The joint synovium: A critical determinant of articular cartilage fate in inflammatory joint diseases

被引:93
作者
Bhattaram, Pallavi [1 ]
Chandrasekharan, Unnikrishnan [1 ]
机构
[1] Cleveland Clin, Lerner Res Inst, Dept Cellular & Mol Med, 9500 Euclid Ave,NC-10, Cleveland, OH 44195 USA
基金
新加坡国家研究基金会;
关键词
Articular cartilage; Endothelial cell; Fibroblast-like synoviocyte; Inflammation; Macrophage; Synovit is; ANTITUMOR NECROSIS FACTOR; MESENCHYMAL STEM-CELLS; RHEUMATOID-ARTHRITIS; FIBROBLASTS; MACROPHAGES; ACTIVATION; SYNOVIOCYTES; ANGIOGENESIS; EXPRESSION; PROMOTES;
D O I
10.1016/j.semcdb.2016.05.009
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
The synovium constitutes the envelope of articular joints and is a critical provider of synovial fluid components and articular cartilage nutrients. Its inflammation is a predominant feature and cause of joint degeneration in diseases as diverse as rheumatoid, psoriatic, juvenile and idiopathic arthritis, and lupus, gout and lyme disease. These inflammatory joint diseases (IJDs) are due to a wide variety of genetic, epigenetic and environmental factors that trigger, promote, and perpetuate joint destabilization. In spite of this variety of causes, IJDs share main pathological features, namely inflammation of the joint synovium (synovitis) and progressive degeneration of articular cartilage. In addition to being a driving force behind the destruction of articular cartilage in IJD, synovitis is also increasingly being recognized as a significant contributor of articular cartilage degeneration in osteoarthritis, a disease primarily due to aging- or trauma-related wear and tear of cartilage surfaces. In view of this important role of the synovium in determining the fate of articular cartilage, this review focuses on its underlying mechanisms in the pathology of IJD. We address the roles of synovial fibroblasts, macrophages and endothelial cells in the maintenance of joint health and in the destruction of articular cartilage integrity during IJD. Molecular mechanisms that have been recently shown to govern the pathological activities of the resident synovial cells are highlighted. Finally, advantages and disadvantages of targeting these new molecular mechanisms for preventing cartilage degeneration due to chronic inflammation are also discussed. (C) 2016 Elsevier Ltd. All rights reserved.
引用
收藏
页码:86 / 93
页数:8
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