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

Adrien Boillot, Ryan T. Demmer, Ziad Mallat, Ralph L. Sacco, David R. Jacobs, Joelle Benessiano, Alain Tedgui, Tatjana Rundek, Panos N. Papapanou, Moïse Desvarieux

Research output: Contribution to journalArticlepeer-review

17 Scopus citations

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.

Original languageEnglish (US)
Pages (from-to)418-423
Number of pages6
JournalAtherosclerosis
Volume242
Issue number2
DOIs
StatePublished - Oct 1 2015

Bibliographical note

Funding Information:
This research is supported by NIH grants R01 DE-13094 (Dr. Desvarieux), NS-29993 (Dr. Sacco). Dr. Demmer is also supported by R00 DE-018739 and Dr. Rundek is also supported by NINDS R01 NS-047655 , all from the NIH. This research was also partially supported by an INSERM Chair of Excellence from the Institut National de la Santé et de la Recherche Médicale (INSERM) and a Chair in Chronic Disease, École des Hautes Études en Santé Publique, France (both to Dr. Desvarieux); and a Mayo Chair Endowment, School of Public Health, University of Minnesota (Dr. Jacobs). Patients were seen at the Columbia University General Clinical Research Center, NIH grants UL1 TR000040 and 1UL1RR024156.

Publisher Copyright:
© 2015.

Keywords

  • Atherosclerosis
  • Cardiovascular diseases
  • Periodontitis
  • Phospholipases

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