![]() With immune activation, there is an influx of predominantly macrophages and T-cell lymphocytes, from the vascular compartment in response to cytokines and cell adhesion molecules ( 12) ( 13), with other contributing cells including synoviocytes and chondrocytes ( 14). The synovium in OA is histologically characterized by thickening, hyperplasia, fibrosis and stromal vascularization ( 11). Innate immunity also likely plays a role in the pathogenesis of OA, with a study demonstrating compromised T and B cell immune function in OA patients, beyond that expected for age ( 10). Trauma is a known trigger of local inflammatory mediators, and there is increasing evidence that obesity also increases systemic low-grade inflammatory mediators ( 9). Cartilage breakdown is mediated by both chondrocyte and synovial macrophage-derived inflammatory mediators ( 8). There is increasing evidence that low-grade inflammation induced by a combination of trauma, metabolism, innate immunity and inflammatory factors contributes to the pathogenesis of OA( 6, 7). Emerging applications such as hybrid PET-MRI and molecular imaging are also briefly discussed. We also discuss the utility of MRI as an outcome measure to assess treatment response, particularly with respect to osteoarthritis (OA) and rheumatoid arthritis (RA). The purpose of this article is to summarize the pathophysiology of synovitis and to review the role of qualitative, semi-quantitative and quantitative MRI in the assessment of synovitis and joint fluid. International initiatives such as OMERACT (Outcome Measures in Rheumatology) and EULAR (European League Against Rheumatism) have emphasized standardization of MR assessment of synovial disease ( 2, 3). It allows noninvasive assessment of synovial volume, as well as active inflammation (assessed via increased vascularity detected with dynamic contrast-enhanced techniques). Magnetic resonance imaging (MRI) allows unparalleled assessment of all joint structures including the synovium, cartilage, and bone marrow amongst other articular structures ( 1). The synovial membrane of diarthrodial joints is implicated in the initiation and progression of a wide range of degenerative, inflammatory and crystalline arthropathies. It has emerged as a powerful tool, which enables not only detection of synovitis and effusion, but also allows quantification, detailed characterization and noninvasive monitoring of synovial processes. Magnetic resonance imaging (MRI) allows unparalleled assessment of all joint structures and associated pathology. Earlier detection and accurate assessment of synovial pathology can, therefore, facilitate appropriate clinical management and hence improve prognosis. Synovitis and joint effusion are common manifestations of rheumatic disease and play an important role in the disease pathophysiology.
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