Severe burns can result in resorptive bone loss and endochondral bone formation at ectopic sites. The underlying pathophysiology involves both the systemic inflammatory response and the stress response with excessive endogenous production of glucocorticoids. The inflammatory response results in production of resorptive cytokines, leading to acute bone resorption; by 2 weeks postburn, glucocorticoid- and inflammation-mediated oxidative stress leads to reduced bone formation and reduced bone resorption, resulting in a net loss of trabecular bone for at least 2 years postburn. The role of the initial inflammatory response in the formation of heterotopic bone is incompletely understood at the present time. This chapter discusses the evidence supporting the pathophysiology described as well as current therapy and possible experimental drugs for future clinical trials Burn injury can produce profound metabolic effects on the bone and mineral balance of the body. Acutely, there is an inflammatory phase and a stress phase that affect calcium and other mineral balances. Chronically, we observe consequences for bone health and the hormonal milieu responsible for the body's mineral balance related to the inflammation of the burn injury as well as dysfunction of the organs and tissues that play a role in mineral metabolism. This chapter reviews the mineral homeostasis, the effects of burn injury in disrupting this homeostasis, recent literature on this topic, and evidence-based management of such derangements.
|Title of host publication||Total Burn Care, Fifth Edition|
|State||Published - 1 Jan 2017|
- bone formation
- bone resorption
- heterotopic ossification