The pathogenesis of osteoarthritis (OA) is complex, but likely involves destruction of articular cartilage by endogenous enzymes (Dingle 1979). Factors controlling this are not well understood. Cetabolin, a 21,000 molecular weight peptide structurally end functionally related to interleukin-1, stimulates living but not killed chondrocytes in vitro to degrade their matrix (Fell and Jubb 1977, Saklatvala et al. 1983), suggesting it is not itself a degradative enzyme but functions as a control factor. The work in this thesis investigated the possible role of cetabolin in the pethogenesis of OA by measuring catabolin production by cultures of synovium excised from the canine anterior cruciate ligament transection model of OA. Normal cenine synovium in culture was shown to produce a factor which can stimulate the release of glycoseminoglycens from living cenine articular cartilage in culture. The total emount of cetebolin produced by cultures of synovium from experimentally induced OA synovium is statistically significantly greater (p<0.05) than that produced by normal synovium. When calculated per gram of synovium, there was no statistically significant difference. This suggests that a possible role for cetebolin in the pathogenesis of OA might be related to the degree of synovial hypertrophy. / Medicine, Faculty of / Graduate