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Macrophages are attracting increasing attention in promoting implant-mediated osteogenesis by modulating the microenvironment of the implant site. Biomaterial surface properties including topography and wettability regulate macrophage responses to influence tissue repair. The objective of our present study was to investigate the effects of hydrogenated titanium dioxide nanotube surfaces on the immune response of macrophages in vitro. Hydrogenated titanium dioxide nanotubes (TNTs) were synthesized on Ti surfaces by anodic oxidation and hydrogenation to form super-hydrophilic nanotubular surfaces. Macrophages were seeded directly onto three substrates (hydrogenated TNTs (H2-TNTs), air-annealed TNTs, and commercially pure Ti substrates) and grown under standard or lipopolysaccharide-stimulated culture conditions. Cell proliferation and viability were evaluated by Cell Counting Kit-8 and live/dead staining at 24 and 48 h. Secretion and expression of pro- and anti-inflammatory cytokines were evaluated at 24 and 48 h to determine whether the surfaces elicited differential macrophage behaviors. Gene expression of the M1/M2 surface markers of macrophages was analyzed to assess the effect of the H2-TNT surface on macrophage polarization. The results showed that hydrogenation of the TNT surface resulted in a super-hydrophilic substrate, which exhibited markedly improved wettability attributable to the formation of oxygen vacancies in the nanotubes. The H2-TNT group induced a significantly lower macrophage proliferation rate and up-regulated anti-inflammatory cytokines (interleukin-10, bone morphogenetic protein-2, and transforming growth factor-β1) irrespective of lipopolysaccharide stimulation, while alleviating the secretion of pro-inflammatory cytokines (tumor necrosis factor-α, interleukin-6, nitric oxide, and macrophage chemotactic protein-1) induced by lipopolysaccharide. Moreover, the H2-TNT surface elicited up-regulated gene expression of M2 surface markers and down-regulation of M1 surface markers. We concluded that the hydrogenated TNT surface modulated macrophage immune responses, which could be useful in accelerating inflammation resolution and facilitating tissue repair. [ABSTRACT FROM AUTHOR]

• Superhydrophilic nanostructure was fabricated for improving soft tissue sealing. • The properties of the surface regulate the behavior of human gingival fibroblasts. • FAK/integrin-mediated adhesion seemed to be induced by the hydrogenated surface. Soft tissue integration is critical for the long-term retention of dental implants. The surface properties including topography and wettability can impact soft tissue sealing. In our work, a thermal hydrogenation technique was applied to modify anodized titanium dioxide nanotubes (TNTs). However, the effects of the hydrogenated surface on soft-tissue cells remain unclear. The aim of the present study was to investigate the bioactivities of human gingival fibroblasts (HGFs) on structured surfaces, which determine the early formation of soft tissue sealing. Three groups were examined: commercially pure titanium (Ti), anodized TNTs (air-TNTs) and hydrogenated TNTs (H 2 -TNTs). Scanning electron microscopy showed the nanotubular topography on the titanium surfaces after anodization. Then, hydrogenation ensured that the H 2 -TNTs were superhydrophilic with a contact angle of 3.5 ± 0.8°. In vitro studies such as cell adhesion assays, cell morphology, immunocytochemistry, wound healing assays, real-time PCR and enzyme-linked immunosorbent assays displayed enhanced adhesion, migration, relative gene expression levels, and extracellular matrix synthesis of the HGFs on H 2 -TNTs. Interestingly, focal adhesion kinase activation and integrin-mediated adhesion seemed to be induced by the H 2 -TNT surface. Our results revealed that a superhydrophilic nanostructure modified by anodization and hydrogenation can improve the bioactivity of HGFs and connective tissue regeneration, which will further promote and expand the application of titanium dioxide nanotubes in dental implants. [ABSTRACT FROM AUTHOR]