Boillot Adrien, Demmer Ryan T, Mallat Ziad, Sacco Ralph L, Jacobs David R, Benessiano Joelle, Tedgui Alain, Rundek Tatjana, Papapanou Panos N, Desvarieux Moïse
Department of Periodontology, Rothschild Hospital (AP-HP); University Paris 7, 5 Rue Santerre, Paris, France; INSERM U1018, University of Versailles St Quentin. Centre for research in Epidemiology and Population Health, Villejuif, France.
Department of Epidemiology, Mailman School of Public Health, Columbia University, New York, NY, USA.
Atherosclerosis. 2015 Oct;242(2):418-23. doi: 10.1016/j.atherosclerosis.2015.07.039. Epub 2015 Jul 22.
Periodontal infections have been linked to cardiovascular disease, including atherosclerosis, and systemic inflammation has been proposed as a possible mediator. Secretory phospholipase A2 (s-PLA2) and Lipoprotein-associated PLA2 (Lp-PLA2) are inflammatory enzymes associated with atherosclerosis. No data are available on the association between oral microbiota and PLA2s. We studied whether a relationship exists between periodontal microbiota and the activities of these enzymes.
The Oral Infection and Vascular Disease Epidemiology Study (INVEST) collected subgingival biofilms and serum samples from 593 dentate men and women (age 68.7 ± 8.6 years). 4561 biofilm samples were collected in the two most posterior teeth of each quadrant (average 7/participant) for quantitative assessment of 11 bacterial species using DNA-DNA checkerboard hybridization. Mean concentration of s-PLA2 and activities of s-PLA2 and Lp-PLA2 were regressed on tertiles of etiologic dominance (ED). ED is defined as the level of presumed periodontopathic species/combined level of all eleven species measured, and represents the relative abundance of periodontopathic organisms. Analyses were adjusted for age, sex, race/ethnicity, education, smoking, BMI, diabetes, LDL cholesterol and HDL cholesterol, and systolic blood pressure.
Higher levels of s-PLA2 activity were observed across increasing tertiles of etiologic dominance (0.66 ± 0.04 nmol ml(-1) min(-1), 0.73 ± 0.04 nmol ml(-1) min(-1), 0.89 ± 0.04 nmol ml-1 min-1; p < 0.001), with also a trend of association between Lp-PLA2 activity and ED (p = 0.07), while s-PLA2 concentration was unrelated to ED.
Increasingly greater s-PLA2 activity at higher tertiles of etiologic dominance may provide a mechanistic explanatory link of the relationship between periodontal microbiota and vascular diseases. Additional studies investigating the role of s-PLA2 are needed.
牙周感染与心血管疾病（包括动脉粥样硬化）有关，全身炎症被认为是一种可能的介导因素。分泌型磷脂酶A2（s-PLA2）和脂蛋白相关磷脂酶A2（Lp-PLA2）是与动脉粥样硬化相关的炎症酶。目前尚无关于口腔微生物群与PLA2s之间关联的数据。我们研究了牙周微生物群与这些酶的活性之间是否存在关系。
口腔感染与血管疾病流行病学研究（INVEST）收集了593名有牙的男性和女性（年龄68.7±8.6岁）的龈下生物膜和血清样本。在每个象限的两颗最后面的牙齿中收集4561份生物膜样本（平均每人7份），使用DNA-DNA棋盘杂交法对11种细菌进行定量评估。将s-PLA2的平均浓度以及s-PLA2和Lp-PLA2的活性与病因优势度（ED）的三分位数进行回归分析。ED定义为假定的牙周病原菌水平/所测的所有11种细菌的综合水平，代表牙周病原菌的相对丰度。分析对年龄、性别、种族/民族、教育程度、吸烟、体重指数、糖尿病、低密度脂蛋白胆固醇和高密度脂蛋白胆固醇以及收缩压进行了校正。
随着病因优势度三分位数的增加，观察到s-PLA2活性水平升高（0.66±0.04 nmol ml(-1) min(-1)，0.73±0.04 nmol ml(-1) min(-1)，0.89±0.0 /ml(-1) min(-1)；p<0.001），Lp-PLA2活性与ED之间也存在关联趋势（p = 0.07），而s-PLA2浓度与ED无关。
在病因优势度较高的三分位数中，s-PLA2活性越来越高，这可能为牙周微生物群与血管疾病之间的关系提供一个机制性的解释联系。需要进一步研究s-PLA2的作用。
