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

20Citations
Citations of this article
32Readers
Mendeley users who have this article in their library.

This article is free to access.

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.

Cite

CITATION STYLE

APA

Kwon, J. H., Park, H. C., Zhu, T., & Yang, H. C. (2015). Inhibition of odontogenic differentiation of human dental pulp cells by dental resin monomers. Biomaterials Research, 19(1). https://doi.org/10.1186/s40824-015-0030-6

Register to see more suggestions

Mendeley helps you to discover research relevant for your work.

Already have an account?

Save time finding and organizing research with Mendeley

Sign up for free