Periodontal microbiota and carotid intima-media thickness - The Oral Infections and Vascular Disease Epidemiology Study (INVEST)
Periodontal microbiota and carotid intima-media thickness - The Oral Infections and Vascular Disease Epidemiology Study (INVEST)
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DOI：
10.1161/01.cir.0000154582.37101.15
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发表时间：
2005-02-08
期刊：
影响因子：
37.8
通讯作者：
Papapanou, PN
中科院分区：
文献类型：
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作者：
Desvarieux, M;Demmer, RT;Papapanou, PN
背景-慢性感染，包括牙周感染，可能易患心血管疾病.我们调查了牙周微生物群和亚临床atherosclerosis.Methods和结果之间的关系-1056人（年龄69 +/- 9岁），没有中风或心肌梗死的历史，参加了口腔感染和血管疾病流行病学研究（INVEST），我们分析了657齿状科目。在这些受试者中，收集了4561个龈下菌斑样本（平均7个样本/受试者），并通过DNA-DNA棋盘杂交定量评估了11种已知的牙周细菌。广泛的心血管危险因素测量，高分辨率B型超声颈动脉扫描，白色血细胞计数和C反应蛋白值被获得。在3项独立分析中，平均颈动脉内膜-中层厚度（IMT）回归到（1）所有评估细菌负荷，（2）牙周病致病细菌负荷（病原细菌负荷）和（3）龈下菌斑中致病菌相对于其他细菌的相对优势的三分位数。所有分析均根据年龄、种族/民族、性别、教育、体重指数、吸烟、糖尿病、收缩压、LDL和HDL胆固醇进行调整。总体牙周细菌负荷与颈动脉IMT相关。这种关系是特定的致病菌的负担和优势的病原菌在所观察到的微生物生态位。病原菌优势三分位数的校正平均IMT值分别为0.84、0.85和0.88（P = 0.002）。同样，在病原菌负荷的三分位数中，白色血细胞值从5.57增加到6.09和6.03个细胞x 10（9）/ L（P = 0.01）。C-反应蛋白值与牙周微生物状态无关（P = 0.82）。结论-我们的数据提供了牙周微生物学和亚临床动脉粥样硬化之间直接关系的证据。这种关系独立于C-反应蛋白而存在.
Background - Chronic infections, including periodontal infections, may predispose to cardiovascular disease. We investigated the relationship between periodontal microbiota and subclinical atherosclerosis.Methods and Results - Of 1056 persons ( age 69 +/- 9 years) with no history of stroke or myocardial infarction enrolled in the Oral Infections and Vascular Disease Epidemiology Study ( INVEST), we analyzed 657 dentate subjects. Among these subjects, 4561 subgingival plaque samples were collected ( average of 7 samples/ subject) and quantitatively assessed for 11 known periodontal bacteria by DNA- DNA checkerboard hybridization. Extensive in- person cardiovascular risk factor measurements, a carotid scan with high- resolution B- mode ultrasound, white blood cell count, and C- reactive protein values were obtained. In 3 separate analyses, mean carotid artery intima- media thickness ( IMT) was regressed on tertiles of ( 1) burden of all bacteria assessed, ( 2) burden of bacteria causative of periodontal disease ( etiologic bacterial burden), and ( 3) the relative predominance of causative/ over other bacteria in the subgingival plaque. All analyses were adjusted for age, race/ ethnicity, gender, education, body mass index, smoking, diabetes, systolic blood pressure, and LDL and HDL cholesterol. Overall periodontal bacterial burden was related to carotid IMT. This relationship was specific to causative bacterial burden and the dominance of etiologic bacteria in the observed microbiological niche. Adjusted mean IMT values across tertiles of etiologic bacterial dominance were 0.84, 0.85, and 0.88 ( P = 0.002). Similarly, white blood cell values increased across tertiles of etiologic bacterial burden from 5.57 to 6.09 and 6.03 cells x 10(9)/ L ( P = 0.01). C- reactive protein values were unrelated to periodontal microbial status ( P = 0.82).Conclusions - Our data provide evidence of a direct relationship between periodontal microbiology and subclinical atherosclerosis. This relationship exists independent of C- reactive protein.