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PubMed1984

Embryonic chick cartilage collagens. Differences in the low-Mr species present in sternal cartilage and tibiotarsal articular cartilage.

The collagenous polypeptides present in embryonic chick sternal and tibiotarsal cartilages have been solubilised by digestion with pepsin and separated by salt fractionation. Type II collagen, 1 alpha 2 alpha 3 alpha collagen, and two polypeptides (apparent molecular mass 150 and 42 kDa), which were reducible to a number of smaller peptides, were extracted from both tissues. However, also present in the peptic digests of tibiotarsal cartilages was a major non-reducible highly-soluble polypeptide of 45 kDa. This short-chain collagen is apparently identical to the pepsinized product of G collagen (Mr 59 000), a major low-Mr procollagen-like species previously detected in chick chondrocyte cultures.

Amino Acids↗
PubMed1989

Comparative effects of azapropazone on cellular events at inflamed sites. Influence on joint pathology in arthritic rats, leucocyte superoxide and eicosanoid production, platelet aggregation, synthesis of cartilage proteoglycans, synovial production and actions of interleukin-1 in cartilage resorption correlated with drug uptake into cartilage in-vitro.

Azapropazone (APZ) has been compared with standard NSAIDs in title systems to establish aspects of its mode of action on cellular events at inflamed sites. APZ (150 mg kg-1 day-1) given for 10-13 days exhibited a reduction in joint pathology in established adjuvant arthritis in rats comparable with that of indomethacin (2 mg kg-1 day-1) and clobuzarit (20 mg kg-1 day-1). APZ was shown to be a potent inhibitor of the production of leucocyte superoxide and synovial interleukin-1 (IL-1)-like activity and stimulated articular cartilage proteoglycan synthesis, but was ineffective as an inhibitor of platelet aggregation or IL-1 induced cartilage degradation in-vitro. These in-vitro effects may have relevance to the mode of action of this weak inhibitor of prostaglandin synthesis.

Animals↗
PubMed1996

Increased degradation and altered tissue distribution of cartilage oligomeric matrix protein in human rheumatoid and osteoarthritic cartilage.

We investigated the degradation and tissue distribution of cartilage oligomeric matrix protein in normal, osteoarthritic, and rheumatoid arthritic articular cartilage of the human knee. Cartilage was subjected to sequential extractions with buffers containing neutral salt, with EDTA, and finally with guanidine/HCl and then was analyzed by Western blotting with a polyclonal antiserum to human cartilage oligomeric matrix protein. Western blots of the nine neutral salt extracts from normal cartilage revealed mostly intact pentameric molecules of cartilage oligomeric matrix protein, in contrast to the 13 osteoarthritic and five rheumatoid arthritic cartilage samples that demonstrated marked degradation of cartilage oligomeric matrix protein as noted by a predominance of reduction-sensitive bands at approximately 150 kDa and nonreduction-sensitive bands in the 67-94 kDa range. The EDTA and guanidine/HCl extracts from all groups were similar and showed mostly intact molecules of cartilage oligomeric matrix protein, with smaller amounts of degraded cartilage oligomeric matrix protein identical to those resolved by the Western blots of the neutral salt extracts. Western blots of matched pairs of synovial fluid and cartilage extracts demonstrated cartilage oligomeric matrix protein fragments of the same molecular mass. Competitive enzyme-linked immunosorbent assay revealed significantly less cartilage oligomeric matrix protein in rheumatoid articular cartilage than in either normal or osteoarthritic cartilage. In contrast to normal cartilage, where cartilage oligomeric matrix protein was predominantly localized to the interterritorial matrix throughout all zones of the matrix, with increased staining in the deeper cartilaginous zones, the most intense staining in osteoarthritic cartilage was in the superficial zones of fibrillated cartilage, with little to no immunostaining in the midzones and relatively poor staining in the deeper cartilaginous zones. This distribution was the inverse of that for proteoglycans, as demonstrated by toluidine blue staining, where proteoglycans were depleted primarily from the superficial fibrillated cartilage. In mild to moderately affected rheumatoid cartilage, the tissue distribution of cartilage oligomeric matrix protein was similar to the distribution of proteoglycans, with relatively uniform staining of the interterritorial and territorial matrics. In more severely affected rheumatoid cartilage, the superficial zones demonstrated punctate immunostaining for cartilage oligomeric matrix protein in the interterritorial and territorial matrics, and staining was restricted to the territorial matrix in the deep cartilaginous zones. It is evident from this study that (a) noncollagenous proteins such as cartilage oligomeric matrix protein are greatly affected in arthritis, (b) degradation fragments released from the matrix into the synovial fluid reflect the processes occurring within the matrix, and (c) different zones of the articular cartilage are susceptible to degradation of cartilage oligomeric matrix protein in the different disease processes.

Adult↗
PubMed2002

[Experimental study on laryngeal cartilage defects repair with differently preserved allogeneic cartilages transplantation].

OBJECTIVE: To study the effect of laryngeal cartilage defect repair with differently preserved allogeneic cartilage grafts. METHODS: 16 New Zealand white rabbits were used and divided into two groups. A 6 mm x 3 mm x 1 mm whole thickness cartilage defect was made in each side of the thyroid cartilage of each rabbit. In group one, the tissue-cultured cartilage grafts, preserved in RPMI-1640 medium for 30 days, were implanted in the left defects and the 4% formaldehyde preserved cartilage grafts for 30 days were implanted in the right defects. Fresh autogenous and allogeneic grafts were seprately transplanted into the right and left thyroid cartilage defects of the other group. Thyroid cartilages were taken out at 7, 30, 180 and 360 days after implantation. Samples were observed by macroscopy and prepared for hematoxylin and eosin (H&E) staining and immunohistochemical examination. RESULTS: No marked changes in form and volume were found in the fresh allografts and RPMI-1640 cultured cartilage grafts. The same as the autogenous cartilages, the defects of thyroid cartilage were successfully repaired by the fresh allografts and RPMI-1640 cultured cartilages. Whereas 4% formaldehyde preserved cartilage grafts were completely absorbed and replaced by cicatricial tissues in the thyroid cartilage defects. Histological observation showed that severe inflammatory cellular infiltration in the formaldehyde preserved cartilages at 7 and 30 days. The cartilage matrixes were resorpted and the chondrocytes showed degenerative change. Finally they were replaced by fibrous connective tissue at 360 days. In the RPMI-1640 cultured and fresh allogeneic cartilages only a little inflammatory cellular infiltration was observed and the cartilage matrixes were almost normal from 7 to 360 days. CONCLUSION: It is clinically feasible to use allogeneic grafts stored in RPMI-1640 medium or fresh allogeneic cartilage grafts for repairing laryngeal cartilage defects.

Animals↗
PubMed1999

Vascularization and cartilage mineralization of the thyroid cartilage of Munich minipigs and domestic pigs.

Thyroid cartilages of Munich minipigs and domestic pigs were investigated by polychrome sequential labeling, radiography, intravascular injections, histologic examination and scanning electron microscopy in order to gain further insight into the process of vascularization and cartilage mineralization. The relationship between vascularization and cartilage mineralization has only been studied in chondroepiphyses of long bones. Vessels branch off the perichondrial vascular network and enter parts of the thyroid cartilage with a large transverse diameter. Cartilage canals, which are perichondral invaginations, contain an arteriole, a venule, a capillary network and connective tissue. The capillaries form a glomerulus-like structure deep in the matrix of the cartilage. Neighbouring cartilage canals do not display any anastomoses. Cartilage mineralization occurs in large areas of the thyroid cartilage. It is only found in the interterritorial extracellular matrix. Mineralization of the cartilage is evident in areas supplied with cartilage canals as well as in non-supplied areas. Mineralized interterritorial matrix is composed of circular structures of different sizes fusing to form plaques. In scanning electron microscopy circular structures appear as globules. It is possible to visualize the dynamic process of cartilage mineralization with polychrome sequential labeling; it proceeds up to 4 microm per week. Distribution of cartilage canals reveals their nutritional role for the cartilage. According to investigations in chondroepiphyses, cartilage mineralization starts adjacent to the glomerular end of cartilage canals. In contrast, no correlation between cartilage vascularization and the beginning of cartilage mineralization of the thyroid cartilage of Munich minipigs and of domestic pigs has been found.

Animals↗
PubMed1998

Cartilage damaging activities of fibronectin fragments derived from cartilage and synovial fluid.

OBJECTIVE: To investigate whether fibronectin fragments (Fn-fs), shown to damage cultured cartilage, can be found in cartilage from patients with osteoarthritis (OA) or rheumatoid arthritis, or can be generated from fibronectin (Fn) within synovial fluids or from Fn in the matrix of cultured cartilage. To also determine whether cartilage or synovial fluid Fn-fs are active and, thus, could contribute to cartilage damage in vivo. METHODS: Fn-fs were immunochemically identified in cartilage extracts from patients with OA or rheumatoid arthritis or in bovine cartilage cultured with IL-1 alpha or in bovine synovial fluids treated with stromelysin-1 (MMP-3). The effect of removal of Fn-fs from OA synovial fluids was tested by passing fluids over an anti-Fn column and adding the resultant fluids to bovine cartilage cultures to measure proteoglycan (PG) degradation. Gelatin-Sepharose purified Fns from bovine plasma, synovial fluid or cartilage were digested with MMP-3 and the Fn-fs tested for degradation of PG in cultured cartilage. RESULTS: Extracts of cartilage from patients with rheumatoid arthritis or with OA contained a range of Fn-fs. Removal of Fn-fs from OA synovial fluids significantly reduced the resultant damage when the fluids were added to cultured cartilage. Addition of IL-1 alpha to cultured cartilage or of MMP-3 to synovial fluids enhanced generation of Fn-fs. Fn-fs, whether derived from bovine plasma or synovial fluid or cartilage Fns, damaged cartilage. CONCLUSIONS: These data demonstrate that although Fn-fs could be generated in vivo within synovial fluids and Fn-fs found in OA synovial fluid may contribute to cartilage damage in vivo, Fn-fs could also be generated within cartilage and amplify cartilage damage. Thus, Fn-fs may be both autocrine and paracrine regulators of cartilage metabolism.

Animals↗
PubMed2005

Association of cartilage defects with loss of knee cartilage in healthy, middle-age adults: a prospective study.

OBJECTIVE: The significance of asymptomatic knee cartilage defects in healthy individuals is not known. The aim of this study was to examine the association between cartilage defects in the knee and cartilage volume both cross-sectionally and longitudinally in healthy, middle-age adults. METHODS: Eighty-six healthy men and women (mean +/- SD age 53.8 +/- 8.8 years) underwent T1-weighted fat-suppressed magnetic resonance imaging of their dominant knees at baseline and at the 2-year followup visit. Knee cartilage volume was measured. Cartilage defects were scored according to a grading system (0-4) and as present (a defect score of > or = 2) or absent in the medial and lateral tibiofemoral compartments. RESULTS: Cartilage defects in the medial and lateral tibiofemoral compartments were very common (in 61% and 43% of subjects, respectively). Those with cartilage defects had a 25% reduction in medial tibial cartilage volume, a 15% reduction in lateral tibial cartilage volume, and a 19% reduction in total femoral cartilage volume relative to those with no cartilage defects in cross-sectional analyses (all P < 0.05). In the medial tibiofemoral compartment, the annual loss of tibial cartilage in those with cartilage defects was 2.5% (95% confidence interval [95% CI] 2.2%, 3.1%) compared with an annual loss of tibial cartilage of 1.3% (95% CI 0.5%, 2.0%) in those with no defects (P = 0.028), independent of other known risk factors for osteoarthritis (OA). CONCLUSION: These data suggest that the presence of asymptomatic, non-full-thickness medial tibiofemoral cartilage defects identifies healthy individuals most likely to lose knee cartilage in the absence of radiographic knee OA. Thus, interventions aimed at reducing or reversing cartilage defects may reduce the risk of subsequent knee OA.

Australia↗
PubMed2002

In situ hybridization and immunohistochemistry of bone sialoprotein and secreted phosphoprotein 1 (osteopontin) in the developing mouse mandibular condylar cartilage compared with limb bud cartilage.

Mandibular condylar cartilage is often classified as a secondary cartilage, differing from the primary cartilaginous skeleton in its rapid progress from progenitor cells to hypertrophic chondrocytes. In this study we used in situ hybridization and immunohistochemistry to investigate whether the formation of primary (tibial) and secondary (condylar) cartilage also differs with respect to the expression of two major non-collagenous glycoproteins of bone matrix, bone sialoprotein (BSP) and secreted phosphoprotein 1 (Spp1, osteopontin). The mRNAs for both molecules were never expressed until hypertrophic chondrocytes appeared. In the tibial cartilage, hypertrophic chondrocytes first appeared at E14 and the expression of BSP and Spp1 mRNAs was detected in the lower hypertrophic cell zone, but the expression of BSP mRNA was very weak. In the condylar cartilage, hypertrophic chondrocytes appeared at E15 as soon as cartilage tissue appeared. The mRNAs for both molecules were expressed in the newly formed condylar cartilage, although the proteins were not detected by immunostaining; BSP mRNA in the condylar cartilage was more extensively expressed than that in the tibial cartilage at the corresponding stage (first appearance of hypertrophic cell zone). Endochondral bone formation started at E15 in the tibial cartilage and at E16 in the condylar cartilage. At this stage (first appearance of endochondral bone formation), BSP mRNA was also more extensively expressed in the condylar cartilage than in the tibial cartilage. The hypertrophic cell zone in the condylar cartilage rapidly extended during E15-16. These results indicate that the formation process of the mandibular condylar cartilage differs from that of limb bud cartilage with respect to the extensive expression of BSP mRNA and the rapid extension of the hypertrophic cell zone at early stages of cartilage formation. Furthermore, these results support the hypothesis that, in vivo, BSP promotes the initiation of mineralization.

Animals↗
PubMed2005

Association of prevalent and incident knee cartilage defects with loss of tibial and patellar cartilage: a longitudinal study.

OBJECTIVE: To describe the association between prevalent and incident knee cartilage defects and loss of knee cartilage in male and female adults. METHODS: A convenience sample of 325 subjects (mean age 45 years; age range 26-61 years) was evaluated at baseline and approximately 2 years later. Knee cartilage volume, cartilage defect scores (0-4 scale), and joint surface area were determined using T1-weighted fat-suppression magnetic resonance imaging techniques. Height, weight, and radiographic evidence of osteoarthritis were measured by standard protocols. RESULTS: Multivariable analysis revealed that baseline cartilage defect scores at the medial tibia, lateral tibia, and patella had a dose-response association with the annual rate of change in knee cartilage volume at the corresponding site (beta = -1.3% to -1.2% per grade; P < 0.05 for all comparisons). In addition, an increase in knee cartilage defect score (change of > or =1) was associated with higher rates of knee cartilage volume loss at all sites (beta = -1.9% to -1.7% per year; P < 0.01 for all comparisons). Furthermore, a decrease in the knee cartilage defect score (change of less than or equal to -1) was associated with an increase in knee cartilage volume at all sites (beta = 1.0% to 2.7% per year; P < 0.05 for all comparisons). CONCLUSION: Prevalent knee cartilage defects are predictive of compartment-specific cartilage loss over 2 years. Both increases and decreases in knee cartilage defects are associated with changes in knee cartilage volume, which implies a potential for reversal of knee cartilage loss.

Adult↗
PubMed1996

Cartilage canals in human thyroid cartilage characterized by immunolocalization of collagen types I, II, pro-III, IV and X.

In this study the collagenous composition of cartilage canals in human thyroid cartilage, which are perichondral invaginations of blood vessels and connective tissue, and the surrounding cartilage matrix were investigated by immunolabelling with specific antibodies against type I, II, pro-III, IV and X collagen. During childhood and early adolescence no cartilage canals were detected in thyroid cartilage, and immunolabelling for type IV collagen was restricted to basal lamina components of blood vessels in the perichondrium. First immunolabelling for type IV collagen, belonging to blood vessels in cartilage canals, in both sexes was detected about the end of the second decade; it was localized in the dorsal part of the thyroid cartilage plate. At this time thyroid cartilage has already reached its final form and size. As revealed by von Kossa staining, vascularization preceded mineralization and ossification. In contrast to the male thyroid cartilage plate, no immunostaining for type IV collagen and no ossification was detected in the ventral half of female thyroid cartilage even in advanced age. The extracellular matrix of cells in cartilage canals showed positive immunostaining for collagen types I and pro-III as well as for collagen type II, indicating that the cells in the canal possess fibroblastic and chondrogenic properties. The extracellular matrix of hypertrophic chondrocytes adjacent to cartilage canals showed strong immunoreactivity for type X collagen. First mineralization was detected close to cartilage canals, suggesting that mineralization in human thyroid cartilage starts in the extracellular matrix adjacent to cartilage canals.

Adolescent↗
PubMed2005

Knee cartilage defects: association with early radiographic osteoarthritis, decreased cartilage volume, increased joint surface area and type II collagen breakdown.

OBJECTIVE: To generate hypotheses regarding the associations between knee cartilage defects and knee radiographic osteoarthritis (ROA), cartilage volume, bone size and type II collagen breakdown in adults. METHODS: A cross-sectional convenience sample of 372 male and female subjects (mean age 45 years, range 26-61) was studied. Knee cartilage defect score (0-4) and prevalence (a defect score of > or =2), cartilage volume, and bone surface area were determined using T1-weighted fat saturation MRI. Urinary levels of C-terminal crosslinking telopeptide of type II collagen (U-CTX-II) were measured by enzyme-linked immunosorbent assay. Height, weight and ROA were measured by standard protocols. RESULTS: In multivariate analysis, the severity and prevalence of knee cartilage defects were significantly and independently associated with tibiofemoral osteophytes (regression coefficient (beta): +0.86 to +1.31/unit, odds ratio (OR): 2.97-3.68/unit, all P<0.05 with the exception of OR in lateral tibiofemoral compartment) and tibial bone area (beta: +0.11 to +0.25/cm2; OR: 1.33-1.58/cm2, all P<0.01). Knee cartilage defects were inconsistently associated with joint space narrowing after adjustment for osteophytes but consistently with knee cartilage volume (beta: -0.27 to -0.70/ml; OR: 0.16-0.56/ml, all P<0.01 except for OR at lateral tibial cartilage site P=0.06). Lastly, knee cartilage defect severity was significantly associated with U-CTX-II (Partial r=+0.18, P<0.001 for total cartilage defect score). CONCLUSION: Osteophytes and increasing knee bone size may be causally related to knee cartilage defects. Furthermore, knee cartilage defects may result in increased cartilage breakdown leading to decreased cartilage volume and joint space narrowing suggesting an important role for knee cartilage defects in early knee OA.

Adult↗
PubMed2005

Monopolar radiofrequency treatment of partial-thickness cartilage defects in the sheep knee joint leads to extended cartilage injury.

BACKGROUND: The application of radiofrequency energy to smooth and stabilize the cartilage surface has become increasingly controversial. There is little knowledge on extended-term effects, such as cartilage viability. PURPOSE: To analyze the effect of radiofrequency treatment on artificially created partial-thickness defects in the femoral cartilage of sheep knee joints 24 weeks after surgery. STUDY DESIGN: Controlled laboratory study. METHODS: Grade II cartilage surface defects on the medial and lateral femoral condyles were artificially created in sheep for in vivo analysis. The cartilage lesions were treated alternately on the lateral or the medial condyle using a monopolar radiofrequency probe. Radiofrequency treatment was performed in a freehand technique until surface smoothing without change of cartilage color was seen. At 24 weeks after surgery, cartilage samples were harvested and were processed for macroscopic and histological evaluation. To analyze the effect of radiofrequency at time zero, samples of sheep femoral condyle cartilage with and without artificially created clefts were treated in vitro with radiofrequency. Evaluation was performed by scanning electron and confocal microscopy. RESULTS: At 24 weeks after surgery, grade IV cartilage defects were detected in all radiofrequency-treated samples. The histological findings showed a central ulcer and dead chondrocytes in the radiofrequency-treated regions. The radiofrequency-treated cartilage revealed partial surface irregularities with partial-defect repair. After radiofrequency treatment in vitro, samples at time zero showed smoothing of the artificially created clefts, as seen by scanning electron microscopy. Confocal microscopy showed necrosis of chondrocytes over approximately one fourth of the upper cartilage thickness. CONCLUSION: Even if chondrocyte death is seen only in approximately one fourth of the upper cartilage layers in the sheep femur after in vitro application, radiofrequency treatment can cause damage to cartilage 24 weeks after application. CLINICAL RELEVANCE: Caution is recommended in the application of monopolar radiofrequency energy by visual control to partial-thickness cartilage defects. Irregular fronds of chondromalacia may be unattractive but represent viable articular cartilage. Using radiofrequency to obtain a more visually pleasing smooth surface may be counterproductive.

Animals↗
PubMed2005

[Repair of articular cartilage defects with "two-phase" tissue engineered cartilage constructed by autologous marrow mesenchymal stem cells and "two-phase" allogeneic bone matrix gelatin].

OBJECTIVE: To investigate the effect of "two-phase" tissue engineered cartilage constructed by autologous marrow mesenchymal stem cells(MSCs) and allogeneic bone matrix gelatin(BMG) in repairing articular cartilage defects. METHODS: Thirty-two New Zealand white rabbits were involved in the experiment. "Two-phase" allogeneic BMG scaffold (one side of porous cancellous bone and the other side of cortical bone; 3 mm both in diameter and in thickness) was prepared from iliac bone and limb bone of 5 rabbits by sequentially chemical method. The MSCs were separated from 18 New Zealand white rabbits and induced to express chondrocytic phenotype. The chondrocyte precursor cells were seeded onto "two-phase" allogeneic BMG to construct tissue engineering cartilage. Masson's trichrome staining, PAS staining and scanning electronic microscopic observation were carried out at 1, 3 and 5 weeks. The defects of full thickness articular cartilage (3 mm both in diameter and in depth) were made at both sides of femoral medial condyles in 27 rabbits (including 18 of separated MSCs and the remaining 9). The defects were repaired with the tissue engineered cartilage at the right side (group A, n = 18), with BMG at the left side (group B, n = 18), and without any implant at both sides in the remaining 9 rabbits as a control (group C, n = 18). After 1, 3 and 6 months, the 6 specimens of femoral condyles were harvested in 3 groups, respectively. Gross observation, Masson's trichrome and Alcian blue staining, modified Wakitani scoring and in situ hybridization of collagen type I were carried out to assess the repair efficacy of tissue engineered cartilage. RESULTS: The "two-phase" BMG consisted of the dense cortical part and the loose cancellous part. In cancellous part, the pore size ranged 100-800 microm, in which the chondrocyte precursor cells being induced from MSCs proliferated and formed the cell-rich cartilaginous part of tissue engineered cartilage. In cortical part, the pore size ranged 10-40 microm, on which the cells arranged in a layer and formed the hard part of subchondral bone. After 1 month of transplantation, the cartilage and subchondral bone were regenerated in group A; during observation, the regenerated cartilage gradually thinned, but defect was repaired and the structure of the articular surface and subchondral bone was in integrity. In groups B and C, defects were not repaired, the surrounding cartilage of defect was abrased. According to the modified Wakitani scoring, the indexes in group A were significantly higher than those in group B and C (P < 0.01) except the thickness of cartilage at 6 months. The positive cell rate of in situ hybridization for collagen type II in group A was also higher than those in groups B and C (P < 0.01). CONCLUSION: "Two-phase" allogeneic BMG is a prospective scaffold for tissue engineered cartilage, which combines with autologous chondrocyte precursor cells induced from MSCs to construct the tissue engineering cartilage. The tissue engineered cartilage can repair defects of articular cartilage and subchondral bone.

Animals↗
PubMed2006

Comparison of age-dependent expression of aggrecan and ADAMTSs in mandibular condylar cartilage, tibial growth plate, and articular cartilage in rats.

A disintegrin and metalloproteinase with thrombospondin motif (adamalysin-thrombospondins, ADAMTS) degrades aggrecan, one of the major extracellular matrix (ECM) components in cartilage. Mandibular condylar cartilage differs from primary cartilage, such as articular and growth plate cartilage, in its metabolism of ECM, proliferation, and differentiation. Mandibular condylar cartilage acts as both articular and growth plate cartilage in the growing period, while it remains as articular cartilage after growth. We hypothesized that functional and ECM differences between condylar and primary cartilages give rise to differences in gene expression patterns and levels of aggrecan and ADAMTS-1, -4, and -5 during growth and aging. We employed in situ hybridization and semiquantitative RT-PCR to identify mRNA expression for these molecules in condylar cartilage and primary cartilages during growth and aging. All of the ADAMTSs presented characteristic, age-dependent expression patterns and levels among the cartilages tested in this study. ADAMTS-5 mainly contributed to ECM metabolism in growth plate and condylar cartilage during growth. ADAMTS-1 and ADAMTS-4 may be involved in ECM turn over in articular cartilage. The results of the present study reveal that ECM metabolism and expression of related proteolytic enzymes in primary and secondary cartilages may be differentially regulated during growth and aging.

ADAM Proteins↗
PubMed2002

Repairing large porcine full-thickness defects of articular cartilage using autologous chondrocyte-engineered cartilage.

Large full-thickness defects of articular cartilage remain a major challenge to orthopedic surgeons because of unsatisfactory results of current therapy. Many methods, such as chondrectomy, drilling, cartilage scraping, arthroplasty, transplantation of chondrocytes, periosteum, perichondrium, as well as cartilage and bone, have been tried to repair articular cartilage defects. However, the results are far from satisfactory. In this study, we applied a tissue-engineering approach to the repair of articular cartilage defects of knee joints in a porcine model. Using isolated autologous chondrocytes, polyglycolic acid (PGA), and Pluronic, we have successfully in vivo-engineered hyaline cartilage and repaired articular cartilage defects. The surface of the repaired defects appeared smooth at 24 weeks postrepair. Histological examination demonstrated a typical hyaline cartilage structure with ideal interface healing between the engineered cartilage and the adjacent normal cartilage and underlying cancellous bone. In addition, glycosaminoglycan (GAG) levels in the engineered cartilage reached 80% of that found in native cartilage at 24 weeks postrepair. Biomechanical analysis at 24 weeks demonstrated that the biomechanical properties of the tissue-engineered cartilage were improved compared with those at an earlier stage. Thus, the results of this study may provide insight into the clinical repair of articular cartilage defects.

Animals↗
PubMed2001

ADAM-10 protein is present in human articular cartilage primarily in the membrane-bound form and is upregulated in osteoarthritis and in response to IL-1alpha in bovine nasal cartilage.

The objective of our study was to determine the tissue distribution and localization of ADAM-10 protein in human and bovine cartilage and the changes it undergoes with cartilage degeneration seen in osteoarthritis (OA) and under the influence of interleukin-1 (IL-1). Human normal and OA articular cartilage and bovine nasal cartilage cultured in the presence of IL-1alpha were processed for histology and immunohistochemistry. ADAM-10 protein was extracted from human cartilage and analyzed by Western blotting using anti-ADAM-10 antibodies. Fluor S Image analyzer and Quantity One software program were applied to quantify the total amount of ADAM-10. ADAM-10 protein was detected in both human and bovine cartilage. The strongest immunostaining was found in the cytoplasm and/or cell membranes of the superficial and upper middle layer of normal adult human cartilage, in the clusters and fibrillated areas of OA cartilage, and in IL-1alpha-stimulated bovine nasal cartilage. The distribution of ADAM-10 protein in bovine nasal cartilage was dependent on the length of exposure to IL-1alpha and corresponded to the areas of proteoglycan depletion. By Western blotting analysis of human cartilage, ADAM-10 was primarily detected in the membrane-enriched fraction and its levels were increased in degenerated and OA cartilage compared to normal cartilage. The results of this study suggest that ADAM-10 might be an important factor associated with cartilage degenerative processes. (J Histochem Cytochem 49:1165-1176, 2001)

ADAM Proteins↗
PubMed2003

Pathways of load-induced cartilage damage causing cartilage degeneration in the knee after meniscectomy.

Results of both clinical and animal studies show that meniscectomy often leads to osteoarthritic degenerative changes in articular cartilage. It is generally assumed that this process of cartilage degeneration is due to changes in mechanical loading after meniscectomy. It is, however, not known why and where this cartilage degeneration starts. Load induced cartilage damage is characterized as either type (1)--damage without disruption of the underlying bone or calcified cartilage layer--or type (2), subchondral fracture with or without damage to the overlying cartilage. We asked the question whether cartilage degeneration after meniscectomy is likely to be initiated by type (1) and/or type (2) cartilage damage. To investigate that we applied an axisymmetric biphasic finite element analysis model of the knee joint. In this model the articular cartilage layers of the tibial and the femoral condyles, the meniscus and the bone underlying the articular cartilage of the tibia plateau were included. The model was validated with data from clinical studies, in which the effects of meniscectomy on contact areas and pressures were measured. It was found that both the maximal values and the distributions of the shear stress in the articular cartilage changed after meniscectomy, and that these changes could lead to both type (1) and type (2) cartilage damage. Hence it likely that the cartilage degeneration seen after meniscectomy is initiated by both type (1) and type (2) cartilage damage.

Anisotropy↗
PubMed1997

Cartilage canals in equine articular/epiphyseal growth cartilage and a possible association with dyschondroplasia.

Cartilage canals have been described in most mammals and contain the vascular elements necessary for the maintenance of epiphyseal growth cartilage. The presence and longevity of cartilage canals in developing articular/epiphyseal cartilage of horses is described for the first time. Growth cartilages from 30 normal horses (from 130 days gestation to age 2 years) and 6 cases of dyschondroplasia (age < 15 months) were examined. Cartilage canals were located in the epiphyses of fetuses as early as 130 days gestation. The secondary centres of ossification had developed by 250 days gestation and, at full term (approximately 340 days), the articular/epiphyseal cartilage was highly vascularised. Cartilage canals were closely surrounded by small round chondrocytes even when present in the zone of hypertrophic chondrocytes. From late gestation until at least age 10 weeks, blood vessels surrounded by cartilage were found extending beyond the zone of hypertrophic chondrocytes into the secondary centre of ossification. Cartilage canals were absent from normal articular/epiphyseal cartilage of animals age > 6 months. Cartilage canals were associated with retained cartilage of dyschondroplastic lesions found in animals age < 15 months. The presence of cartilage canals in association with dyschondroplastic lesions suggests they may have a role in the pathogenesis of this important disease.

Animals↗