Talk:Integumentary System - Tooth Development - Revision history

Z8600021 at 20:15, 1 Ocak 2020

2020-01-01T20:15:37Z

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			==2020==

			{{#pmid:31512758}}
			Immortalized Hertwig's epithelial root sheath cell line works as model for epithelial-mesenchymal interaction during tooth root formation.

			Abstract
			Hertwig's epithelial root sheath (HERS) is critical for epithelial-mesenchymal interaction (EMI) during tooth root formation. However, the exact roles of HERS in odontogenic differentiation by EMI have not been well characterized, because primary HERS cells are difficult to obtain. Immortalized cell lines constitute crucial scientific tools, while there are few HERS cell lines available. Our previous study has successfully established immortalized HERS cell lines. Here, we confirmed the phenotype of our HERS-H1 by verifying its characteristics and functions in odontogenic differentiation through EMI. The HERS-H1-conditioned medium (CM-H1) effectively enhanced odontogenic differentiation of dental papilla cells (DPCs) in vitro. Furthermore, Smad4 and p-Smad1/5/8 were significantly activated in DPCs treated with CM-H1, and this activation was attenuated by noggin. In vivo, our implanted recombinants of HERS-H1 and DPCs exhibited mineralized tissue formation and expression of Smad4, p-Smad1/5/8, and odontogenic differentiation markers. Our results indicated that HERS-H1 promoted DPCs odontoblastic differentiation via bone morphogenetic protein/Smad signaling. HERS-H1 exhibits relevant key molecular characteristics and constitutes a new biological model for basic research on HERS and the dental EMI during root development and regeneration.
			© 2019 Wiley Periodicals, Inc.
			KEYWORDS:
			BMP/Smad signaling; Hertwig's epithelial root sheath cell; dental epithelial-mesenchymal interaction; odontogenic differentiation
			PMID: 31512758 DOI: 10.1002/jcp.29174

	==2019==		==2019==

Z8600021 at 01:09, 16 July 2019

2019-07-16T01:09:49Z

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	~~original page : http://embryology.med.unsw.edu.au/Notes/skin10.htm~~		==2019==

	==~~10 Most Recent~~==		===Parathyroid hormone-related peptide (1-34) promotes tooth eruption and inhibits osteogenesis of dental follicle cells during tooth development===
	{{10 ~~Most Recent}}~~		J Cell Physiol. 2019 Jul;234(7):11900-11911. doi: 10.1002/jcp.27857. Epub 2018 Dec 24.

	~~==2019==~~		Zhang J1,2,3, Liao L1,2,4, Li Y1,3, Xu Y1,3, Guo W1,2,4, Tian W1,2,5, Zou S1,3.

			Dental follicle cells (DFCs) activate and recruit osteoclasts for tooth development and tooth eruption, whereas DFCs themselves differentiate into osteoblasts to form alveolar bone surrounding tooth roots through the interaction with Hertwig's epithelial root sheath (HERS). Also during tooth development, parathyroid hormone-related peptide (PTHrP) is expressed surrounding the tooth germ. Thus, we aimed to investigate the effect of PTHrP (1-34) on bone resorption and osteogenesis of DFCs in vitro and in vivo. In vitro studies demonstrated that DFCs cocultured with HERS cells expressed higher levels of BSP and OPN than the DFCs control group, whereas cocultured DFCs treated with PTHrP (1-34) had lower expressions of ALP, RUNX2, BSP, and OPN than the cocultured DFCs control group. Moreover, we found PTHrP (1-34) inhibited osteogenesis of cocultured DFCs by inactivating the Wnt/β-catenin pathway. PTHrP (1-34) also increased the expression of RANKL/OPG ratio in DFCs. Consistently, in vivo study found that PTHrP (1-34) accelerated tooth eruption and inhibited alveolar bone formation. Therefore, these results suggest that PTHrP (1-34) accelerates tooth eruption and inhibits osteogenesis of DFCs by inactivating Wnt/β-catenin pathway.
			© 2018 Wiley Periodicals, Inc.
			KEYWORDS:
			Hertwig's epithelial root sheath cell; dental follicle cell; osteogenesis; parathyroid hormone-related peptide; tooth eruption
			PMID: 30584670 DOI: 10.1002/jcp.27857

	===Development of immortalized Hertwig's epithelial root sheath cell lines for cementum and dentin regeneration===		===Development of immortalized Hertwig's epithelial root sheath cell lines for cementum and dentin regeneration===

Z8600021 at 02:06, 13 Ocak 2019

2019-01-13T02:06:18Z

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 Shh protein; Wnt signaling pathway; conserved sequence; embryonic development; sequence deletion; tooth germ
 PMID: 29481312 DOI: 10.1177/0022034518758642
 ==2017==

Z8600021 at 01:27, 13 Ocak 2019

2019-01-13T01:27:50Z

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	==2018==		==2018==

			===Persistent Wnt/β-catenin signaling in mouse epithelium induces the ectopic Dspp expression in cheek mesenchyme===

			Organogenesis. 2018 Dec 20:1-12. doi: 10.1080/15476278.2018.1557026. [Epub ahead of print]

			Zhou N1, Li N1, Liu J1, Wang Y1, Gao J1, Wu Y1, Chen X1, Liu C1, Xiao J1.
			Author information
			Abstract
			Tooth development is accomplished by a series of epithelial-mesenchyme interactions. Epithelial Wnt/β-catenin signaling is sufficient to initiate tooth development by activating Shh, Bmps, Fgfs and Wnts in dental epithelium, which in turn, triggered the expression of odontogenic genes in the underlying mesenchyme. Although constitutive activation of Wnt/β-catenin signaling in oral ectoderm resulted in the continuous tooth formation throughout the life span, if the epithelial Wnt/β-catenin signaling could induce the mesenchyme other than oral mesenchyme still required to be elucidated. In this study, we found that in the K14-cre; Ctnnb1ex3f mice, the markers of dental epithelium, such as Pitx2, Shh, Bmp2, Fgf4, and Fgf8, were not only activated in the oral ectoderm, but also in the cheek epithelium. Surprisingly, the underlying cheek mesenchymal cells were elongated and expressed Dspp. Further investigations detected that the expression of Msx1 and Runx2 extended from oral to cheek mesenchyme. These findings suggested that epithelial Wnt/β-catenin signaling was capable of inducing Dspp expression in non-dental mesenchyme. Moreover, Dspp expression in the K14-cre; Ctnnb1ex3f oral mesenchyme was activated earlier than that in the wild type littermates. In contrast, although the elongated oral epithelial cells were detected in the K14-cre; Ctnnb1ex3f mice, the Amelogenin expression was suppressed. The differential effects of the persistent epithelial Wnt/β-catenin signaling on ameloblast and odontoblast differentiation might result from the altered BMP signaling. In summary, our findings suggested that the epithelial Wnt/β-catenin signaling could induce craniofacial mesenchyme into odontogenic program and promote odontoblast differentiation.

			KEYWORDS:
			BMP signaling; Wnt/β-catenin signaling; odontogenic differentiation; tissue interaction; tooth development
			PMID: 30570432 DOI: 10.1080/15476278.2018.1557026


	===Phosphophoryn and Dentin Sialoprotein Effects on Dental Pulp Cell Migration, Proliferation, and Differentiation===		===Phosphophoryn and Dentin Sialoprotein Effects on Dental Pulp Cell Migration, Proliferation, and Differentiation===

Z8600021 at 01:00, 13 Ocak 2019

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 ==2019==
 ===Autocrine regulation of mesenchymal progenitor cell fates orchestrates tooth eruption===
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 ==2018==
 ===Upstream Enhancer Elements of Shh Regulate Oral and Dental Patterning===

Z8600021 at 01:47, 9 Ocak 2019

2019-01-09T01:47:54Z

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	{{10 Most Recent}}		{{10 Most Recent}}

	===~~Tooth Development~~===		==2019==
	~~<pubmed limit=5>Tooth Development<~~/~~pubmed>~~
			===Autocrine regulation of mesenchymal progenitor cell fates orchestrates tooth eruption===

			Akira Takahashi, Mizuki Nagata, Aditi Gupta, Yuki Matsushita, Tetsutaro Yamaguchi, Koji Mizuhashi, Koutaro Maki, Antonio C. Ruellas, Lucia S. Cevidanes, Henry M. Kronenberg, Noriaki Ono, Wanida Ono

			Proceedings of the National Academy of Sciences Jan 2019, 116 (2) 575-580; DOI: 10.1073/pnas.1810200115

			https://www.pnas.org/content/116/2/575

			Abstract

			Formation of functional skeletal tissues requires highly organized steps of mesenchymal progenitor cell differentiation. The dental follicle (DF) surrounding the developing tooth harbors mesenchymal progenitor cells for various differentiated cells constituting the tooth root–bone interface and coordinates tooth eruption in a manner dependent on signaling by parathyroid hormone-related peptide (PTHrP) and the PTH/PTHrP receptor (PPR). However, the identity of mesenchymal progenitor cells in the DF and how they are regulated by PTHrP-PPR signaling remain unknown. Here, we show that the PTHrP-PPR autocrine signal maintains physiological cell fates of DF mesenchymal progenitor cells to establish the functional periodontal attachment apparatus and orchestrates tooth eruption. A single-cell RNA-seq analysis revealed cellular heterogeneity of PTHrP+ cells, wherein PTHrP+ DF subpopulations abundantly express PPR. Cell lineage analysis using tamoxifen-inducible PTHrP-creER mice revealed that PTHrP+ DF cells differentiate into cementoblasts on the acellular cementum, periodontal ligament cells, and alveolar cryptal bone osteoblasts during tooth root formation. PPR deficiency induced a cell fate shift of PTHrP+ DF mesenchymal progenitor cells to nonphysiological cementoblast-like cells precociously forming the cellular cementum on the root surface associated with up-regulation of Mef2c and matrix proteins, resulting in loss of the proper periodontal attachment apparatus and primary failure of tooth eruption, closely resembling human genetic conditions caused by PPR mutations. These findings reveal a unique mechanism whereby proper cell fates of mesenchymal progenitor cells are tightly maintained by an autocrine system mediated by PTHrP-PPR signaling to achieve functional formation of skeletal tissues.

	~~===Teeth Development===~~
	~~<pubmed limit=5>Teeth Development</pubmed>~~

	==2018==		==2018==

Z8600021 at 05:15, 16 July 2018

2018-07-16T05:15:25Z

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 ===Teeth Development===
 <pubmed limit=5>Teeth Development</pubmed>
 ==2017==

Z8600021 at 22:05, 30 April 2017

2017-04-30T22:05:02Z

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	<pubmed limit=5>Teeth Development</pubmed>		<pubmed limit=5>Teeth Development</pubmed>

			==2017==

			===PAX9 gene mutations and tooth agenesis: A review===
			Clin Genet. 2017 Feb 2. doi: 10.1111/cge.12986. [Epub ahead of print]

			Bonczek O1,2, Balcar VJ3, Šerý O1,2.

			Abstract

			Paired box 9 (PAX9) is one of the best-known transcription factors involved in the development of human dentition. Mutations in PAX9 gene could, therefore, seriously influence the number, position and morphology of the teeth in an affected individual. To date, over 50 mutations in the gene have been reported as associated with various types of dental agenesis (congenitally missing teeth) and other inherited dental defects or variations. The most common consequence of PAX9 gene mutation is the autosomal-dominant isolated (non-syndromic) oligodontia or hypodontia. In the present review, we are summarizing all known PAX9 mutations as well as their nature and precise loci in the DNA sequence of the gene. Where necessary, we have revised the loci of the mutations in line with the reference sequence of the PAX9 gene as it appears in the current DNA databases.
			© 2017 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.
			KEYWORDS:
			PAX9; gene; hypodontia; mutation; oligodontia

			PMID 28155232

Z8600021 at 11:53, 12 September 2016

2016-09-12T11:53:10Z

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	==2015==		==2015==
			===Coevolutionary patterning of teeth and taste buds===

			Proc Natl Acad Sci U S A. 2015 Nov 3;112(44):E5954-62. doi: 10.1073/pnas.1514298112. Epub 2015 Oct 19.

			Bloomquist RF1, Parnell NF2, Phillips KA2, Fowler TE2, Yu TY3, Sharpe PT3, Streelman JT4.

			Abstract

			Teeth and taste buds are iteratively patterned structures that line the oro-pharynx of vertebrates. Biologists do not fully understand how teeth and taste buds develop from undifferentiated epithelium or how variation in organ density is regulated. These organs are typically studied independently because of their separate anatomical location in mammals: teeth on the jaw margin and taste buds on the tongue. However, in many aquatic animals like bony fishes, teeth and taste buds are colocalized one next to the other. Using genetic mapping in cichlid fishes, we identified shared loci controlling a positive correlation between tooth and taste bud densities. Genome intervals contained candidate genes expressed in tooth and taste bud fields. sfrp5 and bmper, notable for roles in Wingless (Wnt) and bone morphogenetic protein (BMP) signaling, were differentially expressed across cichlid species with divergent tooth and taste bud density, and were expressed in the development of both organs in mice. Synexpression analysis and chemical manipulation of Wnt, BMP, and Hedgehog (Hh) pathways suggest that a common cichlid oral lamina is competent to form teeth or taste buds. Wnt signaling couples tooth and taste bud density and BMP and Hh mediate distinct organ identity. Synthesizing data from fish and mouse, we suggest that the Wnt-BMP-Hh regulatory hierarchy that configures teeth and taste buds on mammalian jaws and tongues may be an evolutionary remnant inherited from ancestors wherein these organs were copatterned from common epithelium.
			KEYWORDS:
			bipotency; placode patterning; plasticity; quantitative trait loci; tooth/taste bud development

			PMID 26483492

	===Tooth and scale morphogenesis in shark: an alternative process to the mammalian enamel knot system===		===Tooth and scale morphogenesis in shark: an alternative process to the mammalian enamel knot system===

Z8600021 at 11:34, 12 September 2016

2016-09-12T11:34:20Z

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	PMID 26755699		PMID 26755699

			==2015==

			===Tooth and scale morphogenesis in shark: an alternative process to the mammalian enamel knot system===

			BMC Evol Biol. 2015 Dec 24;15:292. doi: 10.1186/s12862-015-0557-0.

			Debiais-Thibaud M1, Chiori R2,3, Enault S4, Oulion S5, Germon I6, Martinand-Mari C7, Casane D8,9, Borday-Birraux V10,11.

			Abstract

			BACKGROUND:
			The gene regulatory network involved in tooth morphogenesis has been extremely well described in mammals and its modeling has allowed predictions of variations in regulatory pathway that may have led to evolution of tooth shapes. However, very little is known outside of mammals to understand how this regulatory framework may also account for tooth shape evolution at the level of gnathostomes. In this work, we describe expression patterns and proliferation/apoptosis assays to uncover homologous regulatory pathways in the catshark Scyliorhinus canicula.
			RESULTS:
			Because of their similar structural and developmental features, gene expression patterns were described over the four developmental stages of both tooth and scale buds in the catshark. These gene expression patterns differ from mouse tooth development, and discrepancies are also observed between tooth and scale development within the catshark. However, a similar nested expression of Shh and Fgf suggests similar signaling involved in morphogenesis of all structures, although apoptosis assays do not support a strictly equivalent enamel knot system in sharks. Similarities in the topology of gene expression pattern, including Bmp signaling pathway, suggest that mouse molar development is more similar to scale bud development in the catshark.
			CONCLUSIONS:
			These results support the fact that no enamel knot, as described in mammalian teeth, can be described in the morphogenesis of shark teeth or scales. However, homologous signaling pathways are involved in growth and morphogenesis with variations in their respective expression patterns. We speculate that variations in this topology of expression are also a substrate for tooth shape evolution, notably in regulating the growth axis and symmetry of the developing structure.

			PMID 26704180

	==2014==		==2014==