Secretory stage ameloblasts then enter a maturation phase characterized by the degradation of the vast majority of the enamel matrix proteins and their replacement by expanding hydroxyapatite crystals.ĭefects in enamel formation, classified under amelogenesis imperfecta (AI) in humans, are common and can present with varying degrees of alterations in enamel thickness, enamel hardness, or both. The pre-secretion phase is followed by a secretion phase during which enamel matrix proteins are secreted in a highly structured fashion to form the scaffold of enamel where mineralization is simultaneously initiated. When these cells leave their niche to differentiate into ameloblasts, they migrate towards the distal end of the tooth and go through different phases.
Dental epithelial stem cells are located in the cervical loop at the most proximal end of the incisor. 1 In rodents, all stages of amelogenesis can be tracked along the proximal-distal axis of the continuously growing incisor.
It is produced by ameloblasts through a complex sequential mechanism. © 2016 American Society for Bone and Mineral Research.Įnamel covers the surface of the tooth and is the hardest tissue in the body. Taken together, these results show that DLX3 is indispensable for the regulation of ion transporters and carbonic anhydrases during the maturation stage of amelogenesis, exerting a crucial regulatory function on pH oscillations during enamel mineralization. These molecular findings were consistent with altered pH staining evidenced by disruption of characteristic pH oscillations in the enamel. Most of these affected genes showed binding of DLX3 to their proximal promoter as evidenced by chromatin immunoprecipitation sequencing (ChIP-seq) analysis on rat enamel organ. In contrast, expression of several ion transporters and carbonic anhydrases known to play an important role in enamel pH regulation during maturation was significantly affected in enamel organs lacking DLX3. Interestingly, transcriptomic analysis revealed that major enamel matrix proteins and proteases known to be involved in enamel secretion and maturation were not affected significantly by Dlx3 deletion in the enamel organ. Dlx3 deletion in the dental epithelium resulted in the formation of chalky hypomineralized enamel in all teeth. Here we used a conditional knockout mouse model to investigate the developmental and molecular consequences of Dlx3 deletion in the dental epithelium in vivo.
Patients with tricho-dento-osseous (TDO) syndrome, an ectodermal dysplasia caused by mutations in the homeodomain transcription factor DLX3, exhibit enamel hypoplasia and hypomineralization.
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