Clinical aspects of the effect of NSAID on cartilage.

Tons of nonsteroidal antiinflammatory drugs (NSAID) are used every year around the world. Their use is increasing and some patients have taken these drugs for at least 2 decades. Do NSAID damage the cartilage and cause rather than prevent further joint damage? The concept of "analgesic hip" or "indomethacin hip" cannot be substantiated. (Individuals who develop progressive joint damage may do so regardless of therapy rather than because of it.) Some NSAID have no effect on normal canine cartilage glycosaminoglycan synthesis while others suppress or stimulate the synthesis. Moreover, it seems that NSAID have no effect on proteoglycan catabolism. We know, however, that intraarticular steroids have only minimal effect on cartilage. If anything, they decrease the synovial fluid proteoglycans, perhaps by decreasing the synthesis of proteoglycans or by inhibiting degradation of cartilage. We do not know whether NSAID induce, mediate or perpetuate cartilage damage. And the effect on fibrillation, proteoglycan loss of osteophyte size is unknown. NSAID are good cyclooxygenase inhibitors; they may well affect monocyte/immune function but their anabolic or catabolic effect on cartilage remains unclear. We cannot talk meaningfully about chondroprotection or chondrotoxicity of NSAID. Intuitively, it seems reasonable to assume that antiinflammatory agents decrease inflammation and the mediators that are known to destroy cartilage. It is probable that cartilage benefits rather than suffers from current NSAID.