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成骨细胞系细胞和牙周膜成纤维细胞调节依赖于核因子-κB(NF-κB)激活的正畸牙齿移动。

Osteoblast lineage cells and periodontal ligament fibroblasts regulate orthodontic tooth movement that is dependent on Nuclear Factor-kappa B (NF-kB) activation.

出版信息

Angle Orthod. 2021 Sep 1;91(5):664-671. doi: 10.2319/031520-182.1.

Abstract

OBJECTIVES

To investigate the role of NF-κB in osteoblast lineage cells and periodontal ligament (PDL) fibroblasts during orthodontic tooth movement (OTM).

MATERIALS AND METHODS

Transgenic mice that expressed a dominant negative mutant of the inhibitor of kB kinase (IKK-DN) with lineage specific expression in osteoblastic cells and PDL fibroblasts driven by a response element in the collagen1α1 promoter and matched wild-type (WT) mice were examined. A 10-12 g force was applied by a NiTi coil and maintained for 5 or 12 days. OTM distance, PDL width, and bone volume fraction were measured using micro computed tomography. Osteoclast numbers were counted in tartrate-resistant acid phosphatase-stained sections. Activation of nuclear factor kappa B (NF-kB) was assessed by nuclear localization of p65, and the receptor activator of nuclear factor-κB ligand (RANKL) was measured by immunofluorescence and compared to control specimens with no orthodontic force.

RESULTS

OTM-induced NF-kB activation (p65 nuclear localization) in WT mice was largely blocked in transgenic (TG) mice. OTM was significantly reduced in the TG mice compared to WT mice along with reduced osteoclastogenesis, narrower PDL width, higher bone volume fraction, and reduced RANKL expression.

CONCLUSIONS

Osteoblast lineage cells and PDL fibroblasts are key contributors to alveolar bone remodeling in OTM through IKKβ dependent NF-κB activation.

摘要

目的

研究核因子-κB(NF-κB)在成骨细胞系细胞和牙周膜(PDL)成纤维细胞中的作用,在正畸牙齿移动(OTM)期间。

材料和方法

检查表达抑制κB 激酶(IKK-DN)显性负突变的转基因小鼠,其在成骨细胞和 PDL 成纤维细胞中的谱系特异性表达由胶原 1α1 启动子中的反应元件驱动,并与匹配的野生型(WT)小鼠进行比较。通过 NiTi 线圈施加 10-12g 的力,并持续 5 或 12 天。使用微计算机断层扫描测量 OTM 距离、PDL 宽度和骨体积分数。在抗酒石酸酸性磷酸酶染色的切片中计数破骨细胞数量。通过核定位的 p65 评估核因子 kappa B(NF-kB)的激活,并通过免疫荧光测量核因子-κB 配体(RANKL),并与无正畸力的对照标本进行比较。

结果

WT 小鼠 OTM 诱导的 NF-kB 激活(p65 核定位)在 TG 小鼠中大部分被阻断。与 WT 小鼠相比,TG 小鼠的 OTM 明显减少,同时破骨细胞生成减少,PDL 变窄,骨体积分数增加,RANKL 表达减少。

结论

成骨细胞系细胞和 PDL 成纤维细胞通过 IKKβ 依赖性 NF-κB 激活成为 OTM 中牙槽骨重塑的关键贡献者。

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