Objectives: The aim of this study was to compare among PCNAand Ki-67 as the most reliable immunohistochemical marker for evaluating cell proliferation in ameloblastic tumors. Study Design: Observational, retrospective, and descriptive study of a large series of ameloblastic tumors, composed of 161 ameloblastomas and four ameloblastic carcinomas, to determine and compare PCNA and Ki-67 expression using immunohistochemistry techniques. Results: When analyzing Ki-67 positivity, the desmoplastic ameloblastoma demonstrated a significantly lower proliferation rate (1.9%) compared with the solid/multicystic and unicystic ameloblastomas and ameloblastic carcinomas (p<0.05), whereas the ameloblastic carcinomas displayed a significantly higher rate compared with all of the other ameloblastomas (48.7%) (p<0.05). When analyzing cell proliferation with PCNA, we found significant differences only between the ameloblastic carcinomas (93.3%) and the desmoplastic ameloblastomas (p<0.05). When differences between the immunopositivity for PCNA and Ki-67 were compared, the percentages were higher for PCNA in all types of ameloblastomas and ameloblastic carcinomas. In all cases, the percentages were greater than 80%, whereas the immunopositivity for Ki-67 was significantly lower; for example, the ameloblastic carcinoma expressed the highest positivity and only reached 48.7%, compared to 93.3% when we used PCNA. Conclusions: In the present study, when we used the proliferation cell marker Ki-67, the percentages of positivity were more specific and varied among the different types of ameloblastomas, suggesting that Ki-67 is a more specific marker for the proliferation of ameloblastic tumor cells.

Molar incisor hypomineralization (MIH) is a defect of the dental enamel that predominantly affects first molars and permanent incisors. Identifying the significant risk factors associated with MIH occurrence is essential for the implementation of prevention strategies. The purpose of this systematic review was to determine the etiological factors associated with MIH. A literature search was carried out from six databases until 2022; it covered pre-, peri-, and postnatal etiological factors. The PECOS strategy, PRISMA criteria, and the Newcastle–Ottawa scale were used, and 40 publications were selected for qualitative analysis as well as 25 for meta-analysis. Our results revealed an association between a history of illness during pregnancy (OR 4.03 (95% CI, 1.33–12.16), p = 0.01) and low weight at birth (OR 1.23 (95% CI, 1.10–1.38), p = 0.0005). Furthermore, general illness in childhood (OR 4.06 (95% CI, 2.03–8.11), p = 0.0001), antibiotic use (OR 1.76 (95% CI, 1.31–2.37), p = 0.0002), and high fever during early childhood (OR 1.48 (95% CI, 1.18–1.84), p = 0.0005) were associated with MIH. In conclusion, the etiology of MIH was found to be multifactorial. Children with health disorders in the first years of life and those whose mothers underwent illnesses during pregnancy might be more susceptible to MIH.

Current concepts in ameloblastoma-targeted therapies in B-raf proto-oncogene serine/threonine kinase V600E mutation: Systematic review

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.