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Inhibition of odontogenic differentiation of human dental pulp cells by dental resin monomers

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Authors
Kwon, Ji Hyun; Park, Hee Chul; Zhu, Tingting; Yang, Hyeong-Cheol
Issue Date
2015-04-10
Publisher
BioMed Central
Citation
Biomaterials Research, 19(1):8
Keywords
TEGDMAHEMAHydrogen peroxideHuman dental pulp cellDifferentiationDental resin monomerOdontogenicMAP kinase
Description
This is an Open Access article distributed under the terms of the Creative
Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and
reproduction in any medium, provided the original work is properly credited.
Abstract
Abstract

Background
Dental resin monomers that are leached from the resin matrix due to incomplete polymerization can affect the viability and various functions of oral tissues and cells. In this study, the effects of triethylene glycol dimethacrylate (TEGDMA) and 2-hydroxyethyl methacrylate (HEMA) on odontogenic differentiation of human dental pulp cells (HDPCs) were examined. To mimic clinical situations, dental pulp cells were treated with resin monomers for 24 h prior to the analysis of alkaline phosphatase (ALP) activity and mRNA expression of genes related to pulp cell differentiation. To elucidate the underlying signaling pathways, regulation of mitogen-activated protein (MAP) kinases by resin monomers was also investigated.


Results
The ALP activity of HDPCs was reduced by TEGDMA and HEMA at noncytotoxic concentrations. The mRNA expression of dentin sialophosphoprotein (DSPP), osteocalcin (OCN), and osteopontin (OPN) was also downregulated by resin monomers. However, DSPP expression was not affected by hydrogen peroxide (H2O2). Among the MAP kinases examined, ERK activation (ERK phosphorylation) was not affected by either resin monomers or H2O2, whereas JNK was phosphorylated by TEGDMA and HEMA. Phospho-p38 was upregulated by HEMA, while TEGDMA and H2O2 suppressed p38 phosphorylation.


Conclusions
Exposure to TEGDMA and HEMA for a limited period suppresses differentiation of HDPCs via different signaling pathways.
Language
English
URI
http://hdl.handle.net/10371/100667
DOI
https://doi.org/10.1186/s40824-015-0030-6
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College of Dentistry/School of Dentistry (치과대학/치의학대학원)Dept. of Dentistry (치의학과)Journal Papers (저널논문_치의학과)
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