Tanaka Yoshiya
The First Department of Internal Medicine, School of Medicine, University of Occupational and Environmental Health.
Clin Calcium. 2010 May;20(5):735-42.
Rheumatoid arthritis (RA) is a systemic autoimmune disease characterized by chronic synovitis and bone damage. The bone manifestation in RA consists of joint destruction and systemic osteoporosis, which are brought about by different mechanisms. During the pathological processes, inflammatory cytokines such as TNF are largely produced from inflamed synovium and cause activation of osteoclasts deviated from bone remodelling cycle, resulting in joint destruction. But by the combinational use of methotrexate and TNF-inhibitors, clinical remission, structural remission and functional remission have become possible for the treatment of RA. Especially TNF-inhibitors remarkably suppress the progression of joint destruction in the vast majority of the patients. On the other side, systemic osteoporosis, mainly caused by menopause and glucocorticoid (GC), is often complicated in RA. However, bisphosphonate is well known to be effective for not only treatment but also prevention of GC-induced osteoporosis. Furthermore, anti-RANKL antibody denosumab possesses a potential to inhibit joint destruction as well as systemic and GC-mediated osteoporosis.
类风湿关节炎（RA）是一种以慢性滑膜炎和骨损伤为特征的全身性自身免疫性疾病。RA的骨表现包括关节破坏和全身性骨质疏松，其由不同机制引起。在病理过程中，诸如肿瘤坏死因子（TNF）等炎性细胞因子大量由发炎的滑膜产生，并导致偏离骨重塑周期的破骨细胞活化，从而导致关节破坏。但是通过甲氨蝶呤和TNF抑制剂的联合使用，实现RA的临床缓解、结构缓解和功能缓解已成为可能。特别是TNF抑制剂在绝大多数患者中显著抑制关节破坏的进展。另一方面，主要由绝经和糖皮质激素（GC）引起的全身性骨质疏松在RA中常并发。然而，双膦酸盐不仅对治疗而且对预防GC诱导的骨质疏松均有效。此外，抗核因子κB受体活化因子配体（RANKL）抗体地诺单抗具有抑制关节破坏以及全身性和GC介导的骨质疏松的潜力。
