Department of Oral Medicine and Periodontology, University of Seville, Sevilla, Spain.
Heart Center, Virgen Macarena University Hospital, Sevilla, Spain.
J Periodontal Res. 2020 Aug;55(4):519-528. doi: 10.1111/jre.12739. Epub 2020 Feb 27.
Our aims were to improve the understanding of the pathogenic relationship between cardiovascular diseases and periodontitis and to generate new perspectives in the prevention and treatment of acute myocardial infarction (AMI) and periodontitis. The present study evaluates possible differences in inflammation, oxidative stress, and autophagy markers among subject suffering AMI, periodontitis, or both, to explore possible common pathogenic mechanisms.
A total of 260 subjects were enrolled in the study: 106 subjects that survived to a first AMI (AMI group) and 154 subjects had no cardiac events in their clinical record (control group). A questionnaire was used to assess age, height, weight, blood pressure, and heart rate. The clinical probing depth, clinical attachment loss, number of remaining teeth, and average number of sites with bleeding on probing were assessed. Lipid peroxidation and protein levels of phosphorylated AMP-activated protein kinase (p-AMPK) and microtubule-associated proteins 1A/1B-light chain 3-II (LC3-II) were determined in isolated peripheral blood mononuclear cells by thiobarbituric acid reactive substances (TBARS) assay and Western blot, respectively. Plasma levels of interleukin-1β were determined using a commercial ELISA kit. All the obtained variables were compared between subjects suffering an AMI with or without periodontitis and control subject periodontal healthy or with periodontitis.
A higher proportion of subjects suffering AMI + periodontitis than only AMI (without periodontitis) was found. Higher levels of TBARS were found in subjects with periodontitis than in subjects without periodontitis in both AMI and control subjects. Positive correlations between IL-1β levels and TBARS and between IL-1β levels and LC3-II were found only in control subjects.
Results from the present study are consistent with the suggestion of periodontitis as a potential risk factor for AMI. Periodontitis association with circulating lipid peroxides in both AMI and control subjects were found. The absence of differences in IL-1β levels between AMI subjects (only AMI vs AMI + periodontitis) suggests that oxidative stress could be the main pathogenic link between AMI and periodontitis.
本研究旨在深入了解心血管疾病与牙周炎之间的致病关系，并为急性心肌梗死（AMI）和牙周炎的防治提供新视角。本研究评估了 AMI、牙周炎和两者并存患者的炎症、氧化应激和自噬标志物的差异，以探索可能的共同发病机制。
共纳入 260 例患者：106 例存活的首次 AMI 患者（AMI 组）和 154 例无心脏事件的患者（对照组）。采用问卷调查评估年龄、身高、体重、血压和心率。临床探诊深度、临床附着丧失、剩余牙齿数和探诊出血平均位点数。采用硫代巴比妥酸反应物质（TBARS）法和 Western blot 法分别检测分离的外周血单个核细胞中的脂质过氧化和磷酸化 AMP 激活蛋白激酶（p-AMPK）和微管相关蛋白 1A/1B-轻链 3-II（LC3-II）的蛋白水平。采用商业 ELISA 试剂盒测定白细胞介素-1β（IL-1β）的血浆水平。比较 AMI 伴或不伴牙周炎患者与牙周健康或伴牙周炎的对照组患者的所有获得变量。
发现 AMI+牙周炎患者的比例高于仅 AMI（无牙周炎）患者。AMI 和对照组中，牙周炎患者的 TBARS 水平均高于无牙周炎患者。仅在对照组中发现 IL-1β 水平与 TBARS 和 IL-1β 水平与 LC3-II 之间存在正相关。
本研究结果与牙周炎作为 AMI 潜在危险因素的观点一致。在 AMI 和对照组中均发现牙周炎与循环脂质过氧化物相关。AMI 患者（仅 AMI 与 AMI+牙周炎）之间 IL-1β 水平无差异表明，氧化应激可能是 AMI 与牙周炎之间的主要致病联系。
