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甲磺酸去铁胺通过促进H型血管生成增强下颌前伸诱导的髁突成骨。

Deferoxamine mesylate enhances mandibular advancement-induced condylar osteogenesis by promoting H-type angiogenesis.

作者信息

Hu Yun, Li Hegang

机构信息

Department of Orthodontics, Stomatological Hospital, Southern Medical University, Guangzhou, China.

出版信息

J Oral Rehabil. 2023 Mar;50(3):234-242. doi: 10.1111/joor.13410. Epub 2023 Jan 16.

Abstract

BACKGROUND

The effect of functional orthopaedic treatment for mandibular deficiency relies on mandibular advancement (MA)-induced condylar new bone formation. However, this is not easy to achieve, especially in non-growing patients. Therefore, how to obtain reliable MA-induced condylar osteogenesis is a subject much worthy of study.

OBJECTIVE

To investigate whether deferoxamine mesylate (DFM) enhances MA-induced condylar osteogenesis in middle-aged mice.

METHODS

Forty 30-week-old male C57BL/6J mice were randomly divided into 4 groups: the control (Ctrl), DFM, MA + Ctrl and MA + DFM groups. After a 4-week experimental period, femurs, tibias and condyles were collected for morphological, micro-computed tomography and histological evaluation.

RESULTS

For long bones, DFM reversed osteoporosis in middle-aged mice by promoting H-type angiogenesis. For mandibular condyles, MA promoted condylar osteogenesis in middle-aged mice, thereby allowing the mandible to achieve a stable protruding position. In addition, DFM enhanced the volume and quality of MA-induced condylar new bone formation. Furthermore, histological analysis revealed that DFM enhanced MA-induced condylar subchondral ossification. Mechanistically, it was confirmed that DFM increased the number of H-type vessels and their coupled Osterix osteoprogenitors by upregulating the hypoxia-inducible factor (HIF)-1α signalling pathway, thereby enhancing MA-induced condylar osteogenesis.

CONCLUSION

Applying DFM to enhance MA-induced condylar osteogenesis through H-type angiogenesis is expected to be an effective strategy to achieve favourable functional orthopaedic treatment effectiveness in non-growing patients.

摘要

背景

功能性正畸治疗下颌骨发育不全的效果依赖于下颌前伸(MA)诱导的髁突新骨形成。然而,这并不容易实现,尤其是在非生长发育期的患者中。因此,如何获得可靠的MA诱导的髁突成骨是一个非常值得研究的课题。

目的

研究甲磺酸去铁胺(DFM)是否能增强中年小鼠MA诱导的髁突成骨。

方法

将40只30周龄的雄性C57BL/6J小鼠随机分为4组:对照组(Ctrl)、DFM组、MA + Ctrl组和MA + DFM组。经过4周的实验期后,收集股骨、胫骨和髁突进行形态学、显微计算机断层扫描和组织学评估。

结果

对于长骨,DFM通过促进H型血管生成逆转了中年小鼠的骨质疏松。对于下颌髁突,MA促进了中年小鼠的髁突成骨,从而使下颌骨达到稳定的前突位置。此外,DFM增强了MA诱导的髁突新骨形成的体积和质量。此外,组织学分析显示DFM增强了MA诱导的髁突软骨下骨化。机制上,证实DFM通过上调缺氧诱导因子(HIF)-1α信号通路增加了H型血管及其耦合的osterix骨祖细胞的数量,从而增强了MA诱导的髁突成骨。

结论

应用DFM通过H型血管生成增强MA诱导的髁突成骨有望成为一种有效的策略,以在非生长发育期患者中实现良好的功能性正畸治疗效果。

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