Integumentary System - Tooth Development - Revision history

Z8600021 at 20:17, 1 Ocak 2020

2020-01-01T20:17:41Z

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			* '''Immortalized Hertwig's epithelial root sheath cell line works as model for epithelial-mesenchymal interaction during tooth root formation'''{{#pmid:31512758\|PMID31512758}} "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."

	* '''Parathyroid hormone-related peptide (1-34) promotes tooth eruption and inhibits osteogenesis of dental follicle cells during tooth development'''{{#pmid:30584670\|PMID30584670}} "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."		* '''Parathyroid hormone-related peptide (1-34) promotes tooth eruption and inhibits osteogenesis of dental follicle cells during tooth development'''{{#pmid:30584670\|PMID30584670}} "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."

Z8600021 at 01:22, 16 July 2019

2019-07-16T01:22:33Z

← Older revision		Revision as of 11:22, 16 July 2019
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	{{Tooth Vignette}}		{{Tooth Vignette}}
	<br>		<br>
	'''Links:''' {{Gastrointestinal ~~Tract~~}}		'''Links:''' {{Gastrointestinal tract}}
	<br>		<br>
	{{Integumentary Links}}		{{Integumentary Links}}

Z8600021 at 01:22, 16 July 2019

2019-07-16T01:22:14Z

← Older revision		Revision as of 11:22, 16 July 2019
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	{{tooth stages table}}		{{tooth stages table}}


	Recent molecular animal model studies have shown that epithelial {{Wnt}}/β-catenin signaling is sufficient to initiate tooth development through activating {{Shh}}, {{Bmp}}s, {{Fgf}}s and {{Wnt}}s in the dental epithelium.{{#pmid:30570432\|PMID30570432}} This then initiates the expression of odontogenic genes in the underlying mesenchyme.		Recent molecular animal model studies have shown that epithelial {{Wnt}}/β-catenin signaling is sufficient to initiate tooth development through activating {{Shh}}, {{Bmp}}s, {{Fgf}}s and {{Wnt}}s in the dental epithelium.{{#pmid:30570432\|PMID30570432}} This then initiates the expression of odontogenic genes in the underlying mesenchyme.


	<br>		<br>
			{{Tooth Vignette}}
			<br>
	'''Links:''' [[Gastrointestinal Tract ~~Development]]~~		'''Links:''' {{Gastrointestinal Tract}}
			<br>
	{{Integumentary Links}}		{{Integumentary Links}}

Z8600021 at 01:19, 16 July 2019

2019-07-16T01:19:49Z

Z8600021 at 01:17, 16 July 2019

2019-07-16T01:17:31Z

← Older revision		Revision as of 11:17, 16 July 2019
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	== Textbooks ==		== Textbooks ==
			[[File:Rat-neonatal_teeth.jpg\|thumb\|Neonatal rat teeth]]
	* '''Human Embryology '''(2nd ed.) Larson Chapter 14 p443-455		* '''Human Embryology '''(2nd ed.) Larson Chapter 14 p443-455
	* '''The Developing Human: Clinically Oriented Embryology '''(6th ed.) Moore and Persaud Chapter 20: P513-529		* '''The Developing Human: Clinically Oriented Embryology '''(6th ed.) Moore and Persaud Chapter 20: P513-529

Z8600021 at 01:17, 16 July 2019

2019-07-16T01:17:04Z

← Older revision		Revision as of 11:17, 16 July 2019
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	== Some Recent Findings ==		== Some Recent Findings ==
	[[File:~~Rat-neonatal_teeth~~.jpg\|thumb\|~~Neonatal rat teeth~~]]		[[File:Tooth eruption signaling.jpg\|thumb\|Tooth eruption signaling{{#pmid:30602459\|PMID30602459}}]]
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Z8600021 at 01:12, 16 July 2019

2019-07-16T01:12:18Z

← Older revision		Revision as of 11:12, 16 July 2019
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			* '''Parathyroid hormone-related peptide (1-34) promotes tooth eruption and inhibits osteogenesis of dental follicle cells during tooth development'''{{#pmid:30584670\|PMID30584670}} "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."

	* '''Autocrine regulation of mesenchymal progenitor cell fates orchestrates tooth eruption'''~~<ref>Akira Takahashi, etal. Autocrine regulation of mesenchymal progenitor cell fates orchestrates tooth eruption. 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</ref>~~ "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."		* '''Autocrine regulation of mesenchymal progenitor cell fates orchestrates tooth eruption'''{{#pmid:30509999\|PMID30509999}} "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."

	* '''Persistent Wnt/β-catenin signaling in mouse epithelium induces the ectopic Dspp expression in cheek mesenchyme'''{{#pmid:30570432\|PMID30570432}} "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. ...In summary, our findings suggested that the epithelial Wnt/β-catenin signaling could induce craniofacial mesenchyme into odontogenic program and promote odontoblast differentiation.		* '''Persistent Wnt/β-catenin signaling in mouse epithelium induces the ectopic Dspp expression in cheek mesenchyme'''{{#pmid:30570432\|PMID30570432}} "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. ...In summary, our findings suggested that the epithelial Wnt/β-catenin signaling could induce craniofacial mesenchyme into odontogenic program and promote odontoblast differentiation.

Z8600021 at 07:11, 30 March 2019

2019-03-30T07:11:37Z

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 ==Abnormalities==
 [[File:Inherited_dentine_disorders.jpg|thumb|Inherited dentine disorders{{#pmid:19021896|PMID19021896}}]]
 ===Adontia===

Z8600021 at 23:43, 10 February 2019

2019-02-10T23:43:27Z

← Older revision		Revision as of 09:43, 11 February 2019
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	Four epithelial signaling molecules, Bmp2, Shh, Wnt10a, and Wnt10b, in the early inductive cascade, each signal has a distinct molecular action on the jaw mesenchyme.		Four epithelial signaling molecules, Bmp2, Shh, Wnt10a, and Wnt10b, in the early inductive cascade, each signal has a distinct molecular action on the jaw mesenchyme.

	Mouse (~~E11~~.0 and ~~E12~~.0) - all four genes are specifically expressed in the epithelium.		Mouse ({{ME11.0}} and {{MEE12.0}}) - all four genes are specifically expressed in the epithelium.

	Shh and Wnt10b induce general Hedgehog and Wnt targets, Ptc and Gli for Shh and Lef1 for Wnt10b,		Shh and Wnt10b induce general Hedgehog and Wnt targets, Ptc and Gli for Shh and Lef1 for Wnt10b,

Z8600021 at 05:24, 4 February 2019

2019-02-04T05:24:27Z

← Older revision		Revision as of 15:24, 4 February 2019
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	==Additional Images==		==Additional Images==
	[[:Category:Tooth]] \| [[:Category:Integumentary]]		[[:Category:Tooth]] \| [[:Category:Integumentary]]

	<gallery>		<gallery>
	File:Tooth_development_stage.jpg\|Tooth development stage		File:Tooth_development_stage.jpg\|Tooth development stage
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	File:Rat-neonatal_teeth.jpg\|Rat - neonatal teeth		File:Rat-neonatal_teeth.jpg\|Rat - neonatal teeth
	</gallery>		</gallery>
	===Historic===		===Historic Images===
	[[Book - Human Embryology and Morphology 5\|Development and Morphology of the Teeth (1902)]]		{{Historic Disclaimer}}

			{{Ref- Keith1902}} [[Book - Human Embryology and Morphology 5\|Development and Morphology of the Teeth (1902)]]

	<gallery>		<gallery>
	File:Keith1902 fig047.jpg\|Fig. 47. Showing the parts of an incisor tooth.		File:Keith1902 fig047.jpg\|Fig. 47. Showing the parts of an incisor tooth.
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	File:Keith1902 fig050.jpg\|Fig. 50. A. The tritubercular Type of Tooth.		File:Keith1902 fig050.jpg\|Fig. 50. A. The tritubercular Type of Tooth.
	</gallery>		</gallery>
	[[Book_-_Manual_of_Human_Embryology_17-2#The_Teeth\|The Teeth (1912)]]
			{{Ref-GrosserLewisMcMurrich1912}} [[Book_-_Manual_of_Human_Embryology_17-2#The_Teeth\|The Teeth (1912)]]
	<gallery>		<gallery>
	File:Keibel_Mall_2_262.jpg\|Fig. 262. Section through the dental ridge of the lower jaw of embryos.		File:Keibel_Mall_2_262.jpg\|Fig. 262. Section through the dental ridge of the lower jaw of embryos.
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	File:Keibel_Mall_2_table_teeth.jpg\|Table - Dentition Timeline		File:Keibel_Mall_2_table_teeth.jpg\|Table - Dentition Timeline
	</gallery>		</gallery>
	[[Book_-_Text-Book_of_Embryology_12#The_Teeth\|The Teeth (1921)]]
			{{Ref-Bailey1921}} [[Book_-_Text-Book_of_Embryology_12#The_Teeth\|The Teeth (1921)]]
	<gallery>		<gallery>
	File:Bailey251.jpg\|Fig. 252. Section of developing tooth from a 3 months human fetus.		File:Bailey251.jpg\|Fig. 252. Section of developing tooth from a 3 months human fetus.
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	File:Baileytable05.jpg\|Permanent teeth		File:Baileytable05.jpg\|Permanent teeth
	</gallery>		</gallery>


	==Terms==		==Terms==
	{{Tooth terms}}		{{Tooth terms}}

← Older revision		Revision as of 11:19, 16 July 2019
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	local ectodermal thickening expresses several signaling molecules		local ectodermal thickening expresses several signaling molecules
	these in turn signal to the underlying mesenchyme triggering mesenchymal condensation		these in turn signal to the underlying mesenchyme triggering mesenchymal condensation
	(epithelially expressed ~~Bmp4~~ induces Msx1 and Lef1 as well as itself in the underlying mesenchyme)		(epithelially expressed {{Bmp}}4 induces Msx1 and Lef1 as well as itself in the underlying mesenchyme)

	Four epithelial signaling molecules, Bmp2, Shh, Wnt10a, and Wnt10b, in the early inductive cascade, each signal has a distinct molecular action on the jaw mesenchyme.		Four epithelial signaling molecules, Bmp2, Shh, Wnt10a, and Wnt10b, in the early inductive cascade, each signal has a distinct molecular action on the jaw mesenchyme.

	Mouse ({{ME11.0}} and {{~~MEE12.0~~}}) - all four genes are specifically expressed in the epithelium.		Mouse ({{ME11}} and {{ME12}}) - all four genes are specifically expressed in the epithelium.

	Shh and Wnt10b induce general Hedgehog and Wnt targets, Ptc and Gli for Shh and Lef1 for Wnt10b,		Shh and Wnt10b induce general Hedgehog and Wnt targets, Ptc and Gli for Shh and Lef1 for Wnt10b,

	~~Bmp2~~ is able to induce tooth-specific expression of Msx1.		{{Bmp}}2 is able to induce tooth-specific expression of Msx1.

	(Text above modified from: Hélène R. Dassule and Andrew P. McMahon Developmental Biology, v 202, n 2, October 15, 1998, p215-227)		(Text above modified from: Hélène R. Dassule and Andrew P. McMahon Developmental Biology, v 202, n 2, October 15, 1998, p215-227)

	(More? Developmental Mechanism - Epithelial Mesenchymal Interaction)		(More? [[Developmental Mechanism - Epithelial Mesenchymal Interaction\|Epithelial Mesenchymal Interaction]])

	==Periodontal Ligament==		==Periodontal Ligament==
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	[[File:Inherited_dentine_disorders.jpg\|thumb\|Inherited dentine disorders{{#pmid:19021896\|PMID19021896}}]]		[[File:Inherited_dentine_disorders.jpg\|thumb\|Inherited dentine disorders{{#pmid:19021896\|PMID19021896}}]]

	===Adontia===		===Adontia===
	A total lack of tooth development.		A total lack of tooth development.