taking a higher dose did not see a

reduction in fractures. In addition, a large

number of the subjects did not complete the

study. Hence flaws in the study methods used

do not allow a firm conclusion about

calcitonin’s impact on spine and non-spine

spine fractures (Chesnut et al. 2000). Calcitonin

may have a somewhat unique benefit in

providing pain relief, particularly for women

who have just sustained a spine fracture (Mehta

et al. 2003). Studies looking at this potential

benefit also do not provide a clear-cut answer.

Nasal calcitonin has very few side effects,

namely, nasal stuffiness, nausea, and dry

mouth. It is currently approved at 200 IU per

daily spray for the treatment (not prevention)

of osteoporosis in women who underwent

menopause five or more years ago.

Combination Antiresorptive Therapy.

Although bisphosphonates, hormone therapy,

and SERMs are all antiresorptive drugs, they

work through different mechanisms of action,

implying that they could have an additive effect

if used in combination (i.e., using both would

be more beneficial than would either used alone).
234 Chapter 9

A Report of the Surgeon General

Therefore, antiresorptive drugs have been studied

in combination. One study compared 2-year use

of two antiresorptive therapies together to similar

use of estrogen and alendronate alone in

postmenopausal women with a hysterectomy

(Bone et al. 2000). BMD increased approximately

8 percent at the spine in those on combination

therapy, compared to 6 percent in women taking

alendronate or estrogen. Similar trends were

noted in BMD at the hip, where combination

therapy resulted in a 1–2 percent greater increase

in BMD than either therapy alone. Importantly,

participants in the combination therapy group did

not have additional unexpected side effects. A

recent 3-year study in women age 65 and older

found that using hormone therapy and

alendronate together resulted in greater increases

in bone mass at the spine and hip than did therapy

with either agent alone (Greenspan et al. 2003).

Hormone therapy has also been used in

combination with risedronate in a short-term

study. At the end of a year, the hip BMD (but

not the spine BMD) of participants on

combination therapy was greater than that of

participants receiving hormone therapy or

risedronate alone (Harris et al. 2001). In another

1-year study, hip BMD was greater in

participants taking a combination therapy of

alendronate and raloxifene than in those taking

either agent alone (Johnell et al. 2002). The study

also found that BMD of the spine and hip in

participants taking alendronate alone was

significantly higher than in participants taking

raloxifene alone; however, the study was not

large enough to determine whether there was

any difference in fracture reduction.

Studies have also examined another

important issue—whether combination therapy

is better than single-agent therapy at maintaining

BMD after discontinuation of the treatment.

Investigators who examined BMD in women on

combination therapy (alendronate and estrogen

replacement) and single therapy (alendronate or

hormone therapy) followed them for an

additional year after therapy was discontinued.

Those who had taken combination therapy or

alendronate alone during the first 2 years

maintained BMD of the spine and hip following

discontinuation of therapy. However, women

who gained bone during 2 years on hormone

replacement lost their BMD gains at the spine

and hip during the year after therapy was

discontinued (Greenspan et al. 2002).

Combination therapies (multiple drugs) are

more expensive and, in principle, could cause

more side effects than therapy with single drugs.

Moreover, because these trials did not examine

fracture reduction, it is unclear if combination

therapy is a cost-effective strategy for reducing

risk of fracture. Therefore, in clinical practice

today, combination therapy is generally reserved

for patients who have experienced a fracture

while on therapy with a single drug, those who

start out with a very low BMD and a history of

multiple fractures, and those with very low BMD

who lose more bone mass on therapy with a single

drug. The combination of anabolic and

antiresorptive agents is discussed below.

Anabolic Therapy. Over the last half century,

antiresorptive therapy has been the primary

treatment for osteoporosis. Recent research has

discovered the potential of intermittent

parathyroid hormone (PTH) as a therapeutic

option for patients with severe osteoporosis.

Unlike other available agents, bone-building

therapy with PTH features stimulation of new

bone formation (Rosen and Rackoff 2001).

Eighteen months of PTH therapy causes

thickening of the outer shell of bones, large

increases in connections between bony islands

within the skeleton, and an overall net increase

in bone strength.
Bone Health and Osteoporosis

Prevention and Treatment 235

Every normal person has PTH. It is typically

secreted at a low level, but secretion increases in

response to reduced levels of serum calcium, a

process that appears to contribute to bone

breakdown. In fact, primary hyperparathyroidism, that is, uncontrolled overactivity

of the parathyroid glands, has been known to

contribute to bone loss, particularly of the cortical

(outer shell) of bone (see Chapter 3). Intermittent

injections of PTH as a therapy actually hold

promise as a means of building up bone. Animal

studies have demonstrated that PTH given

intermittently as a daily subcutaneous injection

leads to significant increases in BMD, restoration

of the inner structure of bone, and increases in

bone size (Lotinun et al. 2002). This paradox—

the fact that PTH secreted continuously can

break down bone while intermittent injections

of the same hormone may actually build bone—

has never been fully explained. It may be related

to the intermittent nature of the exposure to the

hormone that occurs during treatment, as

opposed to the exposure to continuous, excessive

levels of PTH that occur in individuals with

hyperparathyroidism.

Human recombinant PTH (1-34), known as

teriparatide, was developed in the 1980s, with

the hope that it could promote bone building in

humans. Clinical trials designed to test the impact

on fracture rates in humans, which were

originally designed to last 3 years, were stopped

early because of animal data showing

osteosarcoma (bone tumor) formation. Despite

early discontinuation the studies demonstrated

significant increases in BMD and reduction in

fractures. For example, in a study with over 1,600

postmenopausal, osteoporotic women, spine

BMD increased by 9.7 percent and hip BMD

increased by 2.6 percent (Neer et al. 2001) after

approximately 21 months on teriparitide. Spine

fractures decreased by 65 percent and non-spine

fractures by 53 percent (Neer et al. 2001).

Teriparatide also increases BMD in men; in an

approximately 10-month study, spine BMD

increased by 5.9 percent and hip BMD by 1.2

percent (Orwoll 1998). The effects on fracture

risk have not been studied in men.

Because of these significant potential benefits,

the FDA approved teriparatide for the treatment

of osteoporosis in postmenopausal women and

in men who are at high risk for fracture. The

approved dose (20Fg daily by subcutaneous

injection) and duration of treatment have not

been found to be associated with an increased

risk of osteosarcoma in humans.

While the PTH administered daily to postmenopausal women and men with osteoporosis

may benefit some patients (particularly those

with very severe disease), there are some limitations to use of the drug. First, it should not be

prescribed to pediatric patients or adult patients

with hypercalcemia (high levels of calcium in the

blood), Paget’s disease (see below), kidney disease, kidney stones, bone metastases (cancers

that have traveled from another part of the body

to bone), or bone cancer. Second, a small subset

of patients may develop high blood calcium as

well as leg cramps and dizziness. Third, it may

increase serum uric acid, which could potentially

lead to gout, although there is no evidence of an

increase in clinical gout. Fourth, there may be

issues related to compliance since a daily injection is required. Finally, it is much more expensive than antiresorptive therapy.

Additional forms of PTH therapy may be

on the horizon. For example, PTH(1-84) has

shown early promise as a treatment for osteoporosis in preliminary bone density studies

(Hodsman et al. 2003).

Combination Antiresorptive/Anabolic

Therapy. The idea of combining an anabolic agent

with an anti-resorptive therapy has been around
236 Chapter 9

A Report of the Surgeon General

for more than a decade. With the advent of PTH,

combination studies have been proposed to

evaluate the impact of PTH therapy with

antiresorptive therapies such as estrogen and

alendronate. PTH plus estrogen has been shown

to have a greater effect on spine and hip BMD

than estrogen alone, but there are no trials

comparing that combination to PTH alone, nor

are there any studies that evaluate differences in

the impact on fracture rates (Cosman et al. 2001).

Two studies examining the effects of simultaneous

PTH and alendronate treatment suggest that

there may actually be smaller BMD increases with

combination therapy than with PTH alone (Black

et al. 2003, Finkelstein et al. 2003). Another recent

study evaluated the impact of sequential treatment

with PTH for a year followed by alendronate for

a year in 66 women with postmenopausal

osteoporosis year. This sequential treatment

method resulted in substantial increases in spinal

BMD (Rittmaster et al. 2000). The response to

PTH treatment may be affected by prior

treatment with different antiresorptive agents.

Like those patients on estrogen therapy (Lindsay

et al 1997), patients previously treated with

raloxifene showed a rapid and complete response

to PTH, while those previously treated with

alendronate had a reduced response in terms of

biochemical markers of bone formation and BMD

(although they did show increases eventually)

(Ettinger et al. 2004). No data on the relative

impact of PTH treatment on fractures are

available for these different groups.

Future Agents. There are several new

antiresorptive and anabolic drugs on the horizon

for the treatment of osteoporosis. Among

antiresorptive agents, progress has been made

both in developing new treatments and in

improving the means of administering

bisphosphonates. For example, intravenous

pamidronate has been available for the treatment

of Paget’s disease and hypercalcemia of

malignancy (high blood calcium due to cancer)

for nearly a decade. Smaller studies have also

demonstrated that it is effective in increasing

bone mass when administered every 3 months

to postmenopausal women with osteoporosis

(Coleman et al. 2000). A newer drug, zoledronic

acid, was recently approved for the treatment of

metastatic breast cancer, myeloma (see below)

and hypercalcemia (Coleman et al. 2000). It is

administered intravenously is extremely effective

in treating these conditions. A recent trial of this

agent, given as a single intravenous dose once

per year, was shown to increase spine BMD in

women with osteoporosis (Reid et al. 2002). A

large phase III trial is in progress to assess its

effectiveness at reducing fractures.

Along with finding new uses for existing

antiresorptive agents, researchers have also uncovered several potential new types of treatments

during the drug discovery process. A newer class

of antiresorptive drugs (known as integrin inhibitors) prevent osteoclasts from anchoring to

bone surfaces and thereby absorbing the underlying bone (Hutchinson et al 2003). Early studies with this therapy are encouraging with respect to both safety and effectiveness. Agents

that mimic the action of osteoprotegerin can also

inhibit bone resorption and could become useful drugs (Onyia et al. 2004). Statins, the cholesterol-lowering drugs, have been found to stimulate bone formation and may also decrease bone

resorption in animals. Some observational studies in humans suggest that statin users have fewer

fractures, while other studies do not. Controlled

cardiovascular trials did not confirm a reduction

in fractures (Bauer et al. 2004). Finally, strontium ranelate is an element that has some

antiresorptive as well as anabolic qualities, but

the method of action is unclear. In initial

studies, strontium has been shown to improve
Bone Health and Osteoporosis

Prevention and Treatment 237

spine bone density and reduce spine fractures

(Meunier et al. 2002, 2004).

Other new anabolic agents are also being

developed and tested. PTH-related peptide

(PTHrP), a naturally occurring relative of PTH

that is normally made in the breast, uterus, and

pancreas, is undergoing clinical trials for the

treatment of osteoporosis. PTHrP is best known

as a secretion of certain cancers that produces

severe hypercalcemia (high calcium levels in the

blood) and bone resorption. However, when

administered as a single dose intermittently, it

has been shown to markedly increase BMD without causing hypercalcemia (Horwitz et al. 2003).

Treatment of Osteoporotic Fractures

For all osteoporotic fractures, the consistent

goal is for patients to regain their pre-fracture

level of function. All patients with low-trauma

fractures should be evaluated for other bone

diseases (see below) and secondary causes of bone

loss (see Chapter 3). They should also be

evaluated with respect to the need for additional

preventive measures (calcium, vitamin D,

exercise, fall prevention) and for drug therapy,

as described earlier in this chapter. What follows

is a review of the various available treatments

for specific types of osteoporotic-related

fractures, including fractures of the hip, spine,

and wrist.

Hip Fractures. Surgery is the most common

treatment for individuals who suffer a hip

fracture. Virtually all intertrochanteric fractures

(those in the major part of the hip) and most

femoral neck fractures (those in the neck section

of the hip) are surgically stabilized with the use

of internal metal devices. A large percentage of

displaced (unconnected) femoral neck fractures

are treated with partial or total replacement of

the hip because of the significant risk of healing

complications (Zuckerman 1996).

Proper management of hip fracture patients

begins before surgery, at the time of admission.

Evaluation and management of pre-existing

medical conditions is necessary before proceeding to surgery. When possible, management of

pre-existing conditions and surgical repair within

24–48 hours of admission has been shown to

decrease the incidence of post-surgery complications and the possibility of death within a year

of surgery by more than 40 percent (Zuckerman

et al. 1995). The procedure should be performed

by a surgeon who has expertise in hip fracture

stabilization, which will allow the initiation of

mobilization immediately after surgery. The vast

majority of hip fracture patients should be encouraged to become mobile by the first or second post-operative day. Mobility can help to

avoid the medical problems associated with prolonged bed rest, such as muscle atrophy, blood

clots in the legs or lungs, pressure sores, skin breakdown, and overall deconditioning.

The use of antibiotics for the first 24–48

hours after surgery is also advisable, as this practice has been shown to be effective in decreasing

post-surgery infections. Use of techniques to thin

• Antiresorptive agents (reduce bone

loss)

~ Bisphosphonates (alendronate,

risedronate)

~ Hormone or estrogen replacement

~ Selective estrogen receptor

modulators (SERMs) (raloxifene)

~ Calcitonin

• Anabolic agents (build bone)

~ Parathyroid hormone (teriparatide)

Osteoporosis Drug Therapy
238 Chapter 9

A Report of the Surgeon General

the blood after surgery has also been shown to

be effective in decreasing the incidence of blood

clots, particularly in patients who are slow to

mobilize (Todd et al. 1995). Adequate pre- and

post-surgery pain control is also important, not

only for patient comfort, but also to promote

active participation in rehabilitation.

Since hip fractures generally occur in elderly patients with other, associated medical and

psychosocial problems, the health care team

should include professionals from many disciplines, including the orthopaedic surgeon, medical specialists (geriatricians, physiatrists [rehabilitation specialists], primary care physicians, and

medical sub-specialists as necessary), nurses,

physical and occupational therapists, nutritionists, and social workers. The in-hospital care of

hip fracture patients should be guided, whenever possible, by the use of evidence-based clinical care pathways (clinical care based on medical studies) that make use of standardized evaluation and management approaches. This approach should also extend to the entire continuum of care, from the acute care hospital into

the post-discharge setting, whether that setting

is an acute or sub-acute rehabilitation facility, a

skilled nursing facility, or a return home. Effective communication across health settings by

health care providers is also important to effective care management (Morris and Zuckerman

2002). Discharge from acute care hospitals and

independent rehabilitation facilities should be

based on patient progress.

Spine Fractures. Spine fractures usually

occur in the middle or lower section of the back

as a result of minor strain, such as lifting a grocery

bag. Some patients develop fractures without any

identifiable trauma. Spine fractures due to

osteoporosis result in the progressive collapse of

bones in these areas, which typically cause

increasing levels of spinal deformity and pain.

However, about two-thirds of spine fractures go

undiagnosed because there is little or no pain, or

the pain is attributed to one of the many other

causes of back pain (Johnell et al. 2002).

Similarly, other signs of a spine fracture,

including deformities and height loss, are often

accepted as a normal part of aging and thus not

investigated further.

It is not unusual for patients to have prolonged pain and disability following spine fractures. Treatment of spine fractures typically focuses on pain control and progressive increases

in levels of mobilization. Back braces are of limited benefit. More recently, procedures have been

developed to treat patients who have prolonged

pain. Vertebroplasty is a technique in which

acrylic cement (or orthopedic cement mixture)

is injected into the spine bone for the purpose of

stabilizing the fracture (Evans et al. 2003).

Kyphoplasty involves using a balloon to re-expand the collapsed bone and then filling the cavity with bone cement. This procedure has the

potential to stabilize the fracture, prevent further collapse, and restore some degree of height

to the bone (Lieberman et al. 2001). Both

vertebroplasty and kyphoplasty have been

shown to provide effective pain relief and stabilization of the fracture (Evans et al. 2003,

Lieberman et al. 2001). Although complications

from these procedures have been infrequent,

they can be significant if the bone cement leaks

out into the blood stream or into the spinal canal, causing nerve damage. Unfortunately, the

potential benefit of these two procedures has not

yet been accurately assessed in RPCTs, where

they might be compared to each other and to

nonsurgical management.

Wrist Fractures. Wrist fractures commonly

occur as a result of osteoporosis. They include

fractures of the radius and/or ulna (the two long

bones in the forearm), as well as of the small
Bone Health and Osteoporosis

Prevention and Treatment 239

bones of the wrist. The term Colles’ fractures

refers to fractures of the end of the radius, which

has a large amount of trabecular bone. Wrist

fractures are usually treated by either surgical

repositioning and casting or placement of an

external fixation device to prevent further

fracture. Depending on the type of fracture, one

of the following will be used to immobilize the

wrist until an x-ray shows evidence of healing

(usually in 4–8 weeks): a brace or splint, cast,

external fixation, internal fixation, or combined

external and internal fixation. Although most

patients return to an adequate level of

functioning, many do experience some loss of

range of motion of the wrist.

Other Fractures. Osteoporotic fractures

occur in other areas of the body, including the

upper arm, thigh, shin, collar bone, and ribs.

These fractures are treated by a variety of

surgical and non-surgical measures.

Rehabilitation of Osteoporotic Fractures

Hip Fractures. As noted previously, hip

fracture patients typically undergo surgery to

reposition the hip through internal fixation (e.g.,

insertion of a metal pin or plate) or to replace the

hip through joint replacement. Immediately

following either type of surgery, in-hospital

rehabilitation focuses on training the patient to

safely move in bed, to get out of bed, and to begin

walking with partial weight-bearing on the

surgical side using either a walker or crutches. A

physician specializing in rehabilitation medicine

or a physical therapist evaluates the patient,

administers or supervises the treatment sessions,

and makes discharge recommendations. An

occupational therapist also may evaluate the

patient and provide training in performing

activities of daily living (e.g., bathing, dressing)

during recovery from the fracture. The

occupational therapist may also provide the

patient with assistive devices, such as longhandled shoe horns and devices that help the

patients put on his or her socks.

Since the inpatient hospital stay typically is

limited to 2–3 days after surgery, most patients

require additional rehabilitation. Transfer to a

rehabilitation facility (a specialty hospital or a

skilled nursing home) is common, with length

of stay in this setting ranging from several days

to several weeks. Following discharge to home,

rehabilitation is continued through in-home

therapy with a physical therapist or visits to an

outpatient facility. This phase of the rehabilitation focuses on general conditioning, strengthening of muscle, and walking longer distances

on different terrains and with less assistance. The

degree to which a patient progresses from relying on the support of assistive devices during

walking to more complete weight-bearing on the

fractured limb will depend on the type of surgery and implanted metal as well as the physical

condition of the patient. The “typical” patient

progresses from a walker to a four-footed cane

to a single-point cane to no assistive device for

walking. However, 85 percent of patients still

use an assistive device for walking 6 months after the fracture (Marotolli et al. 1992).

Nutrition has been shown to be important

during recovery from hip fracture. Supplementation with calcium, vitamin D, and protein (20

grams per day) have been reported to improve

hospital and rehabilitation courses and to increase BMD a year after the fracture (Schurch

et al. 1998).

6 months after hospital discharge, an evaluation should be performed to determine the

patient’s functional status and to set goals for

the future. Many patients require further

therapy to reach these goals, whereas others

may have reached their potential.
240 Chapter 9

A Report of the Surgeon General

Spine Fractures. As noted above, only

about one-third of spine fractures come to

clinical attention, but those that do usually are

painful. Therefore, pain control is a high

priority after the initial spine fractures and

after multiple fractures, when chronic pain

often becomes a problem. Bedrest should be

partial (resting in bed interspersed with 30- to

60-minute periods of erect sitting, standing,

and walking) and limited to 4 days or less.

Individuals should be taught to position

themselves (e.g., while sitting, standing, or

lying down) and to move (e.g., when lifting,

dressing, doing housework) while maintaining

good posture, which reduces loads on the

fracture and minimizes pain. To minimize pain

and decrease risk of a new spine fracture,

family members should be taught to assist

patients in performing tasks without increasing

the loads on the patient’s spine (Bonner et al. 2003).

Walking should be encouraged even in frail

individuals. A gradual progression starting at

only 2–3 minutes and working up to twenty

or more minutes can be achieved by adding a

minute or two to walking sessions each week.

Short-term use of a back brace is recommended when trunk weakness prevents a patient from maintaining an upright posture. An

occupational therapist can fit the proper device. Weaning from the device, as muscle

strength and endurance improve, will maximize recovery. However, in some patients with

chronic pain and deformity, continued use of

a flexible support device that helps maintain

back strength and posture may be helpful in

reducing pain and improving function (Pfeifer

et al. 2004). If walking is limited due to pain,

use of a rolling walker with four wheels and

hand brakes may help the patient stay active

during recovery, thus preventing loss of

muscle strength and bone mass. This type of

walker allows the use of the arms to keep the

trunk erect, thereby shifting the weight of the

upper body away from the newly fractured

bone. Individuals with a new spine fracture

should avoid use of a standard walker, since

each time the walker is lifted the loads on the

vertebral bodies are increased.

Exercising in a way that safely challenges

balance is also important for rehabilitation of

spinal fracture patients, although this exercise

must be accompanied by an assessment of the

risk of falling and the addressing of modifiable

risk factors for falling, such as vision problems,

medications that cause dizziness, and hazards

in the home. Active range of motion exercises

should be continued during recovery, but resistance/strengthening exercises should not be

initiated or resumed until the fracture has

healed (in approximately 8 to 12 weeks). Since

the risk of another spine fracture is high in patients who have had fractures, patients should

be instructed to avoid exercises and activities

that put high loads on the bones of the spine,

such as flexing or rotating the spine (sit ups,

toe touches). Exercises and activities done with

good spine alignment and low to moderate

amounts of weight should be gradually increased, with the goals of regaining muscle

strength and promoting maintenance of bone

mass. Abdominal strengthening (by tightening

the muscles in the abdomen or belly without

moving the back) is safe and important to reducing loads on the low back. Spinal extension

exercise (i.e., stretching backwards) within a

moderate range is safe and can improve

hyperkyphosis (a spine that is bent excessively

forward) and may help prevent new spine fractures (Sinaki et al. 2002).

Wrist Fractures. Rehabilitation of the wrist

after the cast, brace, or surgical metal is removed

requires about 3 months, but reaching maximum
Bone Health and Osteoporosis

Prevention and Treatment 241

levels of recovery can take up to 24 months, and

some problems may persist for years. During

healing of a wrist fracture, all of the following

are important: arm elevation; early mobilization

of the hand, elbow, and shoulder; and control of

swelling. Progressive exercises, taught by either

a physical or occupational therapist, typically

include active and passive range of motion and

resistance and grip strengthening, such as

squeezing a ball (Bonner et al. 2003). A small

number of patients suffer from sympathetic

dystrophy (complex regional pain syndrome)

after a wrist fracture, resulting in swelling,

weakness, and chronic pain in the wrist.

Treatment of Other Diseases of the Bone

There are specific, effective (and often

curative) treatments for a number of bone

diseases other than osteoporosis, including hyperparathyroidism, rickets, and osteomalacia. There

is also treatment available for some congenital

bone disorders and for bone disease associated

with kidney failure. Early recognition and

treatment of all of these conditions is the key to

avoiding crippling deformities and fractures.

What follows is a brief review of treatment

options for the most common of these diseases.

Primary Hyperparathyroidism. Primary

hyperparathyroidism is caused by an excessive

release of PTH from one or more of the

parathyroid glands. (See Chapter 3 for more a

more detailed description.) Surgical removal of

the parathyroid adenoma (benign tumor) or of

three-and-a-half glands (if all four glands are

enlarged) often cures the disease. In 2002, an

NIH-sponsored workshop on the management

of non-symptomatic primary hyperparathyroidism concluded that patients who are

clearly symptomatic with bone disease or kidney

stones should be advised to have surgery

(Bilezikian et al. 2002, Bilezikian and Silverberg

2004). There is considerable controversy

concerning the need for intervention in patients

who have no clear signs or symptoms of the

disease. Treatment guidelines for nonsymptomatic patients relate to the degree of

hypercalcemia (greater than 1 mg/dL serum

calcium above the upper limits of normal),

hypercalciuria (greater than 400 mg per day urine

calcium), and age (under age 50). An

independent panel of experts that convened after

the end of the NIH workshop suggested that

new guidelines for surgery for non-symptomatic

patients with primary hyperparathyroidism

should be based on levels of bone density that

are in line with modern definitions of

osteoporosis. If T-score measurements are below

–2.5 at any site, surgery is now being

recommended. The evidence suggests,

moreover, that parathyroid surgery is effective;

patients who undergo such surgery have

increased their bone mass by 10 percent or more

over the 3- to 4-year period following surgery,

with the largest gains occurring in the spine

(Silverberg et al. 1999). Parathyroid surgery

patients have also experienced a decreased

incidence of fractures (Vestergaard and

Mosekilde 2004). Optimal parathyroid surgery

requires exceptional expertise in being able to

localize and identify abnormal parathyroid

glands and remove them with minimal injury to

other tissues. Recent advances have led to newer

approaches such as minimally invasive

parathyroidectomy for removal of a single

parathyroid adenoma with a small incision and

minimal trauma to other tissues (Udelsman

2002). This approach requires successful presurgery location of the abnormal parathyroid

gland, usually by technetium-99m-sestamibi

scanning and/or ultrasound imaging (Alexander

et al. 2002). Many patients who are not
242 Chapter 9

A Report of the Surgeon General

candidates for surgery for parathyroidectomy

appear to do very well when they are managed

conservatively with appropriate measures to

avoid dehydration and further bone loss

(Silverberg et al. 1999).

Currently, there are no FDA-approved medications for primary hyperparathyroidism. However, medical therapy may be available in the

future. Specifically, calcimimetic (calcium-mimicking) agents, which can inhibit parathyroid

hormone secretion, offer a direct approach to the

medical therapy of primary hyperparathyroidism (Silverberg et al. 1997). Antiresorptive

therapy can be used in patients with primary

hyperparathyroidism and low bone mass who

refuse surgery or for whom surgery is contraindicated (Rubin et al. 2003, Parker et al. 2002,

Chow et al. 2003).

Renal Osteodystrophy. Renal osteodystrophy is a complex bone disease that occurs

because of chronic renal (kidney) failure; a more

detailed description of the disease and its causes

can be found in Chapter 3. Treatment of renal

osteodystrophy depends on the type of

abnormality in the bone and on the stage of the

renal disease. An important aspect of

prevention of renal osteodystrophy is the early

implementation of dietary phosphate and

protein restriction, oral 1,25-dihydroxy vitamin

D (calcitriol) treatment, and adequate oral intake

of calcium and vitamin D. A recent analysis of

hemodialysis patients suggested that treatment

with a vitamin D analog, paricalcitol, resulted

in lower mortality than did treatment with

calcitriol (Teng et al. 2003). All patients

progressing to end-stage renal disease are

offered treatment to control uremia (high levels

of blood urea nitrogen) with dialysis. An

increasing number of patients on dialysis are

offered the option of kidney transplantation.

The incidence of osteoporosis after

transplantation (when bone loss can be

aggravated by the drugs that are used to

suppress the immune response and prevent

rejection of the transplant) can be reduced by

keeping the dose of corticosteroids and antitransplant drugs to a minimum (Cohen and

Shane 2003). However, osteoporosis in posttransplant patients may also be treated in its

own right by anti-osteoporotic therapies such

as bisphosphonates.

Paget’s Disease of Bone. Paget’s disease of

bone is localized, excessive bone remodeling that

leads to increased bone resorption and formation

(see Chapter 3 for more details). The primary

therapy involves use of bisphosphonates, which

decrease bone resorption and slow bone

turnover (Lyles et al. 2001). Alendronate,

risedronate, tiludronate, and etidronate are

bisphosphonates that are approved for the

treatment of Paget’s disease. The doses used

for treatment of Paget’s disease are generally

higher than those used for osteoporosis

treatment. Bisphosphonates lead to a decrease

in alkaline phosphatase and often decrease the

skeletal pain associated with the excessive bone

turnover. Calcitonin (as an under-the-skin

injection or nasal spray) has also been used to

treat Paget’s disease, but is less effective than

bisphosphonates (Deal 2004). PTH should not

be given to patients with Paget’s disease.

Bone Metastases of Cancer. Bone metastases

are common in a number of cancers, and they

contribute heavily to morbidity and mortality,

most prominently in prostate, breast, and

multiple myeloma. Bone metastases are often

associated with severe and frequently

intractable pain (Mundy 2002). The

relationship between prostate cancer and the

bone is unique among cancers. Approximately

90 percent of advanced prostate cancer patients

develop clinically significant bone metastasis,
Bone Health and Osteoporosis

Prevention and Treatment 243

causing osteoblastic remodeling of the bone that

contributes to the morbidity and mortality of

patients. Bone metastases are also frequent in

breast cancer, often leading to both osteoblastic

and osteoclastic lesions. Multiple myeloma can

cause rapid bone loss with pain, fractures, and

increased blood calcium (see Chapter 3 for more

details). The major source of morbidity and

mortality associated with MM are osteolytic

lesions that form throughout the axial skeleton,

resulting from increased osteoclastic bone

resorption that occurs adjacent to the myeloma

cells. New bone formation that normally occurs

at the sites of bone destruction is also absent, as

local factors produced by myeloma cells appear

• Primary hyperparathyroidism

~ Removal of parathyroid adenoma(s)

by surgery if signs or symptoms

meet guidelines

~ Hormone therapy or bisphosphonates

may be helpful

• Renal osteodystrophy (bone disease

from kidney failure)

~ Treatment of kidney problem

(dialysis, transplantation)

~ Special diets

~ Calcitriol

• Paget’s disease of bone

~ Bisphosphonates (alendronate,

risedronate, tiludronate, etidronate)

• Multiple myeloma

∼ Chemotherapy

∼ Stem cell transplantation

∼ Bisphosphonates

• Osteogenesis imperfecta

∼ Rehabilitation

∼ Physical therapy

∼ Bisphosphonates

Treatment of Other Bone Diseases

to induce extensive bone destruction and block

new bone formation.

There are some treatments available to treat

bone metastases caused by cancers.

Bisphosphonates, which are potent inhibitors of

bone resorption, significantly reduce skeletal

morbidity in patients with advanced breast cancer and can reduce metastasis to bone by human breast cancer cells in an experimental model

(Cancer Supplement 2003). Pamidronate, a second generation bisphosphonate, has recently

been approved by the FDA for treatment of

breast cancer osteolysis. Zoledronic acid, a thirdgeneration bisphosphonate, has also been approved for treatment of cancer patients. Another

inhibitor of bone resorption, the protein

osteoprotegerin, has also been shown to be effective in reducing bone metastases in animal

models of breast and prostate cancer and in reducing bone pain in patients (Cancer Supplement 2003). Although bisphosphonates significantly reduce skeletal morbidity associated with

solid tumor metastases to bone, most studies

indicate no improvement in survival (Cancer

Supplement 2003). Thus, in order to improve

therapy and ultimately prevent bone metastases, a more precise understanding of the

pathophysiology of bone metastases is necessary, as the level of current understanding is

very limited (Cancer Supplement 2003).

Osteogenesis Imperfecta. Osteogenesis

imperfecta (OI) is an inherited skeletal disorder

that results from several different genetic

defects (see Chapter 3 for more details). Patients

with OI have low bone mass and brittle bones

that fracture easily. Treatment of patients is

mainly oriented at preventing and treating

fractures in these patients. It involves a team of

health professionals that typically includes

orthopedists, rehabilitation physicians, and

physical therapists. Encouraging results have

been reported with bisphosphonate therapy

(Glorieux et al. 1998).
244 Chapter 9

A Report of the Surgeon General

• What is the effectiveness of pharmacotherapy in treating persons who have

already sustained hip fractures?

• Are combination therapies more effective

than single therapies? Is there any time

when it is best to use a combination of

anti-resorptive and anabolic therapy?

• What doses, schedules, and methods of

administration are most effective in

encouraging compliance and preventing

fractures in the community (not just

within the confines of a clinical trial)? Can

lower doses, shorter courses, or wider

spacing of treatment help?

• What is the efficacy and utility of

vertebroplasty and kyphoplasty?

• How can we improve the therapy of other

bone diseases, particularly osteogenesis

imperfecta, hyperparathyroidism, and

renal osteodystrophy?

Key Questions for Future

Research

There is good evidence that proper nutrition

and lifestyle can promote bone health and that

pharmacotherapy can slow bone loss or even build

new bone. However, there is still no “cure” for

osteoporosis or for most other bone disorders.

Those drugs that do exist, moreover, are still not

ideal in terms of their expense, ease of

administration, and/or side effects. Answers to the

following research questions would help to move

the field closer to the development of “ideal”

therapies that can prevent and/or cure bone disease:

• What are the relative risks and benefits

of different types of drug therapies in

different populations? When is it best to

use bisphosphonates, SERMS, or

anabolic agents?
Bone Health and Osteoporosis

Prevention and Treatment 245

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Chapter 10: Key Messages

• Individuals have a critical role to play in

promoting their own bone health. All health

care professionals, especially primary care

providers, have the opportunity and

responsibility to assist them in this task by

promoting awareness of factors that

influence bone health; identifying patients

at risk of bone disease; and providing lifestyle

and therapeutic interventions to prevent

bone loss and fractures.

• Nurse practitioners, nurse midwives, and

physician assistants can contribute

significantly to the provision of bone health

care. They can educate patients on nutrition

and physical activity recommendations,

ensure proper screening, and monitor

compliance with treatment. Physical

therapists, occupational therapists,

pharmacists, and dietitians can play valuable

roles in helping patients achieve maximal

physical function and bone accrual.

• Childhood is an excellent time to initiate

counseling aimed at encouraging

appropriate nutrition and physical activities

and discouraging the adoption of behaviors

that negatively affect bone health.

• All young and middle-aged adults should

be encouraged to adopt lifestyles that help

prevent bone loss and promote overall

health and the prevention of chronic

disease. Young and middle-aged adult

patients who have medical conditions or

who are taking medications associated

with bone loss should be considered for

bone density testing and drug therapy.

• For older adults and the elderly,

recommended levels of both calcium and

vitamin D increase. Older adults should

engage in regular physical activity, and many

can follow the recommendations for younger

adults. Weight-supporting activities may be

more appropriate in older adults with

compromised bone health, although with

proper supervision and training they can

safely engage in resistance exercises as well.

• Risk factors for bone loss and fracture should

be assessed in all older women. In addition,

all women aged 65 and older should undergo

bone density testing as recommended by the

U.S. Preventive Services Task Force and the

National Osteoporosis Foundation. Bone

density testing should be considered in men

with fragility fractures; those on therapies

that may cause bone loss, notably

glucocorticoids or androgen deprivation;

and men with multiple risk factors.

• Pharmacologic therapy should be

considered in individuals who have

osteoporosis. Individuals with low bone

mass and multiple risk factors should also

be considered for therapy. Selection of a

therapeutic agent can be tailored to the

severity of the patient’s bone loss and other

co-morbid conditions.

• Fall prevention strategies should also be

discussed with every osteoporosis

patient, and hip protectors should be

considered for the frail elderly and

patients at high risk for falling.

• A person of any age (especially an elderly

individual) who represents a challenging

clinical situation may benefit from a referral

to an endocrinologist, rheumatologist, or

other specialist in osteoporosis management.
Bone Health and Osteoporosis

Putting It All Together 255

PUTTING IT ALL TOGETHER FOR THE BUSY

HEALTH CARE PROFESSIONAL

Chapter 10

As noted throughout this report, individuals

have a critically important role to play in

building and maintaining strong, healthy bones

throughout life. All health care professionals,

especially primary care providers, have the

opportunity and responsibility to assist

individuals in achieving this goal by promoting

awareness of factors that influence bone health,

identifying patients at risk of bone disease, and

providing lifestyle and therapeutic interventions

to prevent bone loss and fractures. Even though

most osteoporotic fractures occur in older

individuals, the risks of incurring such fractures

are largely determined much earlier in life—both

by the level of peak bone mass achieved during

childhood and adolescence and by subsequent

lifestyle choices and medical events of adulthood.

As discussed earlier in this report, health care

professionals could do a better job in preventing,

identifying, and treating bone disease;

osteoporosis remains underdiagnosed and

undertreated. Since osteoporosis is a common

disorder that can be diagnosed and treated in the

primary care setting, much of the responsibility

for promoting awareness, diagnosis, prevention,

and treatment of osteoporosis falls on health care

professionals who provide primary care. For

example, pediatricians and other primary care

providers for children and adolescents should

focus on maximizing bone accrual as discussed

below in the section on infancy through

adolescence. Primary care and other providers

for adults can also help their patients maintain

skeletal health by focusing on germane areas

within their respective specialties. For example,

obstetrics and gynecology providers should

include recommendations for skeletal health in

their discussions of nutrition and physical

activity during family planning, lactation,

pregnancy, and menopause, as discussed in the

section on young and middle adulthood.

Internists and specialists such as

rheumatologists, gastroenterologists, oncologists,

pulmonologists, dermatologists, and urologists

should maximize lifestyle interventions and

manage patients on pharmacotherapies,

including oral glucocorticoids and gonadal

hormone suppression therapies, that can cause

bone loss, as discussed in the section on older

adults and the elderly. Geriatricians, internists,

emergency department physicians, and

orthopedists have a unique opportunity to ensure

that patients who present with fractures receive

intensive interventions designed to maximize

recovery and prevent future fractures. Certain

health care professionals, such as nurse

practitioners, nurse midwives, and physician

assistants, can contribute significantly to the care
256 Chapter 10

A Report of the Surgeon General

of many patients and can educate patients on

nutrition and lifestyle recommendations, ensure

proper screening, and monitor compliance with

treatment. Other health care professionals such

as physical therapists, occupational therapists,

pharmacists, dentists, optometrists, and

dietitians can play valuable roles in helping

patients achieve maximal physical function and

bone accrual. For example, pharmacists can

advise patients concerning calcium and vitamin

D supplementation, the best way to take

medications, and any potential drug interactions.

Optometrists can help by ensuring that the

vision of older patients is adequately corrected,

which should decrease the risk of potentially

debilitating falls. For their part, dentists may be

able to detect bone loss in the jaw, which could

lead to further investigation of the potential for

osteoporosis.

Fortunately, recommendations related to

bone health also promote overall health and

therefore fit in well with other preventive

recommendations. This chapter is devoted to

identifying ways that health care professionals can

incorporate recommendations focused on bone

health into the advice they are already providing

patients, and to offering practical advice on how

providers can assist patients in implementing these

recommendations into their lives. These

recommendations are based largely on the evidence

related to the maintenance of bone health, the

diagnosis of bone disease, and the prevention and

treatment of fractures outlined in Chapters 6, 7, 8,

and 9, and therefore references are not included in

this chapter except in cases where material has not

previously been referenced.

Children and Adolescents

The period from infancy through

adolescence is critical for building bones and

developing healthful bone habits that help an

individual to maintain a robust skeleton

throughout life. As noted in Chapter 2, most

individuals reach their “peak bone mass” during

this time, which is determined by genetic factors

and lifestyle choices (e.g., nutrition, physical

activity) made by children with the influence of

their parents during the first 18 years of life. The

first 2 years of life and early adolescence are

particularly important for future bone health, as

they are characterized by rapid bone

accumulation. Health care professionals who are

involved in the health maintenance of infants,

children, and adolescents have an opportunity

to positively influence bone health for the rest

of their patient’s lives. While bone disease is quite

rare in children and adolescents, health care

professionals also need to be aware of the warning

signs of potential problems that could be caused

by genetic factors, lifestyle choices, certain

diseases, or use of certain medications.

Nutrition

Achieving recommended levels of intake for

calcium, vitamin D, and other nutrients during

infancy, childhood, and adolescence is critical

to maintaining healthy bones throughout life.

(See Table 10-1 for a listing of the dietary

calcium and vitamin D requirements for infants,

children, and adolescents.) What follows is a

more detailed discussion of how health care

professionals can assist their patients in achieving

these levels.

Calcium

Adequate calcium intake is critical for infants,

children, and adolescents, as discussed below.

Infants: Nutrition is important to bone health

even before birth. The largest influx of calcium

into the fetal skeleton occurs during the last

trimester of human pregnancy. Most newborns

will receive adequate levels of calcium from their

mothers during full-term pregnancies, and from
Bone Health and Osteoporosis

Putting It All Together 257

breast milk, formula, and/or solid foods during

the first year of life. Infants who are born

prematurely “miss out” on some calcium before

they are born and will likely have lower bone

mass at birth than will a full-term infant. While

breast feeding provides important advantages to

premature infants, it may not provide for all of

their needs. As a result, health care professionals

should encourage parents of premature infants

who are being breast fed to use supplements that

provide added nutrients, particularly calcium,

vitamin D, phosphorus, and protein (Schanler

2001). Health care professionals should advise

the parents of premature infants who are not

being breast fed about the importance of using

infant formulas that are designed to provide

calcium and phosphorus intakes similar to those

that occur in utero during the last trimester of

normal human pregnancy. Even when

premature infants use such formulas, it can take

up to 5 years for their bone mass to catch up

with that of full-term newborns.
258 Chapter 10

A Report of the Surgeon General

Childhood: As shown in Table 10-1, children

between 1 and 3 years old should get 500 mg

per day of calcium, and those between 4 and 8

years old should consume 800 mg per day. Milk

and foods derived from milk (e.g., cheese,

yogurt) serve as the major food sources for

calcium throughout childhood and adolescence.

Any type of milk (whole, lowfat, or nonfat)

provides the same level of calcium, but low-fat

milk is the best choice for children over age 2.

Additional sources include foodstuffs

supplemented with calcium, such as fruit juices,

fortified soy beverage, breads, and other

breakfast foods, which can help to boost overall

dietary calcium intake levels towards the

recommended values. Since foods that contain

calcium also have many other important

nutrients, health care professionals should

encourage parents and their children to strive

for recommended levels of calcium intake

through diet alone.

Adolescence: The second most rapid gains

in bone mass occur with the onset of puberty,

which also marks the time that calcium intake

needs become greatest. As shown in Table 10-

1, children 9 to 18 years old should consume

1,300 mg per day of calcium. Puberty is also

the time that ethnic and gender differences in

bone mass are first seen. As noted in Chapter

3, bone mass tends to be higher in AfricanAmericans than in Caucasians, and higher in

males than in females. Girls and boys

experience their most rapid rate of bone growth

during puberty, and by the end of puberty they

have almost achieved peak mass. Hence the

teenage years are especially critical to

maximizing skeletal growth. Girls and, to a

greater extent, boys also accumulate bone mass

during and after puberty, with some additional

mass being gained even in the third decade of

life. Finally, it is worth noting that a delayed

onset of puberty is associated with a reduction

in peak bone mass attainment.

Few adolescents consume recommended

levels of dietary calcium shown in Table 10-1.

As indicated in Figure 6-4 based on data from

the National Health and Nutrition Examination

Surveys (NHANES), children up to age 9

consume the recommended amount of calcium.

Consumption begins to decline slightly just as

the calcium requirement to sustain pubertal

growth goes up. Health care professionals should

inquire specifically about calcium intake during

check-ups. It is useful to remember that while

fluid milk consumption decreases as children

progress to adolescents, both children and

adolescents consume mixed foods such as pizza

that contain considerable amounts of calcium

through cheese. Calcium intake in children and

adolescents can be enhanced by incorporating

fruit-flavored yogurt, milk-based puddings and

shakes, cheese (including low-fat cheese

products), and fortified foods such as orange juice

into family meals, snacks, and packed school

lunches. It is important to recognize that even in

the context of obesity and other chronic disease

prevention, low-fat and nonfat, calcium-rich

dairy foods can be emphasized as a way to

promote bone health without having a negative

impact on efforts to manage weight. Calcium

supplements may be used for those individuals

who would otherwise have a chronic, suboptimal intake of calcium and are unable to meet

the requirement for calcium through diet alone.

Interactive nutrition, physical activity, and bone

health information geared toward girls and

adolescents can be found on two Centers for

Disease Control and Prevention (CDC)Web sites

related to the Powerful Bones, Powerful Girls

campaign: http://www.cdc.gov/powerfulbones/

index2.html and http:www.cdc.gov/power

fulbones/parents.
Bone Health and Osteoporosis

Putting It All Together 259

Vitamin D

As with calcium, adequate levels of vitamin

D are critical to forming and maintaining healthy

bones throughout infancy, childhood, and

adolescence. Full-term infants who are fed

human breast milk appear to mineralize the

skeleton similarly to infants fed commercial

formulas, including soy-based formulas for

infants with an intolerance to cow’s milk.

However, infants who are exclusively breastfed

and who have limited exposure to sunlight are

at increased risk of developing vitamin D

deficiency. Severe vitamin D deficiency can lead

to rickets. The American Academy of Pediatrics

has suggested that all infants who are exclusively

breastfed receive 200 IU (international units) of

vitamin D daily to lessen the likelihood of

developing rickets.

Vitamin D requirements during childhood

are 200 IU daily, which is the amount contained

in two glasses of fortified milk or in most

children’s multi-vitamins. There are also rare

cases of rickets in children who have congenital

disorders of vitamin D or phosphorus

metabolism and health care professionals should

be alert to this possibility. (See Chapter 3 for

more details.) These bone diseases may not

respond to vitamin D but can be treated by other

means.

Protein, Salt, and Phosphorus

There has been some concern that the high

intakes of protein, salt, and phosphorus that occur

in children and adolescents who eat high-calorie,

low-nutrient foods and drink soda can impair bone

growth and mineralization. This may be true if

these intakes are at the expense of calcium-rich

foods, but studies in adolescents have shown that

intake of the recommended levels of calcium intake

can compensate for high levels of protein, salt, and

phosphorus (Fitzpatrick and Heaney 2003).

Physical Activity

Bone mass may be increased in childhood

by impact-bearing exercise or physical activity.

Thus, health care professionals should

emphasize the importance of physical activity

at every visit and should encourage healthy

children to be active everyday. At a minimum,

they should engage in at least 60 minutes of

moderate to vigorous physical activity on most

days, preferably daily. Unfortunately, many

children and adolescents do not get enough

physical activity. Health care professionals

should inquire about physical activity at each

visit and urge children and adolescents to engage

in physical activity for at least an hour a day.

Health care professionals can also help promote

the importance of physical education in the

schools by speaking out in the community.

Other Lifestyle Factors

Childhood is an excellent time to initiate

counseling aimed at discouraging the adoption of

behaviors that may negatively affect bone health,

including smoking and alcohol consumption.

Such counseling should be continued throughout

adolescence, at which time the dangers of anabolic

steroids (which can increase the risk of

osteoporosis) should also be discussed.

Risk Factor Assessment, Bone Density

Testing, and Specialty Referral

The vast majority of children and adolescents

will have healthy bone development, and the

health care professional’s goal is to encourage and

support these young individuals and their

parents to make the proper lifestyle choices

(adequate nutrition and physical activity) to

promote both bone health and overall health

status. However, health care professionals should

be alert to medical conditions and medications

that place children and adolescents at risk for

poor bone health.
260 Chapter 10

A Report of the Surgeon General

 In young individuals, skeletal disorders may

present as children who fail to maintain their

natural growth curve. While this can be due to

any of a variety of factors, metabolic bone disease

should be considered as part of a full workup.

Eating disorders such as anorexia and

bulimia are uncommon, but can be extremely

debilitating. General practitioners may observe

changes in weight and appearance, as well as a

history of delayed onset or cessation of menstrual

periods. Individuals suspected of having eating

disorders such as anorexia or bulimia should

immediately be referred to an appropriate

specialist or an eating disorders clinic.

All young females should be queried about

onset and regularity of their menstrual periods.

Regular menses signal an intact gonadal axis and

adequate estrogen exposure. If menses have

stopped after menarche for any reason

investigation is warranted. Prolonged periods of

amenorrhea have very serious and long-term

consequences on bone health. In fact, the

cessation of periods in a young, healthy woman

should serve as a red flag, as it can lead to a high

risk of immediate stress fractures as well as an

increased long-term risk of osteoporosis and

osteoporotic fractures. Its most common cause

in young healthy women is participation in a

very strenuous athletic activity like crosscountry running or activities that are both

strenuous and emphasize low-body weight, such

as gymnastics or ballet. The absence of

menstrual periods might be the only sign that

these individuals need attention. The first step

is to increase nutritional intake with caloriedense foods (e.g., nuts, cheese) as part of an

otherwise balanced diet. If the periods do not

return within a couple of months, these

individuals should be encouraged to curtail their

athletic activity. To ensure that the activities are

curtailed, health care professionals should make

the adolescent, parents, and, if necessary, coaches

and trainers aware of the short- and long-term

consequences of amenorrhea to bone health.

Health care professionals should investigate

the causes surrounding any fracture, including

the level of trauma involved. Most fractures will

be the result of common injuries (e.g., due to

sports), but the potential for child abuse should

also be considered. On the other hand, some of

these children may have osteogenesis imperfecta,

and it is also important to make this diagnosis

and therefore avoid wrongful accusations of

abuse. Health care professionals should also

evaluate the potential for bone-related disorders,

especially in children or adolescents who

experience multiple fractures. Fractures are not

uncommon during the early stage of puberty,

which is a period (as discussed in Chapter 6) of

rapid remodeling where the mineralization of

newly formed bone lags behind the increase in

the size of the bones. Nevertheless, any fractures

in teenagers should be reported to their primary

care providers, who should view it as a signal to

further assess risk factors such as family and

personal history to determine if additional steps

are warranted. In some cases, especially fractures

in infants, referral to a pediatric specialist who

deals with metabolic bone disease (often an

endocrinologist, nephrologist, or rheumatologist)

will be necessary.

Children and adolescents taking certain

medications or with certain diseases that are

known to negatively affect bone health should

also be carefully evaluated by a specialist. See

Table 10-2 for a list of these diseases and

medications. One group that is at particularly

high risk of bone disease is the survivors of

childhood cancer (Kaste 2004). In rare cases

children may suffer from primary diseases that
Bone Health and Osteoporosis

Putting It All Together 261

affect the bone due to genetic anomalies or from

metabolic disorders that affect the processes that

regulate systemic mineral homeostasis for

calcium or phosphorus (Table 10-2). Health care

professionals who suspect these problems

because of poor growth, skeletal deformities, or

unexplained fractures should refer the child to a

specialist in pediatric bone disorders.

Bone density testing is not appropriate for

healthy children and must be interpreted with

caution even in at-risk children, since it is an

imperfect approach to assessing bone before peak

bone mass is achieved. If dual x-ray

absorptiometry (DXA) is used, bone density

should be expressed in Z-scores rather than the

T-scores used for adults. T-scores compare

individuals to peak bone mass (which does not

occur until the third decade of life), while Zscores provide an age-matched comparison.

Comparing children or adolescents to adult peak

bone mass rather than age-specific bone mass

will inappropriately underestimate their bone

density. The measurement of bone density in

children is further complicated by the lack of a

large, uniform reference database for pediatric

patients and by the fact that bone age and

chronologic age may not match in children with

chronic diseases. The bones of these children are

more similar to those of younger children, and

thus their bone density may be lower.

Adults

Nutrition

The recommended diet for optimal bone

health is consistent with diets recommended for

the prevention of other diseases. Therefore,

health care providers have opportunities at

many patient encounters to establish and

reinforce nutritional recommendations that

benefit bone and overall health. There are

many very common conditions such as

hypertension, diabetes, and weight management

for which nutritional counseling is vital,

providing health care professionals with an

excellent opportunity to also incorporate

recommendations for bone health.
262 Chapter 10

A Report of the Surgeon General

Calcium

Calcium intake should be 1,000 mg per day

during early and middle adulthood. A quick assessment of calcium intake can be made by estimating that a diet without dairy products contains approximately 250–300 mg per day of calcium (Weinberg et al. 2004). Calcium intake from

dairy products, calcium-fortified foods, and

supplements can be added to this baseline to

obtain a rapid, reasonable estimate of the total

daily intake. See Chapter 7 for a quick assessment tool that patients can use.

Common food sources of calcium have the

added benefit of providing additional nutrients

as well. Significant food sources of calcium include dairy products, calcium-set tofu, canned

fishes with bones, and other calcium-fortified

foods (see table 10-3). Some individuals with lactose intolerance can consume lactose-reduced

milk, live culture yogurt, fortified soy beverage,

tofu, and hard cheeses. For maximum calcium

nutrition, health care professionals should encourage consumption of low-oxalate vegetables

such as broccoli, kale, mustard greens, and turnip greens, as oxalates can impair calcium absorption. Vegetarians and vegans can consume

tofu brands that are set with calcium (this type

of tofu can be identified by checking the label),

vegetables with calcium, almonds, and calciumfortified foods and beverages, such as fortified

orange juice and fortified soy beverage. Fortunately, the array of calcium-fortified foods is expanding, providing consumers with a wide variety of options for achieving adequate calcium

intake. A table of calcium-containing foods, organized by calcium content per serving, can be

found in Table 10-3.

To assist individuals in determining how

much calcium they are getting from the food they

consume, food labels express calcium content as

a percentage of 1,000 mg—in other words, an

item with 20 percent of the daily recommended

amount of calcium contains 200 mg of calcium.

The calcium content of foods, including fresh

fruits and vegetables, can be found on the

USDA National Nutrient Database Web site at

http://www.nal.usda.gov/fnic/cgi-bin/

nut_search.pl.

Calcium supplements can be critical for

those persons who cannot meet calcium requirements through food alone. In the absence

of gastrointestinal disease, all major forms of

calcium supplements are absorbed equally well

when taken with meals. The citrated salts may

be more readily absorbed in individuals with

gastrointestinal disease or decreased stomach

acid production. Since different types of

supplements may contain different amounts of

elemental calcium, it is important to check the

label and to determine the exact amount of calcium in the supplement, in order to achieve the

targeted level of calcium intake. Patients should

be encouraged to check supplement labels to

ensure that their calcium supplement meets

United States Pharmacopoeia lead standards.

Some calcium supplements may contain other

nutrients such as vitamin D or vitamin K. This

should be discussed with individuals on warfarin therapy who need calcium supplements,

since their response to therapy may be altered

by high vitamin K intake. Finally, calcium

supplements should be ingested no less than 4

hours before or after taking iron or thyroid

medications, since calcium may decrease the

absorption of these other medications.

The efficiency of calcium absorption from

supplements is greatest when calcium is taken

in doses of 500 mg or less. In other words, calcium intake, be it through food and/or supplements, should be spread throughout the day, and

the daily requirement should not be consumed

at a single setting.

Finally, it is important to emphasize to patients that the upper tolerable level for calcium
Bone Health and Osteoporosis

Putting It All Together 263
264 Chapter 10

A Report of the Surgeon General

intake recommended by the Institute of Medicine is 2,500 mg per day. In some cases, this limit

should be even lower, since some individuals

who are susceptible can become hypercalciuric

with calcium intakes as low as 1,500 mg per day.

Health care professionals should ask their patients if they regularly take antacids, since many

of them may not know that common antacids

contain high levels of calcium. As a result, those

individuals who take antacids regularly may be

consuming calcium at the higher-than-recommended levels.

Vitamin D

The following recommendations for adequate

intake do not take into account vitamin D that is

absorbed from the sun, since it is difficult for an

individual to determine how much vitamin D

he or she gets from exposure to sunshine. Young

and middle-aged adults should consume about

200 IU per day of vitamin D, although intakes

of up to about 1,000 IU per day are generally

considered safe. Much higher intakes can be toxic

for healthy individuals, although physicians may

prescribe higher dosages for individuals with a

vitamin D deficiency. Primary food sources of

vitamin D are limited to fortified milk (100 IU

per cup), egg yolk (25 IU per yolk), fortified cereals, and fish oils. Sunlight exposure contributes variably to circulating and active vitamin D

formation, depending on age, race, clothing, and

latitude. Sunscreen with an SPF above eight will

block the ultraviolet B radiation that stimulates

vitamin D production; the extent to which this

can lead to vitamin D deficiency is not well defined. However, particularly in northern climates

and among older individuals, vitamin D deficiency is becoming recognized as very common.

Health care professionals should educate individuals about recommended levels and sources

of vitamin D and encourage adequate intake

through food sources, supplements, and appropriate amounts of sun exposure. Physicians should

consider measuring the circulating form of vitamin

D in the blood—25-hydroxy vitamin D—in individuals who have any of the following characteristics: low dietary intake of vitamin D, inadequate

exposure to the sun, signs of poor absorption of vitamin D, or the presence of a gastrointestinal disorder that might decrease their vitamin D supply. Individuals found to be vitamin D deficient by a physician may be given pharmacologic doses of vitamin

D to replenish stores and maximize bone mineralization (Pettifor 2003).

Protein

Adequate dietary protein is important for

bone health. In short-term studies, low protein

intakes have been shown to result in decreased

calcium absorption, while protein supplementation after hip fracture has been shown to speed

healing and decrease mortality. However, increasing protein intake also increases urine calcium excretion. The long-term effect of both high

and low protein diets on skeletal health has yet

to be determined. Following the current dietary

guidelines for servings of protein-containing

foods such as meat, poultry, beans, and dairy

products does not present any problems for calcium and bone health. These guidelines can be

achieved by consuming 2–3 servings of meat or

beans and 2–3 servings of milk and cheese per

day. Higher intakes may be necessary in individuals with a history of low protein intake and

those who are recovering from fracture in order

to bring protein levels back to normal (as long as

they also are getting sufficient levels of calcium

intake). Important sources of protein include lowfat dairy products, which also provide calcium,

phosphorous, and other important nutrients.

Most vegetables provide fiber and minerals in

addition to small amounts of protein, while soy
Bone Health and Osteoporosis

Putting It All Together 265

protein sources such as tempeh, soybeans, and

full-fat tofu provide isoflavones (plant compounds with estrogenic effects), which have been

shown to increase bone density in some shortterm clinical trials (long-term studies are ongoing). Nutritional supplements containing protein

are available for those who cannot get enough

protein from diet.

Other Nutrients

Sodium chloride intake increases urine calcium excretion, and excessive intake of salt may

increase bone resorption in postmenopausal

women, although this effect may be offset by adequate calcium intake. However, bone health is

yet another reason to maximize the intake of fresh,

unprocessed foods and achieve the Institute of

Medicine recommendation for an intake of no

more than 2,400 mg per day of sodium. Individuals can reduce their intake by avoiding canned,

jarred, cured, and processed foods in home cooking. Individuals can reduce their intake of salt by

carefully checking the labels of processed foods

used in the home and choosing fresh fruits, vegetables, and meats without sauces and dressings

when eating away from home. Caffeine consumption leads to a small decrease in calcium absorption; carbonated beverages do not appear to significantly affect calcium excretion independent

of caffeine. As long as adequate levels of calcium

intake are maintained, however, both carbonated

and caffeinated beverages can be consumed in

moderation.

Many other minerals such as phosphorus,

magnesium, copper, and boron also contribute

to bone health to varying degrees. Adequate

amounts of these elements can generally be consumed by focusing on an overall healthful diet

that includes an adequate intake of lean protein,

abundant consumption of fruits and vegetables,

and appropriate intake of calcium and vitamin D

along with moderate consumption of sodium and

caffeine. (See Table 7-5 for more details.)

Physical Activity

Physical activity should be promoted

throughout adulthood, as appropriate to the

physical capabilities of the individual. Physical

activity not only promotes bone health, but it

also helps to optimize weight control, metabolic

parameters, muscle strength, and cardiovascular fitness. Programs that have demonstrated

skeletal benefits have all included impact activities or resistance-training exercises, including

walking, jumping, jogging, running, soccer,

racquet sports, weight lifting, dancing, hiking,

and stair climbing. To promote bone and overall health, adult patients should be encouraged

to accomplish at least 30 minutes per day of

moderate intensity physical activity on most,

preferably all, days of the week. Some strength

or resistance training can be particularly beneficial to bone health. Engaging in longer periods

of moderate activity and/or increasing the intensity of activity (i.e., at least 20 minutes of vigorous intensity activity) are the best ways to promote cardiovascular health.

Initiating and maintaining a program is a significant challenge for sedentary patients. Patients

should be encouraged to engage in even small

amounts of daily activity, since these activities

may have some health benefits. Some individuals may find it easier to start with manageable

goals that incorporate physical activity into their

daily activities, such as parking farther from their

destination or using the stairs instead of the elevator. Long-term compliance with physical activity routines may be enhanced by enlisting the

support of family members or friends, advocating moderate intensity that is within the person’s

capabilities, devising programs that individuals

can accomplish at home, offering flexibility in
266 Chapter 10

A Report of the Surgeon General

activity choices, and providing feedback and incentives. Participating in a physical activity that

the individual enjoys, such as gardening, a walk

with a friend, or a community exercise or dance

class, also helps maintain compliance. Individuals should be encouraged to find an activity they

like enough to continue and to be ready to try a

different program if they lose interest in the current one.

Patient education materials, including pamphlets and videos with specific exercises and instructions for moving safely and maintaining

optimal posture, can be obtained from the National Institute on Aging at http://

www.niapublications.org or from the National

Osteoporosis Foundation at http://www.nof.org.

Other Lifestyle Measures

Excessive alcohol and tobacco use increases

the risk for fracture. Thus, patients should be

encouraged to quit smoking and to limit alcohol

intake to moderate use, not only to optimize bone

health, but also for their overall health and wellbeing. In addition, general safety measures to

reduce the risk of trauma, such as consistent use

of seatbelts, should be advised.

Pregnancy and Lactation

While the data are somewhat limited, it appears

that there is a transient decrease in bone density

during pregnancy and lactation, but the healthy

mother’s skeleton rapidly recovers after lactation is

completed. Thus, there does not appear to be a

long-term detrimental effect of pregnancy and lactation on bone health. Pregnant and lactating

women should follow their obstetrician’s recommendations for optimal nutrition and physical activity. The current recommended intakes during

pregnancy and lactation are 1,000 mg per day of

calcium and 200 IU per day for vitamin D. A higher

intake of 1,300 mg per day of calcium is recommended for women under age 18.

Risk Factor Assessment and Bone Density

Testing

All young and middle-aged adults should be

encouraged to adopt lifestyles that help to prevent bone loss and to promote overall health and

the prevention of chronic disease. Bone density

testing of asymptomatic young and middle-aged

adults without significant risk factors is not recommended. Although the radiation exposure of

testing is very low, this exam should not be performed on women who may be pregnant.

Young and middle-aged adult patients with

medical conditions associated with bone loss,

such as hyperthyroidism, hyperparathyroidism,

hypogonadism (either endogenous or medically

induced), malabsorptive syndromes or eating

disorders, significantly impaired mobility, or

chronic renal or hepatic failure, warrant special

attention. In addition to being strongly encouraged to adopt appropriate nutrition and lifestyle

choices, they should also be considered for bone

density testing and pharmacologic therapy. A

bone density test should be performed on patients requiring medications that can result in

bone loss, such as oral glucocorticoids,

anticonvulsants, immuno-suppressants

(cyclosporine A, tacrolimus, methotrexate), and

heparin for more than a month. Since bone loss

can occur rapidly after the initiation of glucocorticoid therapy, health care professionals

should consider bone density testing prior to the

start of such therapy; patients with low bone

density should be considered for concurrent

antiresorptive therapy.

In addition, younger patients with conditions that increase fracture risk should be encouraged to adhere to maximal nutrition and lifestyle

measures aimed at preventing bone disease. Specific therapy such as antiresorptive drugs should

also be considered in those with significantly low

bone mass based on a bone density test.
Bone Health and Osteoporosis

Putting It All Together 267

Interpretation of bone density exams in this

age group should focus on the T-score values,

even though specific T-score thresholds for the

diagnosis and treatment of osteoporosis have not

been established for younger individuals. Tscores can be interpreted for patients by explaining that the T-score compares their bone density to the average maximum lifetime bone density (peak bone mass) in young adults. Patients

should be advised that a positive T-score means

that their bone density is above the average for a

young adult around age 30, while a negative

number means their bone density is below that

of the average 30-year-old. The World Health

Organization (WHO) has established definitions

of normal (T-score above -1), low bone mass/

osteopenia (T-score between –1 and –2.5), and

osteoporosis (T-score less than –2.5) based on

epidemiologic data. However, it should be remembered that the risk of bone fracture increases

continuously as bone density decreases. In other

words, there are no precipitous changes in fracture risk associated with these “break” points.

The relationship between T-scores and fracture

risk has been conducted primarily in postmenopausal women; data in younger individuals are

limited. It should also be remembered that the

WHO diagnostic definitions were derived from

DXA data and therefore should not be applied

to other bone density testing modalities.

Treatment and Monitoring Therapy

With the exception of glucocorticoid-induced

osteoporosis, there have been few trials of osteoporosis medications in young and middleaged adults. Therapy in this age group should

focus on maximizing nutrition and lifestyle modifications and addressing any underlying medical conditions such as hypogonadism that can

lead to low bone mass. Comorbid conditions that

may affect bone should be treated; for example,

care should be taken to ensure serum thyroid

stimulating hormone (TSH) remains in the normal range in individuals with hypothyroidism

who are on L-thyroxine therapy. Young and

middle-aged adults who have osteoporosis even

after non-pharmacologic therapies have been

employed should be considered for anti-resorptive therapy, options for which are discussed in

Chapter 9.

For individuals who have received bone density testing prior to menopause, additional bone

density exams should be conducted only if the

results could prompt a change in therapeutic

plan. Early postmenopausal women with normal or marginally low bone density do not need

repeat bone density scanning for at least 3–5

years, unless an intervening medical condition

that could accelerate bone loss develops. Individuals on anti-resorptive therapy may benefit

from a follow-up DXA scan. However, due to

the variability of densitometry measurements,

at least 18 to 24 months should elapse between

scans to ensure that any changes are large

enough to be clearly detected. Since there is variability between DXA scans even with rigorous

quality assurance and careful technique, care

should be taken not to alter treatment regimens

in response to small changes in bone density

values. While they can be significant in research

trials, changes in hip or spine bone density of 4

percent or less are at the detection limits of office-based densitometry and should be interpreted cautiously in the clinical setting. Osteoporotic patients who cannot readily see signs

that therapy is working or failing often do not

take their prescription drugs appropriately (i.e.,

adherence is poor) and/or they do not stick with

their drug regimen over time (i.e., persistence is

poor). A recent study of osteoporotic patients

showed that monitoring by a nurse, with or without the use of a biochemical marker of bone resorption, could improve both adherence to and persis-
268 Chapter 10

A Report of the Surgeon General

tence with therapy over time. Moreover, better adherence was found to be associated with better outcomes (Clowes et al. 2004).

Specialty Referrals

Specialists can assist primary care providers

with additional expertise in those young and

middle-aged adults who represent challenging

situations, including individuals for whom the

etiology of low bone mass is unknown, those who

require an evaluation for secondary causes of

bone loss, those being considered for long-term

antiresorptive therapy, and those who either do

not tolerate or do not respond to therapy. These

patients may benefit from a referral to an endocrinologist, rheumatologist, or other specialist in

osteoporosis management. Referrals to dietitians

and physical therapists can also be helpful in

implementing nutrition and physical activity

programs, particularly for those individuals with

significant dietary and mobility limitations.

A broad approach to assessing bone health,

preventing bone disease, and managing osteoporosis in adults is illustrated in Figure 10-1.

Older Adults

Nutrition

The nutrition guidance outlined for young

and middle-aged adults also applies to older individuals and the elderly. Specific additional recommendations pertinent to this age group are

discussed below.

Calcium and Vitamin D

Calcium and vitamin D absorption decreases

with aging, and older individuals with limited

mobility tend to receive less sunlight, leading to

rates of vitamin D deficiency (as measured by

serologic testing) of up to 57 percent in this population (Thomas et al. 1998). As a result, recommended levels of both calcium and vitamin D

increase in this population. Total calcium intake

should be 1,200 mg per day after age 50. Older

individuals should be educated in how to read

labels for calcium content, since calcium is expressed as a percent of 1,000 mg on labels (the

recommended level for younger adults). Since

the calcium intake goal for older adults is greater

than 1000 mg per day, these individuals actually need to consume more than 100 percent of

the level recommended on food labels. Since

older persons may suffer constipation as a side

effect of calcium supplements, health care professionals should emphasize food sources of calcium and also recommend increasing fluid and

fiber intake. Inability to secrete acid in the stomach (achlorhydria) may limit the absorption of

calcium carbonate salts; citrated salts may be

absorbed better in these patients, but carbonate

salts will still be absorbed if taken with meals.

Individuals between the ages of 51 and 70

should consume 400 IU per day of vitamin D,

while those over age 70 should get 600 IU per

day. Since it may be difficult for older individuals to achieve these levels of intake through food

alone, many individuals will require multi-vitamins or specific vitamin D supplements. Individuals who have low vitamin D dietary intake

and/or low sun exposure should have their vitamin D level measured. Persons found to have

vitamin D deficiency should receive pharmacologic doses of vitamin D.

Other nutrients

Recommendations for other nutrients for

older adults are the same as those for younger

adults. In addition, protein supplementation has

been shown to speed healing and reduce mortality in older individuals suffering hip fractures.

These patients should have a nutritional evaluation during post-fracture rehabilitation.
Bone Health and Osteoporosis

Putting It All Together 269
270 Chapter 10

A Report of the Surgeon General

Physical Activity

Older adults should maintain as high a functional status as possible and regularly engage in

physical activity. Many older adults can follow

the same recommendations for younger adults

outlined above. Weight-supporting activities

such as stationary bicycling, deep-water walking, and floor exercises may be more appropriate in older adults with compromised bone health

although with proper supervision and training

these individuals can safely engage in resistance

exercises as well. Individualized programs devised by physical therapists or physiatrists can

safely improve strength, mobility, and functional

capacity in vulnerable older adults. Physical

therapists can also train individuals in specific

postural exercises to strengthen back extensor

muscles, which may relieve pain and decrease

development or progression of kyphosis.

Patients with spine fractures should avoid

activities that flex the spine and increase pressure on compromised vertebral bodies. In addition, activities such as golf, bowling, tennis, and

horseback riding place significant force on the

spine and should be avoided in patients with

compromised bone health. People with osteoporosis of the spine should avoid use of exercise machines that involve trunk rotation or forward bending, as these movements can cause a

fracture in individuals with osteoporosis. Machines to avoid include abdominal exercisers,

biceps, rowing, and cross-country ski machines,

stationary bicycles with moving handlebars, or

upper body ergometers.

Physical therapists play an important role in

both fracture prevention and treatment. They

can evaluate balance and the risks of falling and

teach specific exercises and techniques to minimize that risk. Since nearly all hip fractures are

associated with a fall, preventing falls in older

individuals is fundamental to preventing fractures. Occupational therapists can evaluate the

home environment and make modifications that

minimize the risks of falling, including eliminating loose rugs; installing hand rails, shower chairs,

and hand-held nozzles in the bathroom; installing bedside lamps, nightlights in hallways and

bathrooms, and strips of contrasting tape on stair

treads; and recommending the use of canes and

walkers as appropriate as well as the avoidance

of certain types of clothing, including long garments and trailing hems.

Patient education materials, including pamphlets and videos with specific exercises and instructions for exercise, moving safely, and maintaining optimal posture, can be obtained from

the National Institute on Aging at http://

www.niapublications.org/shopdisplay

products.asp?id=17&cat=Exercise+for

+Older+People or from the National Institutes

of Health Osteoporosis and Related Bone

Diseases~National Resource Center (http://

www.osteo.org).

Risk Factor Assessment and Bone Density

Testing

Risk factors for bone loss and fracture should be

assessed in all women over 65. Commonly identified risk factors for fracture are listed in Table 10-4.

One of the best validated instruments to help

identify patients at risk of low bone mineral density (BMD) (and thus in need of a DXA) is the

three-item Osteoporosis Risk Assessment Instrument (ORAI). As shown in Table 10-5, ORAI

uses age, weight, and current use of hormone

therapy to identify women at risk for osteoporosis (Cadarette et al. 2000).

Another easy-to-use tool that many clinicians

and their patients may find appealing is the Osteoporosis Self-Assessment Tool (OST). As

shown in Figure 10-2, this tool combines age and

weight in a simple nomogram. Assuming that
Bone Health and Osteoporosis

Putting It All Together 271

BMDs are performed on those with a score of

less than two (the upper two sections of the

chart), the OST tool identifies over 90 percent

of women with osteoporosis—and 100 percent

of those over age 65—as defined by WHO criteria (Cadarette et al. 2004). This finding not only

helps to validate OST, but it also provides further evidence to support current guidelines recommending BMD testing in all women over age

65. However, as with other risk-assessment tools,

OST has low specificity, as about 55 percent of

the women identified by this tool as needing a

BMD actually do not have osteoporosis

(Cadarette et al. 2004). Since the OST index is

easy to calculate, it may be the most useful available tool in clinical practice at this time.

As noted in Chapter 8, one risk factor that is

not included in these screening instruments is

height loss. Careful measurement of height can

be useful both in assessing risk and in monitoring patients on therapy. A height loss of more

than one inch should serve as a “red flag” for the

potential of osteoporosis and/or spinal fractures.

Both the NOF and USPSTF recommend

bone density testing for women age 65 and older.

The USPSTF also recommends that bone density testing begin at age 60 for women who are

at increased risk for osteoporotic fractures. Expert organizations differ, however, on when to

conduct routine screening in women under age

60. The USPSTF has found evidence that

screening women who are at lower risk for osteoporosis or fracture can identify additional individuals who may be eligible for treatment for

osteoporosis. This evidence also suggests that

such widespread screening would prevent a

small number of fractures, since younger individuals with low BMD and no other risk factors

are at low risk of fracture. The NOF guidelines

recommend bone density testing in postmenopausal women under age 65 with risk factors for

osteoporosis. It should also be noted that the

majority of the evidence upon which these

guidelines are based was obtained in White

women. There is no consensus regarding screening in men; however, bone density testing should

be considered in men with fragility fractures,

those on therapies that may cause bone loss,

notably glucocorticoids or androgen deprivation, and men with multiple risk factors.
272 Chapter 10

A Report of the Surgeon General

Measuring bone density at the hip by DXA is

the best predictor of hip fracture. Some members

of the original WHO working group recommended that the diagnosis of osteoporosis should

be based only on the T-score obtained through

DXA measurement at the hip (Kanis et al. 2000).

These members indicated that while measurements

at other sites and with other technologies may be

useful for assessing risk of fracture, they should

not be used for diagnosis of osteoporosis.

Bone density T-scores can be interpreted for

older individuals in the same way they are for

young and middle-aged adults. Although there

are no data, many experts also evaluate the Zscores in older individuals. The Z-score

compares the patient’s bone density to that

expected for their age, rather than to peak bone

mass. While this approach has not been validated,

many experts will more strongly consider a

laboratory evaluation of vitamin D levels and of

potential secondary causes of osteoporosis in

patients with Z-scores of –2 or less (meaning the

patient’s bone density is two standard deviations

or more below that expected for their age). It is

important to consider the possibility of

secondary causes in all patients with

osteoporosis, even those with Z-scores higher

than -2. Laboratory evaluation for secondary

causes should be guided by clinical judgment as

well as findings from the patient’s history and a

physical examination. There are many different

types of conditions and medications that can lead

to secondary osteoporosis, as summarized in

Tables 3-1 and 3-2 in Chapter 3.

Treatment and Monitoring Therapy

Pharmacologic therapy should be instituted

in individuals who have osteoporosis, as defined

by WHO criteria or the existence of fragility

fractures. Individuals with low bone mass and

multiple fracture risk factors should also be con-
Bone Health and Osteoporosis

Putting It All Together 273
274 Chapter 10

A Report of the Surgeon General

sidered for therapy (in addition to emphasizing

appropriate lifestyle and nutritional intake). The

FDA has approved several anti-resorptive therapies (bisphosphonates, selective estrogen receptor modulators, estrogen, and calcitonin) as well

as a single anabolic agent, teriparatide (PTH),

which is currently available only as a daily injection. Selection of therapeutic agent can be tailored to the severity of the patient’s bone loss

and other comorbid conditions. The risks and

benefits of these agents, as determined by clinical trials, are discussed in Chapter 9. Finally, fall

prevention strategies should be discussed with

every osteoporosis patient, and hip protectors

should be considered for the frail elderly and

patients at high risk for falling.

Combinations of antiresorptive agents have been

tested for their impact on bone density, and results

suggest that this approach produces modestly

greater increases in BMD than do single agents used

alone. There are no data, however, on the efficacy

of combination therapy in reducing the risk of fracture. In addition, using bisphosphonates in conjunction with teriparatide provides no added benefit over

use of each agent individually.

As with younger individuals, follow-up bone

density exams should be conducted only when

the results could prompt a change in therapeutic plan. Older individuals with normal or minimally low bone density likely do not need to repeat bone density scanning for at least 3–5 years,

unless an accelerated rate of bone loss is suspected that might lower their bone density to a

level at which treatment would be considered.

As with younger and middle-aged adults, individuals on anti-resorptive therapy may benefit

from a follow up DXA scan at least 18 to 24

months after the initial scan.

The utility of markers of bone resorption in

monitoring response to therapy shows promise

but has not been firmly established. Some experts use marker measurements in the evaluation of patients with an apparent lack of response

to antiresorptive therapy, but this approach has

not been validated. Much work continues to

determine the clinical utility of using markers of

bone activity. A complete discussion can be

found in Chapter 8.

Non-bone medication use should be evaluated as part of the treatment plan for elderly individuals with low bone density. Medications

associated with dizziness, low blood pressure,

falls in blood pressure upon standing

(orthostasis), and sedation can increase the risk

of falling, and their use should be minimized or

avoided. In addition, alcohol use should be reviewed, as it may cause older individuals to become unsteady and susceptible to falls.

Follow-up for Fractures

There is significant morbidity and mortality

following fractures in older individuals. In

addition, these individuals are at very high risk

for future fractures. Thus, health care providers

should aggressively intervene to maximize bone

health, minimize morbidity, and prevent future

fractures in these patients. All nutrition and

lifestyle modifications should be strongly

encouraged, specific osteoporotic pharmacologic

therapy should be instituted, and appropriate

rehabilitation should be achieved. Identifying

and intervening in patients with osteoporotic

fractures presents an exceptional opportunity to

dramatically reduce the consequences of this

disease. Yet, as noted in Chapter 9, a significant

number of fracture patients do not receive

optimal long-term care focused on bone health.

All health care providers involved in the care of

fracture patients must dedicate themselves to

ensuring not only adequate treatment for the

acute fracture, but also aggressive

implementation of all therapeutic and
Bone Health and Osteoporosis

Putting It All Together 275

rehabilitative measures to prevent further

fractures. Specific post-fracture treatment

recommendations are found in Chapter 9.

Specialty Referrals

Osteoporosis is often diagnosed and treated

in the primary care setting. However, as with

younger individuals, older persons and the elderly with particularly challenging clinical situations can benefit from a referral to an endocrinologist, rheumatologist, or other specialist in osteoporosis management. For example, such referrals may be appropriate in cases where secondary osteoporosis is suspected, therapy is not tolerated, bone density declines, or a fragility fracture occurs during treatment.

Physical therapists and occupational therapists

provide vital assistance in the management of

older patients with osteoporosis by working with

them to increase strength, balance, and physical

activity and to reduce the risk of falls. Referrals to

physical and occupational therapists should be

strongly considered for all osteoporotic individuals at risk for falls and/or with limited exercise capacity. Older individuals at risk for fracture should

also be referred to an eye care professional, who

should perform refraction, cataract removal, and/

or glaucoma therapy as appropriate, as such treatments maximize visual acuity and minimize the

risk of falls.

Elderly individuals with vertebral fractures,

particularly those with persistent pain, may benefit from referral to an orthopedist and to a physical therapist, who can fit them for a back brace

that helps to reduce kyphosis.

Strategies to Maximize Adherence

 Long-term adherence, defined as the percentage of prescribed medication taken, and persistence, defined as the percentage of individuals who take a medication for the prescribed period of time, are poor with any therapy, with

rates for both being around 50 percent (Clowes

et al. 2004). It is not known, moreover, whether

certain strategies, such as feedback to patients on

the results of repeat bone density testing or increased use of biochemical markers of bone turnover, can improve long-term compliance with osteoporosis therapies. In fact, while measurement

of bone resorption markers has been advocated to

improve compliance to therapy, monitoring by

a nurse without such measurements has been

found to be equally effective in improving compliance (Clowes et al. 2004). This study suggests

that the key to maximizing adherence to any

therapy is for health care professionals to follow

up with patients to ensure that they are taking

their medications appropriately.

 Specific follow-up strategies that have been

shown to improve adherence to other types

of medical regimens should be utilized in patients with osteoporosis as well. These include

counseling about the importance of the

planned treatment regimen, enlisting the support of the patient’s social network, sending

reminders about follow-up appointments,

recognizing adherence efforts, simplifying

and organizing the treatment regimen, addressing patient concerns about side effects,

and maintaining an encouraging providerpatient relationship. Many of these approaches are time and labor intensive; nonphysician health care professionals can be invaluable resources in making the most of these

strategies in a busy practice. Patient education materials on many aspects of osteoporosis are available free on-line from the National

Institutes of Health Osteoporosis and Related

Bone Diseases~National Resource Center

(http://www.osteo.org).

Key Questions for Future

Research

Research questions related to the prevention,

diagnosis, and treatment of bone disease are

provided at the end of Chapters 6, 8, 9, and 11.
276 Chapter 10

A Report of the Surgeon General

References

Cadarette SM, Jaglal SB, Kreiger N, McIsaac

WJ, Darlington GA, Tu JV. Development

and validation of the osteoporosis risk

assessment instrument to facilitate selection

of women for bone densitometry. CMAJ

2000 May 2;162(9):1289-94.

Cadarette SM, McIsaac WJ, Hawker GA,

Jaakkimainen L, Culbert A, Zarifa G, Ola E,

Jaglal SB. The validity of decision rules for

selecting women with primary osteoporosis

for bone mineral density testing. Osteoporos

Int 2004 Jan 17.

Clowes, JA, Peel NF, Eastell R. The impact of

monitoring on adherence and persistence

with antiresorptive treatment for

postmenopausal osteoporosis: A randomized

controlled trial. J Clin Endocrinol Metab

2004 Mar; 89(3):1117-23.

Fitzpatrick L, Heaney RP. Got soda? J Bone

Miner Res 2003 Sep;18(9):1570-2.

Kanis JA, Gluer CC. An update on the diagnosis

and assessment of osteoporosis with

densitometry. Committee of Scientific

Advisors, International Osteoporosis

Foundation. Osteoporos Int. 2000;11(3):192-

202.

Kaste SC. Bone-mineral density deficits from

childhood cancer and its therapy: A review

of at-risk patient cohorts and available

imaging methods. Pediatr Radiol 2004 Feb

12.

Pettifor JM. Nutritional and drug-induced

rickets and osteomalacia. In: Favus MJ,

editor. Primer on the metabolic bone diseases

and disorders of mineral metabolism. 5th ed.

Washington, DC: American Society for

Bone and Mineral Research; 2003. p. 399-

407.

Schanler RJ. The use of human milk for

premature infants. Pediatr Clin North Am.

2001 Feb;48(1):207-19.

Thomas MK, Lloyd-Jones DM, Thadhani RI,

Shaw AC, Deraska DJ, Kitch BT, Vamvakas

EC, Dick IM, Prince RL, Finkelstein JS.

Hypovitaminosis D in medical inpatients. N

Engl J Med. 1998 Mar 19;338(12):777-83.

U.S. Department of Agriculture, Agricultural

Research Service. Nutrient Data Laboratory

[homepage on the Internet]. 2002. USDA

Nutrient Database for Standard Reference,

Release 15. Available from: http://

www.nal.usda.gov/fnic/foodcomp/search/.

Weinberg LG, Berner LA, Groves JE. Nutrient

contributions of dairy foods in the United

States, Continuing Survey of Food Intakes

by Individuals, 1994-1996, 1998. J Am Diet

Assoc. 2004 Jun;104(6):895-902.


Bone Health and Osteoporosis

 PART FIVE: Health Systems and Population-Based Approaches 279

This part of the report examines how health systems and populationbased approaches can promote bone health.

Chapter 11 looks at the key systems-level issues and decisions that

affect bone health care, including evidence-based medicine, clinical practice

guidelines, training and education of health care professionals, quality

assurance and quality improvement techniques, coverage policies, and

disparities in prevention and treatment. It also evaluates the key roles of

various stakeholders in promoting a more systems-based approach to bone

health care, including individual clinicians; medical groups; health plans

and other insurers; hospitals and rehabilitation facilities; public health

departments; and other stakeholders, such as academic medical centers

and public and private employers.

Chapter 12 describes the various potential components of populationbased approaches to promoting bone health at the local, State, and Federal

levels and reviews the evidence supporting their use. One of the key messages

of this chapter is that well-crafted population-based interventions should be

highly effective in improving bone health as well as other aspects of health.

To illustrate this point, the chapter includes seven detailed profiles of

innovative and/or effective population-based programs, each of which was

selected to illustrate an important concept in population-based health.

Five

WHAT CAN HEALTH SYSTEMS

AND POPULATION-BASED

APPROACHES DO TO PROMOTE

BONE HEALTH?

Part Five
280 Chapter 11

A Report of the Surgeon General

Chapter 11: Key Messages

• Individual organizations—even very small

ones—can apply a “systems-based” approach to clinical care and other services by

putting into place any of a variety of formal

policies and processes.

• There are four distinct systems-based activities that collectively encompass the

overall goal of improving the bone health

status of Americans:

~ Identifying and developing intervention strategies for various risk levels of

the population.

~ Educating and raising awareness

among clinicians and the public about

bone disease.

~ Ensuring that individuals receive appropriate preventive, diagnostic, and

treatment services based upon their

level of risk.

~ Monitoring and evaluating bone health

outcomes within populations and the

community.

• The most important role for individual clinicians in promoting a systems-based approach to bone health is to educate themselves and their patients about prevention,

assessment, diagnosis, and treatment.

• Medical groups have the opportunity to

implement a systems-based approach as

well. For example, they can dedicate staff to

certain important tasks; use bench-marking

data or academic detailing to promote quality improvement; or implement evidencebased care paths and computerized reminder

systems that promote the provision of timely

and appropriate care. Some groups may be

able to develop specialized osteoporosis clinics or disease management programs.

• Hospitals and rehabilitation facilities can go

beyond their traditional role of simply treating bone-related problems or symptoms by

developing strategies for improving overall

bone health and preventing future falls.

• Skilled nursing homes can institute measures to prevent falls and fractures; to assure that residents receive appropriate

amounts of calcium and vitamin D; and to

include activities that strengthen bones in

their daily regimens.

• Health plans and insurers can get involved

in managing bone health by assessing and

monitoring provider performance; engaging in quality improvement programs;

and/or implementing pay-for-performance initiatives.

• The public health system and other government agencies can play a vitally important role in promoting a systems-based approach to bone health, including:

~ Promote awareness among consumers

and clinicians of bone health and disease.

~ Improve linkages between health care

organizations, community-based organizations, and the public health system.

~ Train health professionals to promote

bone health and recognize and treat

bone disease.

~ Develop strategies to promote bone

health and appropriate treatment.

~ Monitor and evaluate activities within

a community and the Nation as a

whole.

• Other institutions, organizations, and agencies can facilitate a systems-based approach

to bone health through research, education,

and purchasing policies.
Bone Health and Osteoporosis

Systems-Based Approaches To Bone Health 281

SYSTEMS-BASED APPROACHES TO

 BONE HEALTH

Chapter 11

Overview

The health care system in the United States

is not a system per se. Rather, it is a collection of

independent enterprises, some small and some

large, that provide or pay for various aspects of

health care. Despite the fragmented nature of

this system, individual organizations—even very

small ones—can apply a “systems-based” or

“systematic” approach to providing clinical care

and other services in order to function most effectively. Under this approach, health care organizations and other facilitators (such as employers and other purchasers) put into place any

of a variety of formal policies and processes that

are designed to ensure that individual consumers receive timely and appropriate preventive,

diagnostic, and treatment measures to promote

bone health. The nature of these measures is tailored to the underlying risk of bone disease.

For example, an individual clinician’s office

can create a simple protocol or flow sheet to ensure that a consistent approach is taken to a specific health issue, such as administering preventive care. Larger organizations can make use of

more complicated systems such as computerized

reminders and triggers based on clinical indicators and/or prescribing patterns.

Systems-based approaches to the prevention

and treatment of osteoporosis can be exceptionally valuable both in improving the management

of osteoporosis care and in reducing adverse

outcomes from poor bone health. This type of

approach can help to overcome the problems

created by poor communication and a lack of

collaboration among the various components of

the health care system (e.g., government, communities, provider organizations, health plans,

employers, the media, academics). Fragmentation makes the system ill equipped to serve the

chronically ill and to provide population-based

care (IOM 2002). It also means that those who

finance care may not receive the benefits of such

care. With increasing job turnover, employees

commonly change insurers, even while remaining with the same health care provider. As a result, employers and insurers may have little incentive to cover expensive preventive services

(e.g., drug therapy to prevent future osteoporotic

fractures) that may not pay dividends until the

patient is covered by a different plan or by Medicare.

This chapter lays out four distinct systemsbased activities that collectively encompass the

overall goals of the larger health system within

the United States for improving the bone health

status of Americans. The four activities are as

follows:

1. Identifying the various risk levels of the

population being served and developing

an intervention strategy for individuals
282 Chapter 11

A Report of the Surgeon General

in each category of risk, with a particular

focus on high-risk individuals.

2. Educating and raising awareness among

clinicians and the public at large about the

risks of bone disease, as well as the best

ways to prevent, diagnose, and treat it in

the various risk categories identified above.

3. Ensuring that individuals receive appropriate

prevention, diagnostic, and treatment

services based upon their level of risk.

4. Monitoring and evaluating bone health

outcomes within specific populations and

the community to identify problem areas

and assess the impact of strategies and

interventions for improving bone health.

The chapter is organized around each of the

individual entities that make up the overall

system—individual clinicians, medical groups,

health plans/insurers, public health, and other

facilitators of bone health, such as public (e.g.,

Medicare and Medicaid) and private purchasers

(e.g., employers) and academic medical centers.

Separate sections describe each of their respective

roles and responsibilities within each of the

activities listed previously. The individual

organizations within the overall system need to

collaborate and coordinate their activities. To

facilitate this type of collaboration, Table 11-1

summarizes the potential participants in a broad

set of major interventions and activities designed

to promote bone health. It is important to

remember, however, that the distinctions between

the various levels are somewhat arbitrary. For

example, a staff-model health maintenance

organization (HMO) includes both a medical

group and health plan. Thus, while the strategies

discussed within the chapter will appear where

they are most commonly employed, it is perfectly

conceivable that other stakeholders can and should

consider their use as well.

Population-Based Risk Stratification:

A Prerequisite to a Systems-Based

Approach

There is one overriding principle that

governs systems-based approaches to

osteoporosis and bone health—that is, to

focus on populations. A population-based

approach considers the health of a group of

persons (as defined by factors such as age,

gender, geography, or risk factors) who may

have diverse needs rather than the patient

who has individual needs. Good populationbased interventions also accommodate

individual needs. The overall goal is to ensure

that all persons receive the care they need,

especially those at high risk of debilitating

and costly fractures. To that end, two tasks

must be accomplished. The first is to

categorize the population being served into

subgroups defined by their underlying risk

of bone disease, falls, and fractures. The

second is to define appropriate preventive,

assessment, and therapeutic strategies for

each subgroup based on the best available

evidence. These steps should be taken by

each of the various components of the health

system, be it an individual provider assessing

risks among his or her patients, a medical

group assessing risks among its patient

population, a health plan evaluating the risks

of its enrollees, an academic health center

educating providers, or a public health

department surveying risks in the

community at large. When implemented

well, risk-stratification and population-based

approaches provide ample opportunity for

decision-making by providers. For more

information on risk stratification, please see

Chapter 8.
Bone Health and Osteoporosis

Systems-Based Approaches To Bone Health 283
284 Chapter 11

A Report of the Surgeon General

meaning that the net number of individuals

initiating drug therapy was quite small. The

same study also found that certain groups,

including men, non-Whites, and those with other

medical conditions, are less likely than White

women to receive treatment for osteoporosis.

There are also certain characteristics of health

care providers that can predict their rates of

diagnosis and treatment of osteoporosis (Morris

2004), such as gender, specialty, and years since

medical school. However, there are no studies

on the effectiveness of programs to increase

awareness in improving diagnosis and therapy.

Two recent large studies conducted in managed

care settings generated similar findings, with

only a minority of post-menopausal women who

had sustained a fracture receiving pharmacologic

treatment following the fracture (Feldstein et al.

2003b, Andrade et al. 2003). These studies

highlight the important role for physicians in

both prescribing the appropriate therapy and in

encouraging patients to comply.

Evidence alone, even when compelling, is

frequently insufficient to change provider

practice patterns. To overcome the barriers to

change, it might make sense to consider adoption

of a comprehensive model for accelerating the

diffusion of innovations. One such approach,

known as the Rodgers Diffusion model, provides

insight into both the limitations of current

behavioral change techniques and potential

strategies for accelerating diffusion of evidencebased innovations (Rodgers 1995). This model

lays out five stages to the process of deciding

when and how to use a new innovation: 1)

knowledge; 2) persuasion; 3) decision; 4)

implementation; and 5) confirmation.

Knowledge

There are two aspects to the knowledge stage.

The first is the need for consumers to be aware

of the importance of the health issue. While

Finally, examples of systems-based

approaches to osteoporosis and bone health are

provided whenever possible. Since such

approaches are still rare in bone health, examples

of successful systems approaches to other lifelong

or chronic health issues are also included. They

contain valuable lessons that may potentially be

relevant to bone health.

Systems-Based Approaches for

Various Stakeholders

While all components of the health system

should engage in risk stratification, the roles and

responsibilities for different types of organizations

will vary when it comes to implementing systemsbased approaches. This section discusses each of

the key stakeholders, including individual

clinicians, medical groups, insurers, public health

departments, and other facilitators.

Systems-Based Approaches for Individual

Clinicians

Perhaps the most important roles for the

individual clinician in promoting a systemsbased approach to bone health relate to 1)

educating themselves and their patients about

bone health prevention, treatment, and

assessment, and 2) putting into place systems to

ensure that patients receive appropriate services

based on their risks and needs.

Unfortunately, however, clinicians may not

always fulfill these roles. Evidence-based

interventions (i.e., those whose effectiveness has

been demonstrated) are often not used on those

who need them. For example, a recent large-scale

study of older patients who had suffered hip or

forearm fractures found that roughly four out

of five did not fill a prescription for an

osteoporosis medication in the 6 months after

the fracture (Solomon et al. 2003). Moreover,

most individuals who did fill a prescription were

already on a medication before the fracture,
Bone Health and Osteoporosis

Systems-Based Approaches To Bone Health 285

individual clinicians can help in educating their

patients, this public awareness role is best played

by medical groups, health plans/insurers, public

health departments and other government

agencies, and potentially other facilitators, such

as medical societies. It is important to remember,

however, that these awareness campaigns are not

the only sources of information for individual

consumers. They also receive information from

the media (e.g., newspapers, magazines,

television program-ming) and pharmaceutical

companies (e.g., via direct-to-consumer

advertising). For more information on public

awareness campaigns, see the section on the role

of public health.

The second aspect of the knowledge stage

relates to making sure that clinicians are aware of

the evidence related to best practices for bone

health. Individual clinicians can employ a variety

of systems-based approaches to ensure their own

awareness of up-to-date information on best

practices. Among these systems are practice

guidelines and evidence-based medicine reports

that synthesize findings from multiple studies and

sources. These reports and guidelines have been

issued by government agencies (e.g., the U.S.

Preventive Services Task Force [USPSTF], a

panel of experts with representation from the nonFederal sector that is housed at the Agency for

Health Care Research and Quality [AHRQ]) and

by professional and public societies (e.g.,

American Association of Clinical Endocrinology,

the National Osteoporosis Foundation). The

National Guideline Clearinghouse (NGC) serves

as a comprehensive source for credible guidelines

related to bone disease and other diseases.

Sponsored by AHRQ in partnership with the

American Medical Association and America’s

Health Insurance Plans, NGC includes 71 general

and specific guidelines related to osteoporosis and

bone health.

Since the evidence base is often not sufficiently

developed to allow the crafting of comprehensive

guidelines, supplemental information based on

expert opinion is often added, thus leading to

variations across guidelines. This lack of complete

evidence also means that guidelines often do not

answer all clinical questions of interest, including

the applicability of the guideline to important

subpopulations (e.g., minorities, older persons) or

the role of comorbidities. In addition, guidelines

and evidence-based reports often fail to incorporate

patient preferences, although this is changing. In

spite of their limitations, guidelines and evidencebased reports should be seriously considered by

individual clinicians, since they attempt to provide

the best recommendations for what clinicians should

do. See Chapter 8 for more on risk assessment

guidelines and Chapter 9 for more on treatment

guidelines.

In addition, as discussed in Chapters 8 and

10, individual clinicians should also consider the

use of risk assessment tools such as the

Osteoporosis Risk Assessment Instrument

(ORAI) and the Osteoporosis Self-Assessment

Tool (OST). These tools, which are based on risk

factors that have been demonstrated to be

associated with osteoporosis, are helpful in

identifying individuals who are at risk of bone

disease and/or fracture and who therefore might

benefit from further assessment and/or treatment.

Persuasion

Just because guidelines and evidence-based

reports exist, there is no guarantee that clinicians

will read and absorb them. Even if they do, the

evidence suggests that they may not change their

behavior by implementing the recommended

practices. In fact, the gap between evidence-based

care and the actual care provided in the community

(the “knowledge-practice gap”) is well recognized

as a barrier to quality care (Reuben 2002).
286 Chapter 11

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Several steps are needed, therefore, to ensure

that individual clinicians become aware of and

act on the evidence. One common strategy is the

use of professional education to disseminate

guidelines and evolving research, including

presentations at meetings and other common

continuing medical education (CME) activities.

However, these techniques have generally

been ineffective in changing provider behavior

on their own (Grimshaw et al. 2001, Grol and

Grimshaw 2003). In fact, it has proven

remarkably difficult to convince clinicians to

implement evidence-based changes for

improving care within clinical settings. Many

factors related to knowledge, attitudes, and

behaviors contribute to this inertia. These

barriers have been well described (Cabana et al.

1999) and are listed below:

• Lack of awareness or familiarity with the

guidelines

• Disagreement with specific guidelines or

guidelines in general

• Doubt that following the guideline will

lead to desired outcomes

• An inability to overcome existing practice habits

• Patient factors, such as preferences

• Environmental factors, such as lack of

time or resources

The disappointing results from CME and

guidelines has led to the use of other approaches

for persuading providers, including academic

detailing (described in the next section) and

opinion leaders. These techniques have long been

used by the pharmaceutical industry in marketing

new products to prescribers. They also fit within

the model described earlier, which relies on

respected peers to assist with persuasion.

Decision and Implementation

Even after clinicians become convinced of

the merits of adopting an evidence-based

practice, they still may need help in deciding

when and how to implement it on a daily basis.

For that reason, a variety of systems-based

approaches have been developed to assist

individual physicians in practicing evidencebased medicine. One common approach is

computerized reminder systems, which have

been used in a variety of settings, including

hospitals (Dexter et al. 2001). These systems are

commonly employed to promote use of

preventive services such as influenza

immunizations (Gaglani et al. 2001) and to

support adherence to clinical protocols (Demakis

et al. 2000). The same kind of approach can be

taken in bone health. For example, a recent study

demonstrated the usefulness of sending e-mail

messages to primary care providers of patients

who had recently suffered an osteoporotic

fracture but had not yet received a bone mineral

density (BMD) test; 51 percent of the patients

of doctors who received the e-mail message were

given a BMD test or a medication for

osteoporosis, compared to just 6 percent in a

usual care group (Feldstein et al. 2003a). A less

technologically sophisticated but similar

approach involves the use of chart flags (Melville

et al. 1993), which alert physicians on the paper

chart when they should consider a particular

evidence-based course of action for a patient.

Flow diagrams or algorithms represent similar

approaches that have been used to determine

who needs testing (e.g., mammography) and

how often they need it (Melville et al. 1993).

Confirmation

All of these steps outlined above are not enough

to result in lasting behavior change (Rodgers 1995),
Bone Health and Osteoporosis

Systems-Based Approaches To Bone Health 287

unless the clinicians who change behavior receive

confirmation after the fact that they made a wise

decision in doing so. For example, clinicians who

agree to try using a pre-visit questionnaire will need

to see that it has achieved its intended results (and

not caused any unanticipated problems, such as

negatively affecting office work flow) before the

change will be permanent. Without this

confirmation step, innovations tend to be dropped

after a period of time.

Summary

The best approach for individual clinicians

is to adopt a comprehensive behavior-change

plan that targets the different barriers to change

with distinct strategies aimed at each (Grol and

Grimshaw 2003). One example of a multicomponent strategy aimed at individual

physicians was developed during the

intervention phase of the Assessing Care of

Vulnerable Elders (ACOVE) project (a

Reuben

et al. 2003). This intervention is aimed at

changing practice behaviors related to the care

of three geriatric conditions (falls, cognitive

impairment, and urinary incontinence) through

the following:

• Use of medical record prompts via structured visit notes

• Delegation of some tasks to office staff

to encourage performance of essential

care processes by clinicians

• Patient education, including encouraging

the patient to play an active role in follow-up, which may also be quite influential in changing physician behavior

(Maly et al. 1996)

Finally, it is important to remember that

individual clinicians not only need to change

their own behavior, but they also need to

encourage their patients to do the same. To that

end, clinicians should constantly be advising

their patients about appropriate lifestyle changes

related to bone health, as discussed in Chapter

10. In addition, clinicians should provide their

patients with information on resources that can

assist them in changing behavior. For example,

ACOVE provides information to patients about

community-based resources, such as exercise

programs that reduce the risk of falls. (See

Chapter 6 for more information.) These

programs are particularly valuable for high-risk

individuals. Unfortunately, the quality and

availability of community-based programs and

resources varies considerably within and across

geographic areas. Most clinicians do not

currently have readily available information for

their patients about community-based programs

and resources, including where they are located

and how to access them. This represents an area

where public health departments and clinicians

could collaborate.

An Example of a Systems-Based Approach

An action plan for the prevention of

osteoporotic fractures in the European

Community provides an interesting example of

a systems-based approach (Compston 2004). In

2002, the European Union Osteoporosis

Consultation Panel was formed to develop an

action plan to implement recommendations for

the prevention of osteoporotic fractures. Six

action steps were developed to achieve the stated

goal of reducing the social and economic burden

of osteoporotic fractures by 2005: 1) awareness

campaigns targeted at potentially high-risk

individuals, e.g. postmenopausal women; 2)

preventive lifestyle strategies, including the

development of government-backed health

education programs and policies and the

harmonization of public health policies; 3)

evidence-based guidelines, including developing

guidelines in member States, making existing

guidelines more accessible, and providing
288 Chapter 11

A Report of the Surgeon General

government endorsement and financial support

to these efforts; 4) evidence-based fracture care

and fall prevention programs, along with

multidisciplinary approaches to rehabilitation;

5) economic data and analysis, including the

identification of resource needs (particularly

bone densitometry systems) and the analysis of

the cost-effectiveness of interventions; and 6) the

European fracture database, including a survey

of existing data, development of data collection

methods, and economic modeling and planning

of health care resources.

Systems-Based Approaches for Medical

Groups

Medical groups should be able to employ all

of the approaches available to individual

clinicians. In addition, because of their larger

size, medical groups have the opportunity to

implement a greater degree of systematization.

For example, office staff can be assigned to

perform a small number of targeted functions

(e.g., checking visual acuity as a component of

an evaluation of the risk of falls), thereby

reducing the burden on clinicians and allowing

staff to develop expertise in specific tasks. Group

practices also have an additional tool available

to them to promote behavior change—

benchmarking, a process that allows physicians

to compare their performance with that of others

or with a “gold standard.” Benchmarking can

also allow an individual clinician to track his or

her performance over time. When

complemented with other quality improvement

techniques, benchmarking has been shown to

improve performance in managing conditions

such as diabetes (Kiefe et al. 2001). It is important

to note that individual clinicians who are

members of independent practice associations

(IPAs) may also have access to benchmarking

data through the IPA’s central office.

Larger group practices can also employ other

formal quality improvement techniques based on

measurement of processes (Nelson et al. 1998) and

outcomes, with the goal of reducing variations in

care delivery and improving overall outcomes. For

example, medical groups can employ rapid-cycle

improvement techniques such as the “Plan, Do,

Study, Act” (PDSA) cycle. The PDSA cycle

begins with clinicians planning and conducting

small-scale, local tests of change in their own offices

and in the health care organizations in which they

work. After studying the results, clinicians and

health care organizations can then apply relevant

systems-based improvements to everyday practice.

In many cases, PDSA cycles are often more

appropriate and informative in facilitating systemsbased improvement than are formal studies with

experimental designs (such as randomized trials)

or the implementation of changes without

evaluative measurement (Berwick 1998). The

Institute for Health Care Improvement has been

successful using the PDSA approach in the areas

of diabetes and depression.

Medical groups also have the ability to create

registries of patients with specific disorders so

that evidence-based interventions can be

delivered systematically to the population in

need. These registries also allow the monitoring

of patients’ responses to these interventions. For

example, medical groups have used registries to

ensure that patients with diabetes receive

glycosylated hemoglobin testing and eye care

referrals. Within bone health, a registry of

patients with higher-than-average risk for

osteoporotic fractures could help to identify

those who are not taking medications to improve

bone health. Similarly, a registry of those who

have fallen or are at high risk of falling could

facilitate preventive measures such as

environmental modifications (e.g., installation of

grab bars, hand rails, raised toilet seats) and/or

referrals to a fall prevention program. The
Bone Health and Osteoporosis

Systems-Based Approaches To Bone Health 289

registry could also be used to monitor those who

have fallen and/or those who have a fear of falling

to determine whether progress in addressing

these problems has been made.

Medical groups can also implement systematic

education efforts aimed at physicians and other

health professionals, such as academic detailing

(Siegel et al. 2003, Solomon et al. 2001). Academic

detailing involves having trained professionals

advise individual providers in one-on-one sessions

about how to follow evidence-based practice

guidelines in a specific area, such as appropriate

use of a diagnostic test (e.g., dual x-ray

absorptiometry [DXA]) or of pharmacologic

therapies. Some groups may even serve enough

patients to sponsor education classes, Internet

resources, and exercise programs.

Very large groups may be able to develop

specialized clinics for caring for specific

disorders, such as osteoporosis. These clinics can

be a practical approach to ensuring that the

quality of care for the disorder is uniform

throughout the group. They can also allow for

the concentration of expensive resources such

as bone densitometers in a few locations. These

clinics may also allow personnel to develop indepth expertise in caring for patients with

conditions such as osteoporosis. For example,

nurse practitioners have gained such expertise

in treating patients with heart failure (Crowther

2003) and diabetes (Litaker et al. 2003). Although

experience with osteoporosis clinics has been

limited, a nurse practitioner-led Fracture Liaison

Clinic in Glasgow was successful in increasing

the frequency of BMD testing and treatment in

fracture patients as compared to historical

controls. The clinic identifies patients who have

suffered one or more fractures in emergency

departments and then follows up with their

health care providers to encourage BMD testing

and treatment (McLellan and Fraser 2002).

Specialized clinics can also refer patients with

osteoporosis and those at risk of falling to

therapists and community-based exercise

programs with expertise in addressing their

specific needs (as discussed earlier, individual

clinicians can do this as well). The optimal

staffing, referral criteria, and volume of patients

needed to justify an osteoporosis clinic are

unknown. In particular, innovative, effective

strategies for using nurses, nurse practitioners,

physician assistants, physical therapists, and

other health professionals to promote bone

health need to be identified.

Large medical groups may have enough

patients with bone disease to justify the

development of their own disease management

programs. (Smaller groups and individual

clinicians may be able to refer patients to

programs run by health plans, if they exist.) In

disease management programs, persons

identified as having specific medical conditions

are followed more intensely. The goals are to

improve health outcomes and reduce costs by

preventing declines in health status that lead to

the need for costly medical care, including

hospitalizations and emergency department

visits. Disease management programs tend to be

utilized primarily for conditions associated with

frequent hospitalizations and high expenditures,

such as heart failure (Rich et al. 1995), diabetes,

and asthma (Legoretta et al. 2000). These

programs also tend to be relevant for conditions

that require intensive monitoring and frequent

changes in regimens (e.g., diuretics for congestive

heart failure, insulin doses for patients with

diabetes). As they require considerable human

resources (e.g., frequent telephone calls and

visits), the typical disease management programs

are likely to be too expensive for a disease like

osteoporosis, which does not demand frequent

adjustment of medication schedules. A possible
290 Chapter 11

A Report of the Surgeon General

exception, however, is disease management for

those who have had prior falls or are at high risk

for falling. In fact, some fall prevention programs

look very similar to disease management programs

(Tinetti 1986), and it can be argued that the high

risk of fracture among persons who have already

fallen or who have multiple risk factors for falls

merits the intensive monitoring and resources

associated with disease management programs.

As an example, Kaiser Permanente

Northwest (with 450,000 members in Oregon

and Washington) is instituting a comprehensive

program to manage osteoporosis after fractures

and to prevent falls. The program is based on a

pilot study, described earlier in this chapter,

which demonstrated the effectiveness of sending

e-mail reminder notices to the physicians of

patients suffering recent fractures (Feldstein et

al. 2003a). The e-mail reminders include

recommendations on BMD testing and

osteoporosis treatment. If a patient is identified

as being at risk of falling, clinicians can enter an

order for a low- or high-risk referral into Kaiser’s

electronic medical record. For those patients

identified as being at low risk for a fall, Kaiser’s

health education department sends educational

information about osteoporosis and fall

prevention along with a referral to a communitybased exercise program. Those at high risk for a

fall also receive educational materials and a

referral to an exercise program, and they are also

referred to an outpatient falls prevention

program run by the physical therapy

department. This 8-week program provides a

complete assessment of the risk of falling along

with muscle strengthening, balance, and gaittraining programs. This regional, populationbased program is provided through a physician

assistant in Kaiser’s Department of Endocrinology with oversight by an endocrinologist.

Finally, large group practices and vertically

integrated health systems can consider taking a

more population-based approach. For example,

large group practices may implement

community-based screening for osteoporosis.

Such approaches have been employed

successfully in increasing mammography

screening for breast cancer (Reuben et al. 2002).

Systems-Based Approaches for Hospitals

and Post-Acute Rehabilitation Facilities

The consequences of poor bone health and

osteoporosis frequently lead to admission to

hospitals and post-acute rehabilitation facilities.

Osteoporotic fractures of the hip, pelvis, and

spine (if symptoms are severe) frequently require

hospitalization for surgery or symptom control.

A systems-based approach to osteoporosis

requires more than just treating the immediate

problems or symptoms; rather, it should include

efforts to both improve bone health and prevent

future falls. Similar approaches have been

employed in managing coronary artery disease

(Fonarow et al. 2001) to ensure that patients in

the hospital after a heart attack are discharged

on appropriate medications that reduce the risk

of future heart attacks. For osteoporosis, this type

of approach would entail patient education about

nutrition, orders for pharmacologic therapy,

referrals for physical therapy or exercise

programs, and social services (if needed).

A large group of hospitalized patients may

not yet have been diagnosed with osteoporosis,

but their admitting diagnosis (e.g., falls, syncope,

gait instability, failure to thrive) may nonetheless

serve as a “red flag” about a high future risk of

fracture. A systems-based approach to caring for

these patients could involve putting into place a

process for identifying these individuals at

admission and then conducting BMD tests prior

to discharge to determine if they are osteoporotic

or osteopenic. However, the current diagnosis-
Bone Health and Osteoporosis

Systems-Based Approaches To Bone Health 291

related group (DRG) reimbursement system for

fee-for-service Medicare discourages the

performance of screening tests during the

hospital stay, since reimbursement is the same

whether or not these tests are performed.

Furthermore, scheduling additional tests such as

BMD during the hospitalization may delay

discharge. At a minimum, however, clinical risk

factors for osteoporotic fractures should be

assessed using standardized protocols during the

hospital stay or at discharge, unless such action

is precluded by the patient’s acute illness.

Many patients who suffer fractures or falls,

as well as those with gait and balance disorders,

are discharged to skilled nursing facilities to

receive additional rehabilitation. These patients

typically do not qualify for Medicare

reimbursement in an acute inpatient

rehabilitation facility. (Under current Medicare

guidelines, patients must need at least 3 hours

per day of a combination of different types of

rehabilitation, such as physical therapy,

occupational therapy, and speech therapy, to

qualify for reimbursement.) Similar to

hospitalized patients, a systems-based approach

to skilled nursing facility residents who suffer

fractures would consider them as candidates for

specific bone and fall prevention interventions.

Those who are at high risk of falling but who

have not fractured should be considered

candidates for rehabilitation to reduce this risk.

However, the assessment and treatment of frail

patients can be challenging. Although BMD

testing may not be available in many nursing

homes, many of the patients have already

suffered fractures and testing is therefore unlikely

to provide additional, useful information. The

goal for these individuals should be the

prevention of new fractures. Since the frail

elderly are especially prone to falling, residential

settings such as nursing homes should take

advantage of the opportunity for social group

exercise activities that reduce the risk of falling

by building muscle strength and improving

balance. In addition, medication administration

can be challenging in the frail elderly who live

in nursing homes and in the community, since

many of these individuals are cognitively

impaired and therefore may have trouble with

compliance. In these situations, long-acting

medications, including those that could be

administered once a year intravenously (e.g.,

intravenous bisphosphonates are currently

under development) or by injection (e.g., vitamin

D) hold great promise, as do drinks fortified with

calcium and the use of hip protectors in those

most prone to falling.

In addition, other systems-based approaches

to improving bone health in the nursing home

are possible. For example, a nursing home could

implement a policy of “standing” orders for

vitamin D and calcium supplementation (in

those who can tolerate it) that are followed unless

the clinical provider specifically rejects the order.

Similar “standing” orders are common for

laxatives and for mild pain medications (e.g.,

acetaminophen). Another possibility would be

“standing” orders for hip protectors for all

residents at risk of falling (Lauritzen et al.1993).

(See Chapter 9 for more details on hip

protectors.)

Systems-Based Approaches for Health Plans

and Insurers

The role of health plans and insurers in

systems-based approaches to medical conditions

varies considerably from plan to plan and insurer

to insurer. It depends in large part on the degree

to which health plans and insurers hold their

contracted medical groups accountable for

management of specific diseases, including the

processes of care. To date, most health plans and
292 Chapter 11

A Report of the Surgeon General

insurers have played a limited role in promoting

optimal care for patients with bone disease. Some

of these organizations might have limited

incentives to invest today in preventive services

and programs that likely will not yield financial

and/or clinical benefits for many years (perhaps

when those who receive the services have

changed health plans or are covered by

Medicare). Nonetheless, there are ways in which

all health plans and insurers affect bone health—

that is, coverage policies that directly affect the

provision of services, procedures, and

medications used to promote bone health and to

prevent, diagnose, and treat bone disease. In

addition, at least some plans and insurers are

getting more intimately involved in a systemsbased approach to bone health and disease. These

plans are assessing and monitoring performance,

engaging in quality improvement programs, and/

or implementing pay-for-performance initiatives

that reward high-quality, evidence-based care.

The rest of this section covers these various

leverage points for plans and insurers—that is,

coverage, performance measurement, quality

improvement, and pay-for-performance.

Medicare and Private Sector Coverage

The Medicare program tends to set the

standard with respect to coverage policies for

testing and treatment within the area of bone

health. In other words, most private insurers tend

to follow Medicare’s lead.

Coverage of Tests for Screening and Monitoring. Under a provision of the Balanced Budget Act of 1997 (P.L. 105-33), Medicare is required

to cover BMD testing every 2 years for people at

risk of developing osteoporosis or under treatment

for osteoporosis (USDHHS 1998). This law is

applicable to individuals enrolled in Medicare feefor-service and Medicare + Choice plans. Under

this law, BMD testing is defined as radiologic, radioisotopic, or other procedures approved by the

FDA for the purpose of identifying bone mass, detecting bone loss, and interpreting bone quality.

Although many different testing modes and devices

have been approved by the FDA and are covered

by Medicare and some private payers, it is important to remember that not all of these tests have been

shown to have a strong predictive relationship with

fracture risk (see Chapter 8 for a more detailed discussion). The most thoroughly investigated tool is

DXA, which measures bone density at the most

likely sites of fracture, the hip and spine. Since DXA

is expensive and not available everywhere, ultrasound of the heel can be used as an initial screening

tool, to be followed by a DXA test in those identified as having low bone density. Individuals with

the following characteristics are considered at risk

and eligible for Medicare coverage of BMD testing:

• Women who are estrogen deficient as defined by their physicians and who are at risk

for osteoporosis

• Individuals with vertebral abnormalities,

osteoporosis, or spine fracture determined

by x-ray

• Individuals with primary hyperparathyroidism

• Individuals being monitored to assess the

response to or efficacy of an FDA-approved

osteoporosis drug therapy

• Individuals receiving or expecting to receive

glucocorticoid therapy, equivalent to >7.5

mg of prednisone per day, for more than 3

months

Men and minority (especially Black) women

who present with these risk factors are often

not recognized as being in need of BMD testing.

White women are known to have a higher risk

of fracture, but it is important to remember that

individuals in other racial and ethnic groups

need to be tested and, if appropriate, treated if

they exhibit the risk factors cited above or have

suffered a fragility fracture at any site.
Bone Health and Osteoporosis

Systems-Based Approaches To Bone Health 293

Policies for coverage of BMD testing by

private health plans generally follow the

eligibility criteria for Medicare, though

individual plans vary in their coverage. For

example, BlueCross of California considers all

women age 65 and older as eligible regardless of

additional risk factors (BlueCross of California

2002). Likewise the specific tests to assess BMD

that are covered may vary from plan to plan.

Coverage of Pharmacologic Treatment. The

Medicare Modernization Act (MMA) was signed

into law in 2003 and provides beneficiaries with

access to some level of coverage for drugs that treat

bone disorders. In addition, Medicare beneficiaries

enrolled in Medicare Advantage (formerly

Medicare + Choice) plans with pharmacy benefits

typically have some level of coverage for

medications related to bone health. Neither

traditional Medicare or Medicare Advantage

beneficiaries have coverage for nutritional

supplements, such as calcium and vitamin D. Most

private health plans do cover estrogen and at least

one of the bisphosphonates. Coverage for selective

estrogen receptor modulators (raloxifene),

calcitonin, and parathyroid hormone varies among

different plans.

Coverage of Non-Pharmacologic Treatment.

Physical therapy is covered under Medicare Part

B for certain diagnoses related to falls. Medicare

does not cover physical therapy for individuals

solely on the basis of being at high risk of falling.

Effective September 1, 2003, there is a combined

$1,590 annual limit on Medicare coverage of

outpatient physical therapy and therapy for

speech-language pathology. Private health plans

have variable coverage for physical therapy.

Coverage for vertebroplasty and

kyphoplasty under Medicare Part B varies from

state to state. These procedures are generally

covered for painful spine fractures that have not

responded to conventional therapy. The

coverage policies of private health plans for

these procedures is limited, due largely to the

lack of solid evidence on their effectiveness. For

example, BlueCross and BlueShield of Montana

will consider coverage of vertebroplasty and

kyphoplasty on an individual basis for patients

who have failed to respond to standard nonsurgical treatment (BlueCross BlueShield of

Montana 2003). Aetna considers kyphoplasty

to restore bone height lost due to painful

osteoporotic fractures to be an experimental/

investigational intervention and consequently

does not cover this procedure (Aetna 2003).

Performance Assessment

In addition to coverage policies, health plans

and insurers are uniquely positioned to employ

a systems-based approach to improving bone

health through the use of performance

assessment. Health plans can use their data about

diagnoses and utilization of services to assess

whether indicated preventive measures and

treatment are provided to their members,

whether such measures and treatments work,

and whether members are satisfied with the care

that they receive. To date, plan-driven programs

to improve quality have largely focused on the

assessment and reporting of performance for

preventive services and selected chronic diseases.

Osteoporosis has not been a target of

performance assessment, although it may

become a target condition in 2004 with the

introduction of a performance measure for

osteoporosis by the National Committee for

Quality Assurance (NCQA).

NCQA is a nonprofit health care oversight

organization that accredits managed care plans

and has produced a widely used quality reporting

system called the Health Plan Employer Data

and Information Set (HEDIS). HEDIS

measures were initially designed to provide

information to large purchasers about the quality
294 Chapter 11

A Report of the Surgeon General

of care delivered to their employees. More

recently, the audience for HEDIS results has

broadened, and they are often reported in

consumer-oriented report cards. Since HEDIS

has standard measures and uniform data

reporting requirements, comparisons can be

made between various health plans.

With the planned implementation of a

performance measure for osteoporosis in 2004,

health plans and insurers will have an

opportunity to assess performance and promote

quality care for osteoporosis. The measure

reports the percentage of women age 67 or older

who suffer a fracture who receive either a BMD

test or prescription treatment for osteoporosis

within 6 months of the date of the fracture.

A complementary approach to the HEDIS

measures has been the development of quality

indicators (e.g., those developed in the

Assessing Care of the Vulnerable Elderly

[ACOVE] project) that can be used to

identify deficiencies in care provided (Wenger

New HEDIS Performance Measure for

Osteoporosis

A new HEDIS performance measure

related to osteoporosis goes into effect in

2004. The measure will evaluate how

well a health plan does in diagnosing and

treating osteoporosis in elderly women

who suffer a fracture. The measure is

defined as: “The percentage of women

age 67 or older who suffer a fracture who

receive either a BMD test or prescription

treatment for osteoporosis with 6 months

of the date of the fracture.” The new

HEDIS measure will evaluate the care

of women age 67 or older on Medicare

who are enrolled in a managed care plan.

and Shekelle 2001, Shekelle et al. 2001).

While guidelines exist that can assist in

determining appropriate services for other

populations, ACOVE spells out seven

evidence-based quality indicators that

specifically apply to elderly individuals (i.e.,

those over age 75) at high risk of functional

decline due to osteoporosis (Table 11-2).

Some are based on chart review of

documented care and others on data obtained

in interviews with elderly individuals

(Grossman and MacLean 2001, RAND 2004).

Quality Improvement Initiatives

Health plans and insurers that sponsor

performance measurement can and often do

supplement these activities with other programs

designed promote use of evidence-based

medicine. While osteoporosis has generally not

been a major focus of such activities, existing

quality improvement programs could be adapted

to osteoporosis. For example, like some medical

groups, health plans have implemented disease

management programs targeting high-cost,

common diseases such as diabetes, heart failure,

and asthma. Given the high cost of osteoporotic

fractures both in terms of health (Tosteson et al.

2001, OTA 1994) and dollars (Max et al.2002),

disease management programs for osteoporosis

might be beneficial for both plans and patients,

especially if individuals who have already

sustained (or are at high risk for) osteoporotic

fractures are targeted. In fact, some osteoporosis

disease management programs have been

implemented (although the details of most of

these are considered proprietary). For example,

one osteoporosis disease management program

implemented by the BlueShield of Northeastern

New York contains components aimed at both

members and providers. Among the membercentered interventions were mailings, education

days at local pharmacies, and newsletter articles
Bone Health and Osteoporosis

Systems-Based Approaches To Bone Health 295

that were all focused on osteoporosis. These were

supplemented with infomercials on a local cable

channel and posters developed for placement in

local clinicians’ offices. To support providers in

providing evidence-based osteoporosis care, the

plan developed guidelines and encouraged

adherence to them by sending notices and

placing stickers on the patient’s chart alerting

providers when patients had been contacted

about osteoporosis. In addition, providers were

given information about compliance issues

related to specific patients. For example,

providers were notified if a patient did not fill

his or her prescription for osteoporosis drugs at

least 80 percent of the time. Finally, the plan

initiated a requirement that BMD be measured
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A Report of the Surgeon General

before the approval of new prescriptions for

osteoporosis drugs. The program appears to be

working; during its first year BMD usage

doubled and medication compliance rates

increased by almost 60 percent (Paccione 2003).

Despite this anecdotal evidence of success,

disease management for osteoporosis has not yet

been adequately evaluated to determine its costeffectiveness. It may be possible for osteoporosis

disease management programs to be integrated

into similar types of programs for other chronic

diseases, such as heart disease or diabetes.

Pay-for-Performance Initiatives

Reimbursement policies represent one of the

most innovative ways that health plans and

insurers can promote quality and quality

improvement. In fact, the National Health Care

Purchasing Institute, through an initiative of the

Robert Wood Johnson Foundation, identified 11

potential provider incentive models for

improving quality of care (Bailit 2002). Several

plans have recently started to tie reimbursement

to performance within specific conditions.

However, it is important to recognize that

clinical performance is typically not the only

parameter assessed when determining the level

of the incentive payment. Other factors that may

be considered include patient satisfaction,

availability of providers (e.g., office hours that

are favorable to the patient), and use of

educational services.

One example of such an approach comes

from California, where a coalition of health plans

and physician groups has initiated, “Pay for

Performance”. This statewide program will pay

physician groups extra if they can document

strong performance in caring for patients with

certain diseases (Integrated Health Care

Association 2003). Participants include Aetna,

BlueCross of California, BlueShield of

California, CIGNA Health Care of California,

Health Net, and PacifiCare, each of which has

agreed to use common performance measures for

asthma, coronary artery disease, and diabetes.

These plans have also agreed to implement

“significant” financial incentives based on

performance, although the size of the incentive

and the distribution methodology for the

payments will be determined independently by

each plan. The first payments to medical groups

under this plan will be in 2004 based on 2003

performance data.

Systems-Based Approaches for Government

and Public Health Agencies

Federal, State, and local governments,

including the public health system, can play

vitally important roles within many of the four

core activities described earlier. In fact, a recent

Institute of Medicine (IOM) report made a

number of general recommendations on the

appropriate role of governments and public health

agencies that are applicable to bone health and

osteoporosis (IOM 2002). Among these were

urging local health departments to support

community-led, joint efforts between the

corporate community and public health agencies

to strengthen health promotion and disease and

injury prevention programs for employees and

their communities, along with a call for increased

collaboration between public health officials and

local and national entertainment media to facilitate

the communication of accurate information about

diseases and medical and health issues.

As the IOM report suggests, perhaps the

most important role for public health agencies is

to promote awareness among consumers and

clinicians of the importance of bone health, and

of the best methods for preventing, assessing,

and treating bone disease. While the lack of a

cohesive health care system creates challenges

for the prevention and treatment of bone disease,

the public health system can help overcome these

problems by mobilizing to increase awareness.
Bone Health and Osteoporosis

Systems-Based Approaches To Bone Health 297

A better informed and more concerned public

can facilitate adherence to recommended care

management practices by influencing provider

behavior (Maly et al. 1996) and policy changes.

To that end, public health agencies may

sponsor broad-based and targeted public

awareness campaigns, with messages tailored to

different population subgroups. For example, for

younger persons, the emphasis may be on

nutrition (e.g., calcium intake), lifestyle choices

(e.g., smoking avoidance and cessation), and

physical activity to build peak bone-mass. In

contrast, for older persons who have already

suffered an osteoporotic fracture, the message

may focus on whether they are receiving

appropriate medications and fall prevention

measures. The choice of venues should vary

based upon the message. Younger persons might

best be reached through the Internet, advertising

on evening television and billboards, and/or in

magazines oriented at youth. In contrast, the

elderly might best be reached through daytime

television programs, magazines, and senior

centers. Of course, other stakeholders within the

overall health system, including health plans/

insurers, large medical groups, and professional

associations can assist with these awareness

campaigns, while individual clinicians can

reinforce the campaign’s messages during their

interactions with consumers.

Public health agencies may also want to

consider supplementing their awareness

activities with broad-based and/or targeted

screening programs, provided either

independently or in collaboration with health

care delivery systems. Similar types of programs

have been conducted in other areas, including

nationwide programs promoting vaccinations for

influenza and polio and local screening programs

for disorders like hypertension and

hypercholesterolemia.

Another potential role for public health and

government is to improve the linkages between

health care organizations, community-based

organizations, and the public health system. At

present the lack of such linkages makes it difficult

to provide consumers—especially those with

multiple, chronic health conditions—with a full

range of beneficial services. While public health

agencies do not typically provide the continuity

of care that is required for management of

chronic conditions like osteoporosis, they may

be able to play a vital role in bridging the gap

between health care organizations, communitybased and educational resources, and other

complementary services in various aspects of

bone health, including fall prevention and BMD

screening. For example, public health agencies

could partner with community-based

organizations to provide consumers with an

assessment of their risk of bone disease (possibly

including BMD screening). Consumers could

take this information to their health care provider

(a referral could be provided, if necessary), who

could then work with the individual to determine

the appropriate course of action. Some

individuals may need a referral to a specialist or

an osteoporosis clinic, while others can continue

to have their bone health managed by their

primary care provider. By educating consumers

and engaging the health system in this manner,

public health can play a critical role in helping

to ensure that consumers receive appropriate,

evidence-based care.

Yet another area for public health is in helping

to train health care professionals to be more

skilled at promoting bone health and in

recognizing and treating bone disease. Public

health agencies can work with health professional

associations to co-sponsor conferences and

seminars and can work with academic institutions

in the development and promotion of curricula.
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Policy-making represents another strategy

that governmental agencies at the local, State, and

Federal level can use to promote bone health and

appropriate treatment of bone disease. They can

use policies to promote bone health and to

encourage the prevention, timely diagnosis, and

early, appropriate treatment of bone disease and

fractures. For example, regulations could require

the installation of grab bars in the showers of all

retirement communities. Financial incentives

such as tax credits could promote the widespread

availability of fitness centers that provide exercise

classes to seniors at risk for falling. Local urban

planning policies can also promote bone health

by developing public spaces that minimize the risk

of falling and that offer opportunities for outdoor

exercise. Finally, governmental agencies can also

set quality control standards for assessing BMD

tests and certification standards for densitometer

operators.

A final, vitally important role for public health

is in monitoring and surveillance activities. These

activities relate not only to monitoring compliance

with regulations, but also to implementing ongoing

surveillance methods to monitor and assess trends

in the following:

• The prevalence of bone disease and fractures in the community

• The degree to which individuals engage

in bone-healthy behaviors

• The degree to which community-wide

and institution-specific interventions are

influencing consumer and clinician behavior and having an impact on bone

health outcomes

Other Facilitators

Individual clinicians, medical groups, health

care delivery systems, insurers, and public health

departments are the primary drivers of systemsbased approaches to improving bone health and

reducing the consequences of osteoporosis.

Other institutions, organizations, and agencies

can facilitate these efforts through research,

education, and purchasing policies and power.

Diverse entities such as voluntary health

organizations and professional associations,

academic institutions, health care purchasers,

and industry (including pharmaceutical and

technology companies) are all stakeholders in the

system. While they have rarely collaborated in

developing approaches to health care problems

such as osteoporosis, a cohesive approach could

provide substantial momentum towards

optimization of bone health on a large scale.

The Role of Voluntary Health Organizations

and Professional Associations

Voluntary health organizations (or advocacy

groups) and professional associations play

important roles in any systems-based approach

to bone health. They are able to reach the public

and providers with critical information quickly

and often with fewer constraints than can

government organizations.

One of the most important roles for voluntary

organizations is to raise public awareness about

specific health problems such as bone disease. By

including individuals who have personally been

touched by bone disease, these organizations are

uniquely positioned to provide important

guidance to other sectors of the health system

regarding the real-life impact of bone disease on

individuals, families, and communities.

Lacking the label of government and being

composed of persons from the community,

voluntary health organizations also can be quite

effective in persuading local residents—their

peers—to adopt the lifestyle changes necessary

to prevent the onset or progression of bone and

other diseases. For some diseases, the absence of

the government label has also made it possible
Bone Health and Osteoporosis

Systems-Based Approaches To Bone Health 299

for voluntary health organizations to develop

registries of affected individuals, thereby

improving access to information and other

resources related to the treatment of the disease.

Professional associations also play a critical role

in promoting a systems-based approach to bone

health. They are key facilitators in the training of

professionals needed to address public health

problems such as bone health. They also promote

changes in the curricula of professional schools and

provide continuing education to practicing bone

health professionals. These associations can also

be instrumental in the development of evidencebased prevention and treatment guidelines and

standards of care for bone health. These guidelines

help to ensure that individuals who have or are at

risk of getting bone disease can benefit from the

best practices related to prevention, assessment,

diagnosis, and treatment.

The Role of Academic Institutions

Academic institutions can be critical

facilitators through their two core missions of

education and research. Typically, health

professions education has focused more on

teaching the clinical aspects of care than on the

delivery or systems aspects. With respect to

osteoporosis and bone health, various professionals

are essential for promoting bone health, including

physicians, nurses, physician assistants, dietitians,

physical and occupational therapists, social

workers, dentists, ophthal-mologists, optometrists,

and pharmacists. While the amount of training

each professional student receives in bone health

and osteoporosis has not been quantified

systematically, discipline-specific curricula could

be created. For example, some schools have

created “bone curricula” that teach basic science

and clinical aspects related to bone health and

bone diseases such as osteoporosis, osteomalacia,

and bone tumors. Teaching tools such as CDROMs, standardized patient case studies, and

videotapes have been created to help teach this

material. Equally important is the

development of professional skills to become

effective members of a health care team that

focuses on improving bone health and

preventing adverse outcomes. For example,

trainees from different disciplines (e.g., medical

students and residents, nurse practitioners,

physician assistants) could be given the

opportunity to rotate through osteoporosis

clinics. Although a variety of models for

interdisciplinary team training have been

implemented, organizational challenges

(bReuben et al. 2003) and discipline-specific

barriers to such cross-discipline training

(Reuben et al. 2004) may impede these

efforts. Finally, academic institutions may

also serve an important educational role for

the general public by teaching lifestyles that

promote bone health in primary and

secondary schools and colleges. Schools must

begin to play a role in promoting and

supporting good dietary habits and regular

physical activity, beginning in childhood.

The second role of academia is to advance

research on bone health. To date, such

research has focused primarily on clinical

issues, but some academic institutions have

active research programs on health care

delivery. While many of these have focused

on preventive measures (e.g., cancer screening,

smoking cessation), a few have attempted to

improve bone health.

The Role of Health Care Purchasers

Health care purchasers have begun to use their

power both individually and collectively to

influence health care delivery. For example, the

Leapfrog Group, a coalition of major employers

around the country, has attempted to change
300 Chapter 11

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health care delivery by encouraging adoption of

computerized physician order entry (CPOE)

systems, referral of patients to specialized, highvolume centers for some surgical procedures, and

minimum requirements for physician staffing in

intensive care units (Leapfrog Group 2003). If

successful, these types of efforts by purchasers

may be very influential in promoting evidencebased care, and thus may represent a potential

top-down approach to ensuring that good bone

health care is provided. As mentioned previously,

the Federal and State governments in their roles

as purchasers can also influence bone health and

osteoporosis care by coverage and other

purchasing-related decisions. It is important to

remember that the role of purchasers in

promoting better bone health will likely continue

to be limited in a financing environment where

those that pay for prevention, assessment, and

treatment today frequently do not realize the

benefits of such investments, which tend to

materialize over the long term.

The Role of Industry

The pharmaceutical and medical device

industries have been important facilitators in

reducing the consequences of poor bone health

through the development and promotion of

drugs, devices, and other technologies. In fact,

these companies are critical sources of

information for providers and the public on the

use of pharmaceutical agents to prevent and treat

bone disease. This information needs to be

combined with a more comprehensive approach

to promoting bone health, including appropriate

diet and physical activity.

In addition, there are other, independent

companies that focus on disease management that

can promote bone health by contracting with

health plans, insurers, and other organizations to

provide evidence-based care, just as they are doing

now for conditions such as heart failure and

diabetes. As mentioned previously, however, it is

not clear to what extent these companies focus

on osteoporosis today or what type of services

they provide.

Special Populations

Several populations deserve special attention

by all components of the health care system

because they face barriers in accessing care and/

or limitations in medical knowledge that may

prevent them from receiving good care. These

populations include the uninsured and

underinsured, the poor, minority populations,

men, nursing home residents, frail elderly

persons, and rural or other remote populations.

The Uninsured

Thanks largely to government programs such

as Medicare and to commercial insurance, the vast

majority of persons who are at risk of poor bone

health and osteoporosis have or are eligible for

health care coverage. In fact, most persons lacking

insurance in the United States are working ageadults and children who, in the absence of medical

conditions and medications that interfere with

good bone health, are at low risk of short-term

adverse bone health outcomes. Nevertheless,

children and adults without access to health care

may not receive important information about

behaviors that promote peak bone mass (e.g.,

appropriate diet and levels of physical activity,

avoidance of smoking). Those uninsured

individuals who are at high risk of bone disease

represent a particularly vulnerable population,

since all of their costs for medical care and

pharmacotherapy must be borne out of their own

pockets or through uncompensated care

mechanisms. In many cases these individuals fail

to access preventive care services and to obtain

early diagnosis and treatments, waiting instead

until their health deteriorates to the point that they

face an urgent or emergent situation.
Bone Health and Osteoporosis

Systems-Based Approaches To Bone Health 301

The Underinsured

A potentially bigger problem than the

uninsured is the far larger number of Americans

with health insurance coverage who are

“underinsured.” These individuals often face

problems in getting access to appropriate services

to promote bone health and to treat osteoporosis.

Medications designed to treat or prevent bone

loss can be expensive and the costs can be highly

variable. For example, in June 2004, costs ranged

from $25 per month for persons who only receive

conjugated equine estrogens, to $64 per month

for bisphosphonates, to $502 per month for those

receiving teriparatide (Drugstore.com 2004). Of

course, the new Medicare drug benefit will

provide some level of coverage to beneficiaries.

However, hip protectors, which cost only $50–

$100 and may prevent fractures in frail elderly

persons (Kannus et al. 2000, Parker et al. 2001),

are not covered by Medicare, while coverage for

important environmental modifications such

as grab bars, railings, and raised toilet seats

is inconsistent. Items considered to be

durable medical equipment (e.g., raised toilet

seats) are covered under Part B Medicare, but

home modifications (e.g., installation of grab

bars) are not. Some of these modifications

may be provided, typically on a sliding scale

basis, by programs sponsored by the

Administration on Aging.

Minority Groups

Along with the uninsured and underinsured,

people of color also need special consideration

with respect to bone health and osteoporosis. As

noted in earlier chapters, the definition of

osteoporosis and assessments of fracture risk

from BMD test results are based upon standards

developed for Whites. Minority groups that have

different average body and bone size, such as

Asians and Blacks, present some challenges for

the assessment of bone health by standard bone

density tests. Blacks have higher bone density

and a lower risk of fracture than do Whites of

the same age. Nevertheless, the presence of

strong risk factors such as a previous fracture or

the use of glucocorticoid drugs, especially when

combined with low body weight and/or older

age, should be a signal for immediate attention

to the potential need for intervention. In other

words, while a person’s race may suggest a lower

average risk of fracture, it by no means indicates

that there is no risk.

The bone density of Asians is similar to that

of Whites after accounting for a smaller average

body and bone size (Finkelstein et al. 2002).

Nevertheless, standard bone density assessment

does not compensate for these differences, and

thus it is important to evaluate family and

personal history of fracture and other risk factors

in Asians (and small Whites) before determining

if they are at high enough risk to warrant the

initiation of treatment.

With respect to prevention and treatment of

bone disease in minorities, there is no indication

that pharmacologic interventions act differently

or less effectively in minority populations. Blacks

and Asians are more prone to lactose intolerance

than are other groups, and thus they may be at

greater risk of consuming inadequate levels of

calcium and vitamin D. Thus, it is important to

promote alternative sources of calcium and

vitamin D in those who are lactose intolerant.

(See Chapter 7 for more details.)

Another issue facing people of color is timely

access to all health care services. The goal of

better bone health for all Americans cannot be

reached without significant improvements in

preventive services, screening, diagnosis, and

treatment, as well as significant changes in

individual behaviors. This goal will not become
302 Chapter 11

A Report of the Surgeon General

a reality for people of color unless there are major

improvements in their ability to access care on a

timely basis. These minority populations are at

the highest risk for poor health, yet they rely on

an unorganized patchwork of providers for

services that are necessary to prevent illness and

maintain health. Emergency facilities are a major

source of care for people of color, and their

dependence on these often overcrowded facilities

continues to grow (IOM 2002). These facilities

are ill equipped to provide or even facilitate the

coordinated, ongoing preventive and treatment

services that people of color need to maintain

bone health and overall health and well-being.

People of color not only have difficulty in

accessing care, but there are also concerns about

the quality of those services that they do receive.

A recent study by the Institute of Medicine

concluded that people of color tend to receive

lower quality health care than does the majority

population, even after accounting for accessrelated factors (Smedley et al. 2003). These

disparities are consistent across a wide range of

services, including those critical to bone health.

A recent study found that few Black women

(11.5 percent) had been screened for osteoporosis

despite the presence of important risk factors for

low bone density; the study also found that the

prevalence of low bone density among these

Black women was substantial (Wilkins and

Goldfeder 2004). Overcoming these disparities

will require specific strategies and programs

geared towards bringing improvements in bone

health to minority populations.

Men

Men represent another population of

concern, since far less is known about the

epidemiology, risk factors, and treatment of

osteoporosis in males. As noted in Chapter 4,

men account for roughly 20 percent of all hip

fractures. It is unclear whether the diagnostic

criteria for osteoporosis in women should be

applied to men. While aging is associated with

bone loss in men, the pattern of loss does not

appear to be the same as that experienced by

women for several years after menopause. (See

Chapter 3 for more details.) The National

Osteoporosis Foundation recommends BMD

testing for men who present with fractures or

are receiving treatment with a GNRH agonist

for prostate cancer, as well as for all individuals

who have primary hyperparathyroidism or are

on long-term glucocorticoid treatment (NOF

2003). For more details on the evidence related

to BMD in men, see Chapter 8. With respect to

therapy, bisphosphonate and PTH treatments

are effective in men (Finkelstein et al. 2003,

Orwoll et al. 2000). The use of testosterone for

bone and muscle loss in elderly men has been

debated due to the possible increased risk of

prostate cancer (Liverman and Blazer 2004). At

this time, testosterone would not be considered

a first-line treatment to prevent fractures.

The Frail Elderly

As with men, the knowledge base for how

best to manage frail elderly persons with

osteoporosis is not fully developed. As discussed

earlier, the frail elderly living in nursing homes

and retirement communities can benefit greatly

from group-based exercise programs that reduce

the risk of falling by improving muscle strength

and balance. These supervised programs help to

reduce some of the barriers to getting frail

individuals to become more physically active,

including lack of knowledge about what types

of activities are safe and effective and the fear of

falling or becoming injured while exercising. As

noted earlier, the frail elderly also stand to benefit

from the development of long-acting medications

that make compliance problems less of an issue.
Bone Health and Osteoporosis

Systems-Based Approaches To Bone Health 303

Populations in Underserved Rural and Inner

City Areas

Individuals living in areas that lack health

care resources, including rural areas and inner

cities, represent another special population to

be considered. Although many of the

therapeutic options for promoting bone health

are accessible nationwide, some communities

may lack bone densitometry services and/or

specialists with expertise in osteoporosis.

Furthermore, newly developed procedures are

not available in every community.

Conclusions

Major advances in bone health have been

made over the past decade. The knowledge base

needed for clinical decision-making has grown

substantially, resulting in a much better

understanding of the risk factors for poor bone

health outcomes and strategies and interventions

for reducing that risk. Measurement of bone

density has become more widely available as the

hardware for BMD testing has become less

expensive. New, well-tolerated drugs have been

introduced that are effective in increasing BMD

and preventing fractures. Fall prevention

programs have been developed and

demonstrated to be effective, as described in

Chapters 6 and 7. For those individuals who are

at extremely high risk of fracture, rigorously

tested hip protectors can significantly reduce the

risk of fracture from a fall. Some payment

decisions (e.g., Medicare’s decision to cover

BMD testing) have facilitated identification

of those who need specific treatment to help

prevent fracture. Finally, there has been

increased public awareness of the importance

of bone health and the potential

consequences of osteoporosis.

In the context of these advances, systemsbased approaches offer the potential to make

substantial improvements in bone health and to

reduce the adverse outcomes of bone disease.

Historically, a number of barriers have

prevented the widespread application of such

approaches. These barriers include the lack of a

comprehensive evidence base to guide decision

making on osteoporosis and bone health, the

fragmented nature of the delivery system, a

financing and payment system that does not

always create the proper incentives for the

promotion of bone health, a workforce that has

not historically been trained to engage in a crossdisciplinary, systems-based approach to care, and

the lack of a strong push for improvement from

outside facilitators, such as purchasers.

Fortunately, some of these barriers are

being broken down. Further progress is

possible through changes in policy, financing,

organizational management, and education.

Such changes are critically important to

improving the bone health of Americans. As

the evidence base continues to grow, a

piecemeal approach to translating research

findings into practice will no longer suffice.

On the contrary, to benefit the largest

numbers of individuals, it will be essential to

utilize systems-based approaches that

promote use of evidence-base bone health

care for a broad spectrum of Americans,

including the special populations discussed

earlier in this chapter.

Key Questions for Future Research

Many systems-based approaches have been

found to be effective in promoting certain aspects

of health, but few have been specifically tested

in bone health. Key research questions in this

area are listed below:

• What are the most effective methods for

increasing consumer and health care pro-
304 Chapter 11

A Report of the Surgeon General

vider awareness of the need for improving bone health? Do these methods need

to vary depending upon the racial and

ethnic make-up of the target population?

If so, how? How do these differ by age

group and treatment goals (e.g., preventive versus therapeutic)?

• What are the most cost-effective methods for stratifying the population according to risk of bone disease? What role can

measures of bone density and of fall risk

play in the risk-stratification process?

• What are the optimal diagnostic and

therapeutic approaches for special populations (e.g., men, racial and ethnic minorities, nursing home residents) for

whom the evidence base is lacking?

• What are the optimal clinical, educational, and social rehabilitation programs

for persons who have sustained hip or

painful vertebral fractures?

• Which provider incentives and quality

improvement techniques are most effective

in changing current patterns of care for

osteoporosis and bone health to be consistent with commonly accepted guidelines?

• What systems changes (e.g., computerized reminders, registries, standing orders)

can be broadly implemented in various

settings to guide osteoporosis and bone

health care in a manner that is consistent

with commonly accepted guidelines?

• What are the best measures for assessing the

quality of comprehensive osteoporosis care?

• Is the use of specialized osteoporosis clinics a more cost effective way to improve

bone health than attempting to improve

practice patterns among primary care

physicians?

• How can health care providers and systems effectively link with communitybased organizations to reduce the risk of

falling?

• How can the public health system be

most effectively engaged as a partner in

improving bone health?

• How effective are fall prevention clinics

in reducing the risk of future falls?

• What screening tools are most appropriate for provider organizations to use in

primary care settings?

• How is screening and treatment for osteoporosis best integrated into management of other chronic diseases?
Bone Health and Osteoporosis

Systems-Based Approaches To Bone Health 305

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310 Chapter 12

A Report of the Surgeon General

Chapter 12: Key Messages

tions. Public sector (social marketing,

mass media campaigns) and private sector (direct-to-consumer advertising) approaches can be used to reach target

populations.

• This chapter includes seven case examples of successful and/or innovative

interventions that can serve as building

blocks for future population-based approaches to bone health:

∼ Any campaign should be based upon

credible evidence and be evaluated on

a continuing basis to ensure that

objectives are being met and/or that

corrective action can be taken.

∼ A number of evidence-based tools are

available for developing interventions.

∼ Basic education about bone health is

an important component.

∼ Building local partnerships is critical

to success. Health care providers;

education, environmental, and

housing agencies; organizations

serving the aged; churches,

synagogues, and other religious

organizations; and other groups can

help to build a comprehensive

strategy for maximizing the bone

health of community residents.

∼ Useful prevention messages are

available for every age group,

although age should not be the only

variable affecting the design of

interventions.

∼ Health policy and environmental

changes are important tools in

health promotion.

• Population-based interventions are targeted toward promoting the overall

health status of the community by preventing disease, injury, disability, and

premature death. A population-based

health intervention should include the

following: assessment, health promotion, disease prevention, monitoring of

services, and evaluation. Some methods include public education programs, community projects, and media interventions.

• Bone health is particularly amenable to

population- and community-based interventions, for several reasons.

∼ Bone loss and fractures affect a large

portion of the population and can be

prevented during all stages of life.

∼ There is a widespread lack of

knowledge about prevention among

providers and the public.

∼⎯ State and local governments have an

incentive to promote this approach,

since the costs of caring for bone

disease are frequently borne by

government and the benefits from

population-based interventions

extend to other areas of health.

∼ Well-crafted population-based

interventions have been shown to

be effective in improving bone

health and other aspects of health,

including increases in physical

activity and decreases in smoking

within a target population.

• Communication is an essential tool in

many population-based health interven-
Bone Health and Osteoporosis

Population-Based Approaches 311

POPULATION-BASED APPROACHES TO

PROMOTE BONE HEALTH

Chapter 12

This chapter defines and provides examples

of population-based interventions for promoting bone health that are tailored to different

populations, addresses evidence regarding their

effectiveness, and identifies some key aspects

of successful programs.

Definition of Population-Based

Interventions

In contrast to clinical services provided to individual patients in an effort to improve their

health status, population-based interventions are

targeted toward populations to promote the overall health status of the community by preventing disease, injury, disability, and premature

death. A population-based health intervention

should include the following: assessment, health

promotion, disease prevention, monitoring of

services, and evaluation. Some methods to accomplish these goals include public education

programs, community projects, and media interventions. Some programs involve combinations of these approaches.

Most of these interventions are tailored to

reach a subset of a population although some

may be targeted towards the population at large.

Populations and subsets may be defined by geography, culture, race and ethnicity, socioeconomic status, age, or other characteristics. Many

of these characteristics relate to the health of the

described population (Keller et al. 2002).

Bone health is a topic particularly amenable

to population-based interventions, for a variety

of reasons. Bone loss and fractures affect a large

portion of the population, and they can be prevented during all stages of life. As discussed elsewhere in this report, there appears to be a widespread lack of knowledge about prevention approaches among both health providers and the

general population. Finally, State and local governments have an incentive to promote population-based bone health interventions, for several

reasons. First, the complications of osteoporosis

are easily observed, and the costs of caring for

these complications are frequently borne by these

governments. Second, such interventions, including promoting exercise and appropriate diet,

provide many other health benefits to community residents as well.

The most effective population-based approaches in bone health often involve a combination of individual- and population-level initiatives. The story of the Elder Floridian Foundation in the text box below highlights the interplay of individual- and population-level interventions and the importance of reaching beyond

traditional health practices to produce positive

changes in the population’s health.
312 Chapter 12

A Report of the Surgeon General

Personal Perspective of a Volunteer With

the Elder Floridians Foundation

As a teenager, I watched my grandmother and her sisters get shorter. After my

grandmother broke her hip, I spent many

weekends cleaning for my grandparents

while my mother prepared meals for the

upcoming week. Grandmother never fully

recovered from her fracture and died within

a year. I was not able to name the primary

reason for my grandmother’s death until

much later.

I learned about osteoporosis by researching the disease and writing press releases and

background papers as a volunteer for the

Elder Floridians Foundation. These materials were used for a media campaign to support proposed Florida legislation that would

mandate the diagnosis and treatment of osteoporosis. Learning that it is possible to keep

bones healthy and prevent fractures was an

incredible discovery. Although I felt strongly

that all older women should have this information, I did not feel that it applied to me.

After all, I was in my mid-40s and healthy.

During the Governor’s kick-off news conference event, which involved bone density

(DXA) tests for reporters and elected officials, I got a big surprise. Results of my own

DXA indicated low bone density of the hip.

I was alarmed that more than a million

women in Florida might be in a similar situation, and it became my mission to educate

them about their risk for this disabling disease. The media campaign was successful.

Legislation was passed that mandated insurance coverage for medically necessary diagnosis and treatment of osteoporosis for highrisk individuals.

It also resulted, however, in an unfunded

mandate to create an education and awareness program in Florida. To fill this gap, the

Elder Floridians Foundation launched Project

Osteoporosis: Be Smart, Be Dense, Know the

Difference in September 1997.

The goal of Project Osteoporosis is to alert

Florida’s citizens through community-based

education programs to the vital need to prevent, diagnose, and treat osteoporosis. These

programs consist of a risk assessment survey,

an educational slide presentation, a question

and answer opportunity with health care professionals, and a peripheral bone density scan

of the forearm (pDXA). Women’s organizations, civic and faith groups, universities, and

professional associations are among the

Foundation’s grassroots partners. They enthusiastically host Project Osteoporosis programs

in local communities and at regional and State

conventions.

Project Osteoporosis has traveled to 53 of

Florida’s 67 counties, providing hundreds of

thousands of screenings to many grateful Floridians. The program has also shown that osteoporosis happens to people from all walks of

life. Many of the people touched by this campaign have already suffered the consequences

of osteoporotic fractures. Here is the story of

one woman who was meaningfully affected by

Project Osteoporosis:

Lucy was in her early 70s, had lost 5 inches

in height and was no longer capable of growing

new bone. Unfortunately, she suffered three

compression fractures before a physician

recommended a bone density test and

prescribed treatment. By this time, Lucy’s

bones had become so brittle that she had two

more compression fractures of the spine after

beginning treatment. She said two things that

still have a tremendous impact on the

volunteers who work for Project Osteoporosis:

“Be sure to tell people about the pain” and “I

wish I had known.”
Bone Health and Osteoporosis

Population-Based Approaches 313

Evidence of the Effectiveness of

Population-Based Interventions

There is every reason to believe that wellcrafted, population-based interventions can be

highly effective in improving bone health and

other aspects of health. For example, in 1993, it

was estimated that while 10 percent of early

deaths in the United States could be prevented

through medical treatment, 70 percent could be

prevented through programs that reduce health

risks such as tobacco, drug, and alcohol use; sedentary lifestyle; poor nutrition; violence and environmental factors (McGinnis and Foege 1993).

Over the past two decades, a variety of public

health and health care professionals and organizations have developed methods for conducting

standardized reviews of the effectiveness of interventions, including population-based interventions. These standardized assessments of an

entire body of evidence for a specific intervention are known as “systematic reviews.” Systematic reviews have contributed to methods for

translating evidence into recommendations for

practice (Canadian Task Force on the Periodic

Health Examination 1994, Preventive Services

Task Force [U.S.] 1996, Briss et al. 2000, Fiore

et al. 2000). These “evidence-based recommendations” provide a method for linking the

strength of a recommendation to the availability

and quality of supporting evidence.

The Guide to Community Preventive Services (the Community Guide) provides systematic reviews on the effectiveness of various population-based interventions for a variety of public

health topics, and then translates the evidence

of effectiveness into evidence-based recommendations (Truman et al. 2000, Zaza et al. 2000).

To date, the Task Force on Community Preventive Services has published reviews and recommendations on population-based interventions for nine public health topics (Guide to

Community Preventive Services 2003).

The Community Guide includes completed

reviews of interventions on two topics directly

related to improving bone health: increasing

physical activity (Task Force on Community

Preventive Services 2002) and reducing tobacco

use and exposure to environmental tobacco

smoke (Task Force on Community Preventive

Services 2001). These reviews and recommendations provide an initial set of population-based

intervention options for communities and health

care systems, and illustrate the range of settings

and strategies to consider when developing

population-based approaches to promote bone

health.

Population-Based Interventions To Increase

Physical Activity

Regular physical activity is associated with

improved health and reduced risk of overall

mortality (Lee et al. 1995, Paffenbarger et al.

1993). Physical activity and fitness have many

bone health benefits, including reduced risk of

osteoporosis and fractures (Bonaiuti et al. 2002,

Karlsson 2004) and fall-related injuries (Carter

et al. 2001, Robertson et al. 2002).

The Task Force on Community Preventive

Services selected and reviewed 11 interventions

related to physical activity. Recommendations

were based primarily on the demonstration of

changes in physical activity behaviors or aerobic capacity. As shown in Table 12-1, the task

force found sufficient or strong evidence on the

effectiveness of six interventions (Task Force on

Community Preventive Services 2002), including community-wide, multi-component information campaigns; point-of-decision prompts to

encourage stair use; school-based physical education; social support interventions in the community; health-behavior change programs
314 Chapter 12

A Report of the Surgeon General
Bone Health and Osteoporosis

Population-Based Approaches 315

adapted for individual needs; and environmentally

enhanced access to places for physical activity.

Evidence was insufficient to assess the effectiveness of five interventions selected for review, meaning that there is not enough information to conclude whether these strategies

are effective. These five interventions include

the following: classroom-based health education focused on information provision (due to

inconsistent results); family-based social support (inconsistent results); mass media campaigns when implemented alone (insufficient

number of studies); college-based physical and

health education (insufficient number of studies); and classroom-based health education focused on reducing television viewing and video

game playing (insufficient evidence of an increase in physical activity). For a more detailed

explanation of the evidence for these interventions as well as others that were evaluated, see

http://www.thecommunityguide.org/pa/

pa.pdf. Conclusions from the task force document the strength of the available evidence and

demonstrate that a variety of communitybased interventions lead directly to increases

in physical activity within the targeted population. These increases should ultimately lead

to bone-health benefits, given the direct link

between regular physical activity and stronger, healthier bones. The recommendations

identify and support a range of effective, population-based options for schools, businesses,

health care systems, and communities to increase physical activity. Programs, planners,

and decision-makers can review the information, identify the efforts most appropriate for

their local circumstances (setting, goals, target

population, and resources), and translate the

selected recommendations into specific, actionable interventions.

Population-Based Interventions To Reduce

Tobacco Use

Smoking can be detrimental to bones, and

therefore tobacco prevention and control efforts

can have a positive impact on bone health. More

broadly, these programs provide an excellent

model for understanding how to assess, translate, and apply evidence on the effectiveness of

population-based interventions.

The Community Guide reports strong evidence-based conclusions on the effectiveness of

population-based interventions in tobacco control (Task Force on Community Preventive Services 2001). Table 12-2 lists task force recommendations developed from 14 population-based

interventions. These recommendations illustrate

several important points.

First, policies themselves are effective interventions. The concept of policies as interventions

is firmly established in tobacco prevention and

control programs. Laws and/or ordinances related to clean indoor air and excise taxes on tobacco products have proven to be effective

population-based policy interventions. (See the

Michigan case study later in this chapter for an

example of the use of State polices to improve

bone health.) Second, health care systems can

be important settings for population-based interventions. Policies and programs implemented

by health care systems, or by large employers

or other entities that purchase health care for

large groups of people, can target both patients

and providers. Evidence of the effectiveness of

clinical interventions that were documented in

previous reviews (U.S. Preventive Services Task

Force 1996, Fiore et al. 2000) enabled the Task

Force on Community Preventive Services to

focus on interventions designed to motivate patients and/or providers to make greater use of

such interventions. (See Chapter 11 for addi-
316 Chapter 12

A Report of the Surgeon General
Bone Health and Osteoporosis

Population-Based Approaches 317

tional discussion of the role of health systems in

population health.)

Third, interventions are often implemented

and evaluated in combination. Four of the 14

interventions reviewed in Table 12-2 consist of

multiple components. In many cases, the independent effects of the various components of the

interventions cannot be determined based on the

available body of evidence. The Michigan example described later in this chapter illustrates

the use of a combination of interventions to improve bone health.

The concept of a comprehensive populationbased approach to address a public health problem has become essential to tobacco prevention

and control programs (Centers for Disease Control and Prevention 1999). Comprehensive multicomponent efforts acknowledge that reducing

tobacco use requires a population-based change

in attitudes as well as behaviors (National Cancer Institute 2000). Bone health advocates can

benefit from examining the multifaceted programs used in community tobacco interventions.

Communication Tools for

Population-Based Interventions

Communication is an essential tool in many

population-based health interventions. Its role

and effectiveness are described extensively in the

Institute of Medicine report, “The Future of the

Public’s Health in the 21st Century” (Committee on Assuring the Health of the Public in the

21st Century 2003). Public sector (social marketing, mass media campaigns) and private sector

(direct-to-consumer advertising) approaches can

be used to communicate with target populations

in order to improve health.

Social Marketing

Social marketing, which has been used since

the 1970s, is based on the principles of commercial marketing. It involves the planning and

implementation of an orchestrated marketing

effort, usually involving multiple organizations

and institutions, with the ultimate goal of generating behavior change. It is commonly described

as being based on the “four Ps”: product, price,

place, and promotion. “Product” is the targeted

behavior, which may be the initiation of a new

behavior or the cessation of a current behavior.

“Price” is the individual’s perception of what

may be lost or given up for the sake of behavior

change. “Place” is where individuals have access

to the products or services or where they engage in the desired behaviors. “Promotion” is

communicating to target audiences about behavior change through a variety of ways, including

media relations, personal selling, and special

events (McKee 1992, Siegel and Donor 1998).

The development of effective social marketing campaigns requires extensive formative research, including qualitative and quantitative

methods that are used throughout the process

to understand the specific needs, desires, beliefs,

and attitudes of the target audience (Andreason

1995). (For an example of formative research for

social marketing purposes, see the description

of the National Bone Health Campaign in this

chapter.) Currently, the Robert Wood Johnson

Foundation is sponsoring a Social Marketing

Collaborative in its Turning Point program to

develop social marketing resource guides for U.S.

agencies and organizations (Social Marketing

Collaborative 2002).

Direct-to-Consumer Advertising

Direct-to-consumer advertising (DTCA) has

become a common way for pharmaceutical companies to market new products. In 1997, the Food

and Drug Administration released guidelines on

consumer-oriented drug marketing. Since then,

DTCA has become a multibillion-dollar aspect
318 Chapter 12

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In addition, the vast memberships and

State chapters of its Coordinating Committee partners carried out many of their own

initiatives via their far-reaching collective

channels.

The impact has been significant. In 1983,

only 35 percent of Americans said they had

had their cholesterol checked. By 1995, that

figure jumped to 75 percent. In other words,

some 70–80 million Americans who were unaware of their blood cholesterol levels in 1983

took action to find out where they stood and

what they needed to do to protect their hearts.

Physicians became more aware of cholesterol

detection and treatment as well, as core

NCEP clinical guidelines are now firmly established in everyday practice. The average

total cholesterol level of American adults has

fallen significantly, and coronary heart disease mortality has continued to decline. These

indicators show the considerable impact that

cholesterol education has had (NCEP 2003).

Ten Lessons Learned From the National

 Cholesterol Education Program

The lessons learned from the NCEP are

valuable for any national campaign being

developed to improve health:

1. Establish a solid scientific base that can

bring credibility and persuasion to

effort.

With input from its partners, the program

developed television public service announcements, print ads and other media

materials, public health information publications, and patient guides. It also produced

physician kits and clinical guidelines.

2. Create a multidisciplinary and far-reaching partnership that includes interested

organizations with State and local chapters.

3. Make sure partners and target audiences have input at the concept stage,

not just the dissemination stage.

Learning From Other Campaigns: The

National Cholesterol Education Program

Successful national educational campaigns for other diseases can serve as useful

models for what might be achievable through

coordinated efforts to improve bone health.

One such model is the National Cholesterol

Education Program (NCEP), launched in

the fall of 1985 and modeled after another

successful program—the National High

Blood Pressure Education Program. NCEP

was administered and coordinated by the

NIH National Heart, Lung, and Blood Institute (NCEP 2003). More than 35 national

medical, public health, and voluntary health

organizations and Federal agencies served as

active partners and members of the

program’s coordinating committee. The

multidisciplinary partnership included researchers, clinicians, public health officials,

and policy advocates at the national, State,

and local levels. NCEP had a number of objectives. First, it attempted to keep health

providers up to date on science-based clinical guidance. Second, it promoted awareness

in the general population of the consequences of uncontrolled high blood cholesterol and urged individuals to “know your

number” and what it means to you. The ultimate goal was to lower elevated cholesterol

levels as a means of reducing heart attacks

and heart attack deaths.

The Basics of Bone in Health and Disease
Bone Health and Osteoporosis

Population-Based Approaches 319

Ten Lessons Learned From the National

Cholesterol Education Program (cont.)

4. Pursue collaboration with outside interests, such as industry, as appropriate opportunities arise.

5. Develop a comprehensive program

plan that includes roles for all partners.

6. Reach a consensus on consistent key

messages that can be repeated and reaffirmed by many partners through

many channels and outlets.

7. To reach desired goals and objectives,

make sure the effort has the type of

long-term commitment in terms of

leadership and funding from sponsoring organizations that is necessary to

make it sustainable over the long term.

8. Both population and clinical approaches will be needed in order to

change behavior at the personal, family, and community level, and choices

between these two types of interventions should not be made.

9. Establish or acquire baseline data pertinent to established goals and objectives so progress, or lack thereof, can

be measured and program direction

can be altered as needed.

10. Build in a reassessment and renewal process to keep the effort vital and current.

1. The first symptom often can be a

serious event (a fracture in one

case, a heart attack in the other).

2. Osteoporosis is now and cholesterol was then underdetected,

underdiagnosed, undertreated,

and underappreciated.

3. Osteoporosis does and cholesterol

did require a two-prong approach,

e.g., lifestyle change and early detection and control.

4. The ability to assess, educate, and

monitor each respective condition

by knowing one’s number, i.e.

blood cholesterol level on one

hand, T-score on the other.

5. There did exist with cholesterol

and does exist with osteoporosis

a tremendous need to increase

awareness that these conditions

are common with potentially serious consequences that can be

prevented and/or treated.

Similarities Between Osteoporosis

 and Cholesterol

There are similarities in expression of

the two risk factors, osteoporosis and elevated cholesterol, that suggest that a

program comparable to the NCEP has

the potential to be effective in improving

bone health. These include:

of pharmaceutical marketing (Rosenthal et al.

2002). Theorists argue for and against its use,

with debate usually centered on whether DTCA

informs and empowers consumers or encourages

them to seek inappropriate and expensive care.

Several surveys have demonstrated that consumers are aware of DTCA and take action as a result of it (such as asking doctors about products)

(Lyles 2002). Evidence of direct health benefits from DTCA, however, is limited

(Weissman et al. 2003).

The mass media, including television programming, movies, radio, newspapers, and

magazines, represents another communication
320 Chapter 12

A Report of the Surgeon General

tool for the promotion of bone health. Health

campaigns for other causes, including those

aimed at reducing cholesterol levels, smoking

rates, and the incidence of sexually transmitted diseases, have been successful in having their

messages and/or desired behaviors portrayed

in the mass media. Specialty and niche media

can be used to reach racial and ethnic groups.

One common approach for television and cinema is to suggest story lines and/or character

portrayals that reinforce the intended message

to the target audience. Similar efforts could be

made in bone health. An example of a promising effort in social marketing is the VERBTM.

It’s what you do. campaign, a national,

multicultural, social marketing campaign initiated in 2002 by the Centers for Disease Control and Prevention (CDC) to encourage young

people between 9 and 13 years old to be physically active every day. Telephone surveys of

youth and their parents conducted before the

launch of the campaign and a year later indicate a 34 percent increase in the number of times

each week that 9- and 10-year-olds engage in

physical activity during their free time. There

are 8.6 million children in the United States in

this age group (Potter et al. 2004).

Population-Based Interventions:

Conclusions

Despite challenges in mobilizing populations

to improve health by addressing risk behaviors,

a number of population-based interventions have

been found to be effective. Evidence reviews

provide a concise summary of the evidence on

effectiveness and help decision-makers and program planners to weigh intervention options for

local applications. Evidence reviews do not replace the important steps of conducting local

assessments and enlisting community participation. Interventions should be well matched to

local conditions (settings, needs, goals, target

populations, and resources) and carefully implemented and evaluated.

As the evidence on different approaches continues to grow, several recurring themes and strategies emerge. While innovative application of new

theories, strategies, and interventions will remain

important to improving bone health, evidencebased reviews of what is already being done can

play a significant role in supporting populationbased program planning and decision-making.

Program Examples

Many of the following examples of population-based interventions in the area of bone

health represent evidence-based interventions

that draw upon research findings that have been

presented in previous chapters of this report. In

other cases, the examples illustrate innovative

approaches where the evidence base is not yet

fully developed. As a result, formal evaluation

results are not available for some programs. In

these cases, other evidence of the program’s impact have been highlighted, including data related to “process” outcomes, such as number of

Web site “hits,” or proxy measures for bone

health, such as the percentage of program participants who increased their calcium intake.

Regardless of the evidence base for the programs, they were chosen for inclusion in this

report because they each illustrate one or more

key concepts in population-based interventions,

which are summarized at the end of the chapter. However, this chapter is not intended to

provide a comprehensive review of all successful population-based bone health interventions.

The included examples are illustrative of the

vast array of innovative programs that exist

throughout the country.
Bone Health and Osteoporosis

Population-Based Approaches 321

Primary Prevention Messages for Young

Girls:

The National Bone Health Campaign

The National Bone Health Campaign illustrates both the need and the ability to use population-based approaches early in life in an effort

to reduce the chance of developing bone disease

later. It also illustrates how a specific audience

(in this case, girls age 9–12) can be the target of a

prevention program.

Background

The National Bone Health Campaign

(NBHC) is a multiyear national campaign created in 1998 by congressional mandate. Managed in partnership by the Centers for Disease

Control and Prevention CDC, the Office on

Women’s Health (OWH) of U.S. Department

of Health and Human Services, and the National

Osteoporosis Foundation, this campaign uses a

social marketing approach to educate preadolescent girls, their parents, and other adult

influencers about behaviors that will help to prevent low bone density, thereby reducing the risk

of osteoporosis later in life.

Before the campaign’s materials were developed, formative research was conducted to get a

better understanding of how information about

calcium consumption and physical activity

would be most effectively conveyed to this age

group, a subject that was poorly understood.

Racial- and ethnic-specific focus groups were the

primary method for this research, along with a

baseline survey of parents and daughters. The

results indicated that bone health was neither

well understood by, nor considered to be important to, girls and their parents.

The research also found that girls and their

parents wanted messages that offer information,

motivate them to act, provide action steps, and

address the environments in which desired behaviors occur (USDHHS 2001). Girls also want

messages provided in a context of fun, power,

and social interaction.

The Intervention

The overall goal of the campaign is to educate and encourage girls to establish lifelong

healthy habits—particularly increased calcium

consumption and physical activity—that build

and maintain strong bones. In the short term,

the campaign is striving to increase girls’ and

parents’ knowledge about how calcium intake

and physical activity relate to bone health. Over

the long term, the focus will shift to building on

this increased knowledge in order to change behaviors.

To reach these goals, the campaign developed six main messages: 1) bone health is an

important part of fitness, strength, and power;

2) calcium-rich foods and regular physical activity build strong bones; 3) calcium can be obtained

from a variety of tasty and easily accessible foods;

4) there are a variety of easy and fun ways to get

physical activity every day; 5) being more physically active is fun, and provides energy, fitness,

health, and social interaction; 6) good nutrition

helps you stay fit and active. All campaign materials are designed to convey easy ways to consume 1,300 mg of calcium and to participate in

weight-bearing physical activity every day. To

appeal to the girls’ desire for inner strength, all

six messages are held together by the campaign

tag line: Powerful Bones. Powerful Girls.TM

The cornerstone of the campaign is a Web

site that helps girls understand how calcium and

weight-bearing physical activity can be a fun,

important part of everyday life. The site’s

spokes-character, Carla (Figure 12-1), emphasizes

the basics of a bone-healthy lifestyle. The site

also includes interactive games and quizzes, reci-
322 Chapter 12

A Report of the Surgeon General

pes for tasty foods with calcium, and tips on ways

to get weight-bearing physical activity (Centers

for Disease Control and Prevention 2003).

The campaign also uses other channels to

reach young girls, including paid advertisements

in children and youth magazines (such as Nickelodeon, Sports Illustrated Kids, and Girls Life),

radio advertisements (434 radio ads ran between

July and December 2001), a radio media tour

(which included 200 interviews), and print materials such as calendars with stickers, presentations, and fact sheets.

For parents, four main messages are consistently used in the campaign: 1) as part of your

daughter’s healthy development and future, it

is vital to build strong bones early in her life; 2)

foods with calcium are an essential part of a

healthy, balanced diet; 3) your actions do make

a difference, participating in your daughter’s

activities or sports programs actively or as an

observer is a way to spend time with her and be

part of her healthy lifestyle; and 4) creating an

environment to facilitate your daughter’s calcium consumption and physical activity is an

easy way to ensure her health in the future. The

four messages are distributed through tip sheets,
Bone Health and Osteoporosis

Population-Based Approaches 323

shopping lists, and checklists that include specific action steps for parents. Paid print advertisements were placed in women’s magazines

such as Essence, Family Circle, and Ladies’

Home Journal. A Web site (http://www.cdc.gov/

powerfulbones/parents) has been launched to

reinforce these key messages.

Partners

Several organizations that work directly with

girls have tailored the NBHC materials to their

needs. The Girl Scouts developed troop activity cards, a videotape, and a bone health patch,

and Girls Inc. created activity guides and facilitator manuals. The National Association of

School Nurses developed materials for use in

schools. In addition, the NBHC partners with

several local, State, and Federal agencies and

nonprofit organizations.

Results, Evaluation, and Challenges

The focus of evaluation of the campaign to

date has been on tracking “process measures”

that gauge the extent to which people are being

exposed to new materials and messages. As of

spring 2004, the campaign had more than 122

million print media mentions and more than 3.1

million Web site visits. The plan going forward

is to expand the target age of girls to 18 in order

to reinforce messages initially introduced to

younger girls.

Culture and Health:

Living Healthy: The Asian American

Osteoporosis Education Initiative of the

National Asian Women’s Health

Organization

This initiative illustrates the compelling need

to understand each community’s resources, leadership, and culture before designing and implementing a community-based health intervention.

Background

Most post-menopausal Asian women are at

high risk for developing osteoporosis due to low

calcium diets, low body weight, and small bones.

Asian Americans often suffer from lactose intolerance, making it difficult to digest calcium-rich

dairy foods. There are more than 30 distinct

Asian-American ethnic groups with varying levels of English proficiency, cultural integration,

and economic status. Many Asian Americans

face economic and social hardships and require

health intervention programs tailored to their linguistic and cultural needs. The lack of such programs, as well as language barriers, low literacy,

financial constraints, and other concerns, leave

Asian-American women with little incentive to

seek health information and services (National

Asian Women’s Health Organization 1997).

The Intervention

The National Asian Women’s Health Organization (NAWHO) has attempted to address

these widespread, complex barriers to osteoporosis information through its community-driven

education project Living Healthy: The Asian

American Osteoporosis Education Initiative.

NAWHO created a guide, “Living Healthy: The

Asian American Women’s Osteoporosis Education Implementation Kit,” which offers a model

program for health and social service agencies to

plan, implement, and evaluate educational seminars on osteoporosis for Asian-American

women.

NAWHO’s program aims to raise awareness

of osteoporosis among pre- and post-menopausal

Asian-American women and to empower them

to engage in positive lifestyle behaviors that promote bone health. The “Living Healthy” kit offers a mix of topics, exercises, cultural perspectives, and examples to enable organizations to

tailor workshop agendas to the needs of ethni-
324 Chapter 12

A Report of the Surgeon General

cally diverse Asian groups. The kit includes three

major sections:

• Section One: Osteoporosis Messages.

This section provides key messages in

osteoporosis prevention for Asian-American women, combining scientific fact (using materials developed by the National

Institutes of Health (NIH) Osteoporosis

and Related Bone Diseases~ National

Resource Center) with culturally specific

content.

• Section Two: Conveying the Message.

This section includes step-by-step instructions for planning and implementing the education seminar, such as partnership-building, agenda development,

program promotion, participant recruitment, logistics preparation, use of Asian

language interpreters, and evaluation and

follow-up.

• Section Three: Resources. This section

lists several resources, including contact

information for obtaining more information on osteoporosis; a review of health

and cultural beliefs shared by many

Asian cultures as well as barriers to outreach, education, and screening; and

guidelines for working with language interpreters.

Partners

NAWHO worked closely with the NIH

Osteoporosis and Related Bone Diseases ~ National Resource Center in developing this campaign. NAWHO also collaborated with three

community-based organizations—the Asian

American Senior Citizens Service Center, the

Lao Family Community of Stockton, and the

Southeast Asian Community Center—to test the

“Living Healthy” kit with Asian-American

women in three California sites. Criteria for selecting community-based partners included

knowledge of Asian-American health needs, access to post-menopausal Asian-American

women, and adequate infrastructure and programmatic capacity in the local community.

Results, Evaluation, and Challenges

NAWHO has evaluated the impact of the

forums and workshops through surveys and interviews of the participants. This evaluation suggests that use of the “Living Healthy” kit has

had positive results. For example, the community forums have increased overall knowledge

about osteoporosis (i.e., understanding what the

disease is), enhanced specific knowledge about

the disease (such as screening and exercise as

prevention strategies), and strengthened behavioral intentions (such as talking to the doctor and

increasing calcium intake).

The evaluation also highlighted specific challenges and barriers for Asian-American women,

many of which are being addressed by the “Living Healthy” program:

• Illiteracy among target population. Many

participants had limited reading and

writing capabilities in their native language, which created challenges in completing evaluation forms. To resolve this

barrier, evaluations were structured as

simple true/false questions that could be

read out loud to the participants. In addition, outreach efforts were extended to

younger women who were educated to

teach their mothers and other elderly relatives about osteoporosis.

• Duration of presentation and audience.

Feedback suggested that the seminars

should be shorter for older participants

(those over age 75). Based on this feedback, an abbreviated 90-minute presentation was developed for this audience,

rather than the normal 4-hour format.
Bone Health and Osteoporosis

Population-Based Approaches 325

• Importance of delivery. Delivery style can

make a difference in terms of how well

information is understood. For example,

many participants failed to understand

the key messages when they were delivered by a well-known doctor who

couched his remarks in difficult-to-grasp

medical terms.

• Lactose intolerance among Asian Americans. To address this issue, the “Living

Healthy” kit provides information on alternative high-calcium foods that AsianAmerican women can include in their

diets, such as tofu, bok choy, sea weed,

and soybeans.

State Policies and Health Promotion:

Michigan Department of Community Health

Osteoporosis Program

This example illustrates the importance of

partnerships across multiple community sectors

in implementing comprehensive health interventions and demonstrates how a State health deprogram is underscored by a 2000 economic assessment that found that Michigan citizens suffered 38,614 osteoporosis-related fractures that

year, with total related medical care costs being

$410 million (Burge et al. 2000).

Intervention

The Michigan Public Health Institute, a nonprofit organization under contract with the

Michigan Department of Community Health,

manages the program’s initiatives, which are focused on reducing the prevalence of osteoporosis and osteoporosis-related fractures through

consumer awareness and education programs,

environmental interventions, and provider support, including education and tools. The initiative also includes assessment and evaluation components. Examples of specific interventions are

described below.

In-School Education: A key recommendation in the Strategic Plan was to incorporate lessons about bone health into the existing Michigan Model for Comprehensive School Health

Education Curriculum. Initiatives were designed

to help youth achieve peak bone mass and lay

the groundwork for continuing healthy behaviors into adulthood. Educational lessons for children in grades two and three were developed in

2000 and pilot-tested in 2001. A parent component was created to complement the information presented to students.

Community Screening: Michigan established

a community screening initiative that combines

a written risk assessment, individualized education, and a bone mineral density (BMD) screening test for those at risk for osteoporosis. Those

individuals identified as having low bone mass

are referred for further medical evaluation, and

follow-up telephone calls are placed to check on

the outcome from these referrals. Over 3,000

partment can promote bone health.

Background

The Michigan Osteoporosis Strategic Plan,

released in 1999, included 18 recommendations

that were part of a detailed plan to reduce the

human and economic burden of osteoporosis;

the plan called for a variety of activities to be

directed at improving the bone health of Michigan residents of all ages (Michigan Department

of Community Health 1999). As a result of the

strategic planning process, the Michigan Legislature dedicated State funds in 1999 to create

the Michigan Osteoporosis Program. The program was launched under the leadership of the

Department of Community Health and the guidance of the Michigan Osteoporosis Strategic Plan

Advisory Committee. The importance of this
326 Chapter 12

A Report of the Surgeon General

individuals completed a risk assessment and received education between 2000 and 2002. Almost two-thirds of them were identified as being at risk for osteoporosis and therefore received

a BMD screening test and follow-up referrals if

indicated.

Fall Prevention Program: Through a 3-year

grant from the CDC, the Injury Prevention Section of the Department of Community Health is

developing, implementing, and evaluating hospital-based geriatric fall prevention clinics at two

Michigan hospitals. Patients who come to the

emergency departments of these hospitals because of a fall or fall injury will be screened using a validated fall risk assessment tool. Eligible

patients will be referred to the clinics, which will

provide a comprehensive set of interventions to

reduce the risk of future falls. These interventions include counseling and education of patients and families; provision of a fall-related home

hazard assessment; a review of medications; lessons in Tai Chi; and referrals to other Medicarereimbursable hospital services, including vision

testing, physical therapy (for gait, balance, and

muscle strengthening), treatment of chronic and

acute conditions that can lead to falls, and BMD

testing. A final component of the project is the

development of training courses for providers

(nurses, physicians, physical therapists, and occupational therapists) on how to improve their

skills in identifying and managing adults over

age 65 with fall injuries.

Health Department Education: In October

2001, Michigan began integrating osteoporosis

education and risk-reduction initiatives into existing health department programs, such as the

Breast and Cervical Cancer Control Program,

WIC, and Senior Screening.

Partners

Partnerships became critical in late 2002 when

State funding for the osteoporosis program was

eliminated due to a budget crisis. Fortunately, by

that time the program had alternative sources of

funding that allowed several smaller initiatives to

move forward, including the development of the

fall prevention program and State quality assurance standards for bone densitometry providers.

Another project that was done in partnership with other organizations was the Partnership for Better Bones Project, a two-pronged initiative that includes both professional training

and community education designed to make

health care professionals and the general public

more aware of osteoporosis and its risk factors.

Educators from existing networks are trained and

receive program materials to implement a standardized osteoporosis education program, “Better Bones, Brighter Futures.”

Results, Evaluation, and Challenges

From the beginning, the program included

an extensive evaluation component. Baseline data

were collected to determine where education,

prevention, and treatment efforts should be targeted. In 2000 and 2001, a statewide random

telephone survey of 1,108 adults (age 18 and

older) and 1,101 women (age 50 and older) was

conducted using a survey instrument that included questions on osteoporosis knowledge and

attitudes, risk factors, functional limitations, and

self-reported prevalence. The survey was repeated in 2003 and will be regularly repeated in

the future in an effort to allow evaluation of the

overall program’s efficacy.

The effectiveness of individual components

of the overall initiative is also being evaluated.

For example, the school health program, which
Bone Health and Osteoporosis

Population-Based Approaches 327

included pilot lessons in three school districts,

used intervention and control groups to assess

the educational impact. Each group took a preand post-education test, the results of which suggest that the education had a meaningful impact.

A post-lesson survey with parents indicated students had made behavior changes related to eating foods high in calcium and increasing weightbearing physical activity. The impact of the fall

prevention program will be tested through a controlled group study. Patients who meet the eligibility criteria for referral to the fall prevention

clinic will be randomly assigned to intervention

and control groups. Both groups will be followed

for 1 year, with an assessment of risk factors and

documentation of subsequent falls and fall injuries taking place at 6 months and 12 months after entry into the study. The evaluation will also

assess quality-of-life issues for older adults and

their caregivers, along with changes in health

professionals’ knowledge and behavior regarding fall risk assessment and management.

Perhaps the biggest challenge facing the

Michigan Osteoporosis Program came when the

State government, faced with budgetary problems, decided to eliminate funding for the initiative. Thanks to strong partnerships, the program

has been able to continue even in the absence of

financial support from the State.

Health Messages for Older Adults:

Project Healthy Bones

New Jersey Department of Health and

Senior Services

The program demonstrates opportunities for

health promotion messages and activities among

older citizens, as well as the use of peer leaders

as advocates for bone health.

Background

The New Jersey Department of Health and

Senior Services (NJDHSS) began osteoporosis

prevention activities in 1991 under a grant from

the CDC. These efforts continue to this day, as

the State still suffers tremendously from the impact of osteoporosis. There were over 36,000

osteoporosis-related fractures in New Jersey in

2000, leading to total medical expenses of $469

million and total nursing home costs of $137

million (Burge and Worley 2001).

NJDHSS’s initial efforts focused on educational programs throughout the State, but it

quickly became apparent that education alone

was not enough. Based on scientific research

showing that osteoporosis and osteoporosis-related disability can be prevented or slowed by

balance and strength training exercises, diet,

appropriate medications, and a safe environment,

Project Healthy Bones was developed This

project was directed toward older women and

men who are at risk for or have osteoporosis.

Intervention

The objectives of ProjectHealthy Bones are to:

• Train peer advocates as leaders for

Project Healthy Bones;

• Educate older adults on the importance

of exercise, nutrition, safety, drug

therapy, and lifestyle factors relating to

osteoporosis; and

• Improve strength, balance, and flexibility in older adults, using weight-training

exercises (Figure 12-2).

Project Healthy Bones includes both education and exercise components. The 24-week curriculum provides information on exercise, nutrition, safety, drug therapy, and lifestyle factors related to osteoporosis. Classes are interactive, with
328 Chapter 12

A Report of the Surgeon General

peer leaders facilitating information exchange.

The peer leaders are older adults who guide

and support group participants as they exercise

and learn. Peer leaders understand the beliefs,

limitations, and concerns of the participants and

work in pairs to provide both class instruction

and individualized assistance. Project Healthy

Bones includes exercises that target the body’s

larger muscle groups to improve strength, balance, and flexibility. Participants receive weight

cuffs with 1-pound pellets that allow for individualized progression.

More than 1,700 older New Jerseyans currently participate in the program as either a peer

leader or class member in 125 sites throughout

the State. Waiting lists exist in most counties, as

classes often elect to continue to meet after completing the 24-week cycle.

Partners

Project Healthy Bones is a partnership of

NJDHSS, the New Jersey Association of Retired and Senior Volunteer Program Directors,

Inc. (RSVP), and the Saint Barnabas Health

Care System. NJDHSS administers Project

Healthy Bones, acting as liaison among the three

partners, developing policies for program operation and managing program funds. NJDHSS

also develops and distributes peer leader and

participant manuals and other educational materials.

RSVP’s primary focus is local project administration, including recruiting volunteer peer

leaders, linking at-risk older adults with classes

in or near their communities, securing sponsors

and sites for classes, and ensuring that classes

operate smoothly on a daily basis.

The third partner in Project Healthy Bones

includes two departments of the Saint Barnabas

Health Care System. The Saint Barnabas Osteoporosis and Metabolic Bone Disease Center

(OMBDC) functions as the program’s technical

advisor, maintaining and updating educational

materials. OMBDC staff educate peer leaders

about osteoporosis and Project Healthy Bones

curriculum. The Saint Barnabas Center for

Health and Wellness provides exercise training

to peer leaders. Trainers are certified exercise

Strength Training for Older Adults

New Jersey’s Project Healthy Bones was

developed based on research at Tufts University investigating the use of strength training exercises to improve bone density in older

adults. This and other research resulted in

several educational programs for enhancing

strength training. One example is “Growing

Stronger: Strength Training for Older

Adults” (Seguin et al. 2002). This self-instructional workbook on strength training

includes exercise instructions, a progression

logbook, safety advice, and information on

additional resources.

Another example is the “Strong Women

Tool Kit: A National Fitness Program for

Women” (Nelson and Seguin 2002). This

tool kit for program leaders of strength training programs for women includes recommendations on physical space and equipment for

classes, screening of participants, tracking

participants’ progress, and use of leadership

techniques to encourage class members. Like

the “Growing Stronger” book, the material

is evidence-based.

Additional information regarding

strength training is available on the CDC

Web site. “Growing Stronger: Strength

Training for Older Adults” can be found at

http://www.cdc.gov/nccdphp/dnpa/physical/

growing_stronger.
Bone Health and Osteoporosis

Population-Based Approaches 329

physiologists who possess extensive experience

with older adults.

Results, Evaluation, and Challenges

The impact of Project Healthy Bones is being evaluated through exercise tracking forms.

Preliminary data suggest that the programs are

making a difference. In 2001, a program review

based on 217 forms revealed that 90 percent of

the participants who completed at least 12 weeks

of the program increased the amount of weight

lifted, and 68 percent increased their calcium

intake (NJDHSS 2000). Looking ahead, a more

rigorous evaluation that examines the program’s

impact on strength, balance, and individual behavior change is warranted. Such information

can be used as feedback to guide program revision and development.

Building Community Capacity and Group

Support in Bone Health:

North Carolina

North Carolina was one of the first States to

develop a program oriented at osteoporosis.

While the State is involved in a variety of initiatives, two are profiled below. The first is a “trainthe-trainer” model to build community capacity to address osteoporosis, and the second is a

support-group program that helps individuals

cope with the effects of osteoporosis.
330 Chapter 12

A Report of the Surgeon General

Background

Low bone density and osteoporosis pose a

threat to at least 1,300,000 North Carolinians age

50 and over. Each year more than 13,000 residents are hospitalized for osteoporosis-related

fractures, resulting in over $145 million in direct

medical costs from hip fractures alone. In addition, there are costs associated with the non-hospital treatment of fractures (wrist and spine being the most prevalent) and other health problems caused by osteoporosis. By 2020, it is projected that the number of North Carolinians with

osteoporosis will exceed 400,000, while an additional million individuals will have low bone density (Borisov et al. 2002).

The Osteoporosis Coalition of North Carolina was established in 1996 to promote education and support for prevention, diagnosis, and

treatment of osteoporosis; to reduce its prevalence, severity, and economic consequences; and

to advocate for public and private support to

achieve these goals. In 1997, the State legislature created the Osteoporosis Task Force to assess surveillance, create awareness, and develop

a State plan.

Interventions and Partners

Train-the-Trainer Program: The Bone

Health/Body Health (BH/BH) Initiative seeks to

teach community leaders how to train others

about bone health. More specifically, goals for

the program include:

• Identify and train community leaders, both

volunteer and professional, in techniques for

communicating information about osteoporosis prevention, diagnosis, and treatment;

• Train community leaders in how to motivate and teach others the same skills; and

• Provide all training materials and educational

support necessary for the community leaders to conduct their efforts effectively.

The BH/BH project targeted health professionals, administrators, and other community

leaders in seven counties. The curriculum emphasized workshops on osteoporosis and health

communication, with participants completing

assignments between workshops. In addition,

participants received a training manual, “Carrying Bone Health/Body Health to Your Community” (NCDPH 2001), “Making Health Communication Programs Work” (NCI 1989), a

National Cancer Institute document, and a collection of excerpts drawn from the 2000 edition

of TST Associates’ “Media Relations and Promotion Training Handbook” (TST 2002).

The BH/BH program was conducted as a

partnership with the North Carolina Division

of Public Health, Osteoporosis Program, and the

Regional Area Agency on Aging, Health Promotion and Disease Prevention Program. In addition, multiple community groups and individuals provided training, educational resources, and

local venues for educating the communities.

Support Group Program: Public health staff

developed a support group curriculum and a support group leader’s handbook in 1997 (Condelli

2000). This effort led to the establishment of support groups in a wide variety of geographical settings by a diverse group of leaders.

During 2000–2001, there were 17 active osteoporosis support groups throughout the State,

with groups holding meetings every 2 or 3 months.

Groups are most active in urban areas, as limited

State funding has largely prevented the establishment of groups in more rural areas. Topics for the

meetings have included fall prevention, stress management, long-term care, diet, emergency preparedness, exercise, and self-esteem. Group leaders receive

up-to-date information through the NOF’s quarterly publication, “The Osteoporosis Report” (NOF

2002). In each session, participants are encouraged

to share their thoughts and experiences in coping
Bone Health and Osteoporosis

Population-Based Approaches 331

with the effects of osteoporosis. In addition, pharmacists, exercise physiologists, physicians, nurses,

nutritionists, wellness coordinators, physical therapists, and others give informational presentations

and answer questions from participants.

Results, Evaluation, and Challenges

While no formal evaluation of the programs

has been conducted, process measures have been

used to track the number of participants in group

presentations and free bone density screenings,

the number of exhibits displayed at churches,

hospitals, and senior centers, and the kinds of

media used for advertising programs. In addition, the support group participants have written about their own perceptions of osteoporosis.

These vignettes will be compiled in a storybook

and used as a resource for future programs. Future plans also include establishing support

groups in new counties, providing technical assistance to established groups, and developing an

organizational structure that allows groups to receive updated information on osteoporosis and

to communicate with “sister” support groups.

Evaluating Community Health Programs:

Missouri Take Our Trail Physical Activity

Program

This example illustrates the importance of

developing a well-planned evaluation of the effectiveness of an intervention program and of

establishing linkages with local community

groups, both of which are critical to the success

of community bone health programs.

Background

In 1997, Missouri State survey data showed

that 65 percent of the State’s population did not

engage in adequate levels of physical activity to

meet public health recommendations. To address

this health problem, the State health department

helped to fund the construction of walking trails

in two communities through the Department of

Transportation (DOT) (Brownson et al. 1996).

A year later, in response to requests from other

communities to build trails, the State asked for

evidence to determine if further investment

would be worthwhile.

Although there had not been a formal evaluation of trail use, anecdotal reports indicated that

the trails were underutilized because of safety

concerns and lack of amenities such as playground equipment and clean restrooms. The

State provided funds to the health department

to conduct the Take Our Trail campaign, which

was designed to enhance trail activities and to

conduct an awareness campaign in one of the

communities with a year-old trail. If community

members were not more physically active after

this awareness effort, the State indicated that it

would probably not fund additional trails.

Intervention

The Take Our Trail campaign was conducted

for 3 months and led by the health department

and a community health coalition. A variety of

initiatives were aimed at increasing awareness of

the trail and of the value of physical activity. The

campaign kicked off with a 3-mile Family Fun

Walk. For the duration of the campaign, signs

were placed in busy areas throughout the community to promote the trail. A brochure was

developed and provided to all programs in the

local health department for distribution to clients, clinics, physician offices, church leaders,

and the coalition. The brochure included information on walking and physical activity, safety,

the trail, and contact names for walking clubs.

The local television station created a public

service announcement to promote the trail and

the importance of regular physical activity. The
332 Chapter 12

A Report of the Surgeon General

public transportation system placed signs inside

buses, encouraging riders to “Take Our Trail.”

The community coalition helped develop walking clubs in work sites, churches, and social organizations. To address concerns about safety

issues, local law enforcement officials patrolled

the trail, and local business, city government, and

churches raised money to add lights, along with

other amenities such as benches, mile markers,

painted lanes, and a water fountain.

Partners

The Take Our Trail campaign and its evaluation included multiple stakeholders. Participating government agencies included the local public health department, the city government, the

Department of Transportation, Department of

Parks and Recreation, and the Department of

Education. Several local businesses and nonprofit organizations supported the campaign

through donated goods, services, and publicity.

Many volunteers also helped to build and support use of the trail, including walking, jogging,

and cycling clubs; nearby employers; and community members who donated land, money, or

other resources.

Results, Evaluation, and Challenges

Since the outcomes of the awareness campaign would directly influence future State budget policy, an extensive campaign evaluation was

planned, including process measures that could

help to replicate the campaign in the future,

along with short- and long-term “outcomes”

measures to gauge whether behaviors or intended

behaviors changed.

Four primary evaluation questions were identified: 1) What activities were actually conducted

as part of the Take Our Trail campaign? 2) Did

trail use increase as a result of the Take Our Trail

campaign? 3) Who used the trail, both before

and after the campaign? 4) To what extent do

trails increase physical activity levels of community members?

Since there were two communities with trails

in place, the evaluation was designed as a quasiexperimental trial. Conducting the Take Our

Trail campaign in one community but not the

other allowed an assessment of whether trail use

appeared to increase due to the campaign. A third

geographically distinct community with similar

sociodemographics and no walking trail or campaign was used as an additional comparison

group. Data collection included electronic

counter monitoring of trail usage; interviews with

trail users and other key stakeholders in the community; event logs to capture activities at the trail

such as formation of walking clubs, trail enhancements, and related events; media review to identify campaign announcements and news coverage; and community surveys immediately before and a year after the campaign.

The 3-month walking trail counter results indicated increased trail usage in the Take Our Trail

community. The Take Our Trail community had

a 35 percent increase in trail use between a month

before and a month after the campaign, compared

with a 10 percent increase experienced by the

community without the campaign. Interviews

revealed that individuals in the campaign community felt safer while walking than did those in

the community with a trail and no campaign.

More than 60 percent of trail users in both

communities indicated an increase in walking

since the building of the trail. All types of people

used the trail. Those who walked were more

likely to be women, older adults, athletes recovering from injuries, and individuals with medical conditions that require a low-impact activity. Many of these groups are people at high risk

for osteoporosis. The 1-year follow-up phone

survey indicated a 5 percent increase in the number of individuals meeting the physical activity
Bone Health and Osteoporosis

Population-Based Approaches 333

recommendations in the Take Our Trail community, compared to a 2 percent increase in the

other community with a trail and a 1 percent

decrease in the community without a trail. While

this level of increase may seem small, it could

result in meaningful changes if similar increases

were to occur for the next few years.

There have been some challenges for the

program. Some organizations and community

leaders felt “left out of the loop” despite efforts

to achieve broad community support. In addition, evaluation efforts also proved to be challenging, particularly labor-intensive surveying

of busy community leaders. In the future, the

use of focus groups might be a more efficient

way to collect similar information.

Despite these challenges, based on this evaluation and other evidence, the Task Force on

Community Preventive Services strongly recommends that communities invest in increasing access to places for physical activity, combined

with informational outreach activities to promote

use of such places. This approach is advocated

as an effective way for communities to increase

physical activity levels among the population at

large (USDHHS 2002) (see Table 12-1).

Using a Multimedia Approach in a National

Campaign:

Milk Matters Campaign

The National Institute of Child Health and

Human Development

This example illustrates the use of multiple

communication channels to communicate health

messages in a national campaign.

Background

Based on 1) strong scientific evidence showing that adequate calcium intake during childhood is necessary for healthy bones throughout

a lifetime, 2) consensus among scientific and

public health communities on optimal calcium

intake, and 3) data indicating that young people

were not consuming sufficient amounts of calcium, the National Institute of Child Health and

Human Development (NICHD) began the Milk

Matters public health campaign in 1997. The

campaign was directed toward all segments of

the population and particularly young people.

Intervention

The long-range goal of the Milk Matters campaign is to encourage consumption of recommended daily amounts of calcium, with an emphasis on the importance of lowfat milk and dairy

products as good sources of calcium. The more

immediate goal is to increase awareness about

the importance of calcium in the diets of young

children and adolescents, which is seen as a critical step in the process of behavior change.

The campaign used multiple approaches to

increase public awareness. Examples include:

• “A Crash Course on Calcium” is an inschool program, which included a video,

featuring Olympic Gold medalists Amy

Van Dyken and Kristi Yamaguchi, along

with a teacher’s guide, poster, and brochure. The course was designed to teach

teens about bone health, calcium, and

how getting enough calcium can help

prevent injury now and osteoporosis later

in life.

• “Milk Matters with Buddy Brush” is a

coloring book for children age 4–8 that

teaches the importance of milk for building strong teeth and bones. More than

1.7 million copies were distributed to

dentists and health educators around the

country.

• “Milk Matters for Your Child’s Healthy

Mouth” is a booklet about milk and calcium for parents. Its goal is to let parents

know that calcium is important for a
334 Chapter 12

A Report of the Surgeon General

healthy mouth and to suggest ways to

include calcium-rich foods such as milk

and dairy products in their child’s diet.

The booklet is distributed to parents

through WIC and Head Start programs,

to State dental directors, and at meetings

for health care professionals.

• “Bone Up on Bone Loss!” is a one-page

brochure for health care professionals to

distribute to parents and children that

emphasizes the importance of weightbearing exercise and calcium on building strong bones.

• Two other brochures were developed for

parents, along with a brochure for health

professionals. Available in both English

and Spanish, these three resources have

been distributed to health professionals

at a number of meetings.

The Milk Matters Web site is designed to be

an interactive, comprehensive resource for the

public that can be viewed in English or Spanish

(http://www.nichd.nih.gov/milk). Users can read

Milk Matters publications online or order them

online at no charge. Among other things, the

Web site provides in-depth information about

foods that are good sources of calcium, facts on

lactose intolerance, and scientific abstracts on

calcium research. The latest addition to the Web

site is the “Kids and Teens” page, which includes

puzzles and coloring pages for younger audiences and video games for older children.

Partners

Early in the campaign, NICHD established

partnerships with several organizations that

could help the campaign reach its primary audience. The campaign also collaborated with several of these organizations in developing its educational resources, including the American Academy of Orthopedic Surgeons (AAOS), the Milk

Processor Education Program (MilkPEP), the

National Dairy Council (NDC), and the National Institute of Dental and Craniofacial Research (NIDCR).

Results, Evaluation, and Challenges

Evaluation of the Milk Matters campaign has

focused primarily on collecting information to

improve the program, not on assessing its impact with respect to increasing awareness and

consumption of calcium. Bounce-back card enclosures are included with outgoing orders for

campaign materials. Recipients use these cards

to indicate, for example, which materials they

requested, how they used the materials, how they

learned about the campaign, and if they are a

health professional, parent, or teacher. Analysis

of this information has influenced Milk Matters

in several ways. For example, it pointed out the

need to reach a Spanish-speaking audience and

the need for publications that are easy to read.

This feedback led to the development of several

new publications, including a coloring book for

children.

The Milk Matters campaign posed new marketing challenges to NICHD, and these challenges increased the importance of reaching out

to new partners. As noted, NICHD worked

closely with commercial partners to develop educational materials. At the same time NIHCD also

partnered with other non-commercial organizations, such as professional societies, in order to

avoid the perception that it was endorsing these

commercial entities.

Building on Success

The case examples included in this chapter

provide critical observations that can serve

as building blocks for population-based interventions:

• Since scientific evidence is an important
Bone Health and Osteoporosis

Population-Based Approaches 335

aspect of effective decision-making

(Eisenberg 2002), it is critical that any

population-based campaign be based

upon credible evidence suggesting that

the proposed approach is likely to be effective in meeting its stated goals. In addition, ongoing, rigorous evaluation activities should test whether the interventions succeed in meeting these objectives.

• Basic education about bone health is an

important aspect of population-based interventions. Almost every example cited

in this chapter noted that most people do

not know that calcium and physical activity are critical to protecting bone

health, that fragile bones are not an inevitable aspect of aging, and that the peak

time to build bone mass is during childhood and adolescence. Unlike the situation for some other health risk factors,

such as smoking or driving under the influence of alcohol, most people remain

unaware of the factors that increase or

decrease the risks of poor bone health.

• Including health care providers as partners in population-based interventions

accomplishes several useful functions, as

illustrated in the Elder Floridian Foundation activities and the Michigan Osteoporosis Program. Health providers

themselves need education on bone

health and its assessment, as well as on

population approaches to prevention.

Health providers are recipients of referrals from community screening programs, so they need to understand and

support these programs. Their support

enhances the credibility of these interventions.

• Useful prevention messages on bone

health are available for every age group.

Examples include drinking milk for

preschoolers (Milk Matters campaign),

building powerful bones for preadolescent girls (National Bone Health Campaign), or weight-lifting for older adults

(Project Healthy Bones). Opportunities

abound for tailoring bone health messages to populations at greatest risk.

• Age is not the only variable affecting the

design of population interventions. The

Living Healthy: The Asian American

Women’s Osteoporosis Education Initiative illustrates the need to address cultural and community concerns. It is significant that a national Asian-American

health organization was not satisfied to

take its own knowledge of Asian culture

into the field. Instead, NAWHO

partnered with Asian-American community-based organizations that were even

better informed about local Asian ethnic

groups and cultures.

• A number of evidence-based tools can be

used in building population interventions

for bone health. As noted previously, effective interventions exist for addressing

specific bone health risk factors, such as

tobacco use or lack of physical activity

(the Take Our Trail campaign). Strategies such as social marketing have also

proved to be useful across multiple health

topics and are likely to work in addressing bone health as well.

• Health policy and environmental

changes are important tools in health

promotion, as illustrated in the section on

tobacco prevention and in the Michigan

Osteoporosis Program and the Take Our

Trail program.

• Building partnerships is usually essential
336 Chapter 12

A Report of the Surgeon General

to intervention success. The right partners provide credibility and resources,

access to networks and communities, collaboration with other health campaigns

and programs, advocacy for health policies, staffing for special projects, and

multiple other advantages. For bone

health, building strong partnerships, especially at the community level, may be

as critical as determining the best population interventions.

• Local culture and circumstances are also

part of the decision-making process.

Policy may be influenced by a

community’s choice of interventions, efficiency in using limited resources, and

equity in health status, especially with

respect to disadvantaged populations.

There are additional factors to consider in

developing and implementing population-based

bone health interventions. While some evidencebased interventions exist, many more are needed.

As new interventions are developed, it will be necessary to design evaluation plans, or even a formal

research design, to assess their effectiveness. Since

the ultimate outcome of these interventions may

not occur for a long period of time (e.g., especially

for interventions among younger adults and children), it will be necessary to develop and validate

proxy measures to assess effectiveness. For older

citizens, however, measuring reductions in osteoporotic fragility fractures can allow for the direct assessment of health outcomes.

Another concern relates to financial support,

both for assessing new interventions and for conducting new interventions at a population level.

Several of the examples cited in this chapter

highlight the difficulty of maintaining financial

support for these programs. An economic analysis of the benefits of preventing bone disease may

help make the case for support.

Despite these concerns, there is reason for

hope. Education and public awareness campaigns may be the most easily understood aspect of population-based interventions and thus

may provide the best opportunities for success.

While education is essential, it usually cannot

change the behavior of the population on its

own. Thus, there is also a need for a change in

cultural attitudes and in formal policies to support positive behavior changes. Social marketing can assist in creating these types of changes.

The good news is that because the essential components of prevention in bone health—good

nutrition and physical activity—are also important to many other aspects of health, there is an

opportunity for the development of synergistic

public health programs to address multiple diseases including not only osteoporosis, but also

obesity, diabetes, and heart disease. This multipronged emphasis on cultural changes has

proven effective in restricting smoking in public

settings, increasing use of seat belts in moving

vehicles, and making use of designated drivers

an accepted social practice.

Though much remains to be learned, enough

is known about bone health to move forward

with population-based interventions, so that

bone disease can become a rare event rather than

an everyday occurrence.
Bone Health and Osteoporosis

Population-Based Approaches 337

National Bone Disease Organizations as

Partners in Population-Based Interventions

The national bone disease organizations

can be important partners in populationbased interventions to promote bone health.

As national nonprofit organizations, they play

key roles in educating the public and health

care professionals about the prevention and

treatment of bone diseases and can serve as

resources for many of the public and private

organizations working at the community and

State levels toward improving bone health.

There are four leading national bone disease

organizations, each with distinct missions, but

all working collaboratively to promote bone

health. The American Society for Bone and

Mineral Research promotes excellence in

bone and mineral research and the translation of basic science to clinical practice. The

three other organizations—the National OsFor More Information:

American Society for Bone and Mineral

Research

2025 M Street, NW, Suite 800

Washington, DC 20036-3309

Phone: (202) 367-1161

Fax: (202) 367-2161

Toll-Free: (800) 981-2663

http://www.asbmr.org

National Osteoporosis Foundation

1232 22nd Street, NW

Washington, DC 20037-1292

Phone: (202) 223-2226

http://www.nof.org

Osteogenesis Imperfecta Foundation

804 West Diamond Avenue, Suite 210

Gaithersburg, MD 20878

Phone: (301) 947-0083

Fax: (301) 947-0456

Toll-Free: (800) 981-2663

http://www.oif.org

The Paget Foundation

120 Wall Street, Suite 1602

New York, NY 10005-4001

Phone: (212) 509-5335

Fax: (212) 509-8492

Toll-Free: (800) 23-PAGET

http://www.paget.org

teoporosis Foundation, the Osteogenesis

Imperfecta Foundation, and the Paget Foundation for Paget’s Disease of Bone and Related

Disorders—promote education, awareness,

research, and support for patients and

health care professionals related to their

specific diseases.

In addition to promoting public and professional awareness, the national bone disease

organizations are powerful advocates for research funding and public policy through the

Federal government to improve the prevention and treatment of bone diseases. They coordinate their advocacy efforts through their

participation in the National Coalition for Osteoporosis and Related Bone Diseases, also

known as the Bone Coalition. The Bone

Coalition’s accomplishments in improving

bone health have been in the areas of research,

policy, legislation, funding, and national guidelines and standards.
338 Chapter 12

A Report of the Surgeon General

Key Questions for Future

Research

While many population-based interventions

have been found to be effective in promoting

specific healthy behaviors, such as smoking cessation and promoting physical activity, relatively

little is known about how best to tailor these approaches to promoting bone health. Key, unanswered research questions appear below:

• What population-based bone health interventions are most effective in reducing the long-term incidence and burden

of osteoporosis and other bone diseases?

• What combinations of health messages

are most effective for a bone health camThe National Institutes of Health

Osteoporosis and Related Bone The National Resource Center offers a range

of services to provide links to resources and information on metabolic bone diseases that are

geared to both professionals and the public. An

in-house database contains references to print

materials, organizations, and programs. A cumulative index of metabolic bone diseases literature contains the latest clinical research and

studies, and customized bibliographies can be

developed from this index. New materials have

been developed to fill important gaps in information for specific populations, including those

who do not speak English, low literacy populations, and the visually impaired.

For more information:

National Institutes of Health Osteoporosis

and Related Bone Diseases

~National Resource Center

1232 22nd Street, NW

Washington, DC 20037-1292

Phone: (202) 223-0344

Toll Free: (800) 624-BONE

Fax: (202) 293-2356

TTY: (202) 466-4315

http://www.osteo.org

paign, including those messages that

have been used in other health campaigns?

• Given the long-term nature of population-based bone health interventions,

what are valid “proxy” measures that

can be used to assess them when targeted at younger adults and children?

• What are the most effective means of

educating the public and providers

about the importance of bone health

and about basic preventive measures?

• What are the best methods for encouraging providers to take a more active role in

promoting bone health with their patients?

Diseases~~National Resource Center:

A Resource for Population-Based

Interventions

A valuable resource for population-based

interventions is the National Institutes of

Health Osteoporosis and Related Bone

Diseases~National Resource Center (NIH

ORBD~NRC). The National Resource Center was established in 1994 to provide patients,

health professionals, and the public with an

important link to resources and information on

metabolic bone diseases, including osteoporosis, Paget’s disease of the bone, osteogenesis

imperfecta, and hyperparathyroidism. The

National Resource Center is operated by the

National Osteoporosis Foundation, in collaboration with The Paget Foundation and the Osteogenesis Imperfecta Foundation. It is supported by the National Institute of Arthritis and

Musculoskeletal and Skin Diseases (NIAMS)

of the National Institutes of Health, with contributions from other Federal offices.
Bone Health and Osteoporosis

Population-Based Approaches 339

• What are the most effective populationbased interventions in schools, businesses, health care systems, and communities to increase physical activity to recommended levels throughout the

lifespan?

• What are the most effective populationbased interventions to increase calcium

and vitamin D consumption to recommended levels throughout the lifespan?

• What population-based interventions are

most effective for improving bone health

in racial and ethnic minorities?

• What are the most effective social marketing interventions to promote bone

health?

• What are the best measures of bone

health to be used for surveillance?

• What environmental modifications are

most effective in preventing fractures?
340 Chapter 12

A Report of the Surgeon General

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Six

Bone Health and Osteoporosis

 PART SIX: Challenges and Opportunities: A Vision for the Future 345

Part Six

The final chapter summarizes the key themes of the report, highlights

those opportunities that have been identified for promoting bone health,

and lays out a vision for how these opportunities can be realized so that

bone health can be improved today and far into the future. The key to

success will be for public and private stakeholders—including individual

consumers; advocacy groups; health care professionals; health systems;

academic medical centers; researchers; health plans and insurers; public

health departments; and all levels of government—to join forces in

developing a collaborative national action plan for promoting timely

prevention, assessment, diagnosis, and treatment of bone disease throughout

life. To that end, these stakeholders need to work together to broaden the

public’s and providers’ understanding of the importance of bone health

and its relevance to general health and well-being and to ensure that existing

and future preventive, diagnostic, and treatment measures for bone diseases

and disorders are made available to all Americans.

CHALLENGES AND

OPPORTUNITIES:

A VISION FOR THE FUTURE

Bone Health and Osteoporosis

A Vision for the Future 347

A VISION FOR THE FUTURE:

A FRAMEWORK FOR ACTION TO PROMOTE

BONE HEALTH

Chapter 13

The major messages of this Surgeon

General’s report are as follows: 1) that bone

health is essential to the general health and wellbeing of all Americans; 2) that great progress

has been made in the last several decades in

understanding and promoting bone health and

in preventing, diagnosing, and treating bone

disease; 3) that most individuals have the

opportunity to make lifestyle choices that can

result in stronger, healthier bones throughout

life; and 4) that health care professionals, health

systems, communities, and a variety of other

stakeholders have critical roles to play in

supporting individuals in making appropriate

choices and in promoting timely preventive,

diagnostic, and therapeutic interventions in

those who have or who are at risk of developing

bone disease.

However, these messages are not yet widely

understood. As a result, the bone health status of

Americans remains in jeopardy today, and without

concerted action it will get worse in the future. Far

too few Americans follow the dietary and physical

activity guidelines that can help promote bone (and

overall) health. Health care professionals can do a

better job in paying attention to the bone health of

their patients. Many individuals do not receive

timely diagnostic tests and preventive and

therapeutic measures that can serve to minimize

the impact of bone disease. The net result is

unnecessary pain, suffering, and

complications that can imperil overall health

and well-being, along with financial and social

costs that diminish the quality of life for

individuals and burden both individuals and

society at large.

Improving the bone health and well-being

of Americans requires actions at all levels of

society, including individuals and

neighborhoods, local communities, health

systems, cities, States, and the Nation as a

whole. A coordinated effort can overcome the

barriers—be they educational, social,

systemic, policy-related, or financial—that

have created a population whose bone health

status is at risk.

A Framework for Action

This Surgeon General’s report looks upon

the Nation’s at-risk bone health status as an

opportunity to do better. A national action plan

for bone health can benefit all Americans. This

plan can be aimed at improving overall health

and quality of life by enhancing the underlying

bone health of all individuals, including men,

racial and ethnic minorities, the uninsured, and
348 Chapter 13

A Report of the Surgeon General

the underinsured. Everyone has a role to play

in improving and promoting bone health,

including families and individuals, health care

professionals, hospitals and rehabilitation

centers, academic medical centers, the research

community, health systems, managed care

organizations and insurance companies, public

and private purchasers, private industry,

community-based organizations, State and local

public health departments, voluntary health

organizations, professional associations,

policymakers, and agencies at all levels of

government. These stakeholders can work

together to broaden the public’s and providers’

understanding of the importance of bone health

and its relevance to general health and well-being

and to promote policies and programs to ensure

that existing and future preventive, assessment,

diagnostic, and treatment measures for bone

diseases and disorders are made available on a

timely basis to all Americans. This approach can

serve as the primary vehicle for improving bone

health in this country.

Key Action Steps

 Increase awareness of the impact of

osteoporosis and related bone diseases and how

they can be prevented and treated throughout

the lifespan.

While much valuable work is already underway,

more needs to be done to change the perception

that osteoporosis is an inevitable part of aging.

On the contrary, like heart disease, it needs to

be thought of as a preventable chronic disease,

the roots of which begin at a fairly young age

even though symptoms may not manifest until

later in life. Like heart disease and other chronic

conditions, there needs to be a better

understanding of how much can be done

throughout life to prevent its eventual onset.

 Change the paradigm of preventing and

treating fractures.

Fractures, especially in the elderly, need to be

thought of by both the public and practitioners as a

sentinel event that probably signals the presence of

a frail skeleton and an increased risk of future

fractures. Much as a first heart attack is thought of

as an opportunity to intervene to prevent future heart

attacks, an individual’s first fracture must be seized

upon as an opportunity to intervene to prevent

future fractures. Suffering one fracture is more than

enough for any individual, and therefore treating

fractures should go beyond the orthopedic aspect

of setting and fixing the bone. Rather, fractures

should be considered a red flag for the potential for

bone disease and therefore should be a catalyst for

further assessment, diagnosis, prevention, and

treatment of bone disease. Patients who suffer nonspine fractures represent one of the easiest high-risk

groups to identify and target for intervention, since

most fracture patients seek medical care for their

injury. Health care practitioners and the public at

large must recognize that fractures caused by

weakened bones do not always manifest as broken

arms, broken wrists, or other easy-to-recognize

problems. Rather, they can occur “silently” in the

spine with the collapse of spinal vertebrae. Individual

patients may not recognize them as fractures, but

rather may come into the office complaining of back

pain or discomfort. Today these warning signs are

too often dismissed by individuals and health

professionals. As a result, too many patients end up

suffering multiple fractures before anyone considers

the possibility of bone disease. Individuals, especially

elderly individuals, must recognize that recurrent

back pain could be a signal of a bone-related

problem, and practitioners that attend to individuals

with back pain must consider the possibility of a

spine compression fracture and hence the need for

further assessment of the potential for metabolic bone

disease.
Bone Health and Osteoporosis

A Vision for the Future 349

 Continue to build the science base on the

prevention and treatment of bone diseases.

Further work is needed in the area of basic

research, clinical and epidemiological research,

health system-based research, and populationbased research, including community

intervention trials. Specific research questions in

each of these areas are discussed in relevant

chapters of this report. A broad message of this

report is that the Nation is not doing equally well

in all areas of research and prevention. While

extensive work is being done in the area of basic

research, the translation of this research to clinical

practice often lags behind. Clinical and

epidemiological research and evaluation enjoy

significant support as well. More needs to be done,

especially with respect to research related to men

and racial and ethnic minorities and how best to

translate basic and clinical research findings into

everyday practice. While much of this basic,

clinical, and epidemiological research will be

focused on osteoporosis, it is important to

remember that research breakthroughs in

osteoporosis (e.g., the development of

bisphosphonates) are already paying dividends

for the treatment of other bone diseases, and these

benefits will likely continue in the future. More

health system- and population-based research in

the area of bone health is needed as well. One of

the biggest voids is in the area of population-based

research on behavior change, where little is known

about how to get people to adopt bone-healthy

behaviors. Fortunately, many of the behaviors

that promote bone health also promote other

aspects of health, including cardiovascular health.

The goal going forward should be to integrate

bone and musculoskeletal health into larger

studies that are evaluating these behavioral issues

in other disease areas. Within the area of health

systems-based research, much more needs to be

known about the most efficient and effective ways

to use the various risk assessment, diagnostic, and

therapeutic tools available in bone health today.

As noted, insights from basic and clinical research

need to find their way into everyday practice.

There are two components to this issue. First,

within a given disease area, many insights from

basic and clinical research are never applied in

practice. For example, research might show that

a particular drug, administered in a particular

dose, is effective in treating a specific population.

Once these findings are published, practitioners

often do not know how to use this populationbased information when assessing and treating

individual patients. They may not know if a

specific patient’s situation applies and, if so, how

long to use the drug in question. Second, in some

situations insights from research into the

prevention of other chronic diseases will have

applications in the prevention of bone disease.

These insights frequently do not become known

to health care professionals responsible for bone

health. Much more needs to be done to address

both of these problems. Work should focus on

stimulating the translation and application of basic

research into clinical research and to promote the

use of basic and clinical research findings in

everyday practice. The research community

should be encouraged to play a larger role in

translating their findings into usable knowledge

that helps a health care professional.

 Support the integration of health messages

and programs on physical activity and nutrition

relating to other chronic diseases.

As noted earlier, many of the behaviors that

prevent bone disease are also critical for

preventing other diseases and chronic conditions,

including asthma, diabetes, obesity, heart disease,

and stroke. Thus, it is absolutely essential that

information directed toward the public and

physicians about the behaviors that optimize
350 Chapter 13

A Report of the Surgeon General

health be integrated. These integrated educational

messages need to promote all aspects of health for

individuals in various stages of life, including

infancy, childhood, adolescence, young adults,

middle-aged adults, and the elderly. For the most

part, the critical messages in each of these disease

areas will be the same. The key is to maintain a

healthy weight and diet, avoid smoking, and

engage in regular physical activity. For example,

the bone health community could join forces with

other organizations promoting healthy lifestyles

and the prevention of chronic diseases, such as

the National Cancer Institute’s 5 A Day for Better

Health campaign to advocate consumption of

fruits and vegetables and the American Heart

Association’s efforts to promote cardiovascular

health through physical activity, diet, and

smoking cessation. The goal should be to ensure

that their messages emphasize the bone-health

benefits of whatever is being promoted, be it

following an appropriate diet, exercising on a

regular basis, or other bone-healthy behaviors.

These integrated messages will help both the

public and practitioners to understand that there

is not a different “recipe” for keeping different

parts of the body healthy, and that therefore it is

not an all-consuming task to do what is needed to

maintain one’s health. Rather, the message will

be a much more positive one—that following

healthy behaviors is relatively easy to do and that

focusing on a few critical elements such as nutrition

and physical activity can go a long way toward

achieving overall health and well-being.

 Act now, as we know more than enough.

While there will always be a need for more

research and a greater understanding of bone

health and bone disease, more than enough is

known today to get started on any of a variety

of critical actions that are needed to enhance the

bone health status of Americans.

The Roles of Key Stakeholders

Many fruitful activities are already underway

in the area of bone health. Advocacy groups,

medical and science organizations, and others have

been working diligently to promote better bone

health for all Americans, including underserved

populations. This Surgeon General’s report can

be a catalyst to build upon, broaden, and expand

these efforts. To that end, this report calls for

public and private stakeholders in the area of bone

health to join forces in the development of a

national action plan. The goal of this effort would

be to forge consensus on the different action steps

that are needed and to determine which

stakeholders are best equipped to take

responsibility for their execution. Because every

stakeholder has an important role to play, this

comprehensive effort should include a wide

variety of organizations, including those

representing families and individuals, health care

professionals, hospitals and rehabilitation centers,

skilled nursing facilities, academic medical centers,

the research community, health systems, managed

care organizations and insurance companies,

public and private purchasers, private industry,

community-based organizations, State and local

public health departments, voluntary health

organizations, professional associations,

policymakers, and agencies at all levels of

government. Some of the most important action

steps for the key stakeholders are highlighted

below:

Individuals and Families

Because many individuals may not realize

that they are at risk of bone disease and may not

take action (e.g., begin engaging in physical

activity) until they are motivated to do so,

individuals and families need to:

• Educate themselves on the importance of

bone health and to recognize that bone
Bone Health and Osteoporosis

A Vision for the Future 351

health is a lifelong issue and that

osteoporosis is not just a women’s disease.

• Set the stage during infancy, childhood,

and adolescence for their children to have

healthy bones throughout their lives.

• Encourage their middle-aged and elderly

parents to take actions to maintain

healthy bones and to prevent bone

disease and fractures later in life.

• Recognize that, regardless of their age,

gender, or racial and ethnic background,

they are at risk of getting bone disease

and therefore should consider making a

lifelong commitment to doing what is

necessary (e.g., getting adequate nutrition

and physical activity) to maintain strong

bones. Doctors cannot do this for their

individual patients, although health care

professionals clearly have a role in

encouraging their patients to adopt bonehealthy behaviors.

Health Care Professionals

All health care professionals, including

physicians, nurses, nurse practitioners, physician

assistants, dietitians/nutritionists, physical and

occupational therapists, social workers, dentists,

optometrists, and pharmacists can play a critical

role in promoting the bone health of their

patients. They need to recognize the potential

for bone disease in men and racial and ethnic

minorities. While the underlying risk in these

population groups may be lower than for White

women, the potential for bone disease is still real,

particularly in the elderly and the poor.

Primary care providers have an especially

critical role to play. They need to:

• Pay close attention to bone health issues

when conducting wellness visits and

treating people with other illnesses.

• Emphasize the basics of good bone health

during their interactions with patients,

including appropriate nutrition and levels

of physical activity.

• Recognize red flags and risk factors that

might signal the potential for osteoporosis

and other bone diseases and take necessary

action or refer at-risk patients to other

providers for the appropriate work-up.

Health care professionals working in

emergency departments and orthopedic

practices also have an important role. They must:

• Recognize that many bone fractures signal

the potential for metabolic bone disease.

• Go beyond fixing patients’ bones by

referring them, when appropriate, to

another health care professional for further

assessment of the potential for bone disease.

Finally, regardless of the setting, consideration

should be given to increasing the role of mid-level

providers as a way of promoting bone health and

minimizing the impact of bone diseases.

Health Systems

Health systems, including hospitals,

organized delivery systems, and health plans and

insurers, can do much to promote bone health

in the populations they serve, including:

• Help individuals practice bone-healthy

behaviors.

• Assist health care professionals in

promoting such behaviors in all patients

and in identifying and treating bone

disease in a timely manner. For example,

these organizations can help practitioners

to identify and implement tools that aid

in the diagnosis and treatment of bone

disease and can point them to credible

sources of information on prevention,

assessment, diagnosis, and treatment.

• Implement a comprehensive, systemsbased approach to promoting bone

health (assuming they have a large

enough population of at-risk individuals
352 Chapter 13

A Report of the Surgeon General

to justify it). This approach may include:

reminder systems that alert providers of

the need for certain services in individual

patients; systematic quality measurement

and improvement; disease management

programs focused on bone health; and/or

the setting of appropriate financial

incentives for providers and individuals.

• Consider adoption of coverage policies that

provide payment for appropriate,

evidence-based preventive, diagnostic, and

therapeutic services within the area of

bone health.

Health Care Purchasers

Health care purchasers, including public and

private employers that buy health coverage on

behalf of their employees, can use their power

both individually and collectively to influence

bone health. More specifically, they can do the

following:

• Like health plans and insurers, consider

adoption of coverage policies that allow

for the appropriate provision of

evidence-based preventive, diagnostic,

and therapeutic services to all who need

them.

• Use their purchasing clout to encourage

providers to adopt policies and programs

that promote bone health and overall health.

• Develop on-site physical activity and

nutrition programs.

Communities and Community-Based

Organizations

Communities consist of multiple components,

including individuals, faith-based and other community organizations, employers, and government agencies. Working together these organizations can:

• Develop a forum in which the public can

discuss bone health status and the burden of bone disease and fractures in their

community.

• Assess the resources currently available

for improving the bone health status of

the community, including public education and treatment.

• Evaluate, and if necessary refine, current

policies and programs for enhancing the

bone health status of the community.

• Promote daily physical activity in schools

at all grade levels.

• Make available user-friendly facilities for

physical activity for all age groups, such

as walking trails and gymnasiums.

Government

Governments at every level—local, State, and

Federal—have a vital leadership role to play in

promoting bone health. To play this role effectively, elected policymakers and other government leaders need to recognize the long-term financial and social costs of the status quo (less-thanoptimal bone health status), and appreciate the

potential to reduce these costs and improve quality of life through prevention, early detection, and

early treatment. Local public health departments

and government agencies—especially those serving the elderly—have an especially important role

to play in developing and implementing a public

health approach to bone health promotion at the

community level. Specific roles that government

can play include:

• Promote public education, public

awareness campaigns, and treatment

services.

• Coordinate actions needed to improve

bone health across the public and private

sectors. These actions could include the

formation of State or local task forces,

steering committees, or advisory

committees related to bone health, and
Bone Health and Osteoporosis

A Vision for the Future 353

the development of strategic plans for

improving the bone health status of the

population and at-risk groups.

• Support the creation of an environment

in which bone-healthy dietary and

physical activity options are readily

accessible, and needed preventive,

diagnostic, and therapeutic services are

readily available and affordable to all who

need them.

• Promote research on basic bone biology,

new approaches to diagnosis and treatment

of bone disease, and the translation of

research findings into practice.

• Promote research on the effects of

community- and population-based

interventions on the community and atrisk populations, including their impact

on: the prevalence of bone disease and

fractures; diet and physical activity; and

access to and use of appropriate

preventive, diagnostic, and treatment

measures.

• Communicate with one another and

coordinate activities to ensure that the

actions and policies of various levels of

government are complementary. The

overall goal should be greater

harmonization of government activities,

thus ensuring more cost-effective and

higher-quality services to the public.

• Use the most current, credible evidence

when making policy and program

decisions related to bone health.

 Voluntary Health Organizations

Voluntary health organizations play

important roles in promoting bone health. They

are often able to reach the public and providers

with critical information quickly and with fewer

constraints than can government organizations.

More specifically, they can:

• Raise public awareness about specific

health problems such as bone disease. By

including individuals who have

personally been touched by bone disease,

these organizations are uniquely

positioned to provide important guidance

to other sectors of the health system

regarding the real-life impact of bone

disease on individuals, families, and

communities.

• Work with residents in the local

community to adopt the lifestyle changes

necessary to prevent the onset or

progression of bone and other diseases.

• Promote the availability of information

and resources related to the prevention,

diagnosis, and treatment of bone disease.

Professional Associations

Professional associations play a critical role

in promoting bone health. They can:

• Facilitate the training of health

professionals needed to address the

prevention, diagnosis, and treatment of

bone disease.

• Promote changes in the curricula of

professional schools and provide

continuing education to practicing bone

health professionals.

• Develop evidence-based guidelines along

with standards of care for bone health.

These guidelines help to ensure that

individuals who have or are at risk of

getting bone disease can benefit from the

best practices related to prevention,

assessment, diagnosis, and treatment.

Academic Institutions

Academic institutions can be critical

facilitators through their two core missions of
354 Chapter 13

A Report of the Surgeon General

education and research. With respect to

osteoporosis and bone health, they can:

• Develop bone-health specific curricula for

the education and training of physicians,

nurses, nurse practitioners, physician assistants, dietitians/nutritionists, physical and

occupational therapists, social workers, dentists, optometrists, and pharmacists.

• Develop the professional skills needed to

become effective members of a health care

team that focuses on improving bone

health and preventing adverse outcomes.

For example, trainees from different disciplines (e.g., medical students and residents, nurse practitioners, physician assistants) could be given the opportunity

to rotate through osteoporosis clinics.

• Educate the general public by teaching

lifestyles that promote bone health in primary and secondary schools and colleges.

Schools can play a role in promoting and

supporting good dietary habits and regular physical activity, beginning in childhood.

• Advance research on bone health. To

date, such research has focused primarily

on laboratory studies and clinical trials.

Some academic institutions have active

research programs on epidemiology,

health care delivery, and outcomes as

well. These should be expanded to

include research on prevention strategies

and on men and racial and ethnic

minorities.

Industry

Industry also has an important role to play

in promoting bone health. They can:

• Reduce the consequences of poor bone

health through the development and promotion of drugs, devices, and other diagnostic and treatment technologies.

• Provide information to health care professionals and the public on the appropriate use of pharmaceutical agents to

prevent and treat bone disease. This information needs to be part of a comprehensive approach to promoting bone

health that includes education on appropriate diet and physical activity.

• Provide disease-management services

that focus on managing osteoporosis and

bone health in at-risk populations.

The Importance of Partnerships

Among Stakeholders

While the roles and contributions of the

individual stakeholders cited above are

undoubtedly important, public-private

partnerships will also be critical to the successful

development and execution of a national action

plan for bone health. These partnerships can

build and strengthen cross-disciplinary,

culturally competent, community-based efforts

to promote bone-healthy behaviors and support

the early identification and treatment of bone

disease. There is no question that the collective

and complementary talents of both public and

private stakeholders will be vital to achieving the

goal of improving the bone health status of all

Americans.

Conclusion

Significant strides have been made in

understanding bone health and bone disease

over the past few decades. Much is known about

how to keep bones healthy throughout life and

how to prevent and treat bone disease and

fractures in those whose bone health

deteriorates. Yet too few people—individuals
Bone Health and Osteoporosis

A Vision for the Future 355

and health professionals alike—make use of this

information. As a result, too many people have or

are at risk of getting bone disease. The time has

come to address this problem, to “get the word

out” about the importance of bone health and the

serious consequences and significant costs of bone

disease and fractures. The time has come for

everyone—including individual citizens, solo

practitioners, the heads of major public and

private sector organizations, and the leaders of

governmental agencies—to do his or her part in

promoting the bone health of all Americans.

Bone Health and Osteoporosis

Appendix A 357

CONGRESSIONAL LANGUAGE CALLING FOR

SURGEON GENERAL’S REPORT

Appendix A

November 29, 2001

House Labor Report

Osteoporosis is a major health threat for more than 28 million Americans, 80% of whom are

women. In 2001, 10 million individuals have already developed the disease. Osteoporosis is responsible

for 1.5 million fractures annually and is second leading cause of nursing home admissions in the

U.S. The Committee urges the Surgeon General to consider issuing a Report to the Nation on the

status of research and education on osteoporosis and related bone disease and setting forth an action

plan to comprehensively address the urgent need to reverse the increasing toll of this disease.

Senate Labor Report

Report on osteoporosis and related bone diseases. More than 30 million Americans suffer from

some form of bone disease, including osteoporosis, Paget’s disease and osteogenesis imperfecta. The

Committee therefore recommends that the Department commission a Surgeon General’s report on

osteoporosis and related bone diseases, detailing the burden bone diseases places on society, and

highlighting preventive measures to improve and maintain bone health throughout life. The report

should also identify best practices for collecting data about the prevalence, morbidity and disability

associated with bone diseases among minority populations.

Bone Health and Osteoporosis

Appendix B 359

HOW DO WE KNOW WHAT WE KNOW:

THE EVIDENCE BEHIND THE EVIDENCE

Appendix B

The approach of this report is to give the best

evidence and advice available at this time and

also to indicate where more evidence is needed.

The report relies on evidence reports, consensus

conferences, and governmental recommendations that have been developed through a

process that reviews and evaluates all evidence

in a structured, unbiased, and comprehensive

manner.

Research Terms and Study Designs

• Clinical trial (intervention; controlled trial):

A special kind of experimental study that

tests the effectiveness of a substance or be

havior (drug, diet, exercise) using consent

ing human subjects. The conditions of the

study—selection of treatment groups,

nature of interventions, management

during follow-up, etc.—are specified

by the investigator for the purpose of

making unbiased comparisons.

• Double-blinded: Neither the participants

nor the researchers know who receives the

intervention versus the placebo.

• Placebo: An inert or innocuous substance

used especially in controlled experiments

testing the efficacy of another substance.

• Randomized: The study participants have

been assigned to receive the active

intervention or placebo randomly.

• Observational study: A study in which the

practice or factor being studied is observed

in a group of participants who have voluntarily chosen to follow or not follow this

practice, i.e., they are not randomly

assigned.

• Cross-sectional study: Study participants

are observed and measurements are made

at one point in time.

• Longitudinal study: Study participants are

observed and measurements made at multiple points in time.

• Meta-analysis: A technique in which results from several studies are combined to

produce an estimate of the effect of the

factor being studied.

(Fletcher et al. 1988, MedlinePlus 2004.)

It is important for clinicians and consumers

to understand the origins of this evidence and

advice. In fact, the evidence presented in this

report has been collected and analyzed in many

different ways. Some common study designs

include cross-sectional longitudinal studies and

randomized clinical trials. These terms, along

with others that are commonly used in research,

are defined in the box below.
360 Appendix B

A Report of the Surgeon General

The endpoints being measured in the various studies often differ. For example, although

fractures due to osteoporosis are a serious threat

late in life, they are not common in younger individuals. So most studies of young people focus on how much bone mass is accumulated or

how much calcium is retained when the body is

put under the influence of a factor such as physical activity, calcium, or vitamin D.

Since fractures are more common in older

individuals, they are commonly used as an endpoint of interest in studies of this age cohort and

often are studied in older populations. A common approach is to compare two groups of

people with different rates of fractures to determine which characteristics of the group with low

fracture rates are protective of bone health, and/

or which factors in the high-fracture group put

them at risk. These “observational studies” make

very important contributions by generating hypotheses about risky versus protective behaviors

and lifestyle practices. The Study of Osteoporotic Fractures, which began in 1987 (see

box below), has followed a group of 9,904 White

women age 65 and older over a period of years

to collect a variety of information as they age

(Cummings et al. 1995). This study is the largest and one of the most important contributors

to knowledge about the risk of fracture in older

women. See Table 8-1 in Chapter 8 for risk factors that were derived from the Study of Osteoporotic Fractures. In 1997, a similar study,

called Mr. OS, was launched to address the gaps

in knowledge about osteoporosis and fractures

in men.

Observational studies have some biases, including the fact that participants are selecting

what they do. As a result, these studies can only

determine that certain factors (e.g., behaviors,

conditions, nutrients) are associated with lower

or higher risks, not that the factor causes the

change in risks. To get around this problem,

some factors can be tested in an even stronger

experimental design call the “double-blinded

randomized clinical trial” (sometimes also referred to as “controlled” or “intervention” trials). In these studies, two or more groups of

individuals are randomly assigned to receive an

active intervention—such as calcium supplements—or a placebo (a pill or procedure that

appears the same as the active intervention, but

does not contain the active treatment). In this

design, neither the participants nor the scientists conducting the study know who is receiving the active substance or the placebo. When

the groups are large enough, all the other characteristics of the individuals in the study can

be balanced similarly across the groups, thus

eliminating, or at least reducing, the chances of

various biases. This makes it possible to determine the effect of the intervention much more

clearly. For this reason, this type of study has

been called the “gold standard” for evidence.

Drugs approved by the Food and Drug Administration for the treatment of osteoporosis

and the prevention of fractures go through the

rigorous testing of randomized clinical trials.

Lifestyle factors and behaviors are sometimes

tested using this design as well. Sometimes

there are gaps in the evidence because large,

well-designed studies have not yet been carried

out in all different age and ethnic groups and

in both men and women. Nevertheless, judgments can be made by expert groups to provide the best possible advice based on consideration of all available evidence. When developing guidelines for individuals about the diagnosis, prevention, or treatment of a disease

or condition like osteoporosis and fractures,

these experts rate the “strength” of the evidence

using a variety of factors such as the design (e.g.,

was it a randomized controlled clinical trial, an
Bone Health and Osteoporosis

Appendix B 361

The Human Side of Research

It is often easy to forget that clinical research depends upon the willing participation

of real people. Several important studies in the

area of osteoporosis and bone health demonstrate the “human” side of research.

Camp Calcium

Camp Calcium is a unique study supported by the National Institutes of Health and

conducted by the Department of Foods and

Nutrition at Purdue University. Since 1990,

Camp Calcium has brought together teenagers to participate in a 6-week camp in which

their dietary intake of calcium is strictly controlled. Researchers also checked participants’

waste and blood samples each day. The dietary

calcium in the foods was varied to determine

how much calcium teenagers can absorb during their most active growing period. Due to

the higher incidence of osteoporosis in females,

the first six camps (1990, 1993, 1996, 1997,

1999, and 2000) included only girls, with each

camp designed to provide insight into a specific factor, as described below:

• Comparison of calcium metabolism in

adolescents versus young adults (Wastney

et al. 1996).

• Establishment of calcium requirements for

teenage girls. The Food and Nutrition

Board of the National Academy of

Sciences used research from Camp

Calcium in setting such requirements

(Wastney et al. 2003).

• Effect of maturation on calcium metabolism

in teenage girls.

• Effect of race on calcium metabolism

(Bryant et al. 2003).

• Effect of high and low levels of sodium on

calcium retention in two races (Palacios et

al. 2004).

• Determination of whether higher calcium

intakes can negate the negative influences

of sodium.

The 2001 camp was the first to include

males, with the goal of establishing calcium

requirements for teenage boys.

Participants in Camp Calcium hardly think

of themselves as participating in a serious and

important study. The camp itself is designed

to be fun, consisting of mini-sports camps led

by Purdue University athletic department staff

and athletes, along with field trips, movies,

nutrition and health classes, and other

educational opportunities. The interaction of

the young people with the scientists through

the camp may inspire a few to choose a career

in science. Participants also get the satisfaction

of knowing that they are helping in the

development of important scientific findings

that will have a significant impact on the health

of future generations.

observational study, or a report of a single

case?), study size, and characteristics of the

study population (e.g., gender, age, severity of

illness). Sometimes they combine results from

several studies using a technique called “metaanalysis.”

It is important to remember that the scientific knowledge that fuels recommendations and

public policy is built on the contributions of not

only dedicated scientists, but also thousands of

volunteers—men, women, and children—who

decide to participate.
362 Appendix B

A Report of the Surgeon General

The Study of Osteoporotic Fractures

The SOF study began in 1986, when

women over age 65 living in four different

communities (Baltimore, MD; Portland, OR;

Minneapolis, MN; and the Monongahela Valley outside of Pittsburgh, PA) were invited

to participate in a study designed to determine the long-term impact of physical activity on osteoporotic fractures and other more

general health measures, including mortality.

The study has generated important findings,

including recently released data indicating

that women who become or stay physically

active after age 65 were only half as likely as

those who are sedentary to die from cardiovascular disease, cancer, or other causes during a 7-year follow-up period (Gregg et al.

2003).

These findings would not have been possible, however, were it not for the dedication

of the nearly 10,000 women who signed up

for SOF, many of whom are still alive and actively participating today. For as long as 17

years, the “women of SOF” have attended

clinic visits, filled out questionnaires/postcards,

and received home visits or phone calls from

SOF staff, all with the purpose of allowing researchers to track their health status and activity levels and to conduct blood and other tests.

Many who have relocated to other parts of the

country still participate by filling out and

sending in their questionnaires and/or by

scheduling visits to the SOF clinic when they

are visiting home.

Many do so out of a sense that what they

are doing is important, if not for themselves,

then for others. As an 87-year-old who was

the 15th person to enter the SOF study noted,

“I am happy to be involved in a study that will

help others.” Many also find participation itself

to be a rewarding experience, not only because

it inspires them to become more physically

active, but also because the clinic visits and

other activities make them feel important and

appreciated. A 78-year-old participant has had

such a good experience with SOF that she has

joined two other studies at the same clinic.

The organizers of SOF make a concerted

effort to make participants feel appreciated. For

example, they provide lunches during clinic

visits and give participants a framed certificate

documenting their participation. These efforts

have paid off, as participants routinely make

sacrifices to attend their clinic visits. One

participant drives over 150 miles each way to

attend. Others routinely come in despite facing

a variety of health problems and/or mobility

limitations that confine them to a wheelchair

or that require them to use a walker. Sons and

daughters of participants routinely go to great

lengths to help their mothers participate; one

son even flew from Chicago to Pittsburgh to

pick up his mother in a nursing home and take

her to the SOF clinic. Participants make these

sacrifices because being in SOF means

something to them; one participant even left

instructions that her participation in SOF be

mentioned in her obituary.
Bone Health and Osteoporosis

Appendix B 363

References

Bryant RJ, Wastney ME, Martin BR, Wood O,

McCabe GP, Morshidi M, Smith DL, Peacock M, Weaver CM. Racial differences in

bone turnover and calcium metabolism in

adolescent females. J Clin Endocrinol Metab.

2003 Mar;88(3):1043-7.

Cummings SR, Nevitt MC, Browner WS, Stone

K, Fox KM, Ensrud KE, Cauley J, Black D,

Vogt TM; Study of Osteoporotic Fractures

Research Group. Risk factors for hip fracture in white women. N Engl J Med 1995

Mar 23;332(12):767-73.

Fletcher RH, Fletcher SW, Wagner EH. Clinical epidemiology: the essentials. 2nd edition.

Baltimore: Williams & Wilkins, 1988.

Gregg EW, Cauley JA, Stone K, Thompson TJ,

Bauer DC, Cummings SR, Ensrud KE;

Study of Osteoporotic Fractures Research

Group. Relationship of changes in physical

activity and mortality among older women.

JAMA 2003 May 14;289(18):2379-86.

MedlinePlus Dictionary Web site. [database

online]. Bethesda (MD): U.S. National Library of Medicine, National Institutes of

Health. [updated 2004 Feb 04; cited 2004

Mar 16]. Available from: http://

www.nlm.nih.gov/medlineplus/

mplusdictionary.html.

Palacios C, Wigertz K, Martin BR, Jackman L,

Pratt JH, Peacock M, McCabe G, Weaver

CM. Sodium retention in black and white

female adolescents in response to salt intake.

J Clin Endocrinol Metab. 2004

Apr;89(4):1858-63.

Wastney ME, Martin BR, Bryant RJ, Weaver

CM. Calcium utilization in young women:

New insights from modeling. Adv Exp Med

Biol. 2003;537:193-205.

Wastney ME, Ng J, Smith D, Martin BR, Peacock M, Weaver CM. Differences in calcium

kinetics between adolescent girls and young

women. Am J Physiol. 1996 Jul;271(1 Pt

2):R208-16.

Bone Health and Osteoporosis

Appendix C 365

RESOURCES AND RELATED LINKS

Appendix C

This section provides the names of resources and links in government and the private sector related

to bone health. Links to non-Federal organizations do not constitute an endorsement of any organization by the Federal Government, and none should be inferred.

Federal Government

Agency for Healthcare Research and Quality (AHRQ)

Osteoporosis publications and electronic information

http://www.ahrq.gov/news/pubsix.htm

Centers for Disease Control and Prevention (CDC)

Growing Stronger: Strength Training for Older Adults

http://www.cdc.gov/nccdphp/dnpa/physical/growing_stronger

PATCH—CDC’s Planned Approach to Community Health

http://www.cdc.gov/nccdphp/patch/index.htm

Physical Activity and Health: A Report of the Surgeon General

http://www.cdc.gov/nccdphp/sgr/sgr.htm

Powerful Bones, Powerful Girls Web Site

http://www.cdc.gov/powerfulbones/

http:/www.cdc.gov/powerfulbones/parents

Powerful Girls Calendar

http://www.cdc.gov/powerfulbones/games_fun/calendar_2004.pdf

Promoting Better Health for Young People Through Physical Activity and Sports

http://www.cdc.gov/nccdphp/dash/presphysactrpt/index.htm

VERBTM. It’s what you do. Youth Media Campaign

http://www.cdc.gov/youthcampaign/

Wisewoman: Well-Integrated Screening and Evaluation for Women Across the Nation

http://www.cdc.gov/wisewoman
366 Appendix C

A Report of the Surgeon General

National Heart, Lung, and Blood Institute (NHLBI)

DASH (Dietary Approaches to Stop Hypertension) Eating Plan

http://www.nhlbi.nih.gov/health/public/heart/hbp/dash/

Hearts N’ Parks

http://www.nhlbi.nih.gov/health/prof/heart/obesity/hrt_n_pk/index.htm

National Cholesterol Education Program

http://www.nhlbi.nih.gov/about/ncep/

National Institute on Aging (NIA)

Exercise: A Guide from the National Institute on Aging

http://www.nia.nih.gov/exercisebook/index.htm

Exercise: A Video from the National Institute on Aging

http://www.niapublications.org/exercisevideo/index.asp

National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS)

Information Package—Ordering Information

http://www.niams.nih.gov/hi/index.htm#ip

Osteoporosis Prevention, Diagnosis, and Therapy

http://odp.od.nih.gov/consensus/cons/111/111_intro.htm

Osteoporosis: Progress and Promise

http://www.niams.nih.gov/hi/topics/osteoporosis/opbkgr.htm

National Institute of Child Health and Human Development (NICHD)

Milk Matters Educational Campaign

http://156.40.88.3/milk/milk.cfm

National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)

Sisters Together: Move More, Eat Better

http://www.niddk.nih.gov/health/nutrit/sisters/sisters.htm

National Institutes of Health (NIH)

Clinical Trials

http://www.ClinicalTrials.gov

NIH Osteoporosis and Related Bone Disease~National Resource Center

http://www.osteo.org/default.asp

President’s Council on Physical Fitness and Sports

The President’s Challenge

http://www.fitness.gov

http://www.presidentschallenge.org
Bone Health and Osteoporosis

Appendix C 367

U.S. Administration on Aging

Aging Internet Information Notes: Osteoporosis

http://www.aoa.gov/prof/notes/docs/osteoporosis.doc

U. S. Department of Agriculture (USDA)

Dietary Guidelines for Americans

http://www.usda.gov/cnpp/

School Meals

http://www.fns.usda.gov/cnd

USDA Food and Nutrition Service

http://www.fns.usda.gov

United States National Agricultural Library

http://www.nal.usda.gov

U. S. Department of Education (USDOE)

National Institute on Disability and Rehabilitation Research (NIDRR)

http://www.ed.gov/about/offices/list/osers/nidrr/index.html?src=mr

U.S. Department of Health and Human Services (HHS)

Dietary Guidelines for Americans

http://www.health.gov/dietaryguidelines

HealthierUS Initiative

http://www.healthierus.gov

Healthfinder® Gateway to Reliable Consumer Health Information on the Internet

http://www.healthfinder.gov

Healthy People in Healthy Communities: A Community Planning Guide Using Healthy People

2010

http://www.healthypeople.gov/publications/HealthyCommunities2001

Healthy People 2010 Toolkit

http://www.healthypeople.gov/state/toolkit

National Women’s Health Information Center

http://www.4woman.gov

STEPS to a HealthierUS Initiative

http://www.healthierus.gov/steps/index.html

U.S. Food and Drug Administration (FDA)

Guidance on How to Understand and Use the Nutrition Facts Panel on Food Labels

http://www.cfsan.fda.gov/~dms/foodlab.html
368 Appendix C

A Report of the Surgeon General

U.S. Food and Drug Administration—FDA Consumer Magazine (10/02)

http://www.fda.gov/fdac/features/2002/502_men.html

State Government

Association of State and Territorial Chronic Disease Program Directors

Osteoporosis Council

http://www.chronicdisease.org/Osteo_Council/osteo_about.htm

Osteoporosis Council: Contact information for state osteoporosis directors/coordinators

http://www.chronicdisease.org/Osteo_Council/osteo_membership.htm

Osteoporosis State Program Practices That Work

http://www.chronicdisease.org/whc/Practices_that_Work.pdf

Osteoporosis 2000: A Resource Guide for State Programs

http://www.chronicdisease.org/Osteo_Council/publications/Resource_Guide.pdf

State Osteoporosis Web Sites

Alabama Department of Public Health

http://www.adph.org/NUTRITION/default.asp?DeptId=115&TemplateId=2022&

TemplateNbr=0

Arizona Osteoporosis Coalition

http://www.azoc.org

http://www.fitbones.org

California Department of Health Services, Arthritis and Osteoporosis Unit

http://www.dhs.ca.gov/osteoporosis

Colorado Department of Public Health and Environment: Osteoporosis Web Site

http://www.cdphe.state.co.us/pp/Osteoporosis/osteohom.html

Florida Osteoporosis Prevention and Education Program

http://www.doh.state.fl.us/family/osteo/default.html

Georgia Osteoporosis Initiative

http://www.gabones.com

Indiana Osteoporosis Prevention Initiative

http://www.in.gov/isdh/programs/osteo

Kentucky Office of Women’s Physical and Mental Health: Osteoporosis

http://chs.ky.gov/womenshealth/resourcecenter/Resources/osteoporosis.htm

Maryland Department of Health and Mental Hygiene

http://www.strongerbones.org
Bone Health and Osteoporosis

Appendix C 369

Michigan Department of Community Health

http://www.michigan.gov/mdch/0,1607,7-132-2940_2955_2978—,00.html

Mississippi State Department of Health

http://www.msdh.state.ms.us/msdhsite/index.cfm/13,0,225,html

Missouri Department of Health and Senior Services

http://www.dhss.state.mo.us/maop

New Jersey Department of Health and Senior Services

http://www.state.nj.us/health/senior/osteo

New York State Department of Health

http://www.health.state.ny.us/nysdoh/osteo/index.htm

Ohio Department of Health

http://www.odh.state.oh.us/odhprograms/osteo/osteo1.htm

Rhode Island Department of Health

http://www.health.ri.gov/disease/osteoporosis/index.htm

Tennessee Department of Health

http://www2.state.tn.us/health/healthpromotion/osteoporosis.html

Texas Department of Health: Osteoporosis Awareness and Education Program

http://www.tdh.state.tx.us/osteo

Virginia Department of Health

http://www.vahealth.org/nutrition/bones.htm

West Virginia Department of Health and Human Resources

http://www.wvdhhr.org/bph/oehp/hp/osteo/default.htm

Non-Government

American Academy of Orthopaedic Surgeons (AAOS)

http://www.aaos.org

American Academy of Pediatrics (AAP)

Policy Statement on Calcium Requirements of Infants, Children, and Adolescents

http://aappolicy.aappublications.org/policy_statement/index.dtl#C

American Council on Exercise

http://www.acefitness.org

American College of Sports Medicine

http://www.acsm.org
370 Appendix C

A Report of the Surgeon General

American Dietetic Association (ADA)

http://www.eatright.org

American Society for Bone and Mineral Research (ASBMR)

http://www.asbmr.org

ASBMR Bone Curriculum Web Site

http://depts.washington.edu/bonebio/ASBMRed/ASBMRed.html

Bone Builders

http://www.bonebuilders.org/

BoneKEy-Osteovision®

http://www.bonekey-ibms.org

Foundation for Osteoporosis Research and Education (FORE)

http://www.fore.org/

Growing Stronger: Strength Training for Older Adults

http://nutrition.tufts.edu/research/growingstronger

International Bone and Mineral Society (IBMS)

http://www.ibmsonline.org/

International Osteoporosis Foundation (IOF)

http://www.osteofound.org/

International Society for Clinical Densitometry (ISCD)

http://www.iscd.org/osteoblast/index.cfm

National Dairy Council (NDC)

http://www.nationaldairycouncil.org

National Osteoporosis Foundation (NOF)

http://www.nof.org

National Strength and Conditioning Association

http://www.nsca-lift.org

Osteoporosis and Bone Physiology, University of Washington

http://courses.washington.edu/bonephys

Osteoporosis Education, University of Washington

http://www.osteoed.org/faq/index.html#male

http://www.osteoed.org

Osteogenesis Imperfecta Foundation (OIF)

http://www.oif.org
Bone Health and Osteoporosis

Appendix C 371

The Paget Foundation (TPF)

http://www.paget.org

Shape-Up America!

http://www.shapeup.org

U.S. Bone and Joint Decade

http://www.usbjd.org

Bone Health and Osteoporosis

 373

AAOS American Academy of Orthopaedic Surgeons

ACOVE Assessing Care of Vulnerable Elders

ACS American Cancer Society

ACSM American College of Sports Medicine

ACTH adrenocorticotropic hormone

AD autosomal dominant

AGS American Geriatrics Society

AHRQ Agency for Health Care Research and Quality

AI adequate intakes

AIAN American Indian and Alaska Native

AR autosomal recessive

BH/BH Bone Health/Body Health

BMD bone mineral density

BSAP bone specific alkaline phosphatase

BUA broadband attenuation

CDC Centers for Disease Control and Prevention

CEE conjugated equine estrogens

CMAJ Canadian Medical Association Journal

CME continuing medical education

CMS Centers for Medicare and Medicaid Services

CNS central nervous system

COPE computerized physician order entry

CTx C-terminal collagen crosslinked peptides

DASH Dietary Approaches To Stop Hypertension

DNA deoxyribonucleic acid

DOT Department of Transportation

Dpd free deoxypyridoline crosslinks

DRG diagnosis-related group

DTCA direct-to-consumer advertising

DV daily value

DXA dual x-ray absorptiometry

E + P estrogen-progestin combination

ECF extracellular fluid

EPESE Established Populations for Epidemiologic Studies of the Elderly

FDA Food and Drug Administration

fl oz. fluid ounce

FNB Food and Nutrition Board

Abbreviations and Acronyms
374

A Report of the Surgeon General

g/cm2 grams per centimeter squared

GIO glucocorticoid-induced osteoporosis

gm gram

GnRH gonadotrophin-releasing hormone

HEDIS Health Plan Employer Data and Information Set

HIV human immunodeficiency virus

HMO health maintenance organization

HOPE Health, Osteoporosis, Progestin, Estrogen

HRR hospital referral regions

HRSA Health Resources and Services Administration

HT hormone therapy

IGF-1 insulin-like growth factor-1

IOM Institute of Medicine

IPA independent practice association

ISCD International Society for Clinical Densitometry

IU international units

kg kilogram

m-CSF macrophage colony stimulating factor

mg milligram

MilkPEP Milk Processor Education Program

ml milliliter

MM multiple myeloma

MMA Medicare Modernization Act

MPA medroxyprogesterone

NAWHO National Asian Women’s Health Organization

NBHC National Bone Health Campaign

NCDPH North Carolina Department of Public Health

NCEP National Cholesterol Education Program

NCHS National Center for Health Statistics

NCI National Cancer Institute

NCQA National Committee for Quality Assurance

ND not determinable

NDC National Dairy Council

NDDIC National Digestive Diseases Information Clearinghouse

NGC National Guideline Clearinghouse

NHANES National Health and Nutrition Examination Survey

NHDS National Hospital Discharge Survey

NIA National Institute on Aging

NICHD National Institute of Child Health and Human Development

NIDCR National Institute of Dental and Craniofacial Research
Bone Health and Osteoporosis

 375

NIH National Institutes of Health

NIHORBD~NRC National Institutes of Health, Osteoporosis and Related Bone

Diseases~National Resource Center

NJDHSS New Jersey Department of Health and Senior Services

NOF National Osteoporosis Foundation

NORA National Osteoporosis Risk Assessment

NTX N-telopeptide of type I collagen

OI osteogenesis imperfecta

OMBDC Saint Barnabas Osteoporosis and Metabolic Bone Disease Center

OPG osteoprotegerin

ORAI Osteoporosis Risk Assessment Instrument

OST Osteoporosis Self-Assessment Tool

OTA Office of Technology Assessment

OTA Orthopaedic Trauma Association

OWH Office on Women’s Health

oz. ounce

PA physical activity

PDSA Plan, Do, Study, Act

pDXA peripheral dual x-ray absorptiometry

PE physical education

PEPI Postmenopausal Estrogen/Progestin Interventions

PICP carboxyterminal propeptide of type I collagen

PINP aminoterminal propeptide of type I collagen

pkt packet

pQCT peripheral quantitative computed tomography

PROOF Prevent Recurrence of Osteoporotic Fractures

PTH parathyroid hormone

PTHrP parathyroid hormone-related protein

Pyd free and total pyridinolines

QALY quality-adjusted life year

QCT quantitative computed tomography

QOL quality of life

QUS quantitative ultrasound

RA radiographic absorptiometry

RANKL receptor activator of nuclear factor kappa B ligand

RDA recommended daily allowance

RPCT randomized placebo-controlled trial

RSVP New Jersey Association of Retired and Senior Volunteer

Program Directors

SCORE Simple Calculated Osteoporosis Risk Estimation
376

A Report of the Surgeon General

SD standard deviation

SERM selective estrogen receptor modulator

SHPPS School Health Policies and Programs Study

SOS speed of sound

SPF sun protection factor

SXA single x-ray absorptiometry

Tbsp tablespoon

TSH thyroid stimulating hormone

UL upper intake levels

USDA United States Department of Agriculture

USDHHS United States Department of Health and Human Services

USP United States Pharmacopoeia

USPSTF United States Preventive Services Task Force

USRDS United States Renal Data System

WHI Women’s Health Initiative

WHO World Health Organization

WIC Women, Infants, and Children Program

yr year
Bone Health and Osteoporosis

 377

List of Tables and Figures

Chapter 1

A Public Health Approach To Promote Bone

Health

Table 1-1 Healthy People 2010 Osteoporosis

and Bone Health Objectives, 10

Chapter 2

The Basics of Bone in Health and Disease

Table 2-1 Most Critical Systemic Hormones

Regulating Bone, 26

Table 2-2 Causes of Bone Loss and Fractures

in Osteoporosis, 32

Figure 2-1 Front Longitudinal Midsection of

Upper Femur, 20

Figure 2-2 Modeling and Remodeling, 22

Figure 2-3 Bone Remodeling, 23

Figure 2-4 Regulation of the Calcium Levels

in the Body Fluids, 27

Figure 2-5 Normal vs. Osteoporotic Bone, 31

Figure 2-6 How Osteoclasts Are Formed, 34

Chapter 3

Diseases of Bone

Table 3-1 Diseases That Cause or Contribute

to Secondary Osteoporosis, 47

Table 3-2 Medications Associated With Secondary Osteoporosis, 51

Table 3-3 Causes of Drug-Induced Rickets/

Osteomalacia, 54

Table 3-4 Clinical Heterogeneity and Biochemical Defects in Osteogenesis

Imperfecta (OI), 58

Figure 3-1 Bone Fracture Areas in Osteoporosis, 42

Figure 3-2 Progressive Spinal Deformity in

Osteoporosis, 45

Figure 3-3 Schematic Representation of Model

for Bone Loss in Postmenopausal

Women and Aging Men, 46

Figure 3-4 Rapid Increase in Vertebral Fracture Rates in Patients Treated With

Glucocorticoids, 52

Figure 3-5 Paget’s Disease of Bone, 56

Chapter 4

The Frequency of Bone Disease

Table 4-1 Lifetime Risk of Fracture at Age

50 Years, 70

Table 4-2 Prevalence (Per 100 Persons) of Osteoporosis and Hip Fracture in Persons 65 Years of Age and Older, by

Gender and Age: United States,

1988-1994, 78
378

A Report of the Surgeon General

Figure 4-1 Age Specific Incidence Rates for

Proximal Femur (Hip), Vertebral

(Spine), and Distal Forearm (Wrist)

Fractures in Rochester, Minnesota,

Men and Women, 72

Figure 4-2 Hip Fracture Incidence by Race/

Ethnicity Among Women and Men,

55 Years of Age and Older in California, 1983 to 2000, 73

Figure 4-3 Ratio of Hip Fracture Rates to the

U.S. Average (2001), 74

Figure 4-4 Projected Prevalence of Osteoporosis and/or Low Bone Mass of the Hip

in Women, Men, and Both Sexes,

50 Years of Age or Older, 76

Figure 4-5 Mean Bone Mineral Density of the

Femoral Neck by Age for U.S. Men

and Women of Different Racial/

Ethnic Groups, 79

Chapter 5

The Burden of Bone Disease

Table 5-1 Resource Utilization Attributable to

Osteoporotic Fractures Among Persons > 45 Years of Age in the United

States in 1995, by Type of Service

and Type of Fracture, 92

Table 5-2 Disability Resulting From Osteoporotic Fractures, 93

Table 5-3 Direct Health Care Expenditures

for Care of Osteoporotic Fractures

Among Persons > 45 Years of Age

in the United States by Type of Service and Type of Fracture, 1995, 94

Table 5-4 Postfracture Dependency at 12 and 24

Months Among Patients Who Were

Independent Prior to Hip Fracture, 99

Table 5-5 Clinical Consequences of Spine

Fractures, 100

Table 5-6 Costs Per Month Per Patient, Before and After Hip Fracture, Adjusted for Death and Excluding

the Cost of the Initial Hospitalization, 102

Figure 5-1 Observed and Expected Race- and SexSpecific Survival Following Fracture of

the Hip, All Ages Combined, 96

Figure 5-2 Schematic Representation of the Morbidity Associated With Different Osteoporotic Fractures With Age, 97

Chapter 6

Determinants of Bone Health

Figure 6-1 Factors Influencing Bone Mass

Structure, 112

Figure 6-2 Bone Mass Versus Age With Optimal

and Suboptimal Bone Acquisition, 113

Figure 6-3 The Progression of Osteoporosis, 114

Figure 6-4 Median Calcium Intakes of Females,

1988-1994, Compared to Adequate

Intake Recommendations, 116

Figure 6-5 Percent of Adults Aged 18 Years

and Over Who Engaged in Regular

Leisure Time Physical Activity, by

Age Group and Sex: United States,

January–September 2003, 123
Bone Health and Osteoporosis

 379

Figure 6-6 Bone Mass Differences in the Playing Arms of Women Racquet Players, 127

Figure 6-7 High-Intensity Jumping Improves

Hip and Lumbar Spine Bone Mass

and Size in Pre-Pubertal Children, 128

Figure 6-8 Rationale for the Use of Hip Protectors To Prevent Fractures, 134

Chapter 7

Lifestyle Approaches To Promote Bone Health

Table 7-1 Adequate Intakes (AI) or Recommended Dietary Allowances

(RDA) and Tolerable Upper Intake

Levels (UL) for Calcium, Vitamin

D, Phosphorus, and Magnesium by

Life-Stage Group for United States

and Canada, 160

Table 7-2 Selected Food Sources of Calcium,

161

Table 7-3 Calcium and Lactose in Common

Foods, 162

Table 7-4 Dietary Sources of Vitamin D, 165

Table 7-5 Other Nutrients and Bone Health

at a Glance, 166-170

Table 7-6 Weight-Bearing Exercise for Kids

and Teens, 173

Table 7-7 Weight-Bearing Exercise for

Adults, 176

Table 7-8 Preventing Falls Among Seniors,

178

Figure 7-1 How To Use the Nutrition Facts

Panel on Food Labels for Calcium,

163

Figure 7-2 General Recommendations for

Physical Activity in Adults, 174

Figure 7-3 Examples of Strength Training Exercises, 175

Figure 7-4 Resources for Strength Training for

Older Adults, 176

Figure 7-5 Fall Risks to Elderly in the Home,

179

Chapter 8

Assessing the Risk of Bone Disease and Fracture

Table 8-1 Risk Factors for Hip Fracture

Among Elderly White Women, 195

Table 8-2 FRACTURE Index Questions and

Scoring, 197

Table 8-3 Techniques for Bone Mass Measurement, 203

Table 8-4 Currently Available Bone Biochemical Markers, 209

Figure 8-1 5-Year Hip Fracture Rates for

Women With T-Score of -2 Without

Previous Hip Fracture, by Age, 193

Figure 8-2 Clinical Risk Factors Independently

Predict Hip Fracture Risk, 196

Figure 8-3 Five-Year Risk of Hip Fracture by

Quintiles of FRACTURE Index,

197
380

A Report of the Surgeon General

Figure 8-4 Bone Mineral Density (BMD) Measurements at Spine and Hip, 200

Figure 8-5 Distribution of Bone Mineral Density in Healthy Women Aged 30-

40 Years, 201

Figure 8-6 Distribution of Bone Mineral Density in Women of Different Ages

and the Prevalence of Osteoporosis (Shaded Area), T-Score Below

-2.5=Osteoporosis, 205

Figure 8-7 T-Scores and Z-Scores, 207

Chapter 9

Prevention and Treatment for Those Who Have

Bone Diseases

Figure 9-1 The Osteoporosis Pyramid for Prevention and Treatment, 221

Chapter 10

Putting It All Together for the Busy Health Care

Professional

Table 10-1 Summary Recommendations for

Bone Health, 257

Table 10-2 Representative Disorders of the Pediatric Skeleton: Developmental Disorders of Bone and Cartilage, 261

Table 10-3 Calcium-Containing Foods by Calcium Content Per Serving With 100

mg, 263

Table 10-4 Risk Factors for Fracture, 271

Table 10-5 Scoring System for Osteoporosis Risk

Assessment Instrument (ORAI), 272

Figure 10-1 Assessment of Bone Health and

Management of Osteoporosis, 269

Figure 10-2 Osteoporosis Self-Assessment Tool

(OST) Chart, 273

Chapter 11

Systems-Based Approaches to Bone Health

Table 11-1 Health Systems Intervention for

Osteoporosis and Bone Health That

Can Be Provided at Different Organizational Levels, 283

Table 11-2 ACOVE-2 Quality Indicators for

the Management of Osteoporosis In

Vulnerable Elders, 295

Chapter 12

Population-Based Approaches To Promote Bone

Health

Table 12-1 Recommendations From the Task

Force on Community Preventative

Services, 2001—Use of Selected Interventions To Increase Physical

Activity (PA) Behaviors and Improve Physical Fitness, 314

Table 12-2 Recommendations From the Task

Force on Community Preventative

Services, 2000—Selected Population-Based Interventions To Reduce Tobacco Use and Exposure to

Secondhand Tobacco Smoke, 316

Figure 12-1 Powerful Bones. Powerful Girls. The

National Bone Health Campaign, 322

Figure 12-2 Weight Training Exercises Can

Improve Strength, Balance, and

Flexibility in Older Adults, 329
Index 381

Index

1,25 dihydroxy vitamin D see calcitriol

25-hydroxy vitamin D ................................................................ 53, 54, 117, 191, 223, 264

absorptiometry see dual x-ray absorptiometry

academic detailing ................................................................................................... 283, 289

academic institutions see bone health, promoting

acquired skeletal disorders

prevalence ......................................................................................................... 81-83

acromegaly ..........................................................................................................................47

Actonel see risedronate

adenoma ............................................................................................................. 48, 241, 243

Administration on Aging ............................................................................................ 9, 301

adolescents see also children and adolescents ................................................................258

sex hormone deficiency in ............................................................................ 48, 191

adrenal gland ....................................................................................................... 29, 30, 191

adults see young adults; middle age

adynamic bone disease.......................................................................................................54

Agency for Healthcare Research and Quality (AHRQ).......................... 9, 206, 210, 285

age-related osteoporosis ............................................................................................... 43-46

aging population ........................................................................................4, 6, 76-77, 82-83

aging see also older adults ................................................................................... 21, 29, 114

calcium and...........................................................................................................268

fall risk and ...........................................................................................................133

nutrition and.........................................................................................................268

osteoporosis and ............................................................................................... 43-46

physical activity and ............................................................ 129-130, 174-176, 270

Albright, Fuller ....................................................................................................... 229, 232

alcohol and bone health .......................................................................... 139, 140, 179, 266

alendronate ....................................................................................................... 226-227, 234

alkaline phosphatase................................................................................................ 190, 191

allergic disorders.................................................................................................................49

Alzheimer’s disease ..........................................................................................................133

amenorrhea see also athletic amenorrhea ...................................... 114, 136, 190, 191, 260

American Academy of Orthopedic Surgeons ...............................................................177

American Academy of Pediatrics (AAP) .......................................................................117

American Association of Clinical Endocrinology ..........................................................285
382 Index

American College of Sports Medicine (ACSM) ............................................................171

American Geriatrics Society ...........................................................................................177

American Society for Bone and Mineral Research (ASBMR) .....................................337

anabolic therapy see also teriperatide ............................................... 13, 226, 234-236, 274

androgen insensitivity ........................................................................................................47

anorexia nervosa .............................................................. 43, 47, 48, 50, 136, 190, 191, 260

antacids and bone disease ................................................................................... 53, 54, 264

anticonvulsant medications ................................................................. 51, 52, 138-139, 266

antiresorptive therapy see also hormone therapy (HT).................... 13, 25, 50, 210, 226,

226-234, 235-236, 274

as treatment for hyperparathyroidism ...............................................................242

bisphosphonates........................................................................................... 226-229

calcitonin.......................................................................................... 26, 28, 226, 233

combination ...................................................................................233-234, 235-236

selective estrogen receptor modulators (SERMs)...................... 219, 226, 232-233

arthritis ......................................................................................................... 19, 30, 132, 191

aseptic necrosis ............................................................................................................. 50-51

prevalence ...............................................................................................................81

Assessing Care of Vulnerable Elders (ACOVE) .................................................. 287, 294

assessment tools see risk assessment

athletic amenorrhea ............................................................. 47, 48, 124, 136, 190, 191, 260

autoimmune disorders .......................................................................................................49

avascular necrosis ......................................................................................................... 50-51

back braces........................................................................................................................275

behavior change

barriers to ...................................................................................................... 284-287

need for research on.............................................................................................349

benchmarks of physician performance.................................................................. 283, 288

bisphosphonates see also drug therapy for osteoporosis, antiresorptive therapy ..... 219,

226-229, 243

alendronate ........................................................................................... 226-227, 234

as treatment for osteogenesis imperfecta ............................................................243

as treatment for Paget’s disease of bone ...................................................... 55, 242

etidronate ..............................................................................................................228

guidelines for intake ..................................................................................... 228-229

ibandronate...........................................................................................................228

risedronate ........................................................................................... 226, 228, 234

Blacks see minority groups

blue sclera (manifestation of osteogenesis imperfecta) ....................................................57

body weight .............................................................................. 122, 130-131, 179, 190-191
Index 383

bone

architecture ....................................................................................................... 17,19

biology of .......................................................................................................... 17-35

changes in ............................................................................................. 18, 19, 20-25

composition ............................................................................................................18

formation .......................................................................................................... 20-25

genetic variation in ........................................................................................... 25-26

importance of.................................................................................................... 17-18

life stages....................................................................................................... 113-114

mass................................................................................................................... 18-19

reservoir function ............................................................................................ 17, 18

resorption.................................................................................................... 20-25, 44

structural function .................................................................................................17

bone accrual ......................................................................................................................136

Bone Coalition, The .........................................................................................................337

bone density testing see bone mineral density (BMD) testing

bone disease

burden of ............................................................................................ 4, 89-103, 187

causes ................................................................................................................ 29-30

costs............................................................................................................... 4, 93-95

disability and .............................................................................................. 93, 96-98

emotional impact of see also depression ....................................................... 98-100

family history of as risk factor .................................................................... 190, 199

financial impact of ................................................................................ 6, 93-95, 101

fractures and ..................................................................................................... 74-75

genetic abnormalities and ......................................................................................29

glucocorticoids and ....................................................................... 24, 30, 43, 51, 52

hormonal disorders and .........................................................................................30

identifying individuals at risk.............................................................. 187, 188-198

impact on functional status ............................................................................. 96-98

impact on individual ...................................................................................... 95-101

impact on quality of life ............................................................................... 100-101

impact on society ............................................................................................. 89-95

in children and adolescents ......................................................................... 259-261

lack of awareness ..................................................................................................4, 7

misperception of .......................................................................................................4

morbidity and................................................................................................... 91-93

mortality and ......................................................................................... 89-91, 95-96

nutrition and...........................................................................................................30

oral health and ........................................................................................................59

prevalence ..................................................................................................... 5, 69-83
384 Index

prevention..................................................................................................... 220-226

recommendations for screenings................................................................. 198-199

risk assessment...............................................................................266-267, 270-272

risk factors......................................................................................... 3, 188-192, 271

secondary factors in ......................................................................... 3, 188, 224-225

treatment and therapy ................................................................................. 219-244

underdiagnosis of ............................................................................................ 7, 187

bone health ................................................................................................................... 25-29

advances........................................................................................................ 3-4, 303

awareness..............................................................................................................4, 7

determinants of.................................................................................. 25-26, 111-142

elements ..................................................................................................................25

environmental threats to ............................................................................. 139, 140

general health linked to................................................................................ 349-350

genetic factors .......................................................................................................111

importance ................................................................................................................4

in middle-aged and older adults.......................................................... 113, 119-120

in young adults..................................................................................... 114, 118-119

maintaining see lifestyle measures

menstruation and ................................................................................ 136, 179, 260

need for national action plan ....................................................................... 347-348

nutrition and..................................................................................115-122, 159-171

population-based approach to.............................................................................282

pregnancy and lactation and ......................................................... 21, 117, 135-136

promoting ........................................................................ 8-9, 12, 159-180, 347-355

reproductive factors and .............................................................................. 135-137

status in America ....................................................................................................12

systems-based approach to .......................................................................... 281-304

bone health, promoting .............................................................. 8-9, 12, 159-180, 347-355

academic institutions’ role ........................................................... 283, 299, 353-354

clinicians’ role ....................................................................................... 283, 284-288

community-based organizations’ role .................................................................352

for children and adolescents ........................................................................ 256-259

government role ................................................................... 283, 296-298, 352-353

health care professionals’ role.............................................................. 255-275, 351

health care purchasers’ role ......................................................... 283, 299-300, 352

health plans and insurers’ role ............................................................ 283, 291-296

health systems’ role ...................................................................................... 351-352

hospitals and care facilities’ role .......................................................... 283, 290-291

importance ............................................................................................................347

individual and family role ........................................................................... 350-351
Index 385

industry role ........................................................................................ 283, 300, 354

medical groups’ role ............................................................................. 283, 288-290

population-based approach ................................................................... 13, 311-388

professional associations’ role ..................................................................... 283, 353

public health role ................................................................. 283, 296-298, 352-353

systems-based approach ........................................................................ 13, 281-304

voluntary health organizations’ role ........................................... 283, 298-299, 353

bone loss..............................................................................................................................46

causes ......................................................................................................................44

estimated rate of .....................................................................................................44

bone mass..........................................................................................................................112

ethnic and gender differences in .........................................................................258

physical activity and ................................................................................... 125, 127

measurement ........................................................................................................203

bone matrix .........................................................................................................................24

bone mineral density (BMD) testing .......................................................... 7, 198-208, 219

and consideration of secondary causes...............................................................188

and other bone diseases .......................................................................................206

complements to ............................................................................................ 208-211

for men ..................................................................................................................199

in adults ........................................................................................................ 266-268

gender and ethnic considerations in interpretation of results...........................206

in children and adolescents .................................................................................261

interpretation of results........................................................................ 202-206, 267

interpretation of results in older adults ..............................................................272

limitations .................................................................................................... 192, 208

methods ................................................................................................ 200-202, 203

need for .................................................................................................................198

recommendations ......................................... 192, 198-199, 254, 257, 266, 269-272

time between screenings ............................................................................. 267, 274

uses of.................................................................................................... 200, 206-208

bone morphogenetic protein .............................................................................................33

bone strength

determinants of................................................................................................ 19, 30

bone tumors see also cancer, Ewings sarcoma, osteosarcoma .......................... 57-59, 102

burden of ..............................................................................................................103

mortality and ..........................................................................................................96

osteolytic lesions and osteoblastic lesions .............................................................59

primary and metastatic .................................................................................... 57-59

treatment....................................................................................................... 242-243

bone turnover see resorption, markers of bone turnover
386 Index

BoneHealth/BodyHealth (BH/BH) ................................................................................330

boron ...................................................................................................................... 166, 265

breast cancer .............................................................................................................. 59, 243

prevalence of associated metastatic bone tumors.................................................82

breastfeeding and vitamin D ...........................................................................................259

British Geriatrics Society.................................................................................................177

brittle bone disease see osteogenesis imperfecta

bulimia ..............................................................................................................................260

Burkitt’s lymphoma ...........................................................................................................59

caffeine ..................................................................................................... 120, 169, 171, 265

calcimimetic agents...........................................................................................................242

calcitonin ...................................................................................................... 26, 28, 226, 233

calcitriol .................................................................................................................. 26, 28, 34

as treatment for renal osteodystrophy................................................................242

calcium ....................................................... 3, 6-7, 12, 17, 26, 29-30, 48, 115-120, 159-164

absorption ...................................................................................................... 49, 117

as component of bone ............................................................................................18

deficiency..............................................................................................................190

importance of................................................................................................ 115-120

in antacids .............................................................................................................264

lactose intolerance and ................................................................................ 162, 164

physical activity and ........................................................................... 118, 119, 124

premature infants and..........................................................................................257

recommended intake in adolescents .................................................. 160, 257, 258

recommended intake in adults ................................................... 160, 257, 262, 264

recommended intake in children ....................................................... 160, 257, 258

recommended intake in older adults ......................................... 160, 222, 257, 268

regulation .......................................................................................................... 26-28

role in frailty stage ................................................................................................119

role in growth stage..............................................................................................118

role in maintenance stage ............................................................................ 118-119

self-assessment tools for intake ............................................................................163

sources ..........................................................................160-161, 162, 258, 262, 263

sources for older adults ........................................................................................268

supplementation .................................................................. 116, 120, 163, 219, 262

calcium-regulating hormones see parathyroid hormone, calcitriol, calcitonin

cancer see also bone tumors, malignancy .........................................................................48

breast.............................................................................................................. 59, 243

Burkitt’s lymphoma ...............................................................................................59

in children and adolescents .................................................................................260

leukemia ........................................................................................................... 47, 59
Index 387

lymphoma........................................................................................................ 47, 59

multiple myeloma ............................................................................ 47, 59, 242-243

myeloma ...............................................................................................................236

non-Hodgkins’ lymphoma ....................................................................................59

prostate .......................................................................................................... 59, 243

carbonated beverages .......................................................................................................265

causes of bone disease .................................................................................................. 29-30

bacterial infections .................................................................................................30

genetic abnormalities .............................................................................................29

glucocorticoids........................................................................................................30

hormonal disorders ................................................................................................30

hypogonadism ........................................................................................................30

inflammation...........................................................................................................30

nutritional deficiencies..................................................................................... 29-30

vitamin D deficiency..............................................................................................30

celiac disease .......................................................................................................................49

cement line ..........................................................................................................................24

Centers for Disease Control and Prevention (CDC) ................................. 9, 177-179, 258

Centers for Medicare and Medicaid Services (CMS) ........................................................9

cerebral palsy ......................................................................................................................50

child abuse, similarity to symptoms of osteogenesis imperfecta............................ 57, 260

children and adolescents.......................................................................................... 256-261

bone diseases in ............................................................................................ 260-261

bone growth in ...................................................................................... 20, 113, 118

recommended calcium intake in ................................................. 118, 160, 257-258

recommended vitamin D intake in .................................................... 118, 160, 257

causes of osteoporosis in ........................................................................................43

focus on bone health in........................................................................................256

fractures in ................................................................................................... 191, 260

nutrition in.................................................................................................... 256-259

osteogenesis imperfecta in .....................................................................................57

osteoporosis in ........................................................................................................43

physical activity in ................................ 122-124, 126-127, 128, 172-173, 257, 259

rickets in ............................................................................................................ 53-54

with high risk for bone disease.................................................................... 259-261

cholesterol

as similar problem to osteoporosis ......................................................................319

chronic bronchitis ..............................................................................................................51

cirrhosis ...............................................................................................................................49

clinical knowledge see also research

lack of application of see also knowledge-practice gap ..........................................7
388 Index

range of ...................................................................................................................11

Cochrane Collaboration ...................................................................................................129

collagen ........................................................................................................................ 18, 24

Colles’ fractures ................................................................................................................239

combination antiresorptive therapy ................................................................ 226, 233-234

combination antiresorptive/anabolic therapy ................................................. 226, 235-236

community-based organizations see bone health, promoting

Community Guide see Guide To Community Preventive Services

Congress................................................................................................................................9

contraceptives and bone health ....................................................................... 135, 136-137

copper ...................................................................................................... 121, 166, 171, 265

cortical bone........................................................................................................................19

corticosteroids........................................................................................................... 137-138

cortisol ..................................................................................................................... 26,29, 50

Crohn’s disease ...................................................................................................................49

curriculum development ........................................................................ 297, 299, 353, 354

Cushing’s syndrome ............................................................................................. 30, 47, 48

screening guidelines .............................................................................................224

cyclosporine A ..................................................................................................... 51, 52, 266

cystic fibrosis ............................................................................................................... 47, 48

cystic lesions .......................................................................................................................30

cytokines .............................................................................................................................48

Decade of the Bone and Joint..............................................................................................4

Department of Agriculture..................................................................................................9

depression ...................................................................................................... 47, 50, 97, 100

developmental disabilities ..................................................................................................50

developmental skeletal disorders ................................................................................. 55-57

prevalence ...............................................................................................................81

diabetes ........................................................................................................................ 47, 48

diagnosis of bone disease see also risk assessment, bone mineral density (BMD) testing

advances in ...............................................................................................................3

inadequacies in ................................................................................................ 7, 187

Dietary Approaches To Stop Hypertension (DASH) ................................. 121-122, 159

Dietary Guidelines for Americans ..................................................................................159

differentiation .....................................................................................................................21

direct-to-consumer advertising............................................................................... 317, 319

disease management programs ........................................................ 283, 289-290, 300, 354

doctors see health care professionals

drug therapy for osteoporosis see also treatment and therapy ............. 226-237, 272, 274

anabolic therapy ............................................................................. 13, 234-236, 274

antiresorptive therapy................................................13, 25, 50, 210, 226-234, 274
Index 389

combination antiresorptive therapy ................................................... 226, 233-234

combination antiresorptive/anabolic therapy .................................... 226, 235-236

drugs see medications

dual x-ray absorptiometry (DXA) .................................................. 125, 200-202, 203, 267

use for monitoring ................................................................................ 200, 206-208

Dubbo Osteoporosis Epidemiology Study ...................................................................193

DXA see dual x-ray absorptiometry

eating disorders see anorexia nervosa, bulimia

Elder Floridians Foundation .................................................................................. 312, 335

elderly see older adults

emergency medical workers ............................................................................................351

emphysema .................................................................................................................. 47, 51

endometriosis......................................................................................................................53

endosteal surface ................................................................................................................21

epilepsy ................................................................................................................ 47, 50, 136

estrogen see also sex hormones; hormone therapy (HT)................................. 26, 28, 274

deficiency......................................................................................................... 44, 48

therapeutic use of ................................................................................. 226, 229-231

ethnic groups see also minority groups, underserved populations

variation of fracture frequency across ............................................................ 72-75

variation of osteoporosis frequency across ..................................................... 79-81

etidronate ....................................................................................................................... . 228

European Union Osteoporosis Consultation Panel ......................................................287

evidence-based practices ......................................................................................... 284, 285

Evista see raloxifene

Ewing’s sarcoma .................................................................................................................59

exercises beneficial to bone health see also physical activity .............................. 124, 223

balance exercises ................................................................. 122, 130, 172, 174, 177

impact exercises ...........................................124, 126, 128, 172, 173, 174, 223, 265

mobility exercises .................................................................................................130

strength training ................................. 124, 171, 172, 173, 174, 175, 176, 328, 329

weight bearing ............................................................. 122, 171, 172, 173, 174, 175

fall prevention ........................................................ 3, 132-135, 177-179, 223-224, 270, 275

environmental hazards......................................................................... 133, 177-179

evidence base ................................................................................................ 133-135

importance of........................................................................................................132

measures ........................................................................................177-179, 223-224

occupational therapists’ role ....................................................................... 270, 275

physical activity and ................................................................................... 130, 133

physical therapists’ role .............................................................................. 270, 275

recommendations ........................................................................................ 177, 178
390 Index

fall risk and vitamin D......................................................................................................119

falls and bone health, evidence base ....................................................................... 133-135

falls............................................................................................................................. 131-135

causes ....................................................................................................................132

environmental risk factors ................................................................... 133, 177-179

evidence base ................................................................................................ 133-135

necessity for inclusion as a factor in BMD assessment screening ............ 196-198

prevalence .............................................................................................................132

prevention see fall prevention

risk factors...................................................... 132-133, 196-198, 223-224, 270, 275

fiber ...................................................................................................................................169

fibrous dysplasia .......................................................................................................... 24, 57

fluoride ..................................................................................................................... 121, 166

followup care

importance of........................................................................................................274

Food and Drug Administration (FDA)..............................................................................9

Food and Nutrition Board (FNB) ..................................................................................159

formation markers see markers of bone turnover

formation of bone ......................................................................................................... 20-25

Fosamax see alendronate

FRACTURE index................................................................................................. 195, 197

fractures see also hip fractures; wrist fractures; spine fractures ......................... 30, 31, 42

bone disease and .............................................................................................. 74-75

consequences of ..................................................................................... 5, 91-93, 97

costs of .................................................................................................. 5, 93-95, 102

followup for ..........................................................................................................274

history of as risk factor for bone disease............................................ 190, 195, 199

in children and adolescents ........................................................................ 191, 260

need for change in paradigm of prevention and treatment ..............................348

physical activity and .................................................................................... 124-125

prevalence ........................................................................... 5, 69-73, 74, 76-81, 193

prevention.................................................................................................... 270, 274

rehabilitation........................................................................................... 13, 239-241

risk factors.................................................................................... 195, 198, 270, 271

treatment................................................................................................. 13, 237-239

variations in prevalence across ethnic groups ................................................ 72-75

gastrectomy.................................................................................................................. 49, 53

gastric bypass surgery........................................................................................................49

gastrointestinal diseases and bone disease ............................................................... 49, 191

genetic abnormalities and bone disease ............................................................................29

genetic factors of bone health ..........................................................................................111
Index 391

glucocorticoid-induced osteoporosis (GIO) ........................................................ 24, 51, 52

glucocorticoids..................................................................... 29, 30, 43, 49, 51, 52, 191, 266

gonadotrophin-releasing hormone (GnRH) agonists ....................................... 51, 53, 138

government see bone health, promoting

growth hormones see also insulin-like growth factor ......................................... 25, 26, 29

guideline development .................................................................................... 283, 299, 353

Guide To Community Preventive Services ...................................................................313

gynecologists see health care professionals

health care

fragmented nature of ...........................................................................................281

problems with current system ............................................................................281

health care professionals see also bone health, promoting ............ 6, 12-13, 187, 255-275

need for improvement in prevention and identification .......................................7

health care providers see also bone health, promoting

necessity for long-term coverage.........................................................................292

health education .............................................................................................. 283, 299, 354

Health Plan Employer Data and Information Set (HEDIS) ............................... 293-294

health plans and insurers see also Medicare .......................................................................8

coverage ................................................................................................... 8, 101, 283

Health Resources and Services Administration (HRSA) .................................................9

Healthy People 2010........................................................................... 5, 9, 10, 71, 122, 130

height loss ............................................................................ 43, 96, 140, 190, 194, 195, 271

hematological disorders see also leukemia, multiple myeloma .......................................51

heparin ..............................................................................................................................266

hepatitis...............................................................................................................................49

hip fractures see also fractures..................................................................................... 97-99

mortality and ..........................................................................................................91

rehabilitation.........................................................................................................239

treatment....................................................................................................... 237-238

hip protectors.................................................................................................... 134-135, 224

Hispanic see minority groups

HIV .....................................................................................................................................49

hormonal disorders ............................................................................................................30

hormone therapy (HT) see also estrogen ................................... 13, 28, 229-233, 234, 243

background...........................................................................................................229

evidence base ................................................................................................ 229-231

future of ........................................................................................................ 231-233

hormones see regulatory hormones, sex hormones, growth hormone, thyroid hormone

hydroxyapatite ...................................................................................................................18

hypercalcemia ................................................................................................... 191-192, 236

hypercalcemia of malignancy ............................................................................................21
392 Index

hyperparathyroidism see also primary hyperparathyroidism .................. 24, 30, 47, 190,

191-192, 199, 223, 266

hypocalcemia ....................................................................................................................191

hypogonadism ........................................................................................................... 30, 266

hypothyroidism ................................................................................................................267

hysterectomy and bone health ........................................................................................137

ibandronate .......................................................................................................................228

idiopathic hypercalciuria ............................................................................................ 47, 48

idiopathic primary osteoporosis ........................................................................................43

causes of ..................................................................................................................43

immobilization ............................................................................................. 47, 51, 172, 191

immuno-suppressants see medications, not bone health-related

infancy ...................................................................................................................... 256-257

calcium intake in .................................................................................. 118, 256-257

inflammation .......................................................................................................................49

Institute of Medicine (IOM)........................................... 120, 159, 160, 164, 265, 296-297

insulin .................................................................................................................................29

Insulin-like growth factor-1 (IGF-1) see also growth hormone ............................... 26, 29

insurance see health plans and insurers

integrin inhibitors.............................................................................................................236

International Osteoporosis Foundation..........................................................................211

International Society for Clinical Densitometry (ISCD) ..............................................206

iron ................................................................................................................... 121, 166, 171

isoflavones................................................................................................................ 166, 265

joints ....................................................................................................................................19

juvenile osteoporosis ..........................................................................................................43

Kaiser Permanente Northwest ........................................................................................290

Kallman’s syndrome ..........................................................................................................48

kidney disease see renal osteodystrophy

Klinefelter’s syndrome ................................................................................................ 47, 48

knowledge-practice gap ...................................................................................... 6, 7, 8, 285

kyphoplasty ............................................................................................................. 238, 293

kyphosis ................................................................................... 43, 45, 56, 71, 100, 114, 275

lactation see pregnancy and lactation

lactose intolerance and calcium intake ................................................... 115, 116, 161, 164

lead ........................................................................................................................... 139, 140

leptin ...................................................................................................................................30

leukemia ..............................................................................................................................47

lifestyle measures...................................................................... 111, 159-180, 222-224, 351

lining cells ...........................................................................................................................21

Lipoprotein Receptor Related Protein 5.................................................................... 33, 34
Index 393

lipoxygenase .......................................................................................................................33

liver disease .........................................................................................................................49

Living Healthy ................................................................................................. 323-325, 335

load bearing see mechanical loading

low bone mass see osteopenia

lupus .......................................................................................................................... 47, 49

lymphoma ...........................................................................................................................47

macrophage colony stimulating factor (M-CSF) ...................................................... 32, 33

magnesium ....................................................................... 120-121, 160, 165, 166, 171, 265

major depression see depression

malabsorption ........................................................................................ 49, 50, 53, 191, 266

malignancy.............................................................................................................. 51, 57-59

manganese........................................................................................................ 121, 167, 171

markers of bone turnover ................................................................................ 209-211, 274

to estimate fracture risk........................................................................................210

to estimate rate of bone loss .................................................................................210

to monitor effectiveness of therapy ........................................................... 211, 274

to select individuals for therapy .................................................................. 210-211

types.............................................................................................................. 209-210

uses ................................................................................................................ 210-211

marrow fibrosis...................................................................................................................59

mechanical loading ...........................................................................................................122

and bone strength ..................................................................................................18

medical conditions that influence bone health................... 47-51, 137-140, 179, 190, 267

Medicare ................................................................................................94-95, 101, 291-293

coverage limitations..............................................................................................293

coverage of medications .......................................................................................293

coverage of testing ................................................................................................293

eligibility for testing .............................................................................................292

inadequacies in coverage .....................................................................................291

role as leader for private insurers ........................................................................292

medications, bone health-related see drug therapy for osteoporosis

medications, not bone health-related ..................................................... 179, 190, 191, 266

bone loss and .......................................................................... 51, 137-139, 261, 266

fall risk and ........................................................................................... 132-133, 274

interactions with bone density therapy..............................................................274

role of health care professionals in monitoring ..................................................274

men, osteoporosis in ......................................................................................... 8, 44-46, 189

menopause and bone health ....................................................................................... 28, 31

menstruation and bone health see also amenorrhea ..................................... 136, 179, 260

meta-analysis.....................................................................................................................225
394 Index

metabolic bone disease .....................................................................................................261

prevalence ...............................................................................................................81

metastatic bone tumors see also bone tumors ............................................................ 57-59

treatment....................................................................................................... 242-243

methotrexate ........................................................................................................ 51, 52, 266

Michigan Osteoporosis Program .................................................................... 325-327, 335

micro-architecture ..............................................................................................................32

micro-damage .....................................................................................................................25

middle age .........................................................................................................................257

bone loss and frailty in................................................................................. 119-120

nutrition in.................................................................................................... 261-265

Milk Matters Campaign ........................................................................... 160, 333-334, 335

minerals

regulation of...................................................................................................... 25-28

minority groups see also ethnic groups, underserved populations

disparities in access to care ...................................................................... 8, 301-302

disparities in knowledge ..........................................................................................8

disparities in quality of care ........................................................................... 8, 302

fracture prevalence in .................................................................................. 5, 72-75

modeling ....................................................................................................................... 20-22

monitoring and surveillance activities.................................................................... 283, 298

monitoring therapy .................................................................................. 206-208, 211, 274

monoclonal gammopathy ..................................................................................................59

multiple myeloma ......................................................................................... 47, 59, 242-243

mortality and ..........................................................................................................96

prevalence ...............................................................................................................82

multiple sclerosis ......................................................................................................... 47, 50

muscle

activity and bone function ....................................................................................19

muscular dystrophy ...........................................................................................................47

musculoskeletal system ......................................................................................................19

myelofibrosis.......................................................................................................................59

national action plan for bone health ....................................................................... 347-355

building of science base .......................................................................................349

change in paradigm of care for fractures ............................................................348

importance of stakeholder partnerships .............................................................354

increase in awareness of bone diseases ...............................................................348

integration of health messages and programs ............................................ 349-350

National Asian Women’s Health Organization (NAWHO) see Living Healthy

National Bone Health Campaign ............................................................ 258, 321-323, 335

National Cholesterol Education Program (NCEP) ............................................... 318-319
Index 395

National Committee for Quality Assurance (NCQA) .......................................... 293-294

National Guideline Clearinghouse (NGC) ....................................................................285

National Health and Nutrition Examination Survey (NHANES) ... 10, 77, 78, 80, 258

National Hospital Discharge Survey ...............................................................................10

National Institute of Aging (NIA) ......................................................................... 266, 270

National Institute of Child Health and Human Development (NICHD)

see also Milk Matters Campaign............................................................................. 333, 334

National Institutes of Health Osteoporosis and Related Bone

Diseases ~National Resource Center (NIH ORBD~NRC) ...................... 270, 275, 338

National Osteoporosis Foundation (NOF) .................. 192, 193, 194, 199, 206, 211, 271,

285, 302, 337

checklist for risk .......................................................................................... 192, 199

nerve and muscle disease ...................................................................................................50

neurologic disorders ........................................................................................................... 49

New Jersey Department of Health and Senior Services see Project Healthy Bones

non-Hodgkins’ lymphoma ................................................................................................59

North Carolina Osteoporosis Support Group............................................... 329, 330-331

nurses see health care professionals

nutrition see also calcium; vitamin D; protein ...................... 12, 29-30, 115-122, 159-171

deficiency and bone disease ............................................................................ 29-30

in children and adolescents ................................................................. 160, 256-259

in older adults .............................................................................................. 160, 268

in young and middle-aged adults ....................................................... 160, 261-265

recommended nutrients....................................................................... 165-168, 171

OB/GYNs see health care professionals

occupational therapists............................................................................................ 270, 275

Office of Disease Prevention and Health Promotion (ODPHP) .....................................9

Office on Minority Health (OMH) ....................................................................................9

Office on Women’s Health..................................................................................................9

older adults see also aging ........................................................................ 254, 257, 268-275

bone loss and frailty in................................................................. 112, 119-120, 129

nutrition in.................................................................................................... 160,268

physical activity in ........................................................................129-130, 174-176

specialty referrals for............................................................................................275

strength training .......................................................................................... 328, 329

oncogenic osteomalacia ......................................................................................................54

oophorectomy and bone health ............................................................................. 135, 137

oral health and bone disease ..............................................................................................59

orthopedists see also health care professionals ...............................................................351

osteitis fibrosa cystica .........................................................................................................48

osteoblastic lesions..............................................................................................................59
396 Index

osteoblasts ..................................................................................................................... 21-24

formation ................................................................................................................21

osteochondroma .................................................................................................................59

osteoclasts................................................................................................................ 21-25, 34

formation ......................................................................................................... 24, 34

osteocytes......................................................................................................... 19, 23, 24, 25

osteogenesis imperfecta (OI) ...................................... 19, 23, 29, 47, 55-57, 102, 260, 261

burden of ....................................................................................................... 90, 103

causes ............................................................................................................... 29, 56

child abuse symptoms and ........................................................................... 57, 260

need for awareness of.............................................................................................57

prevalence ...............................................................................................................80

treatment...............................................................................................................243

types ................................................................................................................. 56, 58

Osteogenesis Imperfecta Foundation (OIF) ..................................................................337

osteolytic lesions ........................................................................................................ 59, 243

osteomalacia ........................................................... 12, 19, 30, 49, 53-54, 80, 102, 206, 223

causes ............................................................................................................... 50, 53

osteomyelitis .......................................................................................................................30

osteonecrosis ................................................................................................................. 50-51

osteopenia ........................................................................................................ 5, 56, 77, 204

prevalence .................................................................................................... 6, 76, 79

osteopetrosis................................................................................................................. 29, 57

burden of ..............................................................................................................103

prevalence ...............................................................................................................81

Osteoporosis Risk Assessment Instrument (ORAI) ............................. 192, 270, 272, 285

Osteoporosis Self-Assessment Tool (OST) ................................... 193, 270-271, 273, 285

osteoporosis see also age-related osteoporosis; prevention .................5-6, 41-53, 204, 205

burden of ................................................................................................. 90, 98, 187

causes .......................................................................................................... 30-32, 48

classical case ............................................................................................................41

definition.................................................................................................. 30, 41, 204

development of ................................................................................................. 31-32

drug therapy for ................................................................................ 24-25, 226-237

fractures and ..................................................................................................... 74-75

glucocorticoid-induced ........................................................................ 24, 43, 51-52

idiopathic primary .................................................................................................43

perception of.............................................................................................................4

prevalence ......................................................................................... 5, 6, 75-81, 205

primary ....................................................................................................... 43-45, 46

secondary.......................................................................................................... 46-53
Index 397

underdiagnosis of .............................................................................................. 7, 77

osteoprotegerin .................................................................................................... 33, 34, 243

osteosarcoma ........................................................................................................ 55, 59, 102

prevalence ......................................................................................................... 81-82

overweight and bone health ............................................................................................131

oxalates..............................................................................................................................169

Paget Foundation for Paget’s Disease of Bone and Related Disorders, The (TPF) ...337

Paget’s disease of bone .........................................................4, 7, 12, 24, 30, 54-55, 56, 102

causes .......................................................................................................... 30-31, 55

burden of ..............................................................................................................102

prevalence ...............................................................................................................81

treatment...................................................................................................... 242, 243

pamidronate ......................................................................................................................236

parathyroid cancer .............................................................................................................48

parathyroid hormone (PTH) ............................................................... 26, 34, 44, 192, 234

therapeutic use of ......................................................................................... 234-236

parathyroid hormone related protein (PTHrP) ............................................... 26, 59, 237

parathyroidectomy................................................................................................... 241-242

patient education materials ............................................................................. 266, 270, 275

patient registries ....................................................................................... 283, 288-289, 299

pay-for-performance initiatives .............................................................................. 283, 296

pediatricians see health care professionals

performance assessments ................................................................................. 283, 293-294

periodontal disease .............................................................................................................30

periosteal surface ................................................................................................................21

peripheral DXA (pDXA) ................................................................................ 201-202, 203

peripheral quantitative computed tomography (pQCT) ..................................... 202, 203

pharmacologic therapy see drug therapy for osteoporosis

pharmacists see health professionals

phosphate deficiency .........................................................................................................53

phosphorus .......................................... 17, 26, 120-121, 160, 165, 167, 169, 171, 259, 265

as component of bone ............................................................................................18

danger of excess .................................................................................. 121, 169, 171

sources ..................................................................................................................171

physical activity see also exercises beneficial to bone health .3, 6, 7, 12, 19, 20, 122-130,

171-177, 223

bone mass and ......................................................................................................125

building sustainability in ............................................................................. 265-266

calcium and.................................................................................................. 118, 119

challenges in studying impact on bone health ...................................................125

evidence base ................................................................................................ 124-130
398 Index

falls and fall prevention........................................................................................130

for sedentary patients .................................................................................. 265-266

fractures and ................................................................................................. 124-125

in adults ......................................................... 123, 127-129, 173-174, 175, 265-266

in children and adolescents .......................... 122-124, 126-127, 128, 172-173, 259

in older adults ....................................................................... 129-130, 174-176, 270

in those with fragility fractures ...........................................................................177

physical therapists’ role in ...................................................................................270

population-based interventions for............................................................. 313-315

recommendations ........................................................ 172, 223, 257, 259, 265, 270

resources ...............................................................................................................328

weight and ............................................................................................................122

physical therapists ................................................................................................... 270, 275

physician assistants see health care professionals

Plan, Do, Study, Act (PDSA) cycle ...............................................................................288

policymaking ................................................................................................... 283, 298, 353

poliomyelitis........................................................................................................................50

population-based interventions ......................................................................... 11, 311-338

appropriacy to bone health .................................................................................311

communication tools............................................................................ 317, 319-320

cultural competence in......................................................................... 323-325, 335

definition...............................................................................................................311

evidence base ........................................................................................................313

factors in successful.............................................................................. 334-335, 337

health care systems and .......................................................................................335

in combination......................................................................................................311

policies as ..............................................................................................................335

program examples ........................................................................................ 320-334

systematic reviews.................................................................................................... 313-317

factors in successfulpopulation-based risk stratification................................................282

postmenopausal osteoporosis see primary osteoporosis

potassium ................................................................................................................. 121, 167

pregnancy and lactation ....................................................................................................21

breastfeeding and vitamin D ...............................................................................259

bone health during............................................................................... 117, 135-136

calcium intake during .................................................................................. 159-160

recommended nutrients during ..........................................................................266

premature infants and calcium ........................................................................................257

President’s Council on Physical Fitness and Sports (PCPFS) .........................................9

prevention see also treatment and therapy; bone health, promoting ....................... 3, 6-7

advances in ...............................................................................................................3
Index 399

as treatment ..........................................................................................................220

in older people ..........................................................................................................6

inadequacy of ...........................................................................................................7

primary ......................................................................................................... 220-224

pyramid approach to ................................................................................... 221-226

secondary.............................................................................. 188, 220, 221, 224-225

tertiary .......................................................................................... 220, 221, 226-244

primary bone tumors ................................................................................................... 57-59

primary care providers see also health care professionals .................................... 255, 351

primary hyperparathyroidism ................................................................................... 48, 81

burden of ....................................................................................................... 96, 102

treatment....................................................................................................... 241-243

primary osteoporosis ................................................................................................... 42, 43

primary prevention .................................................................................................. 220-224

product development .............................................................................................. 300, 354

professional associations see bone health, promoting

professional education...............................................13, 283, 286, 289, 297, 299, 353, 354

progesterone see also sex hormones................................................................................229

Project Healthy Bones ..................................................................................... 327-329, 335

Project Osteoporosis ........................................................................................................312

prostate cancer ........................................................................................................... 59, 243

prevalence of associated metastatic bone tumors.................................................82

protein ...................................................................................................... 121, 259, 167, 170

as component of bone ............................................................................................18

recommended intake............................................................................................264

role in healing fractures .............................................................................. 264, 268

sources .......................................................................................................... 264-265

psychiatric disorders see also anorexia nervosa, major depression.................................50

puberty see children and adolescents

public awareness campaigns............................. 283, 284-285, 296-297, 298-299, 352, 353

public health see bone health, promoting

pulmonary disease..............................................................................................................51

purchasing power............................................................................................. 299-300, 352

pyramid approach to prevention ...................................................................... 13, 221-226

quality improvement initiatives....................................................................... 288, 294-296

quality of life ....................................................................................................... 12, 100-107

quantitative computed tomography (QCT) ................................................. 202, 203, 208

quantitative ultrasounds (QUS)............................................................................. 202, 203

radiogrammetry....................................................................................................... 202, 203

radiographic absorptiometry (RA) ........................................................................ 202, 203

raloxifene .................................................................................................................. 226, 232
400 Index

receptor activator of nuclear factor kappa B ligand (RANKL) ............................... 33, 34

“red flags” see also risk assessment .................................................................. 12, 190-192

Regional Health Administrators .........................................................................................9

regulatory hormones see also parathyroid hormone, calcitriol, calcitonin, sex hormones

growth hormones, thyroid hormone, cortisol .......................................... 17, 25-29

and mechanical loading .........................................................................................26

rehabilitation of fractures......................................................................................... 239-241

reimbursement policies see pay-for-performance initiatives

reminder systems .................................................................................................... 283, 286

remodeling .................................................................................................................... 20-25

activation phase ......................................................................................................23

as damage repair ......................................................................................... 21, 24-25

as lifelong process ...................................................................................................21

reversal phase .................................................................................................. 23, 24

renal osteodystrophy ......................................................................... 4, 12, 54, 81, 102-103

treatment...................................................................................................... 242, 243

reproductive factors and bone health see also menstruation and bone health,

amenorrhea, pregnancy and lactation, oophorectomy .......................................... 135-137

evidence base ................................................................................................ 135-137

research ....................................................................................................... 3-4, 11, 353, 354

lack of application see knowledge-practice gap

design issues .........................................................................................................225

need for continuation...........................................................................................349

population-based ..................................................................................................349

resorption ............................................................................................................... 21, 24, 44

resorption markers see markers of bone turnover

rheumatic diseases ..............................................................................................................49

rheumatoid arthritis .............................................................................................. 47, 49, 51

rickets ............................................................................ 4, 12, 19, 30, 53-54, 102, 223, 259

causes ......................................................................................................................53

risedronate ....................................................................................................... 226, 228, 234

risk assessment.................................................................................. 187-212, 266-267, 269

“red flags” signaling need for evaluation .................................................... 190-192

advances in ...............................................................................................................3

current limitations of............................................................................................194

formal tools ....................................................................... 3, 192-198, 270, 272, 273

importance of........................................................................................................187

in adults ........................................................................................................ 266-267

in children and adolescents ......................................................................... 259-261

in older adults............................................................................................... 270-272

inadequacies in .....................................................................................................187
Index 401

next-generation models................................................................................ 211-212

risk factors..................................................................................................... 188-192

warning signs....................................................................................... 260, 266, 271

risk factors for bone disease ......................................................................... 3, 188-192, 271

amenorrhea .......................................................................... 114, 136, 190, 191, 260

body weight.................................................................................................. 190-191

family history of bone disease .................................................................... 190, 199

genetic factors............................................................................................... 211-212

height loss ............................................................................................ 190, 194, 195

history of fractures .............................................................................. 190, 195, 199

kyphosis................................................................................................................190

medical conditions ............................................................... 191, 199, 260-261, 266

medications........................................................................... 190-191, 195, 260, 266

sex hormone deficiency .......................................................................................199

smoking .................................................................................................................199

vitamin D deficiency................................................................................... 191, 199

risk factors for fracture .................................................................................... 195, 270, 271

Rodgers Diffusion Model ........................................................................................ 284-287

ruffled border .....................................................................................................................24

salt see also sodium.................................................................................................. 259, 265

sarcopenia ......................................................................................................... 122, 129-130

science base see research

sclerosing bone disorders ...................................................................................................57

screenings......................................................................................................... 283, 290, 297

secondary causes of bone disease ....................................................................... 3, 188, 191

importance of treating..........................................................................................224

secondary osteoporosis ............................................................................................. 46, 191

secondary prevention....................................................................... 188, 220-221, 224-225

selective estrogen receptor modulators (SERMs) ......................................... 219, 226, 232

raloxifene .............................................................................................. 226, 232-233

tamoxifen ..............................................................................................................233

serum calcium measurement ........................................................................... 191-192, 224

sex hormone binding globulin ..........................................................................................44

sex hormones see also estrogen, testosterone ........................................... 25, 26, 28-29, 48

deficiency and osteoporosis .......................................................................... 48, 191

Simple Calculated Osteoporosis Risk Estimation (SCORE) ........................................193

single x- ray absorptiometry (SXA) ...................................................................... 202, 203

small bowel resection .........................................................................................................53

smoking .......................................................................................................... 6, 12, 179, 266

effect on bone health.................................................................................... 139-140

population-based interventions to reduce .................................................. 315-317
402 Index

social marketing ................................................................................................................317

sodium ...................................................................................................... 121, 170, 171, 265

specialty clinics ........................................................................................................ 283, 289

specialty referrals............................................................................................. 268, 275, 351

for adults at risk ....................................................................................................268

for older adults .....................................................................................................275

to occupational therapists ....................................................................................275

to orthopedists ......................................................................................................275

to physical therapists ...........................................................................................275

spinal cord injury ...............................................................................................................49

spinal cord lesions ..............................................................................................................51

spine fractures

costs.......................................................................................................... 91, 98, 100

rehabilitation.........................................................................................................240

treatment...............................................................................................................238

standing orders for supplements ............................................................................ 283, 291

statins ...............................................................................................................................236

STEPS to a HealthierUS ....................................................................................................5

steroids see anabolic therapy

stroke .................................................................................................................................49

strontium ralenate .................................................................................................... 236-237

Study of Osteoporotic Fractures ............................................................................ 194-195

supplementation ........................................................................................ 3, 7, 12, 257, 268

Surgeon General .................................................................................................... 9-11, 124

sympathetic dystrophy ....................................................................................................241

systematic risk assessment and intervention .................................................. 283, 290-291

systemic hormones see regulatory hormones

systems-based approach to bone health ................................................... 13, 281-304, 351

academic detailing ....................................................................................... 283, 289

benchmarks of physician performance ..................................................... 283, 288

creation of discipline-specific curricula ..................................... 297, 299, 353, 354

development of guidelines .................................................................. 283, 299, 353

disease management programs............................................ 283, 289-290, 300, 354

evidence-based care .................................................................................... 283, 284

health education .................................................................................. 283, 299, 354

improving links between organizations ..................................................... 283, 297

insurance coverage ...............................................................................................283

monitoring compliance with regulations ................................................... 283, 298

patient registries ........................................................................... 283, 288-289, 299

pay-for-performance initiatives...........................................................................296

performance assessments..................................................................... 283, 293-294
Index 403

policymaking ....................................................................................... 283, 298, 353

product development.................................................................................. 300, 354

professional education ........................................ 283, 286, 289, 297, 299, 353, 354

public awareness campaigns ................ 283, 284-285, 296-297, 298-299, 352, 353

purchasing power ................................................................................ 299-300, 352

quality improvement initiatives .......................................................... 288, 294-296

reminder systems ........................................................................................ 283, 286

research ........................................................................................ 283, 299, 353, 354

screenings ............................................................................................ 283, 290, 297

specialty clinics............................................................................................ 283, 289

stakeholders see bone health, promoting

standing orders for supplements................................................................ 283, 291

systematic risk assessment and intervention ...................................... 283, 290-291

T-scores.....................................................................................201, 204-207, 261, 267, 272

tacrolimus............................................................................................................. 51, 52, 266

Take Our Trail Physical Activity Program ................................................... 331-333, 335

tamoxifen ..........................................................................................................................233

teriparatide ................................................................................................ 226, 235-236, 274

tertiary prevention ................................................................................... 220, 221, 226-244

testosterone ...................................................................................................... 26, 28, 44, 48

thyroid hormone ......................................................................................... 26, 29, 138, 190

excess see thyrotoxicosis

thyrotoxicosis....................................................................................................... 47, 48, 138

thyrotropin (TSH).............................................................................................................29

tobacco use

population-based interventions to reduce .................................................. 315-317

trabecular bone ............................................................................................................ 19, 30

treatment and therapy see also drug therapy for osteoporosis

as prevention ........................................................................................................220

disparities in..............................................................................................................8

future of .........................................................................................231-233, 236-237

non-bone medications and ..................................................................................274

of bone disease...........................................................................3, 219-244, 272-275

strategies to maximize adherence to ................................................... 267-268, 275

study design issues of ..........................................................................................225

Turner’s syndrome ..................................................................................................... 47, 48

U.S. Preventive Services Task Force (USPSTF) .................198-199, 206, 254, 271, 285

ulcerative colitis ..................................................................................................................49

underserved populations see also minority groups, ethnic groups ..................................8

frail elderly............................................................................................................302

men........................................................................................................................302
404 Index

minorities ...................................................................................................... 301-302

rural and inner-city ..............................................................................................303

underinsured ........................................................................................................301

uninsured..............................................................................................................300

underweight and bone health ................................................................................. 130-131

VERBTM It’s What You Do campaign............................................................................320

vertebral fracture see spine fracture

vertebroplasty .......................................................................................................... 238, 293

vitamin A ................................................................................................... 52, 121, 170, 171

vitamin C.......................................................................................................... 121, 168, 171

vitamin D ......................................................... 3, 6-7, 12, 115-120, 160, 164-165, 222-223

25 hydroxy vitamin D measurement .......................................... 53, 117, 191, 224

breastfeeding and .................................................................................................259

deficiency....................................... 29-30, 49, 50, 53, 191, 199, 223, 259, 264, 268

disorder of and bone disease ...............................................................................259

importance of................................................................................................ 115-120

recommended intake in adults ............................................ 118-119, 160, 257, 264

recommended intake in children ............................................... 118, 160, 257, 259

recommended intake in infants ........................................................... 160, 257,259

recommended intake................................... 160, 164, 222-223, 257, 259, 264, 268

sources .................................................................................. 164-165, 222, 259, 264

sunlight and ....................................................................28, 116-117, 164, 222, 264

supplementation .................................................. 120, 165, 219, 222-223, 264, 268

vitamin K ................................................................................................. 121, 168, 171, 262

voluntary health organizations see bone health, promoting

warning signs see “red flags”, risk assessment

weight loss and bone health .................................................................................... 130-131

Women’s Health Initiative (WHI) ..................................................................................120

World Health Organization ................................................. 5, 6, 41, 76, 78, 204, 206, 267

wrist fractures

costs.........................................................................................................................95

rehabilitation................................................................................................. 240-241

treatment....................................................................................................... 238-239

X-linked hypophosphatemic rickets .................................................................................53

young adults ............................................................................................................ 254, 257

bone maintenance in ........................................................................... 114, 118, 129

nutrition in.................................................................................................... 261-265

osteoporosis in ......................................................................................................189

Z scores ............................................................................................ 204, 206, 207, 261, 272

zinc .............................................................................................................. 121, 168, 171

zoledronic acid ......................................................................................................... 236, 243