Failure of the blood supply to the end of a bone, resulting in ischaemic necrosis of bone and marrow

Aetiology

• Greater incidence in males
• Typical age 35-50 years
• Most commonly affects the head of the femur, but can affect other bones too e.g. wrist, head of humerus

Pathophysiology

Idiopathic AVN

1. Coagulation of the intraosseous microcirculation
2. Venous thrombosis causes retrograde arterial occlusion
3. Intraosseous hypertension
4. Decreased blood flow results in necrosis of a segment of bone
5. There will be patchy sclerosis before subchondral collapse and irregularity of the articular surface occurs
6. Resultant bone and joint damage can lead to significant structural collapse of the bone → secondary OA
   1. Can also secondarily affect osteoarthritic joints causing collapse of the articular surface and rapid deterioration

Risk factors

• Irradiation
• Trauma
• Increased coagulability - thrombophilia, sickle cell disease, antiphospholipid deficiency in SLE, pregnancy
• Dysbaric disorders (decompression sickness - Caisson disease)
  • Rare cause which causes AVN from nitrogen gas bubbles forming in the circulation after too rapid a depressurization after deep sea diving
• Alcoholism and steriod (ab)use
  • Alter fat metabolsim which can result in mobilisation of fat into the circulation
  • Sludges up the capillary system and promotes coagulation within prone areas of bone
  • Increased fat content of the marrow can compress venous outflow from the bone causing stasis and ischaemia
• Hyperlipidaemia - increased fat in circulation