ArticleJournal of dental sciences2025
Triethylene-glycol-dimethacrylate induces caspase-mediated apoptotic cell death in cementoblasts by the regulation of JNK and p38 pathways-an in vitro study.
Article in Journal of dental sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background/Purpose: Triethylene-glycol-dimethacrylate (TEGDMA) is one of the monomers used in composite resin matrix. Residual TEGDMA can be eluted from bulk fill composite resins and the amounts also increased with time. Composite resin used as root-end filling materials may invoke the critical biologic reactions in surrounding tissues. However, little is known about the effects of TEGDMA on cementoblasts. The aim of this study was to investigate the possible detrimental effects of murine cementoblast (OCCM.30) by TEGDMA in vitro. Materials and methods: OCCM.30 cells were exposed to TEGDMA (0, 1, 2, 4 mM) for 24 h. Cell viability was determined by microculture tetrazolium assay. Flow cytometry was conducted to evaluate the cell cycle distribution and the type of cell death. Caspase-mediated apoptotic cascade and mitogen-activated protein kinase (MAPK) pathways were analyzed by Western blot. Results: The concentrations of TEGDMA≧1 mM were found to significantly inhibit OCCM.30 cell viability in a dose-dependent manner ( Conclusion: Taken together, our results demonstrated that TEDGMA decreased cell viability and induced the apoptotic cell death in cementoblast. In addition, caspase-mediated cell apoptosis was found to be associated with JNK and p38 signal transduction pathways.
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