Effect of Ni ions on expression of intercellular adhesion molecule 1 by endothelial cells

Abstract

Previous studies have shown that Ni-based alloys implanted into soft tissues cause an infiltration of inflammatory cells around the implant. This phenomenon is potentially important to dental alloys which are adjacent to oral tissues. To help define the mechanisms by which Ni causes an infiltration of inflammatory cells, we exposed endothelial cells in vitro to Ni ions and measured the expression of intercellular adhesion molecule 1 (ICAM-1). ICAM-1 is known to be involved in the recruitment of inflammatory cells from the bloodstream. We also exposed macrophages to Ni ions to test the hypothesis that Ni might alter cytokine secretion and subsequently cause expression of ICAM-1 on endothelial cells. The results showed that Ni ions could promote the expression of ICAM-1 on endothelial cells, but only at concentrations which were high enough (850 mumol/L for 24 h) to suppress cell metabolic activity. Although we had previous evidence that Ni could cause macrophages to secrete cytokines such as interleukin 1 beta, Ni-exposed macrophage supernatants did not induce expression of ICAM-1 on endothelial cells at concentrations subtoxic to the macrophages (85 mumol/L). At subtoxic concentrations, Ni ions were able to suppress ICAM-1 expression on endothelial cells which were stimulated with lipopolysaccharide. Thus, Ni ions either promoted or suppressed the expression of ICAM-1 depending on their concentration. This dual action of Ni ions may be important in vivo where a gradient of concentrations of released ions is likely to exist around the implanted biomaterial. Further studies are necessary to determine the effect of time of exposure and the molecular mechanisms of increased ICAM-1 expression.

Corrosion Susceptibility and Nickel Release of Nickel Titanium Wires during Clinical Application

“…Nickel's effect has been investigated systemically in cell cultures, tissues, organs and organisms, and biological reactions associated with nickel have been analyzed [8-11, 34, 35]. Concentrations of nickel as contained in dental products can activate monocytes and endothelial cells by increasing or decreasing the discharge of the intercellularadhesion molecule 1 by endothelial cells dependent on the ionic concentration [39,40]. Moreover, complexes of nickel within arsenides or sulfides have long been categorized as carcinogenic, allergenic, and mutagenic [32,41].…”

Allergic reactions and nickel-free braces: a systematic review

“…20,21 In this context, nickel binding to endogenous macromolecules can stimulate macrophages and cytotoxic cells, up-regulating the expression of adhesion molecules. [22][23][24] The differential quantification of leukocytes in the current research shows that the difference in the total number of leukocytes was caused by an increase in the number of monocytes. It has been reported that low-dose exposure to nickel can alter the metabolism of monocytes.…”

The connective tissue response to Ti, NiCr and AgPd alloys.

“…The protein overcoat created on the surface of titanium implants is what changes the properties of the passivised surface [14] and this protein, fibronectine and collagen overcoat can be created on titanium implants [15]. The surface of implanted titanium is almost stoichiometrically coated by titanium oxide, which is subject to conversion by hydroxyl, acidic and alkaline groups.…”