The role of the musculoskeletal system in post-burn hypermetabolism.

Burn injury results in a triad of inter-related adaptive responses: a systemic inflammatory response, a stress response, and a consequent hypermetabolic state which supports the former two. Details of what precisely triggers these responses as well as the sequence of events leading up to these responses are not clear. We review the musculoskeletal effects of burn injury to determine the precise contributions of this system in the generation and sustenance of this post-burn triad as well as the possible effects of pharmacologic intervention in the musculoskeletal response to burns on the resulting hypermetabolism. Inflammation-associated bone resorption liberates calcium, which may either prolong or intensify the systemic inflammatory response. Phosphate and magnesium liberated from bone could contribute to sustaining the increased ATP turnover in skeletal muscle that accompanies burn hypermetabolism. Reduced bone formation resulting from both pro-inflammatory cytokines and elevated endogenous glucocorticoid production results in reduced bone mass and therefore reduced osteocalcin production, which may contribute to reduced glucose uptake by skeletal muscle. Moreover, bone resorption liberates muscle catabolic factors such as transforming growth factor β, which contribute to the muscle wasting of burn hypermetabolism. Pharmacologic intervention with anti-resorptive agents early in the process preserve bone and muscle mass post-burn and future research should address the consequences for the hypermetabolic triad duration and intensity accompanying burn injury.