Publication Details
Issue: Vol 18, No (2025)
Visit Journal Website

Abstract

Reactive inflammation of the synovial membrane, which occurs with activation of metalloproteinases and overexpression of proinflammatory cytokines against the background of a deficiency of anti-inflammatory cytokines, exacerbates dystrophic and destructive processes in cartilage tissue. Thus, synovitis, which is secondary in nature, contributes to the progression of osteoarthritis (OA), and with a recurrent torpid course, it can determine a violation of joint function. It has been established that the only energy substrate for chondrocytes is glucose. It has been proven that in patients with diabetes mellitus (DM), synthetic processes in cartilage tissue are disrupted, and chronic hyperglycemia increases damage to muscles and periarticular tissues in OA. In GA, uncompensated chronic hyperglycemia with a glycated hemoglobin content of 10.5% or more contributes to the development of synovitis with intense arthralgia, pronounced exudation, proliferation of the synovial membrane and edema of the collateral ligaments. Synovitis also activates receptors for interleukin-1 (IL-1), fibronectin, and leptin.