Evaluation of cell activation promoted by tantalum and tantalum oxide coatings deposited by reactive DC magnetron sputtering

Abstract

Previous studies have shown both Ta and TaeO to be bioactive, rapidly forming a strongly-bonded surfaceadherent layer of bone-like hydroxyapatite (HAp) when immersed in simulated body fluid (SBF). Consequently, Ta and TaeO coatings are promising for the surface-modification of Ti or stainless steel endodontic endosseous implants, being conducive to a reduction in the risk of developing post-operatory infection and/or peri-implantitis disease. That said, few studies have investigated the effect of Ta or TaeO coatings on such phenomena as cell activation, adhesion, and proliferation. To that effect, Ta, and TaeO films were deposited onto type 316L stainless steel (SS 316L) substrates by reactive DC magnetron sputtering, after which their biological response was evaluated following co-incubation with the murine macrophage-like cell line RAW 264.7. Cell morphology after adhesion was observed by SEM, whereas cell viability and proliferation were evaluated by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) colorimetric assay. Lastly, inflammatory response was assessed by quantification of the cytokines interleukin-6 (IL-6) and interleukin-10 (IL-10). In terms of phase composition, Ta showed a mixture of the α-Ta and β-Ta phases, whereas TaeO showed a nanocrystalline structure. Moreover, a decrease in average roughness (Ra) from 21 nm to 7 nm was observed between Ta and TaeO, accompanied by a decrease in water contact angle (θW) from 106° to 83°. In vitro studies showed that cells exhibited significantly better adhesion to Ta, in comparison with both TaeO and SS 316L. Furthermore, both Ta and TaeO were shown to be non-cytotoxic, with Ta outperforming TaeO in terms of relative cell viability, both at 24 h and 48 h. Lastly, both Ta and TaeO showed vastly inferior IL-6 and IL-10 levels to those obtained for cells treated with bacterial lipopolysaccharides (LPS)—prompting the conclusion that the coatings do not in any way induce an inflammatory response from macrophage cells.