The effects of niobium ions released from 60CaO-30P(2)O(5)-(10-x)Na(2)O-xNb(2)O(5) (mol %, x = 0-10) glasses on MC3T3-E1 cell functions were evaluated by culture tests with two systems; cell culture on glass plates, or in culture media containing glass extracts. Alkaline phosphatase (ALP) activity in the cells cultured on the glass plates containing 3 and 5 mol % of Nb(2)O(5) was significantly higher than that on the Nb(2)O(5)-free glass, although proliferation was not enhanced on all glasses containing Nb(2)O(5). Cells cultured in the medium containing 3 × 10(-7) M niobium ions showed the highest ALP activity in comparison with other Nb-containing media or normal medium, regardless of the presence of osteogenic factors (ascorbic acid, β-glycerophosphate and dexamethasone) in the media. Calcium deposition by the cells cultured in the medium containing 3 × 10(-7) M niobium ions was twice as high as those cultured in medium containing no niobium ions. The effects of niobium ions were thought to depend on ion concentration, and to enhance differentiation and mineralization of osteogenic cells rather than their initial adhesion or proliferation.

Nickel, cobalt, and chromium are well known to be causal agents of allergic contact dermatitis. Palladium (Pd) can also cause allergic disease and exposure results from wide use of this metal in dental restorations and jewelry. Metal allergy is categorized as a delayed-type hypersensitivity, and metal-responsive T cell clones have been isolated from allergic patients. However, compared to nickel, little is known about the pathology of allergic disease mediated by Pd, and pathogenic T cells are poorly understood. To identify the pathogenic T cells that are responsible for onset of Pd allergy, we enriched metal-responsive lymphocytes by sequential adoptive transfer of involved lymph node cells. Here we show that sequential adoptive transfer gradually increased the incidence and the intensity of Pd allergy, and CD8+ T cells are responsible for the disease as CD8+ T cell-depleted mice and β2-microglobulin-deficient mice did not develop Pd allergy. In addition, we found that draining lymph node cells skewed toward CD8+ T cells in response to Pd challenge in 8th adoptive transferred recipient mice. The CD8+ T cells expressed NKG2D, a costimulatory molecule involved in the production of IFN-γ. NKG2D ligand was also induced in Pd-injected tissues. Furthermore, both NKG2D ligand-transgenic mice, where NKG2D is downmodulated, and IFN-γ-deficient mice showed impaired Pd allergy. Taken together, these results indicate that IFN-γ-producing NKG2D+ CD8+ T cells are responsible for Pd allergy and suggest that NKG2D is a potential therapeutic target for treatment of metal allergy.

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Calcium phosphate films were prepared on titanium substrates by radiofrequency (RF) magnetron sputtering at RF powers from 75 to 150 W. Hot-pressed -tricalcium phosphate (-TCP) plates with a high density (>99:6%) were used as a sputtering target. The substrate was not intentionally heated. The films consisted of amorphous calcium phosphate and oxyapatite (Ca 10 (PO 4 ) 6 O) phases. The ratio of the oxyapatite phase depended on the sputtering conditions of RF power, oxygen gas concentration in the sputtering gas (C O2 ) and total pressure in the chamber. The (002) preferred orientation of oxyapatite phase was observed. The deposition rate of films increased with increasing RF power and decreasing C O2 . The highest deposition rate was 0.143 nmÁs À1 (0.515 mmÁh À1 ).

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SHINGO MINETA, SHIGENOBU NAMBA, TAKASHI YONEDA, KYOSUKE UEDA, and TAKAYUKI NARUSHIMA The microstructures of as-cast and heat-treated biomedical Co-Cr-Mo (ASTM F75) alloys with four different carbon contents were investigated. The as-cast alloys were solution treated at 1473 to 1548 K for 0 to 43.2 ks. The precipitates in the matrix were electrolytically extracted from the as-cast and heat-treated alloys. An M 23 C 6 type carbide and an intermetallic r phase (Co(Cr,Mo)) were detected as precipitates in the as-cast Co-28Cr-6Mo-0.12C alloy; an M 23 C 6 type carbide, a r phase, an g phase (M 6 C-M 12 C type carbide), and a p phase (M 2 T 3 X type carbide with a b-manganese structure) were detected in the as-cast Co-28Cr-6Mo-0.15C alloy; and an M 23 C 6 type carbide and an g phase were detected in the as-cast Co-28Cr-6Mo-0.25C and Co-28Cr-6Mo-0.35C alloys. After solution treatment, complete precipitate dissolution occurred in all four alloys. Under incomplete precipitate dissolution conditions, the phase and shape of precipitates depended on the heat-treatment conditions and the carbon content in the alloys. The p phase was detected in the alloys with carbon contents of 0.15, 0.25, and 0.35 mass pct after heat treatment at high temperature such as 1548 K for a short holding time of less than 1.8 ks. The presence of the p phase in the Co-Cr-Mo alloys has been revealed in this study for the first time.

Calcium phosphate films were fabricated on titanium substrates heated up to 773 K using radiofrequency (RF) magnetron sputtering. The deposition rate, phase and preferred orientation of the calcium phosphate films were studied. Immersion tests for the films were conducted using Hanks' solution and PBS(-), and the surface reactions on the specimens coated with the calcium phosphate films were investigated. The bonding strength between the coating films and the titanium substrates before and after the immersion tests was evaluated; the bonding strength decreased after the immersion tests. The alkaline phosphatase (ALP) activity of SaOS-2 cells on a titanium plate coated with a calcium phosphate film was examined by conducting a culture test. Calcium phosphate coating increased the ALP activity of SaOS-2 cells cultured for 3 and 7 days. Titanium cylinders were coated with an amorphous calcium phosphate film and implanted into the mandibles of beagle dogs. An increase in the extent of bone-implant contact for the coated titanium cylinders was confirmed 8 to 12 weeks after implantation and compared with the case for uncoated titanium cylinders.