OSTEOARTHRITIS: FUNDAMENTAL AND APPLIED ASPECTS OF THE DISEASE’S ETIOPATHOGENESIS. NOTHING EVER STANDS STILL
Summary. Summary. Article is devoted to the modern paradigm of osteoarthritis (OA), which is based on evidence derived inflammatory disease theory. OA has long been considered a «wear and tear» disease leading to loss of cartilage. OA used to be considered the sole consequence of any process leading to increased pressure on one particular joint or fragility of cartilage matrix. Progress in molecular biology in the 1990s has profoundly modified this paradigm. The discovery that many soluble mediators such as cytokines or prostaglandins can increase the production of matrix metalloproteinases by chondrocytes led to the first steps of an «inflammatory» theory. However, it took a decade before synovitis was accepted as a critical feature of OA. Today the pathogenesis of OA represented as abnormal remodeling of joint tissues (bone, cartilage, synovial, connective tissue), which is initiated and determined by pro-inflammatory mediators to the development of metabolic and later functional dysfunction of articular structures. Subchondral bone and synovium are a source of proinflammatory mediators. Etiopathogenic and clinical phenotypes of the disease have been identified and separated. This fact will play an important role in the stratification of patients into groups to improve treatment outcomes.
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