Constitutive activation of β-catenin in odontoblasts induces aberrant pulp calcification in mouse incisors.

Abstract

During dentin formation, odontoblast polarization ensures that odontoblasts directionally secrete dentin matrix protein, leading to tubular dentin formation; however, little is known about the major features and regulatory mechanisms of odontoblast polarization. In a study of epithelial cell polarization, β-catenin was shown to serve as a structural component of cadherin-based adherens junctions to initiate cell polarity. However, the role of β-catenin in odontoblast polarization has not been well investigated. In this study, we explored whether β-catenin participated in odontoblast polarization to regulate the secretion of mineralization proteins. We established Col1-CreErt2; β-catenin exon3fl/fl (CA-β-catenin) mice, which constitutively activate β-catenin in odontoblasts. CA-β-catenin mice exhibited disorganization and depolarization of incisor odontoblasts. Moreover, the incisor dentin was hypomineralized, and ectopic calcification was found in mouse incisor pulp. In addition, by constitutive activation of β-catenin, the expression levels of the core polarity molecule Cdc42 and its downstream polarity protein complex Par3-Par6-aPKC were decreased in the incisors of CA-β-catenin mice. These findings suggest that β-catenin plays an essential role in dentin formation by regulating odontoblast polarization.