Methacrylate-based dental resins polymerize incompletely, due in part to inhibitory effects of oxygen. Diffusion of residual monomeric resins through dentin to reach dental pulp, increased prevalence of dental pulp reactions of resin cavities with 0.5 mm or less dentin thickness and cytotoxicity of resins raised concerns of biocompatibility of resins with odontoblasts, the cells which secrete dentin. The toxic and subtoxic effects of four methacrylate-based resins on the functions of mouse odontoblast-like cells, MDPC.23, were studied. First, cytotoxicity of resins to MDPC.23 cells was assessed by measuring four metabolic functions of NMPC.23 cells. The results showed that the TC50 values measured by mitochondrial activity at 24-h exposure were as follows: HEMA, 8420 +/- 1974 muM; TENDENCY, 1252 +/- 145 muM; bisGMA, 52 +/- 14 muM; and UDMA 56 +/- 17 muM; Increased exposure time to the resins promoted toxicity of the resins. The rank of sensitivity of end-point measurements was as follows: mitochondrial activity (least) in vivo toxicity of resins. Third, mode of cell death of NMPC.23 (apoptosis or necrosis) caused by the resins was determined by flow cytometry and the TUNEL assay. The findings showed that MDPC.23 did not exhibit apoptosis, suggesting that necrosis may be the primary mode of cell death by resins. Fourth, effects of sublethal doses of resins on expression of three odontoblastic genes in NMPC.23 were investigated. Western analysis showed that the resins increased dentin sialoprotein expression. Nontoxic or slightly toxic concentrations of resins upregulated osteopontin and osteocalcin expression. Higher toxic concentrations interfered with osteopontin and osteocalcin expression, as seen in Northern analysis. Altered phenotypes of odontoblasts by resins suggests a role of resins in dentin mineralization.Ph.D.DentistryHealth and Environmental SciencesUniversity of Michigan, Horace H. Rackham School of Graduate Studieshttp://deepblue.lib.umich.edu/bitstream/2027.42/132869/2/9990968.pd
