Biological aging mediates the association between periodontitis and cardiovascular disease: results from a national population study and Mendelian randomization analysis

Aug 24, 2024Clinical epigenetics

Biological aging may explain the link between gum disease and heart disease

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Abstract

is associated with a higher risk of cardiovascular disease (CVD).

Participants with periodontitis exhibited increased levels of .
Elevated biological aging levels were linked to a heightened risk of CVD.
Biological aging partially mediates the relationship between periodontitis and CVD risk, with mediation effects of 44.6% for phenotypic age and 22.9% for biological age.
analysis indicated that periodontitis has a causal role in increasing the risk of small vessel stroke.
There is a two-way causal relationship between CVD and biological aging, where phenotypic aging can increase the risk of periodontitis.

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BACKGROUND: The relationship between and cardiovascular disease (CVD) has been extensively studied, but the role of in this relationship remains poorly understood. This study is dedicated to investigating the effect of periodontitis on the incidence of CVD and to elucidating the potential mediating role of biological aging. Furthermore, this study will seek to elucidate the causal association between periodontitis, CVD, and biological aging.

METHODS: We included 3269 participants from the National Health and Nutrition Examination Survey (2009-2014) with diagnostic information on periodontitis and composite CVD events. Biological aging was evaluated by utilizing both the Klemera-Doubal method's calculated biological age (KDMAge) and phenotypic age (PhenoAge). Logistic regression, restricted cubic spline (RCS) analysis, and subgroup analysis were used for data analysis. Mediation analysis was employed to explore the mediating role of biological aging. Subsequently, (MR) analyses were performed using genome-wide association study databases to explore potential causal relationships between periodontitis, CVD, and biological aging.

RESULTS: Periodontitis was associated with a higher risk of CVD. Participants with periodontitis were found to have increased levels of biological aging, and elevated levels of biological aging were associated with increased CVD risk. Mediation analyses showed a partial mediating effect of biological aging (PhenoAge: 44.6%; KDMAge: 22.9%) between periodontitis and CVD risk. MR analysis showed that periodontitis played a causal role in increasing the risk of small vessel stroke, while myocardial infarction was found to increase the risk of periodontitis. In addition, reverse MR analysis showed that phenotypic aging can increase the risk of periodontitis, and there is a two-way causal relationship between CVD and biological aging.

CONCLUSIONS: Periodontitis is associated with an increased CVD risk, partially mediated by biological aging, with a complex causal interrelationship. Targeted interventions for periodontal health may slow the biological aging processes and reduce CVD risk.

Key numbers

2.72

Increase in CVD Risk

Odds ratio for severe vs. CVD risk

44.6%

Mediation

Percentage of mediation effect by

1.056

Causal Effect on Small Vessel Stroke

Odds ratio from analysis

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Biological aging mediates the association between periodontitis and cardiovascular disease: results from a national population study and Mendelian randomization analysis

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