Avascular necrosis or osteonecrosis of femoral head is a sequale of a series of derangment that bring about decreased
blood flow to the femoral head and result in cell death in the femoral head.
Age: usually 20 -50 years ( mean age is 38 years)
Condition was first described by Alexander Munro in 1738.
- Corticosteroid use.
- Alchol use
- sickle cell anemia
- Systemic lupus erythematosus
- Organ transplantation
- Chronic pancreatitis
- Gauchers disease.
- Caissons disease.
- Intramedullary hemorrhage.
High Doses of steroids >30mg/day and more than 400 mL of alchol per week are implicated.
Early stages sjhow bone marrow necrosis which are probably the result of early insult.
Resorption of dead osteocytes then result in formation of empty lacunaes.
Osteoclasts are stimulated to resorb the dead bone and the osteoblasts then lay down the new bone by aprocess known as
If the area of affection is small, the reparative process ensues and the dead bone is replaced by the new bone.
If however the insult continues, the necrotic area enlarges and the histologic changes progresses. A zone of vascular ingrowth
is produced at the periphery of the lesion and the bone and bone marrow is replaced leading to increased sclerosis being visible
As the vasacularity doesnot reaches the innermost areas of necrosis, it remains weak and fractures on stress. The superficial
chondral bone being strong doesnot collapse and a radiographical "crescent sign" of subchondral collapse and fracture
thus appears obn the radiograph.
With time, even the subchondral bone collapses and teh femoral head flattens and deforms.
As the congruent articulation is no longer maintained between the femoral head and acetabulum, the secondary artritic changes
including sclerosis, cysts, obliteration of joint space and marginal osteophyte are produced.