SUMMARYObjective: The current study assessed the efficacy of three current bleaching methods.Methods: Seventy-five healthy subjects (45♀; 30♂) with anterior teeth, having a Vita Shade score of A2 or darker, participated in the study. The subjects were randomly assigned to one of three treatment groups: Group A: home-bleaching (Illumine Home, 10% carbamide peroxide, trays, overnight, for two weeks), Group B: inoffice bleaching (Illumine Office, 15% hydrogen peroxide, trays for 45 minutes, three times over three weeks), Group C: Whitestrips (strips, twice a day, 30 minutes each for two weeks).Following the screening visit, three weeks prior to the baseline examination, all subjects received a dental prophylaxis. Clinical RelevanceThe efficacy of vital bleaching depends on the two aspects-viz, bleaching agent and the bleaching method. Results from this in vivo study show that 10% carbamide peroxide home-bleaching and 15% hydrogen peroxide in-office bleaching were more effective than a 6% hydrogen peroxide home-bleaching over-the-counter product up to three months after completion of the bleaching treatment. M Bizhang • Y-HP Chun • K Damerau P Singh • WH-M Raab • S ZimmerThe color of the teeth was determined using a colorimeter (ShadeEye NCC) and a custom-made stent at baseline (E 0 ), immediately after completion of the bleaching (E 3 ) and three months after treatment (E 4 ). All subjects received oral hygiene instructions and a toothbrush and toothpaste for oral home care during the study period.The change of tooth color was determined for each treatment regimen between baseline and E 3 and baseline and E 4 and was statistically analyzed performing the Kruskal Wallis test and the Mann-Whitney-U test. The significance level was set at p<0.01.Results: The dropout rate was 0%. Mean (SD) ∆E* (overall color change) from baseline to immediately after treatment was 6.57 (2.13) for Group A, 5.77(1.72) for Group B and 3.58 (1.57) for Group C. The mean (SD) tooth color change from baseline to three months after treatment ∆E* was: 4.98(1.34) for Group A, 4.59 (1.42) for Group B and 2.99 (1.39) for Group C. Significant differences were found between home bleaching and Whitestrips, as well as between in-office bleaching and Whitestrips, but not between homebleaching and in-office bleaching during the same time.Conclusion: Using an objective color measurement device, home bleaching and in-office bleaching were found to be superior to Whitestrips. Home bleaching and in-office bleaching were equally efficient for bleaching teeth and maintaining the results for up to three months.

Ameloblastin is a secreted phosphorylated glycoprotein that is processed by protease(s) during enamel formation. We test the hypothesis that Mmp-20 catalyzes the cleavages that generate the Ambn cleavage products that accumulate in developing enamel. We isolated a 23-kDa Ambn cleavage product from developing enamel and determined its N-terminus sequence started at Tyr223. Ameloblastin was stably expressed and secreted from HEK293-H cells, purified and digested with Mmp-20 or Klk4. The digests were analysed by SDS-PAGE and Western blotting, and the cleavage products were characterized by N-terminal sequencing. Six fluorescent peptides were digested with Mmp-20 and Klk4 and analyzed by RP-HPLC and by mass spectrometry. Mmp-20 cleaved each peptide exactly at the sites correspsonding to Ambn cleavages catalyzed in vivo: on the N-terminal sides of Met32, Gln131, Leu171, Tyr223, Leu301, and Tyr343. Klk4 cleaved Ambn and the fluorescent peptides at many sites not observed in vivo, and was only able to cleave at a single correct site: before Leu171. We conclude that Mmp-20 is the enzyme that processes Ambn during the secretory stage of amelogenesis.

Ambn−/− mice fail to make an enamel layer, but the defects could be due to an absence of functional Ambn or to the secretion of a potential toxic mutant Ambn. We hypothesized that the enamel phenotype could be rescued by the transgenic expression of normal Ambn in Ambn−/− mice. We established and analyzed five transgenic lines that expressed Ambn from the amelogenin (AmelX) promoter. We identified transgenic lines that express virtually no transgene, slightly less than normal (Tg+), somewhat higher than normal (Tg++), and much higher than normal (Tg+++) levels of Ambn. All lines expressing detectable levels of Ambn protein at least partially recovered the enamel phenotype. When Ambn expression was only somewhat higher than normal, the enamel covering the molars and incisors was of normal thickness, looked normal, had clearly defined rod and interrod enamel, and held up well in function. We conclude that Ambn is essential for dental enamel formation.