Galler, K. M. and Schweikl, H. and Hiller, K. -A. and Cavender, A. C. and Bolay, C. and D'Souza, R. N. and Schmalz, G. (2011) TEGDMA Reduces Mineralization in Dental Pulp Cells. JOURNAL OF DENTAL RESEARCH, 90 (2). pp. 257-262. ISSN 0022-0345, 1544-0591
Full text not available from this repository. (Request a copy)Abstract
Direct application of dentin bonding agents onto the exposed pulp has been advocated, but in vivo studies indicate a lack of reparative dentin formation. Our objective was to investigate the role of triethylene glycol dimethacrylate (TEGDMA), a commonly used compound in dentin bonding agents, as a potential inhibitor of mineralization. Human pulp cells were exposed to different concentrations of TEGDMA, and expression of the mineralization-related genes collagen I, alkaline phosphatase, bone sialoprotein, osteocalcin, Runx2, and dentin sialophosphoprotein was analyzed. Gene expression studies by real-time polymerase chain-reaction revealed a concentration-and time-dependent decrease of mineralization markers. A subtoxic TEGDMA concentration (0.3 mM) reduced expression levels by 5 to 20% after 4 hrs and by 50% after 12 hrs. Furthermore, alkaline phosphatase activity and calcium deposition were significantly lower in dental pulp cells treated with TEGDMA over 14 days. These findings indicate that even low TEGDMA concentrations might inhibit mineralization induced by dental pulp cells, thus impairing reparative dentin formation after pulp capping with dentin bonding agents.
| Item Type: | Article |
|---|---|
| Uncontrolled Keywords: | OSTEOBLASTIC DIFFERENTIATION; IN-VITRO; INDUCED APOPTOSIS; BONDING SYSTEM; BONE-CELLS; RESIN; CYSTEINE; TEETH; HEMA; VIVO; triethylene glycol dimethacrylate (TEGDMA); dental pulp cells; mineralization |
| Subjects: | 600 Technology > 610 Medical sciences Medicine |
| Divisions: | Medicine > Lehrstuhl für Zahnerhaltung und Parodontologie |
| Depositing User: | Dr. Gernot Deinzer |
| Date Deposited: | 26 Jun 2020 11:19 |
| Last Modified: | 26 Jun 2020 11:19 |
| URI: | https://pred.uni-regensburg.de/id/eprint/21362 |
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