Periodontal microbiota and carotid intima-media thickness - The Oral Infections and Vascular Disease Epidemiology Study (INVEST)

被引:361
作者
Desvarieux, M
Demmer, RT
Rundek, T
Boden-Albala, B
Jacobs, DR
Sacco, RL
Papapanou, PN
机构
[1] Univ Minnesota, Sch Publ Hlth, Div Epidemiol, Minneapolis, MN 55455 USA
[2] Univ Minnesota, Sch Med, Dept Med, Minneapolis, MN 55455 USA
[3] Columbia Univ Coll Phys & Surg, Dept Neurol, New York, NY 10032 USA
[4] Columbia Univ, Mailman Sch Publ Hlth, Dept Sociomed Sci, New York, NY USA
[5] Columbia Univ, Mailman Sch Publ Hlth, Dept Epidemiol, New York, NY USA
[6] Columbia Univ, Sch Dent & Oral Surg, Div Periodont, New York, NY USA
关键词
infection; inflammation; atherosclerosis; epidemiology; carotid arteries;
D O I
10.1161/01.CIR.0000154582.37101.15
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
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.
引用
收藏
页码:576 / 582
页数:7
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