scholarly journals Symmetry and fluctuation of cell movements in neural crest-derived facial mesenchyme

Development ◽  
2021 ◽  
pp. dev.193755
Author(s):  
Adrian Danescu ◽  
Elisabeth G. Rens ◽  
Jaspreet Rehki ◽  
Johnathan Woo ◽  
Takashi Akazawa ◽  
...  
Keyword(s):  
Neural Crest ◽  
Cleft Lip ◽  
Mesenchymal Cell ◽  
Migration Routes ◽  
Temporal Fluctuations ◽  
Cell Movements ◽  
Cell Velocity ◽  
The Face ◽  
Facial Midline ◽  
Frontonasal Mass

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.

Craniofacial growth and development

2018 ◽  
Author(s):  
T.J. Gillgrass ◽  
R. Welbury
Keyword(s):  
Neural Crest ◽  
Cleft Lip ◽  
Neural Crest Cells ◽  
Signs And Symptoms ◽  
Postnatal Growth ◽  
Prenatal Development ◽  
Routine Care ◽  
Developing Heart ◽  
Frontal Process ◽  
The Face

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.

Aspects of orthodontic protocol in cleft lip and palate patients

2020 ◽  
Vol 20 (2) ◽  
pp. 137-142
Author(s):  
O. V. Dudnik ◽  
Ad. A. Mamedov ◽  
O. I. Admakin ◽  
A. A. Skakodub ◽  
Y. O. Volkov ◽  
...  
Keyword(s):  
Oral Hygiene ◽  
Orthodontic Treatment ◽  
Cleft Lip ◽  
Cleft Lip And Palate ◽  
Comprehensive Approach ◽  
Maxillofacial Region ◽  
Indirect Methods ◽  
Indirect Bonding ◽  
The Face ◽  
Direct And Indirect Methods

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.

TGF-beta-3 Promotes Scarless Repair of Cleft Lip in Mouse Fetuses

2002 ◽  
Vol 81 (10) ◽  
pp. 688-694 ◽  
Author(s):  
K. Kohama ◽  
K. Nonaka ◽  
R. Hosokawa ◽  
L. Shum ◽  
M. Ohishi
Keyword(s):  
Cell Proliferation ◽  
Cyclin D1 ◽  
Cleft Lip ◽  
Ex Vivo ◽  
Fetal Surgery ◽  
Mesenchymal Cell ◽  
Tenascin C ◽  
Cleft Lip Repair ◽  
Mouse Fetuses ◽  
Mesenchymal Transformation

TGF-β3 mediates epithelial-mesenchymal transformation during normal fusion of lip and palate, but how TGF-β3 functions during cleft lip repair remains unexplored. We hypothesize that TGF-β3 promotes fetal cleft lip repair and fusion by increasing the availability of mesenchymal cells. In this investigation, we demonstrated that cleft lips in mouse fetuses were repaired by fetal surgery, producing scarless fusion. At the site of the operation, we first observed an infusion of platelets expressing TGF-β3, followed by increased expression of cyclin D1 and tenascin-C, and coupled with increased mesenchymal cell proliferation. In an ex vivo serumless culture system, cleft lip explants fused in the presence of exogenous TGF-β3. Cultured lips also showed up-regulation in cyclin D1 and tenascin-C expression. These findings suggest that microsurgical repair of cleft lip in the fetus that produced scarless fusion is mediated by TGF-β3 regulation of mesenchymal cell proliferation and migration at the site of repair.

Temporally-regulated retinoic acid depletion produces specific neural crest, ocular and nervous system defects

Development ◽  
1997 ◽  
Vol 124 (16) ◽  
pp. 3111-3121 ◽  
Author(s):  
E.D. Dickman ◽  
C. Thaller ◽  
S.M. Smith
Keyword(s):  
Nervous System ◽  
Retinoic Acid ◽  
Neural Crest ◽  
Female Rats ◽  
Retinoid Receptor ◽  
Knock Out ◽  
The Face ◽  
Normal Males ◽  
Temporal Events ◽  
Null Mutant Mice

Both retinoid receptor null mutants and classic nutritional deficiency studies have demonstrated that retinoids are essential for the normal development of diverse embryonic structures (e.g. eye, heart, nervous system, urogenital tract). Detailed analysis of retinoid-modulated events is hampered by several limitations of these models, including that deficiency or null mutation is present throughout gestation, making it difficult to isolate primary effects, and preventing analysis beyond embryolethality. We developed a mammalian model in which retinoid-dependent events are documented during distinct targeted windows of embryogenesis. This was accomplished through the production of vitamin A-depleted (VAD) female rats maintained on sufficient oral retinoic acid (RA) for growth and fertility. After mating to normal males, these RA-sufficient/VAD females were given oral RA doses which allowed for gestation in an RA-sufficient state; embryogenesis proceeded normally until retinoids were withdrawn dietarily to produce a sudden, acute retinoid deficiency during a selected gestational window. In this trial, final RA doses were administered on E11.5, vehicle at E12.5, and embryos analyzed on E13.5; during this 48 hour window, the last RA dose was metabolized and embryos progressed in a retinoid-deficient state. RA-sufficient embryos were normal. Retinoid-depleted embryos exhibited specific malformations of the face, neural crest, eyes, heart, and nervous system. Some defects were phenocopies of those seen in null mutant mice for RXR alpha(−/−), RXR alpha(−/−)/RAR alpha(−/−), and RAR alpha(−/−)/RAR gamma(−/−), confirming that RA transactivation of its nuclear receptors is essential for normal embryogenesis. Other defects were unique to this deficiency model, showing that complete ligand ‘knock-out’ is required to see those retinoid-dependent events previously concealed by receptor functional redundancy, and reinforcing that retinoid receptors have separate yet overlapping contributions in the embryo. This model allows for precise targeting of retinoid form and deficiency to specific developmental windows, and will facilitate studies of distinct temporal events.

The cephalic neural crest provides pericytes and smooth muscle cells to all blood vessels of the face and forebrain

Development ◽  
2001 ◽  
Vol 128 (7) ◽  
pp. 1059-1068 ◽  
Author(s):  
H.C. Etchevers ◽  
C. Vincent ◽  
N.M. Le Douarin ◽  
G.F. Couly
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Neural Crest ◽  
Muscle Cells ◽  
Embryonic Cell ◽  
Avian Embryo ◽  
Connective Tissues ◽  
The Face ◽  
Mesodermal Origin ◽  
The Central Nervous System

Most connective tissues in the head develop from neural crest cells (NCCs), an embryonic cell population present only in vertebrates. We show that NCC-derived pericytes and smooth muscle cells are distributed in a sharply circumscribed sector of the vasculature of the avian embryo. As NCCs detach from the neural folds that correspond to the future posterior diencephalon, mesencephalon and rhombencephalon, they migrate between the ectoderm and the neuroepithelium into the anterior/ventral head, encountering mesoderm-derived endothelial precursors. Together, these two cell populations build a vascular tree rooted at the departure of the aorta from the heart and ramified into the capillary plexi that irrigate the forebrain meninges, retinal choroids and all facial structures, before returning to the heart. NCCs ensheath each aortic arch-derived vessel, providing every component except the endothelial cells. Within the meninges, capillaries with pericytes of diencephalic and mesencephalic neural fold origin supply the forebrain, while capillaries with pericytes of mesodermal origin supply the rest of the central nervous system, in a mutually exclusive manner. The two types of head vasculature contact at a few defined points, including the anastomotic vessels of the circle of Willis, immediately ventral to the forebrain/midbrain boundary. Over the course of evolution, the vertebrate subphylum may have exploited the exceptionally broad range of developmental potentialities and the plasticity of NCCs in head remodelling that resulted in the growth of the forebrain.

scholarly journals How is the face formed and when it goes wrong: In relation to Cleft Lip/Palate

2021 ◽  
Vol 3 (1) ◽  
Author(s):  
Fozia Khan
Keyword(s):  
Cleft Lip ◽  
Normal Development ◽  
Cleft Lip And Palate ◽  
Complex Structure ◽  
First Trimester ◽  
Facial Defect ◽  
Facial Defects ◽  
The Face ◽  
Embryonic Life ◽  
Cleft Lip Palate

The normal development of the face relies upon the correct morphogenesis of structures in utero that usually occurs within the first trimester of embryonic life. The face is a very complex structure involving many genes and factors and with it being such a crucial part of life, both physically and aesthetically and therefore mentally, its important for everything to be just right. However, when the normal process doesn’t go to plan this results in dysmorphogenesis, which cleft lip and palate (CLP) is an example of as the lip/palate doesn’t fuse together and the infant is left with a gap. Although the exact cause of CLP is unknown, it is thought to be a mixture of genetics, environment and the teratogens the mothers are exposed to within the environment. This report will demonstrate the normal development of the face for the purpose of understanding how it goes wrong, resulting in CLP. Since there is still a lot to be understood about CLP it will also shed light on recent advances in relating SHH and certain genes as a possible cause for this dysmorphogenesis. The report will also briefly look at the relation of CLP with the genes associated with syndromic and non-syndromic diseases and the different types of CLP. There are many other facial defects that are a result of dysmorphogenesis, however as CLP is one of the most common yet poorly understood facial defect, it will be the main focus of this report.

The aetiology and pathogenesis of craniofacial deformity

Development ◽  
1988 ◽  
Vol 103 (Supplement) ◽  
pp. 207-212
Author(s):  
David Poswillo
Keyword(s):  
Neural Crest ◽  
Animal Studies ◽  
Cleft Lip ◽  
Cleft Lip And Palate ◽  
Treacher Collins Syndrome ◽  
Apert Syndrome ◽  
Craniofacial Malformations ◽  
Craniofacial Microsomia ◽  
Animal System ◽  
Isolated Cleft Palate

Craniofacial malformations have been recorded since time immemorial. While observational studies have assisted in the recognition of syndromes, little light has been shed on the causal mechanisms which interfere with craniofacial development. Animal studies in which malformations occur spontaneously or have been induced by teratogenic agents have permitted step-by-step investigation of such common deformities as cleft lip and palate. The role of the ectomesenchymal cells of the neural crest and the possible phenomenon of disorganized spontaneous cell death are described in relation to lip clefts. The factors associated with isolated cleft palate, Pierre Robin syndrome and submucous clefts are described by reference to animal models. The haemorrhagic accident preceding the onset of craniofacial microsomia is discussed as is the distinctly different phenomenon of disturbance to the migration or differentiation of neural crest cells in the pathogenesis of Treacher Collins syndrome. The more severe anomalies of the calvarium such as plagiocephaly, Crouzon and Apert syndrome still defy explanation, in the absence of an appropriate animal system to study; some thoughts on the likely mechanism of abnormal sutural fusions are discussed.

The developmental fate of the cephalic mesoderm in quail-chick chimeras

Development ◽  
1992 ◽  
Vol 114 (1) ◽  
pp. 1-15 ◽  
Author(s):  
G.F. Couly ◽  
P.M. Coltey ◽  
N.M. Le Douarin
Keyword(s):  
Neural Crest ◽  
Neural Crest Cells ◽  
Paraxial Mesoderm ◽  
Avian Embryo ◽  
Facial Skeleton ◽  
Developmental Fate ◽  
Prechordal Mesoderm ◽  
The Face ◽  
Neural Crest Origin ◽  
Neurula Stage

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.

Cochlear Nucleus

2017 ◽  
pp. 415-424
Author(s):  
Eric D. Young ◽  
Donata Oertel
Keyword(s):  
Cochlear Nucleus ◽  
Background Noise ◽  
Acoustic Properties ◽  
Acoustic Cues ◽  
Neuronal Circuits ◽  
Acoustic Environment ◽  
Temporal Fluctuations ◽  
The Face ◽  
Thalamocortical System ◽  
The Brain

Neuronal circuits in the brainstem convert the output of the ear, which carries the acoustic properties of ongoing sound, to a representation of the acoustic environment that can be used by the thalamocortical system. Most important, brainstem circuits reflect the way the brain uses acoustic cues to determine where sounds arise and what they mean. The circuits merge the separate representations of sound in the two ears and stabilize them in the face of disturbances such as loudness fluctuation or background noise. Embedded in these systems are some specialized analyses that are driven by the need to resolve tiny differences in the time and intensity of sounds at the two ears and to resolve rapid temporal fluctuations in sounds like the sequence of notes in music or the sequence of syllables in speech.

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