Periodontitis Is Associated with Endothelial Dysfunction in a General Population: A Cross-Sectional Study

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.

Periodontitis and Endothelial Dysfunction: Periodontal Clinical Parameters and Levels of Salivary Markers Interleukin‐1β, Tumor Necrosis Factor‐α, Matrix Metalloproteinase‐2, Tissue Inhibitor of Metalloproteinases‐2 Complex, and Nitric Oxide

“…In the current literature, few studies have been conducted to investigate an association between periodontitis and ED. Five studies reported a positive association, 11–15 and only one reported a lack of association 16 . The present study demonstrates that presence of periodontitis was associated with higher ED.…”

“…In addition, several types of medications, particularly antihypertensive and anti‐inflammatory drugs, may affect ED 23 . Thus, by properly adopting these exclusion criteria in the present study, 215 individuals were excluded, demonstrating the difficulty of obtaining large samples in studies with this characteristic methodology, as in previous studies 11–16 . Another important issue to be considered is the high‐cost equipment necessary to perform the examination, requiring an extensively trained operator for the standardization and implementation of the technique 24 …”

“…Few studies have associated periodontitis to ED 11–16 . It is believed that products of inflammation, IL‐1β, TNF‐α, C‐reactive protein (CRP), MMPs, and prostaglandins, expressed in chronic periodontitis (CP) are released into the systemic circulation and can stimulate endothelial cells to produce other inflammatory markers inducing or exacerbating ED 17 .…”

Relationship between periodontal disease and cardiovascular risk factors among young and middle-aged Brazilians. Cross-sectional study

“…[6][7][8] The inflammation process of PD may trigger systemic inflammation that could be involved in the progression of atherosclerosis and consequently in CVD outcomes such as myocardial infarction or stroke. 9 However, it is not totally clear what the causal pathway between PD and CVD risk is.…”

The Influence of Age in the Relationship between Cerebral Small Vessel Disease and Edentulism. The Atahualpa Project

“…Enhanced expression of inflammatory mediators in response to a chronic infection, endothelial dysfunction and atherosclerosis are the most likely pathogenetic mechanisms underlying these complications [4,5] . In this view, the link between edentulism and stroke has been extensively studied but results have been inconsistent.…”