bluuebunny/crossref_metadata_2025_split huggingface dataset:
Expression of type‐X collagen in osteoarthritis
Authors: Walker Gordon D. , Fischer Mark , Gannon James , Thompson Roby C. , Oegema Theodore R. 
Published: February 2005

AbstractThe present study was undertaken to examine how osteoarthritis affects the expression of type‐X collagen, a hypertrophic chondrocyte‐specific collagen in articular cartilage. A well characterized sheep polyclonal antiserum, as well as three mouse monoclonal antibodies against canine type‐X collagen, was used to immunolocalize type‐X collagen in human and canine joints. Its expression in osteoarthritic cartilage was altered in several locations. In the canine osteoarthritic joints, type‐X collagen increased in and just above the zone of calcified cartilage and was present diffusely throughout the calcified matrix. In both the human and canine cartilage, type‐X collagen was localized around cell clones in the transitional zone of cartilage. This is surprising, since that region of the cartilage does not calcify and one of the proposed roles of type‐X collagen is in mineralization. Thus, the osteoarthritic process may damage the matrix in the superficial layer and induce changes leading to the expression of the hypertrophic chondrocyte phenotype.
Lysyl oxidase and Maillard reaction‐mediated crosslinks in aging and osteoarthritic rabbit cartilage
Authors: Pokharna Hemlata K. , Monnier Vincent , Boja Betty , Moskowitz Roland W. 
Published: February 2005

AbstractAlterations in the integrity of the extracellular matrix play an important role in osteoarthritis. Matrix crosslinks in articular cartilage of the knee were studied in partially meniscectomized rabbits to compare changes due to osteoarthritis with those occurring during aging. Pyridinoline, a lysyl oxidase‐initiated crosslink, and pentosidine, a crosslink formed by the Maillard/glycation reaction, were assayed separately on reverse‐phase high performance liquid chromatography. A significant increase in the percentage of insoluble collagen was observed in normal 12‐month‐old rabbits compared with the levels in 3‐month‐old animals, whereas osteoarthritis was associated with a shift toward more soluble fractions. Total pyridinoline content did not change with age or osteoarthritis. Total pentosidine, however, increased significantly with age but remained constant with osteoarthritis. Analysis of the distribution of crosslinks among solubility fractions indicated a significant shift of pyridinoline from the pepsin‐released fraction to the insoluble fraction with osteoarthritis, but no changes were observed with age. Pentosidine distribution shifted toward the pepsin‐released fraction in osteoarthritis, with a shift toward the insoluble fraction with age. Because of the low levels of pentosidine present, its precise location, whether collagenous or noncollagenous, remains unclear. However, since pentosidine represents a marker for the overall Maillard reaction, the results of our studies support a role for Maillard reaction products in the aging of extracellular matrix. The shift of pentosidine toward more soluble fractions suggests the presence of matrix degradation and repair in osteoarthritis.
Diminished material properties and altered bone structure in rat femora during pregnancy
Authors: Leopold Seth S. , Boskey Adele L. , Doty Stephen B. , Gertner Joseph M. , Peterson Margaret G. E. , Torzilli Peter A. 
Published: February 2005

AbstractPregnancy and lactation are known to cause structural and mechanical changes in bone, but the effects of pregnancy alone have not been evaluated thoroughly. This study used radiographic measurements, torsion testing, mineral analyses, and histological evaluation to determine whether there are changes in bone material and geometric properties during pregnancy in the growing rat, as implied by earlier biochemical and histological studies. The bones of pregnant 9 to 12‐week‐old rats and controls that were not pregnant and were matched by age (but not weight) were evaluated at times corresponding to 5, 10, 15 and 20 days of the 23‐day gestation period to address the following questions: (a) How is the growth of whole bone affected by pregnancy in the growing rat (as determined by radiographic analyses)? (b) How are the mechanical properties (structural and material) of whole bone affected by pregnancy (as assessed by torsion testing)? (c) Are there changes in the characteristics of bone mineral during pregnancy (as determined by measurement of mineral content and x‐ray diffraction analyses)? and (d) Are there detectable morphological or ultrastructural differences between the bones of pregnant and control rats (as assessed by analyses based on histology and back‐scattered electron imaging)? The presence of statistically significant differences in this study was determined initially on the basis of a two‐factor analysis of variance. In general, significant differences were noted only at late gestation (day 20), when the bones were longer and had a greater outer radius and cortical thickness; this indicates that more growth occurred during pregnancy. At day 20, biomechanical testing showed that the femora of pregnant rats had a 20% decrease in rotational angle to failure and a 30% increase in shear stiffness. No alterations in maximum torque or energy to failure were noted. Calculation of the properties of bone material revealed a 54% decrease in ultimate shear stress, a 50% decrease in shear modulus, and no alteration in shear strain when the bones from rats pregnant for 20 days were compared with controls. The bones of the pregnant rats at day 20 also differed from controls in terms of both mineral characteristics and morphology. X‐ray diffraction showed larger mineral crystallites in the specimens from pregnant rats as compared with controls, whereas the mineral contents (ash weights) were similar. Scanning electron microscopy revealed qualitative differences, including increased periosteal vascularity and numerous large cortical cavities thought to be areas of resorption in the bones from rats pregnant for 20 days as contrasted with controls. These changes are consistent with the observed alteration in mechanical properties.
Platelet‐derived growth factor in fibrous musculoskeletal disorders: A study of pathologic tissue sections and in vitro primary cell cultures
Authors: Alman Benjamin A. , Naber Stephen P. , Terek Rick M. , Jiranek William A. , Goldberg Michael J. , Wolfe Hubert J. 
Published: February 2005

AbstractDespite the great variability in the clinical behavior of fibrous lesions of the musculoskeletal system, they are composed of cytologically similar fibrocytes. Receptors for estrogen or progesterone, or both, are present in some of these lesions and some increase their rate of growth during periods of high levels of sex steroid hormones. The platelet‐derived growth factor‐B (PDGF‐B) proto‐oncogene encodes the B chain of PDGF, a mitogen for fibrocytes. Tissue from aggressive fibromatosis, fibrous dysplasia, plantar fibromatosis, and recurrent plantar fibromatosis was analyzed with use of the polymerase chain reaction and in situ hybridization for the expression of PDGF‐B and PDGF beta receptor. Cell culture was used to determine if estrogen and progesterone stimulation modulated the expression of PDGF‐B. Aggressive fibromatosis, fibrous dysplasia, and recurrent plantar fibromatosis expressed PDGF‐B; plantar fibromatosis, normal plantar fascia, normal fascia lata, and mature scar did not. All of the tissues expressed PDGF beta receptor. The level of expression in aggressive fibromatosis and fibrous dysplasia was four times that in the recurrent plantar fibromatosis. Estrogen and progesterone stimulation in aggressive fibromatosis resulted in an increase in the level of expression. Therefore, the detection of PDGF‐B may be an adjunct in the pathologic identification of locally invasive lesions. Its production may be a common mechanism leading to a fibroproliferative response through deregulation of the control of growth by both paracrine and autocrine mechanisms.
Comparison of healing of allograft/endoprosthetic composites with three types of gluteus medius attachment
Authors: Markel Mark D. , Wood Suzanne A. , Bogdanske John J. , Rapoff Andrew J. , Kalscheur Vicki L. , Bouvy Bernard M. , Rock Michael G. , Chao Edmund Y. S. , Vanderby Ray 
Published: February 2005

AbstractThis study compared three methods of gluteus medius tendon attachment to an allograft/endoprosthetic composite of the proximal 25% of the femur in a canine model. The three methods were bone to bone, tendon tobone, and tendon to tendon attachment. In anin vivostudy, 24 dogs were assigned to three groups of eight dogs each, and serial radiography and weight‐bearing analyses were performed throughout the study. The dogs were killed at 6 months, and the specimens were tested in tension to failure and were analyzed histologically. In anin vitrostudy, each repair was done on six limbs, with a contralateral limb serving as a control for each. In these specimens, the bone to bone attachments were significantly stronger (99.1% of the controls) than the tendon to bone attachments (71.8% of the controls) and the tendon to tendon attachments (40.0% of the controls); there were no differences in tensile stiffness among the three types of attachment. By 6 months, the tensile strength of the tendon to tendon attachments increased significantly and that of the tendon to bone attachments decreased significantly. There were no significant differences in tensile strength among the three types of attachment. The tensile stiffness of the bone to bone attachments (91.0% of the controls) was significantly greater than that of the tendon to bone attachments (40.8% of the controls) but not significantly different from that of the tendon to tendon attachments (63.2% of the controls). The bone to bone attachment was associated with increased bone resorption, bone remodeling, and bone porosity, accompanied by thinner allograft cortices, when compared with the other types of attachment. In dogs with a bone to bone attachment, weight‐bearing increased more slowly than in dogs with either of the other two attachments. These changes associated with the bone to bone attachment may merely be secondary to healing of the bone to bone attachment to the greater trochanter; therefore, they may only be temporary phenomena or they may be the portents for long‐term complications. Longer term studies of at least 1–2 years must be performed before these questions can be answered.
Growth of severed flexor tendons in chickens
Authors: Nishijima Naoki , Fujio Keiji , Yamamuro Takao 
Published: February 2005

AbstractTo examine tendon growth in both the distal and proximal portions of severed tendons, we investigated the growth of severed flexor tendons within the fibro‐osseous tunnel in young chickens. When the tendon was severed at the proximal site in the sole, dynamic tension applied by the muscle was lost. Growth in the distal tendon was retarded considerably, although passive tension initially was maintained through the residual vincula and later by adhesion to the chiasma of adjacent flexors. When the tendon was severed at the insertion, passive tension from the extensors was lost. Proximal tendon growth continued if active tension was maintained through the residual vincula. If not, the tendon was markedly shortened and degenerated. Maintaining normal tension may be the most important factor in longitudinal tendon growth.
Integrin display increases in the wounded rabbit medial collateral ligament but not the wounded anterior cruciate ligament
Authors: Schreck Paul J. , Kitabayashi Linda R. , Amiel David , Akeson Wayne H. , Woods Virgil L. 
Published: February 2005

AbstractThe differential capacities of the anterior cruciate and medial collateral ligaments to heal may be related to differences in cellular function. This study tested the hypothesis that differential expression of integrins occurs in these ligaments after injury. The integrins are a family of cell surface receptors that mediate adhesion, migration, and other cellular functions critical to the healing of a wound. A similar complement and amount of the β1 subfamily of integrins are known to be present on the unperturbed anterior cruciate and medial collateral ligaments in humans and rabbits. A partial laceration was surgically created in these two ligaments in 12 anesthetized New Zealand White rabbits. Immunohistochemistry was performed on sections from the ligaments at 1, 3, 7, and 10 days after injury, using monoclonal antibodies directed against the integrin subunits β1, α5, α6, and αv. Between 3 and 7 days, the wounded medial collateral ligament demonstrated a striking increase in staining for the β1, α5, and αv subunits on the fibroblasts, within the repair site, and on capillary endothelium. Increased staining was most marked for the β1 subunit and less marked for the α5 and αv subunits. The α6 subunit stained exclusively vascular structures within the healing medial collateral ligament. In marked contrast, the anterior cruciate ligament, which does not mount an effective repair response, demonstrated no comparable alteration of integrin expression from baseline levels. This study demonstrates that increased expression of integrins occurs coincident with wound healing in the medial collateral ligament, whereas this expression remains at baseline levels in the nonhealing wounded anterior cruciate ligament. This observation suggests that a failure to alter expression of integrins subsequent to injury may play a role in the defective healing of the anterior cruciate ligament.
Serum fractions and related agonists with calcium‐mobilizing activity in the bovine growth plate chondrocyte
Authors: Bulman W. A. , Iannotti J. P. , Glowacki K. , Bleuit J. , Clark C. C. 
Published: February 2005

AbstractLongitudinal growth of bone involves a complex sequence of cellular events in the cartilaginous epiphysis. Whole blood serum has been shown previously to be a potent stimulus to the cells of the growth plate, as demonstrated by its ability to activate the inositol phosphate‐calcium second messenger system resulting in a rise in intracellular Ca2+. By manipulating the preparation of serum to functionally separate it into its constituent parts, we have shown that the processes of platelet lysis and activation of the clotting cascade are responsible for the generation of factors that stimulate this signaling mechanism in isolated bovine growth plate chondrocytes. Through a subsequent trial of bioactive agents generated in these processes, we identified and partially characterized several novel agonists of growth plate chondrocytes: adenosine triphosphate and adenosine diphosphate, the purine energy substrates, and bradykinin, the bioactive peptide generated in a side reaction of the clotting cascade, each induces a rise in intracellular Ca2+ via release from intracellular ion stores. Additionally, the three distinct isoforms of platelet‐derived growth factor (AA, AB and BB), also released on platelet lysis, were compared with respect to their ability to stimulate the inositol phosphate‐calcium second messenger system in growth plate chondrocytes.
Immunolocalization and expression of bone morphogenetic proteins 2 and 4 in fracture healing
Authors: Bostrom Mathias P. G. , Lane Joseph M. , Berberian Wayne S. , Missri Albert A. E. , Tomin Emre , Weiland Andrew , Doty Stephen B. , Glaser David , Rosen Vicki M. 
Published: February 2005

AbstractRecently, it has become increasingly evident that fracture healing involves a complex interaction of many local and systemic regulatory factors. The roles of some of these growth factors have been described; however, little is understood about the presence of the bone morphogenetic proteins in fracture repair, despite the fact that they are the most potent osteoinductive proteins known. This study defines and characterizes the physiologic presence, localization, and chronology of the bone morphogenetic proteins in fracture healing with an established rat fracture healing model. With use of a recently developed monoclonal antibody against bone morphogenetic proteins 2 and 4 developed with standard avidin‐biotin complex/immunoperoxidase protocols, frozen undecalcified fracture calluses were analyzed semiquantitatively for the percentage of various types of fracture cells staining positively. During the early stages of fracture healing, only a minimum number of primitive cells stained positively in the fracture callus. As the process of endochondral ossification proceeded, the presence of bone morphogenetic proteins 2 and 4 increased dramatically, especially in the primitive mesenchymal and chondrocytic cells. While the cartilaginous component of the callus matured with a concomitant decrease in the number of primitive cells, there was a concomitant decrease in both the intensity and the number of positively staining cells. As osteoblasts started to lay down woven bone on the chondroid matrix, these osteoblastic cells exhibited strong positive staining. The intensity of this staining decreased, however, as lamellar bone replaced the primitive woven bone. A similar observation was noted for the areas of the callus undergoing intramembranous ossification. Initially, within several days after the fracture, periosteal cells and osteoblasts exhibited intense staining for bone morphogenetic proteins 2 and 4. As the woven bone was replaced with mature lamellar bone, this staining decreased. These data, and the awareness of the strong osteoinductive capacities of bone morphogenetic protein, suggest that bone morphogenetic proteins 2 and 4 are important regulators of cell differentiation during fracture repair.
Healing of the medial collateral ligament after a combined medial collateral and anterior cruciate ligament injury and reconstruction of the anterior cruciate ligament: Comparison of repair and nonrepair of medial collateral ligament tears in rabbits
Authors: Ohno Kazunori , Pomaybo Amy S. , Schmidt Christopher C. , Levine Rebecca E. , Ohland Karen J. , Woo Savio L‐Y. 
Published: February 2005

AbstractThe optimal treatment for a combined injury of the medial collateral and anterior cruciate ligaments is controversial, and the question remains as to whether repair of the medial collateral ligament and reconstruction of the anterior cruciate ligament improves healing of the medial collateral ligament. We compared reconstruction of the anterior cruciate ligament with and without repair of the medial collateral ligament in a rabbit model of a combined injury of these two ligaments. The anterior‐posterior translation and varus‐valgus rotation of the knee, the structural properties of the femur‐medial collateral ligament‐tibia complex, and the mechanical properties of the midsubstance of the medial collateral ligament were evaluated immediately after surgery and at 6 and 12 weeks postoperatively. Repair of the medial collateral ligament led to significantly less varus‐valgus rotation of the knee than did no repair, but the anterior‐posterior translation of the knees in the repair and nonrepair groups were not significantly different at any study time. At 12 weeks, the cross‐sectional area and ultimate load in the repair group were 60 and 53% greater, respectively, than in the nonrepair group. Among 12 specimens that were repaired (six specimens at 6 weeks and six specimens at 12 weeks), failure occurred within the midsubstance in four (two at each time period); in all of the specimens that were not repaired, failure occurred at the tibial insertion site. There was no significant difference between the modulus of the midsubstance in the repaired and the nonrepaired medial collateral ligaments. Thus, the improved structural properties of the femur‐medial collateral ligament‐tibia complexes that were repaired resulted from an increase in cross‐sectional area of the repaired medial collateral ligament and healing of the tibial insertion site. Postoperative healing time had little effect on the tensile properties. In this rabbit model, repair of the medial collateral ligament with reconstruction of the anterior cruciate ligament may lead to better healing of the medial collateral ligament in the early phase than does reconstruction of the anterior cruciate ligament alone.
Contact areas in the thumb carpometacarpal joint
Authors: Ateshian Gerard A. , Ark Jon W. , Rosenwasser Melvin P. , Pawluk Robert J. , Soslowsky Louis J. , Mow Van C. 
Published: February 2005

AbstractThe thumb carpometacarpal joint is a common site of osteoarthritis. It has been hypothesized that peaks of localized stress on the dorsoradial or volar‐ulnar regions, or both, of the articular surfaces of the trapezium and metacarpal lead to erosion of cartilage and may be responsible for the progression of the disease. The objective of this study was to determine the contact areas in this joint under the functional position of lateral (key) pinch and in the extremes of range of motion of the joint. These contact areas were assessed relative to the observed sites of cartilage thinning. Eight hands from cadavers of women and five from cadavers of men were tested in vitro with the thumb under a 25 N load in the lateral pinch position, and under small muscle loads (0–5 N) with the thumb in flexion, extension, abduction, adduction, and neutral positions. Contact areas of articular surfaces of the thumb carpometacarpal joint were determined for these positions using a stereophotogrammetric technique. The lateral pinch position produced contact areas predominantly on the central, volar, and volar‐ulnar regions of the trapezium and the metacarpal. In three specimens, contact areas were distinctly separated between the dorsoradial and volar‐ulnar regions, and in one specimen, from a man, contact occurred exclusively on the dorsoradial region of the trapezium. Using stereophotogrammetry, maps of cartilage thickness also were determined for a subset of nine specimens. The volar‐ulnar, ulnar, and dorsoradial regions of the trapezium were the most common sites of thin cartilage, and these may be sites of cartilage wear. The results of this study indicate that the lateral pinch position produced stresses in the same regions where cartilage thinning was observed; this lends support to the hypothesis that high stresses can lead to osteoarthritis in this joint.
Autogenous intrasynovial and extrasynovial tendon grafts: An experimental study of pro α1(I) collagen mRNA expression in dogs
Authors: Amiel David , Harwood Frederick L. , Gelberman Richard H. , Chu Constance R. , Seiler John G. , Abrahamsson Sven 
Published: February 2005

AbstractOn the basis of recent evidence that the healing processes of tendon grafts are donor‐tissue specific, in situ hybridization, using a 372 bp cDNA fragment complementary to a portion of pro α1(I) collagen mRNA, was utilized to compare the cellular responses to transplantation exhibited by autogenous intrasynovial and extrasynovial flexor tendon grafts. Intrasynovial and extrasynovial tendons from the hindpaw were transferred to synovial sheaths in the forepaw of 12 mongrel dogs (24 tendons) and treated with immediate controlled passive motion. The tendon grafts were harvested at 2, 4, and 6 weeks, and each was divided into a proximal, central (8 mm), and distal portion. Sections from the central portion were embedded in paraffin and subjected to in situ hybridization, autoradiography, and staining; levels of procollagen mRNA then were assessed by microscopic examination. The two types of tendon grafts exhibited different levels of pro α1(I) collagen mRNA expression at all three time points. Intrasynovial tendon grafts displayed no areas of increased type‐I procollagen mRNA at 2, 4, and 6 weeks. The extrasynovial tendon grafts displayed increased surface levels of type‐I procollagen mRNA at 2 and 4 weeks; the levels decreased to background levels by 6 weeks. The high levels of procollagen mRNA exhibited by the extrasynovial grafts suggest increased collagen synthetic activity, indicative of a cellular response to injury, whereas the preservation of low levels of expression in the intrasynovial grafts may signify a less inflammatory cellular response.