Cytotoxicity of the dental composite component TEGDMA and selected metabolic by-products in human pulmonary cells.

Abstract Objectives The comonomer triethyleneglycoldimethacrylate (TEGDMA) is a commonly used constituent of resin-based dental materials. Upon placement, light-cured dental polymers may release a wide spectrum of residual compounds due to incomplete monomer-conversion during polymerization. Apart from liberating unreacted monomers, additional compound release might occur due to mechanical wear and enzymatic degradation on the salivary surface of resin fillings. Following delivery into the local bio phase, leached compounds may encounter a variety of different enzymes, which might be present in their oral or systemic environment. Metabolic by-products formerly associated with TEGDMA-degradation include triethylene glycol (TEG), methacrylic acid (MA), 2,3-epoxymethacrylic acid (2,3-EMA), and formaldehyde. Methods Cytotoxicitiy of TEGDMA-derived intermediates was measured as mitochondrial dehydrogenase activity assessed by colorimetric measurement of formazan formation as a cleavage-product from the tetrazolium salt XTT by metabolically active A549 cells. EC 50 -values were calculated by using curve fitting software (GraphPad Prism). Results The following EC 50 -values (mmol/L) (95% confidence interval) were obtained: 2,3-EMA 1.65 (1.28–2.13), TEGDMA 1.83 (1.46–2.30), MA 4.91 (4.22–5.71), and paraformaldehyde (PFA) 5.48 (4.56–6.58). For TEG no cytotoxic effects up to a concentration of 10 mM could be found. Significance The epoxy compound 2,3-EMA induced comparable toxic effects as the raw comonomer TEGDMA. It is therefore concluded that the formation of toxic intermediates might significantly contribute to TEGDMA-induced cytotoxicity in human pulmonary cells.