IADR Abstract Archives
Toxic Effects of TEGDMA and HEMA on Dental Pulp Cells
Objectives: TEGDMA (triethylene glycol dimethacrylate) and HEMA (2-hydroxyethyl methacrylate), two common components of dentin bonding agent, may potentially affect the viability and biological activities of the dental pulp. However, the underlying mechanisms remain largely unknown. This study aimed to investigate the influences of TEGDMA and HEMA on the expression of matrix (type I collagen), cell cycle-related molecules (cdc2, p21), Nrf2 and heme oxygenase-1 (HO-1), inflammatory molecules (cyclooxygenase-2 [COX-2] and related drug-metabolizing proteins’ expression (NQO-1, superoxide dismutase-1 [SOD-1]).
Methods: Primary human dental pulp cells were treated with different concentrations of TEGDMA (0-5 mM), and HEMA (0-10 mM) for 24 hours. Cell viability was measured by3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Changes in cellular mRNA expression were determined by reverse-transcription polymerase chain reaction (RT-PCR). Changes in protein production of pulp cells were evaluated by western blot.
Results: TEGDMA and HEMA may induce cytotoxic effect by impairing cell viability on human dental pulp cells at higher concentrations. The expressions of collagen type I, and cdc2 in dental pulp cells were down-regulated after exposure to TEGDMA and HEMA for 24 hours. The expressions of p21, NQO-1, Nrf2, HO-1, and COX-2 showed up-regulation, whereas SOD-1 showed no marked change by both monomers.
Conclusions: This study provides an insight into the mechanism of TEGDMA- and HEMA-induced toxicity toward human dental pulp cells. Impairment of matrix turnover and cell cycle, as well as induction of Nrf2, HO-1, NQO-1, and COX-2 inflammatory response by TEGDMA and HEMA, may contribute to the response of dental pulp to dentin bonding agents and composite resin materials after clinical operative procedures.
Methods: Primary human dental pulp cells were treated with different concentrations of TEGDMA (0-5 mM), and HEMA (0-10 mM) for 24 hours. Cell viability was measured by3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Changes in cellular mRNA expression were determined by reverse-transcription polymerase chain reaction (RT-PCR). Changes in protein production of pulp cells were evaluated by western blot.
Results: TEGDMA and HEMA may induce cytotoxic effect by impairing cell viability on human dental pulp cells at higher concentrations. The expressions of collagen type I, and cdc2 in dental pulp cells were down-regulated after exposure to TEGDMA and HEMA for 24 hours. The expressions of p21, NQO-1, Nrf2, HO-1, and COX-2 showed up-regulation, whereas SOD-1 showed no marked change by both monomers.
Conclusions: This study provides an insight into the mechanism of TEGDMA- and HEMA-induced toxicity toward human dental pulp cells. Impairment of matrix turnover and cell cycle, as well as induction of Nrf2, HO-1, NQO-1, and COX-2 inflammatory response by TEGDMA and HEMA, may contribute to the response of dental pulp to dentin bonding agents and composite resin materials after clinical operative procedures.