Cell death effects of resin-based dental material compounds and mercurials in human gingival fibroblasts.

In order to test the hypothesis that released dental restorative materials can reach toxic levels in human oral tissues, the cytotoxicities of the resin-based dental (co)monomers hydroxyethylmethacrylate (HEMA), triethyleneglycoldimethacrylate (TEGDMA), urethanedimethacrylate (UDMA), and bisglycidylmethacrylate (BisGMA) compared with methyl mercury chloride (MeHgCl) and the amalgam component mercuric chloride (HgCl2) were investigated on human gingival fibroblasts (HGF) using two different test systems: (1) the modified XTT-test and (2) the modified H 33342 staining assay. The HGF were exposed to various concentrations of the test-substances in all test systems for 24 h. All tested (co)monomers and mercury compounds significantly (P<0.05) decreased the formazan formation in the XTT-test. EC50 values in the XTT assay were obtained as half-maximum-effect concentrations from fitted curves. Following EC50 values were found (mean [mmol/l]; s.e.m. in parentheses; n=12; * significantly different to HEMA): HEMA 11.530 (0.600); TEGDMA* 3.460 (0.200); UDMA* 0.106 (0.005); BisGMA* 0.087 (0.001); HgCl2* 0.013 (0.001); MeHgCl* 0.005 (0.001). Following relative toxicities were found: HEMA 1; TEGDMA 3; UDMA 109; BisGMA 133; HgCl2 887; MeHgCl 2306. A significant (P<0.05) increase of the toxicity of (co)monomers and mercurials was found in the XTT-test in the following order: HEMA < TEGDMA < UDMA < BisGMA < HgCl2 < MeHgCl. TEGDMA and MeHgCl induced mainly apoptotic cell death. HEMA, UDMA, BisGMA, and HgCl2 induced mainly necrotic cell death. The results of this study indicate that resin composite components have a lower toxicity than mercury from amalgam in HGF. HEMA, BisGMA, UDMA, and HgCl2 induced mainly necrosis, but it is rather unlikely that eluted substances (solely) can reach concentrations, which might induce necrotic cell death in the human physiological situation, indicating that other (additional) factors may be involved in the induction of tissue (pulp) inflammation effects after dental restauration.