Craniofacial growth and development

Author(s):  
T.J. Gillgrass ◽  
R. Welbury

This chapter describes, in general terms, the prenatal development and postnatal growth of the craniofacial skeleton, and the occlusal development of the primary and permanent dentitions. Understanding of embryological development is essential for the dental practitioner who may frequently face patients with common craniofacial anomalies such as cleft lip and/or palate. For routine care, an understanding of their development and aetiology will bring insight to their likely presenting signs and symptoms. This section will include a brief summary of the development of the face, including the neural crest and pharyngeal arches. It is not the intention of this summary to be in any way a complete or thorough description but simply to describe some of the key cells/interactions and structures. Neural crest cells are derived from the neural fold, and are highly migratory and specialized cells capable of predetermined differentiation. The differentiation occurs after their migration and is essential for the normal development of face and teeth. By week 4 the primitive mouth or stomatodeum is bordered laterally and from the developing heart inferiorly by the pharyngeal or branchial arches. These are six bilateral cylindrical thickenings (although the fifth and sixth are small) which form in the pharyngeal wall and into which the neural crest cells migrate. They are separated externally by the branchial grooves and internally by the pharyngeal pouches. The first groove and pouches are involved in the formation of the auditory apparatus and the Eustachian tube. Each arch has a derived cartilage rod, muscular, nervous, and vascular component. The first two arches and their associated components are central to the development of the facial structures. This period is also characterized by the development of the organs for hearing, sight, and smell, namely the otic, optic, and nasal placodes. By the end of week 4, thickenings start to develop in the frontal process. The medial and lateral frontonasal processes develop from these, together with the nasal placodes. The maxillary process develops from the first pharyngeal arch and grows forward to meet the medial and nasal processes, from which it is separated by distinct grooves at week 7.

Development ◽  
1992 ◽  
Vol 114 (1) ◽  
pp. 1-15 ◽  
Author(s):  
G.F. Couly ◽  
P.M. Coltey ◽  
N.M. Le Douarin

The developmental fate of the cephalic paraxial and prechordal mesoderm at the late neurula stage (3-somite) in the avian embryo has been investigated by using the isotopic, isochronic substitution technique between quail and chick embryos. The territories involved in the operation were especially tiny and the size of the transplants was of about 150 by 50 to 60 microns. At that stage, the neural crest cells have not yet started migrating and the fate of mesodermal cells exclusively was under scrutiny. The prechordal mesoderm was found to give rise to the following ocular muscles: musculus rectus ventralis and medialis and musculus oblicus ventralis. The paraxial mesoderm was separated in two longitudinal bands: one median, lying upon the cephalic vesicles (median paraxial mesoderm—MPM); one lateral, lying upon the foregut (lateral paraxial mesoderm—LPM). The former yields the three other ocular muscles, contributes to mesencephalic meninges and has essentially skeletogenic potencies. It contributes to the corpus sphenoid bone, the orbitosphenoid bone and the otic capsules; the rest of the facial skeleton is of neural crest origin. At 3-somite stage, MPM is represented by a few cells only. The LPM is more abundant at that stage and has essentially myogenic potencies with also some contribution to connective tissue. However, most of the connective cells associated with the facial and hypobranchial muscles are of neural crest origin. The more important result of this work was to show that the cephalic mesoderm does not form dermis. This function is taken over by neural crest cells, which form both the skeleton and dermis of the face. If one draws a parallel between the so-called “somitomeres” of the head and the trunk somites, it appears that skeletogenic potencies are reduced in the former, which in contrast have kept their myogenic capacities, whilst the formation of skeleton and dermis has been essentially taken over by the neural crest in the course of evolution of the vertebrate head.


Development ◽  
2021 ◽  
pp. dev.193755
Author(s):  
Adrian Danescu ◽  
Elisabeth G. Rens ◽  
Jaspreet Rehki ◽  
Johnathan Woo ◽  
Takashi Akazawa ◽  
...  

In the face, symmetry is established when bilateral streams of neural crest cells leave the neural tube at the same time, follow identical migration routes and then give rise to the facial prominences. However developmental instability exists, particularly surrounding the steps of lip fusion. The causes of instability are unknown but inability to cope with developmental fluctuations are a likely cause of congenital malformations such as non-syndromic orofacial clefts. Here, we tracked cell movements over time in the frontonasal mass which forms the facial midline and participates in lip fusion using live-cell imaging. Our mathematical examination of cell velocity vectors uncovered temporal fluctuations in several parameters including order/disorder, symmetry/asymmetry and divergence/convergence. We found that treatment with a RhoGTPase inhibitor completely disrupted the temporal fluctuations in all measures and blocked morphogenesis. Thus we discovered that genetic control of symmetry extends to mesenchymal cell movements and that these movements are of the type that could be perturbed in in asymmetrical malformations such as non-syndromic cleft lip.


2020 ◽  
Vol 11 ◽  
Author(s):  
Anthony-Samuel LaMantia

Mesenchephalic and rhombencephalic neural crest cells generate the craniofacial skeleton, special sensory organs, and subsets of cranial sensory receptor neurons. They do so while preserving the anterior-posterior (A-P) identity of their neural tube origins. This organizational principle is paralleled by central nervous system circuits that receive and process information from facial structures whose A-P identity is in register with that in the brain. Prior to morphogenesis of the face and its circuits, however, neural crest cells act as “inductive ambassadors” from distinct regions of the neural tube to induce differentiation of target craniofacial domains and establish an initial interface between the brain and face. At every site of bilateral, non-axial secondary induction, neural crest constitutes all or some of the mesenchymal compartment for non-axial mesenchymal/epithelial (M/E) interactions. Thus, for epithelial domains in the craniofacial primordia, aortic arches, limbs, the spinal cord, and the forebrain (Fb), neural crest-derived mesenchymal cells establish local sources of inductive signaling molecules that drive morphogenesis and cellular differentiation. This common mechanism for building brains, faces, limbs, and hearts, A-P axis specified, neural crest-mediated M/E induction, coordinates differentiation of distal structures, peripheral neurons that provide their sensory or autonomic innervation in some cases, and central neural circuits that regulate their behavioral functions. The essential role of this neural crest-mediated mechanism identifies it as a prime target for pathogenesis in a broad range of neurodevelopmental disorders. Thus, the face and the brain “predict” one another, and this mutual developmental relationship provides a key target for disruption by developmental pathology.


2017 ◽  
Vol 54 (4) ◽  
pp. 381-390 ◽  
Author(s):  
Hannah Neiswender ◽  
Sammy Navarre ◽  
David J. Kozlowski ◽  
Ellen K. Lemosy

Objective Tinagl1 has a weak genetic association with craniosynostosis, but its functions in cartilage and bone development are unknown. Knockdown of Tinagl1 in zebrafish embryos allowed an initial characterization of its potential effects on craniofacial cartilage development and a test of whether these effects could involve Wnt signaling. Results Tinagl1 knockdown resulted in dose-dependent reductions and defects in ventral pharyngeal arch cartilages as well as the ethmoid plate, a zebrafish correlate to the palate. These defects could be correlated to reduced numbers of cranial neural crest cells in the pharyngeal arches and could be reproduced with comanipulation of Tinagl1 and Wnt3a by morpholino-based knockdown. Conclusions These results suggest that Tinagl1 is required early in the proliferation or migration of cranial neural crest cells and that its effects are mediated via Wnt3a signaling. Because Wnt3a is among the Wnts that contribute to nonsyndromic cleft lip and cleft palate in mouse and man, further investigation of Tinagl1 may help to elucidate mechanisms underlying these disorders.


2021 ◽  
Author(s):  
Sabrina Shameen Alam ◽  
Shruti Kumar ◽  
Marie-Claude Beauchamp ◽  
Eric Bareke ◽  
Alexia Boucher ◽  
...  

Heterozygous mutations in SNRPB, an essential core component of the five small ribonucleoprotein particles of the spliceosome, are responsible for Cerebrocostomandibular Syndrome (CCMS). However, the underlying pathophysiology of CCMS remains a mystery. We generated mouse embryos with heterozygous deletion of Snrpb and showed that they arrest shortly after implantation. We also showed that heterozygous deletion of Snrpb in the developing brain and neural crest cells models many of the craniofacial malformations found in CCMS, and results in death shortly after birth. Abnormalities in these mutant embryos ranged from cleft palate to a complete absence of the ventral portion of the face and are due to apoptosis of the neural crest cells in the frontonasal prominence and pharyngeal arches. RNAseq analysis of mutant embryonic heads prior to morphological defects revealed increased exon-skipping and intron-retention in association with increased 5' splice strength. Mutant embryonic heads had increased exon-skipping in Mdm2 and Mdm4 negative regulators of the P53-pathway and a increased nuclear P53 and P53-target genes. However, removing one or both copies of P53 in Snrpb heterozygous mutant neural crest cells did not rescue craniofacial development. We also found a small but significant increase in exon-skipping of several transcripts required for head and midface development, including Smad2 and Rere. Furthermore, mutant embryos exhibited ectopic or missing expression of Fgf8 and Shh, which are required to coordinate face and brain development. Thus, we propose that mis-splicing of transcripts that regulate P53-activity and craniofacial-specific genes both contribute to craniofacial malformations.


2016 ◽  
Vol 2 (8) ◽  
pp. e1600060 ◽  
Author(s):  
Marketa Kaucka ◽  
Evgeny Ivashkin ◽  
Daniel Gyllborg ◽  
Tomas Zikmund ◽  
Marketa Tesarova ◽  
...  

Cranial neural crest cells populate the future facial region and produce ectomesenchyme-derived tissues, such as cartilage, bone, dermis, smooth muscle, adipocytes, and many others. However, the contribution of individual neural crest cells to certain facial locations and the general spatial clonal organization of the ectomesenchyme have not been determined. We investigated how neural crest cells give rise to clonally organized ectomesenchyme and how this early ectomesenchyme behaves during the developmental processes that shape the face. Using a combination of mouse and zebrafish models, we analyzed individual migration, cell crowd movement, oriented cell division, clonal spatial overlapping, and multilineage differentiation. The early face appears to be built from multiple spatially defined overlapping ectomesenchymal clones. During early face development, these clones remain oligopotent and generate various tissues in a given location. By combining clonal analysis, computer simulations, mouse mutants, and live imaging, we show that facial shaping results from an array of local cellular activities in the ectomesenchyme. These activities mostly involve oriented divisions and crowd movements of cells during morphogenetic events. Cellular behavior that can be recognized as individual cell migration is very limited and short-ranged and likely results from cellular mixing due to the proliferation activity of the tissue. These cellular mechanisms resemble the strategy behind limb bud morphogenesis, suggesting the possibility of common principles and deep homology between facial and limb outgrowth.


2007 ◽  
Vol 27 (1) ◽  
pp. 45-52
Author(s):  
Koh-ichi Atoh ◽  
Manae S. Kurokawa ◽  
Hideshi Yoshikawa ◽  
Chieko Masuda ◽  
Erika Takada ◽  
...  

Author(s):  
O. V. Dudnik ◽  
Ad. A. Mamedov ◽  
O. I. Admakin ◽  
A. A. Skakodub ◽  
Y. O. Volkov ◽  
...  

Relevance. Cleft lip and palate is one of the severe malformations of the face and jaw, requiring a comprehensive approach to the rehabilitation of the patients, including doctors of various specialties, one of which is orthodontists. A feature of orthodontic treatment is difficulty of fixing bracket systems, as well as lowering the level of oral hygiene, caused by deformation and displacement of fragments of the maxillofacial region.Purpose. Improving the effectiveness of orthodontic treatment and hygiene of the oral caviti in patients with cleft lip and palate in permanent bite period.Materials and methods. A comparison was made of the effetctiveness of fixing brackets systmes with direct and indirect bonding techniques and the effectiveness of oral hygiene during orthodontic treatment using irrigators.Results. The results of the study showed a difference in the effectiveness of using direct and indirect methods of fixing bracket systems in patients with cleft and palate. The use of irrigators as additional means of oral hygiene has demonstrated a positive dynamic of hygiene indices.Conclusions. Results of the study demonstrate the advantages of fixation the brackets by indirect bonding and use additional hygiene products irrigator for improving of oral hygiene.


Sign in / Sign up

Export Citation Format

Share Document