Talk:Musculoskeletal System - Skull Development
| About Discussion Pages |
|---|
Glossary Links
Cite this page: Hill, M.A. (2024, June 23) Embryology Musculoskeletal System - Skull Development. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Talk:Musculoskeletal_System_-_Skull_Development |
2012
The BMP Ligand Gdf6 Prevents Differentiation of Coronal Suture Mesenchyme in Early Cranial Development
PLoS One. 2012;7(5):e36789. Epub 2012 May 31.
Clendenning DE, Mortlock DP. Source Department of Molecular Physiology and Biophysics, Center for Human Genetics Research, Vanderbilt University School of Medicine, Nashville, Tennessee, United States of America.
Abstract
Growth Differentiation Factor-6 (Gdf6) is a member of the Bone Morphogenetic Protein (BMP) family of secreted signaling molecules. Previous studies have shown that Gdf6 plays a role in formation of a diverse subset of skeletal joints. In mice, loss of Gdf6 results in fusion of the coronal suture, the intramembranous joint that separates the frontal and parietal bones. Although the role of GDFs in the development of cartilaginous limb joints has been studied, limb joints are developmentally quite distinct from cranial sutures and how Gdf6 controls suture formation has remained unclear. In this study we show that coronal suture fusion in the Gdf6-/- mouse is due to accelerated differentiation of suture mesenchyme, prior to the onset of calvarial ossification. Gdf6 is expressed in the mouse frontal bone primordia from embryonic day (E) 10.5 through 12.5. In the Gdf6-/- embryo, the coronal suture fuses prematurely and concurrently with the initiation of osteogenesis in the cranial bones. Alkaline phosphatase (ALP) activity and Runx2 expression assays both showed that the suture width is reduced in Gdf6+/- embryos and is completely absent in Gdf6-/- embryos by E12.5. ALP activity is also increased in the suture mesenchyme of Gdf6+/- embryos compared to wild-type. This suggests Gdf6 delays differentiation of the mesenchyme occupying the suture, prior to the onset of ossification. Therefore, although BMPs are known to promote bone formation, Gdf6 plays an inhibitory role to prevent the osteogenic differentiation of the coronal suture mesenchyme.
PMID 22693558
The human calvaria: a review of embryology, anatomy, pathology, and molecular development
Childs Nerv Syst. 2012 Jan;28(1):23-31. Epub 2011 Nov 27.
Tubbs RS, Bosmia AN, Cohen-Gadol AA. Source Department of Neurosurgery, Children's Hospital, Ambulatory Care Center, 1600 7th Avenue South, Birmingham, AL 35294, USA. shane.tubbs@chsys.org
Abstract
INTRODUCTION: The human skull is a complex structure that deserves continued study. Few studies have directed their attention to the development, pathology, and molecular formation of the human calvaria. MATERIALS AND METHODS: A review of the medical literature using standard search engines was performed to locate studies regarding the human calvaria. RESULTS: The formation of the human calvaria is a complex interaction between bony and meningeal elements. Derailment of these interactions may result in deformation of this part of the skull. CONCLUSIONS: Knowledge of the anatomy, formation, and pathology of the human calvaria will be of use to the clinician that treats skull diseases. With an increased understanding of genetic and molecular biology, treatment paradigms for calvarial issues may change.
PMID 22120469
2010
Design and construction of a brain phantom to simulate neonatal MR images
Comput Med Imaging Graph. 2010 Dec 10. [Epub ahead of print]
Kazemi K, Moghaddam HA, Grebe R, Gondry-Jouet C, Wallois F.
Department of Electrical and Electronics Engineering, Shiraz University of Technology, Shiraz, Iran; GRAMFC EA 4293, Faculty of Medicine, University of Picardie Jules Verne, 80036 Amiens, France. Abstract This paper presents the design and construction of a 3D digital neonatal neurocranial phantom and its application for the simulation of brain magnetic resonance (MR) images. Commonly used digital brain phantoms (e.g. BrainWeb) are based on the adult brain. With the growing interest in computer-aided methods for neonatal MR image processing, there is a growing demand a digital phantom and brain MR image simulator especially for the neonatal brains. This is due to the pronounced differences between adult and neonatal brains not only in terms of size but also, more importantly, in terms of geometrical proportions and the need to subdivide white matter into two different tissue types in neonates. Therefore the neonatal brain phantom created in the here presented work consists of 9 different tissue types: skin, fat, muscle, skull, dura mater, gray matter, myelinated white matter, nonmyelinated white matter and cerebrospinal fluid. Each voxel has a vector consisting of 9 components, one for each of these nine tissue types. This digital phantom can be used to map simulated magnetic resonance signal intensities resulting in simulated MR images of the newborns head. These images with controlled degradation of the image data present a representative, reproducible data set ideal for development and evaluation of neonatal MRI analysis methods, e.g. segmentation and registration algorithms.
Copyright © 2010 Elsevier Ltd. All rights reserved. PMID: 21146956
Fibroblast growth factor receptor signaling crosstalk in skeletogenesis
Sci Signal. 2010 Nov 2;3(146):re9.
Miraoui H, Marie PJ.
Laboratory of Osteoblast Biology and Pathology, INSERM UMR606 and University Paris Diderot, Paris 75475, Cedex 10, France. Abstract Fibroblast growth factors (FGFs) play important roles in the control of embryonic and postnatal skeletal development by activating signaling through FGF receptors (FGFRs). Germline gain-of-function mutations in FGFR constitutively activate FGFR signaling, causing chondrocyte and osteoblast dysfunctions that result in skeletal dysplasias. Crosstalk between the FGFR pathway and other signaling cascades controls skeletal precursor cell differentiation. Genetic analyses revealed that the interplay of WNT and FGFR1 determines the fate and differentiation of mesenchymal stem cells during mouse craniofacial skeletogenesis. Additionally, interactions between FGFR signaling and other receptor tyrosine kinase networks, such as those mediated by the epidermal growth factor receptor and platelet-derived growth factor receptor α, were associated with excessive osteoblast differentiation and bone formation in the human skeletal dysplasia called craniosynostosis, which is a disorder of skull development. We review the roles of FGFR signaling and its crosstalk with other pathways in controlling skeletal cell fate and discuss how this crosstalk could be pharmacologically targeted to correct the abnormal cell phenotype in skeletal dysplasias caused by aberrant FGFR signaling.
PMID: 21045207 The BMP antagonist noggin regulates cranial suture fusion STEPHEN M. WARREN, LISA J. BRUNET, RICHARD M. HARLAND, ARIS N.,ECONOMIDES & MICHAEL T. LONGAKER
"During skull development, the cranial connective tissue framework undergoes intramembranous ossification to form skull bones (calvaria). As the calvarial bones advance to envelop the brain, fibrous sutures form between the calvarial plates. Expansion of the brain is coupled with calvarial growth through a series of tissue interactions within the cranial suture complex. Craniosynostosis, or premature cranial suture fusion, results in an abnormal skull shape, blindness and mental retardation. Recent studies have demonstrated that gain-of-function mutations in fibroblast growth factor receptors ( fgfr ) are associated with syndromic forms of craniosynostosis. Noggin, an antagonist of bone morphogenetic proteins (BMPs), is required for embryonic neural tube, somites and skeleton patterning. Here we show that noggin is expressed postnatally in the suture mesenchyme of patent, but not fusing, cranial sutures, and that noggin expression is suppressed by FGF2 and syndromic fgfr signalling. Since noggin misexpression prevents cranial suture fusion in vitro and in vivo , we suggest that syndromic fgfr -mediated craniosynostoses may be the result of inappropriate downregulation of noggin expression."
