Steroid-induced osteonecrosis

Abstract

Osteonecrosis associated with the use of glucocorticoids is a severe, potentially debilitating complication. In broader terms, it commonly involves the femoral head with secondary hip osteoarthritis. Osteonecrosis can also be caused by trauma and other non-traumatic factors besides steroid treatment. Nonetheless, glucocorticoid use is frequently observed in clinical settings in which this represents a common therapeutic option, including general practice, rheumatology and clinical immunology, among others. The pathogenesis involves genetic components, vascular impairment, adipocyte hypertrophy, and increased intraosseous pressure, ultimately leading to marrow and bone ischemia and necrosis and the process rapidly becomes irreversible. Osteonecrosis manifests with pain and impaired motility while the diagnosis is usually made with magnetic resonance imaging allowing early detection and potentially (dependent on the patient's needs for steroids and stage) timely management with conservative options, followed by joint replacement at late stages. In this review we discuss the pathogenesis, risk factors, diagnosis, staging, and management of this complication associated with glucocorticoid treatment.

Keywords: Adverse event; Aseptic osteonecrosis; Chronic inflammation; Prosthesis; Safety.

Fig. 1

Schematic representation of the main risk factors for osteonecrosis (blue boxes), measures to be taken for prevention (red boxes), and proposed treatments in early and late stages (green boxes).

Fig. 2

T1-weighted coronal (A) and axial (B) images of a woman with steroid-induced osteonecrosis showing an area of low signal intensity in the anterior-superior right femoral head.

Fig. 3

T2-weighted fat suppressed coronal (A) and axial (B) image of a woman with steroid-induced osteonecrosis showing a crescentic area of subchondral edema of the anterior part of the right femoral head, associated with a low signal intensity peripheral rim. A subchondral cyst may also be seen.