PURPOSE: This study evaluated color stability of Dentca 3D-printed denture teeth, in comparison to color stabilities of four conventional types of denture teeth, upon being immersed in various colorants.MATERIALS AND METHODS: Four types of conventional prefabricated denture teeth (Surpass, GC, Artic 6, Heraeus Kulzer, Premium 6, Heraeus Kulzer, Preference, Candulor), 3D-printed denture teeth (Dentca); and Z250 (Filtek Z250, 3M ESPE) were prepared for testing. The samples were immersed in erythrosine 3%, coffee, cola, and distilled water (DW) at 37℃. Color change (ΔE) was measured by spectrophotometer before immersion and at 7, 14, and 21 days after immersion. One-way analysis of variance was performed along with Tukey's honestly significant difference multiple comparisons test (P<.05).RESULTS: No great difference was observed between the color change of Dentca denture teeth and that of conventional denture teeth in most cases (P>.05). The color change of Dentca denture teeth immersed in erythrosine 3% was greater than that of Surpass (ΔE = 0.67 ± 0.25) after 1 week; Artic 6 (ΔE = 1.44 ± 0.38) and Premium 6 (ΔE = 1.69 ± 0.35) after 2 weeks; and Surpass (ΔE = 1.79 ± 0.49), Artic 6 (ΔE = 2.07 ± 0.21), Premium 6 (ΔE = 2.03 ± 0.75), and Preference (ΔE = 2.01 ± 0.75) after 3 weeks (P<.05).CONCLUSION: A color change was observed in Dentca denture teeth when immersed in some colorants; however, the maximum value of ΔE for Dentca denture teeth was within the clinically acceptable range.
Coffee ; Cola ; Dentures ; Erythrosine ; Immersion ; Printing, Three-Dimensional ; Tooth ; Water

Parkinson's disease is a neurological disorder characterized by tremor, bradykinesia, akinesia, postural instability, and muscular rigidity, which is caused by the depletion of neurotransmitters such as dopamine. Cooperative dental treatment is more challenging because of tremor of Parkinson's disease. In this case, a 47-year-old Parkinson's disease patient with chronic periodontitis was treated with full-mouth rehabilitation using conventional fixed prostheses and implant fixed partial denture, which attained satisfactory outcomes functionally and esthetically. Short term periodic follow-ups will be needed with consideration for the characteristics of Parkinson's disease such as decreased manual dexterity.

BACKGROUND: Non-alcoholic fatty liver disease is the most common form of chronic liver disease in industrialized countries. Recent studies have highlighted the association between peroxisomal dysfunction and hepatic steatosis. Peroxisomes are intracellular organelles that contribute to several crucial metabolic processes, such as facilitation of mitochondrial fatty acid oxidation (FAO) and removal of reactive oxygen species through catalase or plasmalogen synthesis. Statins are known to prevent hepatic steatosis and non-alcoholic steatohepatitis (NASH), but underlying mechanisms of this prevention are largely unknown. METHODS: Seven-week-old C57BL/6J mice were given normal chow or a methionine- and choline-deficient diet (MCDD) with or without various statins, fluvastatin, pravastatin, simvastatin, atorvastatin, and rosuvastatin (15 mg/kg/day), for 6 weeks. Histological lesions were analyzed by grading and staging systems of NASH. We also measured mitochondrial and peroxisomal FAO in the liver. RESULTS: Statin treatment prevented the development of MCDD-induced NASH. Both steatosis and inflammation or fibrosis grades were significantly improved by statins compared with MCDD-fed mice. Gene expression levels of peroxisomal proliferator-activated receptor α (PPARα) were decreased by MCDD and recovered by statin treatment. MCDD-induced suppression of mitochondrial and peroxisomal FAO was restored by statins. Each statin's effect on increasing FAO and improving NASH was independent on its effect of decreasing cholesterol levels. CONCLUSION: Statins prevented NASH and increased mitochondrial and peroxisomal FAO via induction of PPARα. The ability to increase hepatic FAO is likely the major determinant of NASH prevention by statins. Improvement of peroxisomal function by statins may contribute to the prevention of NASH.
Animals ; Atorvastatin Calcium ; Catalase ; Cholesterol ; Developed Countries ; Diet ; Fatty Liver* ; Fibrosis ; Gene Expression ; Hydroxymethylglutaryl-CoA Reductase Inhibitors* ; Inflammation ; Liver Diseases ; Liver* ; Metabolism ; Mice* ; Non-alcoholic Fatty Liver Disease ; Organelles ; Peroxisomes ; Pravastatin ; Reactive Oxygen Species ; Rosuvastatin Calcium ; Simvastatin