4.6 Article

Mineral trioxide aggregate enhances the odonto/osteogenic capacity of stem cells from inflammatory dental pulps via NF-κB pathway

Journal

ORAL DISEASES
Volume 20, Issue 7, Pages 650-658

Publisher

WILEY
DOI: 10.1111/odi.12183

Keywords

dental pulp stem cells; differentiation; inflammation; mineral trioxide aggregate; nuclear factor kappa B

Funding

  1. Medical Elitist Project of Jiangsu Province [RC2011140]
  2. Key Project of National Natural Science Fund [81230022]
  3. Natural Science Foundation of Jiangsu Province [BK20131392]
  4. Priority Academic Program Development of Jiangsu Higher Education Institutions (PAPD) [2011-137]

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ObjectiveThis study was designed to investigate the effects of mineral trioxide aggregate (MTA) on the osteo/odontogenic differentiation of inflammatory dental pulp stem cells (iDPSCs). Materials and Methodsinflammatory DPSCs were isolated from the inflammatory pulps of rat incisors and cocultured with MTA-conditioned medium. MTT assay and flow cytometry were performed to evaluate the proliferation of iDPSCs. Alkaline phosphatase (ALP) activity, alizarin red staining, real-time RT-PCR, and Western blot assay were used to investigate the differentiation capacity as well as the involvement of NF-B pathway in iDPSCs. ResultsMineral trioxide aggregate-treated iDPSCs demonstrated the higher ALP activity and formed more mineralized nodules than the untreated group. The odonto/osteoblastic markers (Alp, Runx2/RUNX2, Osx/OSX, Ocn/OCN, and Dspp/DSP, respectively) in MTA-treated iDPSCs were significantly upregulated as compared with untreated iDPSCs. Mechanistically, cytoplastic phos-P65 and nuclear P65 in MTA-treated iDPSCs were significantly increased in a time-dependent manner. Moreover, the inhibition of NF-B pathway suppressed the MTA-induced odonto/osteoblastic differentiation of iDPSCs, as indicated by decreased ALP levels, weakened mineralization capacity and downregulated levels of odonto/osteoblastic genes (Osx, Ocn, and Dspp). ConclusionsMineral trioxide aggregate enhances the odonto/osteogenic capacity of DPSCs from inflammatory sites via activating the NF-B pathway.

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