The First Clinical Medical College, Shandong University of Traditional Chinese Medicine, Jinan, China.
The First Clinical Medical College, Nanjing University of Chinese Medicine, Nanjing, China.
Clin Epigenetics. 2024 Aug 24;16(1):116. doi: 10.1186/s13148-024-01732-9.
The relationship between periodontitis and cardiovascular disease (CVD) has been extensively studied, but the role of biological aging 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.
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, Mendelian randomization (MR) analyses were performed using genome-wide association study databases to explore potential causal relationships between periodontitis, CVD, and biological aging.
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.
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.
牙周炎与心血管疾病（CVD）之间的关系已得到广泛研究，但生物学年龄在这种关系中的作用仍知之甚少。本研究致力于探讨牙周炎对 CVD 发病的影响，并阐明生物学年龄的潜在中介作用。此外，本研究将试图阐明牙周炎、CVD 和生物学年龄之间的因果关系。
我们纳入了来自国家健康和营养调查（2009-2014 年）的 3269 名参与者，这些参与者具有牙周炎和复合 CVD 事件的诊断信息。利用 Klemera-Doubal 方法计算的生物年龄（KDMAge）和表型年龄（PhenoAge）来评估生物学年龄。采用逻辑回归、限制立方样条（RCS）分析和亚组分析进行数据分析。采用中介分析探讨生物学年龄的中介作用。随后，利用全基因组关联研究数据库进行孟德尔随机化（MR）分析，以探讨牙周炎、CVD 和生物学年龄之间潜在的因果关系。
牙周炎与 CVD 风险增加相关。患有牙周炎的参与者表现出更高的生物学年龄水平，并且较高的生物学年龄水平与 CVD 风险增加相关。中介分析显示生物学年龄（表型年龄：44.6%；KDMAge：22.9%）在牙周炎和 CVD 风险之间存在部分中介作用。MR 分析表明，牙周炎在增加小血管卒中风险方面起因果作用，而心肌梗死则增加了牙周炎的风险。此外，反向 MR 分析表明表型老化会增加牙周炎的风险，CVD 和生物学年龄之间存在双向因果关系。
牙周炎与 CVD 风险增加相关，部分通过生物学年龄介导，存在复杂的因果相互关系。针对牙周健康的靶向干预可能会减缓生物学年龄的进程并降低 CVD 风险。
