Correlation between periodontal disease and endothelial dysfunction
Date
2002
DOI
Authors
Morgan, Sonia
Version
OA Version
Citation
Abstract
Periodontitis and coronary heart disease have complex etiologies, genetic and gender predispositions, and potentially share many risk factors. The mechanism for this association remains largely unknown. Epidemiological studies have suggested that bacterial pathogens residing in the dental flora may participate in the development of atherosclerotic vascular disease through direct vascular injury during periods of bacteremia or via the triggering of systemic immune responses that lead to vascular inflammation. The vascular endothelium normally prevents vasospasm and thrombosis inside blood vessels by production and release of endothelium-derived substances including nitric oxide, it is also a likely target for circulating cytokines and oral pathogens, which plays a central role in the regulation of vascular homeostasis. Activation of endothelial cells by inflammatory cytokines promotes a pro-atherogenic phenotype with increased expression of adhesion molecules and loss of the antithrombotic, growth inhibitory, and vasodilator properties of the endothelium, including a decrease in the biological activity of nitric oxide. These changes occur early in the development of atherosclerosis and to contribute to the clinical expression of the disease. Support for the clinical importance of endothelial dysfunction is provided by recent studies demonstrating increased cardiovascular disease risk in patients with endothelial dysfunction in coronary and peripheral arteries. A non-invasive, ultrasound-based method to examine flow-mediated, nitric-oxide dependent vasodilation of the forearm brachial artery has great promise as a clinical and investigative tool to evaluate vascular endothelial function. The aim of this current proposal is to determine whether individuals with periodontal disease have increased markers of systemic inflammation and impaired vascular endothelial function as compared to normal controls. The study hypothesizes that individuals with periodontal disease may have increased cardiovascular risk. Also, the greater the severity of the periodontal disease the greater the cardiovascular risk, in part, due to impaired vascular function. In the present study, we sought to test this hypothesis using a case-control design and brachial artery flow-mediated dilation as an indicator of endothelial function.
A total of 62 subjects were enrolled in this study. The experimental group comprised 36 subjects affected by periodontal disease, and the control group comprised 26periodontally and systemically healthy individuals. Adjustment by age and sex-matched subjects was done. All periodontal subjects had at least 3 teeth affected by periodontal disease as determined by clinical attachment, probing depth measurements, and radiographic evaluation. Control patients had no sign of periodontal disease. The experimental group subjects were further stratified according to their periodontal condition, and disease severity -moderate or advanced- as defmed by the American Dental Association. The moderate periodontitis group comprised 12 subjects and the advanced periodontitis group 24 subjects. All subjects (periodontal and control) underwent non-invasive endothelium derived nitric oxide (EDNO) determination along with blood tests, which, included LDL, HDL, triglyceride, cholesterol, fasting glucose, and C reactive protein levels. The results demonstrated a statistically significant elevation of the serum levels of C reactive protein of the advanced periodontal disease patients (0.23mg/dl) and moderate periodontal disease patients (0.27mg/dl) when compared to healthy controls (0.07mg/dl) (p[less than].05), a finding that is consistent with the hypothesis that endothelial dysfunction in this setting is attributable to a state of systemic inflammation. The sample size was relatively modest to be able to draw any significance in regard to the endothelium function as evidenced by the endothelium-derived nitric oxide for the moderate periodontal group.
The median values of the levels of amylase, fasting glucose, cholesterol, triglyceride, LDL and HDL showed no statistically significant differences between periodontitis patients and healthy controls. The mean value of FMD % for the experimental group (advanced and moderate) and the control group was 8.21± 5.2, 11.9 ±5.11, 11.6 ±5.1 respectively. (p[less than]0.05) between advanced disease and control group. The average value of nitroglycerine NTG % for the advance periodontal moderate and the control group was 17.8±8.9, 21.5±5.2 and 20.8±10.4 respectively. (P=0.30) between advance disease group and control group. These findings provide a potential mechanistic explanation for prior epidemiological studies suggesting a link between periodontitis and cardiovascular disease and are consistent with the very strong evidence that chronic inflammatory states are associated with cardiovascular disease.
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Thesis (M.S.D.)--Boston University, Henry M. Goldman School of Dental Medicine, 2002 (Oral Biology).
Includes bibliographical references (leaves 57-79).
Thesis (M.S.D.)--Boston University, Henry M. Goldman School of Dental Medicine, 2002 (Oral Biology).
Includes bibliographical references (leaves 57-79).
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This work is protected by copyright. Downloading is restricted to the BU community. If you are the author of this work and would like to make it publicly available, please contact open-help@bu.edu.