Glucocorticoid-Induced Avascular Bone Necrosis: Diagnosis and Management

Abstract

Glucocorticoid use is one of the most important causes of avascular bone necrosis (AVN). The pathogenesis of glucocorticoid-induced AVN is not fully understood but postulated mechanisms include fat hypertrophy, fat emboli and intravascular coagulation that cause impedance of blood supply to the bones. Data regarding the relationship between AVN and dosage, route of administration and treatment duration of glucocorticoids are conflicting, with some studies demonstrating the cumulative dose of glucocorticoid being the most important determining factor. Early recognition of this complication is essential as the prognosis is affected by the stage of the disease. Currently, there is no consensus on whether universal screening of asymptomatic AVN should be performed for long-term glucocorticoid users. A high index of suspicion should be exhibited for bone and joint pain at typical sites. Magnetic resonance imaging (MRI) or bone scintigraphy is more sensitive than plain radiograph for diagnosing early-stage AVN. Conservative management of AVN includes rest and reduction of weight bearing. Minimization of glucocorticoid dose or a complete withdrawal of the drug should be considered if the underlying conditions allow. The efficacy of bisphosphonates in reducing the rate of collapse of femoral head in AVN is controversial. Surgical therapy of AVN includes core decompression, osteotomy, bone grafting and joint replacement. Recent advances in the treatment of AVN include the use of tantalum rod and the development of more wear resistant bearing surface in hip arthroplasty.

The Prevalence of Avascular Necrosis in Adults With Sickle Cell Disease in King Fahad Hospital.

“…Glucocorticoid induced AVN prevalence reach 10% in USA [29]. Most of these cases associated with post kidney transplantation and SLE [29]. Moreover, in this study we noted a relationship between SLE and presence of AVN, this relationship may partly be explained by the long-term use of steroids by SLE patients.…”

“…Another important finding was that 34.9% of SCA patients take Steroids. The long-term use of high dose steroid is reported to be an iatrogenic condition associated with AVN [29]. Although the pathogenesis of glucocorticoid induced AVN is not totally understood, many hypotheses were studied in animal models include fat cell hypertrophy, fat embolism, intravascular coagulation and osteocyte apoptosis [30].…”

“…Although the pathogenesis of glucocorticoid induced AVN is not totally understood, many hypotheses were studied in animal models include fat cell hypertrophy, fat embolism, intravascular coagulation and osteocyte apoptosis [30]. Glucocorticoid induced AVN prevalence reach 10% in USA [29]. Most of these cases associated with post kidney transplantation and SLE [29].…”

Bone Scintigraphy Scanning Safety and Necessity for Silent and Multifocal Osteonecrosis in Sickle Cell Disease

“…In SCD also, the high sensitivity of a bone scan is required to detect bone involvement. In a multicenter study of symptomatic multifocal osteonecrosis, various authors suggested that a total body BSc may be the most cost-effective means of screening for multifocal involvement [26], when the multifocal lesions are not recognizable on plain radiography before localized by BSc technology [27]. The SCD osteonecrosis could be completely clinically silent [28].…”

Predictors of Avascular Necrosis after Kidney Transplantation

“…AVN, a pathological condition defined as death of all cellular elements and progressive destruction of the bone, occurs because of bone vasculature disruption, death of osteocytes and fat cells, and bone architecture alterations (5,6). Generally, various factors such as corticosteroid administration, alcohol use, smoking, radiation, hyperlipidemia, thrombophlebitis, and intravascular coagulation have been proposed as risk factors for AVN throughout the population (7)(8)(9).…”