In this work the surface modification of Ti ndash

From a corrosion point of view, materials implanted in vivo initially come in contact with extracellular body fluids such as blood and interstitial fluids. It has been observed that the chloride ion concentrations in blood plasma and interstitial fluid, 113 mEq/l and 117 mEq/l [5], respectively, are sufficiently high to corrode metallic materials. In addition, body fluids contain ABT-538 and proteins that tend to accelerate corrosion [6] and [7]. However, the pH level decreases to about 5.2 in hard tissue after implantation and recovers to 7.4 within 2 weeks [8]; consequently, corrosion due to an abrupt change in body fluid pH appears to be negligible. Toxicity and allergy may occur in vivo if implant materials are corroded by body fluid, leading to the release of metal ions into the body fluid for a prolonged period and the combination of ions with biomolecules such as proteins and enzymes [3]. On the other hand, wear in mechanical parts is important which is needed to assess the reliability of a material in medical implant applications because an implant has to withstand not only onetime peak stresses but also the several million load cycles that it typically experiences throughout its lifetime [9]. Ti–6Al–4V alloy is reported to have notoriously poor wear resistance due to its low resistance to plastic shearing and the low level of protection imparted by surface oxides [10]. Recently, research on the tribological properties and mechanisms of Ti–6Al–4V alloy under different sliding speeds and loads was conducted [11] and [12]. According to these studies, a transition from oxidative wear to delamination wear occurred with an increase in sliding speed and that low wear resistance was due, in part, to the weak protection afforded by surface oxides. Qiu et al. [13] examined the effect of friction heat on the friction and wear performance of Ti–6Al–4V alloy under high sliding speeds. The authors observed that TiO, TiO2, and V3O4 oxides were formed on the worn surfaces as the friction temperature increased. This behavior originated from the rapid decrease in the wear resistance of Ti–6Al–4V alloy with an increase in sliding speed, which led to the formation of a loose oxide layer. It is clear that loose oxides do not provide a protective effect because of the unfavorable Pilling-Bedworth ratio and the internal stresses owing to the mismatch in thermal expansion between the oxide and the subsurface alloy [14]. In other comparative studies, Ohidul Alam and Haseeb [15] investigated the tribological properties of Ti–6Al–4V and Ti–24Al–11Nb alloys subjected to dry sliding wear against hardened steel and reported that severe delamination was responsible for the low wear resistance of Ti–6Al–4V. The authors suggested that the lower wear rate of Ti–24Al–11Nb was linked to the ability of this alloy to form a Ti–Nb oxide-based protective layer. Thus improving the wear resistance and corrosion behavior of metallic implants by various surface treatments is a challenging task but one that can help expand the use of titanium and titanium alloys in biomedical applications [3]. According to the literature [16], [17], [18], [19] and [20], the fabrication of self-organized oxide nanotube layers as a suitable surface treatment can improve the fundamental specifications of titanium alloys. In terms of corrosion resistance, TiO2 nanotube layers on titanium exhibit better corrosion resistance in simulated biofluids than does smooth-Ti [21]. In addition, recent work has shown that, on TiO2 nanotube layers, hydroxyapatite growth can be further enhanced [22]. A promising biomedical application of these nanotubular arrays has been reported recently by Park et al. [23], who studied cell responses to a highly defined spacing variation involving vertically aligned TiO2 nanotubes with six different diameters ranging between 15 and 100 nm. The findings support those reported in recent studies on cells reacting sensitively to nanoscale roughness on silicon or silica substrates [24] and [25], indicating that cell responses to biomimetic surfaces depend not only on the chemistry of a biomaterial but also on the geometry of the nanoscale microenvironment. Cell interactions with extracellular surfaces are mediated by the clustering of integrins into focal adhesion complexes and the activation of intracellular signaling cascades in the nucleus and the cytoskeleton.