Non-severe burn injury leads to depletion of bone volume that can be ameliorated by inhibiting TNF-α

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.