Maria–Alexandra Martu, Liliana Pasarin, Ana-Maria Sciuca, Cristina Popa, George-Alexandru Maftei, Ovidiu Nicolaiciuc, Oana Butnaru, Ruxandra Stan, Silvia Martu, Ionut Luchian
Abstract
Periodontitis patients are known to have increased circulating lipopolysaccharide activity and metabolic disturbances, which may be either the cause or effect of endotoxemia.
This review approaches endotoxemia as a possible molecular mediator between periodontitis and increased risk of cardiometabolic disorders. Observations that bacteria disseminate into circulation after toothbrushing and periodontal procedures and assumptions that endotoxin may disseminate through inflamed periodontium and bleeding gums support the idea of endotoxemia in periodontitis. However, the evidence that periodontitis-associated dysbiosis contributes to endotoxemia is not as strong as in the case of gut microbiome dysbiosis.
Although the causality is insufficiently demonstrated thus far, many studies have associated changes of the gut microbiome composition, function, and specific bacterial metabolites with cardiometabolic diseases, whereas research on the oral microbiome has severely fallen behind.
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