CAJ | 학술논문

背景：骨折周围神经损伤能够有效抑制破骨细胞活动，促进骨折早期愈合。 　　目的：观察了大鼠肢体骨折合并脑损伤对骨密度、骨微结构、骨生物力学特征和骨代谢影响。 　　方法：63只大鼠随机分为假手术组、单纯骨折组和脑损伤合并骨折组。在术后3周、6周和3个月分批麻醉处死动物保存骨骼和血清标本，检测骨密度、骨微结构和生物力学性能以及血清Ⅰ型胶原氨基末端肽和骨钙素水平的变化。 　　结果与结论：与单纯骨折组相比，在造模3周和6周后，脑损伤合并骨折组胫骨近端的骨密度、松质骨微结构骨体积分数、骨小梁厚度、胫骨皮质骨截面总面积和骨髓腔面积、胫骨极限载荷和极限应力、血清原氨基末端肽和骨钙素水平均显著增高(P<0.05)，造模后3个月，3组间上述指标均差异无显著性意义。结果证实，脑损伤可增加骨折局部骨密度，改善骨微结构，提高生物力学性能，以此促进骨折局部的骨愈合和骨代谢。
배경：골절주위신경손상능구유효억제파골세포활동，촉진골절조기유합。 　　목적：관찰료대서지체골절합병뇌손상대골밀도、골미결구、골생물역학특정화골대사영향。 　　방법：63지대서수궤분위가수술조、단순골절조화뇌손상합병골절조。재술후3주、6주화3개월분비마취처사동물보존골격화혈청표본，검측골밀도、골미결구화생물역학성능이급혈청Ⅰ형효원안기말단태화골개소수평적변화。 　　결과여결론：여단순골절조상비，재조모3주화6주후，뇌손상합병골절조경골근단적골밀도、송질골미결구골체적분수、골소량후도、경골피질골절면총면적화골수강면적、경골겁한재하화겁한응력、혈청원안기말단태화골개소수평균현저증고(P<0.05)，조모후3개월，3조간상술지표균차이무현저성의의。결과증실，뇌손상가증가골절국부골밀도，개선골미결구，제고생물역학성능，이차촉진골절국부적골유합화골대사。
BACKGROUND:Peri-fracture nerve injury can inhibit osteoclast activity and promote early fracture healing. OBJECTIVE:To investigate dynamical y the effects of traumatic brain injury on the bone mineral density, microstructure, biomechanics property and bone metabolism in rat models of fractures. METHODS:Sixty-three male rats were randomly divided into three groups:sham group, simple fracture group and fracture combined with brain injury group. After 3, 6, and 3 months, the animals were sacrificed in batches under anesthesia, and then, the bones and serum specimens were used to detect the bone mineral density, microstructure, biomechanics property, serum cross-linked N-telopeptide of col agen type I and osteocalcin levels. RESULTS AND CONCLUSION:Compared with the simple fracture group, the fracture combined brain injury group had significantly increased bone mineral density of the proximal tibia, bone volume fraction of the cancel ous bone, trabecular thickness, cross-sectional area of tibial cortical bone and total area of the bone marrow, ultimate load and stress of the tibia, serum cross-linked N-telopeptide of col agen type I and osteocalcin levels at 3 and 6 weeks after modeling (P<0.05), but no differences in the above-mentioned indexes were found among the three groups at 3 months after modeling. These findings indicate that traumatic brain injury can increase the bone mineral density at the fracture site, improve bone microstructure and enhance biomechanical properties, thereby promoting bone healing and bone metabolism at the fracture site.