Effect of charcoal dentifrices on tooth whitening and enamel surface roughness.

PURPOSE: To evaluate tooth color change and surface roughness after the use of charcoal dentifrices. METHODS: Bovine teeth (n= 64) used for color measurements were stained in tea solution and embedded in acrylic resin. Specimens were randomized into four groups of 16 specimens each. Cavity Protection (Colgate-Palmolive) was the negative control. Whitening dentifrices used were Black is White (Curaden AG); and My Magic Mud (Carbon and Clay Company) containing activated charcoal and Optic White (Colgate-Palmolive) containing hydrogen peroxide. Instrumental color measurements were performed at baseline, 1-week post-brushing, 30-day post-brushing, and 1-month follow-up. Another set of bovine teeth (n= 64) used for roughness measurements were embedded in acrylic resin and the surface ground flat. The experimental groups and brushing protocol were the same as for the color evaluation part. Surface roughness was measured with a contact type profilometer at baseline and after the last brushing session. Kruskal-Wallis procedure tested changes in color and surface roughness among the different groups. All post-hoc comparisons were conducted with Bonferroni corrections. Tests of hypotheses were two-sided with an alpha level at 0.05. RESULTS: Overall color change was not significantly different among groups at 1-week post-brushing and at 1-month follow-up. However, the hydrogen peroxide group had a significantly higher reduction in chroma in the yellow-blue axis when compared to negative control group at 30-day post-brushing and 1-month follow-up (P< 0.05). There was no significant difference in roughness among the groups at baseline (P= 0.2973) and post treatment (P= 0.8169). CLINICAL SIGNIFICANCE: The use of charcoal dentifrices did not have the claimed whitening effect but did not increase enamel surface roughness.

Stratification of pediatric ALL by in vitro cellular responses to DNA double-strand breaks provides insight into the molecular mechanisms underlying clinical response.

The molecular basis of different outcomes in pediatric acute lymphoblastic leukemia (ALL) remains poorly understood. We addressed the clinical significance and mechanisms behind in vitro cellular responses to ionizing radiation (IR)-induced DNA double-strand breaks in 74 pediatric patients with ALL. We found an apoptosis-resistant response in 36% of patients characterized by failure to cleave caspase-3, -7, -9, and PARP1 by 24 hours after IR and an apoptosis-sensitive response with the cleavage of the same substrates in the remaining 64% of leukemias. Resistance to IR in vitro was associated with poor early blast clearance at day 7 or 15 and persistent minimal residual disease (MRD) at day 28 of induction treatment. Global gene expression profiling revealed abnormal up-regulation of multiple prosurvival pathways in response to IR in apoptosis-resistant leukemias and differential posttranscriptional activation of the PI3-Akt pathway was observed in representative resistant cases. Importantly, pharmacologic inhibition of selected prosurvival pathways sensitized apoptosis-resistant ALL cells to IR in vitro. We suggest that abnormal prosurvival responses to DNA damage provide one of the mechanisms of primary resistance in ALL, and that they should be considered as therapeutic targets in children with aggressive disease.