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. This article is part of a Special Issue entitled "Osteoarthritis".

Carla R Scanzello

Steven R Goldring

Bone

BONE 是一个跨学科论坛，用于快速发表有关骨和矿物质代谢的基础、转化和临床方面的原创文章和评论。该杂志还鼓励提交有关骨骼与其他器官系统相互作用的论文，包括软骨、内分泌、肌肉、脂肪、神经、血管、胃肠道、造血和免疫系统。特别注意将实验研究应用于临床实践。

BONE is an interdisciplinary forum dedicated to the rapid publication of original articles and reviews concerning the fundamental, translational, and clinical aspects of bone and mineral metabolism. The journal also encourages submissions on the interactions between bone and other organ systems, including cartilage, endocrine, muscle, fat, nerve, vascular, gastrointestinal, hematopoietic, and immune systems. Special emphasis is placed on applying experimental research to clinical practice.

BONE 是一个跨学科的论坛，旨在快速发表关于骨骼和矿物质代谢的基础研究、转化研究和临床研究的原创文章和评论。该杂志还鼓励提交关于骨骼与其他器官系统相互作用的论文，包括软骨、内分泌、肌肉、脂肪、神经、血管、胃肠道、造血和免疫系统。特别关注将实验研究应用于临床实践。

The role of synovitis in osteoarthritis pathogenesis.

Most studies have concluded that the presence of synovitis in OA is associated with more severe pain and joint dysfunction, and may be predictive of faster rates of cartilage loss in certain patient populations.

Category	Quartile
医学	2
医学, 内分泌学与代谢	2

The role of synovitis in osteoarthritis pathogenesis.

ivySCI AI Smartly Parses PDF, Answers Researchers' Questions, and Helps You Understand Papers in Seconds

Journal Info

Category	Quartile
ENDOCRINOLOGY & METABOLISM	2