Turner syndrome (TS) is a chromosomal disorder caused by monosomy of the X chromosome, with complete or partial absence of the second sex chromosome. Anomalies of root morphology have been found to occur more often in patients with TS, which make endodontic treatment challenging and requires special handling. The patients with TS may also have systematic problems such as cardiac or renal malformations, so in treating these patients it is important for clinicians not only to be aware of the characteristic intraoral findings, but also to make the patients have regular dental check-ups to prevent oral complications in advance.An 12-year-old girl who had been diagnosed with TS at the age of 10 years was referred due to discomfort in the bilateral mandibular premolar regions. Dens evaginatus and taurodontism were detected in all the mandibular premolars characteristically. The bilateral mandibular first premolars had three roots and the bilateral mandibular second premolars had periapical lesion with two roots. Due to the complexity of the root canal anatomy, root canal treatment were completed with a dental microscope to ensure adequate visualization. After 2 years of regular follow-up examinations, there were no clinical sign or symptom associated with the teeth, and no periapical lesion, was found.This case report describes the characteristic oral features and dental management of TS patients.
Bicuspid ; Child ; Chromosome Disorders ; Dental Pulp Cavity ; Female ; Follow-Up Studies ; Humans ; Monosomy ; Sex Chromosomes ; Tooth ; Turner Syndrome ; X Chromosome

Benzo[a]pyrene (B[a]P) is a polycyclic aromatic hydrocarbon and ubiquitous environmental toxin with known harmful effects to human health. Abnormal phenotypes of keratinocytes are closely associated with their exposure to B[a]P. Resorcinol is a component of argan oil with reported anticancer activities, but its mechanism of action and potential effect on B[a]P damage to the skin is unknown. In this study, we investigated the effects of resorcinol on B[a]P-induced abnormal keratinocyte biology and its mechanisms of action in human epidermal keratinocyte cell line HaCaT. Resorcinol suppressed aryl hydrocarbon receptor (AhR) activity as evidenced by the inhibition of B[a]P-induced xenobiotic response element (XRE)-reporter activation and cytochrome P450 1A1 (CYP1A1) expression. In addition, resorcinol attenuated B[a]P-induced nuclear translocation of AhR, and production of ROS and pro-inflammatory cytokines. We also found that resorcinol increased nuclear factor (erythroid-derived 2)-like 2 (Nrf2) activity. Antioxidant response element (ARE)-reporter activity and expression of ARE-dependent genes NAD(P)H dehydrogenase [quinone] 1 (NQO1), heme oxygenase-1 (HO-1) were increased by resorcinol. Consistently, resorcinol treatment induced nuclear localization of Nrf2 as seen by Western analysis. Knockdown of Nrf2 attenuated the resorcinol effects on ARE signaling, but knockdown of AhR did not affect resorcinol activation of Nrf2. This suggests that activation of antioxidant activity by resorcinol is not mediated by AhR. These results indicate that resorcinol is protective against effects of B[a]P exposure. The mechanism of action of resorcinol is inhibition of AhR and activation of Nrf2-mediated antioxidant signaling. Our findings suggest that resorcinol may have potential as a protective agent against B[a]P-containing pollutants.