Department of Internal Medicine 3, University of Erlangen-Nuremberg, Krankenhausstrasse 12, 91054 Erlangen, Germany.
Nat Rev Rheumatol. 2012 Nov;8(11):656-64. doi: 10.1038/nrrheum.2012.153. Epub 2012 Sep 25.
Bone erosion is a central feature of rheumatoid arthritis and is associated with disease severity and poor functional outcome. Erosion of periarticular cortical bone, the typical feature observed on plain radiographs in patients with rheumatoid arthritis, results from excessive local bone resorption and inadequate bone formation. The main triggers of articular bone erosion are synovitis, including the production of proinflammatory cytokines and receptor activator of nuclear factor κB ligand (RANKL), as well as antibodies directed against citrullinated proteins. Indeed, both cytokines and autoantibodies stimulate the differentiation of bone-resorbing osteoclasts, thereby stimulating local bone resorption. Although current antirheumatic therapy inhibits both bone erosion and inflammation, repair of existing bone lesions, albeit physiologically feasible, occurs rarely. Lack of repair is due, at least in part, to active suppression of bone formation by proinflammatory cytokines. This Review summarizes the substantial progress that has been made in understanding the pathophysiology of bone erosions and discusses the improvements in the diagnosis, monitoring and treatment of such lesions.
骨侵蚀是类风湿关节炎的一个核心特征，与疾病严重程度和不良功能结局相关。骨侵蚀发生于骨皮质，是类风湿关节炎患者平片上的典型表现，是由局部骨吸收过度和骨形成不足引起的。关节骨侵蚀的主要触发因素是滑膜炎，包括促炎细胞因子和核因子 κB 配体（receptor activator of nuclear factor κB ligand，RANKL）的产生，以及针对瓜氨酸化蛋白的抗体。事实上，细胞因子和自身抗体都能刺激破骨细胞的分化，从而刺激局部骨吸收。虽然目前的抗风湿疗法能抑制骨侵蚀和炎症，但现有骨损伤的修复虽然在生理上可行，但很少发生。修复缺乏的原因至少部分是由促炎细胞因子对骨形成的主动抑制所致。本文总结了在理解骨侵蚀病理生理学方面取得的重大进展，并讨论了这些病变的诊断、监测和治疗的改善。
