Institute of Stomatology, Nanjing Medical University, 140 Hanzhong Road, Nanjing, Jiangsu 210029, China; Endodontic Department, The Affiliated Stomatological Hospital of Soochow University, Suzhou Stomatological Hospital, 1505 Renmin Road, Suzhou, Jiangsu 215005, China.
Arch Oral Biol. 2013 Nov;58(11):1709-17. doi: 10.1016/j.archoralbio.2013.09.001. Epub 2013 Sep 10.
Traumatic pulp exposure can bring about some permanent damages to tooth tissues including dental pulps. This study was designed to evaluate the effects of traumatic pulp exposure on the osteo/odontogenic capacity of dental pulp stem cells (DPSCs).
Rat incisors were artificially fractured and dental pulps were exposed to the oral environment for 48 h. Then, multi-colony-derived DPSCs from the injured pulps (iDPSCs) were isolated. Their osteo/odontogenic differentiation and the involvement of NF-κB pathway were subsequently investigated.
iDPSCs presented a lower proliferative capacity than normal DPSCs (nDPSCs), as indicated by MTT and FCM assay. ALP levels in iDPSCs were significantly higher (P<0.01) than those in nDPSCs. Alizarin red staining revealed that iDPSCs exhibited an increased capacity of calcium deposition. Moreover, iDPSCs expressed stronger osteogenic markers (Runx2/RUNX2 and Ocn/OCN) and less odontogenic gene/protein (Dspp/DSP) than nDPSCs in vitro. In vivo transplantation showed that nDPSCs implants generated the typical dentine-pulp complex while all iDPSCs pellets formed the osteodentin-like tissues which were immunopositive for OCN. Mechanistically, iDPSCs expressed the higher levels of cytoplasmic phosphorylated IκBα/P65 and nuclear P65 than nDPSCs, indicating an active cellular NF-κB pathway in iDPSCs. After the inhibition of NF-κB pathway, the osteogenic potential in iDPSCs was significantly down-regulated while odontogenic differentiation was up-regulated, as indicated by the decreased Alp/Runx2/Ocn and uprised Dspp expression.
Pulp exposure for 48 h decreased the odontogenic capacity and enhanced the osteogenic potential of DPSCs via the NF-κB signalling pathway.
外伤性牙髓暴露会对牙髓等牙齿组织造成永久性损伤。本研究旨在评估外伤性牙髓暴露对牙髓干细胞(DPSCs)成骨/成牙能力的影响。
将大鼠切牙人为折断,使牙髓暴露于口腔环境中 48 小时。然后,从受伤牙髓中分离出多集落衍生的 DPSCs(iDPSCs)。随后研究了它们的成骨/成牙分化和 NF-κB 途径的参与情况。
与正常 DPSCs(nDPSCs)相比,iDPSCs 的增殖能力较低,MTT 和 FCM 检测结果表明这一点。iDPSCs 的 ALP 水平明显高于 nDPSCs(P<0.01)。茜素红染色显示 iDPSCs 具有更强的钙沉积能力。此外,iDPSCs 在体外表达更强的成骨标志物(Runx2/RUNX2 和 Ocn/OCN)和更少的成牙标志物/蛋白(Dspp/DSP)。体内移植显示,nDPSCs 植入物产生了典型的牙本质牙髓复合体,而所有 iDPSCs 小球都形成了免疫阳性的骨牙本质样组织。在机制上,iDPSCs 表达的细胞质磷酸化 IκBα/P65 和核 P65 水平高于 nDPSCs,表明 iDPSCs 中存在活跃的细胞 NF-κB 途径。抑制 NF-κB 途径后,iDPSCs 的成骨潜能显著下调,而成牙分化上调,表现为 Alp/Runx2/Ocn 下调和 Dspp 表达上调。
牙髓暴露 48 小时可通过 NF-κB 信号通路降低 DPSCs 的成牙能力,增强其成骨能力。