Talk:Palate Development - Revision history

Z8600021 at 00:15, 7 November 2019

2019-11-07T00:15:21Z

← Older revision		Revision as of 11:15, 7 November 2019
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	==2019==		==2019==

			===Short stature homeobox 2 (SHOX2) regulates osteogenic differentiation and pattern formation during hard palate development in mice===
			J Biol Chem. 2019 Oct 24. pii: jbc.RA119.008801. doi: 10.1074/jbc.RA119.008801. [Epub ahead of print]

			Xu J1, Wang L2, Li H3, Yang T4, Zhang Y5, Hu T6, Huang Z5, Chen Y7.
			Author information
			1
			West China School of Public Health and West China Fourth Hospital, Sichuan University; Tulane University, China.
			2
			Sichuan University and Tulane University, China.
			3
			Fujian Normal University and Tulane University, China.
			4
			Tulane University, United States.
			5
			Southern Center for Biomedical Research, Fujian Key Laboratory of Developmental and Neural Biology, College of Life Sciences, Fujian Normal University, China.
			6
			West China Hospital of Stomatology, Sichuan University, China.
			7
			Cell and Molecular Biology, Tulane University, United States.
			Abstract
			During mammalian palatogenesis, cranial neural crest-derived mesenchymal cells undergo osteogenic differentiation and form the hard palate, which is divided into palatine process of the maxilla and the palatine. However, it remains unknown whether these bony structures originate from the same cell lineage and how the hard palate is patterned at the molecular level. Using mice, here we report that deficiency in short stature homeobox 2 (Shox2), a transcriptional regulator whose expression is restricted to the anterior palatal mesenchyme, leads to a defective palatine process of the maxilla, but does not affect the palatine. Shox2 overexpression in palatal mesenchyme resulted in a hyperplastic palatine process of the maxilla and a hypoplastic palatine. RNA-Seq and assay for transposase-accessible chromatin (ATAC)-Seq analyses revealed that SHOX2 controls the expression of pattern-specification and skeletogenic genes associated with accessible chromatin in the anterior palate. This highlighted a lineage-autonomous function of SHOX2 in patterning and osteogenesis of the hard palate. H3K27ac ChIP-Seq and transient transgenic enhancer assays revealed that SHOX2 binds distal-acting cis-regulatory elements in an anterior palate-specific manner. Our results suggest that the palatine process of the maxilla and palatine arise from different cell lineages and differ in ossification mechanisms. SHOX2 evidently controls osteogenesis of a cell lineage and contributes to the palatine process of the maxilla by interacting with distal cis-regulatory elements to regulate skeletogenic gene expression and to pattern the hard palate. Genome-wide SHOX2 occupancy in the developing palate may provide a marker for identifying active anterior palate-specific gene enhancers.
			Published under license by The American Society for Biochemistry and Molecular Biology, Inc.
			KEYWORDS:
			cell differentiation; craniofacial development; epigenetics; gene regulation; hard palate; lineage-specific chromatin accessibility; osteogenesis; patterning; short stature homeobox 2 (SHOX2); transcription factor
			PMID: 31649032 DOI: 10.1074/jbc.RA119.008801


	==2018==		==2018==

Z8600021 at 22:59, 12 March 2019

2019-03-12T22:59:47Z

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-==10 Most Recent==
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 ==2018==
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 In the present study, it was aimed to perform the morphometric analysis of the hard and soft palate in fetal cadavers and evaluate hard palate asymmetry during the fetal development. The development of the palate was investigated in 40 (21 males, 19 females) fetal materials aged between the 17th and 40th gestational week. In this study, distances between the incisive papilla-staurion (Ip-Sr), staurion-posterior nasal spine (Sr-Pns), incisive papilla-greater palatine foramen (Ip-Gpf) on the right and left sides, Sr-Gpf, and Pns-Gpf were measured. In cases with asymmetry, the ratio of asymmetry was determined in percentage using the asymmetry index. Moreover, angular values between Ip-Sr-Gpf and Ip-Pns-Gpf on the right and left sides were measured, and the right and left side values were compared with each other. The hard and soft palate lengths were measured on the planum medianum. Upon comparing the measured parameters between males and females, the mean values of male fetuses were higher in all parameters, but a significant difference was found only in the Sr-Pns distance among these parameters. Upon comparing the angular data and asymmetry index data on the hard palate between the trimester groups, a significant difference was found only in the Ip-Sr-Gpf (left) parameter. The mean ratio of the hard palate to the soft palate was found as 1.90. It is believed that the obtained data will contribute to studies to be conducted in fields such as plastic surgery, maxillofacial surgery, intrauterine surgery, fetopathology, embryology, anatomy, and obstetrics.
 PMID: 30320695 DOI: 10.1097/SCS.0000000000005016

Z8600021 at 20:21, 23 November 2018

2018-11-23T20:21:56Z

← Older revision		Revision as of 07:21, 24 November 2018
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	===Cleft Palate===		===Cleft Palate===
	<pubmed limit=5>Cleft+Palate</pubmed>		<pubmed limit=5>Cleft+Palate</pubmed>

			==2018==

			===TGF-β Signaling and the Epithelial-Mesenchymal Transition during Palatal Fusion===

			Int J Mol Sci. 2018 Nov 19;19(11). pii: E3638. doi: 10.3390/ijms19113638.

			Nakajima A1, F Shuler C2, Gulka AOD3, Hanai JI4,5.
			Author information
			Abstract
			Signaling by transforming growth factor (TGF)-β plays an important role in development, including in palatogenesis. The dynamic morphological process of palatal fusion occurs to achieve separation of the nasal and oral cavities. Critically and specifically important in palatal fusion are the medial edge epithelial (MEE) cells, which are initially present at the palatal midline seam and over the course of the palate fusion process are lost from the seam, due to cell migration, epithelial-mesenchymal transition (EMT), and/or programed cell death. In order to define the role of TGF-β signaling during this process, several approaches have been utilized, including a small interfering RNA (siRNA) strategy targeting TGF-β receptors in an organ culture context, the use of genetically engineered mice, such as Wnt1-cre/R26R double transgenic mice, and a cell fate tracing through utilization of cell lineage markers. These approaches have permitted investigators to distinguish some specific traits of well-defined cell populations throughout the palatogenic events. In this paper, we summarize the current understanding on the role of TGF-β signaling, and specifically its association with MEE cell fate during palatal fusion. TGF-β is highly regulated both temporally and spatially, with TGF-β3 and Smad2 being the preferentially expressed signaling molecules in the critical cells of the fusion processes. Interestingly, the accessory receptor, TGF-β type 3 receptor, is also critical for palatal fusion, with evidence for its significance provided by Cre-lox systems and siRNA approaches. This suggests the high demand of ligand for this fine-tuned signaling process. We discuss the new insights in the fate of MEE cells in the midline epithelial seam (MES) during the palate fusion process, with a particular focus on the role of TGF-β signaling.
			KEYWORDS:
			TGF-β signaling; cleft palate; collective epithelial migration; crowding; epithelial-mesenchymal transition (EMT); midline epithelial seam (MES); palatal fusion; palatal medial edge epithelial (MEE) cells
			PMID: 30463190 DOI: 10.3390/ijms19113638

			===Development of Hard and Soft Palate During the Fetal Period and Hard Palate Asymmetry===

			J Craniofac Surg. 2018 Nov;29(8):2358-2362. doi: 10.1097/SCS.0000000000005016.

			Dursun A1, Öztürk K, Albay S.
			Author information
			Abstract
			In the present study, it was aimed to perform the morphometric analysis of the hard and soft palate in fetal cadavers and evaluate hard palate asymmetry during the fetal development. The development of the palate was investigated in 40 (21 males, 19 females) fetal materials aged between the 17th and 40th gestational week. In this study, distances between the incisive papilla-staurion (Ip-Sr), staurion-posterior nasal spine (Sr-Pns), incisive papilla-greater palatine foramen (Ip-Gpf) on the right and left sides, Sr-Gpf, and Pns-Gpf were measured. In cases with asymmetry, the ratio of asymmetry was determined in percentage using the asymmetry index. Moreover, angular values between Ip-Sr-Gpf and Ip-Pns-Gpf on the right and left sides were measured, and the right and left side values were compared with each other. The hard and soft palate lengths were measured on the planum medianum. Upon comparing the measured parameters between males and females, the mean values of male fetuses were higher in all parameters, but a significant difference was found only in the Sr-Pns distance among these parameters. Upon comparing the angular data and asymmetry index data on the hard palate between the trimester groups, a significant difference was found only in the Ip-Sr-Gpf (left) parameter. The mean ratio of the hard palate to the soft palate was found as 1.90. It is believed that the obtained data will contribute to studies to be conducted in fields such as plastic surgery, maxillofacial surgery, intrauterine surgery, fetopathology, embryology, anatomy, and obstetrics.
			PMID: 30320695 DOI: 10.1097/SCS.0000000000005016

Z8600021 at 23:46, 17 March 2016

2016-03-17T23:46:57Z

← Older revision		Revision as of 10:46, 18 March 2016
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	==2015==		==2015==

			===Cellular and Molecular Mechanisms of Palatogenesis===

			Curr Top Dev Biol. 2015;115:59-84. doi: 10.1016/bs.ctdb.2015.07.002. Epub 2015 Oct 1.

			Lan Y1, Xu J2, Jiang R3.

			Abstract

			Palatogenesis involves the initiation, growth, morphogenesis, and fusion of the primary and secondary palatal shelves from initially separate facial prominences during embryogenesis to form the intact palate separating the oral cavity from the nostrils. The palatal shelves consist mainly of cranial neural crest-derived mesenchymal cells covered by a simple embryonic epithelium. The growth and patterning of the palatal shelves are controlled by reciprocal epithelial-mesenchymal interactions regulated by multiple signaling pathways and transcription factors. During palatal shelf outgrowth, the embryonic epithelium develops a "teflon" coat consisting of a single, continuous layer of periderm cells that prevents the facial prominences and palatal shelves from forming aberrant interepithelial adhesions. Palatal fusion involves not only spatiotemporally regulated disruption of the periderm but also dynamic cellular and molecular processes that result in adhesion and intercalation of the palatal medial edge epithelia to form an intershelf epithelial seam, and subsequent dissolution of the epithelial seam to form the intact roof of the oral cavity. The complexity of regulation of these morphogenetic processes is reflected by the common occurrence of cleft palate in humans. This review will summarize major recent advances and discuss major remaining gaps in the understanding of cellular and molecular mechanisms controlling palatogenesis.
			© 2015 Elsevier Inc. All rights reserved.
			KEYWORDS:
			Cleft palate; Fusion; Morphogenesis; Mouse; Palate development; Periderm; Signaling
			PMID 26589921

	===Global Birth Prevalence of Orofacial Clefts: A Systematic Review===		===Global Birth Prevalence of Orofacial Clefts: A Systematic Review===
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	A systematic literature search was conducted using electronic databases through PubMed between 1950 and June 2015 using key words and search terms of cleft lip palate OR orofacial cleft AND prevalence.		A systematic literature search was conducted using electronic databases through PubMed between 1950 and June 2015 using key words and search terms of cleft lip palate OR orofacial cleft AND prevalence.
	RESULTS:		RESULTS:
	There were 45,193 patients with OFCs found in a study population of 30,665,615 live births. According to continents, the OFC birth prevalence (95% confidence interval)from Asia, North America, Europe, Oceania, South America, and Africa were 1.57 (1.54-1.60), 1.56 (1.53-1.59), 1.55 (1.52-1.58), 1.33 (1.30-1.36), 0.99 (0.96-1.02), and 0.57 (0.54-0.60) per 1,000 live births, respectively. The American Indians had the highest prevalence rates of 2.62 per 1,000 live births, followed by the Japanese, the Chinese, and the Whites of 1.73, 1.56, and 1.55 per 1,000 live births, respectively. The Blacks had the lowest rate of 0.58 per 1,000 live births.		There were 45,193 patients with OFCs found in a study population of 30,665,615 live births. According to continents, the OFC birth prevalence (95% confidence interval) from Asia, North America, Europe, Oceania, South America, and Africa were 1.57 (1.54-1.60), 1.56 (1.53-1.59), 1.55 (1.52-1.58), 1.33 (1.30-1.36), 0.99 (0.96-1.02), and 0.57 (0.54-0.60) per 1,000 live births, respectively. The American Indians had the highest prevalence rates of 2.62 per 1,000 live births, followed by the Japanese, the Chinese, and the Whites of 1.73, 1.56, and 1.55 per 1,000 live births, respectively. The Blacks had the lowest rate of 0.58 per 1,000 live births.
	CONCLUSION:		CONCLUSION:
	Observed differences may also be of ethnic origin, genetic, environmental factors, and methods of ascertainment. Further investigations are needed to manage this global health problem.		Observed differences may also be of ethnic origin, genetic, environmental factors, and methods of ascertainment. Further investigations are needed to manage this global health problem.

Z8600021 at 13:15, 24 February 2016

2016-02-24T13:15:52Z

← Older revision		Revision as of 00:15, 25 February 2016
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	==2015==		==2015==

			===Global Birth Prevalence of Orofacial Clefts: A Systematic Review===
			J Med Assoc Thai. 2015 Aug;98 Suppl 7:S11-21.

			Panamonta V, Pradubwong S, Panamonta M, Chowchuen B.

			Abstract

			BACKGROUND:
			A birth prevalence of orofacial clefts (OFCs) worldwide has been documented to vary. However a systematic assessment is lacking.
			OBJECTIVE:
			To assess the evidence in the literature for the birth prevalence of OFCs.
			MATERIAL AND METHOD:
			A systematic literature search was conducted using electronic databases through PubMed between 1950 and June 2015 using key words and search terms of cleft lip palate OR orofacial cleft AND prevalence.
			RESULTS:
			There were 45,193 patients with OFCs found in a study population of 30,665,615 live births. According to continents, the OFC birth prevalence (95% confidence interval)from Asia, North America, Europe, Oceania, South America, and Africa were 1.57 (1.54-1.60), 1.56 (1.53-1.59), 1.55 (1.52-1.58), 1.33 (1.30-1.36), 0.99 (0.96-1.02), and 0.57 (0.54-0.60) per 1,000 live births, respectively. The American Indians had the highest prevalence rates of 2.62 per 1,000 live births, followed by the Japanese, the Chinese, and the Whites of 1.73, 1.56, and 1.55 per 1,000 live births, respectively. The Blacks had the lowest rate of 0.58 per 1,000 live births.
			CONCLUSION:
			Observed differences may also be of ethnic origin, genetic, environmental factors, and methods of ascertainment. Further investigations are needed to manage this global health problem.
			PMID 26742364

	===Folic acid supplements and risk for oral clefts in the newborn: a population-based study===		===Folic acid supplements and risk for oral clefts in the newborn: a population-based study===

Z8600021 at 07:36, 22 September 2015

2015-09-22T07:36:05Z

← Older revision		Revision as of 18:36, 22 September 2015
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	PMID: 17693063		PMID: 17693063

			==1979==

			===Anatomy of musculus levator veli palatini in the 15-week human fetus===
			Acta Anat (Basel). 1979;105(1):94-105.

			Klueber K, Langdon HL.

			Abstract

			The morphology of musculus levator veli palatini in the 15-week fetus was analyzed using 30-micrometer subserial sections. The sample included 26 specimens, of which 9 each were sectioned coronally and sagittally while 8 were sectioned in the transverse plane. At this stage of development m. levator veli palatini takes a general attachment to the precursor of the petrous part of the temporal bone, and, in some cases, auxiliary attachments to the auditory tube complex were also observed. At its origin, the muscle is located anterior to the tube. It then runs medially, passing beneath the auditory tube prior to entering the velum. As it nears the region of the lateral pharyngeal wall, a small fascicle trails posteriorly and inferiorly to the main muscle mass and occasionally runs into the upper margin of m. constrictor pharyngis superior. The levator muscle is more localized within the velum at this stage of development than it has been reported to be in the adult, being confined here to the central third of the soft palate. Most of the fibers of the muscle appear to form a sling within the central 20% of the velum, although some were seen to take attachment to loose connective tissue and the palatine raphe. Upon its entry into the velum, m. levator veli palatini is intersected vertically by bundles of both mm. palatoglossus and palatopharyngeus.

			PMID 525252

	==1977==		==1977==

Z8600021 at 07:34, 22 September 2015

2015-09-22T07:34:31Z

← Older revision		Revision as of 18:34, 22 September 2015
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	PMID: 17693063		PMID: 17693063

			==1977==

			Development and peripheral innervation of the palatal muscles.
			Acta Anat (Basel). 1977;97(1):4-14.

			Doménech-Ratto G.

			Following the observation of 51 embryos and human fetuses of between 9 and 190 mm vertex/coccys length, cut transversally, frontally, or sagittally, depending on the case, and coloured with HE, Azan, or by the Bielschowsky method, we studied the development, and peripheral innervation of the palatal muscles. We reached a series of conclusions which we put forward in this paper. The m. tensor veli palatini is the one which develops earliest. It derives from the sam blastematic mass as the muscles of mastication, and it is innervated by a branch of the n. mandibularis. The m. levator veli palatini and m. pharyngopalatinus coincide chronologically with the appearance of the m. cephalopharyngeus. They derive from the pharyngeal musculature, and are innervated by fibres proceeding from the n. glossopharyngeus, in the case of the first one, and, in the case of the second, by direct branches from the n. glossopharyngeus and n. vagus, which penetrate the muscle directly, without prior contact with any nerve plexus. The m. uvulae is first formed, at the time the palatine processes close. In the first place, two outlines may be seen; but after 50 mm approximately it is formed by one muscle only, on the medial line; it is innervated by branches which proceed from the posterior n. palatinus. The m. glossopalatinus is the last to appear. It is closely linked to the musculature of the tongue and, therefore, we think that it derives from the hypobranchial musculature, and that is innervated in the body of the tongue itself, by means of the n. hypoglossus.

			PMID 66841


	==ICD - Cleft Palate==		==ICD - Cleft Palate==

Z8600021 at 00:14, 9 September 2015

2015-09-09T00:14:57Z

← Older revision		Revision as of 11:14, 9 September 2015
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	PMID 26343883		PMID 26343883

			===Classification of Cleft Lip/Palate: Then and Now===
			Cleft Palate Craniofac J. 2015 Sep 4. [Epub ahead of print]

			Allori AC, Mulliken JB, Meara JG, Shusterman S, Marcus JR; CleftKit Collaboration.

			Abstract

			Cleft lip and/or palate (CL/P) is phenotypically diverse, making classification difficult. This article explores the evolution of ideas regarding CL/P classification and includes the schemes described by Davis and Ritchie (1922), Brophy (1923), Veau (1931), Fogh-Andersen (1943), Kernahan and Stark (1958), Harkins et al. (1962), Broadbent et al. (1968), Spina (1973), and others. Based on these systems, a longhand structured form is proposed for describing CL/P in a way that is clear, comprehensive, and consistent. A complementary shorthand notation is also described to improve the utility and convenience of this structured form.
			KEYWORDS:
			CleftKit; classification; cleft lip; cleft palate; nomenclature; nosology; ontology; taxonomy; terminology

			PMID 26339868

Z8600021 at 00:13, 9 September 2015

2015-09-09T00:13:36Z

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 ===Cleft Palate===
 <pubmed limit=5>Cleft+Palate</pubmed>
 ==2014==

Z8600021 at 03:27, 19 Haziran 2014

2014-06-19T03:27:27Z

← Older revision		Revision as of 14:27, 19 Haziran 2014
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	==2014==		==2014==

			===Signaling networks in palate development===
			Wiley Interdiscip Rev Syst Biol Med. 2014 May-Jun;6(3):271-8. doi: 10.1002/wsbm.1265. Epub 2014 Mar 18.

			Lane J, Kaartinen V.

			Abstract

			Palatogenesis, the formation of the palate, is a dynamic process regulated by a complex series of context-dependent morphogenetic signaling events. Many genes involved in palatogenesis have been discovered through the use of genetically manipulated mouse models as well as from human genetic studies, but the roles of these genes and their products in signaling networks regulating palatogenesis are still poorly known. In this review, we give a brief overview on palatogenesis and introduce key signaling cascades leading to formation of the intact palate. Moreover, we review conceptual differences between pathway biology and network biology and discuss how some of the recent technological advances in conjunction with mouse genetic models have contributed to our understanding of signaling networks regulating palate growth and fusion. For further resources related to this article, please visit the WIREs website. Conflict of interest: The authors have declared no conflicts of interest for this article.
			© 2014 Wiley Periodicals, Inc.

			PMID 24644145

	===Neural crest-specific deletion of Ldb1 leads to cleft secondary palate with impaired palatal shelf elevation===		===Neural crest-specific deletion of Ldb1 leads to cleft secondary palate with impaired palatal shelf elevation===