Teeth: malignant neoplasms in the dental pulp?

Neuhaus, Klaus W.

doi:10.1016/s1470-2045(06)71013-0

Cited by 18 publications

(19 citation statements)

References 33 publications

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“…However, PTEN is not a molecular or functional signature of BM-MSCs when compared to placenta MSCs, adipose MSCs, hematopoietic stem and progenitor cells, skin fibroblasts, or osteoblasts 12,13 . We believe that the characteristics of DP-MSCs, including extremely low tumorigenic potential 14 and unique cell fate, are critical for the development of novel functional signatures between DP-MSCs and BM-MSCs.…”

Section: Discussionmentioning

confidence: 99%

“…Osteosarcoma with its cell-of-origin as BM-MSC accounts for the most prevalent primary bone sarcoma. However, there is no report of dental pulp sarcoma 14 . Although MSCs from different tissues recapitulate their original phenotypes; however, the machinery that regulates cell commitment and tumorigenesis remains mostly unknown and it is not clear whether a single endogenous or exogenous factor is able to link both.…”

Section: Introductionmentioning

confidence: 99%

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Methylation and PTEN activation in dental pulp mesenchymal stem cells promotes osteogenesis and reduces oncogenesis

et al. 2019

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Lineage commitment and tumorigenesis, traits distinguishing stem cells, have not been well characterized and compared in mesenchymal stem cells derived from human dental pulp (DP-MSCs) and bone marrow (BM-MSCs). Here, we report DP-MSCs exhibit increased osteogenic potential, possess decreased adipogenic potential, form dentin pulp-like complexes, and are resistant to oncogenic transformation when compared to BM-MSCs. Genome-wide RNA-seq and differential expression analysis reveal differences in adipocyte and osteoblast differentiation pathways, bone marrow neoplasm pathway, and PTEN/PI3K/AKT pathway. Higher PTEN expression in DP-MSCs than in BM-MSCs is responsible for the lineage commitment and tumorigenesis differences in both cells. Additionally, the PTEN promoter in BM-MSCs exhibits higher DNA methylation levels and repressive mark H3K9Me2 enrichment when compared to DP-MSCs, which is mediated by increased DNMT3B and G9a expression, respectively. The study demonstrates how several epigenetic factors broadly affect lineage commitment and tumorigenesis, which should be considered when developing therapeutic uses of stem cells.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Methylation and PTEN activation in dental pulp mesenchymal stem cells promotes osteogenesis and reduces oncogenesis

et al. 2019

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“…Disrupted pulp homeostasis can progress to root resorption detectable early by altered levels of DMP-1, DSP (dentin sialoprotein) and DPP (dentin phosphoprotein) in gingival crevicular fluids [17]. Since BMPs are associated with hard tissue formation, higher odontogenic differentiation and DSPP level by BMP-2 responsive HSP-treated DPSCs may favor pulpal deposition of calcified materials that normally occur in response to external forces, dental caries and pulpal inflammation [31; 32]. This BMP-mediated response suggests enhanced differentiation capacity of surviving HSP-treated DPSCs and possible role of BMP signaling in sustaining pulp vitality despite increased mineral deposition.…”

Section: Discussionmentioning

confidence: 99%

Dynamic hydrostatic pressure promotes differentiation of human dental pulp stem cells

Damek-Poprawa

Nicoll

et al. 2009

Biochemical and Biophysical Research Communications

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The masticatory apparatus absorbs high occlusal forces, but uncontrolled parafunctional or orthodontic forces damage periodontal ligament (PDL), cause pulpal calcification, pulp necrosis and tooth loss. Morphology and functional differentiation of connective tissue cells can be controlled by mechanical stimuli but effects of uncontrolled forces on intra-pulpal homeostasis and ability of dental pulp stem cells (DPSCs) to withstand direct external forces are unclear. Using dynamic hydrostatic pressure (HSP), we tested the hypothesis that direct HSP disrupts DPSC survival and odontogenic differentiation. DPSCs from four teenage patients were subjected to HSP followed by assessment of cell adhesion, survival and recovery capacity based on odontogenic differentiation, mineralization and responsiveness to bone morphogenetic protein-2 (BMP-2). HSP down-regulated DPSC adhesion and survival but promoted differentiation by increasing mineralization, in vivo hard tissue regeneration and BMP-2 responsiveness despite reduced cell numbers. HSP-treated DPSCs displayed enhanced odontogenic differentiation, an indication of favorable recovery from HSP-induced cellular stress. KeywordsDental pulp stem cells; hydrostatic pressure; pulp calcification; tooth; cellular stress AbstractThe masticatory apparatus absorbs high occlusal forces, but uncontrolled parafunctional or orthodontic forces damage periodontal ligament (PDL), cause pulpal calcification, pulp necrosis and tooth loss. Morphology and functional differentiation of connective tissue cells can be controlled by mechanical stimuli but effects of uncontrolled forces on intra-pulpal homeostasis and ability of dental pulp stem cells (DPSCs) to withstand direct external forces are unclear. Using dynamic hydrostatic pressure (HSP), we tested the hypothesis that direct HSP disrupts DPSC survival and odontogenic differentiation. DPSCs from four teenage patients were subjected to HSP followed by assessment of cell adhesion, survival and recovery capacity based on odontogenic differentiation, mineralization and responsiveness to bone morphogenetic protein-2 (BMP-2). HSP down-regulated DPSC adhesion and survival but promoted differentiation by increasing mineralization, in vivo hard tissue regeneration and BMP-2 responsiveness despite reduced cell numbers. HSP-treated DPSCs displayed enhanced odontogenic differentiation, an indication of favorable recovery from HSPinduced cellular stress.

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“…34 Some authors proposed that the proliferation-enhancing effect of arsenic is consistent with its role as tumor promoter 30 which leads to uncontrolled proliferation and carcinogenesis. 35 Due to the ability of arsenic in transforming normal stem cells into cancer stem cells, 35 coupled with the fact that pulpal stem cells might have the potential to undergo neoplastic alteration, 36 one must exercise caution and avoid overzealous interpretation of the viability test results obtained in our study. Low levels of As 2 O 3 rendered the pulpal cells slightly hypertrophic; recently, Samanta et al demonstrated an in vitro hypertrophic effect of 1 µM arsenic when applied for 24 hours on rat cardiomyocytes.…”

Section: Discussionmentioning

confidence: 95%

The Hormetic Effect of Arsenic Trioxide on Rat Pulpal Cells: An In Vitro Preliminary Study

et al. 2020

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Objectives Despite the agreement that there is no longer any indication for arsenic use in modern endodontics, some concerns are surfacing about the minute amount of arsenic trioxide (As2O3) released from Portland cement-based materials. The present study investigated the effect of different concentrations of As2O3 on rat pulpal cells and the efficacy of N-acetylcysteine (NAC) in preventing As2O3-mediated toxicity. Materials and Methods Cytotoxicities of 50, 10, or 5 µm As2O3 and the effect of cells co-treatment with 50 µm As2O3 and 5,000 µm NAC or 500 µm NAC were tested at 24 hours or 3 days. Cell viability was assessed by means of MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) assay and cellular morphological changes were observed under phase contrast microscope. Statistical Analysis Two-way analysis of variance with Tukey’s post-hoc test was used to evaluate differences between the groups (α = 0.05). Results At both exposure times, 50 µm As2O3 resulted in lower optical density (OD) values when compared with 10 or 5 µm As2O3. At 24 hours, 10 µm As2O3 resulted in a higher OD value compared with the control; however, at 3 days the difference was statistically insignificant. At each exposure time, the OD value of 5 µm As2O3 group was comparable to the control and 10 µm As2O3 group. There were no significant differences between 50 µm As2O3 group and 500 NAC+50 µm As2O3 group; however, these two groups had lower OD values when compared with 5,000 NAC + 50 µm As2O3 group at 24 hours and 3 days. The latter group showed significantly lower OD value in comparison with the control at 24 hours and 3 days. Control cells were polygonal-shaped while 50 µm As2O3-treated cells exhibited contracted and spherical morphology with increased intercellular spaces. At 24 hours, 10 μm and 5 µm As2O3-treated cells were slightly hypertrophic. Cells co-treated with NAC and As2O3 showed increased intercellular spaces and lower cellular density compared with the control. Conclusions As2O3 displayed a hormetic effect on pulpal cells; however, the proliferative effect induced by low As2O3 concentrations should be interpreted with caution. NAC did not prevent As2O3-mediated toxicity; however, it demonstrated potential for ameliorating this toxicity.

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Teeth: malignant neoplasms in the dental pulp?

Cited by 18 publications

References 33 publications

Methylation and PTEN activation in dental pulp mesenchymal stem cells promotes osteogenesis and reduces oncogenesis

Methylation and PTEN activation in dental pulp mesenchymal stem cells promotes osteogenesis and reduces oncogenesis

Dynamic hydrostatic pressure promotes differentiation of human dental pulp stem cells

The Hormetic Effect of Arsenic Trioxide on Rat Pulpal Cells: An In Vitro Preliminary Study

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