Cytotoxicity of nickel-chromium alloys: bulk alloys compared to multiple ion salt solutions

Objective. Nickel-based alloys have been in use since the 1930s; however, there are concerns regarding the biocompatibility of the metallic ions released from these alloys to surrounding tissues. The objective of this study was to better understand nickel-based alloy cytotoxicity as well as determine if multiple ion salt solutions can be used to model the cytotoxic effects of bulk implant alloys. Methods. This study evaluated cellular morphology, viability, membrane integrity, and alterations in metabolic activity, including DNA synthesis, RNA synthesis, protein synthesis, oxygen consumption, intracellular ATP levels, and glucose-6-phosphate dehydrogenase in response to bulk alloys and multiple ion salt solutions. Results. Over a 24- or 72-h exposure time, the nickel-based alloys released a total ion concentration in the parts per billion range and caused alterations in DNA, RNA, and protein synthesis, intracellular ATP levels, and glucose-6-phosphate dehydrogenase activity. Interestingly, cellular responses to the salt solutions representing the ions released from the alloys were not consistently significantly similar to those elicited from the alloys. Significance. From these studies, it was shown that a number of cellular functions are altered in response to ions released from these implant alloys. However, cellular functions were not similarly altered in response to salt solutions representing the ions released from the alloys. These results demonstrated salt solutions cannot be easily used to represent alloy cytotoxicity, and ionic release from alloys is a complex process dependent on variables including ion chemistry, ion valence, and dose-time dependence. This study provides a better understanding of the metabolic response of fibroblasts to ions released from dental alloys; and is a good first step towards developing a more reliable cell culture model of cytotoxicity. (C) 2000 Academy of Dental Materials. Published by Elsevier Science Ltd. All rights reserved.