Dental bleaching has become one of the most frequently requested esthetic treatments in dental offices. Despite the high clinical success observed with this procedure, some adverse effects have been reported, including a potential for developing premalignant lesions, root resorption and tooth sensitivity, especially when misused. The aim of this study was to evaluate the genotoxic response using a micronucleus (MN) assay, after the application of two concentrations of carbamide peroxide. Thirty-seven patients were divided into two groups and randomly received either a 10% carbamide peroxide (CP) (19) or a 16% carbamide peroxide (18) concentration for 21 days in individual dental trays. Gingival margin cells were collected immediately before the first use (baseline), and then 15 and 45 days after baseline. The cells were placed on a histological slide, stained by the Feulgen technique, and evaluated by an experienced blinded examiner. One thousand cells per slide were counted, and the MN rate was determined. The two groups were analyzed by the Wilcoxon rank-sum test and the Kruskal-Wallis equality-of-populations rank test. A slight increase in MN was observed for both groups, in comparison with the baseline, at 15 days. However, no difference was observed between the two groups (10% and 16%), at either 15 or 45 days (p = 0.90). When bleaching is not prolonged or not performed very frequently, bleaching agents containing carbamide peroxide alone will not cause mutagenic stress on gingival epithelial cells.
Introduction: Obesity is characterized by extreme body fat accumulation related to lean body mass. The low-grade systemic inflammation induced by weight gain may influence wound healing. This study assessed the association between obesity and alveoli repair after tooth extraction. Methods: Forty-two male Wistar rats were randomly divided into two groups: weight gain (n = 21), animals fed with hyperlipidic cafeteria diet in order to gain weight; and control (non-obese; n = 21) regularly fed rats. After twelve weeks, the upper right central incisor was extracted and animals were sacrificed after 7, 14 and 28 days. Slides were obtained for histological analysis. Bone formation and protein expression at the different periods were compared using Kruskal-Wallis test and Dunn post-test. Results: Bone area was higher in the control group all over the experiment with more TRAP-positive cells and TRAP-positive labeling in the weight gain group. RANKL was homogeneously expressed along the experiment with no differences among the groups; conversely OPG levels reduced in the weight gain groups 14 and 28 days after tooth extraction. Osteocalcin labeling was higher in the control group after 7 days of extraction, with no differences at later time points. VEGF labeling was higher in the control group after 14 days of tooth extraction while the strongest immunolabeling in the weight gain group was observed 21 days post-extraction. Conclusion: Weight gain induced a delay in bone repair after tooth extraction. The increase in the number of TRAP-positive cells observed in the extraction site seems to be mediated by the reduction in the expression of OPG rather than an overexpression of RANKL. In addition, the late expression of VEGF in the weight gain group might have delayed osteoblast migration and differentiation.
Sustained inflammation in tumor microenvironment promotes tumor growth and progression. We previously demonstrated the inflammasome activation and autoinflammation associated with the development of human melanoma. In this study, we investigated how tumor autoinflammation/ inflammasome activation affects the expression of immune checkpoints (ICP) molecules (PD-L1 and PD-L2) in melanoma. Compared to early-stage melanoma, late-stage human melanoma expressed higher ICP molecules. The expression of ICP molecules greatly increased upon the stimulation of pro-inflammatory cytokines, whereas the inhibition of autoinflammation, especially the NLRP3 inflammasome-IL-1 signaling pathway, decreased the expression of ICP molecules. This inhibitory effect was more evident on PD-L2 expression, suggesting PD-L2 expression is more related with autoinflammation/inflammasome activation in human melanoma. Further analysis revealed that the inflammasome activation augmented IFNg-induced ICP molecules through STAT-IRFand NLRP3-IL1B pathways. We found that epigallocatechin gallate (EGCG), the most abundant catechin in tea, inhibited both STAT-IRF and NLRP3-IL1B pathway and deceased the autoinflammation and ICP expression both in vitro and in vivo. To investigate anti-tumor immune responses, B16F10 mouse melanoma cells were used. EGCG increased CD8+ T cell killing against B16F10 cells in vitro. EGCG also inhibited tumor PD-L1 expression and tumor progression of B16F10 in C57BL/6 mice, and this suppressive effect was equivalent PD-1 antibody treatment. In summary, these findings for the first time associate the autoinflammation/inflammasome and ICP molecules expression. Inhibition of both autoinflammation and ICP molecules expression with EGCG might serve as a novel cancer therapy.
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