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The aim of this research was to evaluate the effect of polyethylene terephthalate (Woven Dacron) on the expression of endothelial integrins. Human umbilical vein endothelial cells were cultured on the material for 24 h. The integrins VLA-2 (α2β1-CD49b/CD29), receptor for laminin and collagen, VLA-5 (α5β1-CD49e/CD29), receptor for fibronectin, VLA-6 (α6β1-CD49f/CD29), receptor for laminin, and αVβ3-CD51/CD61 (receptor for vitronectin) were evaluated by flow cytometry. After contact with polyethylene terephthalate, a slight but significant decrease in the percentage of both CD29 and CD49e positive cells was observed, which suggests a lower number of cells expressing the fibronectin receptor α5β1. Moreover, a significant increase in the mean channel for CD49b and for the vitronectin receptor CD51/CD61 was observed. The reduction in the fibronectin receptor could account for the poor endothelialization observed in vivo on polyethylene terephthalate. The increased expression of the vitronectin receptor, favoring the migration of smooth muscle cells, could give some information about the pathogenesis of intimal hyperplasia, which is a complication of vascular grafts. © 2001 Kluwer Academic Publishers

Ten PMMAbased bone cements used in prosthetic surgery have been studied with respect to the induction of programmed cell death i.e., apoptosis in HL60 cells, which are remarkably sensitive to various apoptotic stimuli. Annexin V binding and propidium iodide PI exclusion were the methods for detection of early apoptotic changes, while PI entry was considered as a marker of necrosis. Hoechst 33342 staining was used to detect DNA fragmentation and Alamar blueTMwas applied to measure oxidereduction activity of cells. The production of reactive oxygen species ROS related to cell damage was verified using dichlorofluoresceindiacetate DCFHDA oxidation to DCF. Under our experimental conditions, the cements tested, for the most part, were not toxic to leukemic cells at 4 and 24 h. After 24 h, three cements were able to induce cell death, with two eliciting both apoptosis and necrosis, and one cement acting mainly via apoptosis. Both processes of cell death are likely to be mediated by the production of oxygenfree radicals. These findings provide potential leads for investigation into the molecular mechanisms of cell death, which are responsible for tissue damage by cements and intolerance of cemented prostheses. © 2000 John Wiley & Sons, Inc. J Biomed Mater Res, 52, 338–345, 2000.

The genotoxicity of three glass ionomer cements used in dentistry, manufactured by American (Vitrebond™), Japanese (Fuji I™), and European (Ketac Cem™) companies were examined. The cement components were mixed according to the manufacturers' instructions and allowed to set for two defined times: 1 h or 1 week, before extracting them, as established by ISO standard 10993 part 12. To highlight sister chromatid exchange during mitosis, the extracts then were tested with human peripheral lymphocytes in the presence or absence of metabolic activation with S9 mix. The test performed was a genotoxicity test as provided for in standard EN 30993 part 3. Vitrebond™ resulted in direct genotoxicity and was strongly cytotoxic both in the extracts performed at 1 h and those at 1 week if they were allowed to set without photoactivation. Fuji I™ was noncytotoxic and showed only uncertain indirect genotoxicity in the extracts at 1 h; genotoxicity was not present in the extracts at 1 week. Ketac Cem™ cement was not genotoxic nor was it cytotoxic either at 1 h or 1 week. The authors concluded that of the three cements tested the European cement Ketac Cem™ passed one of the tests suggested by the EEC standard for assessing genotoxicy. © 1998 John Wiley & Sons, Inc. J Biomed Mater Res, 40, 545–550, 1998.

The mutagenic potential of three commercially available glass–ionomer cements used in dentistry was examined. The cement components were mixed according to the manufacturers indications and set for two defined times: 1 h or, alternatively, 1 wk. Cements B and C set spontaneously; in the case of cement A, the manufacturer suggests the use of a lamp to trigger also a photopolymerization. Photopolymerization, however, was not used. Ames tests were performed on the dimethyl sulphoxide extracts of cements by using Salmonella typhimurium strains TA 98, TA 100, TA 1535, TA 1537, TA 1538 and TA 102. Cement A showed mutagenicity only against TA 1537 strain, either in the presence or absence of metabolic activation with microsomial fraction S9. The other two cements showed no mutagenic potential. We conclude that glass–ionomer cements are, on the whole, safe materials from the viewpoint of genotoxicity, and hypothesize that the mutagenicity observed in cement A could depend on its polymerization performed without light activation. © 1998 Chapman & Hall

We have evaluated if the cytotoxic effects of metals released from implants are due to necrosis or apoptosis. Peripheral blood mononuclear cells were exposed to different concentrations of chromium, nickel and cobalt extracts and the characteristics of both apoptosis and necrosis were evaluated by flow-cytometry at different culture endpoints. In order to define the prevalence of apoptosis or necrosis, the ratio cell death/apoptosis was calculated. A ratio of ≤1 means the prevalence of apoptotic events; a ratio >1 indicates the acute toxicity of the tested substance (necrosis). The extracts of chromium, cobalt and nickel had a cytotoxic effect on the mononuclear cells; high concentrations of cobalt and nickel produced cell necrosis, whereas by lowering the extract concentration apoptotic phenomena were observed. High chromium concentrations can induce cell death by apoptosis. Our data suggest that when large amounts of nickel and cobalt are released from implanted metal devices, necrosis is produced and consequently a strong inflammatory tissue reaction is likely to occur. The release of either chromium or limited amounts of nickel and cobalt induces toxicity characterized by apoptotic phenomena, which allows an adaptation of the tissue to the implant.

This study was undertaken to evaluate whether the pyrolytic carbon coating of polyethylene terephthalate induces complement activation. Complement activation induced by pyrolytic carbon-coated polyethylene terephthalate (PET+PC) in comparison with uncoated polyethylene terephthalate (PET) was assessed on whole blood collected with heparin. The activation of the classic pathway was evaluated by C4d fragment enzyme immunoassay. The activation of the alternative pathway was evaluated with Bb fragment enzyme immunoassay. The results show that uncoated PET activates the alternative pathway, but not the classic one. PET+PC does not induce complement activation, not even through the alternative pathway. Pyrolytic carbon coating therefore contributes to improving blood compatibility.