Abstract 14351: Low-Level Inflammation in the Prevalent Oral Disease Gingivitis Induces Surrogate Markers of Atherosclerosis in Young Healthy Individuals. A Single-Subject Interventional Study
Background: Gingivitis is a low-level oral infection induced by bacterial deposits on the teeth with a high prevalence within Western populations. A potential link between the more severe oral disease periodontitis and cardiovascular disease has already been shown. We now investigated for the first time whether Gingivitis may promote surrogate markers of atherosclerotic plaque development.
Methods and Results: 37 non-smoking young volunteers with no inflammatory disease or any cardiovascular risk factors participated in this single-subject interventional study with an intra-individual control. Intentionally experimental oral inflammation was induced by the interruption of oral hygiene for 21 days, followed by a 21-days resolving phase after reinitiating of oral hygiene. Primary outcome measures at baseline, day 21 and 42 were plasma levels of IL-6, hsCRP and MCP-1, as well as oxLDL uptake and the adhesion capacity of isolated blood monocytes. The partial cessation of oral hygiene procedures was followed by the significant increase of gingival bleeding (-32.62%, 95% CI -38.27 to -26.96%; P<0.0001). This local low-level inflammation was associated with a systemic increase in hsCRP (0.092 Log10 (hsCRP+1) ml/l, 0.004 to -0.180; P=0.041), IL-6 (2.742 Log10 (IL-6) ng/l, 1.710 to 4.395; P<0.0001) and MCP-1 (13.42 ng/l, -0.303 to 27.15; P=0.055) in plasma samples at day 21, which decreased at day 42. Monocytes showed an enhanced adherence to endothelial cells and an increase in lipid uptake (P<0.050) at day 21 of gingivitis.
Conclusions: Bacterial-induced gingival low-level inflammation induced an acute systemic increase in surrogate markers of atherosclerotic plaque development in young and healthy volunteers. Adequate dental hygiene almost completely reversed this inflammatory process suggesting that appropriate dental prophylaxis limits risk factors for atherosclerosis.
- © 2012 by American Heart Association, Inc.