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Crown formation during tooth development and tissue engineering
Author(s) -
Nait Lechguer Adnane,
KuchlerBopp Sabine,
Lesot Herve
Publication year - 2009
Publication title -
journal of experimental zoology part b: molecular and developmental evolution
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.823
H-Index - 63
eISSN - 1552-5015
pISSN - 1552-5007
DOI - 10.1002/jez.b.21256
Subject(s) - enamel organ , enamel paint , molar , ameloblast , crown (dentistry) , dental papilla , odontoblast , microbiology and biotechnology , tissue engineering , mesenchyme , amelogenesis , morphogenesis , incisor , biology , dentin , dentistry , chemistry , anatomy , medicine , mesenchymal stem cell , biochemistry , genetics , gene
Considering tooth crown engineering, three main parameters have to be taken into account: (1) the relationship between crown morphology and tooth functionality, (2) the growth of the organ, which is hardly compatible with the use of preformed scaffolds, and (3) the need for easily available nondental competent cell sources. In vitro reassociation experiments using either dental tissues or bone marrow‐derived cells (BMDC) have been designed to get information about the mechanisms to be preserved in order to allow crown engineering. As the primary enamel knot (PEK) is involved in signaling crown morphogenesis, the formation and fate of this structure was investigated (1) in heterotopic reassociations between embryonic day 14 (ED14) incisor and molar enamel organs and mesenchymes, and (2) in reassociations between ED14 molar enamel organs and BMDC. A PEK formed in cultured heterotopic dental tissue reassociations. The mesenchyme controls the fate of the EK cells, incisor or molar‐specific using apoptosis as criterion, and functionality to drive single/multiple cusps tooth development. Although previous investigations showed that they might differentiate as odontoblast‐ or ameloblast‐like cells, BMDC reassociated to an enamel organ could not support the development of multicusp teeth. These cells apparently could neither maintain nor stimulate the formation of a PEK. J. Exp. Zool. (Mol. Dev. Evol.) 312B:399–407, 2009 . © 2009 Wiley‐Liss, Inc.