TRANSECTION OF THE ANTERIOR CRUCIATE LIGAMENT IN THE DOG - A MODEL OF OSTEOARTHRITIS
TRANSECTION OF THE ANTERIOR CRUCIATE LIGAMENT IN THE DOG - A MODEL OF OSTEOARTHRITIS
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DOI：
10.1016/0049-0172(91)90037-z
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发表时间：
1991-12-01
影响因子：
5
通讯作者：
BRANDT, KD
中科院分区：
文献类型：
--
作者：
BRANDT, KD
对人类骨关节炎(OA)早期阶段的研究存在许多困难，因为患者通常直到病理变化非常严重且关节软骨已经广泛丧失时才寻求医疗救治。因此，研究人员使用动物模型来获取有关关节软骨、骨和滑膜早期变化的信息。在这些模型中，研究最广泛的是十字缺陷犬。这份报告证实了十字韧带缺陷犬是进行性骨性关节炎的模型，并强调，在关节软骨全层丧失之前，骨性关节炎的特点是软骨肥大，伴随着软骨细胞合成基质大分子的显著增加(代偿性修复)。综述了一些非类固醇抗炎药(NSAIDs)和不稳定肢体去传入可能加速骨关节炎软骨丢失的证据，并探讨了滑膜炎和软骨下骨改变与关节软骨改变的关系。
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 anti-inflammatory 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.