口腔医学研究

口腔医学研究 ›› 2020, Vol. 36 ›› Issue (6): 534-538.DOI: 10.13701/j.cnki.kqyxyj.2020.06.008

• 口腔生物学研究 • 上一篇    下一篇

釉基质蛋白衍生物调节牙龈卟啉单胞菌感染牙周膜干细胞成骨分化的作用及机制

邬扬绚1, 向黎1, 黄志强2, 褚金海1*   

  1. 1.武汉市红十字会医院口腔科 湖北 武汉 430015;
    2.武汉大学口腔医院牙周科 湖北 武汉 430079
  • 收稿日期:2019-09-23 出版日期:2020-07-03 发布日期:2020-07-06
  • 通讯作者: *褚金海,E-mail:904776804@qq.com
  • 作者简介:邬扬绚(1972~ ),女,浙江人,本科,主治医师,研究方向:口腔正畸。
  • 基金资助:
    湖北省科学技术攻关项目(编号:2007AA301B37-3 )

Effect and Mechanism of Enamel Matrix Protein Derivatives on Osteogenic Differentiation of Periodontal Ligament Stem Cells Infected with Porphyromonas Gingivalis

WU Yangxuan1, XIANG Li1, HUANG Zhiqiang2, CHU Jinhai1*   

  1. 1. Department of Stomatology, Wuhan Red Cross Hospital, Wuhan 430015, China;
    2. Department of Periodontology, Stomatological Hospital, Wuhan University. Wuhan 430079, China
  • Received:2019-09-23 Online:2020-07-03 Published:2020-07-06

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摘要： 目的: 釉基质蛋白衍生物调节牙龈卟啉单胞菌感染牙周膜干细胞(PDLSCs)成骨分化的作用及机制。方法: 原代培养PDLSCs后消化传代,取第3~4代细胞进行分组,对照组进行常规处理及成骨诱导,感染组用牙龈卟啉单胞菌感染24 h后进行成骨诱导,釉基质蛋白衍生物组用牙龈卟啉单胞菌感染24 h后进行成骨诱导并在成骨诱导过程中加入25、50、100 mg/L釉基质蛋白衍生物,100 mg/L釉基质蛋白衍生物+TNF-α组用牙龈卟啉单胞菌感染24 h后进行成骨诱导并在成骨诱导过程中加入100 mg/L釉基质蛋白衍生物及10 ng/mL TNF-α。检测矿化结节数量、ALP活性、成骨标志基因Runx2、OCN、COL-I及信号通路分子NF-κB p65、p-IκB、IκB的表达量。结果: 25、50、100 mg/L釉基质蛋白衍生物组的矿化结节数量、ALP活性及Runx2、OCN、COL-I、IκB的表达量均明显高于感染组,NF-κB p65、p-IκB的表达量均明显低于感染组;100 mg/L釉基质蛋白衍生物+TNF-α组的矿化结节数量、ALP活性及Runx2、OCN、COL-I、IκB的表达量均明显低于100 mg/L釉基质蛋白衍生物组,NF-κB p65、p-IκB的表达量均明显高于100 mg/L釉基质蛋白衍生物组。结论: 釉基质蛋白衍生物能够通过抑制NF-κB通路促进牙龈卟啉单胞菌感染PDLSCs的成骨分化。

关键词: 牙周膜干细胞, 牙龈卟啉单胞菌, 釉基质蛋白衍生物, 成骨分化

Abstract: Objective: To investigate the effect and mechanism of enamel matrix protein derivatives on osteogenic differentiation of porphyromonas gingivalis-infected periodontal ligament stem cells (PDLSCs). Methods: PDLSCs were digested and passaged after primary culture. The cells of the 3rd-4th generation were divided into groups. The control group was treated routinely and osteoblast differentiated. The infected group was osteoblast differentiated after 24 hours of porphyromonas gingivalis infection. The enamel matrix protein derivative group was osteoblast differentiated after 24 hours of porphyromonas gingivalis infection and added with 25 mg/L, 50 mg/L, and 100 mg/L enamel matrix protein derivatives during differentiation. 100 mg/L enamel matrix protein derivatives+TNF-α group was osteoblast differentiated after 24 hours of porphyromonas gingivalis infection and added with 100 mg/L enamel matrix protein and 10 ng/mL TNF-α derivatives during differentiation. The number of mineralized nodules, ALP activity, and expression of osteogenic marker genes Runx2, OCN, COL-I and signal pathway molecules p65 NF-κB, p-I κB and I κB were detected. Results: The number of mineralized nodules, ALP activity, and the expression of Runx2, OCN, COL-I, and I-κB in 25 mg/L, 50 mg/L and 100 mg/L enamel matrix protein derivatives groups were significantly higher than those in the infected group, while the expression of p65 NF-κB and p-I κB were significantly lower than those in the infected group. The number of mineralized nodules, ALP activity, and the expression of Runx2, OCN, COL-I and I-κB in 100 mg/L enamel matrix protein derivatives+TNF-α group were significantly lower than those in the 100 mg/L enamel matrix protein derivatives group, while the expression of p65 NF-κB and p-I κB were significantly higher than those in the 100 mg/L enamel matrix protein derivatives group. Conclusion: Enamel matrix protein derivatives can promote the osteogenic differentiation of porphyromonas gingivalis infected PDLSCs by inhibiting the NF-κB pathway.

Key words: periodontal ligament stem cells, porphyromonas gingivalis, enamel matrix protein derivatives, osteogenic differentiation