The role of lipid peroxidation in the pathogenesis of patients with secondary osteoarthritis depending on the stage of the volume of articular cartilage degeneration

Background. At the current stage of development, the problem of the pathogenesis of secondary osteoarthritis (OA) is attributed to the products of lipid peroxidation (LPO) and their toxic-destructive effect on the cellular tissue structures of articular cartilage. In addition, there are changes in membrane proteins and surface lipids, cell potentials and intercellular connections that characterize the early phase of activation of LPO processes depending on the stage of the volume of cell-tissue degeneration structures and progression of chronic sluggishly progressing inflammation of the joints and switch to activation of the final products of POL – malondealdehyde, which leads to the development of an autoimmune complex in this contingent of patients. Purpose – is to study the changes in LPO in the pathogenesis of patients with secondary OA depending on the stage of the volume of articular cartilage degeneration. Materials and Methods. The study was conducted in 117 patients aged 19 to 45 years who were undergoing inpatient treatment at Artz Klinic (Kharkov) for secondary OA. The diagnosis of OA was established according to the IKX-X. All patients according to the classification of the International Society for the Study of OA (OARSI) were divided into 4 groups depending on the stage of damage to the articular cartilage volume (%) of degenerative changes: stage 1 (< 10%); stage 2 (10–25%); stage 3 (25–50%); stage 4 (> 50%). Special studies were conducted to determine the levels of: primary diene conjugates (DK) and secondary end products of the LPO reaction – malondialdehyde (MDA) in plasma, erythrocytes and synovial fluid, as well as enzymes of antioxidant protection: catalase, superoxide dismutase; glutathione-dependent antioxidant system: glutathione, glutathione peroxidase, glutathione – S-transferase. Results. The obtained data confirmed an increase in LPO and a decrease in antioxidant defense enzymes depending on the degree of articular cartilage degeneration. An increase in primary lipid products, namely DK, was determined in groups of patients with stage 1 and 2 both in plasma, erythrocytes, and synovial fluid, and their subsequent decrease in groups of patients with stage 3 and 4 of the degenerative process in articular cartilage against the background of growth levels of final (secondary) products, namely MDA. The shown processes trigger the destruction of cellular tissue structures of articular cartilage. Against this background, depression of the glutathione-dependent antioxidant system progresses, especially demonstrably in groups of patients with stage 3 and 4 degeneration of articular cartilage, transferring the chronic inflammatory process to an autoimmune basis and apoptosis. Conclusions. In patients with secondary OA, an increase in the primary products of LPO – DK was determined in the groups of patients with stage 1 and 2, and the end products of LPO – MDA in the groups with stage 3 and 4 of the degenerative process in articular cartilage in blood plasma, erythrocytes and synovial fluid. Against the background of an increase in the level of lipids, there is a breakdown of the enzyme system of antioxidant protection, which increases in groups from 2 to 4 stage of articular cartilage degeneration, which leads to the progression of chronic inflammation, strengthening of the autoimmune component, and apoptosis of articular cartilage cells.