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Journal ArticleDOI

The role of synovitis in pathophysiology and clinical symptoms of osteoarthritis

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TLDR
As synovitis is associated with clinical symptoms and also reflects joint degradation in OA, synovium-targeted therapy could help alleviate the symptoms of the disease and perhaps also prevent structural progression.
Abstract
Osteoarthritis (OA), one of the most common rheumatic disorders, is characterized by cartilage breakdown and by synovial inflammation that is directly linked to clinical symptoms such as joint swelling, synovitis and inflammatory pain The gold-standard method for detecting synovitis is histological analysis of samples obtained by biopsy, but the noninvasive imaging techniques MRI and ultrasonography might also perform well The inflammation of the synovial membrane that occurs in both the early and late phases of OA is associated with alterations in the adjacent cartilage that are similar to those seen in rheumatoid arthritis Catabolic and proinflammatory mediators such as cytokines, nitric oxide, prostaglandin E(2) and neuropeptides are produced by the inflamed synovium and alter the balance of cartilage matrix degradation and repair, leading to excess production of the proteolytic enzymes responsible for cartilage breakdown Cartilage alteration in turn amplifies synovial inflammation, creating a vicious circle As synovitis is associated with clinical symptoms and also reflects joint degradation in OA, synovium-targeted therapy could help alleviate the symptoms of the disease and perhaps also prevent structural progression

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Citations
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Journal ArticleDOI

Osteoarthritis: an update with relevance for clinical practice

TL;DR: In the coming years, a better definition of osteoarthritis is expected by delineating different phenotypes of the disease, and treatment targeted more specifically at these phenotypes might lead to improved outcomes.
Journal ArticleDOI

Osteoarthritis as an inflammatory disease (osteoarthritis is not osteoarthrosis

TL;DR: Low-grade inflammation induced by the metabolic syndrome, innate immunity and inflammaging are some of the more recent arguments in favor of the inflammatory theory of OA and highlighted in this review.
Journal ArticleDOI

Inflammation in osteoarthritis

TL;DR: This review focuses on the novel stress-induced and proinflammatory mechanisms underlying the pathogenesis of osteoarthritis, with particular attention to the role of synovitis and the contributions of other joint tissues to cellular events that lead to the onset and progression of the disease and irreversible cartilage damage.
Journal ArticleDOI

Local clearance of senescent cells attenuates the development of post-traumatic osteoarthritis and creates a pro-regenerative environment.

TL;DR: It is found that SnCs accumulated in the articular cartilage and synovium after ACLT, and selective elimination of these cells attenuated the development of post-traumatic OA, reduced pain and increased cartilage development, which support the use of SnCs as a therapeutic target for treating degenerative joint disease.
Journal ArticleDOI

The role of synovitis in osteoarthritis pathogenesis

TL;DR: 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.
References
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Vascular Endothelial Growth Factor

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Osteoarthritis, an inflammatory disease: Potential implication for the selection of new therapeutic targets

TL;DR: There is now strong evidence that the structural changes globally observed in OA are due to a combination of factors, ranging from the mechanical to the biochemical, including endogenous factors such as type II collagen mutation or dysplastic conditions.

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TL;DR: In this paper, skeletal status was evaluated in 2850 females aged 7 to 77 yr using quantitative ultrasound (QUS amplitude-dependent speed of sound [Ad-SoS]), and the peak value (2121 m/s) was achieved in 19-yr-old females.
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Human interleukin-17: A T cell-derived proinflammatory cytokine produced by the rheumatoid synovium.

TL;DR: It is indicated that IL-17 contributes to the active, proinflammatory pattern that is characteristic of RA through the contribution of some Th1-like T cells appear to mediate synovial inflammation.
Journal ArticleDOI

Synovial tissue inflammation in early and late osteoarthritis

TL;DR: Increased mononuclear cell infiltration and overexpression of mediators of inflammation were seen in early OA, compared with late OA; these observations may have important therapeutic implications for some patients during the early evolution of OA
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