类风湿关节炎中的骨损伤：机制见解与预防方法。
Bone damage in rheumatoid arthritis: mechanistic insights and approaches to prevention.
机构信息
Division of Rheumatology, Department of Medicine, University of Massachusetts Medical School, UMass Memorial Medical Center, Lazare Research Building, Suite 223, 364 Plantation Street, Worcester, MA 01605, USA.
出版信息
Rheum Dis Clin North Am. 2010 May;36(2):385-404. doi: 10.1016/j.rdc.2010.03.003.
Abstract
In rheumatoid arthritis (RA), cells within the inflamed synovium and pannus elaborate a variety of cytokines, including tumor necrosis factor (TNF) alpha, interleukin (IL)-1, IL-6, and IL-17, that contribute to inflammation, and may directly affect bone. The receptor activator of NF-kappaB (RANK) ligand/RANK/osteoprotegerin pathway plays a critical role in regulating osteoclastogenesis in articular bone erosions in RA. Proinflammatory cytokines can modulate this pathway, and may also affect the ability of the osteoblast to repair bone at sites of articular erosion. In this review, the authors discuss the current understanding of pathogenic mechanisms of bone erosion in RA and examine current therapeutic approaches to prevent this damage.
摘要
在类风湿关节炎 (RA) 中，炎症滑膜和血管翳中的细胞产生多种细胞因子，包括肿瘤坏死因子 (TNF)α、白细胞介素 (IL)-1、IL-6 和 IL-17，这些细胞因子有助于炎症的发生，并可能直接影响骨骼。核因子-κB 受体激活剂 (RANK) 配体/RANK/骨保护素途径在调节 RA 关节骨侵蚀中的破骨细胞生成中起着关键作用。促炎细胞因子可以调节这条途径，也可能影响成骨细胞在关节侵蚀部位修复骨骼的能力。在这篇综述中，作者讨论了对 RA 中骨侵蚀发病机制的现有理解，并研究了预防这种损伤的当前治疗方法。
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