Patients who undergo heart transplantation (HT) have increased loss of bone mineral density (BMD) [g/cm2]. The greatest drop in BMD occurs within the first year after HT with a decrease 3.5-8.5% in the lumbar spine and 5.6-10.5% in the femoral neck. Thereafter, BMD tend to stabilize or even recover to some degree. Accordingly, risk of fracture correlates to BMD evolution, with the highest rate of fractures during the first year, with a cumulative incidence of 12-36%. Fragility fractures contributes to increased morbidity and increased mortality.

The pathophysiology behind BMD impairment in HT patients is complex and involves side-effects of the immunosuppressive therapy and of heart failure medications, as well as organ failure. Of the immunosuppressive agents, corticosteroids (CS) exerts the greatest impact on BMD through multiple cellular pathways. Also, calcineurin inhibitors seem have a negative impact on BMD, mainly mediated through enhancement of bone resorption. Additionally, kidney dysfunction has a significant effect on bone homeostasis and is frequently present in HT patients.

The optimal timing and type of pharmacological treatment of osteoporosis in HT patients are not yet known. However, bisphosphonates and monoclonal antibody against RANK ligand (Denosumab) may have beneficial effects on bone metabolism in HT patients. However, their efficacy and safety in have not been thoroughly studied in this particular patient population. Therefore, careful individual evaluation of prescription, frequency, and possible treatment options is advisable in this patient population.