1. The destruction of articular cartilage in human rheumatoid and other arthritides is the result of diverse mechanical, inflammatory and local cellular factors. A tissue-culture model for studying cartilage-synovial interactions that may be involved in the final common pathway of joint destruction is described. 2. Matrix breakdown was studied in vitro by using bovine nasal-cartilage discs cultivated in contact with synovium. Synovia were obtained from human and animal sources. Human tissue came from patients with ;classical' rheumatoid arthritis, and animal tissue from rabbits with antigen-induced arthritis. 3. Cartilage discs increased their proteoglycan content 2-3-fold during 8 days in culture. Proteoglycan was also released into culture medium, approx. 70% arising from cartilage breakdown. 4. Synovial explants from human rheumatoid and rabbit antigen-induced arthritis produced equivalent stimulation of proteoglycan release. After an initial lag phase, the breakdown rate rose abruptly to a maximum, resulting in a 2-fold increase of proteoglycan accumulation in culture medium after 8-10 days. 5. High-molecular-weight products shed into culture media were characterized chromatographically and by differential enzymic digestion. Proteoglycan-chondroitin sulphate accounted for 90% of the released polyanion, and its partial degradation in the presence of synovial explants was consistent with limited proteolytic cleavage. 6. Rheumatoid synovium applied to dead cartilage increased the basal rate of proteoglycan release. Living cartilage was capable of more extensive autolysis, even in the absence of synovium. However, optimal proteoglycan release required the interaction of living synovium with live cartilage. These findings support the view that a significant component of cartilage breakdown may be chondrocyte-mediated.
The in vitro breaking forces of the distal femoral growth plates of young rabbits were measured as a background to the design of a bone lengthening method, using epiphyseal distraction. The mean breaking force in 16 femora was 12.98 +/- 3.48 kg and the mean strain was 0.91 +/- 0.33 mm. The mean stress in 10 femora was 14.51 +/- 3.88 kg/cm2. The procedure was repeated, after applying a 1.0 kg dead weight to 6 femora for 24 hours and the breaking force was then 15.01 +/- 4.70 kg, with a mean strain of 0.85 +/- 0.62 mm. A further 8 rabbits then underwent epiphyseal distraction for 2 days in vivo, with 1 or 2 kg forces delivered to two parallel K wires by a pair of spring devices, whereupon the femora were removed and tested as before. The breaking force on the distracted side was now only 8.91 +/- 3.71 kg, compared with 13.99 +/- 3.40 kg on the control side. Although not fractured, these plates had obviously been weakened. The clinical implication of this is discussed.
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