The American Heart Association (AHA) has released an updated scientific statement reviewing the evidence linking periodontal disease with atherosclerotic cardiovascular disease (ASCVD). Published in Circulation, the statement updates a 2012 AHA report and reflects advances in epidemiologic, mechanistic, genetic, and interventional research over the past decade.
ASCVD remains the leading cause of death worldwide and in the United States, accounting for approximately 30% of all U.S. deaths. Periodontal disease, a chronic inflammatory condition affecting the supporting structures of the teeth, is also highly prevalent. U.S. surveillance data indicate that 42% of adults aged 30 years or older have periodontitis, including 7.8% with severe disease. Globally, more than 1 billion individuals are affected, with prevalence continuing to rise.
The statement notes that periodontal disease and ASCVD share several established risk factors, including older age, cigarette smoking, diabetes, hypertension, obesity, and lower socioeconomic status. While these shared factors may partially explain observed associations, the writing group reviewed evidence suggesting that periodontal disease may also be independently associated with ASCVD through both direct and indirect biological pathways. The authors emphasize, however, that a causal relationship has not been definitively established.
“Since the publication of the prior scientific statement, there has been growing literature highlighting associations between periodontal disease and atherosclerotic cardiovascular disease (ASCVD), especially with large cohort studies and meta-analyses,” said Andrew H. Tran, MD, MPH, MS, FAAP, FAHA, lead author on the study. “Additionally, there have been new studies evaluating subclinical cardiovascular disease measures such as carotid intima media thickness and studies in youth.”
Direct mechanisms discussed in the statement include bacteremia and vascular infection. Periodontal disease is characterized by inflamed periodontal pockets that may bleed during routine activities or dental procedures, allowing oral bacteria to enter systemic circulation. These bacteria may contribute to endothelial dysfunction, an early process in atherogenesis. Periodontal pathogens and their genetic material have also been identified in atherosclerotic plaques, supporting biological plausibility for an association between periodontal disease and ASCVD.
Indirect mechanisms focus on systemic inflammation. Individuals with periodontal disease consistently demonstrate elevated circulating inflammatory markers, including C-reactive protein, interleukins, tumor necrosis factor, and altered adipokines. These inflammatory pathways are also implicated in the development and progression of atherosclerosis. Additional indirect mechanisms reviewed include autoimmune responses to bacterial heat shock proteins, platelet activation, and alterations in the oral microbiome.
Epidemiologic studies summarized in the statement demonstrate associations between periodontal disease and a range of cardiovascular outcomes, including coronary artery disease, myocardial infarction, stroke, peripheral artery disease, and cardiovascular mortality. Meta-analyses also report associations between periodontal disease and subclinical vascular measures such as increased carotid intima–media thickness, impaired endothelial function, and increased arterial stiffness.
“While studies have yet to identify a direct causal link, the available literature shows that periodontal disease contributes to chronic inflammation,” Dr. Tran explained. “Identifying and treating periodontal disease may help decrease inflammation and promote cardiovascular health. These findings should also spur clinicians and researchers towards further study to better understand the association between periodontal disease and ASCVD.”
The statement also highlights disparities in periodontal disease prevalence. Severe periodontitis is more common among individuals with lower income, reduced access to dental care, and in certain racial and ethnic populations. These disparities overlap with those observed in ASCVD, underscoring the role of social determinants of health in both conditions.
Interventional studies assessing whether periodontal treatment reduces cardiovascular events have yielded inconclusive results. Randomized trials and systematic reviews have not demonstrated definitive reductions in primary or secondary ASCVD events following periodontal therapy. However, several studies show improvements in intermediate outcomes, including inflammatory markers, blood pressure, lipid levels, and endothelial function.
Mendelian randomization studies included in the review have produced mixed findings. Some analyses suggest associations between periodontal disease and specific stroke subtypes, while others do not demonstrate significant genetic evidence linking periodontal disease with coronary artery disease or subclinical atherosclerosis. Methodological differences and limited statistical power are noted as contributing factors.
“Several areas are important to focus on in future studies. Pediatric and longitudinal studies from childhood into adulthood are needed to help clarify the mechanisms for the association between periodontal disease and ASCVD,” said Dr. Tran. “Mendelian randomization techniques may also help clarify the link. More studies evaluating the effects of treating periodontal disease and cardiovascular outcomes are also needed.”
The AHA concludes that while substantial evidence supports an association between periodontal disease and ASCVD, further research is needed to clarify causality and clinical implications. The statement calls for additional longitudinal studies, randomized clinical trials, mechanistic investigations, and interdisciplinary collaboration.
Source: Circulation