Associations of periodontitis with biological aging among US adults: An exploratory mediation analysis via lactate

To investigate the potential role of lactate in the relationship between periodontitis and biological aging. Cross-sectional data from 9,652 participants in the National Health and Nutrition Examination Survey 2009-2014 were analyzed. Periodontitis was categorized based on the Centers for Disease Control and Prevention and American Academy of Periodontology (CDC/AAP) classification. Biological aging was assessed based on KDM-BA acceleration and PhenoAge acceleration, while lactate levels were assessed using lactate dehydrogenase (LDH). Weighted multivariable linear regression analyses were conducted to examine the association between periodontitis and biological aging. Additionally, exploratory mediation analyses were carried out to determine the mediating effect of LDH on this association. Participants with moderate/severe periodontitis showed accelerated biological aging and higher serum LDH levels. Similarly, mean attachment loss (AL) and probing pocket depth (PPD) were positively associated with biological aging and serum LDH levels. Furthermore, serum LDH was found to mediate 8.4% and 3.8% of the associations between periodontitis and KDM-BA acceleration and PhenoAge acceleration, respectively. LDH also explained 11.0% and 4.4% of the association between mean PPD and KDM-BA acceleration and PhenoAge acceleration, respectively. However, the role of LDH in the relationship between mean AL and biological aging was not observed. These findings indicate that LDH, an enzyme that converts pyruvate to lactate, mediates the association between periodontitis and biological aging. However, additional longitudinal or interventional studies are needed to more effectively assess causality and confirm our findings.