Haugeberg Glenn, Ørstavik Ragnhild E, Kvien Tore K
Oslo City Department of Rheumatology, Diakonhjemmet Hospital, Norway.
Curr Opin Rheumatol. 2003 Jul;15(4):469-75. doi: 10.1097/00002281-200307000-00016.
The effects of rheumatoid arthritis on bone include structural joint damage (erosions) and osteoporosis. The latter may lead to increased risk for fractures, which are associated with increased morbidity and mortality. Osteoporosis in rheumatoid arthritis is characterized by a complexity of risk factors, including primary osteoporosis risk factors in addition to inflammation, immobilization, and use of corticosteroids. Quantitative assessment of periarticular and generalized bone loss in rheumatoid arthritis may be reliable indicators of future disease course and potential response variables in intervention studies. The osteoclast cell in rheumatoid arthritis plays a crucial role in the development of erosions and periarticular and generalized osteoporosis, suggested to be mediated through the osteoprotegerin/receptor activator of Nuclear Factor (NF)-kappabeta/receptor activator of NF-kappabeta ligand signaling system. Based on an improved understanding of this biology, new treatment opportunities exist.
类风湿关节炎对骨骼的影响包括关节结构损伤(侵蚀)和骨质疏松症。后者可能导致骨折风险增加,而骨折与发病率和死亡率的上升相关。类风湿关节炎中的骨质疏松症具有多种风险因素,除炎症、制动和使用皮质类固醇外,还包括原发性骨质疏松症的风险因素。类风湿关节炎中关节周围和全身性骨质流失的定量评估可能是未来疾病进程的可靠指标,也是干预研究中潜在的反应变量。类风湿关节炎中的破骨细胞在侵蚀以及关节周围和全身性骨质疏松症的发展中起关键作用,这一过程可能是通过骨保护素/核因子(NF)-κB受体激活剂/NF-κB配体受体激活剂信号系统介导的。基于对这一生物学特性的深入了解,出现了新的治疗机会。