Hip

Avascular Necrosis of the Femoral Head

Avascular necrosis (AVN) of the femoral head (also called osteonecrosis) is a progressive and potentially devastating condition in which the blood supply to the ball of the hip joint is disrupted, causing bone cells to die. Without treatment, the femoral head can collapse, leading to severe arthritis. But when caught early, joint-preserving procedures can halt progression and avoid or delay hip replacement. At Maryland Orthopedic Specialists, our adult reconstruction team has the expertise to evaluate every stage of AVN and tailor treatment to preserve your hip as long as possible.

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What is avascular necrosis of the femoral head?

Avascular necrosis of the femoral head is death of bone in the ball of the hip joint caused by loss of its blood supply. Over time the weakened bone can collapse, leading to pain and arthritis. Risk factors include steroid use, heavy alcohol use, and prior hip injury.

The femoral head relies on a precise vascular supply (primarily the medial femoral circumflex artery) to maintain bone viability. When this supply is interrupted or reduced, ischemia leads to osteocyte death. Over time, the dead bone loses its structural integrity and is prone to fracture from normal weight-bearing loads, causing the round surface of the femoral head to "collapse" inward. This subchondral collapse destroys articular cartilage and leads to end-stage hip arthritis.

Causes and risk factors:

  • Traumatic: Femoral neck fracture, hip dislocation
  • Corticosteroid use: Systemic lupus, organ transplant, asthma (high-dose, prolonged use)
  • Alcohol use: Chronic heavy alcohol consumption
  • Hematologic: Sickle cell disease, coagulopathy
  • Infectious: HIV (and antiretroviral therapy — protease inhibitors)
  • Idiopathic: No identifiable cause (~20% of cases)

Incidence: An estimated 10,000–20,000 new cases are diagnosed in the United States annually. AVN accounts for approximately 10% of total hip replacements performed.

Staging (Ficat / ARCO classification):

  • Stage I: Normal X-ray; MRI shows marrow edema and early ischemia. Femoral head round and intact.
  • Stage II: Sclerosis or cysts on X-ray; MRI shows necrotic lesion; head still spherical.
  • Stage III: "Crescent sign" on X-ray: a thin radiolucent line beneath the subchondral bone indicating early collapse; head deforming but joint space preserved.
  • Stage IV: Femoral head collapsed with articular step-off; secondary acetabular changes; end-stage arthritis.

Symptoms — do you recognize these?

**Early (Stages I–II):**

  • Often asymptomatic — a critical window for joint preservation
  • Groin pain that may be present in some patients; others have none until collapse
  • Pain with weight-bearing and hip rotation
  • Progressive groin and hip pain, increasingly constant
  • Antalgic gait
  • Markedly restricted hip range of motion, especially internal rotation
  • Symptoms resemble hip OA

Call us at (301) 515-0900. Same-day appointments available at our Bethesda and Germantown locations.

How we diagnose it

X-rays (AP pelvis and lateral hip views) are the first study ordered:

  • Stages I–II: May appear normal or show subtle sclerosis
  • Stage III: Crescent sign (thin radiolucent line below the subchondral plate)
  • Stage IV: Femoral head collapse, loss of sphericity, joint-space narrowing

MRI is the most sensitive and specific test for early AVN (sensitivity ~97% for Stages I–II where X-rays are normal). Characteristic finding: a "double-line sign" on T2-weighted sequences, a low-signal outer rim with a high-signal inner rim representing the necrotic-reactive interface. MRI also:

  • Quantifies the size and location of the necrotic lesion (critical for prognosis)
  • Assesses for bilateral involvement (~70% of AVN cases are bilateral)

Bone scan (technetium-99m): Less specific than MRI; may show early AVN as a "cold" lesion progressing to "hot" reactive uptake. Largely superseded by MRI.

Laboratory studies: Directed by clinical history: CBC, lipid panel, coagulation studies, sickle cell screen, and workup for lupus or hypercoagulable states.

Treatment options

Treatment is staged to the severity of disease and the size of the necrotic lesion.

Stage I and II (Pre-collapse): Joint Preservation

Core decompression is the most established joint-preserving procedure for early AVN. One or more small-diameter drill channels are made from the lateral femoral cortex into the necrotic zone, reducing intraosseous pressure, stimulating a vascular healing response, and removing necrotic bone. Most effective for small-to-medium lesions in the non-weight-bearing zone Can be combined with autologous bone grafting, demineralized bone matrix, or concentrated bone marrow aspirate (stem cells) to augment healing Outpatient procedure with crutch walking for 4–6 weeks Vascularized fibular graft: A pedicled segment of fibula (with its blood supply intact) is transferred into the necrotic zone to provide structural support and vascular ingrowth. Technically demanding; used for larger lesions in younger patients with high demand for joint preservation. Non-operative management: Protected weight-bearing (crutches) alone does not halt progression in most patients. Reserved for very small asymptomatic lesions or when surgery is contraindicated. Bisphosphonates and lipid-lowering agents have been studied but not definitively proven.

Stage III (Crescent Sign / Early Collapse)

This is a critical decision point. The femoral head is beginning to deform but the joint space remains intact. Core decompression is less effective once collapse has begun but may still be considered for very early Stage III Femoral head osteotomy (rotational or varus/valgus) repositions the necrotic segment away from the primary weight-bearing zone; highly technical, reserved for select young patients at centers with expertise Resurfacing arthroplasty or total hip arthroplasty is increasingly considered for Stage III when the lesion is large and the femoral head is significantly deformed

Recovery & rehabilitation

  • Core decompression: Toe-touch weight-bearing 4–6 weeks; return to full activity 3–4 months; MRI surveillance at 6 and 12 months to monitor progression
  • Total hip arthroplasty for AVN: Similar recovery to standard THA. Weight-bearing within 1 day; full recovery 3–6 months

Frequently Asked Questions

Can AVN be cured?
Early-stage AVN can be arrested with core decompression in a significant proportion of patients, preventing collapse and preserving the native joint for many years. Once the femoral head has collapsed (Stage III–IV), the goal shifts to pain relief and function through hip replacement.
I've been on prednisone for years. Should I be screened for AVN?
Yes. Any patient with prolonged systemic corticosteroid use (particularly at doses > 20 mg/day for > 3 months) has a substantially elevated risk. A baseline MRI of the hips is warranted, especially if hip or groin pain develops.
Does stopping steroids reverse AVN?
Not reliably. Once ischemic damage has occurred, discontinuing the precipitating cause does not necessarily restore blood flow or prevent collapse. Early diagnosis and joint preservation procedures are the priority.
Is bilateral hip replacement needed?
Approximately 70% of AVN cases are bilateral, though they may be at different stages. Each hip is evaluated and treated individually.
What non-surgical treatments are available for AVN, and how effective are they?
Non-surgical options for early-stage AVN include protected weight-bearing, bisphosphonate medications, lipid-lowering agents, and vasodilators, though evidence for their long-term effectiveness in halting collapse is limited. Core decompression (a minimally invasive procedure that relieves pressure inside the femoral head) is the most established joint-preserving intervention and is most successful when performed before the femoral head collapses. At MOS, your surgeon will stage your AVN with MRI to determine whether you are likely to benefit from a joint-preserving approach or whether reconstruction is a better choice. In advanced stages with femoral head collapse, total hip replacement remains the most reliable way to eliminate pain and restore function.

Meet the specialists

John J. Christoforetti, MD

John J. Christoforetti, MD

Orthopedic Surgery · Sports Medicine · Hip, Knee & Shoulder Arthroscopy · Shoulder Replacement

Meet Dr. Christoforetti
Brian McCormick, MD

Brian McCormick, MD

Adult Reconstruction · Hip and Knee Replacement

Meet Dr. McCormick

Related conditions

Medically reviewed by John J. Christoforetti, MD, FAAOS
Last reviewed May 1, 2026

References

  1. Mont MA, Hungerford DS. Non-traumatic avascular necrosis of the femoral head. J Bone Joint Surg Am. 1995;77(3):459–474. https://doi.org/10.2106/00004623-199503000-00020
  2. Marker DR, Seyler TM, Ulrich SD, Srinivasan A, Mont MA. Do modern techniques improve core decompression outcomes for hip osteonecrosis? Clin Orthop Relat Res. 2008;466(5):1093–1103. https://doi.org/10.1007/s11999-008-0184-9
  3. Plenk H Jr, Hofmann S, Eschberger J, et al. Histomorphology and bone morphometry of the bone marrow edema syndrome of the hip. Clin Orthop Relat Res. 1997;(334):73–84. https://doi.org/10.1097/00003086-199701000-00009
  4. Moya-Angeler J, Gianakos AL, Villa JC, Ni A, Lane JM. Current concepts on osteonecrosis of the femoral head. World J Orthop. 2015;6(8):590–601. https://doi.org/10.5312/wjo.v6.i8.590
  5. Assouline-Dayan Y, Chang C, Greenspan A, Shoenfeld Y, Gershwin ME. Pathogenesis and natural history of osteonecrosis. Semin Arthritis Rheum. 2002;32(2):94–124. https://doi.org/10.1053/sarh.2002.33995
  6. American Academy of Orthopaedic Surgeons. Osteonecrosis of the Hip. OrthoInfo. https://orthoinfo.aaos.org/en/diseases--conditions/osteonecrosis-of-the-hip/
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