Keynote Address: Dental Acrylates Inhibit Biomineralization

Biomineralization is one of the key characteristics of dental pulp leading to the generation of tertiary dentin to compensate for dentin loss; e.g. due to caries or trauma. Early approaches to induce tertiary dentin formation included the application of calcium hydroxide on healthy exposed pulps. Recently, the use of dentin adhesives for direct pulp capping has been advocated. However, in vitro experiments show that exposure of pulp cells to acrylate monomers like TEGDMA lead to a down-regulation of biomineralization markers. Odontogenic differentiation and mineralization processes in pulp-derived (stem) cells were shown to be down-regulated. Furthermore, TEGDMA or HEMA induced a depletion of the non-enzymatic antioxidant glutathione (GSH) and a consecutive increase of ROS formation in pulp cells and in macrophages. The consequence was oxidative DNA damage, upregulation of energy-consuming cellular repair mechanisms and potentially apoptosis. The application of N-acetyl-cysteine, a GSH precursor, however, can reduce ROS formation and monomer-induced apoptosis and compensate for the down-regulation of biomineralization markers. Together with recent animal studies, this data suggests that dental acrylates inhibit tertiary dentin formation.