Tooth development involves signaling crosstalk between the embryonic oral epithelium and the underlying neural-crest-derived mesenchyme. Odontogenic epithelial-mesenchymal interactions repeatedly recruit basic organogenic cascades involving Fgf, Bmp, Shh, and Wnt signaling. Any disturbances in the tightly balanced signaling cascades may result in tooth anomaly which is the most prevalent craniofacial congenital birth defect in humans. Here we investigated the role of retinoic acid (RA) signaling in odontogenesis by using tamoxifen inducible ubiquitous Cre mice to conditionally delete Rdh10, a rate limiting enzyme for producing active all-trans RA. We revealed that eliminating Rdh10 by tamoxifen administration at E7.0 or E7.5 results in missing or split upper incisor placodes. The upper incisors that did develop in mutants were hypoplastic compared to controls. Furthermore, RA deficient embryos exhibited lack of stratification and decreased cell proliferation of the Sox2 expressing dental lamina which regulates the progenitor state of dental epithelial cells. In order to uncover the signaling pathways underlying this etiology, we focused on Shh and Bmp4 which are critical for embryonic tooth development. Noticeably reduced expression of these genes was detected in the upper incisor region of Rdh10 mutants. Taken together, our data indicate that upper incisor defects caused by reduced RA signaling were associated with decreased stratification and proliferation of Sox2 expressing dental epithelium which is caused by downregulation of Shh, Bmp4.