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非血管性运输牵张成骨在骨形成和再生中的作用。这是一种偶然现象吗?

Nonvascular transport distraction osteogenesis in bone formation and regeneration. Is it an accidental phenomenon?

作者信息

Guo Peng, Zeng Jing-Jing, Zhou Nuo

机构信息

College of Stomatology, GuangXi Medical University, Nanning Guangxi, China.

College of Stomatology, GuangXi Medical University, Nanning Guangxi, China.

出版信息

J Craniomaxillofac Surg. 2015 Jan;43(1):21-7. doi: 10.1016/j.jcms.2014.10.004. Epub 2014 Oct 17.

DOI:10.1016/j.jcms.2014.10.004
PMID:25457741
Abstract

PURPOSE

To explore the osteogenic mechanism of nonvascular transport distraction osteogenesis (NTDO) by constructing mandibular defects in dogs.

METHODS

Sixty adult dogs were randomly divided into three groups with 20 dogs in each group. Canine mandibular defect models of NTDO were constructed. Animals were euthanized 1, 4 and 12 weeks after distraction, and the transport disc and surrounding tissue were collected and fixed. Histochemical staining using hematoxylin and eosin (H&E) and electron microscopic observations were used to examine bone regeneration.

RESULTS

Distraction bone regeneration was observed in the distraction gap and around the transport disc, and osseous connections had formed between new bone and the transport disc after one week. Osteoclasts gathered around the transport disc, and bone absorption pit formation could be seen. After 4 weeks of distraction, the new bone around the transport disc was close to maturity with thick sclerostin on the middle of the transport disc. After 12 weeks the new bone and the transport disc were fully integrated, and were difficult to distinguish by H&E staining and electron microscopy.

CONCLUSIONS

Canine mandibular defects were successfully repaired by NTDO resulting in ideal new bone formation and fully recovered mandibular physiological function. The surrounding tissues, including musculoskeletal tissues, the periosteum and other soft tissues and the nonvascular transport disc, together contribute to bone regeneration and neovascularization in NTDO.

摘要

目的

通过构建犬下颌骨缺损模型,探讨非血管运输牵引成骨(NTDO)的成骨机制。

方法

将60只成年犬随机分为三组,每组20只。构建犬NTDO下颌骨缺损模型。在牵引后1、4和12周对动物实施安乐死,并收集运输盘及周围组织进行固定。采用苏木精-伊红(H&E)组织化学染色和电子显微镜观察来检测骨再生情况。

结果

在牵引间隙和运输盘周围观察到牵引性骨再生,1周后新骨与运输盘之间形成了骨连接。破骨细胞聚集在运输盘周围,可见骨吸收陷窝形成。牵引4周后,运输盘周围的新骨接近成熟,运输盘中部有厚的硬化蛋白。12周后新骨与运输盘完全融合,通过H&E染色和电子显微镜难以区分。

结论

NTDO成功修复了犬下颌骨缺损,形成了理想的新骨,下颌骨生理功能完全恢复。包括肌肉骨骼组织、骨膜和其他软组织以及非血管运输盘在内的周围组织共同促进了NTDO中的骨再生和新血管形成。

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