Endodontic Treatment of Chronic Apical Periodontitis Ameliorates Systemic Inflammation and Restores Impaired Cellular Responses to Insulin in an In Vitro Model

Abstract

Introduction

A growing body of research supports an association between periapical inflammation and an increased risk of developing systemic diseases. There is currently no scientific evidence to support a causal effect of inflammation on the onset of insulin resistance (IR) in patients with apical periodontitis (AP). The aim of this in vitro study was to evaluate any association between AP and levels of serum inflammatory factors potentially associated with the onset of IR, and to investigate the effect of root canal treatment (RCT) on these systemic inflammation markers and on the response in vitro to insulin.

Methods

A total of 27 control subjects and 27 patients with AP were enrolled. Patients with AP underwent RCT and were followed-up 6 and 12 months post-treatment. Enzyme-linked immunosorbent assays were used to evaluate serum levels of proinflammatory cytokines interleukin (IL)-1, IL-6, IL-8, and tumor necrosis factor (TNF)-α. The response in vitro to insulin was assessed by measuring glucose consumption in a human pancreatic epithelioid carcinoma cell line treated with sera from healthy and AP subjects.

Results

At baseline AP was associated with significant higher levels of IL-1, IL-6, and IL-8 in the serum of untreated (AP) patients vs controls (P < .001). Glucose consumption decreased in pancreatic cells incubated with baseline serum from patients with AP, in a manner proportional to total cytokines amount. Notably, endodontic treatment was associated with reduced levels of cytokines (P < .001) and improved response to insulin in AP group (P < .001).

Conclusions

Our findings suggest that AP may promote inflammatory-driven IR in an in vitro model, and that RCT may ameliorate inflammatory mediators in vivo and the cellular response to insulin in vitro.