Inactivation of Tgfbr2 in Osterix-Cre expressing dental mesenchyme disrupts molar root formation.
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ABSTRACT: It has been difficult to examine the role of TGF-ß in post-natal tooth development due to perinatal lethality in many of the signaling deficient mouse models. To address the role of Tgfbr2 in postnatal tooth development, we generated a mouse in which Tgfbr2 was deleted in odontoblast- and bone-producing mesenchyme. Osx-Cre;Tgfbr2(fl/fl) mice were generated (Tgfbr2(cko)) and post-natal tooth development was compared in Tgfbr2(cko) and control littermates. X-ray and μCT analysis showed that in Tgfbr2(cko) mice radicular dentin matrix density was reduced in the molars. Molar shape was abnormal and molar eruption was delayed in the mutant mice. Most significantly, defects in root formation, including failure of the root to elongate, were observed by postnatal day 10. Immunostaining for Keratin
SUBMITTER: Wang Y
PROVIDER: S-EPMC3783640 | biostudies-literature | 2013 Oct
REPOSITORIES: biostudies-literature
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