The role of synovitis in osteoarthritis pathogenesis.

The role of synovitis in osteoarthritis pathogenesis.
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DOI:
10.1016/j.bone.2012.02.012
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发表时间:
2012-08
期刊:
影响因子:
4.1
通讯作者:
Goldring, Steven R.
Goldring, Steven R.
中科院分区:
医学2区
文献类型:
--
作者:
Scanzello, Carla R.;Goldring, Steven R.

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对骨关节炎(OA)的病理生理学的研究集中在软骨和关节骨周围,但是人们对OA的识别越来越多,OA会影响所有关节组织,包括正常生理条件。具有巨噬细胞和成纤维细胞的表型特征的细胞薄层。对于正常软骨和关节功能所必需的滑动流体(SF)的重要来源。增生,巨噬细胞和淋巴细胞的浸润,新血管生成和纤维化。其他关节组织的代谢和结构变化。结论是,OA中的滑膜炎与更严重的疼痛和关节功能障碍有关。在某些患者人群中的软骨损失率。软骨和其他关节组织的细胞外质量。趋化因子。在关节组织中检测到一些炎症介质,并在OA中进行SF,并对软骨细胞具有分解代谢作用。
Research into the pathophysiology of osteoarthritis (OA) has focused on cartilage and peri-articular bone, but there is increasing recognition that OA affects all of the joint tissues, including the synovium (SM). Under normal physiological conditions the synovial lining consists of a thin layer of cells with phenotypic features of macrophages and fibroblasts. These cells and the underlying vascularized connective tissue stroma form a complex structure that is an important source of synovial fluid (SF) components that are essential for normal cartilage and joint function. The histological changes observed in the SM in OA generally include features indicative of an inflammatory “synovitis”; specifically they encompass a range of abnormalities, such as synovial lining hyperplasia, infiltration of macrophages and lymphocytes, neoangiogenesis and fibrosis. The pattern of synovial reaction varies with disease duration and associated metabolic and structural changes in other joint tissues. Imaging modalities including Magnetic Resonance (MRI) and ultrasound (US) have proved useful in detecting and quantifying synovial abnormalities, but individual studies have varied in their methods of evaluation. Despite these differences, most studies have concluded that the presence of synovitis in OA is associated with more severe pain and joint dysfunction. In addition, synovitis may be predictive of faster rates of cartilage loss in certain patient populations. Recent studies have provided insights into the pathogenic mechanisms underlying the development of synovitis in OA. Available evidence suggests that the inflammatory process involves engagement of Toll-like receptors and activation of the complement cascade by degradation products of extracellular matrices of cartilage and other joint tissues. The ensuing synovial reaction can lead to synthesis and release of a wide variety of cytokines and chemokines. Some of these inflammatory mediators are detected in joint tissues and SF in OA and have catabolic effects on chondrocytes. These inflammatory mediators represent potential targets for therapeutic interventions designed to reduce both symptoms and structural joint damage in OA.
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