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 language||English (US)|
|Number of pages||6|
|State||Published - Oct 1 2015|
Bibliographical noteFunding 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.
- Cardiovascular diseases