Ono Kumiko, Ohashi Satoru, Tanaka Sakae
Department of Orthopaedic Surgery, The University of Tokyo Hospital, Japan.
Clin Calcium. 2013 Feb;23(2):249-55.
In rheumatoid arthritis (RA) , the osteoclast pathway is activated by an abnormal immune condition accompanied by chronic inflammation, resulting in periarticular osteoporosis and local bone destruction around joints. In addition, multiple factors including pharmacotherapies such as steroids, and reduced physical activity, lead to systemic osteoporosis. These conditions expose patients to increased fracture risk. In RA treatment, it is important to achieve suppression of fracture risk by controlling inflammation, which is associated with periarticular osteoporosis and bone destruction, using disease-modifying anti-rheumatic drugs or biologic agents and by improving systemic osteoporosis using anti-osteoporotic agents.
在类风湿关节炎（RA）中，破骨细胞途径因伴有慢性炎症的异常免疫状况而被激活，导致关节周围骨质疏松以及关节周围局部骨质破坏。此外，包括类固醇等药物治疗以及体力活动减少在内的多种因素会导致全身性骨质疏松。这些情况使患者面临更高的骨折风险。在类风湿关节炎的治疗中，通过使用改善病情抗风湿药物或生物制剂控制与关节周围骨质疏松和骨质破坏相关的炎症，并使用抗骨质疏松药物改善全身性骨质疏松，从而实现对骨折风险的抑制，这一点很重要。
