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

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.

Fig. 1

Distribution of s-PLA2 activity across tertiles of etiologic, putative and health-associated burdens. s-PLA2: Secretory phospholipase A2. EB: Etiologic burden; PB: Putative burden; HAB: Health-associated burden. Adjustment for gender, age, race, education, diabetes, smoking, BMI, mean systolic blood pressure, HDL-cholesterol, LDL-cholesterol. Bacterial burdens are mutually adjusted. Tertile 1: n = 197; Tertile 2: n = 198; Tertile 3: n = 198. p for linear trend (1 d.f.): EB = 0.14; PB = 0.07; HAB = 0.43. p for global null hypothesis of any difference in outcome (2 d.f.): EB = 0.22; PB = 0.14; HAB = 0.60.

Fig. 2

Distribution of Lp-PLA2 and s-PLA2 activities across tertiles of etiologic dominance. s-PLA2: Secretory phospholipase A2; Lp-PLA2: Lipoprotein-associated phospholipase A2. Adjustment for gender, age, race, education, diabetes, smoking, BMI, mean systolic blood pressure, HDL-cholesterol, LDL-cholesterol. Tertile 1: n = 197; Tertile 2: n = 198; Tertile 3: n = 198. p for linear trend (1 d.f.): Lp-PLA2: 0.10; s-PLA2 < 0.001. p for global null hypothesis of any difference in outcome (2 d.f.): Lp-PLA2: 0.07; s-PLA2 < 0.001.