Idiopathic Osteonecrosis and Atypical Femoral Fracture in Systemic Lupus Erythematosus

Abstract

Osteonecrosis and osteoporosis are frequent adverse efects of glucocorticoid therapy of systemic lupus erythematosus (SLE). Idiopathic osteonecrosis (ION) of the femoral head occurs in 3-40% of patients receiving glucocorticoid, and can also develop in other bones. Higher doses of glucocorticoid and steroid pulse therapy are considered to be risk factors for ION of the femoral head. To analyze these risk factors, it seems important to detect early changes in the femoral head by magnetic resonance imaging and to monitor early clinical events atributable to steroid therapy. Prophylaxis with statins and warfarin remains debatable. The use of glucocorticoid is increase the risk of bone fractures. Bisphosphonate (BP) is used for its prevention and treatment of osteoporosis. Atypical femoral fracture (AFF) has been recently recognized as a complication associated with BP use. AFF is considered to be a form of stress fracture; localized periosteal thickening of the lateral cortex is often present at the fracture site. The thickening has been recently recognized as a complication associated with the use of antiresorptive agents such as BP and denosumab. As long-term BP/glucocorticoid use is a risk factor for beaking in patients with SLE , temporary withdrawal of BP administration should be considered.