Suppr超能文献

过氧化物酶体增殖物激活受体γ调节小鼠腭中缝扩展后的骨重塑。

Peroxisome proliferator-activated receptor gamma regulates bone remodeling after midpalatal suture expansion in mice.

作者信息

Wu Jing, Ru Nan, Li Song

出版信息

Int J Oral Maxillofac Implants. 2015 Nov-Dec;30(6):1423-30. doi: 10.11607/jomi.3916. Epub 2015 Oct 16.

Abstract

PURPOSE

The effectiveness of rapid maxillary expansion is adversely affected by failure and relapse. It is important to identify key factors that increase new bone formation and improve bone remodeling of midpalatal sutures to improve the stability and effectiveness of this commonly used orthodontic procedure. Peroxisome proliferator-activated receptor gamma (PPARγ) plays an important role in modulating osteogenesis and bone resorption in long bones. This study was designed to explore the function of PPARγ in bone remodeling and tissue engineering of midpalatal sutures.

MATERIALS AND METHODS

Pioglitazone, a PPARγ agonist, and osteoclast PPARγ knockout mice were used to explore the impact of PPARγ activation and inactivation, respectively, on bone remodeling in a mouse model of midpalatal suture expansion (MSE). Histologic analysis including staining with hematoxylin-eosin, tartrate-resistant acid phosphatase, and alkaline phosphatase was used to evaluate tissue remodeling. Reverse-transcriptase quantitative polymerase chain reaction was used to measure gene expression.

RESULTS

Pioglitazone decreased new bone formation after MSE. This was accompanied by an increased amount of osteoclasts and expression of genes promoting osteoclastogenesis, as well as a decreased amount of osteoblasts and expression of genes promoting osteoblastogenesis in midpalatal sutures. Conversely, osteoclast PPARγ knockout mice increased new bone formation and decreased the amount of osteoclasts and expression of genes promoting osteoclastogenesis.

CONCLUSION

In the process of bone remodeling after MSE, PPARγ, particularly in osteoclasts, is an important regulator of osteoblast and osteoclast homeostasis and bone remodeling in midpalatal sutures. Blockade of PPARγ might be an effective strategy to improve stability and decrease relapse in the practice of rapid maxillary expansion.

摘要

目的

快速上颌扩弓的有效性会受到失败和复发的不利影响。识别增加新骨形成和改善腭中缝骨重塑的关键因素,对于提高这种常用正畸手术的稳定性和有效性至关重要。过氧化物酶体增殖物激活受体γ(PPARγ)在调节长骨的成骨作用和骨吸收中起重要作用。本研究旨在探讨PPARγ在腭中缝骨重塑和组织工程中的功能。

材料与方法

使用PPARγ激动剂吡格列酮和破骨细胞PPARγ基因敲除小鼠,分别探讨PPARγ激活和失活对腭中缝扩展(MSE)小鼠模型骨重塑的影响。采用苏木精-伊红染色、抗酒石酸酸性磷酸酶染色和碱性磷酸酶染色等组织学分析方法评估组织重塑。使用逆转录定量聚合酶链反应测量基因表达。

结果

吡格列酮减少了MSE后的新骨形成。这伴随着腭中缝破骨细胞数量增加和促进破骨细胞生成的基因表达增加,以及成骨细胞数量减少和促进成骨细胞生成的基因表达减少。相反,破骨细胞PPARγ基因敲除小鼠增加了新骨形成,减少了破骨细胞数量和促进破骨细胞生成的基因表达。

结论

在MSE后的骨重塑过程中,PPARγ,特别是在破骨细胞中,是腭中缝成骨细胞和破骨细胞稳态以及骨重塑的重要调节因子。阻断PPARγ可能是提高快速上颌扩弓稳定性和减少复发的有效策略。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验