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Bone resorption control of tooth eruption and root morphogenesis: Involvement of the receptor activator of NF‐κB (RANK)
Authors:Beatriz Castaneda  Yohann Simon  Jaime Jacques  Estelle Hess  Yong‐Wong Choi  Claudine Blin‐Wakkach  Christopher Mueller  Ariane Berdal  Frédéric Lézot
Institution:1. INSERM UMR 872, Cordeliers Research Center, Team 5, Laboratory of Oral Molecular Physiopathology, Paris, France;2. Faculty of Odontology, Department of Basic Studies, University of Antioquia, Medellin, Colombia;3. CNRS, UPR 9021, Laboratory of Therapeutic Immunology and Chemistry, IBMC, University of Strasbourg, Strasbourg, France;4. Department of Pathology and Laboratory Medicine, Abramson Family Cancer Research Institute, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania;5. INSERM U576, Laboratory of Regulation of Immune and Inflammatory Reactions, L'Archet Hospital, Nice, France
Abstract:Activation of the receptor activator of NF‐κB (RANK) is a crucial step in osteoclastogenesis. Loss‐ and gain‐of‐function mutations in the Rank gene cause, respectively, osteopetrosis and several forms of extensive osteolysis. Tooth and alveolar bone alterations are associated with these pathologies but remain to be better characterized. The aim of the present study was to establish the tooth and alveolar bone phenotype of a transgenic mouse model of RANK over‐expression in osteoclast precursors. Early tooth eruption and accelerated tooth root elongation were observed subsequent to an increase in osteoclast numbers surrounding the tooth. The final root length appeared not to be affected by RANK over‐expression, but a significant reduction in root diameter occurred in both control and root‐morphogenesis‐defective Msx2 null mutant mice. These results indicate that root length is independent of the surrounding bone resorption activity. In contrast, root diameter is sensitive to the activity of alveolar bone osteoclasts. These data suggest that early eruption and thin root are phenotypic features that could be associated with extensive osteolytic pathologies. J. Cell. Physiol. 226: 74–85, 2010. © 2010 Wiley‐Liss, Inc.
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