The Role of Cytokines in Osteoarthritis

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Inflammation and accompanying dysregulated cytokine catabolic activities play key roles in OA pathogenesis in addition to the effects of age and excessive mechanical loading (for review, see [70,74,121] (Fig. 3.2). Osteoarthritis is not considered a classical inflammatory arthropathy, because of the absence of neutrophils in the synovial fluid and the lack of systemic manifestations of inflammation. Nevertheless, synovial inflammation is common in both early and late stages of OA [19]. The expression of proinflammatory cytokines is observed in patients with early OA, and synovitis is common in advanced OA, where it involves infiltration of activated B cells and T lymphocytes [156]. There appears to exist a relationship between the levels in OA synovial fluids and joint tissues of catabolic enzymes and inflammatory mediators such as prostaglandins and nitric oxide and the levels of interleukin-1

Cartilage matrix

Cartilage matrix

Osteoarthritis Cytokines

Figure 3.2. The loss of balance between cartilage matrix degradation and synthesis in osteoarthritis. The figure shows potential roles and sources of inflammatory cytokines, such as interleukin-1 (IL-1), tumor necrosis factor-a (TNF-a), and oncostatin M (OSM), and anabolic growth factors, such as insulin-like growth factor-1 (IGF-1) and bone morphogenetic proteins (BMPs), that regulate cartilage metabolism.

Figure 3.2. The loss of balance between cartilage matrix degradation and synthesis in osteoarthritis. The figure shows potential roles and sources of inflammatory cytokines, such as interleukin-1 (IL-1), tumor necrosis factor-a (TNF-a), and oncostatin M (OSM), and anabolic growth factors, such as insulin-like growth factor-1 (IGF-1) and bone morphogenetic proteins (BMPs), that regulate cartilage metabolism.

(IL-1) and tumor necrosis factor-a (TNF-a). Therefore therapies that interfere with the expression or actions of these cytokines have been explored [68,167].

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