BackgroundThe objective of the present study was to determine the prevalence and severity of dental fluorosis and to evaluate exposure to fluoridated products in students in the southwest part of the Federal District (Mexico City).Material/MethodsStudents between 10 and 12 years of age who were born and raised in the study zone were evaluated. The level of dental fluorosis was determined using the modified Dean index (DI) using criteria recommended by the World Health Organization (WHO). A bivariate analysis was performed with the χ2 test, and odds ratios (OR) and 95% confidence intervals (CI) are presented. Logistic regression was performed to evaluate the association between dental fluorosis and the independent variables.ResultsA total of 239 students were evaluated. Their mean age was 11±0.82 years, and there were 122 (51%) males. Overall, dental fluorosis was found in 59% of participants; 29.3% had very mild fluorosis, 20.9% had mild fluorosis, 6.7% had moderate fluorosis, and 2.1% had severe fluorosis. The mean fluorosis score was 0.887±0.956. In the final logistic regression model, dental fluorosis was significantly associated with frequency of brushing (OR: 0.444; 95% CI: 0.297–0.666) and with the absence of parental supervision (OR: 0.636; 95% CI: 0.525–0.771).ConclusionsThe association found with frequency of brushing and lack of parental supervision may be contributing to the prevalence and severity of dental fluorosis.

Cell proliferation assays are performed using antibodies against nuclear proteins associated with DNA replication. These nuclear proteins have gained special interest to predict the biological and clinical behaviors of various tumors. The aim of this study was to analyze the presence of Ki-67 protein and the minichromosome maintenance-2 (MCM2) and maintenance-3 (MCM3) proteins in ameloblastoma. Materials and Methods. Cell proliferation marker expression levels were assessed via immunohistochemistry in 111 ameloblastoma cases (72 unicystic ameloblastoma samples, 38 solid/multicystic ameloblastoma samples, and 1 ameloblastic carcinoma). The label index was performed as described previously. Results. MCM2 and MCM3 showed higher proliferation indexes in all variants of ameloblastoma compared to the classic marker Ki-67. No correlation between the proliferation index and the clinical and protein expression data was observed. Conclusion. The results suggest that clinical features do not directly affect tumor cell proliferation. Moreover, the high levels of cellular proliferation of MCM2 and MCM3 compared with Ki-67 may indicate that MCM2 and MCM3 are more sensitive markers for predicting the growth rate and eventually might be helpful as a tool for predicting aggressive and recurrent behaviors in these tumors.

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This manuscript provides an update to the literature on molecules with roles in tumor resistance therapy in head and neck squamous cell carcinoma (HNSCC). Although significant improvements have been made in the treatment for head and neck squamous cell carcinoma, physicians face yet another challenge—that of preserving oral functions, which involves the use of multidisciplinary therapies, such as multiple chemotherapies (CT) and radiotherapy (RT). Designing personalized therapeutic options requires the study of genes involved in drug resistance. This review provides an overview of the molecules that have been linked to resistance to chemotherapy in HNSCC, including the family of ATP-binding cassette transporters (ABCs), nucleotide excision repair/base excision repair (NER/BER) enzymatic complexes (which act on nonspecific DNA lesions generated by gamma and ultraviolet radiation by cross-linking and forming intra/interchain chemical adducts), cisplatin (a chemotherapeutic agent that causes DNA damage and induces apoptosis, which is a paradox because its effectiveness is based on the integrity of the genes involved in apoptotic signaling pathways), and cetuximab, including a discussion of the genes involved in the cell cycle and the proliferation of possible markers that confer resistance to cetuximab.

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