Pro-inflammatory cytokine release and cell growth inhibition in primary human oral cells after exposure to endodontic sealer

被引:59
作者
Diomede, F. [1 ]
Caputi, S. [1 ]
Merciaro, I. [1 ]
Frisone, S. [1 ]
D'Arcangelo, C. [1 ]
Piattelli, A. [1 ]
Trubiani, O. [1 ]
机构
[1] Univ G DAnnunzio, Dept Med Oral & Biotechnol Sci, I-66100 Chieti, Italy
关键词
cytokines; endodontic sealer; human oral cells; inflammation; HUMAN GINGIVAL FIBROBLASTS; ROOT-CANAL SEALERS; IN-VITRO; RESIN; CYTOTOXICITY; TOXICITY; TISSUE; VIVO;
D O I
10.1111/iej.12230
中图分类号
R78 [口腔科学];
学科分类号
100302 [口腔临床医学];
摘要
Aim To assay the toxicity of the single-methacrylate-based sealer urethane dimethacrylate (UDMA) (EndoRez) in terms of cell growth and pro-inflammatory cytokines release, in expanded ex vivo human dental pulp stem cells (hDPSCs), human periodontal ligament stem cells (hPDLSCs), human gingival fibroblasts (hGFs) and human osteoblasts (hOSTs). Methodology Dental pulp and periodontal ligament stem cells, osteoblasts and fibroblasts were derived from five young donors. After in vitro isolation, hDPSCs, hPDLSCs, hGFs and hOSTs were seeded to resin-based sealers for 24, 48, 72 h up to 1 week. The morphological features and the cell growth and the release of pro-inflammatory interleukin (IL) 6, IL8, IL12 and tumour necrosis factor (TNF) alpha were analysed. Differences in cell growth and in interleukin secretion were analysed for statistical significance with two-way ANOVA tests for multiple comparisons. Results Exposure to endodontic sealer based on UDMA resulted in a 50% decrease in survival oral cells at 24 h of incubation. No evident morphological changes were present in cell cultures examined. After 48 h, 72 h and 1-week culture time, a progressive cell growth was evident. A significant up-regulation of IL6, IL8, IL12 and TNF alpha cytokines in cells in contact with the dental sealer compared to the control was observed. Conclusion In vitro, EndoRez interacted with primary human hDPSCs, hPDLSCs, hGFs and hOSTs causing damage to biological system evidenced through cell growth inhibition and up-regulation of IL6, IL8, IL12 and TNF alpha proinflammatory mediators.
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收藏
页码:864 / 872
页数:9
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