Evaluation of Extrusion and Apical Seal of Thermafil™ Obturation with and without MTA as an Apical Barrier in Comparison with Lateral Condensation Technique: An In Vitro Study.

AIM AND OBJECTIVE: This study aimed to compare the apical sealing ability and periapical extrusion in the Thermafil™ obturation technique, with and without an apical barrier of MTA, with lateral condensation technique. MATERIALS AND METHODS: Sixty freshly extracted human central incisors were instrumented with the crown down technique and divided into three experimental groups. Group I: lateral condensation technique obturation, group II: Thermafil obturation (DENTSPLY Tulsa), and group III: this group was obturated into two parts; first MTA (ProRoot) was placed in apical 3 mm and later the remaining canal was obturated with Thermafil™ obturation technique (DENTSPLY Tulsa). AH Plus sealer was used in all the groups. Specimens of all the groups were layered with nail paint excluding the apical 3 mm. Twenty-four hours later, all the teeth were suspended in Black India ink for 48 hours. Finally, all the teeth were decalcified, rendered transparent and linear dye leakage and periapical extrusion was measured using ×60 magnification of stereomicroscope with an in-built ruler. RESULTS: A Chi-square test done to evaluate periapical extrusion showed there was a significant difference found among all the groups (p < 0.05), whereas in case of linear apical dye leakage using a Student's "t" test showed there was no significant difference among all the groups (p > 0.05). CONCLUSION: Despite showing apical leakage, the thermo-plasticized gutta-percha obturation technique can be advantageous when used with MTA as an apical barrier since there is no scope for apical extrusion along with the benefit of three-dimensional obturation of the root canal system when compared with the lateral condensation technique. HOW TO CITE THIS ARTICLE: Rao AS, Mathur R, Shah NC, et al. Evaluation of Extrusion and Apical Seal of Thermafil™ Obturation with and without MTA as an Apical Barrier in Comparison with Lateral Condensation Technique: An In Vitro Study. Int J Clin Pediatr Dent 2020;13(S-1):S40-S44.

TCF7L1 promotes skin tumorigenesis independently of ß-catenin through induction of LCN2.

The transcription factor TCF7L1 is an embryonic stem cell signature gene that is upregulated in multiple aggressive cancer types, but its role in skin tumorigenesis has not yet been defined. Here we document TCF7L1 upregulation in skin squamous cell carcinoma (SCC) and demonstrate that TCF7L1 overexpression increases tumor incidence, tumor multiplicity, and malignant progression in the chemically induced mouse model of skin SCC. Additionally, we show that downregulation of TCF7L1 and its paralogue TCF7L2 reduces tumor growth in a xenograft model of human skin SCC. Using separation-of-function mutants, we show that TCF7L1 promotes tumor growth, enhances cell migration, and overrides oncogenic RAS-induced senescence independently of its interaction with ß-catenin. Through transcriptome profiling and combined gain- and loss-of-function studies, we identified LCN2 as a major downstream effector of TCF7L1 that drives tumor growth. Our findings establish a tumor-promoting role for TCF7L1 in skin and elucidate the mechanisms underlying its tumorigenic capacity.

Tcf3 promotes cell migration and wound repair through regulation of lipocalin 2.

Cell migration is an integral part of re-epithelialization during skin wound healing, a complex process involving molecular controls that are still largely unknown. Here we identify a novel role for Tcf3, an essential transcription factor regulating embryonic and adult skin stem cell functions, as a key effector of epidermal wound repair. We show that Tcf3 is upregulated in skin wounds and that Tcf3 overexpression accelerates keratinocyte migration and skin wound healing. We also identify Stat3 as an upstream regulator of Tcf3. We show that the promigration effects of Tcf3 are non-cell autonomous and occur independently of its ability to interact with ß-catenin. Finally, we identify lipocalin-2 as the key secreted factor downstream of Tcf3 that promotes cell migration in vitro and wound healing in vivo. Our findings provide new insights into the molecular controls of wound-associated cell migration and identify potential therapeutic targets for the treatment of defective wound repair.