Resin monomers induce apoptosis of the pulp-dentin complex through the mitochondrial pathway.

Abstract

Numerous studies have confirmed that the apoptosis induced by the methacrylate resin monomers triethyleneglycol-dimethacrylate (TEGDMA), 2-hydroxy ethyl methacrylate (HEMA), etc., in pulp cells and odontoblast-like cells is caused mainly by oxidative stress (OS). Reactive oxygen species (ROS), recognized as the most important risk factor for apoptosis in cells of the pulp-dentin complex, are produced mainly via the mitochondrial respiratory chain. When the free resin monomers in the oral cavity and pulp reach a toxic level, the monomers induce oxidative DNA damage, activate ATM-p53 in the nucleus, and mediate the intrinsic apoptotic pathway in the presence of Bcl-2 family proteins. A vicious cycle is established between OS cellular responses and abnormalities in mitochondrial dynamics that accelerate apoptosis. Despite numerous products generated via iteration, complete polymerization of resin monomers is not currently possible. The cytotoxicity of free monomers may lead to adverse reactions, such as pulp sensitivity. This review is based on the most important papers describing the roles of resin monomers in mediating apoptosis in the pulp-dentin complex and provides an overview of the precise mechanisms related to mitochondrion-mediated cytotoxicity, suggesting ways to reduce or eliminate their cytotoxicity in the future through advancements in material technology.