Corrosion of phosphate-enriched titanium oxide surface dental implants (TiUnite) under in vitro inflammatory and hyperglycemic conditions.

Endosseous dental implants use is increasing in patients with systemic conditions that compromise wound healing. Manufacturers recently have redesigned implants to ensure more reliable and faster osseointegration. One design strategy has been to create a porous phosphate-enriched titanium oxide (TiUnite) surface to increase surface area and enhance interactions with bone. In the current study, the corrosion properties of TiUnite implants were studied in cultures of monocytic cells and solutions simulating inflammatory and hyperglycemic conditions. Furthermore, to investigate whether placement into bone causes enough mechanical damage to alter implant corrosion properties, the enhanced surface implants as well as machined titanium implants were placed into human cadaver mandibular bone, the bone removed, and the corrosion properties measured. Implant corrosion behavior was characterized by open circuit potentials, linear polarization resistance, and electrical impedance spectroscopy. In selected samples, THP1 cells were activated with lipopolysaccharide prior to implant exposure to simulate an inflammatory environment. No significant differences in corrosion potentials were measured between the TiUnite implants and the machined titanium implants in previous studies. TiUnite implants exhibited lower corrosion rates in all simulated conditions than observed in PBS, and EIS measurements revealed two time constants which shifted with protein-containing electrolytes. In addition, the TiUnite implants displayed a significantly lower corrosion rate than the machined titanium implants after placement into bone. The current study suggests that the corrosion risk of the enhanced oxide implant is lower than its machined surface titanium implant counterpart under simulated conditions of inflammation, elevated dextrose concentrations, and after implantation into bone.

Corrosion of machined titanium dental implants under inflammatory conditions.

The effects of hyperglycemia, altered cell function, or inflammatory mediators on implant corrosion are not well studied; yet, these effects are critical to implant biocompatibility and osseointegration. Because implant placement is burgeoning, patients with medically compromising systemic conditions such as diabetes are increasingly receiving implants, and the role of other inflammatory diseases on implant corrosion also needs investigation. In the current study, the corrosion properties of commercially available, machined titanium implants were studied in blood, cultures of monocytic cells, and solutions containing elevated dextrose concentrations. Implant corrosion was estimated by open circuit potentials, linear polarization resistance, and electrical impedance spectroscopy (EIS) for 26 h. In selected samples, THP1 monocytic cells were activated for 2 h with Lipopolysaccharide prior to implant exposure, and IL-1beta secretion was measured to assess the affect of the implants on monocyte activation. Implants under conditions of inflammatory stress exhibited more negative E(corr) values, suggesting an increased potential for corrosion. Linear polarization measurements detected increased corrosion rates in the presence of elevated dextrose conditions over PBS conditions. EIS measurements suggested that implants underwent surface passivation reactions that may have limited corrosion over the short term of this test. This result was supported by cyclic polarization tests. IL-1beta secretion was not altered under conditions of corrosion or implant exposure. The results suggest that inflammatory stress and hyperglycemia may increase the corrosion of dental endosseous titanium-based implants, but that longer, more aggressive electrochemical conditions may be necessary to fully assess these effects.

Interactions between stainless steel, shear stress, and monocytes.

Angioplasty with stent placement is commonly used to treat coronary atherosclerosis. However, 20-40% of stainless steel stents restenose within 6 months via a prolonged inflammatory response mediated by monocytic infiltration and cytokine secretion. In the current study, we tested a hypothesis that blood flow and monocytes interact to alter stent corrosion. We assessed the effects of THP1 monocytes on the corrosion rate of 316L stainless steel (316LSS) under shear stress (0.5-50 dyn/cm(2)). In addition, THP1 cytokine secretion was determined using cytokine arrays and ELISA analyses. Data were compared using ANOVA and Tukey post hoc analysis (alpha = 0.05). Monocytes significantly lowered 316LSS corrosion rates without limiting current density. However, shear stress alone did not alter the corrosion rate of 316LSS. THP1 cells adhered to the 316LSS surface at all flow rates. Exposure to the 316LSS/corrosion test under high fluid flow rates increased (>twofold) the secretion of 7 of the 42 cytokines tested (angeogenin, GRO, I309, interleukin 8, interleukin 6, interleukin 1beta, and macrophage chemoattractant protein-1). Each of these cytokines play a role in wound healing, macrophage differentiation, and cell proliferation, all hallmarks of in-stent restenosis. Furthermore, only IL8 levels were significantly higher than any of the system controls during the 316LSS/corrosion test conditions. The IL8 levels from the 316LSS/corrosion tests were not significantly different from the +LPS control. Together, these data suggest that monocytic cells maybe activated by exposure to 316LSS stents and could contribute to in-stent restenosis and altered corrosion of the stent.

Corrosion rates of stainless steel under shear stress measured by a novel parallel-plate flow chamber.

A unique parallel-plate flow chamber has been engineered to assess the corrosion properties of implant materials in biological environments under shear flow. This parallel-plate flow chamber provides a novel approach to investigate hypotheses regarding cellular-material-mechanical-force interactions that influence the success or failure of implant devices. The results of the current study demonstrated that physiological stresses (0.5-50 dynes/cm2) from laminar flow from cell culture media did not significantly alter corrosion rates of stainless steel, providing baseline information for an extensive study of the cellular-material-mechanical-force interactions. Furthermore, this study demonstrated that this device is electrochemically stable and provides reproducible results within test parameters. In addition, the results were not significantly different from corrosion tests on bulk samples. Therefore, this system will be useful for investigating cell-material interactions under shear stress for implant alloys or other opaque materials. This information is currently lacking. The results of the present study also support further development of this test system to assess cellular responses to these materials under shear stresses.