Dataset Information

A physico-mechanical model of postnatal craniofacial growth in human.

ABSTRACT: Our fundamental understanding of the physico-mechanical forces that drive the size and shape changes of the cranium during ontogeny are limited. Biomechanical models based on finite element method present a huge opportunity to address this critical gap in our knowledge. Here, we describe a validated computational framework to predict normal craniofacial growth. Our results demonstrated that this approach is capable of predicting the growth of calvaria, face, and skull base. We highlighted the crucial role of skull base in antero-posterior growth of the face and also demonstrated the contribution of the maxillary expansion to the dorsoventral growth of the face and its interplay with the orbits. These findings highlight the importance of physical interactions of different components of the craniofacial system. The computational framework described here serves as a powerful tool to study fundamental questions in developmental biology and to advance treatment of conditions affecting the craniofacial system such as craniosynostosis.

SUBMITTER: Liang C

PROVIDER: S-EPMC11365398 | biostudies-literature | 2024 Sep

REPOSITORIES: biostudies-literature

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A physico-mechanical model of postnatal craniofacial growth in human.

Liang Ce C Marghoub Arsalan A Profico Antonio A Buzi Costantino C Didziokas Marius M van de Lande Lara L Khonsari Roman Hossein RH Johnson David D O'Higgins Paul P Moazen Mehran M

iScience 20240729 9

Our fundamental understanding of the physico-mechanical forces that drive the size and shape changes of the cranium during ontogeny are limited. Biomechanical models based on finite element method present a huge opportunity to address this critical gap in our knowledge. Here, we describe a validated computational framework to predict normal craniofacial growth. Our results demonstrated that this approach is capable of predicting the growth of calvaria, face, and skull base. We highlighted the cr ...[more]

PMID: 39220256

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Project description:BackgroundThe Epstein-Barr virus is widespread in all human populations and is strongly associated with human disease, ranging from infectious mononucleosis to cancer. In infected cells the virus can adopt several different latency programs, affecting the cells' behaviour. Experimental results indicate that a specific genetic switch between viral latency programs, reprograms human B-cells between proliferative and resting states. Each of these two latency programs makes use of a different viral promoter, Cp and Qp, respectively. The hypothesis tested in this study is that this genetic switch is controlled by both human and viral transcription factors; Oct-2 and EBNA-1. We build a physico-chemical model to investigate quantitatively the dynamical properties of the promoter regulation and experimentally examine protein level variations between the two latency programs.ResultsOur experimental results display significant differences in EBNA-1 and Oct-2 levels between resting and proliferating programs. With the model we identify two stable latency programs, corresponding to a resting and proliferating cell. The two programs differ in robustness and transcriptional activity. The proliferating state is markedly more stable, with a very high transcriptional activity from its viral promoter. We predict the promoter activities to be mutually exclusive in the two different programs, and our relative promoter activities correlate well with experimental data. Transitions between programs can be induced, by affecting the protein levels of our transcription factors. Simulated time scales are in line with experimental results.ConclusionWe show that fundamental properties of the Epstein-Barr virus involvement in latent infection, with implications for tumor biology, can be modelled and understood mathematically. We conclude that EBNA-1 and Oct-2 regulation of Cp and Qp is sufficient to establish mutually exclusive expression patterns. Moreover, the modelled genetic control predict both mono- and bistable behavior and a considerable difference in transition dynamics, based on program stability and promoter activities. Both these phenomena we hope can be further investigated experimentally, to increase the understanding of this important switch. Our results also stress the importance of the little known regulation of human transcription factor Oct-2.

Project description:Humans and other jawed vertebrates rely heavily on their craniofacial skeleton for eating, breathing, and communicating. As such, it is vital that the elements of the craniofacial skeleton develop properly during embryogenesis to ensure a high quality of life and evolutionary fitness. Indeed, craniofacial abnormalities, including cleft palate and craniosynostosis, represent some of the most common congenital abnormalities in newborns. Like many other organ systems, the development of the craniofacial skeleton is complex, relying on specification and migration of the neural crest, patterning of the pharyngeal arches, and morphogenesis of each skeletal element into its final form. These processes must be carefully coordinated and integrated. One way this is achieved is through the spatial and temporal deployment of cell signaling pathways. Recent studies conducted using the zebrafish model underscore the importance of the Transforming Growth Factor Beta (TGF-β) and Bone Morphogenetic Protein (BMP) pathways in craniofacial development. Although both pathways contain similar components, each pathway results in unique outcomes on a cellular level. In this review, we will cover studies conducted using zebrafish that show the necessity of these pathways in each stage of craniofacial development, starting with the induction of the neural crest, and ending with the morphogenesis of craniofacial elements. We will also cover human skeletal and craniofacial diseases and malformations caused by mutations in the components of these pathways (e.g., cleft palate, craniosynostosis, etc.) and the potential utility of zebrafish in studying the etiology of these diseases. We will also briefly cover the utility of the zebrafish model in joint development and biology and discuss the role of TGF-β/BMP signaling in these processes and the diseases that result from aberrancies in these pathways, including osteoarthritis and multiple synostoses syndrome. Overall, this review will demonstrate the critical roles of TGF-β/BMP signaling in craniofacial development and show the utility of the zebrafish model in development and disease.

Dataset Information

A physico-mechanical model of postnatal craniofacial growth in human.

Publications

A physico-mechanical model of postnatal craniofacial growth in human.

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