Effects of the concentration and composition of in-office bleaching gels on hydrogen peroxide penetration into the pulp chamber.

UNLABELLED: In tooth whitening, the hydrogen peroxide (HP) diffuses in the enamel and dentin, reaching the pulp. This in vitro study aimed to quantify the penetration of HP in the pulp chamber in teeth submitted to bleaching agents of different concentrations of HP without calcium (HP 20% [20CF], HP 35% [35CF]) and with calcium (HP 20% [20CC], HP 35% [35CC]). METHOD: Fifty human premolars were sectioned 3 mm from the cemento-enamel junction and the pulp tissue was removed. The teeth were divided into five groups according to treatment and with a control group (n=10). An acetate buffer solution was placed in the pulp chamber of all teeth. The control group was exposed only to distilled water, while the other groups were treated with a bleaching procedure, according to the manufacturer's recommendations. After treatment, the acetate buffer solution was transferred to a glass tube in which leuco-crystal violet and peroxidase solutions were added, resulting in a blue solution. The optical density of this blue solution was determined spectrophotometrically and converted into micrograms equivalent to the HP. Data were analyzed using analysis of variance and Tukey tests (α=0.05). RESULTS: The HP concentration did not affect the HP inside the pulp chamber, but the presence of calcium significantly reduced it (p<0.0001). CONCLUSION: The amount of HP that reaches the pulp chamber depends on the bleaching protocol and the product employed, and it seems to be less affected by HP concentration.

Prevalence, serologic and genetic studies of high expressers of the blood group A antigen on platelets*.

OBJECTIVE/AIM: The aim of this study is to describe the distribution of the platelet blood group A antigenicity in Euro-Brazilians (EUBs) and Afro-Brazilians (AFBs). BACKGROUND: A small but significant proportion of individuals express high levels of A or B antigen on their platelets corresponding to the erythrocyte ABO group. The mechanism of increased antigen expression has not been elucidated. MATERIAL/METHODS: A cohort of 241 blood group A donors was analysed by flow cytometry. Although mean fluorescence intensity (MFI) is a typical continuous variable, platelets were screened and divided into two categories: low expressers (LEs) and high expressers (HEs). A three-generation family was investigated looking for an inheritance mechanism. RESULTS: The prevalence of the HE platelet phenotype among group A(1) donors was 2%. The mean of MFI on platelets of A(1) subgroup of EUBs differs from that of AFBs (P = 0·0115), whereas the frequency of the HE phenotype was similar between them (P = 0·5251). A significant difference was found between sexes (P = 0·0039). Whereas the serum glycosyltransferase from HE family members converted significantly more H antigen on group O erythrocytes into A antigens compared with that in LE serum, their ABO, FUT1 and FUT2 genes were consensus. The theoretically favourable, transcriptionally four-repeat ABO enhancer was not observed. CONCLUSION: The occurrence of HE in several members suggests familial aggregation. Indeed, in repeated measures, stability of the MFI values is suggesting an inherited condition. Factors outside the ABO locus might be responsible for the HE phenotype. Whether the real mechanism of inheritance is either of a polygenic or of a discrete Mendelian nature remains to be elucidated.