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

Objective This 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 Methods inflammatory DPSCs were isolated from the inflammatory pulps of rat incisors and cocultured...

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Veröffentlicht in:Oral diseases 2014-10, Vol.20 (7), p.650-658
Hauptverfasser: Wang, Y, Yan, M, Fan, Z, Ma, L, Yu, Y, Yu, J
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Sprache:eng
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Zusammenfassung:Objective This 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 Methods inflammatory 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‐κB pathway in iDPSCs. Results Mineral 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‐κB 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). Conclusions Mineral trioxide aggregate enhances the odonto/osteogenic capacity of DPSCs from inflammatory sites via activating the NF‐κB pathway.
ISSN:1354-523X
1601-0825
DOI:10.1111/odi.12183