Paradontitis is associated with the risk of developing cardiovascular diseases as a pathogenic factor. The onset and spread of periodontitis occurs as a result of dysbacteriosis of commensal oral microbiota, that is further interacts with the hosts immune system, being the cause of development of low rank systemic inflammation and the most frequent cause of cardiovascular diseases. An important virulence factor of gram-negative bacteria that dominate in the oral microbiota in periodontitis is lipopolysaccharides, which are part of their cell membranes and being endotoxins. In humans, lipopolysaccharides play a central role in host immune responses, which is characterized by cytokine synthesis, activation of the immune system and provokes the risk of atherosclerotic changes and thromboembolic processes. At the same time, serum lipopolysaccharide activity correlates with serum IgG levels against P. gingivalis, the main causative agent of periodontitis. Lipopolysaccharides are the molecular association between oral dysbacteriosis and cardiometabolic disorders. Saliva lipopolysaccharides correlate with serum lipopolysaccharide activity and this association is enhanced in the presence of periodontitis. The oral microbiota is stably associated with such cardiovascular diseases as acute coronary syndrome and atherosclerosis. Certain types of microflora associated with cardiovascular diseases are identified. Some types associated with periodontitis, such as Porphyromonas gingivalis, are able to invade epithelial cells and multiply in them. Inflammation associated with endotoxemia in periodontitis explains the association with the clinical manifestations of cardiovascular diseases. All bacterial structural components and virulence factors are recognized in the host organism as antigens. They lead to the formation of antibodies, however, the mechanisms of their participation in the pathogenesis of periodontitis and other chronic diseases associated with paradontium are not yet clear. The contribution of cross-reactive antibodies obtained against host antigens is investigated as a response to the similarity of their epitopes with the antigens of bacteria, which is called molecular mimicry and which promotes inflammation. One of the most frequently studied epitopes is present in heat shock proteins (HSP), therewith eight members of the HSP family are associated with the development of cardiovascular diseases and mortality from them. Proteins of the HSP60 family are identified as major antigens in a number of bacterial species associated with periodontitis. The levels of antibodies to A. actinomycetemcomitans and P. gingivalis, which dominate in the oral microbiota in periodontitis are being studied. Serum positivity of IgA to these species is a predictor of recurrent stroke, myocardial infarction and other cardiovascular diseases. The high combined IgG response to A. actinomycetemcomitans and P. gingivalis is combined with calcification of the coronary artery. The combined effect of some oral pathogens causes a more significant impact on the development of cardiovascular diseases than the effect of a single microbe. Thus, both direct and indirect mechanisms are involved in the development of cardiovascular diseases that are associated with periodontitis, while patients are constantly exposed to dysbiotic bacteria and their virulence, which causes and maintains systemic low rank inflammation. Endotoxemia and antibody response are mediators that connect oral dysbacteriosis with an increased risk of cardiovascular diseases

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