Materials Science Unit, Division of Oral Bioscience, Dublin Dental University Hospital, Trinity College Dublin, Lincoln Place, Ireland.
Dent Mater. 2011 Dec;27(12):1295-306. doi: 10.1016/j.dental.2011.09.013. Epub 2011 Oct 11.
To develop an enhanced, reproducible and discriminatory biocompatibility testing model for non-precious dental casting alloys, prepared to a clinically relevant surface finishing condition, using TR146 oral keratinocyte cells.
Comparative biocompatibility was determined following direct and indirect exposure of TR146 cells to two nickel-chromium (Ni-Cr) and a cobalt-chromium (Co-Cr) alloy-discs. The surface roughness of the discs was determined using a contact stylus profilometer and the elemental ion release by inductively coupled plasma mass spectrometry (ICP-MS). Subsequent biocompatibility analysis included cell morphology, cell density measurements with Trypan blue exclusion assay, inflammatory cytokine expression with ELISAs, cellular metabolic activity using XTT and cellular toxicity using lactate dehydrogenase (LDH) release assay.
TR146 cell morphology was altered following direct and indirect exposure to the Ni-Cr alloys but not the Co-Cr alloy. Significant reductions (all P<0.001) in viable cell density measurements, cellular metabolic activity, significant increases inflammatory cytokine expression and cellular toxicity were observed when TR146 cells were exposed to the Ni-Cr alloys. Significant decreases in cell density measurements, cellular metabolic activity, significant increases inflammatory cytokine expression and cellular toxicity for the Ni-Cr d.Sign(®)15 alloy compared with d.Sign(®)10 alloy were identifiable (all P<0.001). Cellular toxicity was attributed to nickel ion release levels in solution detected by ICP-MS analysis.
Nickel ions from the Ni-Cr alloys permeated the epithelial cells and activated a proinflammatory response, namely IL-1a, IL-8 and PGE2 expression. Further evidence of nickel ioninduced cell death was supported by the decreased biocompatibility of the highest nickel ion releasing alloy (d.Sign(®)15 compared with d.Sign(®)10) and the increased biocompatibility of the Co-Cr (d.Sign(®)30) alloy where nickel ions were absent.
开发一种增强的、可重复的和有区别的非贵金属牙科铸造合金生物相容性测试模型，使用 TR146 口腔角质细胞，制备到临床相关的表面抛光条件。
通过 TR146 细胞直接和间接暴露于两种镍铬（Ni-Cr）和钴铬（Co-Cr）合金盘，确定比较生物相容性。使用接触式轮廓仪测定圆盘的表面粗糙度，通过电感耦合等离子体质谱（ICP-MS）测定元素离子释放。随后的生物相容性分析包括细胞形态、台盼蓝排除试验测量细胞密度、酶联免疫吸附试验（ELISA）测定炎症细胞因子表达、XTT 测定细胞代谢活性和乳酸脱氢酶（LDH）释放试验测定细胞毒性。
TR146 细胞形态在直接和间接暴露于 Ni-Cr 合金后发生改变，但在暴露于 Co-Cr 合金后没有发生改变。当 TR146 细胞暴露于 Ni-Cr 合金时，观察到活细胞密度测量值、细胞代谢活性显著降低（均 P<0.001），炎症细胞因子表达显著增加，细胞毒性增加。与 d.Sign(®)10 合金相比，Ni-Cr d.Sign(®)15 合金的细胞密度测量值、细胞代谢活性、炎症细胞因子表达和细胞毒性均显著降低（均 P<0.001）。细胞毒性归因于 ICP-MS 分析检测到的溶液中镍离子的释放水平。
Ni-Cr 合金中的镍离子渗透到上皮细胞中，激活了炎症反应，即 IL-1a、IL-8 和 PGE2 的表达。镍离子诱导细胞死亡的进一步证据得到支持，最高镍离子释放合金（d.Sign(®)15 与 d.Sign(®)10 相比）的生物相容性降低，以及不存在镍离子的 Co-Cr（d.Sign(®)30）合金的生物相容性增加。
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