Background: The ectodysplasin A ( EDA) gene plays a crucial role in tooth development by regulating epithelial–mesenchymal interactions during odontogenesis. Genetic variations in this pathway may influence susceptibility to congenital tooth agenesis, including non-syndromic mandibular incisor agenesis, a specific dental phenotype with a complex genetic basis. Aim: To investigate the association between EDA rs12853659 polymorphism and susceptibility to non-syndromic mandibular incisor agenesis in the South Indian population. Materials and methods: A case–control study was conducted among 60 unrelated individuals comprising 30 cases with non-syndromic mandibular incisor agenesis and 30 controls with complete permanent dentition, aged 13–40 years. Genomic deoxyribonucleic acid (DNA) was isolated from peripheral blood samples, and EDA rs12853659 genotyping was performed using amplification-refractory mutation system polymerase chain reaction (ARMS-PCR). Genotype frequencies, allele frequencies, and allele-carrier frequencies were analyzed and Hardy–Weinberg equilibrium was assessed. Results: The CT genotype was predominant among cases (80%), whereas the TT genotype was absent among affected individuals. C-allele carrier frequency was significantly higher in cases than controls (100% vs. 83.3%; χ 2 = 5.45, p = 0.02). T-allele carrier frequency was identical in both groups (80%; χ 2 = 0.00, p = 1.00). The control group was in Hardy–Weinberg equilibrium, whereas the case group showed deviation from equilibrium. Conclusion: The findings suggest C-allele carrier status of the EDA rs12853659 polymorphism may be associated with susceptibility to non-syndromic mandibular incisor agenesis in the studied South Indian population.
Background The relative influence of age, sex, and site on craniofacial suture/synchondrosis patency after maxillary skeletal expansion is unclear. We evaluated these predictors across four sites, accounting for within-subject correlation. Methods In this cross-sectional study, 108 adults (age 18–58 years) were assessed by CBCT for patency (closed/fused vs. open) at the pterygomaxillary, sphenovomerine, frontonasal, and frontozygomatic sutures (432 observations). Generalized estimating equations (binomial, logit link, exchangeable correlation) modeled patency by age and site, with secondary age-by-site, site-by-separation-status, and site-by-sex interaction models. Results Age was not significantly associated with patency after adjusting for site (OR = 0.98, 95% CI: 0.96–1.01, p = 0.166). Site significantly predicted patency (Wald χ2(4) = 27.98, p < 0.001): frontonasal patency was significantly lower than the other three sites (all p < 0.001), which did not differ from each other, across the observed age range. Separation status was positively associated with pterygomaxillary patency (OR = 2.36, p = 0.042) and similarly at the frontozygomatic suture, but inversely with frontonasal patency (interaction p = 0.021). Sex showed no uniform association with patency (p = 0.214), but a site-by-sex interaction revealed higher patency odds in males at the frontonasal (OR = 4.06, 95% CI: 1.51–10.96, p = 0.006) and sphenovomerine sutures (OR = 2.34, 95% CI: 1.03–5.30, p = 0.041), with no effect elsewhere. Conclusions The frontonasal suture was more resistant to opening than the other sites, independent of age, with an inverse relationship to separation success and a male-predominant sex effect absent elsewhere. These findings suggest the frontonasal and, to a lesser extent, sphenovomerine sutures follow a distinct pathway shaped by sex and treatment outcome, warranting confirmation in larger, prospective studies.
Background The ectodysplasin A (EDA) gene plays a crucial role in tooth development by regulating epithelial–mesenchymal interactions during odontogenesis. Genetic variations in this pathway may influence susceptibility to congenital tooth agenesis, including non-syndromic mandibular incisor agenesis, a specific dental phenotype with a complex genetic basis. Aim To investigate the association between EDA rs12853659 polymorphism and susceptibility to non-syndromic mandibular incisor agenesis in the South Indian population. Materials and methods A case–control study was conducted among 60 unrelated individuals comprising 30 cases with non-syndromic mandibular incisor agenesis and 30 controls with complete permanent dentition, aged 13–40 years. Genomic deoxyribonucleic acid (DNA) was isolated from peripheral blood samples, and EDA rs12853659 genotyping was performed using amplification-refractory mutation system polymerase chain reaction (ARMS-PCR). Genotype frequencies, allele frequencies, and allele-carrier frequencies were analyzed and Hardy–Weinberg equilibrium was assessed. Results The CT genotype was predominant among cases (80%), whereas the TT genotype was absent among affected individuals. C-allele carrier frequency was significantly higher in cases than controls (100% vs. 83.3%; χ2 = 5.45, p = 0.02). T-allele carrier frequency was identical in both groups (80%; χ2 = 0.00, p = 1.00). The control group was in Hardy–Weinberg equilibrium, whereas the case group showed deviation from equilibrium. Conclusion The findings suggest C-allele carrier status of the EDA rs12853659 polymorphism may be associated with susceptibility to non-syndromic mandibular incisor agenesis in the studied South Indian population.
Objectives The clinical performance of root-end filling materials may influence the success of endodontic microsurgery. This in-vitro study evaluated two placement techniques using bioceramic materials under dry, synthetic tissue fluid (STF), and blood-contaminated conditions. Methods Seventy-two maxillary anterior teeth were subjected to standardized endodontic therapy, followed by root-end resection and retro-preparation. The specimens were randomly allocated to dry, STF, and blood (n = 24 per condition) conditions, and subdivided by root-end filling technique (n = 12): traditional packing (T), using Bio-C Repair, and deep putty packing (DPP), using Bio-C Repair with Bio-C Sealer incorporation. Following a 28-days incubation period, the two outermost 1-mm obtained discs containing the retrograde filling were evaluated by SEM for marginal adaptation and push-out bond strength (POBS) test. The data were analyzed using one-way ANOVA with post-hoc comparison and independent T-test, P < 0.05. Results Under STF condition, the traditional protocol produced significantly larger interfacial gaps (4.310 ± 1.221 μm), than under dry and blood contaminated condition (p < 0.001). No significant differences in marginal adaptation were detected among contamination conditions with the DPP protocol (p = 0.806). Blood contamination significantly reduced the push-out bond strength in both placement groups (P < 0.05), while the two protocols showed comparable bond strengths under all conditions (p > 0.05). Conclusion DPP demonstrated greater consistency in marginal adaptation across the tested contaminations, whereas POBS adversely affected by the blood contamination in both placement techniques. Neither packing technique demonstrated a significant overall advantage in POBS.
Objective(s) To evaluate the effect of aluminum chloride (AlCl3)–based hemostatic agent contamination and various decontamination protocols on the shear bond strength (SBS) of a universal adhesive applied in self-etch mode, and to assess resin–dentin interface adaptation using scanning electron microscopy (SEM). Materials and methods Eighty-four extracted human molars were prepared and randomly assigned to seven groups (n = 12): control, contaminated, and five decontamination groups (water, sodium hypochlorite [NaOCl], chlorhexidine [CHX], phosphoric acid, and ethylenediaminetetraacetic acid [EDTA]). Following contamination and respective surface treatments, Prime & Bond Universal adhesive was applied in self-etch mode. Composite cylinders were bonded to dentin surfaces, and SBS was measured. One specimen from each group was subjected to SEM analysis to evaluate the resin–dentin interface. Data was analyzed using one-way analysis of variance (ANOVA) and Tukey's post hoc test (p < 0.05). Results Contamination with the hemostatic agent significantly reduced SBS (p < 0.001). Decontamination with NaOCl, phosphoric acid, and CHX restored bond strength to values comparable to the control group (p > 0.05). In contrast, water and EDTA groups showed significantly lower SBS than the control (p < 0.05). SEM analysis supported these findings, demonstrating improved interfacial adaptation in NaOCl, phosphoric acid, and CHX-treated groups. Conclusion(s) AlCl3-based hemostatic agent contamination adversely affected bonding performance. Decontamination with NaOCl, phosphoric acid, and CHX effectively restored bond strength and interfacial integrity, whereas water and EDTA were less effective.
