Biocompatibility of nickel-titanium shape memory metal and its corrosion behavior in human cell cultures

190

108

Nickel-titanium (NiTi) alloy derives its biocompatibility and good corrosion resistance from a homogeneous oxide layer mainly composed of TiO(2), with a very low concentration of nickel. In this article, we described the corrosion behavior of NiTi alloys after mechanical polishing, electropolishing, and sterilization processes using cyclic polarization and atomic absorption. As a preparative surface treatment, electropolishing decreased the amount of nickel on the surface and remarkably improved the corrosion behavior of the alloy by increasing the mean breakdown potential value and the reproducibility of the results (0.99 +/- 0.05 V/SCE vs. 0.53 +/- 0. 42). Ethylene oxide and Sterrad(R) sterilization techniques did not modify the corrosion resistance of electropolished NiTi, whereas a steam autoclave and, to a lesser extent, peracetic acid sterilization produced scattered breakdown potential. In comparing the corrosion resistance of common biomaterials, NiTi ranked between 316L stainless steel and Ti6A14V even after sterilization. Electropolished NiTi and 316L stainless-steel alloys released similar amounts of nickel after a few days of immersion in Hank's solution. Measurements by atomic absorption have shown that the amount of released nickel from passive dissolution was below the expected toxic level in the human body. Auger electron spectroscopy analyses indicated surface contamination by Ca and P on NiTi during immersion, but no significant modification in oxide thickness was observed.

Section: Discussionmentioning

confidence: 83%

“…[12][13][14] NiTi alloy derives its good corrosion behavior from a homogeneous oxide layermainly TiO 2 -which spontaneously covers the surface of NiTi alloy in presence of oxygen. This passive surface layer, similar to those observed on titanium-based alloys, enhances NiTi high stability in most corrosive environments.…”

Section: Introductionmentioning

confidence: 99%

Effect of surface treatment and sterilization processes on the corrosion behavior of NiTi shape memory alloy

Thierry

Tabrizian

Trépanier³

et al. 2000

190

108

“…Most of the current quantitative analyses of metal corrosion toxicity or biocompatibility use a combination method of incubating cultured cells in metal-immersed media. [3][4][5][6][7][8] Alloy discs, 3 wires, 4 particulates 5 of test metals have been used in cell cultures to explore the dose-effect relationship. 4 The cell growth around pieces of metal in culture dishes was observed and compared with that in control cultures.…”

Section: Introductionmentioning

confidence: 99%

“…The release of oxides and metal ions could be detected in the first few days immediately after the stent implantation. 3 However, corrosive breakdown might take place any time, even several years after implantation. At the tissue contact interface, the released ions may be "burst-out" locally, accumulated, and then taken up by the adjacent cells.…”

Section: Introductionmentioning

confidence: 99%

The cytotoxicity of corrosion products of nitinol stent wire on cultured smooth muscle cells

Shih¹,

Lin

Chen

et al. 2000

180

Although nitinol is one of most popular materials of intravascular stents, there are still few confirmative biocompatibility data available, especially in vascular smooth muscle cells. In this report, the nitinol wires were corroded in Dulbecco's modified Eagle's medium with constant electrochemical breakdown voltage and the supernatant and precipitates of corrosion products were prepared as culture media. The dose and time effects of different concentrations of corrosion products on the growth and morphology of smooth muscle cells were evaluated with [(3)H]-thymidine uptake ratio and cell cycle sorter. Both the supernatant and precipitate of the corrosive products of nitinol wire were toxic to the primary cultured rat aortic smooth muscle cells. The growth inhibition was correlated well with the increased concentrations of the corrosion products. Although small stimulation was found with released nickel concentration of 0.95 +/- 0.23 ppm, the growth inhibition became significant when the nickel concentration was above 9 ppm. The corrosion products also altered cell morphology, induced cell necrosis, and decreased cell numbers. The cell replication was inhibited at the G0-G1 to S transition phase. This was the first study to demonstrate the cytotoxicity of corrosion products of current nitinol stent wire on smooth muscle cells, which might affect the postimplantation neointimal hyperplasia and the patency rate of cardiovascular stents.

“…1 Intimal hyperplasia is one of the major mechanisms responsible for poststenting restenosis, and is mainly caused by the proliferation of vascular smooth muscle cells. 1,2 But the effects of electrochemical corrosion of stent materials on the tissue response, especially on the growth of vascular smooth muscle cells, had not been well studied. The release of oxides and metal ions could be detected in the first few days immediately after the stent implantation.…”

Section: Introductionmentioning

confidence: 99%

Growth inhibition of cultured smooth muscle cells by corrosion products of 316 L stainless steel wire

Shih

Chen³

et al. 2001

The potential cytotoxicity on vascular smooth muscle cells of corrosion products from 316 L stainless steel, one of most popular biomaterials of intravascular stents, has not been highlighted. In this investigation, 316 L stainless steel wires were corroded in Dulbecco's modified eagle's medium with applied constant electrochemical breakdown voltage, and the supernatant and precipitates of corrosion products were prepared as culture media. The effects of different concentrations of corrosion products on the growth of rat aortic smooth muscle cells were conducted with the [3H]-thymidine uptake test and cell cycle sorter. Both the supernatant and precipitates of corrosion products were toxic to the primary culture of smooth muscle cells. The growth inhibition was correlated well with the increased nickel ions in the corrosion products when nickel concentration was above 11.7 ppm. The corrosion products also changed cell morphology and induced cell necrosis. The cell growth inhibition occurred at the G0/G1 to S transition phase. Similar to our recent study of nitinol stent wire, the present investigation also demonstrated the cytotoxicity of corrosion products of 316 L stainless steel stent wire on smooth muscle cells, which might affect the poststenting vascular response.