| Dokumentenart: | Artikel | ||||
|---|---|---|---|---|---|
| Titel eines Journals oder einer Zeitschrift: | Journal of Dental Research | ||||
| Verlag: | SAGE PUBLICATIONS INC | ||||
| Ort der Veröffentlichung: | THOUSAND OAKS | ||||
| Band: | 85 | ||||
| Nummer des Zeitschriftenheftes oder des Kapitels: | 10 | ||||
| Seitenbereich: | S. 870-877 | ||||
| Datum: | 2006 | ||||
| Institutionen: | Medizin > Lehrstuhl für Zahnerhaltung und Parodontologie > Prof. Dr. rer. nat. Helmut Schweikl | ||||
| Identifikationsnummer: |
| ||||
| Stichwörter / Keywords: | NF-KAPPA-B; HUMAN GINGIVAL FIBROBLASTS; OXIDATIVE DNA-DAMAGE; TRIETHYLENE GLYCOL DIMETHACRYLATE; ELECTROPHORESIS COMET ASSAY; IN-VITRO CYTOTOXICITY; ACETYL-L-CYSTEINE; FILLING MATERIALS; PULP CELLS; GLUTATHIONE CONCENTRATION; dental materials; oxidative stress; genotoxicity; cell cycle; apoptosis | ||||
| Dewey-Dezimal-Klassifikation: | 600 Technik, Medizin, angewandte Wissenschaften > 610 Medizin | ||||
| Status: | Veröffentlicht | ||||
| Begutachtet: | Ja, diese Version wurde begutachtet | ||||
| An der Universität Regensburg entstanden: | Ja | ||||
| Dokumenten-ID: | 69772 |
Web of ScienceZusammenfassung
Monomers are released from dental resin materials, and thus cause adverse biological effects in mammalian cells. Cytotoxicity and genotoxicity of some of these methacrylates have been identified in a vast number of investigations during the last decade. It has been well-established that the comonomer triethylene glycol dimethacrylate (TEGDMA) causes gene mutations in vitro. The formation of ...
Zusammenfassung
Monomers are released from dental resin materials, and thus cause adverse biological effects in mammalian cells. Cytotoxicity and genotoxicity of some of these methacrylates have been identified in a vast number of investigations during the last decade. It has been well-established that the comonomer triethylene glycol dimethacrylate (TEGDMA) causes gene mutations in vitro. The formation of micronuclei is indicative of chromosomal damage and the induction of DNA strand breaks detected with monomers like TEGDMA and 2-hydroxyethyl methacrylate (HEMA). As a consequence of DNA damage, the mammalian cell cycle was delayed in both G1 and G2/M phases, depending on the concentrations of the monomers. Yet, the mechanisms underlying the genetic and cellular toxicology of resin monomers have remained obscure until recently. New findings indicate that increased oxidative stress results in an impairment of the cellular pro-and anti-oxidant redox balance caused by monomers. It has been demonstrated that monomers reduced the levels of the natural radical scavenger glutathione (GSH), which protects cell structures from damage caused by reactive oxygen species (ROS). Depletion of the intracellular GSH pool may then significantly contribute to cytotoxicity, because a related increase in ROS levels can activate pathways leading to apoptosis. Complementary, cytotoxic, and genotoxic effects of TEGDMA and HEMA are inhibited in the presence of ROS scavengers like N-acetylcysteine (NAC), ascorbate, and Trolox (vitamin E). Elevated intracellular levels of ROS can also activate a complex network of redox-responsive macromolecules, including redox-sensitive transcription factors like nuclear factor kappaB (NF-kappa B). It has been shown that NF-kappa B is activated probably to counteract HEMA-induced apoptosis. The induction of apoptosis by TEGDMA in human pulp cells has been associated with an inhibition of the phosphatidylinositol 3-kinase (PI3-K) cell-survival signaling pathway. Although the details of the mechanisms leading to cell death, genotoxicity, and cell-cycle delay are not completely understood, resin monomers may be able to alter the functions of the cells of the oral cavity. Pathways regulating cellular homeostasis, dentinogenesis, or tissue repair may be modified by monomers at concentrations well below those which cause acute cytotoxicity.
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