Literature DB >> 23354247

Systemic inflammation induced by a thoracic trauma alters the cellular composition of the early fracture callus.

Stefan Recknagel1, Ronny Bindl, Christoph Brochhausen, Melanie Göckelmann, Tim Wehner, Philipp Schoengraf, Markus Huber-Lang, Lutz Claes, Anita Ignatius.   

Abstract

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 osteoclasts was 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.

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Year:  2013        PMID: 23354247     DOI: 10.1097/TA.0b013e318278956d

Source DB:  PubMed          Journal:  J Trauma Acute Care Surg        ISSN: 2163-0755            Impact factor:   3.313


  27 in total

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7.  Current Concepts in Orthopedic Management of Multiple Trauma.

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8.  Exposure to 100% Oxygen Abolishes the Impairment of Fracture Healing after Thoracic Trauma.

Authors:  Julia Kemmler; Ronny Bindl; Oscar McCook; Florian Wagner; Michael Gröger; Katja Wagner; Angelika Scheuerle; Peter Radermacher; Anita Ignatius
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9.  Impaired bone healing in multitrauma patients is associated with altered leukocyte kinetics after major trauma.

Authors:  Okan W Bastian; Anne Kuijer; Leo Koenderman; Rebecca K Stellato; Wouter W van Solinge; Luke Ph Leenen; Taco J Blokhuis
Journal:  J Inflamm Res       Date:  2016-05-18

10.  Duffy antigen receptor for chemokines regulates post-fracture inflammation.

Authors:  Charles H Rundle; Subburaman Mohan; Bouchra Edderkaoui
Journal:  PLoS One       Date:  2013-10-17       Impact factor: 3.240

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