P8-alteration of tooth development in two-phase organotypic cultures by transient glycogen synthase kinase-3 (GSK-3) inhibition.

Introduction Regulation of intercellular signalling pathways is a key question in tooth organogenesis. Wnt pathway is essential for patterning tooth development, and for controlling the shape of individual teeth (Liu et al., 2008). Moreover, conditional overexpression of β‐catenin leading to an overactivation of the canonic Wnt pathway of the dental epithelium, (Järvinen et al., 2006), or conditional inactivation of Apc (Wang et al., 2009) produces a phenotype whereby multiple extra teeth are formed. In addition, Lef1 (a Wnt activator) knockout or Wnt inhibitor‐Dkk1 overexpressing mouse models present altered tooth development characterized by the accumulation of dental germs at bud stage (Andl et al., 2002). In the absence of Wnt signals, a multiheteromeric destruction complex formed by protein GSK‐3 (Glycogen Synthase Kinase 3), among others, phosphorylates and triggers β‐catenin degradation in the proteasome (Seidensticker and Behrens, 2000). All together data support the importance of the Wnt pathway on odontogenesis. The aim of this work was to characterize the implication of the Wnt signalling pathway on tooth development by means of Wnt activation in mouse first molar cultures.