The peculiarities of arthrosis itself

Osteoarthritis (OA) affects 240 million people worldwide [1] and is one of the ten most disabling diseases in developed countries. The most common form of arthritis is osteoarthritis (OA).In the Global Burden of Disease 2010 study, hip and knee OA ranked11th in global disability (Cross et al., 2014). The prevalence of OA will increase in parallel with the increase in the number of people aged 60 years and older and the increase in obesity worldwide. Cohort studies have shown that after aging, obesity and metabolic disorders are the main risk factors for developing OA (Aspden et al., 2001; Felson et al.,1988).Conversely,

OA is a risk factor for metabolic syndrome and cardiovascular disease, suggesting that effective treatment of OA may prevent or delay the development of a large number of comorbidities (Haugen et al., 2013; Prior et al.,2014) [ 2 ]. There is growing evidence that there are different phenotypes of OA, reflecting different mechanisms of pathology.In 2016, evidence from six potential clinical phenotypes was presented in theliterature: those occurring with chronic pain; with inflammation;withmetabolic syndrome; bone and cartilagemetabolism;mechanical overload; and minimaljoint involvement[3]. These researchers subsequently examined the prevalence of these phenotypes in the OA Biomarker Consortium (OAI/FNIH) Foundation datasetof the National Institutes of Health [4] ]. Another review focused on molecular/mechanicalendotypes, particularly those associated with inflammation (characterized, for example, by c-reactive protein and interleukin-6), bone (e.g., c-terminal collagen telopeptide I [CTX-I]), metabolic syndrome (e.g., adipokines, advanced glycation end products), and aging (markers of aging) [5]]. Recent efforts have been made to standardize the conduct and reporting of phenotypic studiesin OA [6], in which it has been noted that phenotypes are "subtypes of OA that have various underlying pathobiological and pain mechanisms and their structural and functional consequences" [7]. Metabolic syndrome is a term encompassing a complex of hormonal and metabolic disorders, a serious medical and social problem of our time. Due to its prevalence among the adult population, MC is called the "syndrome of the new era" [8]. For the first time in 1988. J.M.Riven formulated the concept of MC as "X-syndrome".Thus, in 1989, abdominal obesity was identified as the most important etiological factor in the formation of insulin resistance, and obesity, especially in the upper body, increased glucose tolerance in hypertension. Thus, this combination is most indicative for increasing mortality from cardiovascular diseases [9].Adipose tissue is a type of connective tissue made up of blood vessels, collagen fibers, fibroblasts, and an extensive network of the immune system surrounded by lipid cells called adipocytes [10]. According to the classification, adipose tissue is divided into two types: white and gray. They are characterized by different anatomical localization, structure and functions. Adipose tissue produces many biologically active substances, among which an important role is played by adipokines and adipocytokines [11].More than 50 adipokines are known, including leptin, adiponectin, resistin, visfatin, etc., whichsecrete anti-inflammatory cytokines, such as tumor necrosis factor a (TNFa), interleukin 6 (IL6), inhibitor 1 of the plasminogen activator and others. Adipokines are biologically active substances produced by white adipose tissue and have a pleiotropic effect. They are involved in a wide range of metabolic processes, including not only carbohydrate x and fatmetabolism, but also modulationandimmune and inflammatory responses.Adipokines contribute to the chronic inflammatory process and interact with other cytokines, which together enhance degenerative processes in the joints [12]. Due to synergistic relationships with IL1, adipokines can enhance catabolic processes in cartilage and increase the synthesis of pro-inflammatory mediators in joint tissues [13].Thus, obesity, cardiovascular lesions and other pathogenetic metabolic disorders are associated with OA, which can be viewed as a systemic disease. Adipokine levels in patients with OA were significantly higher than in the control group. In particular, high levels of adiponectin and leptin areassociatedwith female sex and high BMI [14].Odin of the main adipokines involved in metabolic processes in OAis Leptin, itis produced bywhite fat cells. And itscirculation directly depends on the amountof fat in the body. Itis not only the main regulator of body weight,butalso suppresses appetite,stimulates energy expenditure using the receptorof thehypothalamus. As we understand it,obesity is a mild inflammatory process, causingsystemic metabolic dysfunction. In obesity OA, the production of adipokines with pro-inflammatory functions increases, which contributes to the progression of the disease[26]. Recent evidence suggests that adipokines produced by white adipose tissue may provide a link between obesity and