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Supernumerary teeth and tooth agenesis are common morphological anomalies in humans. We previously obtained evidence that supernumerary maxillary incisors form as a result of the successive development of the rudimentary maxillary incisor tooth germ in  Usag-1  null mice. The development of tooth germs is arrested in  Runx2  null mice, and such mice also exhibit lingual epithelial buds associated with the upper molars and incisors. The aim of this study is to investigate the potential crosstalk between  Usag-1  and  Runx2  during tooth development. In the present study, three interesting phenomena were observed in double null  Usag-1  -/- / Runx2  -/-  mice: the prevalence of supernumerary teeth was lower than in  Usag-1  null mice; tooth development progressed further compared than in  Runx2  null mice; and the frequency of molar lingual buds was lower than in  Runx2  null mice. Therefore, we suggest that RUNX2 and USAG-1 act in an antagonistic manner. The lingual bud was completely filled with odontogenic epithelial Sox2-positive cells in the  Usag-1  +/+ / Runx2  -/-  mice, whereas almost no odontogenic epithelial Sox2-positive cells contributed to supernumerary tooth formation in the rudimentary maxillary incisors of the  Usag-1  -/- / Runx2  +/+  mice. Our findings suggest that RUNX2 directly or indirectly prevents the differentiation and/or proliferation of odontogenic epithelial Sox2-positive cells. We hypothesize that RUNX2 inhibits the bone morphogenetic protein (BMP) and/or Wnt signaling pathways regulated by USAG-1, whereas RUNX2 expression is induced by BMP signaling independently of USAG-1.

Antagonistic Functions of USAG-1 and RUNX2 during Tooth Development