Conclusions
HEMA inhibits the migration of dental pulp cells in vitro, suggesting that poor pulpal wound healing under resin-based dental materials may be caused, in part, by the inhibition of cell migration by HEMA.
Methods
Cell viability was assessed using the MTT (3-(4, 5-dimethylthiazolyl-2)-2, 5-diphenyltetrazolium bromide) assay, and cell migration was evaluated using the wound scratch assay and transwell migration assay at noncytotoxic doses. The Western blot was used to examine pathways associated with migration such as focal adhesion kinase, mitogen-activated protein kinase, and glycogen synthase kinase 3.
Results
There were no drastic changes in the cell viability below 3 mmol/L HEMA. When DPSCs were treated with HEMA at 0.5, 1.0, and 2.5 mmol/L, cell migration was diminished. HEMA-treated DPSCs exhibited the loss of phosphorylated focal adhesion kinase in a dose-dependent manner. The HEMA-mediated inhibition of cell migration was associated with phosphorylation of p38 but not glycogen synthase kinase 3, Extracellular signal-related kinase (ERK), or c-Jun N-terminal kinase (JNK) pathways. When we inhibited the p38 signaling pathway using a p38 inhibitor, the migration of DPSCs was suppressed. Conclusions: HEMA inhibits the migration of dental pulp cells in vitro, suggesting that poor pulpal wound healing under resin-based dental materials may be caused, in part, by the inhibition of cell migration by HEMA.