Abstract
Osteoarthritis (OA) is the most common joint disease worldwide and is a major ca use of joint pain and disability. Traditionally OA was considered primarily as a disease determined by progressive articular cartilage breakdown, caused by exposure to different mechanical and biological factors. The contemporary concept of OA emphasizes the complex pathogenesis of the disease, as a disorder of the joint as a whole organ, which involves not only hyaline cartilage, but also underlying bone and synovial tissue (synovium). Histological examination of synovial membrane have shown in most OA patients, infiltration of inflammatory cells into the synovium (synovitis), thickening of the synovium, increased production of pro-inflammatory cytokines. Significant inflammatory changes might be observed in the synovium even before evident cartilage damage occurs, however synovitis is present in all stages of OA. The histopathological and molecular examinations a well as modern imaging modalities (magnetic resonance, ultrasound) support the relevance of synovitis in OA. Synovial inflammation seems to be pivotal in the pathogenesis of OA, it is significantly associated with clinical symptoms (pain, morning stiffness), impairment of physical function. Synovitis could be an independent risk factor indicating progressive structural damage of OA and associated radiological changes. The goal of OA therapy is the reduction of pain and at least in some patients it is achie ved with anti-inflammatory treatment, using non-steroidal anti-inflammatory drugs (NSAIDs) or intra-articular glucocorticosteroid injections. The research of other treatment is in progress, looking for therapeutics of long-term anti-inflammatory effect, inhibiting the low-grade inflammation and the progress of degenerative change.
Published Version
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