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Open AccessJournal ArticleDOI

Role of inflammation in the pathogenesis of osteoarthritis: latest findings and interpretations

TLDR
This review will discuss a wide range of evolving data leading to the current hypotheses regarding the role of immune activation and inflammation in OA onset and progression as this is the joint most well characterized by epidemiologic, imaging, and translational studies investigating the association of inflammation with OA.
Abstract
Osteoarthritis (OA) has traditionally been classified as a noninflammatory arthritis; however, the dichotomy between inflammatory and degenerative arthritis is becoming less clear with the recognition of a plethora of ongoing immune processes within the OA joint and synovium. Synovitis is defined as inflammation of the synovial membrane and is characteristic of classical inflammatory arthritidies. Increasingly recognized is the presence of synovitis in a significant proportion of patients with primary OA, and based on this observation, further studies have gone on to implicate joint inflammation and synovitis in the pathogenesis of OA. However, clinical OA is not one disease but a final common pathway secondary to many predisposing factors, most notably age, joint trauma, altered biomechanics, and obesity. How such biochemical and mechanical processes contribute to the progressive joint failure characteristic of OA is tightly linked to the interplay of joint damage, the immune response to perceived damage, and the subsequent state of chronic inflammation resulting in propagation and progression toward the phenotype recognized as clinical OA. This review will discuss a wide range of evolving data leading to our current hypotheses regarding the role of immune activation and inflammation in OA onset and progression. Although OA can affect any joint, most commonly the knee, hip, spine, and hands, this review will focus primarily on OA of the knee as this is the joint most well characterized by epidemiologic, imaging, and translational studies investigating the association of inflammation with OA.

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Journal ArticleDOI

Low-grade inflammation as a key mediator of the pathogenesis of osteoarthritis

TL;DR: Osteoarthritis has long been viewed as a degenerative disease of cartilage, but accumulating evidence indicates that inflammation has a critical role in its pathogenesis, and increasing insight into the inflammatory underpinnings of OA holds promise for the development of new, disease-modifying therapies.
Journal ArticleDOI

Synovitis in osteoarthritis: current understanding with therapeutic implications.

TL;DR: Current knowledge on the prevalence of synovial inflammation in OA and its role in symptoms and structural progression is reviewed, and lessons learnt from targeting synovitis therapeutically are explored.
Journal ArticleDOI

Damage-Associated Molecular Patterns in Inflammatory Diseases.

TL;DR: Current research on the role of DAMPs in inflammatory diseases, including rheumatoid arthritis, systemic lupus erythematosus, osteoarthritis, atherosclerosis, Alzheimer's disease, Parkinson's disease and cancer are reviewed.
Journal ArticleDOI

Platelet-rich plasma for managing pain and inflammation in osteoarthritis

TL;DR: Understanding PRP in molecular terms could help to exploit its therapeutic potential, and aid the development of novel treatments and tissue-engineering approaches, for the different stages of joint degeneration.
Journal ArticleDOI

Aging and osteoarthritis: Central role of the extracellular matrix

TL;DR: This review will systematically analyze cellular and structural changes taking place in the articular cartilage and bone in the pathogenesis of OA which are linked to aging and place a particular emphasis on age-related changes in the phenotype of theArticular chondrocytes.
References
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TL;DR: Recent advances that have been made by research into the role of TLR biology in host defense and disease are described.
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Gout-associated uric acid crystals activate the NALP3 inflammasome

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Inflammation in Atherosclerosis

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TL;DR: Interactions ofHMGB1 with TLR 2 and TLR 4 may provide an explanation for the ability of HMGB1 to generate inflammatory responses that are similar to those initiated by LPS.
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