Phulpin Bérengère, Dolivet Gilles, Marie Pierre-Yves, Poussier Sylvain, Gallet Patrice, Leroux Agnès, Graff Pierre, Groubach Frederique, Bravetti Pierre, Merlin Jean-Louis, Tran Nguyen
Head and Neck and Dental Surgery Units, Oncologic Surgery Department, Centre Alexis Vautrin; ; Tumor Biology Unit, EA4421 SIGReTO UHP-Nancy University, Centre Alexis Vautrin;
Exp Ther Med. 2010 Jul;1(4):553-560. doi: 10.3892/etm_00000087. Epub 2010 Jul 1.
Radiotherapy is successfully used to treat neoplastic lesions, but may adversely affect normal tissues within the irradiated volume. However, additional clinical and para-clinical data are required for a comprehensive understanding of the pathogenesis of this damage. We assessed a rat model using clinical records and medical imaging to gain a better understanding of irradiation-induced tissue damage. The hindlimbs of the rats in this model were irradiated with a single dose of 30 or 50 Gy. Sequential analysis was based on observation records of stage and planar scintigraphy. Additional radiography, radiohistology and histology studies were performed to detect histological alterations. All animals developed acute and late effects, with an increased severity after a dose of 50 Gy. The bone uptake of (99m)Tc-HDP was significantly decreased in a dose- and time-dependent manner. Histologically, significant tissue damage was observed. After the 50 Gy irradiation, the animals developed lesions characteristic of osteoradionecrosis (ORN). Radiographic and histological studies provided evidence of lytic bone lesions. Our rat model developed tissue damage characteristic of radiation injury after a single 30 Gy irradiation and tissue degeneration similar to that which occurs during human ORN after a 50 Gy irradiation. The development of this animal model is an essential step in exploring the pathogenesis of irradiation-induced tissue damage, and may be used to test the efficacy of new treatments.
放射疗法已成功用于治疗肿瘤性病变，但可能会对照射区域内的正常组织产生不利影响。然而，要全面了解这种损伤的发病机制，还需要更多的临床和临床旁数据。我们使用临床记录和医学成像评估了一个大鼠模型，以更好地了解辐射诱导的组织损伤。该模型中的大鼠后肢接受了单次30或50 Gy的照射。序贯分析基于分期观察记录和平面闪烁显像。还进行了额外的放射摄影、放射组织学和组织学研究以检测组织学改变。所有动物均出现了急性和晚期效应，50 Gy剂量后严重程度增加。(99m)Tc-HDP的骨摄取以剂量和时间依赖性方式显著降低。组织学上，观察到明显的组织损伤。50 Gy照射后，动物出现了放射性骨坏死（ORN）的特征性病变。放射摄影和组织学研究提供了溶骨性骨病变的证据。我们的大鼠模型在单次30 Gy照射后出现了辐射损伤特征性的组织损伤，在50 Gy照射后出现了与人类ORN期间相似的组织退变。这个动物模型的建立是探索辐射诱导组织损伤发病机制的重要一步，可用于测试新治疗方法的疗效。
