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

  • Kwon, Ji Hyun (Department of Dental Biomaterials Science and Dental Research Institute, School of Dentistry, Seoul National University) ;
  • Park, Hee Chul (Department of Dental Biomaterials Science and Dental Research Institute, School of Dentistry, Seoul National University) ;
  • Zhu, Tingting (Department of Dental Biomaterials Science and Dental Research Institute, School of Dentistry, Seoul National University) ;
  • Yang, Hyeong-Cheol (Department of Dental Biomaterials Science and Dental Research Institute, School of Dentistry, Seoul National University)
  • Received : 2015.02.02
  • Accepted : 2015.03.26
  • Published : 2015.06.30

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 ($H_2O_2$). Among the MAP kinases examined, ERK activation (ERK phosphorylation) was not affected by either resin monomers or $H_2O_2$, whereas JNK was phosphorylated by TEGDMA and HEMA. Phospho-p38 was upregulated by HEMA, while TEGDMA and $H_2O_2$ suppressed p38 phosphorylation. Conclusions: Exposure to TEGDMA and HEMA for a limited period suppresses differentiation of HDPCs via different signaling pathways.

Keywords

Acknowledgement

Supported by : Ministry of Health & Welfare

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