Healthy Gums May Lead to Healthier Hearts

Atherosclerotic cardiovascular disease (ASCVD) is a condition in which plaque builds up in the arteries, leading to reduced blood flow and increased risk of heart attack and stroke. It is the leading cause of death in the United States and worldwide and is greatly affected by long-term inflammation occurring throughout the body, not just in one specific organ.^1-6 Recently, the American Heart Association (AHA) updated its scientific statement related to periodontal diseases and ASCVD. This report brings together growing evidence showing a clear association between periodontal diseases and negative cardiovascular outcomes, while noting that a direct cause-and-effect relationship has not been proven.⁷ Simultaneously, the AHA Healthy Smiles, Healthy Hearts™ initiative elevates the dental setting as a key touchpoint for cardiovascular screening and referrals, positioning dental hygienists to lead standardized blood pressure screening, patient education, and interdisciplinary coordination with family practitioners and cardiac specialists.⁸

While heart disease has significant comorbidities and health consequences, periodontal diseases affect more than 40% of US adults aged 30 and older, with higher prevalence among men, older adults, individuals with poor oral hygiene, and individuals whose health is negatively affected by social, economic, or environmental factors beyond their control.^9-10 These characteristics mirror traditional cardiovascular risk determinants, reinforcing the plausibility of shared pathways while also supporting an independent association between periodontal status and ASCVD risk. Newer observational analyses have strengthened this association. Song et al,¹¹ in a National Health and Nutrition Examination Survey-based study, found moderate to severe periodontitis was associated with elevated 10-year ASCVD risk and tooth loss showed similar associations.

The 2012 AHA statement included observational studies that showed an association independent of confounders, but they did not establish a cause-and-effect relationship. Further, there was no direct evidence that periodontal treatment modified cardiovascular events.¹² The 2025 update revisited these concepts with broader mechanistic and interventional insights but retains caution about causality.

Biologic Mechanisms

The 2025 update report delineates two complementary mechanisms for how periodontal diseases may exacerbate cardiovascular risk including direct and indirect pathways. A direct pathway occurs when oral pathogens and bacteremia may seed vascular compartments, contributing to endothelial injury and local inflammatory responses.⁷ Indirect pathways occur through chronic systemic inflammation, such as elevated C-reactive protein (CRP) and interleukins (IL), which can form plaques in the intima layer of arteries,¹³ constrict blood vessels,¹⁴ and cause pathological changes in the composition, distribution, or metabolism of lipids.^7,15 Emerging evidence also links periodontitis with hypertension, a dominant ASCVD driver. Meta-analyses and case-control data demonstrate higher systolic and diastolic blood pressure among individuals with periodontitis, even in otherwise healthy adults.^16-17

Association of Periodontal Diseases and Atherosclerotic Cardiovascular Disease

The 2025 AHA scientific statement frames periodontal diseases as conditions consistently associated with increased risk of ASCVD, including atherosclerosis, coronary artery disease (CAD) and acute coronary syndromes, cerebrovascular disease, and peripheral artery disease (PAD). This interpretation reflects observational data, mechanistic evidence, and current research gaps.

The AHA statement emphasizes that atherosclerosis underlies many clinical manifestations of ASCVD including CAD, stroke, and PAD, and that periodontal diseases are associated with subclinical and clinical markers of atherosclerotic vascular disease. As noted in the scientific statement, epidemiologic studies link periodontal diseases with greater plaque burden and vascular inflammation, supporting an association between oral inflammatory burden and systemic vascular pathology.⁷

In the context of CAD, the updated statement highlights that individuals with periodontal diseases have a higher likelihood of CAD events, such as myocardial infarction and angina, compared to those without periodontal diseases. This association persists despite controlling for traditional risk factors such as smoking, hypertension, high cholesterol, diabetes, obesity, and sedentary lifestyle, suggesting that periodontal diseases could act as an independent risk marker for CAD. However, periodontal treatment has not yet been demonstrated to reduce the incidence of CAD events in clinical trials.⁷

The scientific statement also notes an association between periodontal diseases and increased risk of cerebrovascular events such as ischemic stroke. In addition, for those individuals with a history of stroke, the presence of periodontal diseases increases the risk for recurrent stroke.¹⁸ Periodontal diseases are also associated with an increased risk of dementia and cognitive impairment.¹⁹ While the AHA cautions that causation has not been established and that periodontal treatment has not been shown to conclusively prevent strokes, there is a consistent association that supports the idea that periodontal diseases may serve as a marker of elevated risk for cerebrovascular ASCVD outcomes, particularly among individuals with other cardiovascular risk factors.⁷

Similarly, periodontal diseases are associated with peripheral artery disease, which represents atherosclerotic narrowing of arteries supplying the limbs. The statement highlights that individuals with periodontal diseases tend to have higher rates of PAD independent of shared risk factors. Potential causes of this association are the release of inflammatory cytokines and the direct effect of periodontal pathogens. However, data related to PAD and periodontal diseases are insufficient to determine causality, largely due to a lack of well conducted longitudinal studies and little understanding of the biologic mechanisms underlying PAD and periodontal diseases.⁷

Across these ASCVD manifestations, the AHA concludes there is consistent epidemiologic evidence supporting an association between periodontal diseases and ASCVD outcomes. Shared risk factors partially explain this association, yet there are independent associations after adjustments for major confounders. However, definitive causality has not been established, and periodontal treatment has not yet been shown to reduce ASCVD events in randomized clinical trials.

Evidence for Intervention

While definitive cardiovascular outcomes remain under study, nonsurgical periodontal therapy (NSPT) consistently improves periodontal parameters and favorable shifts in systemic biomarkers, such as reduced CRP and low-density lipoprotein (LDL) and increased high-density lipoprotein (HDL). However, there is general low certainty in this evidence.⁷ Targeted clinical studies in hypertensive populations report reduced inflammatory cytokines, such as IL-6 and vascular endothelial growth factor, and improved periodontal inflamed surface area after NSPT.²⁰ In patients with established cardiovascular disease, randomized pilot data show periodontal therapy improves periodontal outcomes and yields within-group changes in endothelial function and carotid intima-media thickness (ultrasound measurements on the inner layers of the carotid artery walls), though between-group differences may be limited.²¹ The updated AHA statement’s synthesis aligns with these signals: treating periodontal diseases appears to improve cardiovascular-related markers, such as blood pressure, HDL-C, and inflammatory mediators, but causality remains unproven and event-level reductions are not yet established.⁷

The Dental Hygienist’s Role in Integrated Cardiovascular Prevention

Dental hygienists have an opportunity to apply the evidence provided in the AHA statement through risk assessment, patient education, and care coordination. Risk assessment can be addressed through blood pressure screening and oral systemic risk questions as part of the health history. Dental hygienists should implement standardized blood pressure screening at routine visits and follow protocols for staging, re-measurement, and referral recommended by the AHA.⁸

Ensure that the proper cuff size is used for taking blood pressure, the individual is seated and rested, and that elevated readings are confirmed with repeat measurements.⁸ Because many people are seen in a dental practice setting vs a physician during the course of a year, patients should be advised that blood pressure checks are routine and that oral health professionals will provide referrals for medical care if needed based on the AHA hypertension guidelines.

Oral-systemic risk assessment questions can be implemented in the health history intake at initial appointments and throughout maintenance appointments. Questions should include reference to smoking/vaping, diabetes control, physical activity, diet, and sleep. Quick checks for medication adherence, home blood pressure monitoring, oral hygiene habits, and recare intervals that align with systemic risk and readiness can be embedded in the intake questions. Asking what medications patients take, why they take it, and whether it was taken as prescribed at the current appointment provides valuable insight into how well they follow medical recommendations. Another consideration is to address disparities by screening for social determinants that impede regular care and connecting patients to community resources.²² These procedures align closely with the profession’s Standards for Clinical Dental Hygiene Practice.²³

Clinical care can be enhanced for individuals who present with risk factors for or known heart disease with comorbidities. Dental hygienists can track periodontal inflamed surface area (PISA) to monitor the inflammatory burden. The PISA is an index for clinical assessment that represents the inflammation status of patients. This procedure requires six-point probing depth measurements on 28 teeth measuring bleeding on probing combined with either probing depth or clinical attachment levels and gingival recession. A calculation formula is used to determine the total inflamed surface area in square millimeters, providing a comprehensive measure of periodontal inflammation. Findings show an association between PISA and systemic markers of low-grade inflammation such as CRP,^21,22 and it can be compared with blood pressure and lipid markers shared by medical teams when available.^20,21 The PISA index can be used to correlate periodontal diseases with noncommunicable maladies such as cardiovascular diseases, cancers, chronic respiratory disease, diabetes, and chronic kidney disease.^24,25

With regard to patient education, dental hygienists should communicate how gingival inflammation and oral pathogens contribute to systemic inflammation and potentially to elevated blood pressure and vascular injury. Transparency with the evidence should be shared so individuals understand that periodontal therapy can improve systemic inflammatory markers but has not yet been proven to prevent heart attacks or strokes. Also, as part of self-care instruction, the need for oral hygiene and maintenance therapy should be emphasized. Evidence-based strategies for toothbrushing, interproximal biofilm management, and antiseptic mouthrinses should be used and follow-up appointments recommended to evaluate individuals’ ability to appropriately perform self-care recommendations.

Care coordination is another important consideration in the provision of care. Dental hygienists should establish referral pathways to primary care and/or cardiology specialists for hypertension or other suspected ASCVD risk. Included in this process is confirming follow-up with recommended physicians and integrating feedback into continuing care and oral hygiene maintenance schedules.⁸ Equally important, dental hygienists should document shared risk factors and periodontal status in interprofessional communications highlighting the potential role of periodontal therapy in lowering CRP and LDL levels and raising HDL keeping in mind current limits of evidence on ASCVD event reduction.⁷

Conclusion

The updated AHA statement advances the oral-cardio conversation, confirming stronger associations between periodontal diseases and ASCVD-related outcomes while retaining appropriate caution regarding causality. For dental hygienists, the implications are immediate: provide chairside cardiovascular screening, educate patients about the oral-systemic link, and coordinate care to reduce the inflammatory burden. Integrating standardized screening, incorporating referral protocols and implementing high-quality periodontal prevention and therapy can position dental hygienists as a frontline partner in cardiovascular risk reduction while using transparent communication about the evidence.

References

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