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Although the reported percentage of bone-implant contact is far lower than 100%, the cause of such low levels of bone formation has rarely been investigated. This study tested the negative biological effect of hydrocarbon deposition onto titanium surfaces, which has been reported to be inevitable. Osteogenic MC3T3-E1 cells were cultured on titanium disks on which the carbon concentration was experimentally regulated to achieve carbon/titanium (C/Ti) ratios of 0.3, 0.7, and 1.0. Initial cellular activities such as cell attachment and cell spreading were concentration-dependently suppressed by the amount of carbon on the titanium surface. The osteoblastic functions of alkaline phosphatase activity and calcium mineralization were also reduced by more than 40% on the C/Ti (1.0) surface. These results indicate that osteoblast activity is influenced by the degree of hydrocarbon contamination on titanium implants and suggest that hydrocarbon decomposition before implant placement may increase the biocompatibility of titanium.

The increasing use of nanomaterials in consumer and industrial products has aroused concerns regarding their fate in biological systems. An effective detection method to evaluate the safety of bio-nanomaterials is therefore very important. Titanium dioxide (TiO2), which is manufactured worldwide in large quantities for use in a wide range of applications, including pigment and cosmetic manufacturing, was once thought to be an inert material, but recently, more and more studies have indicated that TiO2 nanoparticles (TiO2 NPs) can cause inflammation and be harmful to humans by causing lung and brain problems. In order to evaluate the safety of TiO2 NPs for the environment and for humans, sensor cells for inflammation detection were developed, and these were transfected with the Toll-like receptor 4 (TLR4) gene and Nuclear Factor Kappa B (NF-κB) reporter gene. NF-κB as a primary cause of inflammation has received a lot of attention, and it can be activated by a wide variety of external stimuli. Our data show that TiO2 NPs-induced inflammation can be detected by our sensor cells through NF-κB pathway activation. This may lead to our sensor cells being used for bio-nanomaterial safety evaluation.

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Microfluidic devices can sort viable mammalian cells by size. In this study, we investigated size-based sorting of cells using flow splitting microfluidic devices based on hydrodynamic filtration for noninvasive cell cycle synchronization. Two different types of mammalian cell lines, HepG2 (human hepatocellular liver carcinoma cell line) and NIH/3T3 (mouse embryonic fibroblast cell line) were sorted by microfluidic device and its DNA contents were analyzed. Our results showed that a microfluidic device can synchronize the cell cycle after size separation. The damage-free separation of living cells in different phases of the cell cycle represents a potentially promising technology for the investigation of gene transfection and gene expression.

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The corrosion behavior of the Ti-33.5Nb-5.7Ta alloy (Ti-Nb-Ta) as a biocompatible β-type Ti alloy during long-term immersion in simulated body fluid was investigated. Like pure Ti, pitting corrosion did not occur on Ti-Nb-Ta during anodic polarization. Thus, alloying of Ti with Nb and Ta did not change the chloride-ion sensitivity. Metal ion release of Ti, Nb, and Ta was detected after 7-d immersion in the solution; however, the amounts of ions were much smaller than those from Type316L stainless steel. X-ray photoelectron spectroscopy revealed that the fractions of Nb and Ta in the passive layer increased during the immersion while that of Ti decreased. The corrosion rate of Ti-Nb-Ta determined by electrochemical impedance spectroscopy kept decreasing over a period of 15 d while the thickness of the passive layer did not change after 1 d. Thus, the reconstruction of the passive layer of the alloy was proven to be important for metal ion release during long-term implantation in a living body. Thus, Ti-Nb-Ta has sufficient corrosion resistance as a biocompatible β-type Ti alloy.

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