PDF(Pubmed)
Abstract：
Traumatic brain injury (TBI) and long bone fractures are a common injury pattern in polytrauma patients and modulate each other\'s healing process. As only a limited number of studies have investigated both traumatic sites, we tested the hypothesis that brain-bone polytrauma mutually impacts neuro- and osteopathological outcomes. Adult female C57BL/6N mice were subjected to controlled cortical impact (CCI), and/or osteosynthetic stabilized femoral fracture (FF), or sham surgery. Neuromotor and behavioral impairments were assessed by neurological severity score, open field test, rotarod test, and elevated plus maze test. Brain and bone tissues were processed 42 days after trauma. CCI+FF polytrauma mice had increased bone formation as compared to FF mice and increased mRNA expression of bone sialoprotein (BSP). Bone fractures did not aggravate neuropathology or neuroinflammation assessed by cerebral lesion size, hippocampal integrity, astrocyte and microglia activation, and gene expression. Behavioral assessments demonstrated an overall impaired recovery of neuromotor function and persistent abnormalities in anxiety-related behavior in polytrauma mice. This study shows enhanced bone healing, impaired neuromotor recovery and anxiety-like behavior in a brain-bone polytrauma model. However, bone fractures did not aggravate TBI-evoked neuropathology, suggesting the existence of outcome-relevant mechanisms independent of the extent of brain structural damage and neuroinflammation.
摘要：
创伤性脑损伤(TBI)和长骨骨折是多发伤患者常见的损伤模式,它们相互调节愈合过程。由于只有有限数量的研究调查了这两个创伤部位，我们检验了脑骨多发性创伤相互影响神经和骨病理学结果的假设.对成年雌性C57BL/6N小鼠进行受控皮质冲击（CCI），和/或骨合成稳定的股骨骨折（FF），或者假手术.神经运动和行为障碍通过神经严重程度评分进行评估，露天试验,旋转杆试验,和高架加迷宫测试。创伤后42天处理脑和骨组织。与FF小鼠相比，CCIFF多发性创伤小鼠的骨形成增加，骨唾液酸蛋白（BSP）的mRNA表达增加。骨折并没有加重神经病理学或神经炎症通过脑病灶大小评估，海马完整性,星形胶质细胞和小胶质细胞激活，和基因表达。行为评估表明，多发性创伤小鼠的神经运动功能总体恢复受损，焦虑相关行为持续异常。这项研究显示骨愈合增强，脑-骨多发性创伤模型中神经运动恢复受损和焦虑样行为。然而,骨折没有加重TBI诱发的神经病理学，提示结局相关机制的存在与脑结构损伤和神经炎症的程度无关。
