Avascular necrosis

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Avascular necrosis is a disease resulting from the temporary or permanent loss of the blood supply to the bones.[1] Without blood, the bone tissue dies and causes the bone to collapse.[1] If the process involves the bones near a joint, it often leads to collapse of the joint surface. This disease also is known as osteonecrosis, aseptic (bone) necrosis, and ischemic bone necrosis.[1]

There are many theories about what causes avascular necrosis. Proposed risk factors include alcoholism[2], excessive steroid use,[3] post trauma,[4][5] caisson disease (decompression sickness),[6][7] vascular compression,[8] hypertension, vasculitis, thrombosis, damage from radiation, bisphosphonates (particularly the mandible),[9] sickle cell anaemia,[10] and Gaucher’s Disease.[11] In some cases it is idiopathic (no cause is found).[12] Rheumatoid arthritis and lupus are also common causes of AVN.

While it can, by definition, affect any bone, and half of cases show multiple sites of damage, this disease primarily affects the joints at the shoulder, knee, and hip.

Although it can happen in any bone, avascular necrosis most commonly affects the ends (epiphysis) of long bones such as the femur, the bone extending from the knee joint to the hip joint. Other common sites include the humerus (the bone of the upper arm),[13][14] knees,[15][16] shoulders,[13][17] ankles and the jaw.[18] The disease may affect just one bone, more than one bone at the same time, or more than one bone at different times.[19] Avascular necrosis usually affects people between 30 and 50 years of age; about 10,000 to 20,000 people develop avascular necrosis of the head of the femur in the US each year. When it occurs in children at the femoral head, it is known as Legg-Calvé-Perthes syndrome.[20]

Orthopaedic doctors most often diagnose the disease except when it affects the jaws, when it is usually diagnosed and treated by dental and maxillofacial surgeons.

Because early x-rays are usually normal in the early stage of the disease, bone scintigraphy[21] and MRI[22] are the diagnostic modalities of choice since both can detect minimal changes at early stages of the disease. Late radiographic signs include a radiolucency area following the collapse of subchondral bone (crescent sign) and ringed regions of radiodensity resulting from saponification and calcification of marrow fat following medullary infarcts.

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