A proposed conceptual model of cardiovascular disease pathogenesis resulting from burn injury

While prolonged stress may contribute to cardiovascular dysfunction, it is possible that inflammation-induced bone loss may play a significant role in setting conditions for the development of significant post-burn cardiovascular disease. This narrative review of selected conditions brought about by burn injury in adults and children raises the possibility that these conditions are more prone to develop in these individuals than in age-matched controls, as has already been demonstrated. In this review I demonstrate that bone resorption releases transforming growth factor-beta (TGF-β) that has paracrine catabolic effects on skeletal muscle protein breakdown. These effects are entirely prevented by early administration of anti-resorptive agents such as bisphosphonates. Moreover, it is presently known that significant myocardial dysfunction exists following burn injury, much of which is initiated by TGF-β. It has yet to be resolved whether the source of the myocardial TGF-β is cardiac or skeletal. In addition, the body's handling of calcium and phosphate post-burn could lead to increased calcium phosphate precipitation in the blood vessels, promoting cardiac ischemia. Further studies on the use of anti-resorptives may tell us how much of a role bone resorption plays in the pathogenesis of long-term cardiovascular dysfunction.