Abstract

Eugenol (mixed with zinc oxide powder) is widely used as direct capping material during pulp therapy in primary teeth. The aim of the present study was to evaluate the effect of eugenol on diverse genes involved in inflammatory and cell apoptosis processes. The regulatory effect of eugenol on the expression of inflammation and apoptotic genes was evaluated in dental pulp fibroblasts from extracted third molars, cultured under concentration of eugenol of 13 μM. Eugenol allowed the expression of inflammatory and apoptotic genes when compared with positive and negative controls. Eugenol is a proinflammatory agent when it is in direct contact with healthy tissues and behaves as an anti-inflammatory agent in tissues undergoing inflammatory/apoptotic processes, as in cases of pulp inflammation in primary teeth. These findings are relevant for dentistry, when considering the application of safer pulp treatments to grossly carious children's teeth.

Highlights

  • Dental caries is the most common chronic disease in childhood caused mainly by a poor, long-term oral hygiene

  • The remaining tissue was cultured for explant, together with 3 mL of Dulbecco’s Modified Eagle Medium (DMEM) culture medium enriched with 10% Fetal Bovine Serum (FBS) and an antibiotic combination (1,000 U/mL Penicillin, 1 mg/mL Streptomycin, and Amphotericin B 2.5 mg/μL); the mixture was incubated at 37∘C, 5% CO2, and 95% humidity, and the culture medium was replaced every other day

  • To assess whether there were differences among fibroblast gene expressions, comparisons were made as follows: (a) negative control versus cell groups treated with eugenol and (b) positive control (LPS) versus cell groups treated with eugenol

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Summary

Introduction

Dental caries is the most common chronic disease in childhood caused mainly by a poor, long-term oral hygiene. The disease can be preventable and reversible; without appropriate and timely control, cariogenic bacteria may seriously destroy the hard dental tissues and affect the dental pulp [1]. LPS can activate the pulp immune system, inducing the segregation of proinflammatory chemokines and cytokines, with an increase in capillary permeability [3]. The pulp’s role during the inflammatory response is to fight against infection and tissue damage through immune cells, such as fibroblasts and other cells that recognize damage from cariogenic bacteria [4]; fibroblasts activate the recognition of bacterial surface receptors, which initiates the inflammatory response by stimulating the production of cytokines, including proinflammatory, anti-inflammatory, and regulatory cytokines [5]. Recruitment of neutrophils and polymorphonuclear cells occurs, which increases expression of the interleukins [6]

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