Abstract

The objective of this preclinical in vivo study was to determine changes in vascular inflammatory biomarkers in systemic circulation after injection of lipopolysaccharide (LPS) from Porphyromonas gingivalis (Pg) in rats. Experimental periodontitis was induced by injections of Pg-LPS. Gingival soft and hard tissues changes were analysed by means of magnetic resonance imaging and micro computed tomography. Serum levels of interleukin (IL)-6, IL-10, pentraxin (PTX) 3, and soluble fragment of tumor necrosis factor-like weak inducer of apoptosis (sTWEAK) were determined at baseline and 24 h, 7, 14, and 21 days after periodontal induction. Significant periodontal inflammation and alveolar bone loss were evident at the end of periodontal induction. Experimental periodontitis posed an acute systemic inflammatory response with increased serum levels of IL-6 and PTX3 at 24 h post-induction, followed by a significant overexpression of sTWEAK at 7 days. This inflammatory state was maintained until the end of the experiment (21 days). As expected, IL-10 serum levels were significantly lower during the follow-up compared to baseline concentrations. In the present animal model, experimental periodontitis is associated with increased systemic inflammation. Further studies are needed to confirm whether PTX3 and sTWEAK could be useful biomarkers to investigate potential mechanisms underlying the relationship between periodontitis and atherosclerotic vascular diseases.

Highlights

  • Atherosclerotic vascular diseases (AVDs) such as coronary heart disease and ischemic stroke have been associated with periodontitis [1, 2]

  • In terms of gingival palatal thickness, which we considered as a surrogate measure of oedema, an increase in the relative percentage was found after the induction of LPSinduced experimental periodontitis

  • The relationship between inflammation and AVDs is supported by the high presence of inflammatory cells within the plaque tissue and the circulating levels of inflammatory mediators [4]

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Summary

Introduction

Atherosclerotic vascular diseases (AVDs) such as coronary heart disease and ischemic stroke have been associated with periodontitis [1, 2]. In patients with cardiovascular disease plasma PTX3 is negatively correlated with flow-mediated dilatation (FMD), a hallmark of endothelial dysfunction [8]. Human studies showed that in patients with chronic kidney disease, sTWEAK was associated with impaired FMD [10, 11] and atheromatosis progression [12]. It was found that in artery samples from patients with atherosclerosis, sTWEAK concentrations were correlated with increased carotid intima-media thickness (c-IMT), a hallmark of subclinical atherosclerotic disease [13]

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