Abstract

The intestinal microbiota (IMB) can indirectly affect the course of ostearthritis (OA) at the systemic level by stimulating a chronic nonspecific inflammatory reaction in the synovial membrane and subchondral bone, the cause of which is an increase in the amount of circulating lipopolysaccharides (LPS) of the bacterial wall, as well as provoke the development of metabolic syndrome, which links the two necessary components of the pathogenesis of OA. The result of direct exposure is the formation of leaky gut syndrome with the activation of LPS of the bacterial wall of mild inflammation, provoking the production of proinflammatory cytokines, the effect of which on synoviocytes and chondrocytes leads to their activation with subsequent production of IL-6 and IL-8, which contributes to the persistence of inflammation. By correlation analysis, the relationship of three taxa with OA joint damage was proved, namely, the order Desulfovibrionales and the genus Ruminiclostridium 5 – with knee joint OA, Methanobacteriaceae – with knee joint OA, and OA of any localization, and the appearance and degree of contamination with the genus Streptococcus correlated with the severity of pain syndrome. The metabolic syndrome itself can provoke the development of dysbiosis, so it can also be its consequence. A change in the composition of the microbiota in the form of the predominance of the genus Clostridium and the species Staphylococcus aureus with a decrease in the diversity of microorganisms is associated with an increase in the amount of adipose tissue in the body, dyslipidemia, insulin resistance with impaired carbohydrate metabolism. Low levels of LPS in the blood are found in obese patients even in the absence of an obvious focus of infection due to violations in the CMB, they signal TLR-4, triggering systemic inflammation. Studies have shown a positive effect of prescribing proand prebiotics on the course of OA, which makes IMB a promising target for the treatment and prevention of OA.

Full Text
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