Tooth development hinged on reciprocal interactions between enamel and dentin, shaping tooth structures. Centrioles influenced cellular direction, critical for stem cell differentiation. Aberrant centrioles contributed to conditions like Huntington's disease and cancers. Centriole-related gene mutations, like Pericentrin and Centrosomal P4.1-associated protein (CPAP), led to tooth abnormalities, microcephaly. Our study explored the role of centrioles in ameloblasts during molar growth, shedding light on tooth development mechanisms. Tissue sections underwent immunofluorescence and hematoxylin and eosin staining to observe centriole changes in C57BL/6 mouse molars (1,3,5,7, and 9 days). Emphasis was placed on comparing centrioles in enamel and ameloblasts between Nestin-Cremediated Cpap conditional knockout in p53-deficient mice (Cpap(-/-) mice) and normal mice on the ninth day. In mouse molar tissue, ameloblasts and enamel underwent notable changes during the 1-9 days after birth. Centrioles in ameloblasts exhibited dynamic temporal localization, migrating away from cell nuclei towards enamel generation. Correlation between enamel thickness and centriole quantity suggested a relationship. Comparative analysis of normal and Cpap (-/-) mice on the ninth day revealed differences in enamel thickness, ameloblast elongation, and centriole distribution, highlighting the impact of CPAP deficiency on tooth development. This study affirmed the positive contribution of ciliated centrioles in ameloblasts to enamel growth during the secretory phase. Increased centrioles correlated with enhanced enamel formation. Conversely, CPAP loss disrupted centriole organization, impacting ameloblast morphology and functionality, resembling enamel hypoplasia observed in microcephaly patients. Further research is essential to unravel molecular mechanisms and potential interactions with odontoblast centrioles.
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Pei et al. (2024) studied this question.
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