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拉伸强度抑制炎症微环境中牙周膜细胞的成骨作用。

Tensile strength suppresses the osteogenesis of periodontal ligament cells in inflammatory microenvironments.

作者信息

Sun Chaofan, Liu Fen, Cen Shendan, Chen Lijiao, Wang Yi, Sun Hao, Deng Hui, Hu Rongdang

机构信息

Department of Orthodontics, School of Stomatology, Wenzhou Medical University, Wenzhou, Zhejiang 325027, P.R. China.

Department of Histology and Embryology, School of Basic Medical Sciences, Wenzhou Medical University, Wenzhou, Zhejiang 325027, P.R. China.

出版信息

Mol Med Rep. 2017 Jul;16(1):666-672. doi: 10.3892/mmr.2017.6644. Epub 2017 May 29.

Abstract

The present study aimed to investigate the role of orthodontic force in osteogenesis differentiation, matrix deposition and mineralization in periodontal ligament cells (PDLCs) cells in inflammatory microenvironments. The mesenchymal origin of PDLCs was confirmed by vimentin and cytokeratin staining. PDLCs were exposed to inflammatory cytokines (5 ng/ml IL‑1β and 10 ng/ml TNF‑α) and/or tensile strength (0.5 Hz, 12% elongation) for 12, 24 or 48 h. Cell proliferation and tensile strength‑induced cytokine expression were assessed by MTT assay and ELISA, respectively. Runt‑related transcription factor 2 (RUNX2) and type I collagen (COL‑I) expression were analysed by reverse transcription‑quantitative polymerase chain reaction and western blot analysis. Additionally, alkaline phosphatase activity was measured, and the mineralization profile was evaluated by alizarin red S staining. PDLCs exposed to tensile strength in inflammatory microenvironments exhibited reduced proliferation and mineralization potential. Treatment with the inflammatory cytokines IL‑1β and TNF‑α increased RUNX2 expression levels; however, decreased COL‑I expression levels, indicating that bone formation and matrix deposition involve different mechanisms in PDL tissues. Notably, RUNX2 and COL‑I expression levels were decreased in PDLCs exposed to a combination of an inflammatory environment and loading strength. The decreased osteogenic potential in an inflammatory microenvironment under tensile strength suggests that orthodontic force may amplify periodontal destruction in orthodontic patients with periodontitis.

摘要

本研究旨在探讨正畸力在炎症微环境中对牙周膜细胞(PDLCs)成骨分化、基质沉积和矿化的作用。通过波形蛋白和细胞角蛋白染色证实了PDLCs的间充质起源。将PDLCs暴露于炎症细胞因子(5 ng/ml白细胞介素-1β和10 ng/ml肿瘤坏死因子-α)和/或拉伸强度(0.5 Hz,12%伸长率)下12、24或48小时。分别通过MTT法和酶联免疫吸附测定(ELISA)评估细胞增殖和拉伸强度诱导的细胞因子表达。通过逆转录定量聚合酶链反应和蛋白质免疫印迹分析来分析与 runt 相关的转录因子2(RUNX2)和I型胶原蛋白(COL-I)的表达。此外,测量碱性磷酸酶活性,并通过茜素红S染色评估矿化情况。在炎症微环境中暴露于拉伸强度的PDLCs表现出增殖和矿化潜力降低。用炎症细胞因子白细胞介素-1β和肿瘤坏死因子-α处理可增加RUNX2表达水平;然而,COL-I表达水平降低,表明牙周组织中的骨形成和基质沉积涉及不同机制。值得注意的是,在暴露于炎症环境和加载强度组合的PDLCs中,RUNX2和COL-I表达水平降低。拉伸强度下炎症微环境中成骨潜力的降低表明正畸力可能会加剧牙周炎正畸患者的牙周破坏。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e746/5482070/7fb1f24926fc/MMR-16-01-0666-g00.jpg

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