Bone damage in rheumatoid arthritis: mechanistic insights and approaches to prevention.

Bone damage in rheumatoid arthritis: mechanistic insights and approaches to prevention.
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DOI:
10.1016/j.rdc.2010.03.003
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发表时间:
2010-05
影响因子:
2.3
通讯作者:
Gravallese, Ellen M.
Gravallese, Ellen M.
中科院分区:
医学4区
文献类型:
--
作者:
Karmakar, Sougata;Kay, Jonathan;Gravallese, Ellen M.

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在类风湿性关节炎中,炎症滑膜和血管翳内的细胞产生多种细胞因子,包括TNFα、IL-1、IL-6和IL-17,这些细胞因子可导致炎症,并可能直接影响骨。RANKL/RANK/OPG通路在调节RA关节骨侵蚀中的破骨细胞生成中起关键作用。促炎细胞因子可以调节这一途径,也可能影响成骨细胞修复关节侵蚀部位骨的能力。在这篇综述中,我们讨论了目前对RA骨侵蚀致病机制的认识,并研究了目前预防这种损害的治疗方法。
In rheumatoid arthritis, cells within the inflamed synovium and pannus elaborate a variety of cytokines, including TNFα, IL-1, IL-6 and IL-17, that contribute to inflammation, and may directly impact bone. The RANKL/RANK/OPG pathway plays a critical role in regulating osteoclastogenesis in articular bone erosions in RA. Pro-inflammatory 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, we discuss the current understanding of pathogenic mechanisms of bone erosion in RA and examine current therapeutic approaches to prevent this damage.
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