Toxic Mechanism of Urethane Dimethacrylate on Human Dental Pulp Cells

Method: Dental pulp cells were treated with different concentrations of UDMA for 24 hours with/without pretreatment and co-incubation by N-acetylcysteine (NAC, an antioxidant), catalase (a H₂O₂ degradation enzyme), porcine esterase, Zn- protoporphyrin (a HO-1 inhibitor) or loperamide (a CES-2 inhibitor). Cytotoxicity was evaluated by MTT assay and cell cycle progression was analyzed by propidium iodide flow cytometry. Cellular mRNA (cdc2, cyclin B1, cdc25C, HO-1, cyclooxygenase-2 [Cox-2]) expression was evaluated by reverse transcription polymerase chain reaction (RT-PCR).

Result: UDMA induced morphological changes of pulp cells and decreased cell viability by 30-60% at concentrations of 0.1-0.35 mM. UDMA induced G0/G1, G₂/M cell cycle arrest and apoptosis. The expression of cdc2, cyclinB1, and cdc25C was inhibited by UDMA. Moreover, UDMA stimulated COX-2 and HO-1 mRNA expression of pulp cells. The cytotoxicity of UDMA was attenuated by NAC, catalase and esterase, but enhanced by loperamide and Zn-protoporphyrin.

Conclusion: Exposure of UDMA may potentially induce the inflammation and toxicity of the dental pulp. Toxicity of UDMA is related to decrease of cdc2, cyclinB1 and cdc25C expression as well as the induction of cell cycle arrest and apoptosis. ROS production, HO-1 and CES enzyme activity may affect the UDMA cytotoxicity. This event is important for the clinical response of dental pulp to resin monomers after operative restoration.