The systemic inflammatory response to dental plaque

Abstract

Introduction: Bacteremia involving oral bacteria and the systemic inflammatory responses are mechanisms that could causally link oral and systemic diseases. Objective: To use an experimental gingivitis model (EGM) in 2 clinical studies to 1) examine the systemic inflammatory responses to dental plaque, and assess racial differences in these responses; 2) determine whether dental plaque accumulation causes bacteremia and subsequent systemic responses following toothbrushing. Additionally, a laboratory study was conducted to examine the interaction between circulating human neutrophils and Fusobacterium nucleatum. Methods: For both clinical studies, healthy adults, aged 18-31 years, were recruited. In the first study, black and white, males and females participated in a 21-day EGM; in the second study, white adults participated in a 7-day EGM. In both studies, subjects visited the clinic weekly for: 1) measurement of the plaque index (PI) and gingival index (GI); 2) collection of peripheral blood samples to evaluate systemic markers of inflammation. In the second study, to analyze bacteremic episodes during the experimental phase, peripheral blood samples were collected at baseline and at 0.5, 5, and 30 minutes post-toothbrushing. In the laboratory study, interactions between F. nucleatum and circulating neutrophils were examined using a luminol-enhanced chemiluminescence assay. Results: During the experimental phases of both clinical studies, PI and GI increased (p<0.05) with a correlation between PI and GI ≥0.79. In the first study, dental plaque accumulation resulted in a systemic response that manifested as changes (p<0.05) in the level of inflammatory markers, hematologic factors, markers of lipid metabolism, and markers of metabolic change. This systemic response differed between individuals of different gender and race. In the second study, bacteremic episodes and changes in hematologic factors were observed post-toothbrushing during the experimental phase. Activation of neutrophils with F. nucleatum, in the laboratory study, increased the levels of neutrophil chemiluminescence (p<0.05). Conclusions: Overall, the findings of these investigations may shed light on the mechanistic pathways by which oral infection may impose risk for systemic diseases and provide some evidence to support a possible causal association between oral and systemic diseases. The clinical significance of this in systemic inflammatory diseases requires further investigation.