lntraarticular injections of triamcinolone acetonide resulted in deleterious changes in living rabbit articular knee cartilage. These changes were characterized by an increased frequency of chondrocyte nuclear degeneration and prominent cyst formation as compared with control animals. Degenerative changes were localized to the cartilage of the medial tibia1 plateau. This localization may be related to the different histologic pattern seen i n this cartilage surface as compared to other areas of the knee. The correlation between certain pre-existing patterns of cartilage histology and susceptibility t o degenerative change may provide a clue to the localization of degenerative joint disease i n humans.Clinical (1-5) ges has been attributed to a number of possible factors: increased coagulability (9) , vasculitis ( 5 ) , and local inhibition of pain sensation with secondary degenerative change (2). Mankin and Conger (8) demonstrated in rabbits, a decrease in glycine-H3 incorporation in the presence of intra-articular hydrocortisone acetate. They interpreted these findings as evidence that cortisol caused a decrease in cartilage matrix synthesis. Silberberg et ul ('i), noted that cortisone acetate when administered to mice disturbed organellar development of the cell, with a decrease in chondrocyte size. Their studies suggested a direct cata-I d i c or antianabolic effect of the corticosteroid. The present study, which evaluates the effects of long-acting corticosteroid preparations on living rabbit articular cartilage, was carried out in an effort to elucidate in further detail the pathology and pathogenesis of any steroid-related degenerative changes. Since corticosteroids are used frequently for therapeutic purposes, fur-
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