Wnt signaling in dental pulp homeostasis and dentin regeneration

Kornsuthisopon, Chatvadee; Photichailert, Suphalak; Nowwarote, Nunthawan; Tompkins, Kevin; Osathanon, Thanaphum

doi:10.1016/j.archoralbio.2021.105322

Cited by 14 publications

(15 citation statements)

References 86 publications

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“…Dentin formation can be divided into three steps. First, cell differentiation is initiated by multiple molecular signaling pathways, such as Wnt and TGF‐β, from the inner enamel epithelium (Kornsuthisopon et al, 2022; Lee et al, 2022). Odontoblast precursors, that is, dental papilla cells (Kawashima & Okiji, 2016), differentiate into functional mature odontoblasts that secrete organic dentin matrices, such as collagen and noncollagenous molecules.…”

Section: Introductionmentioning

confidence: 99%

Hereditary dentin defects with systemic diseases

Zhu

Wang

et al. 2023

Oral Diseases

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ObjectiveThis review aimed to summarize recent progress on syndromic dentin defects, promoting a better understanding of systemic diseases with dentin malformations, the molecules involved, and related mechanisms.Subjects and MethodsReferences on genetic diseases with dentin malformations were obtained from various sources, including PubMed, OMIM, NCBI, and other websites. The clinical phenotypes and genetic backgrounds of these diseases were then summarized, analyzed, and compared.ResultsOver 10 systemic diseases, including osteogenesis imperfecta, hypophosphatemic rickets, vitamin D‐dependent rickets, familial tumoral calcinosis, Ehlers‐Danlos syndrome, Schimke immuno‐osseous dysplasia, hypophosphatasia, Elsahy‐Waters syndrome, Singleton‐Merten syndrome, odontochondrodysplasia, and microcephalic osteodysplastic primordial dwarfism type II were examined. Most of these are bone disorders, and their pathogenic genes may regulate both dentin and bone development, involving extracellular matrix, cell differentiation, and metabolism of calcium, phosphorus, and vitamin D. The phenotypes of these syndromic dentin defects various with the involved genes, part of them are similar to dentinogenesis imperfecta or dentin dysplasia, while others only present one or two types of dentin abnormalities such as discoloration, irregular enlarged or obliterated pulp and canal, or root malformation.ConclusionSome specific dentin defects associated with systemic diseases may serve as important phenotypes for dentists to diagnose. Furthermore, mechanistic studies on syndromic dentin defects may provide valuable insights into isolated dentin defects and general dentin development or mineralization.

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Section: Introductionmentioning

confidence: 99%

Hereditary dentin defects with systemic diseases

Zhu

Wang

et al. 2023

Oral Diseases

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“…Evidence suggests that the canonical Wnt signalling pathway is crucial for dental pulp repair process and dentine regeneration (Han et al, 2014; Hara et al, 2021; Kornsuthisopon et al, 2022; Uribe‐Etxebarria et al, 2017; Vijaykumar et al, 2021; Yaemkleebbua et al, 2019; Zhao et al, 2019). Direct pulp capping with calcium or silicon‐based materials such as Mineral trioxide aggregate (MTA) and Biodentine™ activated the reparative dentine formation in animal pulp exposure model also accompanied by β‐catenin nuclear translocation in odontoblast‐like and dental pulp cells underneath suggesting the activation of canonical Wnt signalling during the process (Han et al, 2014; Hara et al, 2021; Yaemkleebbua et al, 2019).…”

Section: Introductionmentioning

confidence: 99%

Wnt3a promotes odonto/osteogenic differentiation in vitro and tertiary dentin formation in a rat model

et al. 2023

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Aim:To investigate the effect of Wnt3a on odonto/osteogenic differentiation of stem cells isolated from human exfoliated deciduous teeth (SHEDs) and reparative dentine formation in a rat model. Methodology:Stem cells isolated from human exfoliated deciduous teeth were cultured in media with Wnt3a (50-200 ng/ml). Wnt activation was confirmed by βcatenin immunocytochemistry. Colony-forming unit assay (normalized percentage area), osteogenic gene expression analysis by real-time polymerase chain reaction and mineralization assays measured by the absorption at 540 nm were performed.Tertiary dentine formation in vivo was evaluated using 8-week-old, male Wistar rats.Cavities with pinpoint pulp exposure by a sharp instrument were prepared at the mesial surface of the first molars. Teeth were divided into (n = 6): (1) distilled water (negative control), (2) phosphate-buffered saline (PBS), (3) lithium chloride in DI (20 μM), and (4) Wnt3a in PBS (200 ng/ml). Collagen sponge was used as a scaffold.The cavity was sealed with glass ionomer restoration. Four weeks later, animals were euthanized by sodium pentobarbital (120 mg/kg body weight). Hard tissue formation was evaluated using micro-computerized tomography. Sixty consecutive slides from the initial plane were analysed and calculated as bone/dentine volume per total tissue volume. Paraffin sections (2 μm) were stained with haematoxylin and eosin and Masson's trichrome for morphological evaluation. Data are presented as the mean ± standard error. Mann-Whitney U test was used for two-group comparison.Kruskal Wallis followed by pairwise comparison was employed for three or more group comparisons. Statistical analysis was performed using GraphPad Prism 7.Differences were considered significant at p < .05.Results: Wnt3a decreased SHEDs colony formation and increased OSX, BMP2, and DMP1 expression, corresponding to an increase in mineralization. Additionally, a significant increase in dentine/bone volume per total tissue volume was observed in Wnt3a treated defects. Dentine bridge formation at the exposure sites treated with Wnt3a demonstrated, while fibrous tissues were observed in the control.

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“…In contrast, YAP upregulation in MCF10A mammary epithelial cells reduced β-catenin protein levels and mediated adipogenesis . Wnt/β-catenin signaling pathway has also been implicated as a key mediator of mechano-transduction. − Rahman et al found that an electrospun polystyrene fibrous (PSF) matrix with nanofibrous topography supported nuclear localization of β-catenin and odontoblast differentiation in DPSCs. However, it is unclear if YAP and Wnt/β-catenin signaling act synergistically or antagonistically during mechano-transduction.…”

Section: Introductionmentioning

confidence: 99%

Topographic Cues of a PLGA Scaffold Promote Odontogenic Differentiation of Dental Pulp Stem Cells through the YAP/β-Catenin Signaling Axis

Yang

et al. 2023

ACS Biomater. Sci. Eng.

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Purpose: The underlying mechanism of how topographic cues of artificial scaffolds regulate cell function remains poorly understood. Yes-associated protein (YAP) and β-catenin signaling have both been reported to play important roles in mechano-transduction and dental pulp stem cells (DPSCs) differentiation. We investigated the effects of YAP and β-catenin in spontaneous odontogenic differentiation of DPSCs induced by topographic cues of a poly(lactic-co-glycolic acid) (PLGA) membrane. Methods: The topographic cues and function of a fabricated PLGA scaffold were explored via scanning electron microscopy (SEM), alizarin red staining (ARS), reverse transcription-polymerase chain reaction (RT-PCR), and pulp capping. Immunohistochemistry (IF), RT-PCR, and western blotting (WB) were used to observe the activation of YAP and β-catenin when DPSCs were cultured on the scaffolds. Further, YAP was inhibited or overexpressed on either side of the PLGA membrane, and YAP, β-catenin, and odontogenic marker expression were analyzed using IF, ARS, and WB. Results: The closed side of the PLGA scaffold promoted spontaneous odontogenic differentiation and nuclear translocation of YAP and β-catenin in vitro and in vivo compared to the open side. The YAP antagonist verteporfin inhibited β-catenin expression, nuclear translocation, and odontogenic differentiation on the closed side, but the effects were rescued by LiCl. YAP overexpressing DPSCs on the open side activated β-catenin signaling and promoted odontogenic differentiation. Conclusion: The topographic cue of our PLGA scaffold promotes odontogenic differentiation of DPSCs and pulp tissue through the YAP/β-catenin signaling axis.

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Wnt signaling in dental pulp homeostasis and dentin regeneration

Cited by 14 publications

References 86 publications

Hereditary dentin defects with systemic diseases

Hereditary dentin defects with systemic diseases

Wnt3a promotes odonto/osteogenic differentiation in vitro and tertiary dentin formation in a rat model

Topographic Cues of a PLGA Scaffold Promote Odontogenic Differentiation of Dental Pulp Stem Cells through the YAP/β-Catenin Signaling Axis

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