Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “CARTILAGE, ARTICULAR”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 685 records · Page 38Linked to original sources
PubMedDate not supplied

Surface fissures in articular cartilage: effect of pathological changes in synovial fluid.

OBJECTIVE: A unified mathematical model of two different modes of inception of fissures at the surface of articular cartilage in healthy and pathological joints. DESIGN: The superficial tangential zone of articular cartilage is modeled as a three-phase medium consisting of collagen fibers, matrix, and of infiltrated thin constituent of synovial fluid. BACKGROUND: The author's general mesomechanical concept is applied to the analysis of deterioration of articular cartilage. METHODS: Theoretical analysis based on the results of the author's preceding paper. RESULTS: The presented analysis shows that superficial fissures in articular cartilage can also be caused by pathological thinning of synovial fluid. CONCLUSIONS: Whereas in healthy joints the probable cause of creation of fissures at the surface of cartilage was shown to be fast impact loading, in joints with inflammatory synovial fluid the fissures can be caused by plain walking. RELEVANCE: Appearance of surface fissures in articular cartilage is a serious, still not fully clarified problem that deserves attention.

Cartilage, Articular↗
PubMed1977

[Study of an articular cartilage in rheumatoid arthritis by the immunofluorescence method].

The immunomorphological examinations of 20 biopsy specimens of articular cartilage in rheumatoid arthritis at various stages of the pathological process showed immunoglobulins of different classes and complement (C'3) to penetrate into the articular cartilage. In early stages mostly IgG was detected, and with increasing destructive processes in the matrix IgM was found. A certain tropism in the distribution of immunoglobulins in the cartilage matrix to the zones of chondrocytic capsules was observed which could be associated with the direction of immune reactions towards chondrocytes. The articular cartilage tissue may be the basis for the development of the autoimmune process and maintain permanent inflammatory process in the synovial membrane of the joint with local antibody synthesis. The process of phagocytosis of the antigenic substances of the articular cartilage or immune complexes deposed in it underlies the distribution of pannus.

Arthritis, Rheumatoid↗
PubMed1998

Type X collagen, a natural component of mouse articular cartilage: association with growth, aging, and osteoarthritis.

OBJECTIVE: To perform a systematic study on the production and deposition of type X collagen in developing, aging, and osteoarthritic (OA) mouse articular cartilage. METHODS: Immunohistochemistry was employed to define the distribution of type X collagen and Northern analyses to determine the messenger RNA levels as an indicator of the synthetic activity of the protein. RESULTS: Type X collagen was observed in the epiphyseal and articular cartilage of mouse knee joints throughout development and growth. Type X collagen deposition in the transitional zone of articular cartilage became evident toward cessation of growth, at the age of 2-3 months. The most intense staining for type X collagen was limited to the tidemark, the border between uncalcified and calcified cartilage. Northern analysis confirmed that the type X collagen gene is also transcribed by articular cartilage chondrocytes. Intense immunostaining was observed in the areas of OA lesions, specifically, at sites of osteophyte formation and surface fibrillation. Type X collagen deposition was also seen in degenerating menisci. CONCLUSION: This study demonstrates that type X collagen is a natural component of mouse articular cartilage throughout development, growth, and aging. This finding and the deposition of type X collagen at sites of OA lesions suggest that type X collagen may have a role in providing structural support for articular cartilage.

Aging↗
PubMed1985

In vitro metabolic response of articular cartilage segments to low levels of hydrostatic pressure.

Bovine and human articular cartilage segments exhibit variable alterations in metabolism following in vitro exposure to hydrostatic pressure. A decrease in incorporation of the labeled substrates 35SO4, 3H-glycine and 3H-uridine to values less than 50% of non-pressurized tissue results from exposure to pressures between 75 and 300 psi. A pressure of 375 psi consistently results in a 10-15% increase in cartilage synthetic activity in the presence or absence of 10% fetal calf serum. Dialyzed fetal calf serum increases the metabolic response at 375 psi from 10% to 55%. The recovery phase following exposure to pressure includes a release (rebound) phenomenon whereby a burst of metabolic activity elevates the metabolic rate to normal levels when the tissues are inhibited (75-300 psi) and accelerates the metabolic rate by 60% in tissues whose metabolism was elevated (375 psi). These data suggest that articular cartilage chondrocytes have the capacity to rapidly and differentially transform mechanical signals derived from application of hydrostatic pressure into metabolic events. The direction of the response is apparently dictated by the magnitude of the applied force and presence of dialyzable components in serum. Although the force applied only partially mimics in vivo forces, the observed responses to pressure support the thesis that pressure modulation of metabolic activity in articular cartilage may be an important factor in its maintenance.

Animals↗
PubMed1994

Histological and immunohistochemical studies on the articular cartilage after experimental discectomy of the temporomandibular joint in rabbits.

Total discectomy was performed experimentally in the rabbit temporomandibular joint (TMJ). In order to evaluate the injury and repair of the articular cartilage of the mandibular condyle after discectomy, both histologic and immunohistochemical observations were made. Immunohistochemical observation by using bromodeoxyuridine (BrdU) and its monoclonal antibody in vivo labelling method was used. The present study demonstrated that the cartilage on the articular surface of the condyle disappeared at 1 week post-operatively. This defect in the injured articular cartilage was not repaired by the cartilage, but was covered by a fibrous connective tissue at 6 weeks post-operatively, where the condylar recontouring by the adjacent articular cartilage, and flattening and hyperplasia of the condyle were observed. Thus, the cartilaginous repair following discectomy was characterized by the proliferation of the adjacent cartilage to the injured site and osteoblastic formation in the bone marrow at the exposed subchondral bone.

Animals↗
PubMed2006

Causes of mechanically induced collagen damage in articular cartilage.

Osteoarthritis (OA) is a multifactorial disease, associated with articular cartilage degeneration and eventually joint destruction. The phases of the disease have been described in detail, and mechanical factors play an important role in the initiation of OA, but many questions remain about its etiology. Swelling of cartilage, one of the earliest signs of damage, is proportional to the amount of collagen damage. This strongly suggests that damage to the collagen network is an early event in cartilage degeneration. The goal of this study was to determine the mechanical cause of early collagen damage in articular cartilage after mechanical overloading. Both the shear strain along the fibrils and the maximum fibril strains were evaluated as possible candidates for causing collagen damage. This evaluation was done by comparing the locations of maximum shear and tensile strains with the locations of initial collagen damage after mechanical overloading in bovine explants as found using antibodies directed against denatured type II collagen (Col2-3/4M). Collagen damage could be initiated by excessive shear strains along the collagen fibrils, and by excessive fibrils strains. The locations of collagen damage after mechanical overloading were highly dependent on the cartilage thickness, with thinner cartilage being more susceptible to damage than thicker samples.

Animals↗
PubMed2005

Impact loading of articular cartilage during transplantation of osteochondral autograft.

Surgical reconstruction of articular surfaces by transplantation of osteochondral autografts has shown considerable promise in the treatment of focal articular lesions. During mosaicplasty, each cylindrical osteochondral graft is centred over the recipient hole and delivered by impacting the articular surface. Impact loading of articular cartilage has been associated with structural damage, loss of the viability of chondrocytes and subsequent degeneration of the articular cartilage. We have examined the relationship between single-impact loading and chondrocyte death for the specific confined-compression boundary conditions of mosaicplasty and the effect of repetitive impact loading which occurs during implantation of the graft on the resulting viability of the chondrocytes. Fresh bovine and porcine femoral condyles were used in this experiment. The percentage of chondrocyte death was found to vary logarithmically with single-impact energy and was predicted more strongly by the mean force of the impact rather than by the number of impacts required during placement of the graft. The significance of these results in regard to the surgical technique and design features of instruments for osteochondral transplantation is discussed.

Animals↗
PubMed1989

Ultrastructural study of articular cartilage in experimental pyogenic arthritis.

Ultrastructural changes of the articular cartilage at the early stage of experimental pyogenic arthritis were studied by electron microscopy. The superficial zone of the cartilage at the site of the cartilage-synovium junction demonstrated far more changes than those at the site of the free surface of the articular cartilage. Changes were observed at the cartilage-synovium junction as early as four hours after the intraarticular injection of the infecting organism. The most interesting finding was migration of erythrocytes and polymorphonuclear leucocytes into the superficial zone of the cartilage at the early stage. The pericellular matrix in the middle zone became so loose in some areas that collagen fibrils were partially exposed after three days. The naked collagen fibrils were tapered, nicked and irregular in size after seven days.

Animals↗
PubMed1996

The development of articular cartilage: II. The spatial and temporal patterns of glycosaminoglycans and small leucine-rich proteoglycans.

Articular cartilage is both morphologically and biochemically heterogeneous. Its susceptibility to degenerative diseases such as arthritis and its limited repair capacity has made cartilage the focus of intense study; surprisingly, little is known of its development. Using a panel of specific antibodies, we have documented the temporal and spatial patterns of the small leucine-rich proteoglycans fibomodulin, decorin and biglycan in the developing knee cartilage of the marsupial South American opposum (Monodelphis domestica) from parturition to adulthood. The major proteoglycan of cartilage, aggrecan, can be substituted with a variety of isomers of chondroitin sulphate (CS) and keratan sulphate (KS) glycosaminoglycans. Consequently, we have used monoclonal antibodies to determine the distribution of the chondroitinase generated epitopes of CS isomers (delta di-6S and delta di-4S oligosaccharide 'stubs'). Other monoclonal antibodies (3B3[-], 7D4) were used to investigate temporal changes in the expression of specific sulphation patterns within native chondroitin sulphate chains in addition to keratan sulphate chains (5D4). We found the distributions of the small proteoglycans (PGs) to be highly dynamic during development. Both fibromodulin and biglycan appeared to specifically label early articular cartilage as opposed to epiphyseal or growth plate cartilage. All 3 small PGs become preferentially distributed to the upper half of the adult articular cartilage depth. Similarly, delta di-6S, delta di-4S oligosaccharide 'stubs', KS and epitope 7D4 were variably distributed during development but all were again preferentially located to the upper depth of the mature tissue. The epitope recognised by antibody 3B3[-] was extensively distributed in the neonate, but became more restricted to hypertrophic chondrocytes by day 19. It was not detected in the adult tissue. These data suggest that in Monodelphis, proteoglycans are preferentially synthesised and elaborated in the upper half of the tissue depth and contrasts with the patterns observed in eutherian mammals. The data also pose questions as to the functional significance of these molecules within the tissues and to the idea that global patterns of matrix components exist in mammalian articular cartilages.

Animals↗
PubMed2003

[Repair of articular cartilage defect with homogeneous chondrocytes combined with pluronic].

OBJECTIVE: To investigate the possibility of repairing the cartilage cartilage defect with homogeneous chondrocytes combined with Pluronic. METHODS: Homogeneous cartilage chondrocytes of adult New Zealand rabbits were harvested and cultured in vitro, which were marked by 3H-TdR and mixed with Pluronic. The medial or lateral condyle defects were made (phi 4 mm, extending down to the calcified zone) in 20 rabbits. In the experimental group, the right defects were repaired by homogeneous chondrocytes combined with Pluronic; in the control group, the left defects were repaired by Pluronic only or were left un-repaired. The animals were sacrificed in the 4th, 8th and 16th weeks after operation respectively. The repair results were observed and the cell source of repair tissue was distinguished. RESULTS: In the experimental group, the cartilage defects were repaired by the cartilage-like tissue after 8 weeks of operation; the defects were completely filled with mature cartilage tissue, which integrated smoothly with articular cartilage 16 weeks later. In the control group, only a small amount fibrous tissues were seen on the surface of defects. Autoradiographic assessment showed that the repair cells came from the implants, but not from self-chondrocytes. CONCLUSION: It is a good way to repair articular cartilage defects with homograft of tissue engineering cartilage. It is a convenient method to mark with 3H-TdR to discriminate the resource of the repair cells.

Animals↗
PubMed1984

Keratan sulfate content and articular cartilage maturation during postnatal rabbit growth.

This article describes the macromolecular changes in keratan sulfate and proteoglycan that occur in rabbit articular cartilage during postnatal development. Articular cartilage glycosaminoglycans from femoral condyles and the tibial plateaus of rabbits at 8, 12, 18, and 26 weeks and 2 years of age were extracted, fractionated, and quantified. The predominant glycosaminoglycan present in articular cartilage at 8 weeks was chondroitin sulfate. During subsequent maturation the relative proportions of keratan sulfate and chondroitin sulfate varied inversely. The greatest increase in the amount of keratan sulfate present in cartilage was observed between 12 and 26 weeks of age. Hyaluronic acid content was measurable at 12 weeks; afterward the amount remained relatively constant with age. Proteoglycans, extracted from 6-, 12-, and 22-week-old rabbit femoral and tibial cartilage in the presence of protease inhibitors, were analyzed on columns of Sepharose CL-2B. Cartilage proteoglycans decreased in hydrodynamic size between 12 and 22 weeks, corresponding to the period of maximal change in content of keratan and chondroitin sulfate.

Age Factors↗
PubMed1990

The viability of articular cartilage in fresh osteochondral allografts after clinical transplantation.

The articular cartilage of four fresh osteochondral allografts was biopsied after transplantation, and its viability was studied by autoradiography. The biopsy specimens were labeled with both 3H-cytidine, for newly synthesized ribonucleic acid, and 35S-sulphate, for newly synthesized proteoglycans. The cartilage of a lateral humeral condylar graft at twelve months had 96 to 99 per cent labeled chondrocytes, the articular cartilage of a medial femoral condylar graft at twenty-four months showed 69 to 78 per cent labeled chondrocytes, and the cartilage of a medial tibial-plateau graft at forty-one months had 90 per cent labeled cells. At six years, a lateral tibial-plateau graft had 37 per cent labeled chondrocytes.

Adult↗
PubMedDate not supplied

Poly(vinyl alcohol) hydrogel as a biocompatible viscoelastic mimetic for articular cartilage.

The prevalence of suboptimal outcome for surgical interventions in the treatment of full-thickness articular cartilage damage suggests that there is scope for a materials-based strategy to deliver a more durable repair. Given that the superficial layer of articular cartilage creates and sustains the tribological function of synovial joints, it is logical that candidate materials should have surface viscoelastic properties that mimic native articular cartilage. The present paper describes force spectroscopy analysis by nano-indentation to measure the elastic modulus of the surface of a novel poly(vinyl alcohol) hydrogel with therapeutic potential as a joint implant. More than 1 order of magnitude decrease in the elastic modulus was detected after adsorption of a hyaluronic acid layer onto the hydrogel, bringing it very close to previously reported values for articular cartilage. Covalent derivatization of the hydrogel surface with fibronectin facilitated the adhesion and growth of cultured rat tibial condyle chondrocytes as evidenced morphologically and by the observance of metachromatic staining with toluidine blue dye. The present results indicate that hydrogel materials with potential therapeutic benefit for injured and diseased joints can be engineered with surfaces with biomechanical properties similar to those of native tissue and are accepted as such by their constituent cell type.

Animals↗
PubMed2003

The distribution of Notch receptors and their ligands during articular cartilage development.

We examined the distribution of Notch family members and their ligands during the development of articular cartilage and the growth plate. Notch 1 was expressed by the chondrocytes of the developing articular surface but became increasingly restricted to the deeper layers after birth whilst expression of this family member was restricted to hypertrophic chondrocytes in the growth plate. Notch 2 and 4, Delta and Jagged 2 showed a broadly similar distribution, being present throughout the articular cartilage during development and becoming increasingly restricted to deeper layers with age. Hypertrophic chondrocytes within the growth plate also expressed Notch 2 and 4, Delta and Jagged 2 (which was also expressed in prehypertrophs). Notch 3 and Jagged 1 were absent from developing articular cartilage but were present in deeper layers at later time points (> 1 month) and both receptor and ligand were expressed in hypertrophic chondrocytes at all ages examined. These results highlight the complex Notch signalling interactions that result in the formation of the heterogeneous articular cartilage and allow for the co-ordinated ossification and elongation of the growth plate. Mechanisms by which these processes are controlled are discussed in light of recent advances in the understanding of Notch signalling pathways.

Animals↗
PubMed2001

High frequency acoustic parameters of human and bovine articular cartilage following experimentally-induced matrix degradation.

Matrix degradation and proteoglycan loss in articular cartilag eare features of early osteoarthritis. To determine the effect of matrix degradation and proteoglycan loss on ultrasound propagation in cartilage, we used papain and interleukin-1alpha to degrade the matrix proteoglycans of human and bovine cartilage samples, respectively. There is also minor collagen alteration associated with these chemical degradation methods. We compared the speed of sound and frequency dependent attenuation (20-40 MHz) of control and experimental paired samples. We found that a loss of matrix proteoglycans and collagen disruption resulted in a 20-30% increase in the frequency dependent attenuation and a 2% decrease in the speed of sound in both human and bovine cartilage. We conclude that the frequency dependent attenuation and speed of sound in articular cartilage are sensitive to experimental modification of the matrix proteoglycans and collagen. These findings suggest that ultrasound can potentially be used to detect morphologic changes in articular cartilage associated with the progression of osteoarthritis.

Adult↗
PubMed1993

In vivo effects of naproxen on composition, proteoglycan metabolism, and matrix metalloproteinase activities in canine articular cartilage.

Naproxen is a nonsteroidal anti-inflammatory drug commonly used in the clinical treatment of joint disease. In this study, its effect in vivo on the biochemical composition, metabolic activities, and metalloproteinase activities of normal canine articular cartilage was analyzed. The articular cartilage from the knee joints of dogs who had been given naproxen for 4 weeks to maintain a serum level of 40-50 micrograms/ml was examined. Control animals were given a placebo. Treatment with naproxen was not found to change the composition (water, collagen, and proteoglycan) of the articular cartilage. The culture studies of cartilage explants indicated that proteoglycan synthesis rates were unaffected by the treatment with naproxen but that proteoglycan release from the tissue was suppressed. Analysis of the cartilage for matrix metalloproteinase activities showed reduced activity of neutral matrix metalloproteinase by 80%, of collagenase by 40%, and of gelatinase by 87%, with no change in activity of acid metalloproteinase or of tissue inhibitor for metalloproteinase. These findings indicate that in vivo treatment with naproxen has the capacity to modulate catabolic activities in articular cartilage.

Animals↗
PubMed2002

Highly sulfated glycosaminoglycans inhibit aggrecanase degradation of aggrecan by bovine articular cartilage explant cultures.

The catabolism of 35S-labeled aggrecan and loss of tissue glycosaminoglycans was investigated using bovine articular cartilage explant cultures maintained in medium containing 10(-6) M retinoic acid or 40 ng/ml recombinant human interleukin-1alpha (rHuIL-1alpha) and varying concentrations (1-1000 microg/ml) of sulfated glycosaminoglycans (heparin, heparan sulfate, chondroitin 4-sulfate, chondroitin 6-sulfate, dermatan sulfate and keratan sulfate) and calcium pentosan polysulfate (10 microg/ml). In addition, the effect of the sulfated glycosaminoglycans and calcium pentosan polysulfate on the degradation of aggrecan by soluble aggrecanase activity present in conditioned medium was investigated. The degradation of 35S-labeled aggrecan and reduction in tissue levels of aggrecan by articular cartilage explant cultures stimulated with retinoic acid or rHuIL-1alpha was inhibited by heparin and heparan sulfate in a dose-dependent manner and by calcium pentosan polysulfate. In contrast, chondroitin 4-sulfate, chondroitin 6-sulfate, dermatan sulfate and keratan sulfate did not inhibit the degradation of 35S-labeled aggrecan nor suppress the reduction in tissue levels of aggrecan by explant cultures of articular cartilage. Heparin, heparan sulfate and calcium pentosan polysulfate did not adversely affect chondrocyte metabolism as measured by lactate production, incorporation of [35S]-sulfate or [3H]-serine into macromolecules by articular cartilage explant cultures. Furthermore, heparin, heparan sulfate and calcium pentosan polysulfate inhibited the proteolytic degradation of aggrecan by soluble aggrecanase activity. These results suggest that highly sulfated glycosaminoglycans have the potential to influence aggrecan catabolism in articular cartilage and this effect occurs in part through direct inhibition of aggrecanase activity.

Aggrecans↗
PubMed1993

The quantitation of a native chondroitin sulfate epitope in synovial fluid lavages and articular cartilage from canine experimental osteoarthritis and disuse atrophy.

OBJECTIVE: Previous studies have shown the presence of a native chondroitin sulfate epitope in articular cartilage proteoglycans from canine knee joints with experimental early osteoarthritis (OA), but not in normal cartilage. The objective of this study was to quantitate the native epitope recognized by monoclonal antibody 3-B-3 in synovial fluids and articular cartilage of diseased joints. METHODS: An immunoassay with monoclonal antibody 3-B-3, which recognizes a native chondroitin-6-sulfate structure, was developed and used to analyze synovial fluid lavage material and extracts of articular cartilage from canine knee joints with early experimental OA or with mild disuse atrophy, and from control animals. RESULTS: The concentration of epitope in the OA fluids was elevated 33-35-fold, and in the OA articular cartilage extracts it was elevated > 200-fold, compared with samples from the control group. No significant difference was detected in the levels of 3-B-3 epitope in the synovial fluid lavage material or cartilage extracts from the joints of the disuse group versus the control group. CONCLUSION: The native 3-B-3 epitope in articular cartilage and synovial fluids may be a specific marker of ongoing anabolic events in early degenerative joint disease.

Animals↗