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实验性咬合紊乱对下颌髁突的退行性和再生性改建反应。

Combined degenerative and regenerative remodeling responses of the mandibular condyle to experimentally induced disordered occlusion.

机构信息

Postgraduate student, Department of Orthodontics, School of Stomatology, Fourth Military Medical University, Xi'an, China.

出版信息

Am J Orthod Dentofacial Orthop. 2013 Jan;143(1):69-76. doi: 10.1016/j.ajodo.2012.08.024.

Abstract

INTRODUCTION

The purposes of this research were to investigate the long-term responses of mandibular condylar cartilage to experimentally induced disordered occlusion and to evaluate changes in the expression of the SDF-1/CXCR4 axis.

METHODS

Experimentally induced disordered occlusions were created in 8-week-old female Sprague-Dawley rats by orthodontic methods. After 24 weeks, remodeling of the mandibular condylar cartilage was assessed by hematoxylin and eosin staining. Protein and mRNA expression of SDF-1, CXCR4, MMP9, IL6, OPG, and RANKL were investigated by means of immunohistochemical staining and real-time polymerase chain reaction.

RESULTS

Obvious cartilage degenerative remodeling responses were observed; they appeared as uneven distributions of cellular disposition, loss of cartilage surface integrity, and cell-free areas. Regenerative responses presenting as thickening of the whole and the calcified cartilage layers in the experimental group were also observed. Compared with the age-matched controls, the protein and mRNA levels of SDF-1, CXCR4, MMP9, IL6, and OPG, but not RANKL, were increased in the experimental group (all, P <0.05). In addition, the mRNA level of RANKL/OPG showed a decreasing trend in the experimental group compared with the age-matched controls (P = 0.052).

CONCLUSIONS

This study demonstrated that long-term experimentally induced disordered occlusion leads to a combined response in degeneration and regeneration of mandibular cartilage, accompanied by active interaction of the SDF-1/CXCR4 axis and local upregulation of MMP9, IL6, and OPG.

摘要

简介

本研究旨在探讨下颌髁突软骨在实验性咬合紊乱后的长期反应,并评估 SDF-1/CXCR4 轴表达的变化。

方法

采用正畸方法在 8 周龄雌性 Sprague-Dawley 大鼠中建立实验性咬合紊乱模型。24 周后,通过苏木精-伊红染色评估下颌髁突软骨的重塑。通过免疫组织化学染色和实时聚合酶链反应检测 SDF-1、CXCR4、MMP9、IL6、OPG 和 RANKL 的蛋白和 mRNA 表达。

结果

观察到明显的软骨退行性重塑反应,表现为细胞分布不均匀、软骨表面完整性丧失和无细胞区。实验组还观察到呈全层和钙化软骨层增厚的再生反应。与同龄对照组相比,实验组 SDF-1、CXCR4、MMP9、IL6 和 OPG 的蛋白和 mRNA 水平均升高(均 P<0.05),但 RANKL 除外。此外,实验组 RANKL/OPG 的 mRNA 水平与同龄对照组相比呈下降趋势(P=0.052)。

结论

本研究表明,长期实验性诱导的咬合紊乱导致下颌软骨退变和再生的综合反应,伴随着 SDF-1/CXCR4 轴的积极相互作用和 MMP9、IL6 和 OPG 的局部上调。

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