Nickan Research Institute Immunopathologia Persa 2423-8015 12 2 2026 07 01 Dysbiosis of the oral microbiome and cardiovascular risk; from endothelial dysfunction to systemic inflammation e44026 e44026 10.34172/ipp.2026.44026 EN Ali Farmanieh https://orcid.org/0009-0007-8002-2742 Afsoon Jalali Ara https://orcid.org/0000-0003-3621-8370 Sara Rashki Ghalehno https://orcid.org/0000-0002-7638-2290 Parsa Malek https://orcid.org/0009-0003-9096-0899 Mitra Rostami https://orcid.org/0009-0002-5162-1256 Seyed Sasan Amiri https://orcid.org/0009-0001-3438-9371 Negar Khaneshi https://orcid.org/0009-0008-3403-7887 Reza Faramarzzadeh https://orcid.org/0000-0002-3201-5261 Golara Abdolmohammadi https://orcid.org/0000-0003-1889-8480 Maryam Onsori https://orcid.org/0009-0005-6733-5862 Journal Article 10.34172/ipp.2026.44026 2025 12 12 2026 03 18 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.