METABOLIC PHENOTYPE OF OSTEOARTHRITIS. MODERN VIEWS ON PATHOGENESIS, MECHANISMS OF PROGRESSION AND APPROACHES TO TREATMENT
Summary. In recent years, there has been a growing interest in metabolic changes in osteoarthritis. The review article summarizes data on the metabolic phenotype of osteoarthritis, the role of obesity, dyslipidemia, diabetes in the development of a metabolic phenotype. Current prospective epidemiological studies demonstrate the existence of clear associations between osteoarthritis and metabolic syndrome components. Some researchers consider metabolic osteoarthritis only as a result of excessive stress on the supporting joints due to obesity. However, many recent studies have demonstrated that adipokines and cytokines produced by fat tissue, hyperglycemia, insulin resistance and dyslipidemia can disrupt the metabolism of the joint tissues. Visceral obesity, dyslipidemia and insulin resistance form a special inflammation — low-level, chronic, associated with metabolic disorders and called «metaflammation». This type of inflammation plays a crucial role in the pathogenesis of obesity, type 2 diabetes and its complications, and multiple signaling pathways bind insulin resistance and immune response. Obesity has a dual effect on the course of osteoarthritis: the mechanical effect on the load-bearing joints, as well as the generation of metaflammation, which disrupts the metabolism of articular tissues of the non-load-bearing joints. Thus, obesity can influence the pathogenesis and progression of osteoarthritis through biomechanical effects, as well as an increase of metaflammation.
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