Brandt K D, Slowman-Kovacs S
Clin Orthop Relat Res. 1986 Dec(213):84-91.
It is clear that some synovial inflammation occurs in joints affected by osteoarthritis (OA) and it is well recognized that many patients with OA experience a decrease in pain and joint stiffness following administration of salicylates or other nonsteroidal antiinflammatory drugs (NSAIDs). However, neither the extent to which synovitis contributes to the cartilage breakdown in OA nor the effects of chronic administration of NSAIDs on the natural history of OA in humans is known. Recent studies indicate that several NSAIDs, including salicylates, suppress proteoglycan synthesis in articular cartilage in vitro. The effect on OA cartilage is more marked than that on normal cartilage. Other studies show that salicylate feeding may suppress proteoglycan metabolism in degenerating cartilage in vivo, aggravating the decrease in proteoglycan content caused by the disease itself. However, no effect of salicylates on normal articular cartilage has been observed in vivo. In damaged cartilage the magnitude of NSAID-induced suppression of proteoglycan metabolism appears to be related inversely to the proteoglycan content of the tissue. In addition, the NSAIDs used in treatment of arthritis today may differ with respect to their in vivo effects on articular cartilage metabolism due, in part, to differences between the molar concentrations of these drugs in synovial fluid.
很明显，骨关节炎（OA）受累关节会出现一些滑膜炎，而且众所周知，许多OA患者在服用水杨酸盐或其他非甾体抗炎药（NSAIDs）后疼痛和关节僵硬会减轻。然而，滑膜炎在OA中对软骨破坏的影响程度以及NSAIDs长期给药对人类OA自然病程的影响尚不清楚。最近的研究表明，包括水杨酸盐在内的几种NSAIDs在体外可抑制关节软骨中蛋白聚糖的合成。对OA软骨的影响比对正常软骨的影响更明显。其他研究表明，喂食水杨酸盐可能会抑制体内退变软骨中蛋白聚糖的代谢，加剧疾病本身导致的蛋白聚糖含量下降。然而，在体内未观察到水杨酸盐对正常关节软骨有影响。在受损软骨中，NSAIDs诱导的蛋白聚糖代谢抑制程度似乎与组织中蛋白聚糖含量呈负相关。此外，如今用于治疗关节炎的NSAIDs在体内对关节软骨代谢的影响可能存在差异，部分原因是这些药物在滑液中的摩尔浓度不同。
