Avascular necrosis (AVN), or osteonecrosis, is an irreversible change of the bone structure leading to bone destruction, and is a terminal event for multiple conditions.

Femoral head is the most common place of avascular necrosis. Fractures, compromised blood supply (thrombi, emboli, vascular compression, vascular injury, vasculitis, sickle cell disease), compromised structure (for example due to the steroid use or Gaucher disease), degenerative bone disease and radiation are the common causes. Diseases of childhood or adolescence resulting in avascular necrosis include: Osgood-Schlatter disease (tibial tuberosity AVN) and Legg-Calve-Perthes disease (femoral head AVN). AVN is a common and serious complication of slipped capital femoral epiphysis.

The nutritional supply of the cartilage is from the synovial fluid, therefore cartilage is unaffected, and hence "subchondral avascular necrosis" is another term used for AVN. Radiographically subchondral fractures, cystic changes, and eventually collapse of the bone (crescent sign) can be appreciated.

Grossly necrosis is wedge-shaped, soft, yellow and well-demarcated. In the acute phase, osteocyte loss from bone lacunae and bone marrow necrosis are seen, however bone marrow cell loss may precede the loss of osteocytes by days. Eventually, a replacement of dead tissue begins at the border with viable tissue. Histiocytes clear necrotic debris, fibroblasts lay down the matrix and new blood vessels are formed. The activity of osteoclasts and osteoblasts is increased. When new bone starts replacing (or creeps over) necrotic bone trabeculae, the term "creeping substitution" is applied. Grossly, new granulation tissue can be appreciated at the edge of the infarct as a rim of hyperemia.

When necrotic bone collapses, a mixture of non-viable and new tissue can be seen histologically. Eventually, secondary osteoarthritis develops as late changes.

See related content for references:

1) Fondi, C., Franchi, A. Clinical Cases in Mineral and Bone Metabolism. 4(1):21-26. 2007.