Introduction
This topic covers aseptic osteonecrosis (avascular necrosis, AVN), death of bone and marrow cells caused by interrupted blood supply without infection. It focuses on how the disease is recognised on imaging, staged, and separated from its mimics, and on what the radiologist must report so the orthopaedic or rheumatology team can choose treatment.
Definition, causes and sites
Osteonecrosis is ischaemic death of all elements of bone, including osteocytes and marrow. The term 'aseptic' distinguishes it from osteomyelitis. Causes are usually divided into traumatic and non-traumatic groups. Aetiology also includes chronic mild trauma, hormonal effects and blood vessel embolism; the disease is common in children and adolescents, and also occurs in some adults.
- Traumatic: femoral neck fractures with disruption of the medial circumflex femoral artery, scaphoid and talar neck fractures, dislocations of the hip.
- Corticosteroids in high or prolonged doses, the commonest non-traumatic cause, probably through fat-cell hypertrophy and intraosseous hypertension.
- Alcohol excess, which raises marrow fat and lipid levels, and caisson disease (nitrogen bubbles after rapid decompression).
- Systemic disease: systemic lupus erythematosus, sickle cell disease and other haemoglobinopathies, Gaucher disease, pancreatitis, HIV infection, hyperlipidaemia, renal transplantation, and coagulopathies.
- Idiopathic forms in children, such as Legg-Calvé-Perthes disease of the femoral head, and Kienböck disease of the lunate. Drug-related osteonecrosis of the jaw from bisphosphonates and denosumab is an important modern cause.
Typical sites are the femoral head (most common, often bilateral in steroid and alcohol cases), the femoral condyles, the humeral head, the scaphoid, the lunate, the talus, the navicular (Köhler disease), the metatarsal heads (Freiberg disease), and the tibial tuberosity (Osgood-Schlatter disease).