Abstract
Constant supplies of dental epithelial cells from stem cell niches in the cervical loop enable mouse incisors to grow continuously through life. Fibroblast growth factor 10 (FGF10) has been shown to be essential for development of mouse incisors and maintenance of incisor cervical loops during prenatal development. Whether its cognate receptor, FGFR2IIIB, in the dental epithelium is required for postnatal tooth development remains unknown because Fgfr2IIIb ablation causes neonatal lethality. Here we report that tissue-specific ablation of Fgfr2 in the dental epithelium led to defective maxillary incisors that lacked ameloblasts and the enamel, and had poorly developed odontoblasts. Although the cervical loop in Fgfr2 null maxillary incisors was formed initially, it failed to continue to develop and gradually diminished soon after birth. The results suggest that the FGFR2 signaling axis plays a role in maintaining the stem cell niche required for incisor development and lifelong growth.