Abstract
A large body of evidence underlines an association between periodontal disease and cardiovascular disease. In contrast, data on its relation with endothelial dysfunction as a marker of early subclinical atherosclerosis is inconclusive and limited to patient-cohort studies. We therefore investigated the association between periodontal disease and flow-mediated dilation of the brachial artery (FMD) as a measure of endothelial dysfunction in a general population, and also addressed a possible mediation via inflammation. The study population comprised 1,234 subjects (50.5% men) aged 25–85 years from the 5-year follow-up of the Study of Health in Pomerania, a population-based cohort study. Clinical attachment loss (CAL) and pocket probing depth (PPD) as measures of periodontal disease were assessed half-mouth at four sites per tooth. Subjects were classified according to the periodontitis case definition proposed by Tonetti and Claffey (2005). Measurements of FMD and nitroglycerin-mediated dilation (NMD) were performed using standardized ultrasound techniques. High-sensitive C-reactive protein, fibrinogen and leukocyte count were measured. Fully adjusted multivariate linear regression analyses revealed significant associations of the percentage of sites with PPD ≥6 mm with FMD (ptrend=0.048), with subjects within the highest category having a 0.74% higher FMD compared to subjects within the lowest category (p<0.05). Consistently, FMD values increased significantly across categories of the percentage of sites with CAL ≥6 mm (ptrend=0.01) and the periodontitis case definition (ptrend=0.006). Restrictions to subjects without antihypertensive or statin medication or current non-smokers confirmed previous results. Systemic inflammation did not seem to mediate the relation. Both PPD and CAL were not consistently associated with NMD. In contrast to previous studies, high levels of periodontal disease were significantly associated with high FMD values. This association was not mediated via systemic inflammation. This study revives the discussion on whether and how periodontitis contributes to endothelial dysfunction.
Highlights
The association between periodontal disease and cardiovascular disease (CVD) is supported by a large body of evidence [1,2,3,4]
There were no differences in smoking status, waist circumference, LDL-C, high-density lipoprotein cholesterol (HDL-C), fibrinogen, and systolic blood pressure
Association between hs-C-reactive protein (CRP) and flow-mediated dilation of the brachial artery (FMD) To further address the role of systemic inflammation as a potential mediator of the link between periodontitis and endothelial dysfunction, we evaluated the association between hs-CRP and FMD
Summary
The association between periodontal disease and cardiovascular disease (CVD) is supported by a large body of evidence [1,2,3,4]. Observational studies suggest that such an association is independent of known confounders, a causative relationship could not be substantiated so far [2]. A potential limitation of previous clinical studies suggesting such a relationship may be confounding by common risk factors of both periodontal disease and cardiovascular disease such as smoking, socioeconomic status, and other cardiovascular risk factors [4]. Periodontitis is a chronic infectious disease involving gingival tissues, the periodontal ligament and the alveolar bone. It is accompanied by increased low grade inflammation and transient bacteremia [5,6,7]. Inflammation plays an important role in the initiation and progression of atherosclerosis [10,11] and may contribute to the development of coronary heart disease [8,12,13]
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