Comparison of additive manufactured models of the mandible in accuracy and quality using six different 3D printing systems.

The aim of this study was to analyze and compare the accuracy and quality of six 3D printing systems available on the market. Data acquisition was performed with 12 scans of human mandibles using an industrial 3D scanner and saved in STL format. These STL files were printed using six different printing systems. Previously defined distances were measured with a sliding caliper on the 72 printed mandibles. The printed models were then scanned once again. Measurements of volumes and surfaces for the STL files and the printed models were compared. Accuracy and quality were evaluated using industrial software. An analysis of the punctual aberration between the template and the printed model, based on a heat map, was also carried out. Secondary factors, such as costs, production times and expendable materials, were also examined. All printing systems performed well in terms of accuracy and quality for clinical usage. The Formiga P110 and the Form 2 showed the best results for volume, with average aberrations of 0.13 ± 0.23 cm3 and 0.12 ± 0.17 cm3, respectively. Similar results were achieved for the heat map aberration, with values of 0.008 ± 0.11 mm (Formiga P110) and 0.004 ± 0.16 mm (Form 2). Both printers showed no significant difference from the optimal neutral line (Formiga P110, p = 0.15; Form 2, p = 0.60). The cheapest models were produced by the Ultimaker 2+, with an average of 5€ per model, making such desktop printers affordable for rapid prototyping. Meanwhile, advanced printing systems with sterilizable and biocompatible printing materials, such as the Formiga P110 and the Form 2, fulfill the high expectations for maxillofacial surgery.

Natural resistance to ascorbic acid induced oxidative stress is mainly mediated by catalase activity in human cancer cells and catalase-silencing sensitizes to oxidative stress.

BACKGROUND: Ascorbic acid demonstrates a cytotoxic effect by generating hydrogen peroxide, a reactive oxygen species (ROS) involved in oxidative cell stress. A panel of eleven human cancer cell lines, glioblastoma and carcinoma, were exposed to serial dilutions of ascorbic acid (5-100 mmol/L). The purpose of this study was to analyse the impact of catalase, an important hydrogen peroxide-detoxifying enzyme, on the resistance of cancer cells to ascorbic acid mediated oxidative stress. METHODS: Effective concentration (EC(50)) values, which indicate the concentration of ascorbic acid that reduced the number of viable cells by 50%, were detected with the crystal violet assay. The level of intracellular catalase protein and enzyme activity was determined. Expression of catalase was silenced by catalase-specific short hairpin RNA (sh-RNA) in BT-20 breast carcinoma cells. Oxidative cell stress induced apoptosis was measured by a caspase luminescent assay. RESULTS: The tested human cancer cell lines demonstrated obvious differences in their resistance to ascorbic acid mediated oxidative cell stress. Forty-five percent of the cell lines had an EC(50) > 20 mmol/L and fifty-five percent had an EC(50) < 20 mmol/L. With an EC(50) of 2.6-5.5 mmol/L, glioblastoma cells were the most susceptible cancer cell lines analysed in this study. A correlation between catalase activity and the susceptibility to ascorbic acid was observed. To study the possible protective role of catalase on the resistance of cancer cells to oxidative cell stress, the expression of catalase in the breast carcinoma cell line BT-20, which cells were highly resistant to the exposure to ascorbic acid (EC(50): 94,9 mmol/L), was silenced with specific sh-RNA. The effect was that catalase-silenced BT-20 cells (BT-20 KD-CAT) became more susceptible to high concentrations of ascorbic acid (50 and 100 mmol/L). CONCLUSIONS: Fifty-five percent of the human cancer cell lines tested were unable to protect themselves against oxidative stress mediated by ascorbic acid induced hydrogen peroxide production. The antioxidative enzyme catalase is important to protect cancer cells against cytotoxic hydrogen peroxide. Silenced catalase expression increased the susceptibility of the formerly resistant cancer cell line BT-20 to oxidative stress.