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单次电离辐射暴露致放射性骨坏死模型的建立及其机制

Establishment of an Osteoradionecrosis Model and its Mechanism Via Single Ionizing Radiation Exposure.

作者信息

Wang Yuetong, Wang Xian, Liu Zhiqing, Li Yuetao, Lu Haoyu, Mo Dongqin, Wang Daiyou

机构信息

College & Hospital of Stomatology, Guangxi Medical University, Nanning, Guangxi, P.R. China; Guangxi Key Laboratory of Oral and Maxillofacial Rehabilitation and Reconstruction, Nanning, Guangxi, P.R. China.

College & Hospital of Stomatology, Guangxi Medical University, Nanning, Guangxi, P.R. China; Guangxi Key Laboratory of Oral and Maxillofacial Rehabilitation and Reconstruction, Nanning, Guangxi, P.R. China.

出版信息

Int Dent J. 2025 Jun;75(3):1672-1682. doi: 10.1016/j.identj.2025.03.006. Epub 2025 Mar 29.

Abstract

INTRODUCTION AND AIMS

The aim of this study was to establish a reliable model of osteoradionecrosis of the mandible in New Zealand white rabbits and systematically examine the impacts of different radiation doses on mandibular tissue, as well as to appraise the inducing role of tooth extraction in the pathogenesis of the disease.

METHOD

In this research, 16 New Zealand white rabbits were randomly allocated to the control group, the 16Gy group, the 18Gy group, and the 20Gy group with a single high-dose radiation. Two weeks after radiotherapy, the teeth were extracted, and the animals were sacrificed four weeks later. Micro CT, scanning electron microscopy, HE staining, Masson staining, TRAP staining, TUNEL staining, and immunohistochemical staining were employed to verify the modelling status and damage mechanism.

RESULTS

Research findings show that, compared to the control group, rabbits exposed to 18Gy and 20Gy radiation doses exhibited significant bone necrosis after tooth extraction. Key observations included extensive bone tissue necrosis, increased osteoclasts (P < .05), reduced vascularization (P < .001), exacerbated fibrosis (P < .001), decreased bone density, disrupted trabecular structure, and damaged bone surface microstructure. In contrast, the 16Gy group showed some bone damage but did not meet bone necrosis criteria.

CONCLUSION

This study established an animal model appropriate for inducing ORNJ with a single large dose of radiation.

CLINICAL RELEVANCE

This work provides a solid experimental basis and a theoretical framework for further studies of ORNJ pathogenesis in particular to explore effective preventive and clinical treatment strategies.

摘要

引言与目的

本研究旨在建立新西兰白兔下颌骨放射性骨坏死的可靠模型,系统研究不同辐射剂量对下颌骨组织的影响,并评估拔牙在该疾病发病机制中的诱导作用。

方法

本研究中,16只新西兰白兔被随机分为对照组、16Gy组、18Gy组和20Gy组,接受单次高剂量辐射。放疗两周后拔牙,四周后处死动物。采用显微CT、扫描电子显微镜、苏木精-伊红染色、Masson染色、抗酒石酸酸性磷酸酶染色(TRAP染色)、末端脱氧核苷酸转移酶介导的缺口末端标记法(TUNEL染色)和免疫组织化学染色来验证建模情况和损伤机制。

结果

研究结果表明,与对照组相比,接受18Gy和20Gy辐射剂量的兔子在拔牙后出现明显的骨坏死。主要观察结果包括广泛的骨组织坏死、破骨细胞增多(P < 0.05)、血管化减少(P < 0.001)、纤维化加剧(P < 0.001)、骨密度降低、小梁结构破坏和骨表面微观结构受损。相比之下,16Gy组显示出一些骨损伤,但未达到骨坏死标准。

结论

本研究建立了一种适合通过单次大剂量辐射诱导放射性颌骨坏死性骨炎(ORNJ)的动物模型。

临床意义

这项工作为进一步研究ORNJ的发病机制,特别是探索有效的预防和临床治疗策略提供了坚实的实验基础和理论框架。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c5a1/11994307/b81ce3c3d379/gr1.jpg

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