scholarly journals Secreted Frizzled-Related Protein 1 Promotes Odontoblastic Differentiation and Reparative Dentin Formation in Dental Pulp Cells

Cells ◽  
2021 ◽  
Vol 10 (9) ◽  
pp. 2491
Author(s):  
Keita Ipposhi ◽  
Atsushi Tomokiyo ◽  
Taiga Ono ◽  
Kozue Yamashita ◽  
Muhammad Anas Alhasan ◽  
...  
Keyword(s):  
Dental Pulp ◽  
Nodule Formation ◽  
Dental Pulp Cells ◽  
Related Protein ◽  
Direct Pulp Capping ◽  
Odontoblastic Differentiation ◽  
Reparative Dentin ◽  
Pulp Cells ◽  
Dentin Formation ◽  
Reparative Dentin Formation

Direct pulp capping is an effective treatment for preserving dental pulp against carious or traumatic pulp exposure via the formation of protective reparative dentin by odontoblast-like cells. Reparative dentin formation can be stimulated by several signaling molecules; therefore, we investigated the effects of secreted frizzled-related protein (SFRP) 1 that was reported to be strongly expressed in odontoblasts of newborn molar tooth germs on odontoblastic differentiation and reparative dentin formation. In developing rat incisors, cells in the dental pulp, cervical loop, and inner enamel epithelium, as well as ameloblasts and preodontoblasts, weakly expressed Sfrp1; however, Sfrp1 was strongly expressed in mature odontoblasts. Human dental pulp cells (hDPCs) showed stronger expression of SFRP1 compared with periodontal ligament cells and gingival cells. SFRP1 knockdown in hDPCs abolished calcium chloride-induced mineralized nodule formation and odontoblast-related gene expression and decreased BMP-2 gene expression. Conversely, SFRP1 stimulation enhanced nodule formation and expression of BMP-2. Direct pulp capping treatment with SFRP1 induced the formation of a considerable amount of reparative dentin that has a structure similar to primary dentin. Our results indicate that SFRP1 is crucial for dentinogenesis and is important in promoting reparative dentin formation in response to injury.

scholarly journals Alcohol Inhibits Odontogenic Differentiation of Human Dental Pulp Cells by Activating mTOR Signaling

2017 ◽  
Vol 2017 ◽  
pp. 1-10 ◽  
Author(s):  
Wei Qin ◽  
Qi-Ting Huang ◽  
Michael D. Weir ◽  
Zhi Song ◽  
Ashraf F. Fouad ◽  
...  
Keyword(s):  
Behavioral Problems ◽  
Dental Pulp ◽  
Nodule Formation ◽  
Dependent Manner ◽  
Dental Pulp Cells ◽  
Human Dental Pulp Cells ◽  
Odontoblastic Differentiation ◽  
Heavy Alcohol Consumption ◽  
Human Dental Pulp ◽  
Pulp Cells

Long-term heavy alcohol consumption could result in a range of health, social, and behavioral problems. People who abuse alcohol are at high risks of seriously having osteopenia, periodontal disease, and compromised oral health. However, the role of ethanol (EtOH) in the biological functions of human dental pulp cells (DPCs) is unknown. Whether EtOH affects the odontoblastic differentiation of DPCs through the mechanistic target of rapamycin (mTOR) remains unexplored. The objective of this study was to investigate the effects of EtOH on DPC differentiation and mineralization. DPCs were isolated and purified from human dental pulps. The proliferation and odontoblastic differentiation of DPCs treated with EtOH were subsequently investigated. Different doses of EtOH were shown to be cytocompatible with DPCs. EtOH significantly activated the mTOR pathway in a dose-dependent manner. In addition, EtOH downregulated the alkaline phosphatase activity, attenuated the mineralized nodule formation, and suppressed the expression of odontoblastic markers including ALP, DSPP, DMP-1, Runx2, and OCN. Moreover, the pretreatment with rapamycin, a specific mTOR inhibitor, markedly reversed the EtOH-induced odontoblastic differentiation and cell mineralization. Our findings show for the first time that EtOH can suppress DPC differentiation and mineralization in a mTOR-dependent manner, indicating that EtOH may be involved in negatively regulating the dental pulp repair.

scholarly journals Lithium Chloride Exerts Differential Effects on Dentinogenesis and Osteogenesis in Primary Pulp Cultures

2021 ◽  
Vol 2 ◽  
Author(s):  
Anushree Vijaykumar ◽  
Mina Mina
Keyword(s):  
Dental Pulp ◽  
Osteoblast Differentiation ◽  
Prolonged Treatment ◽  
Odontoblast Differentiation ◽  
Positive Effects ◽  
Reparative Dentin ◽  
Dentin Formation ◽  
Reparative Dentin Formation

Wnt/β-catenin signaling is known to play essential roles in odontoblast differentiation and reparative dentin formation. Various Wnt activators including LiCl have been increasingly studied for their effectiveness to induce repair of the dentin-pulp complex. LiCl is a simple salt thought to activate Wnt/β-catenin signaling by inhibiting GSK3β. Previous in vitro and in vivo studies showed that LiCl increased odontoblast differentiation and enhanced reparative dentin formation. However, the underlying molecular and cellular mechanisms by which LiCl regulates odontoblast and osteoblast differentiation during reparative dentinogenesis are not well-understood. Our in vitro studies show that exposure of early dental pulp progenitors to LiCl increased the survival and the pool of αSMA+ progenitors, leading to enhanced odontoblast and osteoblast differentiation. The positive effects of LiCl in the differentiation of osteoblasts and odontoblasts from αSMA+ progenitors are mediated by Wnt/β-catenin signaling. Our results also showed that continuous and late exposure of dental pulp cells to LiCl increased the expression of odontoblast markers through Wnt/β-catenin signaling, and the number of odontoblasts expressing DMP1-Cherry and DSPP-Cerulean transgenes. However, unlike the early treatment, both continuous and late treatments decreased the expression of Bsp and the expression of BSP-GFPtpz transgene. These observations suggest that prolonged treatment with LiCl in more mature cells of the dental pulp has an inhibitory effect on osteoblast differentiation. The inhibitory effects of LiCl on osteogenesis and Bsp were not mediated through Wnt/β-catenin signaling. These observations suggest that the effects of LiCl, and GSK3β antagonists on reparative dentinogenesis involve multiple pathways and are not specific to Wnt/β-catenin signaling.

scholarly journals Sclerostin promotes human dental pulp cells senescence

PeerJ ◽  
2018 ◽  
Vol 6 ◽  
pp. e5808 ◽  
Author(s):  
Yanjing Ou ◽  
Yi Zhou ◽  
Shanshan Liang ◽  
Yining Wang
Keyword(s):  
Dental Pulp ◽  
Wnt Signaling Pathway ◽  
Dental Pulp Cells ◽  
Differentiation Potential ◽  
Human Dental Pulp Cells ◽  
Qrt Pcr ◽  
Odontoblastic Differentiation ◽  
Human Dental Pulp ◽  
Pulp Cells

Background Senescence-related impairment of proliferation and differentiation limits the use of dental pulp cells for tissue regeneration. Deletion of sclerostin improves the dentinogenesis regeneration, while its role in dental pulp senescence is unclear. We investigated the role of sclerostin in subculture-induced senescence of human dental pulp cells (HDPCs) and in the senescence-related decline of proliferation and odontoblastic differentiation. Methods Immunohistochemical staining and qRT-PCR analyses were performed to examine the expression pattern of sclerostin in young (20–30-year-old) and senescent (45–80-year-old) dental pulps. HDPCs were serially subcultured until senescence, and the expression of sclerostin was examined by qRT-PCR analysis. HDPCs with sclerostin overexpression and knockdown were constructed to investigate the role of sclerostin in HDPCs senescence and senescence-related impairment of odontoblastic differentiation potential. Results By immunohistochemistry and qRT-PCR, we found a significantly increased expression level of sclerostin in senescent human dental pulp compared with that of young human dental pulp. Additionally, elevated sclerostin expression was found in subculture-induced senescent HDPCs in vitro. By sclerostin overexpression and knockdown, we found that sclerostin promoted HDPCs senescence-related decline of proliferation and odontoblastic differentiation potential with increased expression of p16, p53 and p21 and downregulation of the Wnt signaling pathway. Discussion The increased expression of sclerostin is responsible for the decline of proliferation and odontoblastic differentiation potential of HDPCs during cellular senescence. Anti-sclerostin treatment may be beneficial for the maintenance of the proliferation and odontoblastic differentiation potentials of HDPCs.

scholarly journals Dental pulp cells that express adeno-associated virus serotype 2-mediated BMP-7 gene enhanced odontoblastic differentiation

2014 ◽  
Vol 33 (5) ◽  
pp. 656-662
Author(s):  
Wei QIN ◽  
Haiyan ZHU ◽  
Lingling CHEN ◽  
Xiaoting YANG ◽  
Qiting HUANG ◽  
...  
Keyword(s):  
Dental Pulp ◽  
Dental Pulp Cells ◽  
Adeno Associated Virus ◽  
Odontoblastic Differentiation ◽  
Virus Serotype ◽  
Pulp Cells

The role of SDF-1 and CXCR4 on odontoblastic differentiation in human dental pulp cells

2013 ◽  
Vol 47 (6) ◽  
pp. 534-541 ◽  
Author(s):  
D. S. Kim ◽  
Y. S. Kim ◽  
W. J. Bae ◽  
H. J. Lee ◽  
S. W. Chang ◽  
...  
Keyword(s):  
Dental Pulp ◽  
Dental Pulp Cells ◽  
Human Dental Pulp Cells ◽  
Odontoblastic Differentiation ◽  
Human Dental Pulp ◽  
Pulp Cells

scholarly journals Lipopolysaccharide stimulation improves the odontoblastic differentiation of human dental pulp cells

2014 ◽  
Vol 11 (5) ◽  
pp. 3547-3552 ◽  
Author(s):  
YIHUA HUANG ◽  
HONGWEI JIANG ◽  
QIMEI GONG ◽  
XUYAN LI ◽  
JUNQI LING
Keyword(s):  
Dental Pulp ◽  
Dental Pulp Cells ◽  
Human Dental Pulp Cells ◽  
Odontoblastic Differentiation ◽  
Human Dental Pulp ◽  
Pulp Cells

scholarly journals Induction of reparative dentin by calcium silicate-based material as direct pulp capping agent

2019 ◽  
Vol 12 (4) ◽  
pp. 182-186
Author(s):  
Mozammal Hossain ◽  
Mahmood Sajedeen ◽  
Yukio Nakamura
Keyword(s):  
Calcium Hydroxide ◽  
Calcium Silicate ◽  
Normal Function ◽  
Direct Pulp Capping ◽  
Pulp Tissue ◽  
Pulp Capping ◽  
Exposure Site ◽  
Reparative Dentin ◽  
Dentin Formation ◽  
Reparative Dentin Formation

This study was performed to examine whether calcium silicate could induce reparative dentin formation without eliciting any adverse effect in direct pulp capping of premolar teeth. Twenty participants who need extraction of their 4 healthy permanent premolar teeth for orthodontic reasons were included in this study. Following the surgical procedure, the exposed pulp tissue was treated either with calcium silicate or covered with calcium hydroxide paste. On day 3, 7, 14 and 28, the experimental teeth was extracted and examined using light microscopy and histometric analysis to observe the inflammatory changes and the amount of reparative dentin formation. The results showed that in the calcium silicate treated teeth, substantial amounts of dentine-like tissue was formed on day 14 and mostly located on the exposure site. It was also observed in the calcium hydroxide treated teeth but dentin-like tissue located at a distance from the exposure site. The total amount of reparative dentine formed in the calcium silicate-treated teeth was significantly higher (p<0.005) than in the calcium hydroxide-treated specimens. In conclusion that the calcium silicate indices pulpal wound healing and reparative formation in the exposed teeth without affecting the normal function of the remaining pulp.

17β-Estradiol induces odontoblastic differentiation via activation of the c-Src/MAPK pathway in human dental pulp cells

2015 ◽  
Vol 93 (6) ◽  
pp. 587-595 ◽  
Author(s):  
Su Mi Woo ◽  
Kyung Joo Seong ◽  
Sang Jin Oh ◽  
Hong Ju Park ◽  
Sun Hun Kim ◽  
...  
Keyword(s):  
Dental Pulp ◽  
Mapk Pathway ◽  
Mapk Signaling ◽  
Dental Pulp Cells ◽  
Human Dental Pulp Cells ◽  
Odontoblastic Differentiation ◽  
Alp Activity ◽  
Human Dental Pulp ◽  
Pulp Cells ◽  
17Β Estradiol

The present study is aimed at investigating the effects of the exogenous estrogen 17β-estradiol (E2) on odontoblastic differentiation in human dental pulp cells (HDPCs) immotalized with hTERT gene and their molecular mechanism. Proliferation was detected by BrdU assay, and odontoblast differentiation induction was evaluated by the expression of dentin sialophosphoprotein (DSPP), dentin sialoprotein (DSP) and dentin matrix protein1 (DMP1), and alkaline phosphatase (ALP) activity and mineralization. Estrogen receptor-α (ER-α), c-Src, and mitogen-activated protein kinases (MAPKs) were examined and their inhibitors were used to determine the roles on odontogenic induction. E2 significantly promoted the HDPC proliferation, which was mediated by extracellular signal-related kinase 1/2. E2 upregulated DSPP, DSP, and DMP1 as the odontogenic differentiation markers and enhanced ALP activity and mineralization. E2 increased phosphorylation of ER-α and fulvestrant, an ER downregulator, significantly downregulated DSPP, DMP1, and DSP induced by E2. Moreover, E2 treatment activated c-Src and MAPKs upon odontogenic induction, whereas chemical inhibition of c-Src and MAPKs decreased expression of DSPP, DMP1, and DSP and mineralization augmented by E2. Moreover, fulvestrant reduced E2-induced phosphorylation of c-Src and MAPK and inhibition of c-Src by PP2 attenuated activation of MAPKs during E2-induced odontoblastic differentiation. Taken together, these results indicated that E2 stimulates odontoblastic differentiation of HDPCs via coordinated regulation of ER-α, c-Src, and MAPK signaling pathways, which may play a key role in the regeneration of dentin.

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