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The use of drugs for the treatment of osteoarthritis, with a view to obtain a long-term symptomatic as well as structural benefit, is still in a preliminary state. Nowadays, matricial precursors, such as glucosamine sulfate, are an interesting approach in this indication. They have demonstrated a symptomatic efficacy comparable to that of N.S.A.I.D., with significantly reduced side-effects. Glucosamine sulfate also appears to positively interfere with the structural evolution of osteoarthritis by preventing joint space narrowing which characterizes the evolution of the disease. Encouraging results have also been obtained with chondroitin sulfate and diacerein. As for other molecules, new studies should be undertaken to confirm the results already obtained.

APOPTOSIS IN JOINT CARTILAGE: Apoptosis is the physiologically programmed death of cells to be distinguished from necrosis which caused non-programmed cell death. In joint cartilage, more than 50% of the chondrocytes show signs of apoptosis compared with 10% in normal cartilage. ROLE OF NITRIC OXIDE: In osteoarthritis the production of nitric oxide (NO) appears to be increased, inducing apoptosis of articular chondrocytes stimulated by interleukin 1. NO inhibitors can limit the progression of experimentally induced joint lesions in animal models. IN VITRO RESULTS: The protective effect of the chondroitin sulfates CS4 and CS6 against death of chondrocytes exposed to NO has been demonstrated in vitro. Chondrocytes for New Zealand white rabbits were cultivated in the presence of an NO donor for exposure durations from 12 to 72 hours, with or without adding CS 4&6 to the culture medium. After 3 days of culture, NO induced a significant rise in the number of apoptotic chondrocytes. In 70% of the cases, preventive treatment with 100 micrograms/ml CS 4&6 lowered the number of dead cells. This cytoprotective effect reached a mean 28% and was inversely dependent on the duration of exposure to the NO donor.