Osteonecrosis of the hip, also called avascular necrosis (AVN), is a condition in which bone tissue within the femoral head dies due to a disruption of its blood supply. As the bone dies and weakens, the femoral head eventually collapses, leading to severe pain, deformity, and secondary arthritis. It is a leading cause of hip replacement in younger adults.
AVN is one of the most time-sensitive diagnoses in hip medicine — the window for joint-preserving treatment is only open while the femoral head remains round and intact. Once collapse occurs, the hip develops rapid secondary osteoarthritis and hip replacement becomes unavoidable. AVN must also be distinguished from subchondral insufficiency fracture, which produces a similar MRI appearance and can be confused with early AVN — the distinction matters because management differs. In younger patients, Legg-Calvé-Perthes disease is the pediatric equivalent of AVN and shares the same fundamental mechanism of femoral head ischemia.
Causes
Traumatic causes.
Femoral neck fractures, hip dislocations, and other significant hip injuries can directly damage or shear the delicate blood vessels that supply the femoral head — primarily the medial femoral circumflex artery and its branches, which travel along the femoral neck. Traumatic AVN develops in a significant percentage of displaced femoral neck fractures, even when the fracture itself heals in good alignment, because the vascular injury occurs at the time of the original trauma. The risk is highest with displaced fractures and with delays in surgical reduction.
Non-traumatic causes.
Chronic corticosteroid use and heavy alcohol consumption together account for the large majority of non-traumatic AVN cases — corticosteroids induce fat emboli and impair angiogenesis, while alcohol disrupts lipid metabolism and promotes intraosseous fat accumulation that compresses the vascular sinusoids. Other recognized contributing conditions include sickle cell disease (vascular occlusion from sickling), lupus and other autoimmune conditions, inherited and acquired coagulation disorders, decompression sickness (nitrogen bubble embolism in divers), radiation therapy, chemotherapy agents, Gaucher's disease, and HIV. In some cases no identifiable cause is found — idiopathic AVN. Non-traumatic AVN is frequently bilateral, with the second hip sometimes already showing early MRI changes before the patient develops symptoms on that side, making bilateral imaging essential at the time of diagnosis.
Symptoms
Early osteonecrosis is often entirely asymptomatic and discovered incidentally on imaging obtained for another reason — a critical window for intervention that is frequently missed. As the condition progresses, patients develop a deep, aching groin pain that worsens with weight-bearing and activity and is often indistinguishable from other causes of hip pain in its early stages. Pain may radiate to the thigh or buttock. Once the femoral head begins to collapse — signaled by the appearance of the crescent sign on X-ray — pain becomes severe and constant, range of motion deteriorates rapidly, and a progressive limp develops. The course from symptom onset to femoral head collapse and secondary arthritis often spans months to a few years, making early imaging essential.
Diagnosis
A physical exam by a doctor reveals painful and restricted hip range of motion — particularly internal rotation — and an antalgic gait in more advanced cases. X-rays are frequently normal in the early stages of AVN, which is precisely the stage at which treatment is most effective and joint preservation is possible. An MRI is the gold standard for diagnosing AVN and is far more sensitive than X-ray — capable of detecting necrosis months before any changes appear on plain films. The characteristic MRI finding is a serpiginous (serpentine) low-signal line on T1-weighted sequences demarcating the necrotic segment, with a "double line sign" on T2-weighted images representing the reactive interface between viable and necrotic bone. MRI precisely defines the location, size, and percentage of femoral head involvement — all critical prognostic factors that determine whether joint preservation is feasible. Bilateral hip imaging is mandatory given the high rate of asymptomatic contralateral involvement in non-traumatic cases.
Disease stages (Ficat-Arlet)
Doctors use the Ficat-Arlet staging system to indicate the progression of osteonecrosis and guide treatment decisions. Stage is the most important determinant of whether joint-preserving surgery is appropriate.
- Stage 0: Silent hip with normal X-rays and normal MRI. AVN suspected only based on risk factors. Contralateral hip at elevated risk.
- Stage I: Normal X-rays. Bone marrow edema and early necrosis visible only on MRI. The most favorable stage for joint preservation — core decompression is most effective here.
- Stage II: Sclerotic or cystic changes visible on X-ray without femoral head collapse. Joint space is preserved. Joint-preserving surgery still possible but less predictable.
- Stage III: Subchondral collapse with the characteristic crescent sign on X-ray and flattening of the femoral head contour. Joint-preserving options have largely failed at this stage.
- Stage IV: Significant femoral head collapse with secondary osteoarthritis — joint space narrowing, acetabular involvement, and osteophyte formation. Total hip arthroplasty is the indicated treatment.
Treatments
Treatment depends on the stage of disease, size and location of the necrotic lesion, patient age, and activity level. Early diagnosis is the single most critical factor — joint-preserving options are only effective before the femoral head collapses, and the opportunity narrows rapidly once subchondral bone weakens.
Initial management includes weight-bearing restrictions using crutches or a cane to reduce mechanical stress on the compromised femoral head, activity modification, and anti-inflammatory medications for pain. Addressing modifiable risk factors — discontinuing or minimizing corticosteroids, eliminating alcohol — is essential and may slow progression in early cases.
Early stage AVN (Stages I and II) in young and active patients: Joint-preserving surgery is strongly recommended to delay or prevent femoral head collapse. Core decompression removes a small core of bone from the femoral neck and head to decompress elevated intraosseous pressure and stimulate revascularization. This is frequently augmented with concentrated bone marrow aspirate (stem cell therapy), structural bone grafting (fibular allograft or vascularized fibular autograft), or the placement of a tantalum metal rod to mechanically support the subchondral bone. Outcomes are most favorable when the necrotic lesion occupies less than 30% of the femoral head and the patient is treated before any collapse occurs. After surgery, a structured rehabilitation program with protected weight-bearing is critical to protecting the healing femoral head.
Collapsed AVN (Stages III and IV) in young and active patients
Once the femoral head has collapsed and the articular surface has been disrupted, joint-preserving options are generally ineffective and total hip arthroplasty becomes the treatment of choice. Modern implant designs — including highly cross-linked polyethylene and ceramic bearings — make hip replacement an excellent long-term option even for young, active patients in their 30s and 40s, with implant survival rates exceeding 90% at 20 years in contemporary series.
AVN in older, lower-demand patients
Older patients with symptomatic AVN — particularly those at Stage III or IV — typically proceed directly to total hip arthroplasty, which dramatically improves pain, function, mobility, and quality of life. The excellent outcomes of hip replacement in this setting make it one of the most effective interventions in all of orthopedic surgery.
Bilateral AVN
When both hips are affected — as is common in non-traumatic AVN — treatment is staged based on the severity of disease in each hip. Early-stage AVN in the less symptomatic hip may be treated with core decompression to attempt joint preservation while the more advanced hip undergoes replacement. Vigilant monitoring of the treated hip with follow-up MRI is essential, as progression can occur despite intervention.
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