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Nickel release from orthodontic arch wires and cellular immune response to various nickel concentrations

✍ Scribed by Jia, Wenyi ;Beatty, Mark W. ;Reinhardt, Richard A. ;Petro, Thomas M. ;Cohen, Donald M. ;Maze, Constance R. ;Strom, E. A. ;Hoffman, Melvin


Book ID
101258185
Publisher
John Wiley and Sons
Year
1999
Tongue
English
Weight
156 KB
Volume
48
Category
Article
ISSN
0021-9304

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✦ Synopsis


Aims: Results from two previous clinical studies suggested that exposure to high nickel-containing orthodontic arch wires may induce hypersensitivity in certain individuals. The purpose of this study was to measure the amount of nickel released from three types of nickel-containing arch wires into a synthetic saliva in vitro, and determine if the concentrations were sufficient to elicit either cytotoxic (trypan blue exclusion test) or stimulatory (MTT test) responses in human peripheral blood mononuclear cells (PBMCs) derived from nickelsensitive and nickel-nonsensitive individuals. PBMCs were exposed to five concentrations of nickel sulfate solutions ranging from 0 -29 ppm, and results were compared, particularly at concentrations obtained from nickel release experiments. Findings: The amount of nickel released into synthetic saliva ranged from 0.4 -4.1 ppb. Wires subjected to a combination of soaking and cyclic straining released significantly more nickel than those that were soaked only (p < 0.05), and NiTi wires released significantly more nickel than did stainless steel or nitrogen-implanted NiTi wires (p < 0.05).

For PBMCs, significant increased cell proliferation was not observed for any nickel concentration. PBMC cell death rates were highest at nickel concentrations of 29 ppm when the cells were cultured without a cell growth promoter (p < 0.05), and MTT test values were significantly reduced at both 2.9 and 29 ppm when a growth promoter was included (p < 0.05). Conclusion: The maximum amount of nickel released from all tested arch wires was 700 times lower than the concentrations necessary to elicit cytotoxic reactions in human PBMCs.