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Cranial Base Synchondrosis: Chondrocytes at the Hub

The cranial base is formed by endochondral ossification and functions as a driver of anteroposterior cranial elongation and overall craniofacial growth. The cranial base contains the synchondroses that are composed of opposite-facing layers of resting, proliferating and hypertrophic chondrocytes wit...

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Detalles Bibliográficos
Autores principales: Hallett, Shawn A., Ono, Wanida, Franceschi, Renny T., Ono, Noriaki
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9317907/
https://www.ncbi.nlm.nih.gov/pubmed/35887171
http://dx.doi.org/10.3390/ijms23147817
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author Hallett, Shawn A.
Ono, Wanida
Franceschi, Renny T.
Ono, Noriaki
author_facet Hallett, Shawn A.
Ono, Wanida
Franceschi, Renny T.
Ono, Noriaki
author_sort Hallett, Shawn A.
collection PubMed
description The cranial base is formed by endochondral ossification and functions as a driver of anteroposterior cranial elongation and overall craniofacial growth. The cranial base contains the synchondroses that are composed of opposite-facing layers of resting, proliferating and hypertrophic chondrocytes with unique developmental origins, both in the neural crest and mesoderm. In humans, premature ossification of the synchondroses causes midfacial hypoplasia, which commonly presents in patients with syndromic craniosynostoses and skeletal Class III malocclusion. Major signaling pathways and transcription factors that regulate the long bone growth plate—PTHrP–Ihh, FGF, Wnt, BMP signaling and Runx2—are also involved in the cranial base synchondrosis. Here, we provide an updated overview of the cranial base synchondrosis and the cell population within, as well as its molecular regulation, and further discuss future research opportunities to understand the unique function of this craniofacial skeletal structure.
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spelling pubmed-93179072022-07-27 Cranial Base Synchondrosis: Chondrocytes at the Hub Hallett, Shawn A. Ono, Wanida Franceschi, Renny T. Ono, Noriaki Int J Mol Sci Review The cranial base is formed by endochondral ossification and functions as a driver of anteroposterior cranial elongation and overall craniofacial growth. The cranial base contains the synchondroses that are composed of opposite-facing layers of resting, proliferating and hypertrophic chondrocytes with unique developmental origins, both in the neural crest and mesoderm. In humans, premature ossification of the synchondroses causes midfacial hypoplasia, which commonly presents in patients with syndromic craniosynostoses and skeletal Class III malocclusion. Major signaling pathways and transcription factors that regulate the long bone growth plate—PTHrP–Ihh, FGF, Wnt, BMP signaling and Runx2—are also involved in the cranial base synchondrosis. Here, we provide an updated overview of the cranial base synchondrosis and the cell population within, as well as its molecular regulation, and further discuss future research opportunities to understand the unique function of this craniofacial skeletal structure. MDPI 2022-07-15 /pmc/articles/PMC9317907/ /pubmed/35887171 http://dx.doi.org/10.3390/ijms23147817 Text en © 2022 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
Hallett, Shawn A.
Ono, Wanida
Franceschi, Renny T.
Ono, Noriaki
Cranial Base Synchondrosis: Chondrocytes at the Hub
title Cranial Base Synchondrosis: Chondrocytes at the Hub
title_full Cranial Base Synchondrosis: Chondrocytes at the Hub
title_fullStr Cranial Base Synchondrosis: Chondrocytes at the Hub
title_full_unstemmed Cranial Base Synchondrosis: Chondrocytes at the Hub
title_short Cranial Base Synchondrosis: Chondrocytes at the Hub
title_sort cranial base synchondrosis: chondrocytes at the hub
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9317907/
https://www.ncbi.nlm.nih.gov/pubmed/35887171
http://dx.doi.org/10.3390/ijms23147817
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