Oxygen plasma with different treatment powers and durations was utilized to modify the biomedical pure titanium (Ti) surface in the present study. The superficial, microstructural and biological properties of the plasma-oxidized samples were investigated using the electron microscopy, X-ray photoemission spectroscopy, grazing incidence X-ray diffractometer, contact angle goniometer and blood clotting time assay. During different treatment powers and durations, the island-like nanostructural rutile-TiO 2 layer and dimple-like nanostructural rutile-TiO 2 layer were generated on the surfaces of the plasma-oxidized samples, respectively. It was also found that the plasma-oxidized sample with a rough oxide layer resulted in the formation of a higher wettability. Moreover, the blood clotting time assay indicated that the plasma-oxidized samples exhibited the adhesion behaviors of red blood cells. As the Ti surface underwent plasma oxidation at 280 W for 30 min, it not only generates a rough nanostructural rutile-TiO 2 layer, but also presents an excellent hemocompatibility. Therefore, these findings demonstrate that oxygen plasma modification is a potential approach to promote the hemocompatibility of biomedical pure Ti surface.
The aim of the present study was to test the hypothesis that the proliferation of a human osteoblast cell line (HOS cells) stimulated with hydroxyapatite (HA) may be regulated by nitric oxide (NO). The cells were cultured on the surface of HA. Medium or cells alone were used as controls. L-arginine, D-arginine, 7-NI (an nNOS inhibitor), L-NIL (an iNOS inhibitor), L-NIO (an eNOS inhibitor) or carboxy PTIO, a NO scavenger, was added in the HA-exposed cell cultures. The cells were also precoated with anti-human integrin alphaV antibody. The levels of nitrite were determined spectrophotometrically. Cell proliferation was assessed by colorimetric assay. The results showed increased nitrite production and cell proliferation by HA-stimulated HOS cells up to day 3 of cultures. Anti-integrin alphaV antibody, L-NIO, or carboxy PTIO suppressed, but L-arginine enhanced, nitrite production and cell proliferation of HA-stimulated HOS cells. The results of the present study suggest, therefore, that interaction between HA and HOS cell surface integrin alphaV molecule may activate eNOS to catalyze NO production which, in turn, may regulate the cell proliferation in an autocrine fashion.
The purpose of the present study was to examine early tissue response and osseointegration in the animal model. The surface morphologies of SLAffinity were characterized using scanning electron microscopy and atomic force microscopy. The microstructures were examined by X-ray diffraction, and hardness was measured by nanoindentation. Moreover, the safety and toxicity properties were evaluated using computer-aided programs and cell cytotoxicity assays. In the animal model, implants were installed in the mandibular canine-premolar area of 12 miniature pigs. Each pig received three implants: machine, sandblasted, large grit, acid-etched, and SLAffinity-treated implants. The results showed that surface treatment did affect bone-to-implant contact (BIC) significantly. At 3 weeks, the SLAffinity-treated implants were found to present significantly higher BIC values than the untreated implants. The SLAffinity treatments enhanced osseointegration significantly, especially at early stages of bone tissue healing. As described above, the results of the present study demonstrate that the SLAffinity treatment is a reliable surface modification method.
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