Avascular Necrosis of the Femoral Head
Avascular necrosis, also known as aseptic necrosis (AN) of the femoral head, is a pathological process caused by interruption of the blood supply to the bone. Ischemia of the femoral head leads to death of bone marrow and osteocytes, which can ultimately result in collapse of the necrotic segment of the femoral head.

Multifactorial Disease
Aseptic necrosis of the femoral head is often described as a multifactorial condition. Its etiopathogenesis is not yet fully understood, but several risk factors have been identified.
Risk Factors
Genetic predisposition
Some individuals may have an inherited tendency to develop the condition[1].
Corticosteroid use
Prolonged or high-dose corticosteroid use is a major risk factor for AN[2].
Alcohol consumption
High and prolonged alcohol intake is associated with increased risk.
Smoking
Smoking may reduce blood flow to the femoral head and contribute to ischemia.
Chronic diseases
Several chronic diseases are associated with AN, including:
Sickle cell anemia: Can cause obstruction of blood flow in small vessels.
HIV: Increases the risk of AN through both the disease process and medication-related factors.
Hypercoagulable states: For example thrombophilia, which may lead to blood clots and reduced blood supply.
Autoimmune disorders: Conditions such as lupus erythematosus can affect microcirculation in the femoral head[3][4][5].
Stages of Aseptic Necrosis of the Femoral Head
Aseptic necrosis (AN) progresses through four characteristic stages. Each stage reflects ongoing physiological changes in the bone caused by reduced blood flow, bone necrosis and repair processes.
1. Initial Stage / Necrosis
Pathophysiology:
Blood supply to the femoral head is disrupted, leading to ischemia and the onset of necrosis.
Consequences:
The bone remains structurally intact, but bone-marrow cells and osteocytes begin to die.
Clinical signs:
The condition may be asymptomatic or cause mild hip pain.
2. Fragmentation
Pathophysiology:
The body begins to resorb necrotic bone tissue.
Woven bone replaces the necrotic area, but this tissue is weak and vulnerable to fracture and collapse.
Consequences:
Structural weakening increases the risk of femoral-head collapse.
Clinical signs:
Increasing pain and loss of hip function.
3. Reossification
Pathophysiology:
Stronger bone tissue begins to develop and replace woven bone.
The repair process strengthens the structure and increases stability.
Consequences:
Partial restoration of bone structure.
Clinical signs:
Pain may decrease, but function can remain limited.
4. Healed Stage / Remodeling
Pathophysiology:
Bone regeneration is completed and the femoral head assumes its final shape.
Consequences:
The final shape of the femoral head may be normal or deformed depending on the extent of previous damage.
Clinical signs:
Depending on the extent of injury, the patient may range from normal function to persistent pain and reduced mobility.
Early identification of the disease stage allows more targeted treatment and may help prevent progression to irreversible damage.
Progression from necrosis to remodeling takes time and depends on factors such as age, general health and how quickly treatment is initiated.
Diagnostic Procedures for Aseptic Necrosis of the Femoral Head
Early diagnosis of aseptic necrosis (AN) is essential for achieving the best possible treatment outcome. The timing of diagnosis is closely related to treatment effectiveness, particularly in the early stages.
Diagnostic Methods
X-ray Examination
X-rays may identify necrotic changes in moderate to late stages of the disease.
Crescent Sign:
A thin, curved radiolucent line parallel to the cortical margin of the femoral head.
This finding indicates subchondral collapse and is a typical sign of AN in moderate or late stages.
MRI Examination
MRI is the gold standard for detecting early or subclinical osteonecrosis.
Advantages:
High sensitivity and specificity for identifying ischemia and necrotic changes before they become visible on X-ray.
Provides detailed information about the extent of necrosis and may assist treatment planning.
Importance of Early Diagnosis
Disease progression may be slowed or halted with early intervention before extensive damage develops.
Appropriate use of imaging, particularly MRI, can improve the likelihood of successful treatment by identifying disease in its earliest stages.
History and Clinical Examination
Early and accurate identification of aseptic necrosis (AN) of the femoral head requires a detailed history and thorough physical examination. Because symptoms may be vague and resemble other hip-related conditions, the patient's history should be combined with targeted examination techniques.
History
Primary symptoms:
Groin pain is the most common symptom.
Pain may radiate to:
The knee.
The buttock region.
Course of symptoms:
Pain may begin as diffuse and mild but progress to more pronounced discomfort, particularly during weight bearing.
Risk factors:
Known risk factors should be identified before examination, including:
Corticosteroid use.
Alcohol consumption.
Chronic diseases such as sickle cell anemia or hypercoagulable states.
Clinical Examination
Assessment of range of motion:
Restricted range of motion is common, particularly:
Painful internal rotation during forced movement.
Other movements such as flexion and abduction may also be painful.
Bilateral assessment:
Both hips should be examined to rule out bilateral AN because the condition can occur symmetrically.
Awareness of early signs:
AN should be suspected in any patient with:
Hip or groin pain.
Negative radiological findings combined with one or more risk factors.
The combination of a thorough history and targeted physical examination can support early suspicion of AN even before imaging confirms the diagnosis.
Identifying risk factors and less typical symptoms, such as pain radiating to the knee, may improve diagnostic accuracy.
Treatment
Treatment of aseptic necrosis (AN) of the femoral head is complex and should be individualized according to the patient's age, symptom severity, location and extent of necrosis, and any comorbidities. The goals are to prevent progression, reduce pain and preserve joint function.
Treatment Strategies Based on Stage and Severity
Pre-Collapse Stage
Non-operative treatment:
Appropriate for asymptomatic patients or small to medium-sized necrotic lesions.
Measures include:
Physiotherapy: To maintain mobility and strength.
Weight-bearing restriction: Reduces loading of the femoral head.
Lifestyle modifications:
Avoidance of alcohol.
Discontinuation or reduction of corticosteroid treatment when medically appropriate.
Pain relief: NSAIDs or other analgesics may be used for symptom management.
Pharmacological treatment:
Bisphosphonates may reduce bone resorption.
Vascular growth factors may promote blood supply.
Core decompression:
A surgical technique in which a channel is drilled into the necrotic area to:
Reduce intraosseous pressure.
Increase blood flow.
Delay or halt disease progression.
Medium to large lesions
Bone grafting:
May include vascularized or non-vascularized bone grafts to reinforce and reconstruct necrotic bone.
Osteotomy:
The femoral head or proximal femur is surgically repositioned to redistribute load away from the damaged area.
Collapse Stage or Acetabular Involvement
Arthroplasty (hip replacement):
Indicated when the femoral head has collapsed or when there is extensive acetabular damage.
Total hip arthroplasty (THA) generally provides the best functional restoration in such cases.
Time-Critical Treatment
Treatment during the pre-collapse stage is important because untreated AN can progress to subchondral fracture within 2–3 years.
Early diagnosis and an appropriate treatment approach may delay or prevent progression to more severe stages, including collapse of the femoral head. The choice between conservative and surgical treatment depends on disease stage and the patient's individual needs.
Physiotherapy for Aseptic Necrosis of the Femoral Head
Physiotherapy is an important component of conservative management of aseptic necrosis (AN) of the femoral head and can help delay disease progression and improve function. Although physiotherapy alone cannot cure the condition, it can help maintain hip function and prepare the patient for possible surgical treatment.
Goals of Physiotherapy
Reducing load on the hip joint
Weight-bearing restriction:
Use of crutches or walking aids to reduce load on the hip joint.
This may help prevent further damage to necrotic bone and can delay the need for surgery.
Patient education
Provide information about risk factors that should be reduced or eliminated:
Lifestyle modifications:
Smoking cessation.
Reduction or elimination of alcohol consumption.
Weight management to reduce joint loading.
Reduction or discontinuation of corticosteroids under medical supervision.
Improving Range of Motion
Passive exercises:
Passive movement of the hip joint to maintain flexibility.
Stretching exercises to improve mobility without placing excessive stress on the joint.
Active exercises:
Focus on three-dimensional hip movements performed in standing, sitting or lying positions.
Strength Training
Gradual introduction of strengthening exercises targeting the hip and thigh musculature.
Core musculature:
Core training can support hip stability and reduce loading of the necrotic area.
Functional Exercises:
Endurance exercise such as treadmill walking or low-resistance stationary cycling.
Coordination training with increasing complexity, including balance exercises and challenging gait tasks.
Physiotherapy After Surgery
Early mobilization
Begins the day after surgery.
Focus on basic functions:
Getting in and out of bed.
Walking with a walker or crutches.
Further Rehabilitation
Gradual progression with exercises for:
Strengthening of the hip and thigh musculature.
Improving mobility: Focus on increasing range of motion without compromising hip precautions.
Balance training and gait speed to restore function.
Combined with a home exercise program to support continued progress.
Clinical Significance
Physiotherapy provides patients with tools to manage symptoms of AN and prepare for both surgical and conservative treatment pathways. After surgery, physiotherapy is essential for restoring mobility, strength and independence.
Sources:
Adesina O, Brunson A, Keegan THM, Wun T. Osteonecrosis of the femoral head in sickle cell disease: prevalence, comorbidities, and surgical outcomes in California. Blood Adv. 2017;1(16):1287-1295.
Xie XH, Wang XL, Yang HL, Zhao DW, Qin L. Steroid-associated osteonecrosis: Epidemiology, pathophysiology, animal model, prevention, and potential treatments (an overview). J Orthop Translat. 2015 Apr;3(2):58-70.
Jaffré C, Rochefort GY. Alcohol-induced osteonecrosis--dose and duration effects. Int J Exp Pathol. 2012;93(1):78-9
Orthobullets Hip Osteonecrosis Available: https://www.orthobullets.com/recon/5006/hip-osteonecrosis(accessed 15.12.2022)
Mont MA, Jones LC, Hungerford DS. Non-traumatic avascular necrosis of the femoral head: ten years later. J Bone Joint Surg Am. 2006;88:1117-1132
Hsu H, Nallamothu SV. StatPearls. StatPearls Publishing; Treasure Island (FL), 2020. Hip Osteonecrosis. Available from:https://www.ncbi.nlm.nih.gov/books/NBK499954/ (Accessed 25 July 2020)
Mont MA, Hungerford DS. Non-traumatic avascular necrosis of the femoral head. J Bone Joint Surg Am. 1995;77:459-474
Barney J, Piuzzi NS, Akhondi H. Femoral head avascular necrosis. Available:https://www.ncbi.nlm.nih.gov/books/NBK546658/ (accessed 15.12.2022)
Stanford Medicine Core Decompression. Available: https://stanfordhealthcare.org/medical-conditions/bones-joints-and-muscles/avascular-necrosis/treatments/core-decompression.html (accessed 15.12.2022)
Paula Miller, Treating Avascular Necrosis, 21(17):23





