The Relationship Between Oral Health and Cardiovascular Disease: A Narrative Review

Background: Periodontitis is a common chronic inflammatory disease that has been repeatedly investigated in relation to cardiovascular disease (CVD), particularly atherosclerotic cardiovascular disease (ASCVD). Epidemiological studies frequently report an association between periodontitis and cardiovascular outcomes, while mechanistic studies provide several biologically plausible pathways. However, the interpretation of this relationship is complicated by shared risk factors, residual confounding, heterogeneity in periodontal definitions, and limited evidence from cardiovascular-event trials. Objective: To critically summarize current evidence concerning the relationship between oral health, particularly periodontitis, and cardiovascular disease, with emphasis on biological mechanisms, epidemiological associations, causal inference, periodontal treatment, and clinical and public-health implications. Methods: This narrative review was developed primarily through PubMed/MEDLINE searches using terms related to periodontitis, oral health, cardiovascular disease, atherosclerosis, myocardial infarction, stroke, inflammation, endothelial dysfunction, periodontal treatment, randomized controlled trials, and Mendelian randomization. Relevant systematic reviews, meta-analyses, randomized trials, mechanistic reviews, and major scientific statements were prioritized. Additional literature was identified through targeted searches and reference chaining. Results: Current evidence consistently demonstrates an epidemiological association between periodontitis and several cardiovascular outcomes, including myocardial infarction, stroke, and recurrent cardiovascular events. Proposed mechanisms include transient bacteremia, systemic inflammatory signaling, endothelial dysfunction, oxidative stress, immune activation, and thrombo-inflammatory pathways. Nevertheless, observational associations cannot establish causality. Recent Mendelian randomization evidence suggests a possible causal relationship with cardioembolic stroke but no substantial causal association with coronary atherosclerosis. Randomized studies demonstrate changes in selected vascular and inflammatory surrogate measures after periodontal treatment, while evidence that periodontal therapy prevents major cardiovascular events remains insufficient. Conclusions: Periodontitis is consistently associated with cardiovascular disease and has biologically plausible pathways through which it may influence cardiovascular health. However, current evidence does not establish a uniform causal relationship across cardiovascular phenotypes, and cardiovascular-event prevention has not been demonstrated as a consequence of periodontal treatment. Future research should use standardized periodontal phenotyping, rigorous control of confounding, adequately powered randomized trials, and robust causal-inference methods.