Inflammation-induced bone loss: Can it be prevented?
Inflammation-induced bone loss: Can it be prevented?
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DOI：
10.1016/j.rdc.2006.07.004
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发表时间：
2006-11-01
影响因子：
2.3
通讯作者：
Gillespie, Matthew T.
中科院分区：
文献类型：
--
作者：
Romas, Evange;Gillespie, Matthew T.
类风湿性关节炎的炎症过程导致严重的骨丢失，表现为关节骨侵蚀、关节旁骨质减少和全身性骨质疏松。关键的分子发现加上优雅的动物研究强调了破骨细胞在骨破坏中的致病作用。细胞因子的肿瘤坏死因子（TNF）家族，尤其是TNF-α和核因子-κ B配体的受体激活剂（RANKL），对于募集和激活破骨细胞以及诱导骨丢失是关键的。靶向抗TNF治疗或RANKL拮抗作用可预防炎症诱导的骨丢失，而有效的新型双膦酸盐是一种新兴的治疗工具。
The inflammatory process in rheumatoid arthritis elicits intense bone loss that is manifest as articular bone erosions, juxta-articular osteopenia, and systemic osteoporosis. Key molecular discoveries coupled with elegant animal studies have highlighted a pathogenic role of osteoclasts in bone destruction. The tumor necrosis factor (TNF) family of cytokines, especially TNF-alpha and receptor activator of nuclear factor-kappa B ligand (RANKL), are pivotal for recruiting and activating osteoclasts and inducing bone loss. Targeted anti-TNF therapy or RANKL antagonism prevents inflammation-induced bone loss, and the potent new bisphosphonates are an emerging therapeutic tool.