Effects of pulpotomy using mineral trioxide aggregate on prostaglandin transporter and receptors in rat molars

Naoto Ohkura,Hayato Ohshima,Takashi Okiji,Hiroko Ida-Yonemochi,Mariko Ohkura,Ryosuke Takeuchi,Nagako Yoshiba,Kunihiko Yoshiba,Naoki Edanami,Yuichiro Noiri,Aiko Tohma

doi:10.1038/s41598-017-07167-y

Abstract

Mineral trioxide aggregate (MTA) is a commonly used dental pulp-capping material with known effects in promoting reparative dentinogenesis. However, the mechanism by which MTA induces dentine repair remains unclear. The aim of the present study was to investigate the role of prostaglandin E2 (PGE2) in dentine repair by examining the localisation and mRNA expression levels of its transporter (Pgt) and two of its receptors (Ep2 and Ep4) in a rat model of pulpotomy with MTA capping. Ep2 expression was detected in odontoblasts, endothelial cells, and nerve fibres in normal and pulpotomised tissues, whereas Pgt and Ep4 were immunolocalised only in the odontoblasts. Moreover, mRNA expression of Slco2a1 (encoding Pgt), Ptger2 (encoding Ep2), and Ptger4 (encoding Ep4) was significantly upregulated in pulpotomised dental pulp and trigeminal ganglia after MTA capping. Our results provide insights into the functions of PGE2 via Pgt and Ep receptors in the healing dentine/pulp complex and may be helpful in developing new therapeutic targets for dental disease.

Highlights

The dentine-pulp complex possesses high repair capacity and forms reparative dentine in response to various injuries
Our findings indicate that the Mineral trioxide aggregate (MTA)-induced pulpal wound healing process is basically similar to that described in a previous report[8]; that is, the primary process of reparative dentinogenesis after MTA capping involved mild inflammatory and necrotic changes at the exposed site (Fig. 3c,d, Fig. 4c,d), followed by calcified bridge formation, which was first observed in all specimens at 7 days after treatment (Figs 3g,h and 4g,h)
Because damaged pulp tissue initiated the pulpal healing process of calcified bridge formation by 7 days, we were required to observe the progress of reparative dentinogenesis beneath the MTA-capped area until 7 days to analyse the mechanism of primary inflammation and repair

Summary

Introduction

The dentine-pulp complex possesses high repair capacity and forms reparative dentine in response to various injuries. A recent in vitro study demonstrated that PGE2 stimulates Ep2 to mediate cAMP levels in dental pulp cells and that Ep1 and Ep3 are not involved in this process[27]. Both Ep2 and Ep4 stimulate angiogenesis and bone formation, only Ep2 promotes cAMP-dependent neuroprotection in neurons[28]. Ep2 and Ep4 receptors, which bind to PGE2 transported by Pgt, may play an important role in pulpal inflammation and repair. This study aimed to demonstrate the modes of expression of Pgt, Ep2, and Ep4 during reparative dentinogenesis after MTA capping, and to evaluate their functional significance (angiogenesis and neuroprotection) with gene expression assays

Objectives

Results

Conclusion