Title : Periodontal and cardiovascular disease: Shared pathophysiology and therapeutic implications – New insights for 2025
Abstract:
Periodontal disease is increasingly recognized as a significant systemic contributor to atherosclerosis. Key oral pathogens—Porphyromonas gingivalis, Aggregatibacter actinomycetemcomitans, Treponema denticola, and Tannerella forsythia—are implicated in all major stages of atherogenesis. First, these bacteria release phospholipase A2, promoting the formation of small dense LDL particles (sdLDL), which are strongly associated with elevated apolipoprotein B (ApoB), a well-established predictor of atherosclerotic cardiovascular disease (ASCVD). Second, bacterial lipopolysaccharides compromise endothelial integrity by increasing permeability and upregulating adhesion molecules, facilitating monocyte infiltration and triggering systemic inflammation via the innate immune response. Third, negatively charged bacterial components interact electrostatically with positively charged ApoB residues, enhancing lipoprotein retention within the arterial intima—a key step in plaque formation [1].
Moreover, periodontitis correlates with elevated systemic inflammatory markers, including C-reactive protein (CRP), interleukin-1, and fibrinogen, all associated with increased incidence of venous thromboembolism (VTE), including deep vein thrombosis and pulmonary embolism [2] . Notably, CRP levels above 3 mg/L indicate high risk for major cardiovascular events . Clinical studies demonstrate that periodontal therapy—particularly antibiotic regimens such as amoxicillin-metronidazole or tetracyclines—can significantly reduce these markers, indicating a potential cardioprotective effect.
Additionally, oral bacteria like Streptococcus and Staphylococcus species can lead to infective endocarditis, especially in patients with prosthetic valves or congenital heart defects, reinforcing the need for prophylactic antibiotics during invasive dental procedures in high-risk individuals [3].
Current evidence supports a causal role of periodontal disease in ASCVD by influencing three core pathogenic mechanisms. While periodontal disease is primarily managed in dental settings, its systemic effects demand interdisciplinary strategies. Identifying effective treatment pathways may offer a promising route for reducing cardiovascular risk through periodontal intervention.
