Goldring Steven R, Gravallese Ellen M
Harvard Institutes of Medicine, Room 241, 4 Blackfan Circle, Boston, MA 02115, USA.
Curr Rheumatol Rep. 2002 Jun;4(3):226-31. doi: 10.1007/s11926-002-0069-y.
Histopathologic characterization of bone erosions from patients with rheumatoid arthritis (RA) and studies performed in animal models of inflammatory arthritis provide strong evidence that osteoclasts play an important role in focal marginal and subchondral bone loss in inflammatory arthritis. Much has been learned concerning the factors responsible for the induction and activation of osteoclasts associated with the bone erosions in RA. Therapies that target these osteoclast-inducing factors or other aspects of osteoclast-mediated bone resorption represent potential targets for blocking or at least attenuating bone destruction in RA. The demonstration of the role of the newly described osteoclastogenic factor receptor activator of nuclear factor kappaB ligand in RA synovial tissues and the successful prevention of bone erosions in animal models of arthritis with its inhibitor osteoprotegerin provide hope that specific therapies can be developed for preventing bone and joint destruction in RA, particularly in situations in which disease-modifying agents are ineffective in controlling disease activity.
类风湿关节炎（RA）患者骨侵蚀的组织病理学特征以及在炎性关节炎动物模型中进行的研究提供了强有力的证据，表明破骨细胞在炎性关节炎中局灶性边缘和软骨下骨丢失中起重要作用。关于RA中与骨侵蚀相关的破骨细胞诱导和激活的相关因素，人们已经了解很多。针对这些破骨细胞诱导因子或破骨细胞介导的骨吸收其他方面的疗法，是阻断或至少减轻RA中骨破坏的潜在靶点。新描述的破骨细胞生成因子核因子κB受体活化因子配体在RA滑膜组织中的作用得到证实，并且其抑制剂骨保护素在关节炎动物模型中成功预防了骨侵蚀，这让人们看到了开发特异性疗法以预防RA中骨和关节破坏的希望，特别是在病情缓解抗风湿药无法有效控制疾病活动的情况下。
