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Atherosclerosis. 2015 Oct;242(2):418-23. doi: 10.1016/j.atherosclerosis.2015.07.039. Epub 2015 Jul 22.

Periodontal microbiota and phospholipases: the Oral Infections and Vascular Disease Epidemiology Study (INVEST).

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  • 1Department 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.
  • 2Department of Epidemiology, Mailman School of Public Health, Columbia University, New York, NY, USA.
  • 3Inserm U970; Cardiovascular Research Center, and Université Paris-Descartes University, F-75015, Paris, France; Department of Medicine, University of Cambridge, Cambridge, United Kingdom.
  • 4Department of Neurology, Miller School of Medicine, University of Miami, Miami, FL, USA.
  • 5Department of Epidemiology and Community Health, School of Public Health, University of Minnesota, Minneapolis, MN, USA; Department of Nutrition, University of Oslo, Oslo, Norway.
  • 6Service de Biochimie, Hôpital Bichat, Assistance Publique-Hôpitaux de Paris, Paris, France.
  • 7Inserm U970; Cardiovascular Research Center, and Université Paris-Descartes University, F-75015, Paris, France.
  • 8Division of Periodontics, Section of Oral and Diagnostic Sciences, College of Dental Medicine, Columbia University, New York, NY, USA.
  • 9Department of Epidemiology, Mailman School of Public Health, Columbia University, New York, NY, USA; INSERM Epidemiology and Biostatistics Research Center, Sorbonne Paris Cité, INSERM UMR 1153, Paris, France. Electronic address:



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.


Atherosclerosis; Cardiovascular diseases; Periodontitis; Phospholipases

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