Parental acceptability of silver diamine fluoride: The UK and US experiences.

BACKGROUND: International data suggest that parents may have reservations about the use of silver diamine fluoride (SDF). AIM: The aims of this study were to: (1) examine the acceptance of parents/carers towards the use of SDF for the management of caries in children's primary teeth in secondary care dental settings in the UK and the United States and (2) determine which factors may affect the acceptance of the use of SDF. DESIGN: This was a cross-sectional questionnaire of SDF acceptability, completed by parents of young children. It was validated and adapted to local populations. Data were analysed with descriptive and inferential statistics. RESULTS: Of the 113 Sheffield parents, 73% reported that they would accept SDF treatment of children's posterior teeth, with 58% reporting this for anterior teeth. Parents having less concern about posterior aesthetics had a statistically significant effect on reported acceptance of SDF (p = .013). In the Colorado sample (n = 104), 72% reported that they would accept SDF on posterior teeth, and 58% reported that they would accept SDF on anterior teeth. Concerns about aesthetics had an effect on decreasing SDF acceptance overall (p = .0065) in anterior (p = .023) and posterior teeth (p = .108). CONCLUSION: The majority of parents in the two study populations accepted the treatment using SDF. However, concern about aesthetics had an influence on acceptability.

Dithianon exposure induces dopaminergic neurotoxicity in Caenorhabditis elegans.

Dithianon is a conventional broad-spectrum protectant fungicide widely used in agriculture, but its potential neurotoxic risk to animals remains largely unknown. In this study, neurotoxic effects of Dithianon and its underlying cellular and molecular mechanisms were investigated using the nematode, Caenorhabditis elegans, as a model system. Upon chronic exposure of C. elegans to Dithianon, dopaminergic neurons were found to be vulnerable, with significant degeneration in terms of structure and function in a concentration-dependent manner. In examining toxicity mechanisms, we observed significant Dithianon-induced increases in oxidative stress and mitochondrial fragmentation, both of which are often associated with cellular stress. The present study suggests that Dithianon exposure causes dopaminergic neurotoxicity in C. elegans, by inducing oxidative stress and mitochondrial dysfunction. These findings contribute to a better understanding of Dithianon's neurotoxic potential.

Dental abnormalities in individuals with pathogenic germline variation in DICER1.

Pathogenic germline variation in the microRNA processing gene DICER1 gives rise to an autosomal dominant, tumor-predisposition disorder. Conditional deletion of Dicer1 in murine dental epithelium shows that it controls tooth patterning, size, number, and shape. The human dental phenotype of people with germline pathogenic variation in DICER1 is unknown. DICER1-carriers (n = 57) and family controls (n = 55) were evaluated at the NIH Clinical Center dental clinic as part of a comprehensive medical evaluation. Digital panoramic radiographs, bite-wing radiographs, and oral photographs were collected. A single observer, blind to DICER1 status, reviewed the dental records and determined the presence or absence of 11 dental characteristics as described in the clinic notes, radiographs, or oral photographs. Subjective phenotypes were reviewed on radiographs by two examiners (blind to DICER1 status) for the presence or absence of the dental characteristics to reduce inconsistencies. By simple association, bulbous crown, periodontitis, and taurodontism were all significant (p < .05). Logistic regression with chi-square maximum likelihood estimates showed that bulbous crown and periodontitis remained significant. Recognition of these phenotypes may aid identification of individuals and families at risk for DICER1-associated neoplasms. These findings may also guide dental care for individuals with germline DICER1 pathogenic variation.

A fluid secretion pathway unmasked by acinar-specific Tmem16A gene ablation in the adult mouse salivary gland.

Activation of an apical Ca(2+)-activated Cl(-) channel (CaCC) triggers the secretion of saliva. It was previously demonstrated that CaCC-mediated Cl(-) current and Cl(-) efflux are absent in the acinar cells of systemic Tmem16A (Tmem16A Cl(-) channel) null mice, but salivation was not assessed in fully developed glands because Tmem16A null mice die within a few days after birth. To test the role of Tmem16A in adult salivary glands, we generated conditional knockout mice lacking Tmem16A in acinar cells (Tmem16A(-/-)). Ca(2+)-dependent salivation was abolished in Tmem16A(-/-) mice, demonstrating that Tmem16A is obligatory for Ca(2+)-mediated fluid secretion. However, the amount of saliva secreted by Tmem16A(-/-) mice in response to the ß-adrenergic receptor agonist isoproterenol (IPR) was comparable to that seen in controls, indicating that Tmem16A does not significantly contribute to cAMP-induced secretion. Furthermore, IPR-stimulated secretion was unaffected in mice lacking Cftr (Cftr(∆F508/∆F508)) or ClC-2 (Clcn2(-/-)) Cl(-) channels. The time course for activation of IPR-stimulated fluid secretion closely correlated with that of the IPR-induced cell volume increase, suggesting that acinar swelling may activate a volume-sensitive Cl(-) channel. Indeed, Cl(-) channel blockers abolished fluid secretion, indicating that Cl(-) channel activity is critical for IPR-stimulated secretion. These data suggest that ß-adrenergic-induced, cAMP-dependent fluid secretion involves a volume-regulated anion channel. In summary, our results using acinar-specific Tmem16A(-/-) mice identify Tmem16A as the Cl(-) channel essential for muscarinic, Ca(2+)-dependent fluid secretion in adult mouse salivary glands.