Dental Plaque as a Risk Factor for Coronary Heart Disease

Introduction: Interest is increasing in the possible causal link between oral infection and coronary heart disease (CHD). Objectives: We used the Experimental Gingivitis Model to determine the effect of dental plaque accumulation on systemic markers of inflammation that are associated with CHD risk. Moreover, we addressed whether a gender/racial disparity in the systemic inflammatory responses to dental plaque exists. Methods: We recruited 156 healthy adults (aged 18-31 years), comprising black and white males and females. Participants brushed for 21 days (control phase), ceased brushing for 21 days (experimental phase), and resumed brushing for a further 21 days (recovery phase). Plaque levels and gingival inflammation were assessed. In addition, peripheral blood samples were collected at each visit to evaluate systemic markers of inflammation. Paired t-tests and Wilcoxon signed rank tests were used to test for significant changes during the experimental phase. Results: 128 participants completed the study. The correlation between the plaque index and gingival index changes during the experimental phase was 0.79 overall, and was similar across genders/races. During the experimental phase, participants had significant increases (P<0.05) in the plaque index, gingival index, mean corpuscular volume, mean platelet volume, and cortisol levels. In blacks, significant increases (P<0.05) were observed in the neutrophil oxidative activity and mean corpuscular hemoglobin levels. In black males, the erythrocyte sedimentation rate increased (P<0.05). Fibrinogen levels increased (P<0.05) in white males. Significant decreases (P<0.05) occurred in total cholesterol, high density lipoprotein, and red blood cell count. Hematocrit and hemoglobin levels decreased (P<0.05) in blacks. In black males, decreases (P<0.05) were observed in the low density lipoprotein levels. Conclusions: In young healthy adults, accumulation of dental plaque elicited systemic inflammatory responses, some of which are with potential atherogenic consequences. These responses differed between individuals and were dependant upon gender/race. Supported by NIH # R01 DEO15145-01.