Loss of Stat3 in Osterix+ cells impairs dental hard tissues development

Abstract

Background Mutations in the signal transducers and activators of transcription 3 (STAT3) gene result in hyper-IgE syndrome(HIES), a rare immunodeficiency that causes abnormalities in immune system, bones and teeth. However, the role of Stat3 in development of dental hard tissues was yet to investigate. Methods In this study, a transgenic mouse of conditional knockout of Stat3 in dental mesenchymal cells (Osx-Cre; Stat3fl/fl, Stat3 CKO) was made. The differences of postnatal tooth development between control and Stat3 CKO mice were compared by histology, µCT and scanning electron microscopy. Result Compared with the control, Stat3 CKO mice were presented with remarkable abnormal tooth phenotypes characterized by short root and thin dentin in molars and incisors. The enamel defects were also found on mandibular incisors. showed that Ki67-positive cells significantly decreased in dental mesenchymal of Stat3 CKO mice. In addition, β-catenin signaling was reduced in Hertwig's epithelial root sheath (HERS) and odontoblasts of Stat3 CKO mice. Conclusions Our results suggested that Stat3 played an important role in dental hard tissues development, and Stat3 may regulate dentin and tooth root development through the β-catenin signaling pathway.

PRX1-positive mesenchymal stem cells drive molar morphogenesis

“…Osterix (Osx/Sp7) is a specific transcription factor committed to the dentin-forming odontoblastic lineage. 21 The expression levels of Tomato + cells from Osx-cre; R26R tdTomato mice verified that OSX was highly expressed during odontoblast differentiation of dental MSCs, both M1 and M3 (Fig. S3a ).…”