Бюллетень сибирской медицины (Apr 2021)

The role of metabolic syndrome in the pathogenesis of knee osteoarthritis: a new view on the problem

  • G. V. Poryadin,
  • A. N. Zakhvatov,
  • T. V. Tarasova,
  • V. O. Timoshkin

DOI
https://doi.org/10.20538/1682-0363-2021-1-190-199
Journal volume & issue
Vol. 20, no. 1
pp. 190 – 199

Abstract

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Currently, numerous studies undeniably prove the influence of metabolic syndrome on osteoarthritis (OA) progression.In hyperlipidemia, free fatty acids abnormally accumulate in the cartilage tissue and provoke cell dysfunction and necrosis. Studies show that palmitate and stearate have a pronounced proapoptotic effect on chondrocytes of the articular cartilage.Mediators of the systemic inflammatory response produced by the adipose tissue act as a significant link in the pathogenesis of metabolic OA in the knee joint. Metabolic disorders, insulin resistance, and dyslipidemia boost production of inflammatory mediators and glycosylated compounds and formation of free oxygen radicals provoking endothelial dysfunction.A relationship between intra-articular structures (articular cartilage, synovial membrane, subchondral bone and synovial fluid) and the intra-articular infrapatellar fat pad is a local pathogenetic factor in the metabolic OA ofthe knee. It is proven that the intra-articular infrapatellar fat pad increases significantly in obese patients. Due to proximity to the articular cartilage and synovial membrane, the adipose tissue is in close contact with them. The influence of systemic metabolites activates the growth of adipocytes, preadipocytes, macrophages, fibroblasts, and other fat body cells which enhance the production and release of adipokines, such as leptin, adiponectin, visfatin, and cytokines, that in turn stimulate aseptic inflammation resulting in development of synovitis, cartilage degeneration, and gonarthrosis progression.Therefore, the metabolic syndrome has a negative impact on the condition of the joint tissues, contributing to the development of gonarthrosis or its progression. It manifests itself both through systemic effects and the local impact of the hypertrophied infrapatellar fat pad on the components of the synovial joint environment.

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