• Cellular bone death due to vascular insufficiency
    • Can be either traumatic or nontraumatic
  • Also known as:
    • Avascular necrosis (AVN)
    • Ischemic necrosis
    • Idiopathic osteonecrosis
    • Lunatomalacia/Kienböck disease (lunate bone)
    • Subchondral fracture
    • Aseptic necrosis
    • Legg-Calvé-Perthes syndrome (idiopathic necrosis of the femoral head)
    • Osteonecrosis of the jaw (ONJ)


  • Primarily involves the epiphysis of long bones (most commonly femoral head, humeral head, and the femoral condyles), but any bone may be affected
  • System(s) affected: musculoskeletal


  • Predominant age: 3rd to 5th decades
  • Predominant sex: varies depending on comorbidities and etiology


  • 10,000 to 20,000 new cases per year in the United States (1)
  • Osteonecrosis is the most common cause for total hip replacement in young adults. It represents about 10% of all hip replacements (1).
  • Disease is bilateral in at least 50% of all nontraumatic cases and in 75–95% of cases associated with steroid use (1).


  • Hip: occurs in 10% of undisplaced femoral neck fractures, 15–30% of displaced femoral neck fractures, and 10% of hip dislocations
  • Jaw: Over the past 10 years, ONJ has been reported in 5% of cancer patients receiving high-dose IV bisphosphonates.
  • Glucocorticoid-induced osteonecrosis develops in 9–40% of patients on long-term therapy.
  • Osteonecrosis occurs during early postoperative period in 20–25% of patients after renal transplant.

Etiology and Pathophysiology

  • Pathophysiology is multifactorial and not fully understood. The final common pathway is the interruption of blood flow to the bone.
  • Vascular insufficiency leads to demineralization, trabecular thinning, subchondral plate fracture, and fatigue/fracture of the necrotic segment (1).
  • Traumatic: disruption of blood supply due to vessel injury as the result of fracture or dislocation
  • Nontraumatic
    • Impedance of blood flow due to vascular compression/vasospasm
    • Intraluminal obstruction from thromboembolism, nitrogen bubbles (diving), fat emboli, intravascular coagulation, or vascular stasis (1)
    • Long-term high-dose corticosteroid therapy
    • In many, the cause of interrupted blood flow is unknown.

Risk Factors

  • Primary risk factors are a history of trauma, prolonged corticosteroid use, or alcoholism.
  • Other risk factors include bisphosphonate use, sickle cell disease, diabetes mellitus, hyperlipidemia, oral contraceptives, pregnancy, chemotherapy, decompression sickness (“bends”; “caisson disease”), chronic pancreatitis, Crohn disease, gout, myeloproliferative disorders, radiation treatment, rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), chronic renal failure and hemodialysis, chronic liver disease, Gaucher disease, organ transplant, trauma, tobacco use, HIV, hypercoagulable states, fat embolus syndrome, developmental hip dysplasia, and slipped capital femoral epiphysis (SCFE).

General Prevention

  • Limit alcohol use. There is a dose-dependent relationship with alcohol consumption. The relative risk (RR) is 3.3 for <400 mL/week and 17.9 for >1,000 mL/week.
  • Smoking cessation: Smokers have RR of 3.9 versus nonsmokers.
  • Limit corticosteroid use: Serum corticosteroid concentration is cumulatively associated with osteonecrosis.
  • Consider screening bone density for high-risk patients.
  • Consider preventive dental checkup before high-dose bisphosphonate use in chemotherapy patients.

There's more to see -- the rest of this topic is available only to subscribers.