ABSTRACT
INTRODUCTION: Supernumerary teeth in cases of cleft lip and palate do not result from the division of normal germs before the formation of hard tissue. Deciduous and permanent teeth odontogenesis begins after the face has formed, either with or without the cleft. DISCUSSION: The most acceptable hypothesis to enable understanding of the presence of supernumerary teeth on one or both sides of the cleft palate is hyperactivity of the dental lamina in its walls. This hyperactivity, with the formation of more tooth germs, must be attributed to mediators and genes related to tooth formation, under strong influence of local epigenetic factors, whose developmental environment was affected by the presence of the cleft. CONCLUSION: The current concepts of embryology no longer support the fusion of embryonic processes for the formation of the face, but rather the leveling of the grooves between them. All human teeth have a dual embryonic origin, as they are composed of ectoderm and mesenchyme/ectomesenchyme, but this does not make it easy for them to be duplicated to form supernumerary teeth.
Subject(s)
Anodontia , Cleft Lip , Cleft Palate , Tooth, Supernumerary , Cleft Lip/complications , Cleft Palate/complications , Humans , Tooth Germ/diagnostic imaging , Tooth, Supernumerary/complicationsABSTRACT
ABSTRACT Introduction: Supernumerary teeth in cases of cleft lip and palate do not result from the division of normal germs before the formation of hard tissue. Deciduous and permanent teeth odontogenesis begins after the face has formed, either with or without the cleft. Discussion: The most acceptable hypothesis to enable understanding of the presence of supernumerary teeth on one or both sides of the cleft palate is hyperactivity of the dental lamina in its walls. This hyperactivity, with the formation of more tooth germs, must be attributed to mediators and genes related to tooth formation, under strong influence of local epigenetic factors, whose developmental environment was affected by the presence of the cleft. Conclusion: The current concepts of embryology no longer support the fusion of embryonic processes for the formation of the face, but rather the leveling of the grooves between them. All human teeth have a dual embryonic origin, as they are composed of ectoderm and mesenchyme/ectomesenchyme, but this does not make it easy for them to be duplicated to form supernumerary teeth.
RESUMO Introdução: Os dentes extranumerários nas fissuras labiopalatinas não são resultado da divisão dos germes normais antes da formação do tecido duro. A odontogênese dos decíduos e permanentes inicia-se depois de formada a face, com ou sem fissuras. Discussão: A hipótese mais plausível para compreender a presença dos dentes extranumerários em um ou nos dois lados da fissura labiopalatina é a hiperatividade da lâmina dentária em suas paredes. Essa hiperatividade, com formação de mais germes dentários, deve ser atribuída aos mediadores e genes relacionados à formação dos dentes, sob forte influência de fatores epigenéticos locais, cujo ambiente de desenvolvimento foi afetado pela presença da fissura. Conclusão: Os conceitos atuais da embriologia não fundamentam mais a fusão de processos embrionários para a formação da face, e sim o nivelamento dos sulcos entre eles. Todos os dentes humanos têm uma dupla origem embrionária, pois se compõem de ectoderma e mesênquima/ectomesênquima, mas isso não facilita sua duplicação para formar dentes extranumerários.
Subject(s)
Humans , Tooth, Supernumerary/complications , Cleft Lip/complications , Cleft Palate/complications , Anodontia , Tooth Germ/diagnostic imagingABSTRACT
BACKGROUND/AIM: This study analyzed moesin immunoexpression in 91 lip squamous cell carcinomas and its influence in patients' prognosis. MATERIALS AND METHODS: Moesin immunoexpression was evaluated at the invasive tumor front by a semi-quantitative score method. The association of moesin with the clinicopathological variables was analyzed by the Chi-square test, the survival rates were calculated by Kaplan-Meier and the survival curves compared using the log-rank test. RESULTS: The expression of moesin was strong at the invasive tumor front and weak/negative in differentiated cells such as keratin pearls. There was no association between moesin expression and the clinicopathological variables, but there was a tendency for patients with lip cancer and strong moesin expression to have lower 5- and 10-year overall and disease-free survival rates. CONCLUSION: Our results confirm the participation of moesin in oral carcinogenesis and suggest that this protein can influence the survival rates of patients with lip squamous cell carcinoma.
