颌骨放射性骨坏死——当前综述——第1部分:病理生理学及风险和易感因素

Osteoradionecrosis of the jaws--a current overview--part 1: Physiopathology and risk and predisposing factors.

作者信息

Chrcanovic Bruno Ramos, Reher Peter, Sousa Alexandre Andrade, Harris Malcolm

出版信息

Oral Maxillofac Surg. 2010 Mar;14(1):3-16. doi: 10.1007/s10006-009-0198-9.

Abstract

PURPOSE

The aim of this paper is to explore the current theories about definition, classification, incidence and physiopathology of osteoradionecrosis (ORN) of the jaws. Moreover, it is discussed the predisposing and risk factors for the development of osteoradionecrosis based on the literature review.

DISCUSSION

Osteoradionecrosis is one of the most serious oral complications of head and neck cancer treatment. Osteoradionecrosis is a severe delayed radiation-induced injury, characterised by bone tissue necrosis and failure to heal. Osteoradionecrosis either stabilises or gradually worsens and is notoriously difficult to manage. The most widely accepted theory to explain its cause until recently was the theory of hypoxia, hypovascularity and hypocellularity. A new theory for the pathogenesis of osteoradionecrosis was proposed. The clinical presentations of osteoradionecrosis are pain, drainage and fistulation of the mucosa or skin that is related to exposed bone in an area that has been irradiated. The tumour size and location, radiation dose, local trauma, dental extractions, infection, immune defects and malnutrition can predispose its development.

CONCLUSIONS

A better understanding of risk factors for the development ORN and of the underlying pathophysiology may improve our ability to prevent this complication and help to improve the prognosis for those being treated for osteoradionecrosis.

摘要

目的

本文旨在探讨目前关于颌骨放射性骨坏死(ORN)的定义、分类、发病率及病理生理学的理论。此外,基于文献综述讨论了放射性骨坏死发生的诱发因素和风险因素。

讨论

放射性骨坏死是头颈癌治疗最严重的口腔并发症之一。放射性骨坏死是一种严重的迟发性辐射诱导损伤,其特征为骨组织坏死且无法愈合。放射性骨坏死要么稳定,要么逐渐恶化,而且 notoriously difficult to manage(此处原文有误,应改为“ notoriously difficult to manage”,意为“众所周知难以处理”)。直到最近,解释其病因最被广泛接受的理论是缺氧、血管减少和细胞减少理论。一种关于放射性骨坏死发病机制的新理论被提出。放射性骨坏死的临床表现为疼痛、黏膜或皮肤引流及瘘管形成,这与曾接受照射区域暴露的骨组织有关。肿瘤大小和位置、辐射剂量、局部创伤、拔牙、感染、免疫缺陷和营养不良可使其发病。

结论

更好地了解放射性骨坏死发生的风险因素及潜在病理生理学,可能会提高我们预防这种并发症的能力,并有助于改善放射性骨坏死患者的预后。

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