title: Non-severe burn injury leads to depletion of bone volume that can be ameliorated by inhibiting TNF-α.
abstract: Bone loss after severe burn injury is well established, and is thought to be a consequence of the severe hyper-metabolic response as well as changes in cytokine and glucocorticoid levels that decrease bone synthesis and increase rate of loss. However, 90% of presentations are for non-severe burns which do not elicit this response. Little is known about whether these non-severe injuries may also affect bone tissue, and whether other mechanisms may be involved. To investigate whether bone loss occurs after a non-severe burn injury we used a mouse model of an approximately 8% total body surface area (TBSA) full-thickness burn and micro-CT. We also assessed whether blocking TNF-α after a burn injury by administration of an antibody could modulate the impacts of the burn on bone tissue. There was a significant loss of trabecular bone volume of (3.27% compared to 5.27%, p=0.0051) after non-severe burn injury. Trabecular number was significantly decreased (0.57/mm after injury compared to 1.02/mm controls, p=0.0051) and spacing increased after burn injury (0.40 compared to 0.28, p=0.0083). Anti-TNF-α antibodies significantly improved trabecular bone volume (8.53%, p=0.0034) and number after burn injury (1.28/mm, p=0.0034). There was no significant change observed in cortical bone after burn injury or administration of anti-TNF-α antibodies. These findings show that non-severe burn injury can lead to changes in bone metabolism. Monitoring bone density in patients with non-severe injuries and interventions to limit the impacts of the inflammatory storm may benefit patient recovery and outcomes.
authors.affiliation: Burn Injury Research Unit, School of Surgery, University of Western Australia, Perth, Australia.
authors.forename: Emily
authors.initials: E
authors.lastname: O'Halloran
authors.affiliation: School of Pathology and Laboratory Medicine, University of Western Australia, Perth, Australia.
authors.forename: Jasreen
authors.initials: J
authors.lastname: Kular
authors.affiliation: School of Pathology and Laboratory Medicine, University of Western Australia, Perth, Australia.
authors.forename: Jiake
authors.initials: J
authors.lastname: Xu
authors.affiliation: Burn Injury Research Unit, School of Surgery, University of Western Australia, Perth, Australia; The Fiona Wood Foundation, Royal Perth Hospital, Perth, Australia; Burns Service of Western Australia, Department of Health, Perth, Australia.
authors.forename: Fiona
authors.initials: F
authors.lastname: Wood
authors.affiliation: Burn Injury Research Unit, School of Surgery, University of Western Australia, Perth, Australia; The Fiona Wood Foundation, Royal Perth Hospital, Perth, Australia; School of Medicine, University of Notre Dame Australia, Fremantle, Australia. Electronic address: mark@fionawoodfoundation.com.
authors.forename: Mark
authors.initials: M
authors.lastname: Fear
mesh_terms: D000818:Animals; D001851:Bone Diseases, Metabolic / Q000000981:diagnostic imaging / Q000209:etiology / Q000276:immunology*; D002056:Burns / Q000150:complications / Q000276:immunology*; D005269:Femur / Q000000981:diagnostic imaging*; D051379:Mice; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors* / Q000276:immunology; D055114:X-Ray Microtomography
chemical_list: D014409:Tumor Necrosis Factor-alpha
keywords: Bone; Burn injury; TNF-α