Systemic inflammation induced by a thoracic trauma alters the cellular composition of the early fracture callus
Systemic inflammation induced by a thoracic trauma alters the cellular composition of the early fracture callus
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DOI：
10.1097/ta.0b013e318278956d
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发表时间：
2013-02-01
影响因子：
3.4
通讯作者：
Ignatius, Anita
中科院分区：
文献类型：
--
作者：
Recknagel, Stefan;Bindl, Ronny;Ignatius, Anita
背景：我们最近证实，钝性胸部创伤是创伤后全身炎症反应的强烈诱因，也是多发伤患者最严重的创伤之一，它显著延迟了大鼠骨折的愈合，可能是由于全身炎症与骨折局部早期再生过程的相互作用。然而，潜在的细胞机制至今仍不清楚。因此，本研究的目的是分析钝性胸部创伤后早期骨折骨痂的细胞和形态组成。方法：大鼠在胸部钝性创伤后接受外固定器稳定的右侧股骨截骨术。分别于第3、7、35天处死动物，对骨折骨痂进行组织学分析，观察新组织形成、中性粒细胞、巨噬细胞、破骨细胞及致炎细胞因子IL-6的存在。结果：与单纯骨折动物相比，胸部钝挫伤后第3天骨痂中的中性粒细胞数量显著增加。胸部创伤后第3、7天巨噬细胞数量明显减少，破骨细胞数量在术后各时间点均无明显变化。3天后，钝性胸部创伤导致膜内骨化区骨膜骨痂内白细胞介素6的染色明显增强。结论：胸部创伤后全身创伤后炎症反应通过改变骨折局部炎症细胞的募集和细胞因子的表达，破坏了骨折愈合早期的炎症平衡，从而影响骨折愈合。这些发现为严重创伤患者骨折愈合受损的病理机制提供了新的见解。(《创伤急救外科杂志》2013；74：531-537。版权所有(C)2013年，Lippincott Williams&Wilkins)
BACKGROUND: We recently demonstrated that a blunt chest trauma, a strong inducer of the posttraumatic systemic inflammatory response and one of the most critical injuries in polytrauma patients, significantly delayed fracture healing in rats, possibly by the interaction of the systemic inflammation with early regeneration processes locally at the fracture site. The underlying cellular mechanisms, however, have as yet remained unknown. Therefore, the aim of this study was to analyze the cellular and morphologic composition of the early fracture callus after a blunt chest trauma.METHODS: Rats received an osteotomy of the right femur stabilized by an external fixator in combination with a blunt chest trauma or not. The animals were killed after 3, 7, and 35 days, and the fracture calli were analyzed histologically for new tissue formation, polymorphonuclear leucocytes, macrophages, osteoclasts, and the presence of the proinflammatory cytokine interleukin 6.RESULTS: The blunt chest trauma considerably increased the number of polymorphonuclear leucocytes in the callus by Day 3 compared with animals with isolated fractures. The number of macrophages was significantly reduced by the thoracic trauma at Days 3 and 7. The number of osteoclastswas not changed at any postoperative time point. After 3 days, the blunt chest trauma led to a significantly stronger interleukin 6 staining within the periosteal callus in zones of intramembranous ossification. During the time of cortical bridging at Day 35, the amount of newly formed bone was significantly decreased after blunt chest trauma.CONCLUSION: Our results suggest that the systemic posttraumatic inflammation induced by a thoracic trauma disturbed the inflammatory balance during the early healing stage by altering the recruitment of inflammatory cells and cytokine expression locally at the fracture site and thus impaired fracture healing. These findings provide new insights in the pathomechanisms of impaired fracture healing in patients experiencing severe trauma. (J Trauma Acute Care Surg. 2013;74: 531-537. Copyright (C) 2013 by Lippincott Williams & Wilkins)