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Journal articles on the topic 'Craniofacial morphogenesis'

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Published: 10 December 2022
Last updated: 28 January 2023

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1

Klueber, Kathleen M. "Craniofacial Morphogenesis." Ear, Nose & Throat Journal 71, no. 10 (October 1992): 472–76. http://dx.doi.org/10.1177/014556139207101008.

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2

Cobourne, M. "Review: Craniofacial Morphogenesis." European Journal of Orthodontics 25, no. 2 (April 1, 2003): 214–15. http://dx.doi.org/10.1093/ejo/25.2.214.

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3

Solursh, Michael, and Jeffrey Murray. "Craniofacial Morphogenesis Workshop Report." Cleft Palate-Craniofacial Journal 31, no. 3 (May 1994): 230–31. http://dx.doi.org/10.1597/1545-1569(1994)031<0230:cmwr>2.3.co;2.

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4

Solursh, Michael, and Jeffrey Murray. "Craniofacial Morphogenesis Workshop Report." Cleft Palate-Craniofacial Journal 31, no. 3 (May 1994): 230–31. http://dx.doi.org/10.1597/1545-1569_1994_031_0230_cmwr_2.3.co_2.

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The following report highlights the discussions and Interaction at the workshop on craniofacial morphogenesis, sponsored by The Human Frontier Science Program, held in April 1993 at the University of Iowa. A brief summary of selected sessions is Included to exemplify the benefits of bringing together Individuals from various disciplines and backgrounds In order to establish a unified theory of craniofacial morphogenesis. The synthesis of information and experience of a wide range of approaches made the 4-day period an Invaluable experience for the participants from nine different countries.
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5

Radlanski, RJ. "Prenatal craniofacial morphogenesis: four-dimensional visualization of morphogenetic processes." Orthodontics & Craniofacial Research 6 (August 2003): 89–94. http://dx.doi.org/10.1034/j.1600-0544.2003.240.x.

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6

Mundhada, A., U. Kulkarni, V. Swami, S. Deshmukh, and A. Patil. "Craniofacial Muscles-differentiation and Morphogenesis." Annual Research & Review in Biology 9, no. 6 (January 10, 2016): 1–9. http://dx.doi.org/10.9734/arrb/2016/24329.

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7

Helms, J. A. "New insights into craniofacial morphogenesis." Development 132, no. 5 (February 2, 2005): 851–61. http://dx.doi.org/10.1242/dev.01705.

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8

Szabo-Rogers, Heather L., Lucy E. Smithers, Wardati Yakob, and Karen J. Liu. "New directions in craniofacial morphogenesis." Developmental Biology 341, no. 1 (May 2010): 84–94. http://dx.doi.org/10.1016/j.ydbio.2009.11.021.

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9

Chai, Yang, and Robert E. Maxson. "Recent advances in craniofacial morphogenesis." Developmental Dynamics 235, no. 9 (2006): 2353–75. http://dx.doi.org/10.1002/dvdy.20833.

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10

Lu, Chung-Ling, and Jinoh Kim. "Craniofacial Diseases Caused by Defects in Intracellular Trafficking." Genes 12, no. 5 (May 13, 2021): 726. http://dx.doi.org/10.3390/genes12050726.

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Cells use membrane-bound carriers to transport cargo molecules like membrane proteins and soluble proteins, to their destinations. Many signaling receptors and ligands are synthesized in the endoplasmic reticulum and are transported to their destinations through intracellular trafficking pathways. Some of the signaling molecules play a critical role in craniofacial morphogenesis. Not surprisingly, variants in the genes encoding intracellular trafficking machinery can cause craniofacial diseases. Despite the fundamental importance of the trafficking pathways in craniofacial morphogenesis, relatively less emphasis is placed on this topic, thus far. Here, we describe craniofacial diseases caused by lesions in the intracellular trafficking machinery and possible treatment strategies for such diseases.
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11

Partridge, James. "Psycho-social reflections on craniofacial morphogenesis." Seminars in Cell & Developmental Biology 21, no. 3 (May 2010): 333–38. http://dx.doi.org/10.1016/j.semcdb.2010.01.006.

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12

Nassif, Ali, Ibtisam Senussi, Fleur Meary, Sophia Loiodice, Dominique Hotton, Benoît Robert, Morad Bensidhoum, Ariane Berdal, and Sylvie Babajko. "Msx1 role in craniofacial bone morphogenesis." Bone 66 (September 2014): 96–104. http://dx.doi.org/10.1016/j.bone.2014.06.003.

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13

Osumi-Yamashita, Noriko. "Retinoic acid and mammalian craniofacial morphogenesis." Journal of Biosciences 21, no. 3 (May 1996): 313–27. http://dx.doi.org/10.1007/bf02703091.

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14

Agnihotri, Gaurav. "The Fundamentals for Craniofacial Morphogenesis -A review with emphasis on the decisive dynamics." National Journal of Clinical Anatomy 07, no. 01 (January 2018): 052–57. http://dx.doi.org/10.1055/s-0040-1701717.

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AbstractA rekindled need to widerstand details of craniofacial morphogenesis stems from the clinicians requirement to distinguish normal Variation from the effect of abnormal or pathologic processes. The understanding of the developmental blueprint is core to diagnosis, timing, planning of treatment and predicting post treatment outcomes. The morphogenesis works constantly towards a State of composite, architectonic balance among all of the separate growing parts. The various parts, developmentally merge into a functional whole with each part complementing the others as they all grow and function together. The present overview takes into account the principal fundamentals of the morphogenesis and the decisive dynamics involved therein. There is a cephalo-caudal gradient in the craniofacial growth pattern. In accordance with functional matrix theory, the major determinant of growth of maxilla and mandible is enlargement of nasal and oral cavities, which grow in response to functional needs. The craniofacial complex can be divided into four areas that grow rather differently.These are cranial vault, cranial base, nasomaxillary complex and mandible. The craniofacial morphogenesis leads to an aggregate State of structural and functional equilibrium. A thorough understanding of the process and patterns is the 'vital key' for successful therapies in this region.
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15

Lu, M., F. Ping, and J. Hong. "Role of the decoy bone morphogenetic protein receptor in craniofacial morphogenesis." International Journal of Oral and Maxillofacial Surgery 38, no. 5 (May 2009): 549. http://dx.doi.org/10.1016/j.ijom.2009.03.535.

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16

Hu, D., and J. A. Helms. "The role of sonic hedgehog in normal and abnormal craniofacial morphogenesis." Development 126, no. 21 (November 1, 1999): 4873–84. http://dx.doi.org/10.1242/dev.126.21.4873.

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There is growing evidence that implicates a role for Sonic hedgehog (SHH) in morphogenesis of the craniofacial complex. Mutations in human and murine SHH cause midline patterning defects that are manifested in the head as holoprosencephaly and cyclopia. In addition, teratogens such as jervine, which inhibit the response of tissues to SHH, also produce cyclopia. Thus, the loss of SHH signaling during early stages of neural plate patterning has a profound influence of craniofacial morphogenesis. However, the severity of these defects precludes analyses of SHH function during later stages of craniofacial development. We have used an embryonic chick system to study the role of SHH during these later stages of craniofacial development. Using a combination of surgical and molecular experiments, we show here that SHH is essential for morphogenesis of the frontonasal and maxillary processes (FNP and MXPs), which give rise to the mid- and upper face. Transient loss of SHH signaling in the embryonic face inhibits growth of the primordia and results in defects analogous to hypotelorism and cleft lip/palate, characteristics of the mild forms of holoprosencephaly. In contrast, excess SHH leads to a mediolateral widening of the FNP and a widening between the eyes, a condition known as hypertelorism. In severe cases, this widening is accompanied by facial duplications. Collectively, these experiments demonstrate that SHH has multiple and profound effects on the entire spectrum of craniofacial development, and perturbations in SHH signaling are likely to underlie a number of human craniofacial anomalies.
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17

Ogou, Soh-Ichi. "Immunological perturbation of craniofacial morphogenesis in vitro." JOURNAL OF THE STOMATOLOGICAL SOCIETY,JAPAN 54, no. 1 (1987): 37–46. http://dx.doi.org/10.5357/koubyou.54.37.

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18

Baas, Dominique, Maryline Malbouyres, Zofia Haftek-Terreau, Dominique Le Guellec, and Florence Ruggiero. "Craniofacial cartilage morphogenesis requires zebrafish col11a1 activity." Matrix Biology 28, no. 8 (October 2009): 490–502. http://dx.doi.org/10.1016/j.matbio.2009.07.004.

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19

Noden, Drew M., and Philippa Francis-West. "The differentiation and morphogenesis of craniofacial muscles." Developmental Dynamics 235, no. 5 (2006): 1194–218. http://dx.doi.org/10.1002/dvdy.20697.

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20

Heath, Lindsay, and Peter Thorogood. "Keratan sulfate expression during avian craniofacial morphogenesis." Roux's Archives of Developmental Biology 198, no. 2 (June 1989): 103–13. http://dx.doi.org/10.1007/bf02447745.

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21

Percival, Christopher J., Rebecca Green, Ralph Marcucio, and Benedikt Hallgrímsson. "Surface landmark quantification of embryonic mouse craniofacial morphogenesis." BMC Developmental Biology 14, no. 1 (2014): 31. http://dx.doi.org/10.1186/1471-213x-14-31.

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22

Morriss-Kay, Gillian. "Retinoic acid and craniofacial development: Molecules and morphogenesis." BioEssays 15, no. 1 (January 1993): 9–15. http://dx.doi.org/10.1002/bies.950150103.

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23

Veistinen, Lotta, Thomas Åberg, and David P. C. Rice. "Convergent signalling through Fgfr2 regulates divergent craniofacial morphogenesis." Journal of Experimental Zoology Part B: Molecular and Developmental Evolution 312B, no. 4 (June 15, 2009): 351–60. http://dx.doi.org/10.1002/jez.b.21276.

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24

Diewert, Virginia M., and Kang-Yee Wang. "Recent Advances in Primary Palate and Midface Morphogenesis Research." Critical Reviews in Oral Biology & Medicine 4, no. 1 (October 1992): 111–30. http://dx.doi.org/10.1177/10454411920040010201.

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During the sixth week of human development, the primary palate develops as facial prominences enlarge around the nasal pits to form the premaxillary region. Growth of craniofacial components changes facial morphology and affects the extent of contact between the facial prominences. Our recent studies have focused on developing methods to analyze growth of the primary palate and the craniofacial complex to define morphological phases of normal development and to determine alterations leading to cleft lip malformation. Analysis of human embryos in the Carnegie Embryology Collection and mouse embryos of cleft lip and noncleft strains showed that human and mouse embryos have similar phases of primary palate development: first, an epithelial seam, the nasal fin, forms; then a mesenchymal bridge develops through the nasal fin and enlarges rapidly. A robust mesenchymal bridge must form between the facial prominences before advancing midfacial growth patterns tend to separate the facial components as the medial nasal region narrows and elongates, the nasal pits narrow, and the primary choanae (posterior nares) open posterior to the primary palate. In mouse strains with cleft lip gene, maxillary growth, nasal fin formation, and mesenchymal replacement of the nasal fin were all delayed compared with noncleft strains of mice. Successful primary palate formation involves a sequence of local cellular events that are closely timed with spatial changes associated with craniofacial growth that must occur within a critical developmental period.
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25

Wedden, S. E. "Morphogenesis of the head and face: discussion report." Development 103, Supplement (September 1, 1988): 61–62. http://dx.doi.org/10.1242/dev.103.supplement.61.

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The discussion following the session on evolution and morphogenesis of the head and face concentrated upon two major issues: (1) How can one test models of development, particularly at biochemical and molecular levels? (2) Are the cell populations of the early facial primordia heterogeneous and when might this heterogeneity arise? The Chairman, J. Z. Young (London), had suggested in his introductory remarks that research into craniofacial development was at last becoming more specialized, having previously dealt with principles and model systems rather than with issues of practical importance. The ensuing lectures clearly demonstrated the direction and advances in current research, both in evolutionary aspects and at the level of morphogenesis. Robert Greene (Philadelphia) opened the general discussion. He emphasized the need to examine biochemical and molecular aspects of craniofacial development. In his view, the conceptual chasm between the gene and metazoan embryogenesis was wide and deep and had remained so in recent years.
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26

Christian, Laura, Harinath Bahudhanapati, and Shuo Wei. "Extracellular metalloproteinases in neural crest development and craniofacial morphogenesis." Critical Reviews in Biochemistry and Molecular Biology 48, no. 6 (September 25, 2013): 544–60. http://dx.doi.org/10.3109/10409238.2013.838203.

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27

Trainor, Paul A. "Craniofacial morphogenesis: a meeting in memory of Peter Thorogood." BioEssays 22, no. 2 (January 31, 2000): 202–4. http://dx.doi.org/10.1002/(sici)1521-1878(200002)22:2<202::aid-bies12>3.0.co;2-9.

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28

Nonaka, Kazuaki, Yasunori Sasaki, Yoshihisa Watanabe, Ken-ichi Yanagita, and Minoru Nakata. "Effects of Fetus Weight, Dam Strain, Dam Weight, and Litter Size on the Craniofacial Morphogenesis of CL/Fr Mouse Fetuses Affected with Cleft Lip and Palate." Cleft Palate-Craniofacial Journal 34, no. 4 (July 1997): 325–30. http://dx.doi.org/10.1597/1545-1569_1997_034_0325_eofwds_2.3.co_2.

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Objective: This study examined the factors related to the morphogenesis of the craniofacial complex of the CL/Fr mouse fetus affected with CLP based on the findings of a lateral cephalogram. Design: Embryo transfer experiments were performed to determine the effect of the fetus weight, dam strain, dam weight, and litter size on the intra-uterine craniofacial morphogenesis of CL/Fr mouse fetuses. On the 18th gestational day, each pregnant dam that had received CL/Fr mouse embryos was laparotomized to remove the transferred fetuses that had developed in the uteri of the cleft lip and palate (CLP)-susceptible CL/Fr strain dam and the CLP-resistant C57BL strain dam. A cephalometric observation of the craniofacial morphology of each fetus was subsequently performed. Results: Based on a multiple regression analysis, the standardized partial regression coefficients of the affected fetus weight, the dam weight, and the litter size on the maxillary size of the affected CL/Fr fetus were 0.71 (p < .01), 0.03, and −0.07. According to a least-squares analysis of variance, the dam strain effect in addition to the effect of the affected fetus weight on the maxillary size and the cranial size of the affected fetuses was significant (p < .01 for cranial size, p < .05 for maxillary size) and close to a significant level (p = .09) for the mandibular size of the affected fetuses. The adjusted maxillary size and cranial size after statistically eliminating the effects of the affected fetus weight, dam weight, and lifter size on each original craniofacial size of the affected fetuses that had developed in the CL/Er dam strain were also significantly smaller than those of the affected fetuses that had developed in the C57BL dam strain. Conclusions: The present results indicate that the craniofacial growth of the CL/Fr mouse fetus affected with CLP increased in proportion to the fetus weight. The dam strain effect, in addition to the effect of the affected fetus weight, could thus not be ignored when the etiology of the spontaneous CLP was examined, while the uterine environment, provided by the CL/Fr strain dam, retarded the intra-uterine craniofacial growth of the affected fetuses. It was therefore concluded that the dam strain effect, as well as the effect of the affected fetus weight, both play an important role on the craniofacial morphogenesis of the CL/Fr strain of the affected fetuses that developed in both strain dams.
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29

Lyons, K. M., R. W. Pelton, and B. L. Hogan. "Organogenesis and pattern formation in the mouse: RNA distribution patterns suggest a role for bone morphogenetic protein-2A (BMP-2A)." Development 109, no. 4 (August 1, 1990): 833–44. http://dx.doi.org/10.1242/dev.109.4.833.

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Bone morphogenetic protein-2A (BMP-2A) is a member of the transforming growth factor beta (TGF beta) gene family that has been implicated in cartilage and bone formation. Here we use in situ hybridization to show that BMP-2A RNA is expressed in a variety of embryonic epithelial and mesenchymal tissues outside of the developing skeletal system, including cell populations known to play important roles in morphogenesis. Thus, high levels of transcripts are found in developing limb buds (ventral ectoderm and apical ectodermal ridge), heart (myocardium of the atrioventricular canal), whisker follicles (ectodermal placodes, hair matrix and precortex cells), tooth buds (epithelial buds, dental papilla and odontoblasts), and craniofacial mesenchyme, as well as a number of other sites. The expression patterns of BMP-2A are different from those of TGF beta-1, -2 and -3, and this is illustrated in detail in the developing whisker follicles. These results suggest that BMP-2A plays multiple roles in morphogenesis and pattern formation in the vertebrate embryo.
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30

Brault, V., R. Moore, S. Kutsch, M. Ishibashi, D. H. Rowitch, A. P. McMahon, L. Sommer, O. Boussadia, and R. Kemler. "Inactivation of the (β)-catenin gene by Wnt1-Cre-mediated deletion results in dramatic brain malformation and failure of craniofacial development." Development 128, no. 8 (April 15, 2001): 1253–64. http://dx.doi.org/10.1242/dev.128.8.1253.

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('bgr;)-Catenin is a central component of both the cadherin-catenin cell adhesion complex and the Wnt signaling pathway. We have investigated the role of (β)-catenin during brain morphogenesis, by specifically inactivating the (β)-catenin gene in the region of Wnt1 expression. To achieve this, mice with a conditional ('floxed') allele of (β)-catenin with required exons flanked by loxP recombination sequences were intercrossed with transgenic mice that expressed Cre recombinase under control of Wnt1 regulatory sequences. (β)-catenin gene deletion resulted in dramatic brain malformation and failure of craniofacial development. Absence of part of the midbrain and all of the cerebellum is reminiscent of the conventional Wnt1 knockout (Wnt1(−)(/)(−)), suggesting that Wnt1 acts through (β)-catenin in controlling midbrain-hindbrain development. The craniofacial phenotype, not observed in embryos that lack Wnt1, indicates a role for (β)-catenin in the fate of neural crest cells. Analysis of neural tube explants shows that (β)-catenin is efficiently deleted in migrating neural crest cell precursors. This, together with an increased apoptosis in cells migrating to the cranial ganglia and in areas of prechondrogenic condensations, suggests that removal of (β)-catenin affects neural crest cell survival and/or differentiation. Our results demonstrate the pivotal role of (β)-catenin in morphogenetic processes during brain and craniofacial development.
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31

Moiseiwitsch, Julian R. D. "The Role of Serotonin and Neurotransmitters During Craniofacial Development." Critical Reviews in Oral Biology & Medicine 11, no. 2 (April 2000): 230–39. http://dx.doi.org/10.1177/10454411000110020601.

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Several neurotransmitters, in particular serotonin (5-HT), have demonstrated multiple functions during early development and mid-gestational craniofacial morphogenesis. Early studies indicated that 5-HT is present in the oocyte, where it appears to function as a regulator of cell cleavage. Later, it has a significant role during gastrulation, during which there are significant areas of 5-HT uptake in the primitive streak. Subsequently, in association with neurulation, 5-HT uptake is seen in the floor plate of the developing neural tube. During neural crest formation and branchial arch formation, 5-HT has been demonstrated to facilitate cell migration and stimulate cell differentiation. During morphogenesis of the craniofacial structures, 5-HT stimulates dental development and may aid in cusp formation. All of the most commonly prescribed anti-depressant drugs inhibit serotonin uptake, yet they do not appear to cause major craniofacial malformations in vivo. Given the wide spectrum of effects that 5-HT has during development, it is difficult to understand why these anti-depressants are not major teratogens. Redundancy within the system may allow receptor and uptake pathways to function normally even with lower than normal levels of circulating serotonin. Serotonin-binding proteins, that are expressed in most craniofacial regions at critical times during craniofacial development, may have a buffering capacity that maintains adequate 5-HT tissue concentrations over a wide range of 5-HT serum concentrations. Dental development appears to be particularly sensitive to even small fluctuations in concentrations of 5-HT. Therefore, it may be that children of patients who have received selective serotonergic re-uptake inhibitors (such as Prozac and Zoloft) or the less selective tricyclic anti-depressant drugs (such as Elavil) would be at a higher risk for developmental dental defects such as anodontia and hypodontia. In this review, the evidence supporting a role for 5-HT during mammalian craniofacial development is discussed. A series of models is proposed that may explain how the craniofacial effects of 5-HT are mediated.
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32

Neuhauss, S. C., L. Solnica-Krezel, A. F. Schier, F. Zwartkruis, D. L. Stemple, J. Malicki, S. Abdelilah, D. Y. Stainier, and W. Driever. "Mutations affecting craniofacial development in zebrafish." Development 123, no. 1 (December 1, 1996): 357–67. http://dx.doi.org/10.1242/dev.123.1.357.

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In a large-scale screen for mutations affecting embryogenesis in zebrafish, we identified 48 mutations in 34 genetic loci specifically affecting craniofacial development. Mutants were analyzed for abnormalities in the cartilaginous head skeleton. Further, the expression of marker genes was studied to investigate potential abnormalities in mutant rhombencephalon, neural crest, and pharyngeal endoderm. The results suggest that the identified mutations affect three distinct aspects of craniofacial development. In one group, mutations affect the overall pattern of the craniofacial skeleton, suggesting that the genes are involved in the specification of these elements. Another large group of mutations affects differentiation and morphogenesis of cartilage, and may provide insight into the genetic control of chondrogenesis. The last group of mutations leads to the abnormal arrangement of skeletal elements and may uncover important tissue-tissue interactions underlying jaw development.
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33

Lei, Run, Ke Zhang, Yanxia Wei, Min Chen, Lee S. Weinstein, Yang Hong, Minyan Zhu, Hongchang Li, and Huashun Li. "G-Protein α-Subunit Gsα Is Required for Craniofacial Morphogenesis." PLOS ONE 11, no. 2 (February 9, 2016): e0147535. http://dx.doi.org/10.1371/journal.pone.0147535.

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34

Rizzoti, K., and R. Lovell-Badge. "SOX3 activity during pharyngeal segmentation is required for craniofacial morphogenesis." Development 134, no. 19 (October 1, 2007): 3437–48. http://dx.doi.org/10.1242/dev.007906.

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35

Babic, M., M. Micic, N. Jak sic, and S. Micic. "An extra X chromosome effect on craniofacial morphogenesis in men." European Journal of Orthodontics 13, no. 4 (August 1, 1991): 329–32. http://dx.doi.org/10.1093/ejo/13.4.329.

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36

Kraus, Petra, and Thomas Lufkin. "MammalianDlx homeobox gene control of craniofacial and inner ear morphogenesis." Journal of Cellular Biochemistry 75, S32 (1999): 133–40. http://dx.doi.org/10.1002/(sici)1097-4644(1999)75:32+<133::aid-jcb16>3.0.co;2-e.

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37

Wolpert, L. "Craniofacial development: a summing up." Development 103, Supplement (September 1, 1988): 245–49. http://dx.doi.org/10.1242/dev.103.supplement.245.

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It is convenient to distinguish between three related problems in development: cell differentiation; pattern formation, which is about spatial organization; and morphogenesis in the strict sense, which is about change in form, particularly of cell sheets, but includes cell migration (Wolpert, 1981; Wolpert & Stein, 1984). All these need to be linked to gene action. If one looks forward over the next five to ten years then the future of craniofacial biology lies in molecular cell biology. This is not to say that all the problems at the tissue level have been solved, quite the contrary, but rather that the emphasis must now be at the cell and molecular level. One can illustrate some of the problems of cell differentiation – and the approaches involved – with the differentiation of the cells of the haemopoietic system. Here we have a stem cell that can give rise to all the different types of blood cell.
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38

Morris, Zachary S., Kent A. Vliet, Arhat Abzhanov, and Stephanie E. Pierce. "Heterochronic shifts and conserved embryonic shape underlie crocodylian craniofacial disparity and convergence." Proceedings of the Royal Society B: Biological Sciences 286, no. 1897 (February 20, 2019): 20182389. http://dx.doi.org/10.1098/rspb.2018.2389.

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The distinctive anatomy of the crocodylian skull is intimately linked with dietary ecology, resulting in repeated convergence on blunt- and slender-snouted ecomorphs. These evolutionary shifts depend upon modifications of the developmental processes which direct growth and morphogenesis. Here we examine the evolution of cranial ontogenetic trajectories to shed light on the mechanisms underlying convergent snout evolution. We use geometric morphometrics to quantify skeletogenesis in an evolutionary context and reconstruct ancestral patterns of ontogenetic allometry to understand the developmental drivers of craniofacial diversity within Crocodylia. Our analyses uncovered a conserved embryonic region of morphospace (CER) shared by all non-gavialid crocodylians regardless of their eventual adult ecomorph. This observation suggests the presence of conserved developmental processes during early development (before Ferguson stage 20) across most of Crocodylia. Ancestral state reconstruction of ontogenetic trajectories revealed heterochrony, developmental constraint, and developmental systems drift have all played essential roles in the evolution of ecomorphs. Based on these observations, we conclude that two separate, but interconnected, developmental programmes controlling craniofacial morphogenesis and growth enabled the evolutionary plasticity of skull shape in crocodylians.
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39

Dressler, Simone, Philipp Meyer-Marcotty, Nicole Weisschuh, Anahita Jablonski-Momeni, Klaus Pieper, Gwendolyn Gramer, and Eugen Gramer. "Dental and Craniofacial Anomalies Associated with Axenfeld-Rieger Syndrome with PITX2 Mutation." Case Reports in Medicine 2010 (2010): 1–7. http://dx.doi.org/10.1155/2010/621984.

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Axenfeld-Rieger syndrome (ARS) (OMIM Nr.: 180500) is a rare autosomal dominant disorder (1 : 200000) with genetic and morphologic variability. Glaucoma is associated in 50% of the patients. Craniofacial and dental anomalies are frequently reported with ARS. The present study was designed as a multidisciplinary analysis of orthodontic, ophthalmologic, and genotypical features. A three-generation pedigree was ascertained through a family with ARS. Clinically, radiographic and genetic analyses were performed. Despite an identical genotype in all patients, the phenotype varies in expressivity of craniofacial and dental morphology. Screening for PITX2 and FOXC1 mutations by direct DNA-sequencing revealed a P64L missense mutation in PITX2 in all family members, supporting earlier reports that PITX2 is an essential factor in morphogenesis of teeth and craniofacial skeleton. Despite the fact that the family members had identical mutations, morphologic differences were evident. The concomitant occurrence of rare dental and craniofacial anomalies may be early diagnostic indications of ARS. Early detection of ARS and elevated intraocular pressure (IOP) helps to prevent visual field loss.
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40

Richman, Joy M. "The Role of Retinoids in Normal and Abnormal Embryonic Craniofacial Morphogenesis." Critical Reviews in Oral Biology & Medicine 4, no. 1 (October 1992): 93–109. http://dx.doi.org/10.1177/10454411920040010701.

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The objective of this article is to evaluate the role of retinoids in the developing head and face. This article covers two lines of evidence that strongly support a role for retinoids in craniofacial development. First, the specific effects of exogenous retinoids on the head and face are covered and mechanisms for the specificity discussed. Second, the function of endogenous retinoids in facial development is discussed in relation to the distribution of retinoid-binding substances in the face. Finally, the interaction of retinoids with other genes known to be expressed in the face as well as other factors required for facial growth is discussed.
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41

HAYES, CHRISTOPHER, MARY F. LYON, and GILLIAN M. MORRISS-KAY. "Morphogenesis of Doublefoot (Dbf), a mouse mutant with polydactyly and craniofacial defects." Journal of Anatomy 193, no. 1 (July 1998): 81–91. http://dx.doi.org/10.1046/j.1469-7580.1998.19310081.x.

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42

Murray, Stephen A., Kathleen F. Oram, and Thomas Gridley. "Multiple functions of Snail family members in palate development and craniofacial morphogenesis." Developmental Biology 306, no. 1 (June 2007): 305–6. http://dx.doi.org/10.1016/j.ydbio.2007.03.096.

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43

Johnson, Christopher, Weiguo Feng, Trevor Williams, and Kristin B. Artinger. "vgl-2a is required for endodermal pouch morphogenesis in zebrafish craniofacial development." Developmental Biology 319, no. 2 (July 2008): 516. http://dx.doi.org/10.1016/j.ydbio.2008.05.176.

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44

Thesleff, Irma. "Homeobox genes and growth factors in regulation of craniofacial and tooth morphogenesis." Acta Odontologica Scandinavica 53, no. 3 (January 1995): 129–34. http://dx.doi.org/10.3109/00016359509005962.

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45

Melvin, Vida Senkus, Weiguo Feng, Laura Hernandez-Lagunas, Kristin Bruk Artinger, and Trevor Williams. "A morpholino-based screen to identify novel genes involved in craniofacial morphogenesis." Developmental Dynamics 242, no. 7 (June 3, 2013): 817–31. http://dx.doi.org/10.1002/dvdy.23969.

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46

Melvin, Vida Senkus, Weiguo Feng, Laura Hernandez-Lagunas, Kristin Bruk Artinger, and Trevor Williams. "A morpholino-based screen to identify novel genes involved in craniofacial morphogenesis." Developmental Dynamics 242, no. 11 (October 9, 2013): 1345. http://dx.doi.org/10.1002/dvdy.24069.

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47

Reddy, T. Praveen Kumar, B. Sunil Kumar, Gojja Sreedevi, Baratam Srinivas, CMS Krishna Prasad, and R. Satish. "Heritability of Thirty Cephalometric Parameters on Monozygotic and Dizygotic Twins: Twin Study Method." Journal of Contemporary Dental Practice 14, no. 2 (2013): 304–11. http://dx.doi.org/10.5005/jp-journals-10024-1318.

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ABSTRACT Genetic mechanisms are already predominant during embryonic craniofacial morphogenesis, but environment is also thought to influence dentofacial morphology postnatally, particularly during facial growth. A better understanding of the relative effects of genes and environment on dentofacial and occlusal parameters should improve our knowledge on the etiology of orthodontic disorders and therefore also on the possibilities and limitations of the orthodontic treatment and treatment planning. The aim of the present study is to explore the genetic and environmental influence on craniofacial dimensions in a group of 19 pairs of twins using the twin study method. The twin study carried out here clearly indicates that craniofacial matrix is under substantial genetic control and the redirection of a basic growth pattern may be modified only within biological limits which are harmonious for the patient. How to cite this article Sreedevi G, Srinivas B, Reddy TPK, Prasad CMSK, Kumar BS, Satish R. Heritability of Thirty Cephalometric Parameters on Monozygotic and Dizygotic Twins: Twin Study Method. J Contemp Dent Pract 2013; 14(2):304-311.
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48

Lauder, J. M., H. Tamir, and T. W. Sadler. "Serotonin and morphogenesis. I. Sites of serotonin uptake and -binding protein immunoreactivity in the midgestation mouse embryo." Development 102, no. 4 (April 1, 1988): 709–20. http://dx.doi.org/10.1242/dev.102.4.709.

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The possible involvement of the neurotransmitter serotonin (5-HT) in morphogenesis of the craniofacial region in the mouse embryo has been investigated using the method of whole-embryo culture. Day-12 embryos were incubated for 3–4 h in the presence of 5-HT or its precursors L-tryptophan (L-TRP) or 5-hydroxytryptophan (5-HTP), followed by fixation, sectioning and staining with a specific antiserum to 5-HT. Sites of 5-HT immunoreactivity were found in a variety of locations in tissues of the head and neck, which are either epithelia derived from the non-neural ectoderm or are non-neuronal midline brain structures. These sites include the surface epithelia of the head, face, nasal prominences, branchial arches, oral cavity and associated parts of the nasal epithelium, the epithelium covering the eye, parts of the otic vesicle, the epiphysis and roof of the diencephalon. With the exception of the oral cavity, sites of immunoreactivity for serotonin-binding protein were identified in the mesenchyme adjacent to these sites. This mesenchyme consists of ectodermally derived neural crest cells, which are known to receive inductive influences from the epithelia with which they interact during their migration through the craniofacial region. The presence of 5-HT uptake sites in epithelia and adjacent sites of SBP in the underlying mesenchyme raises the possibility that 5-HT might be involved in those epithelial-mesenchymal interactions known to be important for the development of structures in the craniofacial region.
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49

Liu, Z., C. Li, J. Xu, Y. Lan, H. Liu, X. Li, P. Maire, X. Wang, and R. Jiang. "Crucial and Overlapping Roles of Six1 and Six2 in Craniofacial Development." Journal of Dental Research 98, no. 5 (March 24, 2019): 572–79. http://dx.doi.org/10.1177/0022034519835204.

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SIX1 and SIX2 encode closely related transcription factors of which disruptions have been associated with distinct craniofacial syndromes, with mutations in SIX1 associated with branchiootic syndrome 3 (BOS3) and heterozygous deletions of SIX2 associated with frontonasal dysplasia defects. Whereas mice deficient in Six1 recapitulated most of the developmental defects associated with BOS3, mice lacking Six2 function had no obvious frontonasal defects. We show that Six1 and Six2 exhibit partly overlapping patterns of expression in the developing mouse embryonic frontonasal, maxillary, and mandibular processes. We found that Six1 –/– Six2 –/– double-mutant mice were born with severe craniofacial deformity not seen in the Six1 –/– or Six2 –/– single mutants, including skull bone agenesis, midline facial cleft, and syngnathia. Moreover, whereas Six1 –/– mice exhibited partial transformation of maxillary zygomatic bone into a mandibular condyle-like structure, Six1 –/–Six2 +/– mice exhibit significantly increased penetrance of the maxillary malformation. In addition to ectopic Dlx5 expression at the maxillary-mandibular junction as recently reported in E10.5 Six1 –/– embryos, the E10.5 Six1 –/– Six2 +/– embryos showed ectopic expression of Bmp4, Msx1, and Msx2 messenger RNAs in the maxillary-mandibular junction. Genetically inactivating 1 allele of either Ednra or Bmp4 significantly reduced the penetrance of maxillary malformation in both Six1 –/– and Six1 –/– Six2 +/– embryos, indicating that Six1 and Six2 regulate both endothelin and bone morphogenetic protein-4 signaling pathways to pattern the facial structures. Furthermore, we show that neural crest–specific inactivation of Six1 in Six2 –/– embryos resulted in midline facial cleft and frontal bone agenesis. We show that Six1 –/– Six2 –/– embryos exhibit significantly reduced expression of key frontonasal development genes Alx1 and Alx3 as well as increased apoptosis in the developing frontonasal mesenchyme. Together, these results indicate that Six1 and Six2 function partly redundantly to control multiple craniofacial developmental processes and play a crucial neural crest cell–autonomous role in frontonasal morphogenesis.
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50

Forman, Thomas E., Brenna J. C. Dennison, and Katherine A. Fantauzzo. "The Role of RNA-Binding Proteins in Vertebrate Neural Crest and Craniofacial Development." Journal of Developmental Biology 9, no. 3 (August 27, 2021): 34. http://dx.doi.org/10.3390/jdb9030034.

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Cranial neural crest (NC) cells delaminate from the neural folds in the forebrain to the hindbrain during mammalian embryogenesis and migrate into the frontonasal prominence and pharyngeal arches. These cells generate the bone and cartilage of the frontonasal skeleton, among other diverse derivatives. RNA-binding proteins (RBPs) have emerged as critical regulators of NC and craniofacial development in mammals. Conventional RBPs bind to specific sequence and/or structural motifs in a target RNA via one or more RNA-binding domains to regulate multiple aspects of RNA metabolism and ultimately affect gene expression. In this review, we discuss the roles of RBPs other than core spliceosome components during human and mouse NC and craniofacial development. Where applicable, we review data on these same RBPs from additional vertebrate species, including chicken, Xenopus and zebrafish models. Knockdown or ablation of several RBPs discussed here results in altered expression of transcripts encoding components of developmental signaling pathways, as well as reduced cell proliferation and/or increased cell death, indicating that these are common mechanisms contributing to the observed phenotypes. The study of these proteins offers a relatively untapped opportunity to provide significant insight into the mechanisms underlying gene expression regulation during craniofacial morphogenesis.
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