Obesity is considered the most important risk factor for the development of osteoarthritis (ОА) - progressive inflammatory disease of the joints, that is one of the causes of disability and long-term immobilization. Excessively developed adipose tissue not only increases the mechanical load on the joints, but also participates in the maintenance of chronic low-grade inflammation through the production of adipokines, cytokines, hemokines, complement factors and hormones. Adipokines influence cells of synovial tissue, cartilage and bone, which in turn produce some adipokines locally, maintaining an inflammatory microenvironment intraarticularly. Adipokines, including leptin, adiponectin, chemerin, and resistin, regulate inflammatory immune responses in cartilage, also affecting synovial tissue cells and bone. In turn, chondrocytes, osteoblasts and osteoclasts produce some adipokines locally, maintaining an inflammatory microenvironment intra-articularly. Weight loss in OA can improve the patient's quality of life, physical function, lead to reduce pain, and slow or halt the progression of structural degenerative changes. The purpose of this article is to clearly describe the pathogenetic ways between obesity and inflammation, to reveal the mechanisms of the pathological state of adipokines and proinflammatory mediators (IL-6, TNF-á, etc.) on cartilage and bone homeostasis and, as expected, to evaluate their participation in the development of OA. So understanding immune regulation and resolution of inflammation in obesity is critical to developing treatments approaches to OA for these patients. The article also analyzes current researches on the effect of drug therapy (liraglutide, orlistat, sibutramine) and bariatric surgery of obesity on the course of inflammatory joint diseases.