From the Department of Orthopedics, Aachen University Hospital, Aachen, Germany; and the Department of Orthopedics, Johannes-Gutenberg University, Mainz, Germany
Authors’ disclosures of potential conflicts of interest are found at the end of this article.
Address reprint requests to Wolf Drescher, MD, PhD, Department of Orthopaedic Surgery, University Hospital, Aachen, D 52074 Aachen, Germany; e-mail: wolfdrescher{at}hotmail.com
Overview: Osteonecrosis (ON) is a common complication of chemotherapy and defined as death of all cellular elements of bone. It predominantly affects the femoral head but can affect several other sites and occur multifocally. Glucocorticoid seems to be the main etiology, although its pathogenesis is ischemia. The mechanism of ischemia initiation is discussed. Intravascular coagulation obstructing microcirculation has been proposed; raising intraosseous pressure may cause inhibition of microcirculation. Direct cytotoxicity on osteocytes has also been suggested as a probable pathomechanism. The Association of Research on Osseous Circulation (ARCO) has published a detailed classification which is the basis for differential therapy. ARCO stage I seems to be best treated by core decompression, which means drilling a canal from the bone cortex into the necrotic lesion in order to release increased intraosseous pressure. Bone grafting and proximal femur osteotomies have proven to be valid therapies in stages II and III. ARCO stage IV may best be treated by total surface hip replacement or common total joint replacement. Because of the typically young age of patients with ON, joint-preserving techniques are preferred if possible.
