Brandt K D
Indiana University School of Medicine, Indianapolis 46223.
Semin Arthritis Rheum. 1991 Dec;21(3 Suppl 2):22-32. doi: 10.1016/0049-0172(91)90037-z.
Study of the early stages of osteoarthritis (OA) in humans presents numerous difficulties, since the patient commonly does not seek medical attention until pathologic changes are far advanced and articular cartilage has already been extensively lost. Investigators have, therefore, used animal models to obtain information about the early changes in articular cartilage, bone, and synovium. Among the most widely studied of these models is the cruciate-deficient dog. This report validates the cruciate-deficient dog as a model of progressive OA and emphasizes that, before full-thickness loss of articular cartilage, OA is marked by a phase of cartilage hypertrophy associated with a striking increase in synthesis of matrix macromolecules by the chondrocyte (compensatory repair). It reviews evidence that some nonsteroidal antiinflammatory drugs (NSAIDs) and deafferentation of the unstable limb may accelerate cartilage loss in OA, and examines the relationship of synovitis and of changes in subchondral bone to the changes in articular cartilage.
对人类骨关节炎(OA)早期阶段的研究存在诸多困难,因为患者通常直到病理变化非常严重且关节软骨已大量丧失时才就医。因此,研究人员使用动物模型来获取有关关节软骨、骨骼和滑膜早期变化的信息。其中研究最广泛的模型之一是十字韧带损伤犬。本报告验证了十字韧带损伤犬作为进行性OA模型的有效性,并强调在关节软骨全层丧失之前,OA的特征是软骨肥大阶段,伴有软骨细胞合成基质大分子的显著增加(代偿性修复)。报告回顾了一些证据,表明某些非甾体抗炎药(NSAIDs)和对不稳定肢体进行去传入神经处理可能会加速OA中的软骨损失,并研究了滑膜炎以及软骨下骨变化与关节软骨变化之间的关系。