Positive regulators of osteoclastogenesis and bone resorption in rheumatoid arthritis.
Positive regulators of osteoclastogenesis and bone resorption in rheumatoid arthritis.
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DOI：
10.1186/ar3380
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发表时间：
2011-07-28
影响因子：
4.9
通讯作者：
Zwerina J
中科院分区：
文献类型：
--
作者：
Braun T;Zwerina J
骨破坏是类风湿性关节炎（RA）患者常见的临床严重事件。局部关节破坏可导致关节不稳定，通常需要重建或置换手术。此外，炎症诱导的全身性骨丢失与骨折风险增加有关。骨吸收是一个良好控制的过程，依赖于单核细胞分化为骨吸收破骨细胞。RA患者的滑膜细胞，如T细胞、单核细胞和滑膜成纤维细胞等浸润性和驻留性滑膜细胞已被确定为破骨细胞分化信号的来源。促炎细胞因子是驱动这一过程的最重要机制之一。特别是，巨噬细胞集落刺激因子、RANKL、TNF、IL-1和IL-17可能在关节炎相关骨丢失的发病机制中起主导作用。这些细胞因子激活不同的细胞内途径以启动破骨细胞分化。因此，在过去的几年中，已经确定了几个有希望的治疗关节炎性骨破坏的靶点。
Bone destruction is a frequent and clinically serious event in patients with rheumatoid arthritis (RA). Local joint destruction can cause joint instability and often necessitates reconstructive or replacement surgery. Moreover, inflammation-induced systemic bone loss is associated with an increased fracture risk. Bone resorption is a well-controlled process that is dependent on the differentiation of monocytes to bone-resorbing osteoclasts. Infiltrating as well as resident synovial cells, such as T cells, monocytes and synovial fibroblasts, have been identified as sources of osteoclast differentiation signals in RA patients. Pro-inflammatory cytokines are amongst the most important mechanisms driving this process. In particular, macrophage colony-stimulating factor, RANKL, TNF, IL-1 and IL-17 may play dominant roles in the pathogenesis of arthritis-associated bone loss. These cytokines activate different intracellular pathways to initiate osteoclast differentiation. Thus, over the past years several promising targets for the treatment of arthritic bone destruction have been defined.
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