RESUMO
Taurodontism is a dental anomaly caused due to the failure of Hertwig's epithelial sheath to invaginate at the proper horizontal level. A huge pulp chamber, displacement of the pulpal floor apically, and no constriction at the level of the cementoenamel junction are the key features representing a taurodontic tooth. This condition is most commonly associated with permanent molars. This clinical entity occurs in the form of an isolated, singular trait in majority of the cases. However, seldom, it may be associated with syndromes or ectodermal anomalies. The large and deep pulp chamber makes instrumentation of canals difficult, thereby challenging an endodontist. This case report describes the endodontic challenge faced in cases of taurodontism as well as the clinical steps involved in its successful endodontic management. Furthermore, it shows the typical presence of bilateral hypertaurodontism with respect to the maxillary first molar.
RESUMO
Orofacial clefts are the most prevalent craniofacial birth defects and these malformations transform an infant with severe functional and esthetic handicaps. Cleft lip and palate is a common malformation that occurs in about 2 in 1000 live births. The cleft can vary from a hardly visible furrow in the palate or on one side of the lip to bilateral complete clefts of the lip, alveolus and palate. Clefts of the lip, alveolus and palate are highly complicated malformations. The problems associated such as speech, function, esthetic, and socio-psychological and more precisely deleterious effect on the growth and development of teeth, alveolus and jaws. A specialized corrective surgery is mandatory and indicated in early months of life to achieve the best outcome to improve the function and appearance. We are presenting a case of unilateral incomplete cleft lip with primary repair in a 4months and 20days baby boy.
RESUMO
Aim: To explore the molecular pathophysiology that might explain the epidemiologic association between cigarette smoke and age-related macular degeneration (AMD) by examining the effects of hydroquinone (HQ), a toxic compound present in high concentration in cigarette smoke-related tar, on human retinal pigment epithelial cells (ARPE-19), rat retinal neurosensory cells (R-28), and human microvascular endothelial cells (HMVEC). Materials and Methods: ARPE-19, R-28, and HMVEC were treated for 24 h with four different concentrations of HQ (500 μM, 200 μM, 100 μM, 50 μM). Cell viability, caspase-3/7 activation, DNA laddering patterns, and lactate dehydrogenase (LDH) levels were analyzed. Results: At 50 μM HQ, R-28 cells showed a significant decrease in cell viability compared with the dimethyl sulfoxide (DMSO)-treated controls. At the 100–500 μM concentrations, all three cell lines showed significant cell death (P < 0.001). In the ARPE-19, R-28, and HMVEC cultures, the caspase-3/7 activities were not increased at any of the HQ concentration. Conclusion: Our findings suggest that the mechanism of cell death in all three cell lines was through non-apoptotic pathway. In addition, neuroretinal R-28 cells were more sensitive to HQ than the ARPE-19 and HMVEC cultures.