Ability of Ni-containing biomedical alloys to activate monocytes and endothelial cells in vitro

Nickel-containing alloys commonly are used in medical and dental applicatio ns that place them into longterm contact with soft: tissues. The release of Ni ions from these alloys is disturbing because of the toxic, immunologic, and carcinogenic effects that have been documented for some Ni compounds. In particular, Ni ions in solution recently have been shown to cause expres sion of inflammatory mediators, such as interleukin-1 beta (IL-1 beta), tum or necrosis factor-alpha (TNF-alpha), and intercellular adhesion molecules (ICAMs) from keratinocytes, monocytes, and endothelial cells. However, the ability of the solid alloys themselves to induce these inflammatory effects has not been demonstrated. An in vitro system was used to determine if Ni- containing biomedical alloys could cause secretion of either IL-1 beta or T NF-alpha from monocytes or expression of ICAMs on endothelial cells. Pure n ickel, titanium, and three biomedical alloys-18-8 stainless steel, NiTi, an d Rexillium III-were evaluated. First, it was determined whether or not the alloys or pure metals could cause cytotoxicity to THP-1 human monocytes or human microvascular endothelial cells (HMVECs) by measuring the succinic d ehydrogenase (SDH) activity of the cells. Then, using identical conditions of exposure, the secretion of IL-1 beta or TNP-alpha from monocytes or ICAM -1 expression on the HMVECs was determined. Only pure nickel suppressed (by 48% compared to Teflon controls) the SDH activity of the HMVECs or THT-1 m onocytes. No alloy or metal caused the HMVECs to express ICAM-1, but the Ni Ti alloy caused a significant (ANOVA/Tukey) secretion of IL-1 beta from the THP-1 monocytes. Secretion of TNF-alpha induced by NiTi was detectable but not statistically significant. The levels of IL-1 beta secretion from mono cytes were sufficient to induce ICAM-1 expression on HMVECs. The release of Ni from the NiTi was a logical suspect in causing the IL-1 beta secretion by monocytes, but its role was not confirmed since other alloys, such as Re xillium III, released the same quantities of Ni yet did not activate the TH P-1 monocytes. Within the limitations of in vitro conditions, our results i ndicate that NiTi alloys pose a risk of promoting an inflammatory response in soft tissues by activating monocytes. Further study is needed to substan tiate this finding in vivo. (C) 1999 John Wiley & Sons, Inc.