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Genetic Etiology Of Development Alterations Affecting The Number, Size, Form, Structure And Eruption Of The Teeth

Teeth develop in the mammalian embryo via a series of interactions between the odontogenic epithelium and the neural crest-derived ectomesenchyme of the early jaw primordia. The molecular interactions required to generate a tooth are mediated by families of signaling molecules, which often act reiteratively in both a temporal and spatial manner. In humans, the process of odontogenesis lasts approximately 18 years, beginning in the 6th-8th week in the uterus and ending with the formation of the third molars in late adolescence. Each tooth passes through a series of stages that follow the same pattern, beginning with the formation of the bud, then cap and bell, followed by the deposit of enamel and dentin on the crown of the tooth. After the crown is formed, the development of the roots continues and finally the teeth emerge in the oral cavity, when about 2/3 of the roots have formed. Alterations in the indicated processes lead to of the cusps. During cytodifferentiation, in the bell stage, enamel and dentin are synthesized at the epithelial-mesenchymal interface, by the interaction of the same signals present in dental morphogenesis [2,3]. The development of the root begins after the formation of the crown. The apical region of the dental organ elongates and originates the Hertwig's epithelial root sheath (HERS), which grows apically guiding the formation of the root(s) and determining their number, size and shape. The inner layer of the sheath interacts with the mesenchyme, producing laminin-5 and growth factors that induce the differentiation of odontoblasts that secrete root dentin. The cells from HERS control the formation of cementum by the cells of the dental follicle [4]. Abnormalities in the indicated processes lead to a wide range of abnormalities that affect the number, size, shape of teeth and structural defects in mineralized tissues, as well as failures in dental eruption. the knowledge about mammalian odontogenesis comes from studies in animal models, mainly mouse. However, the murine dentition is not equal to human dentition, so there are a series of aspects of tooth development in our species that remain unanswered. In this context, the clinical and molecular genetics study of families with various dentition disorders is a valuable approach that will contribute to improve our knowledge of the phenotype-genotype correlations involved in these abnormalities.