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THE DEGREE OF FRACTURE-ASSOCIATED SOFT TISSUE INJURY MODIFIES SYSTEMIC INFLAMMATION AND REMOTE ORGAN DYSFUNCTION FOLLOWING BILATERAL FEMUR FRACTURE



Abstract

Patients with bilateral femur fractures are known to be at a high risk for the Systemic Inflammatory Response Syndrome; however the impact of fracture-associated soft tissue injury in the induction of systemic inflammation following bilateral femur fracture is poorly understood. To address this, the systemic inflammatory response and remote organ dysfunction following bilateral femur fracture with various degrees of soft tissue injuries were investigated in this study.

6–8 weeks old male C57/BL6 mice (n = 4–8 animals per group) were grouped as follows: Control-group (no anaesthesia, no femoral catheterisation); Sham-group (6 hour anaesthesia, femoral catheterisation); Fx-group (6 hour anaesthesia, femoral catheterisation, bilateral femur fracture with minor soft tissue injury); Fx+STI-group (6 hour anaesthesia, femoral catheterisation, bilateral femur fracture with severe soft tissue injury). Six hours after bilateral femur fracture serum levels of IL-2, IL-4, IL-6, IL-10, IL-12, TNF-α, KC and MCP-1 were measured. Furthermore, IL-6 levels of homogenized liver tissue were assessed. Neutrophil accumulation in liver and lung was determined with a myeloperoxidase (MPO) assay. Changes in liver permeability were assessed by measuring the wet-dry-ratio.

The Fx+STI-group showed significantly increased serum cytokine levels as compared to the Fx- or Sham-group. The homogenized liver tissue of the Fx+STI-group showed significantly increased IL-6 levels as compared to the Sham-group. The MPO activity in lung and liver in the Fx+STI-group was significantly increased in comparison to the Fx- or Sham-group and in the Fx-group in comparison to the Sham-group. The wet-dry-ratio of the liver was significantly increased in the Fx+STI-group as compared to the Sham-group.

The degree of fracture-associated soft tissue injury appears to modify systemic inflammation following bilateral femur fracture and is able to induce remote organ dysfunction. These results may have implications that have been underestimated, thus warranting clinical follow-up studies.

Correspondence should be addressed to: EFORT Central Office, Technoparkstrasse 1, CH – 8005 Zürich, Switzerland. Tel: +41 44 448 44 00; Email: office@efort.org

Author: Philipp Kobbe, Germany

E-mail: Kobbe.Philipp@gmx.de