Periodontal Status and Novel Systemic Inflammatory Markers in INVEST

Objective: To investigate the relationship between clinical periodontal status and novel inflammatory markers relevant to incident coronary artery disease.

Methods: We measured secretory-phospholipase A2 (s-PLA2) activity and lipoprotein-associated PLA2 (Lp-PLA2) activity in 771 baseline participants (60% f; 58% Hispanic, 22% Black, 18% White, 2% other) of mean age(±SD) 69±9 years in The Oral Infections and Vascular Disease Epidemiology Study (INVEST). Dentate subjects (n=678) received a clinical periodontal exam with probing depth (PD) and attachment loss (AL) recorded in up to 192 sites/mouth. We examined the cross-sectional relationship between clinical periodontal status and both s-PLA2 activity and Lp-PLA2 activity. Periodontal status was classified into six levels. The first five levels correspond to quintiles of the % of sites with PD≥3 mm (%PD≥3); edentulous participants comprised the sixth level. A second periodontal status definition substituted quintiles of %AL≥3 for PD quintiles. Multivariable statistical models included: age, gender, race/ethnicity, education, diabetes, smoking, systolic blood pressure, HDL-cholesterol and LDL-cholesterol.

Results: Mean %PD≥3 was 45±27% and was assessed in an average of 107±48 sites/mouth. Mean s-PLA2 activity and Lp-PLA2 activity values were 0.78±0.56 nmol/min/ml and 30.4±11.1 nmol/min/ml, respectively. s-PLA2 values increased across quintiles of %PD≥3 and the edentulous, as follows: Q1=0.68, Q2=0.69, Q3=0.82, Q4=0.81, Q5=0.85 and edentulous=0.87 nmol/min/ml (p for trend=0.0008). Lp-PLA2 values also increased: Q1=27.8, Q2=29.8, Q3=30.1, Q4=31.1, Q5=32.0 and edentulous=31.9 nmol/min/ml (p for trend=0.0008). Results were similar but attenuated across levels of %AL≥3, for both s-PLA2 activity (p for trend=0.006) and Lp-PLA2 activity (p for trend=0.01).

Conclusion: Clinical periodontal status is positively associated with novel inflammatory markers recently shown to have prognostic value for incident coronary artery disease.

Support: NIH-R01DE-13094, InsermR05115DD