Técnica combinada de microabrasión y blanqueamiento dental para tratamiento de pigmentaciones asociadas a fluorosis. Reporte de un caso / Combined technique of microabrasion and teeth whitening for treatment of surface stains associated with fluorosis. Case Report

La fluorosis dental es una condición irreversible originada durante el desarrollo dental que genera pigmentaciones intrínsecas, alteraciones en el esmalte manifestadas a manera de manchas blancas, amarillas o marrones, que perjudican la estética y repercuten en el desenvolvimiento social. El presente reporte de caso clínico describe la combinación de los procedimientos de microabrasión y blanqueamiento dental, como alternativas en la eliminación de pigmentaciones dentales. Después del diagnóstico de la patología, verificación de ausencia de lesiones pulpares y caries, una explicación minuciosa a la paciente y obtención del consentimiento informado, se realizó limpieza de las superficies dentales y, bajo aislamiento absoluto, se procedió a realizar la técnica de microabrasión mediante ácido clorhídrico al 6,6% siguiendo las instrucciones del fabricante. Concluido el procedimiento y, observando que era posible mejorar aún más la estética, se decidió ejecutar el procedimiento de blanqueamiento dental, a base de peróxido de hidrógeno al 40% en el consultorio, seguido por peróxido de carbamida al 10% aplicado en el domicilio. Al finalizar el tratamiento se observó uniformidad en el color dental, conjugados con una evidente mejora en la calidad de vida y relación social de la paciente. La combinación de procedimientos, como el reportado en este caso, constituye una excelente alternativa de tratamiento para eliminar pigmentaciones fluoróticas moderadas

Dental fluorosis is an irreversible condition caused during dental development that generates intrinsic pigmentation, enamel alterations manifested as white, yellow, or brown spots, which impair aesthetics and have an impact on social development. This clinical case report describes the combination of microabrasion and teeth whitening procedures, as alternatives in the elimination of dental pigmentations. After the diagnosis of the pathology, verification of absence of pulpal lesions and caries, a thorough explanation to the patient and obtaining informed consent; dental surfaces were cleaned and, under absolute isolation, the microabrasion technique was performed using 6.6% hydrochloric acid following the manufacturer's instructions. Once the procedure was concluded and observing that it was possible to improve the aesthetics even further, it was decided to perform the teeth whitening procedure, based on 40% hydrogen peroxide, in the dental office, followed by 10% carbamide peroxide applied at home. At the end of the treatment, uniformity in tooth color was observed, combined with an evident improvement in the quality of life and social relationship of the patient. The combination of procedures, such as that reported in this case, constitutes an excellent treatment alternative to eliminate moderate fluorotic pigmentation

La obesidad en niños y adolescentes como factor desencadenante de caries dental, revisión bibliográfica / Obesidade em crianças e adolescentes como fator desencadeante da cárie dentária, revisão de literatura / Obesity in children and adolescents as a trigger factor for dental caries, literature review

Objetivo: Establecer posible relación de la obesidad en niños y adolescentes con la presencia de caries dental. Materiales y métodos: se realizó una revisión bibliográfica de la base de datos PUBMED, empleando como palabras de búsqueda, Caries, Obesity, Child, Adolescent junto con AND como conector booleano, se tomaron en cuenta todos los artículos publicados entre el año 2013 al 2018. Cuarenta artículos fueron encontrados, 29 artículos se Revisiónexcluyeron por referirse a variables no consideradas dentro del estudio, los 11 artículos restantes fueron revisados y los principales hallazgos expuestos. Resultados: la literatura revisada no muestra asociación entre obesidad con la presencia de caries, encontrándose una fuerte influencia de bajo peso con caries dental. Conclusiones: la caries dental en niños y adolescentes muestra ausencia de relación con el aumento de peso.

Objetivo: Estabelecer relação entre a obesidade em crianças e adolescentes com a presença de cárie dentária. Materiais e Métodos: foi executada uma revisão bibliográfica no banco de dados PubMed, empregando como palavras chaves, cárie, obesidade, criança, juntamente com AND como conector booleano, foram considerados todos os artigos publicados entre 2013-2018. Quarenta artigos foram encontrados, 29 excluidos por referir variáveis não consideradas no estudo, os 11 artigos restantes foram revisados e os principais achados foram expostos. Resultados: a literatura revisada não mostra associação entre obesidade com a presença de cárie, encontrando-se uma forte influência do baixo peso com a cárie dentária. Conclusão: A cárie dentária em crianças e adolescentes mostra ausência de relação com o incremento de peso.

Objective: To establish the relationship of obesity in children and adolescents with the presence of dental caries. Materials and methods: A bibliographic review of PUBMED database was carried out, using terms like, Caries, Obesity, Child, adolescent with AND as a boolean connector. All articles published between 2013 and 2018 were taken into account. 40 articles were found, 29 later excluded because they referred variables not considered in the study. The remaining 11 articles were reviewed and the main findings synthesizad. Results: The literature reviewed does not suggest an association between obesity and the presence of caries. A strong influence of low weight with dental caries was identified. Conclusions: Dental caries in children and adolescents does not suggest a relationship with weigth gain.

Arsenic exposure induces the Warburg effect in cultured human cells.

Understanding how arsenic exacts its diverse, global disease burden is hampered by a limited understanding of the particular biological pathways that are disrupted by arsenic and underlie pathogenesis. A reductionist view would predict that a small number of basic pathways are generally perturbed by arsenic, and manifest as diverse diseases. Following an initial observation that arsenite-exposed cells in culture acidify their media more rapidly than control cells, the report here shows that low level exposure to arsenite (75ppb) is sufficient to induce aerobic glycolysis (the Warburg effect) as a generalized phenomenon in cultured human primary cells and cell lines. Expanded studies in one such cell line, the non-malignant pulmonary epithelial line, BEAS-2B, established that the arsenite-induced Warburg effect was associated with increased accumulation of intracellular and extracellular lactate, an increased rate of extracellular acidification, and inhibition by the non-metabolized glucose analog, 2-deoxy-D-glucose. Associated with the induction of aerobic glycolysis was a pathway-wide induction of glycolysis gene expression, as well as protein accumulation of an established glycolysis master-regulator, hypoxia-inducible factor 1A. Arsenite-induced alteration of energy production in human cells represents the type of fundamental perturbation that could extend to many tissue targets and diseases.

Arsenite-induced autophagy is associated with proteotoxicity in human lymphoblastoid cells.

Epidemiological studies of arsenic-exposed populations have provided evidence that arsenic exposure in humans is associated with immunosuppression. Previously, we have reported that arsenite-induced toxicity is associated with the induction of autophagy in human lymphoblastoid cell lines (LCL). Autophagy is a cellular process that functions in the degradation of damaged cellular components, including protein aggregates formed by misfolded or damaged proteins. Accumulation of misfolded or damaged proteins in the endoplasmic reticulum (ER) lumen causes ER stress and activates the unfolded protein response (UPR). In an effort to investigate the mechanism of autophagy induction by arsenite in the LCL model, we examined the potential contribution of ER stress and activation of the UPR. LCL exposed to sodium arsenite for 8-days induced expression of UPR-activated genes, including CHOP and GRP78, at the RNA and the protein level. Evidence for activation of the three arms of the UPR was observed. The arsenite-induced activation of the UPR was associated with an accumulation of protein aggregates containing p62 and LC3, proteins with established roles in the sequestration and autophagic clearance of protein aggregates. Taken together, these data provide evidence that arsenite-induced autophagy is associated with the generation of ER stress, activation of the UPR, and formation of protein aggregates that may be targeted to the lysosome for degradation.

A Comparison of group A Streptococcus versus Streptococcus pneumoniae pneumonia.

BACKGROUND: St reptococcus pyogenes is an uncommon cause of community-acquired pneumonia in children. Further, its clinical course in comparison to pneumonia caused by Streptococcus pneumonia has not been previously highlighted. METHODS: We reviewed medical records of children 0-18 years of age from April 1983 to April 2005, with discharge diagnoses of invasive disease caused by group A streptococcus (GAS) (Streptococcus pyogenes), or Streptococcus pneumonia (SP) or pneumonia. Data were extracted from the charts, and a comparison of clinical characteristics between the 2 etiologies was performed. Confirmed disease required blood or pleural fluid isolates. Patients with single isolates of GAS in tracheobronchial secretions or sputum were classified as having presumed disease caused by GAS. Patients with confirmed disease due to GAS and SP were compared with respect to clinical characteristics. RESULTS: Of 103 patients with invasive GAS disease, 12 (11.6%) had confirmed GAS lobar pneumonia. In addition 7 patients had presumed GAS pneumonia. There were 54 patients with confirmed SP pneumonia. Most children who had GAS pneumonia were healthy and recovered completely. Compared with patients with confirmed SP pneumonia, those with confirmed GAS pneumonia had more frequent and larger effusions, more culture positive effusions, had prolonged fever, and had longer hospitalizations. There was not an increasing trend to GAS pneumonia over the 22-year period. There was not a predominant serotype responsible for the pneumonias. CONCLUSIONS: Lobar GAS pneumonia represents approximately 11% of all cases of invasive disease in this institution during a 22-year period. Compared with patients with SP pneumonia, it appears to cause more effusions and morbidity. The organism is also more frequently recovered from pleural fluid.