Variations of titanium oxide films induced by osteoblast-like cells in a rat calvaria culture system and the influence of an H2O2 pretreatment have been investigated by using X-ray photoelectron spectroscopy and electrochemical impedance spectroscopy. For abraded titanium, the results revealed that phosphate and calcium ions may incorporate into the surface oxide film during the cell culture, forming a precipitate with a Ca/P ratio near that of hydroxyapatite. Oxidized carbon also was found in the surface layer, most likely precipitated hydroxylcarbonated apatite (HCA). The H2O2 pretreatment of titanium in a phosphate-buffered saline solution results in a 10-fold thickened porous oxide film and large amounts of surface hydroxyl groups as well as a certain amount of phosphate ions inside the oxide film. During the cell culture, the H2O2-treated titanium surface favors the ion incorporation and precipitation of the HCA-like compound, which probably is inlaid into the oxide film. Osteoblast-like cells on the H2O2-treated titanium showed a more active morphology during the initial stage compared with cells on abraded titanium. Moreover, bone-like nodule formation and mineralization appear to be related to the precipitation of the HCA-like compound on the surface. The results are discussed with respect to corrosion resistance, ion incorporation and precipitation of the HCA-like compound on the surface, osseointegration, and bioactivity of titanium implants.

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Tendon healing is characterized mostly by slow rehabilitation and, as in tendinopathy, aberrant, protracted sensory nerve ingrowth. This study investigated whether administration of the sensory neuropeptide substance P (SP) could enhance healing and modulate sensory nerve plasticity after Achilles tendon rupture. Fifty-four male Sprague-Dawley rats were allocated to three groups, all receiving six daily injections post-rupture of; (1) SP (10(-6) mol/kg body weight)+endopeptidase inhibitors captopril and thiorphan, (2) captopril/thiorphan only and (3) saline control. At 1, 3 and 6 weeks post-rupture tendon healing was evaluated by assessments of fibroblast proliferation, collagen III-LI (like) occurrence, diameter of newly organized collagen and sensory nerve fiber ingrowth. At 1 week, the SP-treated group exhibited increased occurrence of collagen III-LI (P=0.03) and of organized collagen (P=0.04) compared with control. At 3 weeks, the SP group notably displayed reduced SP-nerve fiber ingrowth (P=0.02), and higher fibroblast density (P=0.004). Both the SP and captopril/thiorphan groups demonstrated increase in collagen fiber organization compared with control (P=0.02 and 0.004, respectively). At 6 weeks, no significant differences were observed between the groups. SP supply in tendon repair promotes early tissue proliferation and regulation of endogenous sensory nerve ingrowth, suggesting implications for novel treatment in tendinopathy.

The in vitro cytotoxic potential of six commonly used methacrylate polymers was evaluated using human oral fibroblast cultures with different cell-material contact systems. A tissue culture insert was introduced to test resin-released components. Both acute and delayed cytotoxic effects of resin were quantified by cellular enzymatic and DNA synthetic activities of fibroblasts over a 6-day exposure period. Resin toxicity was material-dependent. Statistical analysis showed that the experimental conditions significantly contributed to the overall toxicity and the cytotoxicity pattern for a given material. DNA synthesis activity of human oral fibroblasts assayed by 3H-thymidine incorporation was more sensitive to resins than cellular enzyme activity, as determined by tetrazolium bromide reduction. However, extended exposure increased the cytotoxicity of all resins, as measured by tetrazolium bromide reduction, which seemed to be a better indicator of the development of resin toxicity than 3H-thymidine incorporation. Removal of the oxygen inhibition layer on resin specimens partially enhanced cell viability, indicating that this surface layer together with other unknown factors contributed to resin toxicity.

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