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The relationship between periodontitis and cardiovascular disease (CVD) has been extensively studied, but the role of biological ageing in this relationship remains poorly understood.

This study seeks to elucidate the causal association between periodontitis, CVD and biological ageing.

The authors included 3269 participants in the National Health and Nutrition Survey (2009-2014) with diagnostic information on periodontitis and cardiovascular events.

Biological ageing was assessed using both calculated biological age (KDMAge) and phenotypic age (PhenoAge) from the Klemera-Doubal method. Logistic regression, restricted cubic spline (RCS) analysis and subgroup analysis were used to analyse the data. Mediation analysis was used to explore the mediating role of biological ageing. Subsequently, Mendelian randomisation (MR) analyses were performed using genome-wide association study databases to explore potential causal relationships between periodontitis, CVD and biological ageing.

Periodontitis was associated with a higher risk of CVD. Participants with periodontitis had increased levels of biological ageing, and higher levels of biological ageing were associated with an increased risk of CVD. Mediation analyses showed a partial mediating effect of biological ageing (PhenoAge: 44.6%; KDMAge: 22.9%) between periodontitis and CVD risk.

Magnetic resonance analysis showed that periodontitis played a causal role in increasing the risk of small-vessel stroke, while myocardial infarction increased the risk of periodontitis. In addition, inverse MR analysis showed that phenotypic ageing can increase the risk of periodontitis, and that there is a bidirectional causal relationship between CVD and biological ageing.

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


Source(s) :
Zhaoqi Zhang, Xingru Zhao, Shang Gao, An Li, Ke Deng, Kai Yang, Wei Liu , Mi Du ;

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