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At least 145 records · Page 8Linked to original sources
PubMedDate not supplied

Cartilage space width in slipped capital femoral epiphysis: the relationship to cartilage necrosis.

The radiolucent cartilage space of eighty-three patients with unilateral or bilateral slipped capital femoral epiphysis was measured by a standardized technique. In the majority of patients, whether unilateral or bilateral involvement, there was bilateral narrowing of the cartilage space. In the unaffected hip of unilaterally involved patients, there was a progressive narrowing as skeletal maturity was attained. A concomitant anatomical study of cadaver hips, removed at autopsy from adolescent patients, showed a progressive narrowing of the cartilage as the proximal femur matured. Black females showed most narrowing (minimum cartilage space width), had the narrowest final cartilage space widths, and took the longest to attain this final width. While other racial, sexual and therapeutic groups failed to demonstrate statistically significant differences, the general trend was for females, Blacks, and patients treated by osteotomy to have more joint space narrowing. However, rewidening occurred in most of these affected joint spaces, in contrast to the progressive linear decrease observed in unaffected hips and anatomical specimens. On the basis of this study, we feel that cartilage space narrowing may be anticipated in the post-operative period in most patients treated for slipped capital femoral epiphysis. This narrowing appears to improve with time. Narrowing of greater than one-half the original width, in association with pain and limitation of joint function, probably represents "cartilage necrosis," or pathologic joint space narrowing. Unless the narrowing remains less than one-half to two-thirds of the initial cartilage space for more than twenty-four to thirty-six months, probably no specific surgical treatment should be undertaken, other than observation and protected weight bearing during any painful phase. Plotting the roentgenographic cartilage space width during the three month to thirty-six month phase may be useful in monitoring and predicting the outcome.

Adolescent↗
PubMed1997

The role of mandibular condylar cartilage in articular cartilage repair.

The articular hyaline cartilage of synovial joints has a very limited capacity for repair after injury. In contrast, the mandibular condylar cartilage of the temporomandibular joint possesses as intrinsic potential for regeneration. This study aimed to test the hypothesis that cultured allografts of mandibular condylar cartilage could be used to promote biological repair of injured orthotopic joint surfaces. Using a primate animal model, cultures of mandibular condylar cartilage cells were grafted into surgically created defects in a recipient hyaline cartilage joint surface. Articular wound healing was assessed macroscopically and histologically over a postoperative period of 52 weeks. Mandibular condylar cartilage cells scheduled for allogenous transplantation were initially characterised in vitro. Expansion of primary colonies in organ culture provided the allogenic cellular material for in vivo grafting. Grafting of osteochondral articular wounds with 5-week cultures of mandibular cartilage cells led to wound regeneration with complete reconstitution of articular surface continuity by 52 weeks. There was novel synthesis of cartilage collagens and sulphated glycosaminoglycans within the repair tissue and no evidence of immunological rejection. Healing of grafted defects was thought to occur by a combination of donor cell proliferation and ingress of host mesenchymal cells. In contrast, grafted control wounds underwent largely fibrous repair with incomplete articular regeneration. In conclusion, transplanted allografts of cultured mandibular condylar cartilage appeared to have the ability, in this primate model, to promote cartilaginous repair and regeneration of orthotopic articular wounds.

Animals↗
PubMed1998

[Noninvasive analysis of cartilage volume and cartilage thickness in the human elbow joint using MRI].

The aim of the study was to non-invasively analyse the cartilage volume and thickness in the human elbow joint with magnetic resonance imaging. 12 fresh frozen specimens (ages 20 to 69 yrs.) were investigated using a 1.5 T magnet, and a water-excitation FLASH-3D sequence at a resolution of 1 x 0.25 x 0.25 mm3. After linear interpolation to 0.125 x 0.125 mm2 in the image plane, the cartilages were segmented interactively with a Snake algorithm. Following three-dimensional reconstruction, the cartilage volumes were determined, and the mean and maximal cartilage thickness computed by Euclidean distance transformation. The total cartilage volume of the human elbow joint amounted to between 3.90 and 7.17 ml (mean 5.5 ml +/- 20%). The humerus occupied 49 to 60%, the radius 15 to 27% and the ulna 20 to 29% of the total volume. The mean cartilage thickness ranged from an average of 0.9 (proximal part of the ulna) to 1.4 mm (capitulum humeri), and the maximal thickness from 2.3 mm (proximal part of the ulna) to 2.9 mm (distal part of the ulna). The ulnar cartilage showed a more inhomogeneous distribution than that of the humerus and radius. The interindividual variability of the cartilage thickness was less than that of the volume. There was no significant relationship of the volume with age (r = 0.11) or body weight (r = 0.51). However, based on the joint size (r = 0.71-medio-lateral extension of the articular surfaces) about 50% of the variability of the total cartilage volume could be predicted. The technique presented is suitable for designing computer models to investigate the load transmission and functional adaptation of diarthrodial joints, and for diagnosing and monitoring joint disease.

Adult↗
PubMed1997

Enhancement of cartilage matrix protein synthesis in arthritic cartilage.

OBJECTIVE: To investigate whether the synthesis of cartilage matrix protein (CMP) is enhanced in arthritic cartilage. METHODS: The content of CMP in human and pig cartilage was determined by immunoblotting, and CMP-producing chondrocytes in osteoarthritic (OA) and rheumatoid arthritic (RA) joints were immunostained. RESULTS: CMP was undetectable in the condylar cartilage and disc of pigs, whereas it was abundant in the rib and tracheal cartilage of the same animals. By immunohistochemical analysis, CMP was localized in only a few chondrocytes (5%) in normal human joints, whereas numerous chondrocytes (>60%) were immunostained in RA joints. The number of CMP-producing cells was also increased in OA cartilage (>40%). Immunoblotting analyses confirmed that the CMP content in the cartilage from OA and RA patients was much higher than that in normal cartilage. CONCLUSION: These findings demonstrate that articular chondrocytes can synthesize CMP, although it is suppressed under physiologic conditions. The results also suggest that articular chondrocytes express CMP in response to arthritic stimuli.

Adult↗
PubMed1995

Cartilage oligomeric matrix protein: isolation and characterization from human articular cartilage.

Cartilage oligomeric matrix protein was purified in a native form from normal adult human articular cartilage. The key steps in the purification scheme were selective extraction with buffer containing EDTA, wheat germ agglutinin affinity chromatography, and removal of the related protein thrombospondin by heparin affinity chromatography. Particles of cartilage oligomeric matrix protein viewed by electron microscopy after rotary shadowing revealed structures similar to the prototype molecule purified from Swarm rat chondrosarcoma. The protein demonstrated a bouquet-like five-armed structure, with peripheral globular domains connected by thin flexible strands to a central assembly domain. Immunohistochemistry revealed age-dependent differences in the protein's distribution in cartilage. In normal human adult articular cartilage, there was a relatively uniform distribution throughout the interterritorial extracellular matrix, whereas in fetal articular cartilage, immunostaining was localized to the extracellular matrix directly adjacent to the chondrocytes. The isolation and characterization of human cartilage oligomeric matrix protein will facilitate its study in pathological conditions of human cartilage.

Adult↗
PubMed1998

Modulation of IL-1-induced cartilage injury by NO synthase inhibitors: a comparative study with rat chondrocytes and cartilage entities.

Nitric oxide (NO) is produced in diseased joints and may be a key mediator of IL-1 effects on cartilage. Therefore, we compared the potency of new [aminoguanidine (AG), S-methylisothiourea (SMT), S-aminoethylisothiourea (AETU)] and classical [Nomega-monomethyl-L-arginine (L-NMMA), Nomega-nitro-L-arginine methyl ester (L-NAME)] NO synthase (NOS) inhibitors on the inhibitory effect of recombinant human interleukin-1beta (rhIL-1beta) on rat cartilage anabolism. Three different culture systems were used: (1) isolated chondrocytes encapsulated in alginate beads; (2) patellae and (3) femoral head caps. Chondrocyte beads and cartilage entities were incubated in vitro for 48 h in the presence of rhIL-1beta with a daily change of incubation medium to obtain optimal responses on proteoglycan synthesis and NO production. Proteoglycan synthesis was assessed by incorporation of radiolabelled sodium sulphate [Na2(35)SO4] and NO production by cumulated nitrite release during the period of study. Chondrocytes and patellae, as well as femoral head caps, responded concentration-dependently to IL-1beta challenge (0 to 250 U ml(-1) and 0 to 15 U ml(-1) respectively) by a large increase in nitrite level and a marked suppression of proteoglycan synthesis. Above these concentrations of IL-1beta (2500 U ml(-1) and 30 U ml(-1) respectively), proteoglycan synthesis plateaued whereas nitrite release still increased thus suggesting different concentration-response curves. When studying the effect of NOS inhibitors (1 to 1000 microM) on NO production by cartilage cells stimulated with IL-1beta (25 U ml(-1) or 5 U ml(-1)), we observed that: (i) their ability to reduce nitrite level decreased from chondrocytes to cartilage samples, except for L-NMMA and AETU; (ii) they could be roughly classified in the following rank order of potency: AETU > L-NMMA > or = SMT > or = AG > or = L-NAME and (iii) AETU was cytotoxic when used in the millimolar range. When studying the effect of NOS inhibitors on proteoglycan synthesis by cartilage cells treated with IL-1beta, we observed that: (i) they had more marked effects on proteoglycan synthesis in chondrocytes than in cartilage samples; (ii) they could be roughly classified in the following rank order of potency: L-NAME > or = L-NMMA > > AG > SMT > > AETU and (iii) potentiation of the IL-1 effect by AETU was consistent with cytotoxicity in the millimolar range. D-isomers of L-arginine analog inhibitors (1000 microM) were unable to correct nitrite levels or proteoglycan synthesis in IL-1beta treated cells. L-arginine (5000 microM) tended to reverse the correcting effect of L-NMMA (1000 microM) on proteoglycan synthesis, thus suggesting a NO-related chondroprotective effect. However, data with L-NAME and SMT argued against a general inverse relationship between nitrite level and proteoglycan synthesis. Dexamethasone (0.1 to 100 microM) (i) failed to inhibit NO production in femoral head caps and chondrocytes beads whilst reducing it in patellae (50%) and (ii) did not affect or worsened the inhibitory effect of IL-1beta on proteoglycan synthesis. Such results suggested a corticosteroid-resistance of rat chondrocyte iNOS. Data from patellae supported a possible contribution of subchondral bone in NO production. In conclusion, our results suggest that (i) NO may account only partially for the suppressive effects of IL-1beta on proteoglycan synthesis, particularly in cartilage samples; (ii) the chondroprotective potency of NOS inhibitors can not be extrapolated from their effects on NO production by joint-derived cells and (iii) L-arginine analog inhibitors are more promising than S-substituted isothioureas for putative therapeutical uses.

Animals↗