Introduction Based on WHO report, in 2008, the global prevalence of overweight reached over 1.4 billion people aged 20 years and over including more than 200 million men and 300 million women who suffered from obesity in 2012. More than 34 % of U.S. adults are overweight, and more than 27 % are obese. In European countries, the prevalence of obesity is 35–40 % among adult population. More than 30 percent of the Russia’s working population is overweight, 25 percent of whom are obese. Material and methods Search engines used included MEDLINE, the primary component of Pubmed; the Electronic Library System, products from Elsevier and Springer publishing companies; open access articles of PubMed Central; BioMed Central; Free Medical Journals and open access publications using the keywords 'knee osteoarthritis', 'etiology and pathogenesis', 'knee osteoarthritis in obesity'. Results and discussion Osteoarthritis (OA) is multifactorial in origin and closely associated with genetic predisposition, sex and age, greater body mass index (BMI) and obesity. Family history, age, gender, previous injury or abnormal mechanical loading are common risk factors of knee OA. While the above risk factors can increase the chances of developing knee OA, they are not absolute. In clinical practice, in patients with new onset of knee pain 5.1 % of cases are due to previous knee injury and 24.6 % related to being overweight or obese. Such metabolic factors as obesity and dyslipidemia might be involved in the pathophysiology of knee OA. Increased free radical production associated with obesity results in degradation of articular cartilage and synovial involvement. The pathogenesis of knee OA attributable to obesity is predominantly related to unfavorable mechanical environment at the joint; chronic inflammation in adipose tissue and dyslipidemia; pro-inflammatory cytokines and adipokines secreted by the adipose tissue; cytokines secreted by infrapatellar fat pad. Conclusion Inflammatory mediators of adipose origin play a major role in the initiation and perpetuation of the obesity-induced OA. There is a significant multifactorial association between OA and obesity with central roles for LDL oxyforms, HDL synthesis and excessive activation of matrix metalloproteinases, adiponectin synthesis, the release of adipokines and excessive mechanical stress.