Ficat-Arlet Staging of Femoral Head Osteonecrosis

You cannot stage a disease you cannot recognise, and the examiner will expect you to reel off the causes of femoral head osteonecrosis before you ever reach a stage. The causes divide cleanly into traumatic (a mechanical insult to the blood supply) and non-traumatic (a systemic or local insult to the same vessels). Corticosteroids and alcohol together account for the majority of non-traumatic cases worldwide. For the full pathology, epidemiology and management of the disease itself see avascular necrosis of the hip.

Understanding why the femoral head is so vulnerable is a classic basic-science viva that examiners hang off this topic. The femoral head has a precarious, largely end-arterial blood supply, so a single vascular insult produces ischaemia that the head cannot compensate for. (For the anatomy in full see hip blood supply.)

• The deep branch of the medial femoral circumflex artery (MFCA) is the dominant supply. It gives rise to the lateral epiphyseal (superior retinacular) vessels, which run beneath the synovial reflection along the posterosuperior neck and supply the great majority of the weight-bearing femoral head.
• The lateral femoral circumflex artery contributes to the anteroinferior head, and the artery of the ligamentum teres (a branch of the obturator/medial circumflex) supplies only a small foveal region and is insufficient to sustain the head alone in adults.
• Because these are terminal vessels with limited anastomosis, a displaced femoral neck fracture (tearing the retinacular vessels), a dislocation, raised intraosseous pressure (fatty marrow, Gaucher cells), or microvascular occlusion (sickle cells, nitrogen or fat emboli, thrombus) all converge on the same end point: ischaemia of the subchondral weight-bearing bone.

The final common pathway is the same whatever the cause: ischaemia kills osteocytes and marrow, the body mounts a repair response (creeping substitution) in which osteoclastic resorption of dead bone outpaces new bone formation, the subchondral bone is transiently weakened, and under continued load it fractures (the crescent sign) and then collapses. The Ficat-Arlet stages are simply snapshots of this sequence — and the reason early (pre-collapse) intervention works is that it acts before the resorption-weakening-fracture cascade becomes irreversible.

View larger

The Ficat-Arlet system was described by Ficat and Arlet in the 1960s and 1970s as a radiographic staging system for idiopathic avascular necrosis of the femoral head. It was originally designed before MRI was available, so early stages relied on bone scans and functional bone marrow exploration. Modern practice adds MRI to detect Stage 0 and Stage I disease that plain radiographs miss entirely.

Accurate Ficat-Arlet staging requires a combination of plain radiographs and MRI. Bone scan has been superseded by MRI for early detection but may still have a role when MRI is unavailable or contraindicated.

View larger

The Ficat-Arlet stage is the primary determinant of treatment. The fundamental question is whether the femoral head is structurally salvageable or whether collapse has progressed to the point where arthroplasty is the only reliable option.

Beyond the stage-driven algorithm, three adjuncts are worth knowing for the exam. First, risk-factor modification is treatment: minimising corticosteroids (with the prescribing team) and stopping alcohol can halt progression and protect the contralateral hip, and any joint-preserving operation is undermined if ongoing steroid exposure continues. Second, pharmacological and biological adjuncts — bisphosphonates (to reduce osteoclastic resorption during the weakening phase) and, increasingly, augmentation of core decompression with bone marrow aspirate concentrate or other cell therapy — have shown promise in early-stage disease but the evidence remains limited and they are adjuncts, not replacements for sound staging. Third, in the young patient facing arthroplasty, the conversation is about implant longevity and bearing choice: AVN patients are typically decades younger than osteoarthritis patients, historically had higher failure rates, and now do well with modern cementless stems and hard bearings — hip resurfacing is reserved for selected young, active patients with good bone stock and no large necrotic segment in the residual head.

The crescent sign is the radiographic signature of Stage III and the single most important imaging finding that shifts management from joint preservation to arthroplasty. It was first described by Ficat and Arlet and is present on plain radiographs in most Stage III lesions.

View larger

What it is: A curved, radiolucent line beneath the subchondral cortex of the femoral head, most commonly at the superior weight-bearing dome. It represents a fracture plane through the necrotic subchondral bone, filled with gas or joint fluid under pressure.

How to detect it:

• Best seen on the anteroposterior pelvis radiograph; the frog-lateral view may show it in a different plane.
• Look carefully at the superior margin of the femoral head — it appears as a thin dark crescent just beneath the dense subchondral cortex.
• CT is more sensitive than plain radiography and can demonstrate the subchondral fracture line before it becomes radiographically apparent.
• MRI shows it as a low-signal line through the subchondral bone on T1 with surrounding marrow oedema on T2.

Why it matters:

• It signifies that the structural support of the articular cartilage has failed — the necrotic bone cannot bear load and has fractured.
• Once the crescent sign appears, the femoral head will progressively flatten under continued weight-bearing.
• Joint-preserving procedures performed after the crescent sign appears have a significantly higher failure rate because the structural defect cannot be reversed.

The Ficat-Arlet stage alone does not predict outcomes perfectly. The size of the necrotic segment and its location within the femoral head are critical modifiers that affect prognosis at every stage.

Lateral lesion classification (Kerboul angle): The lateral extent of the necrotic segment is measured on MRI by combining the arc of necrosis seen on the coronal and sagittal planes. A combined angle greater than 200 degrees (large lateral lesion) carries a much higher risk of collapse and is the strongest imaging predictor of failure of joint-preserving surgery, even in Ficat-Arlet Stage II.

• The Ficat-Arlet system was developed before MRI, so the original Stages 0 and I were defined by bone scan and functional bone marrow biopsy. Modern MRI has largely replaced bone scan for early detection, but the stage names and definitions remain unchanged.
• The ARCO (Association Research Circulation Osseous) classification adds MRI-based sub-staging and lesion quantification to the Ficat-Arlet framework, and is preferred in some centres. ARCO stages I, II, III, and IV roughly correspond to Ficat-Arlet I through IV, with ARCO Stage 0 equating to Ficat-Arlet 0. The 2019 revised ARCO simplified the system to four stages and made the separation of pre-collapse (stage II) from collapse (stage III, subdivided IIIA early and IIIB late by the degree of depression) the central decision point — the same preserve-versus-replace logic as Ficat-Arlet.
• The Steinberg (University of Pennsylvania) classification is the principal alternative used in North America and in much of the research literature (it is the system the Castro meta-analysis used). Its key advantage over Ficat-Arlet is that it quantifies the disease: it has seven stages (0–VI) and, crucially, each stage is subdivided A (mild, under 15 percent of the head involved), B (moderate, 15–30 percent), and C (severe, over 30 percent), formalising the lesion-size effect that Ficat-Arlet captures only qualitatively.
• Inter-observer reliability is moderate for the four-type system, particularly for distinguishing early Stage II from late Stage II (the degree of sclerosis and cystic change is subjective). The distinction between late Stage II and early Stage III (before the crescent sign is radiographically apparent) is the most difficult.
• The system does not incorporate lesion size, lateral involvement, or aetiology. A steroid-induced lateral lesion occupying 70 percent of the head has a vastly different prognosis from a small post-traumatic medial lesion, yet both may be classified as Ficat-Arlet Stage II.
• Ficat-Arlet applies only to the femoral head. Other sites of osteonecrosis (knee, talus, scaphoid, humeral head) are staged with different systems.

• AAOS Clinical Practice Guideline (US) on osteonecrosis of the femoral head recommends core decompression or core decompression with bone grafting for pre-collapse disease (Ficat-Arlet Stages I-II) and total hip arthroplasty for post-collapse disease (Stages III-IV). The guideline notes the limited evidence for many joint-preserving procedures and emphasises shared decision-making.
• NICE (UK) does not have a specific guideline for osteonecrosis but NICE interventional procedures guidance covers core decompression and vascularised bone grafting as treatment options requiring specialist referral.
• BOA standards (UK) recommend that suspected osteonecrosis be referred to a hip preservation or arthroplasty specialist; staging with MRI is mandatory before any surgical decision.
• ARCO (Association Research Circulation Osseous) international classification builds on the Ficat-Arlet system by incorporating MRI-based lesion quantification and is widely used in research across Europe and Asia.
• Japanese Investigation Committee (JIC) classification divides osteonecrosis by the location of the necrotic segment (Type A, B, C1, C2) and is used extensively in Japan and parts of East Asia alongside Ficat-Arlet staging.
• Global epidemiology: Steroid use and excessive alcohol consumption remain the leading causes worldwide. Sickle cell disease is the dominant aetiology in sub-Saharan Africa and parts of the Caribbean and Middle East. Idiopathic osteonecrosis accounts for a significant proportion in all populations.