1 Department of Periodontology, School of Dental Medicine, Tufts University, Boston, MA, USA.
2 Division of Preventive Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA.
J Dent Res. 2018 Sep;97(10):1106-1113. doi: 10.1177/0022034518782189. Epub 2018 Jun 21.
Periodontal disease (PD) shares common risk factors with cardiovascular disease. Our hypothesis was that having a family history of myocardial infarction (FamHxMI) may be a novel risk factor for PD. Risk assessment based on FamHxMI, conditional on smoking status, was examined given the strong influence of smoking on PD. Exploratory analysis with inflammatory biomarkers and genetic determinants was conducted to understand potential mechanistic links. The Women's Genome Health Study (WGHS) is a prospective cohort of US female health care professionals who provided blood samples at baseline in the Women's Health Study, a 2 × 2 factorial clinical trial investigating vitamin E and aspirin in the prevention of cardiovascular disease and cancer. PD was ascertained via self-report over 12 y of follow-up. Prevalence (3,442 cases), incidence (1,365 cases), and survival analysis of PD were investigated for associations of FamHxMI as well as in strata of FamHxMI by smoking. Kruskal-Wallis, chi-square tests, multivariate regression, and Cox proportional hazard models were used for the analyses. In the WGHS, women with FamHxMI showed higher risk of ever having PD. A particularly high-risk group of having both FamHxMI and smoking at baseline was highlighted in the prevalence and risk of developing PD. PD risk increased according to the following strata: no FamHxMI and nonsmokers (reference), FamHxMI and nonsmokers (hazard ratio [HR] = 1.2, 95% CI = 1.0 to 1.5), smokers without FamHxMI (HR = 1.3, 95% CI = 1.2 to 1.5), and smokers with FamHxMI (HR = 1.5, 95% CI = 1.2 to 1.8). An independent analysis by the dental Atherosclerosis Risk in Communities study ( N = 5,552) identified more severe periodontitis cases among participants in the high-risk group (smokers with FamHxMI). Further examination of interactions among inflammatory biomarkers or genetic exploration with FamHxMI did not explain the risk increase of PD associated with FamHxMI in the WGHS. Future efforts based on an integrative-omics approach may facilitate validation of these findings and suggest a mechanistic link between PD and FamHxMI.
牙周病（PD）与心血管疾病有共同的危险因素。我们的假设是，心肌梗死家族史（FamHxMI）可能是 PD 的一个新的危险因素。鉴于吸烟对 PD 的强烈影响，我们检查了基于 FamHxMI 的风险评估，并在吸烟状况的条件下进行了评估。进行了探索性分析，以了解炎症生物标志物和遗传决定因素之间的潜在机制联系。妇女基因组健康研究（WGHS）是一项前瞻性队列研究，由美国女性医疗保健专业人员组成，她们在妇女健康研究中提供了基线血液样本，这是一项 2×2 因子临床试验，研究维生素 E 和阿司匹林在预防心血管疾病和癌症中的作用。通过 12 年的随访，通过自我报告确定 PD。研究了 FamHxMI 以及 FamHxMI 按吸烟分层的相关性与 PD 的患病率（3442 例）、发病率（1365 例）和生存分析。使用 Kruskal-Wallis、卡方检验、多变量回归和 Cox 比例风险模型进行分析。在 WGHS 中，有 FamHxMI 的女性患 PD 的风险更高。在 PD 的患病率和发病风险方面，突出了一个基线时同时具有 FamHxMI 和吸烟的高风险群体。根据以下分层，PD 风险增加：没有 FamHxMI 和不吸烟（参考）、有 FamHxMI 和不吸烟（风险比[HR] = 1.2，95%CI = 1.0 至 1.5）、没有 FamHxMI 的吸烟者（HR = 1.3，95%CI = 1.2 至 1.5）和有 FamHxMI 的吸烟者（HR = 1.5，95%CI = 1.2 至 1.8）。牙齿动脉粥样硬化风险社区研究（N = 5552）的独立分析确定了高风险组（有 FamHxMI 的吸烟者）中更严重的牙周炎病例。进一步检查炎症生物标志物之间的相互作用或遗传与 FamHxMI 的探索并没有解释与 FamHxMI 相关的 PD 风险增加与 WGHS 中的风险增加。基于综合组学方法的未来努力可能有助于验证这些发现，并提示 PD 与 FamHxMI 之间的机制联系。
