Parathyroid hormone‐related peptide (1–34) promotes tooth eruption and inhibits osteogenesis of dental follicle cells during tooth development

2018 ◽  
Vol 234 (7) ◽  
pp. 11900-11911 ◽  
Author(s):  
Jiawei Zhang ◽  
Lijun Liao ◽  
Yuyu Li ◽  
Yang Xu ◽  
Weihua Guo ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Tooth Development ◽  
Tooth Eruption ◽  
Follicle Cells ◽  
Dental Follicle ◽  
Dental Follicle Cells ◽  
Related Peptide ◽  
Parathyroid Hormone Related Peptide

Secretion of CSF-1 and its inhibition in rat dental follicle cells, implications for tooth eruption

1998 ◽  
Vol 106 (3) ◽  
pp. 808-815 ◽  
Author(s):  
Robert L. Grier IV ◽  
Lihong Zhao ◽  
Charles E. Adams ◽  
Gary E. Wise
Keyword(s):  
Tooth Eruption ◽  
Follicle Cells ◽  
Dental Follicle ◽  
Dental Follicle Cells

Enhancement of gene expression in rat dental follicle cells by parathyroid hormone-related protein

2000 ◽  
Vol 45 (10) ◽  
pp. 903-909 ◽  
Author(s):  
Gary E Wise ◽  
Benito G Que ◽  
Heguang Huang ◽  
Steven J Lumpkin
Keyword(s):  
Gene Expression ◽  
Parathyroid Hormone ◽  
Follicle Cells ◽  
Dental Follicle ◽  
Related Protein ◽  
Dental Follicle Cells ◽  
Parathyroid Hormone Related Protein

Dental Follicle Cells Participate in Tooth Eruption via the RUNX2-MiR-31-SATB2 Loop

2015 ◽  
Vol 94 (7) ◽  
pp. 936-944 ◽  
Author(s):  
J. Ge ◽  
S. Guo ◽  
Y. Fu ◽  
P. Zhou ◽  
P. Zhang ◽  
...  
Keyword(s):  
Tooth Eruption ◽  
Follicle Cells ◽  
Dental Follicle ◽  
Dental Follicle Cells

Cellular, Molecular, and Genetic Determinants of Tooth Eruption

2002 ◽  
Vol 13 (4) ◽  
pp. 323-335 ◽  
Author(s):  
G.E. Wise ◽  
S. Frazier-Bowers ◽  
R.N. D’Souza
Keyword(s):  
Mononuclear Cells ◽  
Alveolar Bone ◽  
Tooth Eruption ◽  
Follicle Cells ◽  
Dental Follicle ◽  
Genetic Determinants ◽  
Dental Follicle Cells ◽  
Parathyroid Hormone Related Protein ◽  
Molecular Events ◽  
Chemotactic Protein

Tooth eruption is a complex and tightly regulated process that involves cells of the tooth organ and the surrounding alveolus. Mononuclear cells (osteoclast precursors) must be recruited into the dental follicle prior to the onset of eruption. These cells, in turn, fuse to form osteoclasts that resorb alveolar bone, forming an eruption pathway for the tooth to exit its bony crypt. Some of the molecules possibly involved in the signaling cascades of eruption have been proposed in studies from null mice, osteopetrotic rodents, injections of putative eruption molecules, and cultured dental follicle cells. In particular, recruitment of the mononuclear cells to the follicle may require colony-stimulating factor-one (CSF-1) and/or monocyte chemotactic protein-1 (MCP-1). Osteoclastogenesis is needed for the bone resorption and may involve inhibition of osteoprotegerin transcription and synthesis in the follicle, as well as enhancement of receptor activator of NFκB ligand (RANKL), in the adjacent alveolar bone and/or in the follicle. Paracrine signaling by parathyroid-hormone-related protein and interleukin -1α, produced in the stellate reticulum adjacent to the follicle, may also play a role in regulating eruption. Osteoblasts might also influence the process of eruption, the most important physiologic role likely being at the eruptive site, in the formation of osteoclasts through signaling via the RANKL/OPG pathway. Evidence thus far supports a role for an osteoblast-specific transcription factor, Cbfa1 (Runx2), in molecular events that regulate tooth eruption. Cbfa1 is also expressed at high levels by the dental follicle cells. This review concludes with a discussion of the several human conditions that result in a failure of or delay in tooth eruption.

Inhibition of osteoclastogenesis by the secretion of osteoprotegerin in vitro by rat dental follicle cells and its implications for tooth eruption

2002 ◽  
Vol 47 (3) ◽  
pp. 247-254 ◽  
Author(s):  
Gary E Wise ◽  
Shaomian Yao ◽  
Quiyang Zhang ◽  
Yi Ren
Keyword(s):  
Tooth Eruption ◽  
Follicle Cells ◽  
Dental Follicle ◽  
Dental Follicle Cells

scholarly journals The expressions of tooth eruption relevant genes are different in incisors and molars dental follicle cells in rat: an in vitro study

2019 ◽  
Author(s):  
Mengting He ◽  
Xiaomeng Dong ◽  
Peiqi Wang ◽  
Zichao Xiang ◽  
Jiangyue Wang ◽  
...  
Keyword(s):  
Gene Expression ◽  
Real Time ◽  
Expression Patterns ◽  
In Vitro Study ◽  
Tooth Eruption ◽  
Follicle Cells ◽  
Dental Follicle ◽  
Dental Follicle Cells ◽  
Real Time Qpcr

Abstract Background The incisors and molars showed different patterns of tooth eruption in rodents and the dental follicle cells play key roles in tooth eruption. Little is known about the differences in incisors and molars dental follicle cells during tooth eruption in rodents. The purpose of this study was to investigate the differences between incisor dental follicle cells and molar dental follicle cells during tooth eruption in rat.Methods Incisor dental follicle cells and molar dental follicle cells were obtained as previously described. Immunofluorescence was used to identify the cells. Gene expression was measured by real-time qPCR and western blot.Results Compared with molar dental follicle cells, the incisor dental follicle cells showed higher expression of OPG, BMP-2 and BMP-3. The molar dental follicle cells showed higher expression of MCP-1 and RANKL.Conclusions The expression patterns of genes related to tooth eruption were different in incisors and molars dental follicle cells in rat.

scholarly journals Dental Follicle Cells: Roles in Development and Beyond

2019 ◽  
Vol 2019 ◽  
pp. 1-17 ◽  
Author(s):  
Tao Zhou ◽  
Jinhai Pan ◽  
Peiyao Wu ◽  
Ruijie Huang ◽  
Wei Du ◽  
...  
Keyword(s):  
Tissue Engineering ◽  
Clinical Application ◽  
Alveolar Bone ◽  
Tooth Development ◽  
Tooth Germ ◽  
Follicle Cells ◽  
Tooth Root ◽  
Dental Follicle ◽  
Mesenchymal Progenitor Cells ◽  
Dental Follicle Cells

Dental follicle cells (DFCs) are a group of mesenchymal progenitor cells surrounding the tooth germ, responsible for cementum, periodontal ligament, and alveolar bone formation in tooth development. Cascades of signaling pathways and transcriptional factors in DFCs are involved in directing tooth eruption and tooth root morphogenesis. Substantial researches have been made to decipher multiple aspects of DFCs, including multilineage differentiation, senescence, and immunomodulatory ability. DFCs were proved to be multipotent progenitors with decent amplification, immunosuppressed and acquisition ability. They are able to differentiate into osteoblasts/cementoblasts, adipocytes, neuron-like cells, and so forth. The excellent properties of DFCs facilitated clinical application, as exemplified by bone tissue engineering, tooth root regeneration, and periodontium regeneration. Except for the oral and maxillofacial regeneration, DFCs were also expected to be applied in other tissues such as spinal cord defects (SCD), cardiomyocyte destruction. This article reviewed roles of DFCs in tooth development, their properties, and clinical application potentials, thus providing a novel guidance for tissue engineering.

scholarly journals CHD7 Regulates Osteogenic Differentiation of Human Dental Follicle Cells via PTH1R Signaling

2020 ◽  
Vol 2020 ◽  
pp. 1-10
Author(s):  
Caojie Liu ◽  
Qiwen Li ◽  
Qingyue Xiao ◽  
Ping Gong ◽  
Ning Kang
Keyword(s):  
Parathyroid Hormone ◽  
Osteogenic Differentiation ◽  
Chromatin Remodeling ◽  
Epigenetic Modification ◽  
Dna Binding Protein ◽  
Follicle Cells ◽  
Dental Follicle ◽  
Rna Seq ◽  
Dental Follicle Cells ◽  
Parathyroid Hormone Receptor

Chromodomain helicase DNA-binding protein 7 (CHD7) is an ATP-dependent chromatin remodeling enzyme, functioning as chromatin reader to conduct epigenetic modification. Its effect on osteogenic differentiation of human dental follicle cells (hDFCs) remains unclear. Here, we show the CHD7 expression increases with osteogenic differentiation. The knockdown of CHD7 impairs the osteogenic ability of hDFCs, characterized by reduced alkaline phosphatase activity and mineralization, and the decreased expression of osteogenesis-related genes. Conversely, the CHD7 overexpression enhances the osteogenic differentiation of hDFCs. Mechanically, RNA-seq analyses revealed the downregulated enrichment of PTH (parathyroid hormone)/PTH1R (parathyroid hormone receptor-1) signaling pathway after CHD7 knockdown. We found the expression of PTH1R positively correlates with CHD7. Importantly, the overexpression of PTH1R in CHD7-knockdown hDFCs partially rescued the impaired osteogenic differentiation. Our research demonstrates that CHD7 regulates the osteogenic differentiation of hDFCs by regulating the transcription of PTH1R.

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