Abstract

AbstractThe in vivo effect of aspirin on degeneration of knee cartilage in a canine model of osteoarthritis was examined. When dogs were fed aspirin daily after anterior cruciate ligament transection, the degeneration of articular cartilage in the unstable knee was more marked 9 weeks later than that in the operated knee of dogs which did not receive aspirin. Compared with samples from the contralateral knees, the thickness of articular cartilage in the operated knees of aspirin‐fed dogs was reduced, while it was increased in the operated knees of dogs not fed aspirin. In addition, the proteoglycan (uronic acid) content and the augmentation of proteoglycan synthesis in cartilage from the unstable knee were significantly lower when the dogs were fed aspirin than when they were not, and Safranin‐O staining of the matrix was less intense. However, cartilage from the contralateral knees of aspirin‐fed dogs was histochemically and biochemically normal in every respect. When metatarsal bones, with their overlying articular cartilage intact, were cultured in the presence of 10−4M and 10−5M salicylate, net glycosaminoglycan synthesis was suppressed by 25% and 15%, respectively. These concentrations of salicylate had previously been shown to have no effect on glycosaminoglycan metabolism in normal cartilage from the weightbearing region of the femoral condyle. Since the uronic acid content of metatarsal cartilage is lower than that of femoral cartilage, and that of osteoarthritic femoral cartilage is lower than that of normal femoral cartilage, the present results are consistent with the concept that cartilage is more permeable to aspirin when its matrix is depleted of proteoglycans.

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