Dysbiosis of the oral microbiome and cardiovascular risk; from endothelial dysfunction to systemic inflammation

A growing body of evidence implicates dysbiosis of the oral microbiome as a significant, modifiable risk factor for cardiovascular disease. This dysbiosis, often manifesting as periodontitis, initiates local inflammation and tissue destruction, however its systemic consequences are profound. Key mechanisms linking oral dysbiosis to cardiovascular disease involve the induction of endothelial dysfunction and chronic systemic inflammation. Pathogens and their virulence factors enter the bloodstream through inflamed periodontal tissues, directly impairing endothelial nitric oxide production and bioavailability, promoting vasoconstriction, leukocyte adhesion, and a pro-thrombotic state. Concurrently, microbial components activate innate immune receptors on endothelial and immune cells, triggering sustained release of pro-inflammatory cytokines and acute-phase proteins. The low-grade, systemic inflammation accelerates atherosclerosis by promoting foam cell formation, plaque instability, and vascular remodeling. Epidemiological studies consistently associate periodontitis with increased risks of myocardial infarction, stroke, and atherosclerosis severity, independent of traditional risk factors.