| [ Summary ] |
The sequential reciprocal signaling interactions between ectodermis-derived epithelial cells and cranial neural crest derived mesenchymal cells regulate cell proliferation and cytodifferentiation during tooth development. The dental epithelium, which is induced by the trigger signaling from the dental mesenchyme at the initiation stage, is differentiated into four distinct layers in the developing enamel organ, stellate reticulum, stratum intermedium, and outer and inner enamel epithelia. Enamel, the hardest structure in our body, is formed by ameloblasts, which differentiate from the inner enamel epithelium in part through multiple signaling pathways, including the BMP, FGF, Shh, WNT, and Notch pathways. Ameloblasts secrete a series of enamel matrices such as amelogenin, ameloblastin, enamelin, and amelotin, as well as the proteases MMP20 and KLK4. The single gene targeted mutant mouse of one of enamel matrix proteins or proteases develop amelogenesis imperfecta. Thus, all these molecules are critical for the development of enamel. Epiprofin, a transcription factor belonging to the Sp family, shows limited expression in dental epithelial cells and inner enamel epithelial cells at the cap and bell stages. Epiprofin-knockout mice do not develop enamel layers on their incisors and molars because of blockage of ameloblast differentiation. The mutant mice keep developing supernumerary teeth because of continuous development of tooth buds. Last, we provide our preliminary data in relation with molar incisor hypomineralization, which may be caused by reduction in serum 1α,25-dihydroxyvitamin D3. |