Mohr W
Abteilung Pathologie, Universität Ulm.
Radiologe. 1996 Aug;36(8):593-9. doi: 10.1007/s001170050116.
Joint destruction, a hallmark of rheumatoid arthritis, is described with respect to different mechanisms: destruction by inflammatory cells of the synovial fluid, pannus tissue and even ischemic bone necroses. Destruction via the synovial fluid is due to polymorphonuclear neutrophils (PMN) that can invade the pannus-free cartilage surface. In the absence of anti-proteases as a result of direct contact between the PMN and cartilage, enzymatic degradation can occur. Pannus tissue usually develops from the synovial insertion. Increased cellular proliferation in this area leads to a superficial pannus tissue that covers the cartilage (Fig. 4b); granulation tissue from the synovial insertion can destroy cortical bone and invade the subchondral tissue. The problem of isolated subchondral inflammatory foci is briefly discussed. The effector cells of cartilage destruction are identified as macrophages, PMN, and mast cells -cells that produce or activate destructive enzymes. Bone destruction is due to osteoclasts and even macrophages. Acute destruction via the granulation tissue may be followed by defect healing-scar tissue or chondroid metaplastic tissue can be present in the final stages of the disease. Ischemic bone necrosis leading to pseudocysts may also contribute to joint destruction.
关节破坏是类风湿性关节炎的一个标志，可根据不同机制进行描述：滑膜液、血管翳组织甚至缺血性骨坏死的炎性细胞所导致的破坏。经由滑膜液的破坏是由于多形核中性粒细胞（PMN）可侵入无血管翳的软骨表面。由于PMN与软骨直接接触而缺乏抗蛋白酶，可能会发生酶促降解。血管翳组织通常从滑膜附着处发展而来。该区域细胞增殖增加会导致覆盖软骨的浅表血管翳组织（图4b）；来自滑膜附着处的肉芽组织可破坏皮质骨并侵入软骨下组织。文中简要讨论了孤立性软骨下炎性病灶的问题。软骨破坏的效应细胞被确定为巨噬细胞、PMN和肥大细胞，即产生或激活破坏酶的细胞。骨破坏是由破骨细胞甚至巨噬细胞引起的。经由肉芽组织的急性破坏之后可能会出现缺损愈合，在疾病的最终阶段可能会出现瘢痕组织或软骨样化生组织。导致假囊肿的缺血性骨坏死也可能导致关节破坏。
