ACUTE PHASE REACTANTS IN PERIODONTITIS AND CARDIOVASCULAR DISEASE

这项分子流行病学研究的目的是阐明，与美国成年人的代表性人群，全身炎症反应的机制，与心血管疾病（CVD）的风险升高，观察牙周病的人。这项巢式横断面研究将从现有的社区动脉粥样硬化风险（ARIC）研究中选择受试者，该研究是一项正在进行的纵向队列研究，随机抽取了四个州16，000名45-64岁的人。ARIC研究的临床牙周状态的现有记录将用于研究不同类型的探诊袋深度（PPD）范围评分中相同数量的受试者。将通过ELISA分析储存的血清样本的C-反应蛋白（CRP-一种非特异性急性期反应物）和脂多糖结合蛋白（LBP-一种内源性载体分子，可将LPS结合至多形核白细胞的CD 14受体，增强炎症介质的释放）。这些数据将与颈动脉和腘动脉内膜壁厚度的现有超声测量、急性CVD事件的医生诊断以及ARIC研究中收集的其他风险因素相关联。此外，目前正在收集数据（本项目无成本）从龈沟液（GCF）和血清中的炎症介质（IL-6，IL-10和TNF α）在相同的主题的测定。统计分析将评估我们的牙周CVD病因学假设模型的关键组成部分。将使用控制其他口腔内疾病和社会人口统计学变量的最小二乘回归模型评价PPD程度和GCF炎症介质之间的关系。将在控制其他介质（CRP、IL-6、IL-10和TNF α）的PPD组之间比较血清炎症介质（CRP、IL-6、IL-10和TNF α）的严重程度（平均水平）和患病率（有临床意义的升高阈值），将在控制其他全身性疾病的PPD组之间比较其他介质（CRP、IL-6、IL-10和TNF α）。最后，多变量模型将评估牙周病和血清LBP对全身炎症介质和普遍CVD之间的假设协同作用。

The purpose of this molecular epidemiological study is to elucidate, with representative populations of US adults, mechanisms of systemic inflammatory response that are associated with elevated risk of cardiovascular disease (CVD) observed among persons with periodontal disease. This nested cross-sectional study will select subjects from the existing Atherosclerosis Risk in Communities (ARIC) study, an ongoing longitudinal cohort study of a random sample of 16,000 people aged 45-64 years in four states. Existing records of clinical periodontal status from the ARIC study will be used to study equal number of subjects across categories of probing pocket depth (PPD) extent scores. Stored serum samples will be analyzed by ELISA for C-reactive protein (CRP- a non-specific acute phase-reactant) and for lipopolysaccharide binding protein (LBP- an endogenous carrier molecule that binds LPS to the CD14 receptor of polymorphonuclear leukocytes, enhancing the release of inflammatory mediators). Those data will be linked to existing ultrasound measurements of intimal wall thickness of the carotid and popliteal arteries, physician diagnoses of acute CVD events, and other risk factors collected in the ARIC study. In addition, data currently are being collected (with no cost to this project) from assays of inflammatory mediators (IL-6, IL-10 and TNFalpha) in gingival crevicular fluid (GCF) and serum in the same subjects. Statistical analyses will evaluate key components of our hypothesized model of periodontal-CVD etiology. Relationships between extent of PPD and GCF inflammatory mediators will be evaluated using least squares regression models that control for other intra-oral conditions and socio-demographic variables. Severity (mean levels) and prevalence (thresholds of clinically meaningful elevation) of serum inflammatory mediators (CRP, IL-6, IL-10 and TNFalpha) will be compared between PPD groups controlling for other mediators (CRP, IL-6, IL-10 and TNFalpha) will be compared between PPD groups controlling for other systemic diseases. Finally, the multivariate models will assess hypothesized synergistic effects between periodontal disease and serum LBP on systemic inflammatory mediators and prevalent CVD.