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Bone resorption: an actor of dental and periodontal development?

Dental and periodontal tissue development is a complex process involving various cell-types. A finely orchestrated network of communications between these cells is implicated. During early development, communications between cells from the oral epithelium and the underlying mesenchyme govern the den...

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Autores principales: Gama, Andrea, Navet, Benjamin, Vargas, Jorge William, Castaneda, Beatriz, Lézot, Frédéric
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4633481/
https://www.ncbi.nlm.nih.gov/pubmed/26594180
http://dx.doi.org/10.3389/fphys.2015.00319
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author Gama, Andrea
Navet, Benjamin
Vargas, Jorge William
Castaneda, Beatriz
Lézot, Frédéric
author_facet Gama, Andrea
Navet, Benjamin
Vargas, Jorge William
Castaneda, Beatriz
Lézot, Frédéric
author_sort Gama, Andrea
collection PubMed
description Dental and periodontal tissue development is a complex process involving various cell-types. A finely orchestrated network of communications between these cells is implicated. During early development, communications between cells from the oral epithelium and the underlying mesenchyme govern the dental morphogenesis with successive bud, cap and bell stages. Later, interactions between epithelial and mesenchymal cells occur during dental root elongation. Root elongation and tooth eruption require resorption of surrounding alveolar bone to occur. For years, it was postulated that signaling molecules secreted by dental and periodontal cells control bone resorbing osteoclast precursor recruitment and differentiation. Reverse signaling originating from bone cells (osteoclasts and osteoblasts) toward dental cells was not suspected. Dental defects reported in osteopetrosis were associated with mechanical stress secondary to defective bone resorption. In the last decade, consequences of bone resorption over-activation on dental and periodontal tissue formation have been analyzed with transgenic animals (RANK(Tg) and Opg(−∕−) mice). Results suggest the existence of signals originating from osteoclasts toward dental and periodontal cells. Meanwhile, experiments consisting in transitory inhibition of bone resorption during root elongation, achieved with bone resorption inhibitors having different mechanisms of action (bisphosphonates and RANKL blocking antibodies), have evidenced dental and periodontal defects that support the presence of signals originating bone cells toward dental cells. The aim of the present manuscript is to present the data we have collected in the last years that support the hypothesis of a role of bone resorption in dental and periodontal development.
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spelling pubmed-46334812015-11-20 Bone resorption: an actor of dental and periodontal development? Gama, Andrea Navet, Benjamin Vargas, Jorge William Castaneda, Beatriz Lézot, Frédéric Front Physiol Physiology Dental and periodontal tissue development is a complex process involving various cell-types. A finely orchestrated network of communications between these cells is implicated. During early development, communications between cells from the oral epithelium and the underlying mesenchyme govern the dental morphogenesis with successive bud, cap and bell stages. Later, interactions between epithelial and mesenchymal cells occur during dental root elongation. Root elongation and tooth eruption require resorption of surrounding alveolar bone to occur. For years, it was postulated that signaling molecules secreted by dental and periodontal cells control bone resorbing osteoclast precursor recruitment and differentiation. Reverse signaling originating from bone cells (osteoclasts and osteoblasts) toward dental cells was not suspected. Dental defects reported in osteopetrosis were associated with mechanical stress secondary to defective bone resorption. In the last decade, consequences of bone resorption over-activation on dental and periodontal tissue formation have been analyzed with transgenic animals (RANK(Tg) and Opg(−∕−) mice). Results suggest the existence of signals originating from osteoclasts toward dental and periodontal cells. Meanwhile, experiments consisting in transitory inhibition of bone resorption during root elongation, achieved with bone resorption inhibitors having different mechanisms of action (bisphosphonates and RANKL blocking antibodies), have evidenced dental and periodontal defects that support the presence of signals originating bone cells toward dental cells. The aim of the present manuscript is to present the data we have collected in the last years that support the hypothesis of a role of bone resorption in dental and periodontal development. Frontiers Media S.A. 2015-11-05 /pmc/articles/PMC4633481/ /pubmed/26594180 http://dx.doi.org/10.3389/fphys.2015.00319 Text en Copyright © 2015 Gama, Navet, Vargas, Castaneda and Lézot. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Physiology
Gama, Andrea
Navet, Benjamin
Vargas, Jorge William
Castaneda, Beatriz
Lézot, Frédéric
Bone resorption: an actor of dental and periodontal development?
title Bone resorption: an actor of dental and periodontal development?
title_full Bone resorption: an actor of dental and periodontal development?
title_fullStr Bone resorption: an actor of dental and periodontal development?
title_full_unstemmed Bone resorption: an actor of dental and periodontal development?
title_short Bone resorption: an actor of dental and periodontal development?
title_sort bone resorption: an actor of dental and periodontal development?
topic Physiology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4633481/
https://www.ncbi.nlm.nih.gov/pubmed/26594180
http://dx.doi.org/10.3389/fphys.2015.00319
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