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Avascular Necrosis of the Hip

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Other Names

  • Osteonecrosis of the Hip
  • Hip osteonecrosis
  • AVN of the hip
  • AVN of the femoral head (AVNFH)
  • Atraumatic necrosis
  • Ischemic necrosis
  • Avascular necrosis (AVN)


  • This page refers to osteonecrosis or avascular necrosis of the femoral head, often referred to as avascular necrosis of the hip



  • Debilitating disease that can affect all ages, but most common in middle age men (ages 35-50)
  • Around 20,000 new cases per year and accounts for roughly 5% - 12% of total hip arthroplasties (THAs) performed[1]
  • Bilateral hips involved roughly 80% of the time (need citation)


  • See: Avascular Necrosis (Main)
  • Can be separated into traumatic versus nontraumatic
  • Denomination “avascular” is very not entirely appropriate
    • Femoral head blood supplying vessels do not disappear
    • They suffer a pathological process which results in blood flow interruption
  • Apoptosis of bone cells (bone marrow, osteoclasts, osteoblasts) results in bone collapse with involvement of overlaying cartilage
    • Leads to flattening of the femoral head surface and development of secondary osteoarthritis
  • Most use the term idiopathic for atraumatic causes, but a metabolic disorder background is the keystone behind the pathophysiology in almost all patients
    • Hepatic metabolism altered by alcohol intake or administration of steroid medication
      • Alcohol disturbs the phospholipid and cytokine metabolism and interrupts blood flow
        • Both alcohol intake and streroid administration are dose dependent and account for more than 80 percent of atraumatic cases [2]
    • Other conditions increase tendency of intravascular coagulation
      • Can be intraosseous (e.g. sickle cell disease) or extraosseous (e.g. Raynaud disease, decompression sickness)
  • Cultural, geographical and genetic circumstances have also been linked to idiopathic cases (Legg Calvé Perthes’ Disease (LCPD))
  • Pathophysiology in adults and children the same process with an ischemic phase and regeneration phase
    • Chilren's course depends on potential capability of the epiphyseal cartilage to synthesize new cartilage matrix
      • Children under 4 have very good prognosis and children older than 9 have poorer prognosis
  • Cases related to trauma have resulting osteonecrosis due to vascularity around the head being severely disturbed
    • Mainly the medial femoral circumflex artery

Risk Factors

  • Indirect[3]
    • Alcohol use
    • Prolonged corticosteroid use (greater than 20-40 mg per day for > 3 months)
      • Usually related to chronic conditions (transplant, rheumatoid arthritis, etc.)
    • Systemic Lupus Erythematosus (SLE)
    • Sickle cell disease (SCD)
    • Coagulation factor abnormalities (hypofibrinolysis or thrombophilia)
    • Virus infection (hepatitis, HIV, CMV)
    • Protease inhibitors (HIV medication)
  • Direct
    • Trauma (fracture)
    • Hip dislocation
    • Gaucher disease
    • Radiation
    • Decompression sickness (Caisson disease)

Differential Diagnosis

Clinical Features

  • History
    • Recognition of risk factors very important
    • Most common presenting symptom is pain
      • Can mimic joint pain with anterior hip pain radiating into groin
      • May also have pain in buttocks and pain exacerbated with weight bearing
      • Around 2/3 have pain at rest and 1/3 have night pain [4]
  • Physical Exam: Physical Exam Hip
    • Can be fairly nonspecific, but some have limitations in motion and pain in hip with passive and active range of motion
  • Special Tests
    • FADIR Test: May suggest hip etiology, not specific to AVN



  • Standard Radiographs Hip
    • Includes AP views and frog leg lateral views
    • Close attention to superior portion of femoral head for subchondral abnormalities
  • Crescent sign
    • Refers to a linear area of subchondral lucency seen most frequently in the anterolateral aspect of the proximal femoral head
    • Sign of imminent collapse


  • MRI is the gold standard with sensitivity up to 100 percent
  • Findings:
    • T1 images appear dark with a low intensity band and T2 images have focal brightness or marrow edema
    • Presence of marrow edema has been shown to predict worsening pain and future progression of disease [5]
    • "Double line” sign that can be seen on T2 Spin echo or turbo spin echo sequences [6]
      • Consists of a low signal intensity outer and a high signal intensity inner rim
      • Sign or scheme was not ever used widely, as it did not correlate with radiographic staging, clinical presentation and prognosis
  • Can be used to predict prognosis or risk of femoral head collapse (Kerboul combined necrotic angle) [7]
    • Calculated by adding the arc of the femoral head necrosis on a midsagittal and mid-coronal MR image
      • Less than 190 degrees can be characterized as low risk
      • Between 190 and 240 degrees moderate risk
      • Greater than 240 are high risk

Bone Scintography

  • Radionuclide testing (Technetium-99m)
    • Can be used in patients with normal x-rays but suspected AVN
    • Increased burn turnover increased uptake with cold surrounding area sometimes called the "doughnut" sign [8]
    • Not used frequently and is less sensitive than MRI


Association Research Circulation Osseous (ARCO) System

  • Stage 0
    • All diagnostic techniques normal
  • Stage 1
    • Plain X-ray and CT-scan are normal but scintigraphy or MRI or positive
    • Subdivided into 3 categories according to location of lesion (medial, central, lateral)
    • Quantitation or area of femoral head involvement can be added: Minimal (<15%), Moderate (15-30%), Extensive (>30%)
  • Stage 2
    • No subchondral fracture or crescent sign
    • Radiography shows a mottled aspect, sclerosis, osteolysis and focal porosis
    • Femoral head remains spherical on AP and lateral views and CT scan.
    • Can add quantitation or sub-classification as in stage 1.
  • Stage 3
    • Crescent sign on x-ray and femoral head fails mechanically
    • Axial x-ray shows subchondral fracture line and spherical configuration starts to deteriorate and flatten
    • Sub-classification and quantitation added (done by calculating the amount of flattening of femoral dome)
    • This is performed by selecting most prominent crescent sign view and measuring depression
      • Minimal = < 15% involvement or a depression of <2 mm.
      • Moderate = 15-30% involvement or a depression of 2-4 mm.
      • Extensive = > 30% involvement or a depression of more than 4 mm.
  • Stage 4
    • Progression to osteoarthritis
    • The femoral articular surface is flattened and joint space narrows
    • Associated with sclerosis, cysts, marginal osteophytes
    • Complete destruction of joint eventually seen and sub-classification not needed
  • ARCO: the most common staging system (need citation)
    • Older staging systems are still used by some and include the Ficat-Arlet staging system, the Hungerford-Lennox system, the Steinberg classification system and the Ohzono system

Steinberg Classification (modification of Ficat classification)

  • Stage: 0
    • Radiographs: normal
    • MRI: normal MRI and bone scan
  • Stage: I
    • Radiographs: normal
    • MRI: abnormal MRI and/or bone scan
  • Stage: II
    • Radiographs: cystic or sclerosis changes
    • MRI: abnormal MRI and/or bone scan
  • Stage: III
    • Radiographs: crescent sign (subchondral collapse)
    • MRI: abnormal MRI and/or bone scan
  • Stage: IV
    • Radiographs: flattening of femoral head
    • MRI: abnormal MRI and/or bone scan
  • Stage: V
    • Radiographs: narrowing of joint
    • MRI: abnormal MRI and/or bone scan
  • Stage: VI
    • Radiographs: advanced degenerative changes
    • MRI: abnormal MRI and/or bone scan



  • Increasing attention to nonoperative interventions aimed at preserving native joint or delaying THA
    • Overall, THA outcome data less satisfactory compared to other indications
    • Primarily related to limited lifetime, durability of THA in such young patients[9]
  • Core decompression (CD)[10]
    • Clinical success rate is only about 63.5%
    • Rate for subsequent THA is about 33%


  • Indications
    • Unclear
    • Somewhat controversial with mixed results
  • Treat & address risk factors
    • Alcohol cessation
    • Discontinue steroids if possible
    • Correct coagulopathies
    • Optimize management of SLE, SSD, etc

Pharmacologic Therapies

  • Bisphosphonates
    • One uncontrolled study showed improvement in pain, clinical function when taking alendronate 10 mg daily at three years, but not eight years[11]
    • Another study with 40 patients showed less collapse [7 vs. 76 percent] while taking alendronate 70 mg weekly[12]
    • However, 2016 meta-analysis concluded bisphosphonate therapy did not significantly reduce the progression to collapse[13]
  • Statins
    • Sometimes used to treat steroid-induced AVN
    • Ongoing trials

Regenerative Therapy

Nonpharmacologic Therapy


  • Indications
    • Most cases
  • Technique
    • Core Decompression +/- bone grafting
    • Total Hip Arthroplasty
    • Rotational Osteotomy
    • Curettage and Bone Grafting
    • Vascularized Free-fibula Transfer
    • Total Hip Resurfacing
    • Hip Arthrodesis

Rehab and Return to Play


  • Needs to be updated

Return to Play

  • Needs to be updated


  • Chronic Pain
  • Inability to return to sport
  • Inability to participate in athletic activities

See Also


  1. Malizos KN, Karantanas AH, Varitimidis SE, Dailiana ZH, Bargiotas K, Maris T (2007) Osteonecrosis of the femoral head: etiology, imaging and treatment. Eur J Radiol 63:16–28.
  2. Mont MA, Hungerford DS. Non-traumatic avascular necrosis of the femoral head. J Bone Joint Surg Am 1995;77:459–74
  3. Shah KN, Racine J, Jones LC, Aaron RK. Pathophysiology and risk factors for osteonecrosis. Curr Rev Musculoskelet Med. 2015;8(3):201–209. doi:10.1007/s12178-015-9277-8
  4. Mont MA, Hungerford DS. Non-traumatic avascular necrosis of the femoral head. J Bone Joint Surg Am 1995;77:459–74
  5. Ito H, Matsuno T, Minami A. Relationship between bone marrow edema and development of symptoms in patients with osteonecrosis of the femoral head. AJR 2006;186:1761–70.162:717.
  6. Mitchell DG, Rao VM, Dalinka MK, et al. Femoral head avascular necrosis: correlation of MR imaging, radiographic staging, radionuclide imaging, and clinical findings. Radiology 1987;162:709–15
  7. Ha YC, Jung WH, Kim JR, Seong NH, Kim SY, Koo KH. Prediction of collapse in femoral head osteonecrosis: a modified Kerboul method with use of magnetic resonance images. J Bone Joint Surg Am. 2006;88 Suppl 3:35–40
  8. Dumont M, Danais S, Taillefer R. "Doughnut" sign in avascular necrosis of the bone. Clin Nucl Med 1984; 9:44
  9. Lau RL, Perruccio AV, Evans HM, Mahomed SR, Mahomed NN, Gandhi R (2014) Stem cell therapy for the treatment of early stage avascular necrosis of the femoral head: a systematic review. BMC Musculoskelet Disord 15:156.
  10. Mont MA, Carbone JJ, Fairbank AC (1996) Core decompression versus nonoperative management for osteonecrosis of the hip. Clin Orthop Relat Res 324:169–178
  11. Agarwala S, Shah S, Joshi VR. The use of alendronate in the treatment of avascular necrosis of the femoral head: follow-up to eight years. J Bone Joint Surg Br 2009; 91:1013.
  12. Lai KA, Shen WJ, Yang CY, et al. The use of alendronate to prevent early collapse of the femoral head in patients with nontraumatic osteonecrosis. A randomized clinical study. J Bone Joint Surg Am 2005; 87:2155.
  13. Yuan HF, Guo CA, Yan ZQ. The use of bisphosphonate in the treatment of osteonecrosis of the femoral head: a meta-analysis of randomized control trials. Osteoporos Int 2016; 27:295.
  14. Malizos KN, Karantanas AH, Varitimidis SE, et al. Osteonecrosis of the femoral head: etiology, imaging and treatment. Eur J Radiol. 2007;63:16-22.
Created by:
John Kiel on 20 March 2020 19:04:15
Last edited:
5 October 2022 13:05:28