Level D· Scientific groundwork from lab and animal studiesLaboratory StudyEurope PMCOpen access

Effects of Aspirin on Odontogenesis of Human Dental Pulp Cells and TGF- β 1 Liberation from Dentin In Vitro

Khampatee V., Zhang C., Chou L.

Laboratory Study, published in Int J Dent (2022) — summary generated from the PubMed abstract.

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Level D· Scientific groundwork from lab and animal studiesEvidence level of this study

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

  • Level A · Stronger Clinical Evidence
  • Level B · Emerging clinical evidence with positive signals
  • Level C · Early human research exploring benefits
  • Level D · Scientific groundwork from lab and animal studies
  • Emerging · Emerging topic under active research
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This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.

Study type
Laboratory Study
Journal
Int J Dent (2022)
Reported sample size
—
Source database
Europe PMC
PMID
36034475
PMCID
PMC9411001
DOI
10.1155/2022/3246811
Citations
6

Abstract (original English)

Aim This in vitro study aimed to investigate the roles of aspirin (ASA) and its concentrations on the odontogenesis of human dental pulp cells (HDPCs) and to investigate the influence of ASA on TGF- β 1 liberation from dentin. Methodology . HDPCs were cultured in a culture medium with 25, 50, 75, 100, and 200 μ ·g/mL ASA and 0 μ ·g/mL ASA as a control. The mitochondrial activity of HDPCs was assessed using an MTT assay. Crystal violet staining and triton were used to evaluate cell proliferation rates. ALP activity was measured with a fluorometric assay. Expressions of DSP and RUNX2 were determined with the ELISA. DSP and RUNX2 mRNA levels were measured with RT-qPCR. Alizarin red staining was conducted to evaluate the mineralized nodule formation. Dentin slices were submerged in PBS (negative control), 17% EDTA (positive control), and ASA before collecting the solution for TGF- β 1 quantification by the ELISA. The data were analyzed by the t- tests and ANOVA, followed by the Tukey post hoc tests. P values Results The results showed that 25-50 μ ·g/mL ASA promoted mitochondrial activity of HDPCs at 72 h ( P P β 1 liberation after conditioning dentin for 5 min (25, 200 μ ·g/mL; P μ ·g/mL; P Conclusions This in vitro study demonstrated that ASA, especially in high concentrations, promoted the odontogenesis of HDPCs and TGF- β 1 liberation from dentin, showing the potential of being

What this study does not prove

  • • This study does not prove SVF is an approved treatment or a replacement for standard care.
  • • This is preclinical work; animal or laboratory results cannot be applied to humans.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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