الفهرس 
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Abstract
OA is a low-grade synovial joint inflammatory disease. It is characterized by cartilage degradation and alteration of the whole joint structure. Because of this, the “OA ” has been changed to ”whole-organ illness.” Pathological changes such as periarticular muscular wasting and ligaments laxity are examples of these pathologic abnormalities. These patients typically have meniscal degeneration with increasing synovial inflammation and subchondral bone alterations and osteophyte formation. In elderly people, it is a main source of persistent discomfort and disability.
OA is significantly more prevalent than RA and other types of joint illness and it is among the most costly and severe types of joint disease. The knee is the most frequent joint disorder, and it is the commonest form of both radiographically visible and symptomatic joint disease.
Synovial inflammation marked by immune cell infiltration and cytokine production, is now commonly recognized as a hallmark of OA. Both innate immune system activation and the T-cell-mediated inflammatory pathway play important roles in disease genesis and progression as damage fuels the fire of inflammation.
Synovial inflammation has a significant and growing role in OA pathogenesis. Synovial inflammation is exacerbated by cartilage breakdown products. The inflamed synovium then creates catabolic and pro-inflammatory mediators, which leads to an increase in the synthesis of proteolytic enzymes that break down cartilage, generating a loop of positive feedback. The inflammatory response is boosted by activated synovial B cells, T cells, and invading macrophages.
Multiple studies have shown that inflammatory cytokines send key biochemical signals to chondrocytes, causing them to produce cartilage-degrading enzymes. Furthermore, chondrocytes have the ability to create and respond to these cytokines via autocrine and paracrine pathways. Furthermore, aberrant mechanical stresses can cause chondrocytes to release a variety of cytokines. Finally, oxidative stress may have a role in cytokine release triggering. TNFα, IL-1, IL-6, IL-15, IL-17, IL-8, and IL-18 are the most important of the many representatives of this cytokine family.