Objectives: The aim of this study was to evaluate the effect of the precipitate that was formed by combining Sodium Hypochlorite (NaOCl) and Chlorhexidine Gluconate (CHX) on the sealing ability of root canal obturation materials.Materials and Methods: The fluid filtration method was conducted on a total of 100 roots. Samples were randomly divided into two control (n=5) and three experimental groups (n=30). The samples in group 1 were irrigated with 1.5 mL of 2.5% NaOCl, and then the smear layers of the teeth were removed by 17% EDTA, while the specimens of group 2 were irrigated by 1.5 mL of 2.5% NaOCl and 1.5 mL of 2% CHX; after the smear layer removal, a final flush with 1.5 mL of 2.5% NaOCl was performed. The samples of group 3 were irrigated the same as group 1 but after the smear layer removal canals were irrigated again with 1.5 mL of 2.5% NaOCl and then a final flush with 1.5 mL of 2% CHX was performed. Teeth were obturated with gutta-percha and AH26 sealer and after seven days, microleakage was evaluated by the fluid filtration technique. The results were analyzed by the ANOVA and Tukey's test.Results: The samples in group 3 had significantly greater microleakage compared to teeth in group 1, 2 (p<0.05), and the specimens in group 1 showed significantly less amount of microleakage than samples in group 2, 3 (p<0.05).Conclusion: The presence of the precipitate that is formed due to interaction between NaOCl and CHX has negative effect on the sealing ability of gutta-percha and AH26 sealer.

Introduction. Tooth avulsion in the young permanent dentition is a frequent finding, and its prognosis depends on the treatment of the avulsed tooth before replantation, the extra-alveolar time, the storage medium, and the patient's general health. The present report describes management of an immature avulsed lower central incisor 90 minutes after the accident. Methods. A right lower central incisor of a 7-year-old girl was avulsed, and it was soaked in a glass of milk. 90 minutes after avulsion, replantation was performed, and the tooth was splinted; but after two weeks the replanted tooth's pulp was necrotic. Thus, endodontic treatment was performed and root canal was filled using a calcium hydroxide and iodoform paste (Metapex). Three months later, the intracanal medication was washed out and the canal was sealed using an apical plug of calcium enriched mixture (CEM) cement. Results. 20 months after replantation the tooth was completely asymptomatic, with physiologic mobility. Also, continued root formation including an apical segment beyond the artificial apical plug was observed. Conclusion. Creation of an appropriate apical barrier following the disinfection of root canal system promoted continued root-end growth in a replanted immature permanent tooth.

Oral cancer presents a major health burden across the globe, specially in developing countries. Kamrup, a district of India, where the KaviKrishna laboratory is located has the highest incidence of oral cancer in the entire world. The mechanism of oral cancer carcinogenesis process is not clearly known. Previous studies indicate the potential role of HPV-16 virus as well as tobacco consumption as major contributing factors of oral cancer. In mouse, the carcinogen agent 4-NQO was found to induce oral cancer having similar phenotype as human oral mucosa cancer. 4-NQO may exert tobacco like oxidative stress toxicity to oral mucosa. Hence, developing both in vitro and in vivo models of HPV-16 and 4-NQO mediated oral carcinogenesis might help to understand the initiating event of oral carcinogenesis. In this study, we propose that oral mucosa stem cells (OMSCs) could be the target of HPV-16, and 4-NQO induced carcinogensis. Thus, in vitro treatment of oral mucosa cells of healthy human volunteers with HPV-16 protein E6, and 4-NQO led to expansion of CD271+ cells, which are enriched in OMSCs. Importantly, the expanded CD271+ cells exhibited high HIF-2alpha, low p53, and high glutathione secretion, a phenotype of stem cell altruism that we recently described in human embryonic stem cells (Das B et al. Stem Cells, 2012). In human ES cells, the altruistic reprogramming served as an initiating event of malignant transformation by altering p53/MDM2 oscillation, in an abnormal state of low p53 and high MDM2. Therefore, we performed a complete evaluation of E6 protein and 4-NQO treated CD271+ oral mucosa cells for altruistic behavior, including low p53 and high MDM2 state. For this purpose, the carcinogen treated oral mucosa cells were subjected to immunomagnetic sorting for CD271+ cells. We found that post-carcinogen treated CD271+ cells exhibited in vitro self-renewal activity, high GSH secretion, and importantly activation of a HIF-2alpha/MYC co-operation. ChiP assay revealed the MYC binding to HIF-2alpha, and Sox-2, an stemness associated transcription factor. Importantly, HIF-2alpha was important for the reversible but prolonged suppression of p53 for more than two weeks. We also found that the high HIF-2alpha and low p53 expressing CD271+ cells could be enriched in a ABCG2+ population. Thus, we were able to enrich a CD271+/ABCG2+ cell population in oral mucosa cells of both human and mouse. Based on these findings we propose to use HPV-16 and 4NQO derived carcinogenesis models to study the potential role of altruistic reprogramming in the malignant transformation of oral mucosa stem cells to oral cancer stem cell like cells. Our study may unravel a novel mechanism of malignant transformation, the failure of altruistic stem cells to sacrifice its fitness (altruism) as a potential initiating event of malignant transformation of stem cells to cancer stem cells. Citation Format: Sukanya Gayan, Hong Li, Rashmi Bhuyan, Sora Sandhya, Joyeeta Talukdar, Bidisha Pal, Jaishree Garhyan, Wael Tasabehji, Manaf Muhammad Alkurdi, Heidar Zohrehei, Seema Bhuyan, Anupam Sarma, Gayatri Gogoi, A.C. Kataki, Rakesh Bhatnagar, Debabrata Baishya, Bikul Das. The potential role of oral mucosa stem cell altruistic behavior as the initiating event of malignant transformation. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 4073.