| Biocompatibility evaluation of nickel-titanium shape memory metal alloy: | ||
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Various studies have shown that the metallic components of the alloys used in orthopedics may be toxic and dissolve in body fluids due to corrosion (Poehler 1983). Every metal has its own intrinsic toxicity to cells, but the corrosion mostly determines the existing concentration. Thus, the corrosion resistance of the alloy and the toxicity of individual metals in the alloy are the main factors determining its biocompatibility.
The corrosion of metals in aqueous solutions takes place via an electrochemical mechanism. Different metals have different intrinsic aptitudes to corrode. The more noble the metal, the lesser is its aptitude to corrode. Reactions taking place on the metal surface and in the specific environment may cause radical changes in this theoretical nobility. After implantation, the metal is surrounded by serum ions, proteins and cells, which may all modify the effect on local corrosion reactions. The corrosion behavior of a metal in non-physiological in vitro studies vs physiological in vitro studies vs in vivo studies may vary dramatically. Every implant metal corrodes inside the human body (Williams et al. 1996). After implantation, elevated metal concentrations are often measured even in distant organs. This is due to ionization, but also to the phagocytosing cells which circulate small metal and metal oxide particles.
Some forms of corrosion are typical of implant use. Corrosion focused to small points is called pitting corrosion. Galvanic corrosion may occur when dissimilar metals are used. The less noble metal becomes anodic and corrodes (stainless steel screws corrode when used with titanium plate). Fretting corrosion occurs when micromotion between two metals breaks their passivation layers (as with screws and plates) (Brown 1987).
There are numerous factors which affect metal corrosion. Porosity and rough surfaces increase the reacting surface area of the implant and thus the total amount of corrosion. The loading areas of the implant are more sensitive to corrosion compared to the less loading areas (Kruger 1983).
The structure, composition and thickness of the passive layer are highly dependent on the metal itself and its environment. Metals contain various elements, such as lattice defects, impurities and contaminants, which may affect the corrosion reaction. The different heat treatments and working processes change the grain size and energy state of the metal and cause surface heterogeneity (Poehler 1983). All these factors may affect the passivation layer.
The corrosion resistance of metals and metal alloys is mainly based on a passivation phenomenon (Kruger 1983). The passivation of a metal is due to the compact coat, the passive layer, which contains hardly any original metal, but forms a metal-oxide layer, a “skin” on the metal. This oxide layer may be amorphic or crystal. The composition of the oxide layer also changes from its outer surface towards the metal. The oxide layer is thicker on implanted metal than on non-implanted metal. Contaminants of Ca and P are generally seen (Kasemo et al. 1991).
The human body is a very demanding environment because it is so salty. When metal ions are dissolved from the points where the oxide layer is not fully developed, they form metal hydroxide. This is immediately surrounded by water molecules and then attaches to the passive layer. When there are chloride ions present, as in human plasma, these replace the water molecules from the passive layer. If the passive layer is not fully developed, the dissolved metal ions form a metal-chloride complex which dissolves into body fluids. This impairs local passivity, and may lead to pitting corrosion (Williams et al. 1996). When the passive layer breaks locally, this anodic area is very small and the surrounding catodic area is very large. This may lead to very rapid local corrosion and unexpectedly fast destruction of the material (Kruger 1983).