Inflammation in osteoarthritis (OA): Review of its role in clinical picture, disease progress, subsets, and pathophysiology

Electroacupuncture versus Diclofenac in symptomatic treatment of Osteoarthritis of the knee: a randomized controlled trial

“…The consequent roughness of the articular cartilage surfaces elicits secondary inflammatory reactions of the synovial membrane and bone. Unlike rheumatoid arthritis and other inflammatory joint diseases, the inflammatory component of OA is relatively mild [2,3]. Clinical manifestations of OA of the knee are joint pain, stiffness in the morning or after rest, pain at night, limited joint motion and/or joint deformity.…”

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“…The accumulation of mononuclear cells in synovial fluid, an increasing concentration of immunoglobulin and pathological findings of OA synovial tissue such as hyperplasia of synovial lining cells and infiltration of inflammatory cells into the sublining layer strongly suggest chronic inflammatory features of OA. These findings resemble the early stage of rheumatoid arthritis [7-9]. We were therefore interested in the immune response to cartilage components such as cartilage intermediate layer protein (CILP) and YKL39 [10,11].…”

Production of the chemokine eotaxin‐1 in osteoarthritis and its role in cartilage degradation

“…Osteoarthritis (OA), characterized by degradation of articular cartilage and inflammation of the synovium [Radin et al, 1991; Muir, 1995; Pelletier et al, 2001], is a chronic degenerative joint disease caused by biomechanical alterations and the aging process [Yuan et al, 2003]. However, recent studies have revealed a role of an inflammatory process in the pathogenesis of OA, with evidence of an inflammatory process reflected in several clinical signs and symptoms of OA, including swelling of affected joints, synovial effusion, and joint stiffness [Peyron, 1980; Pelletier et al, 2001]. Cartilage is normally avascular and, hence, is secluded from immune surveillance.…”