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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).

Author information

  • 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: mdesvarieux@columbia.edu.

Abstract

OBJECTIVE:

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.

METHODS:

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.

RESULTS:

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.

CONCLUSION:

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.

KEYWORDS:

Atherosclerosis; Cardiovascular diseases; Periodontitis; Phospholipases

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