Avascular necrosis (AVN) of the knee — also called osteonecrosis — occurs when the blood supply to the bone is disrupted, causing bone cells to die. Without adequate blood flow, the affected bone gradually weakens, may collapse, and can lead to destruction of the overlying articular cartilage and progressive arthritis. The femoral condyles are the most commonly affected sites in the knee, though the tibial plateau and patella can also be involved.
AVN shares some overlap with other conditions that damage knee bone and cartilage — including Osteochondral Defects and Popliteal Cysts, which can develop secondary to chronic joint stress and cartilage breakdown.
Types of Knee AVN
Spontaneous Osteonecrosis of the Knee (SONK): The most common form, typically affecting older patients — particularly women over 55. SONK most often involves the medial femoral condyle and tends to present suddenly with the acute onset of pain. Despite the name, SONK is now understood to frequently be triggered by insufficiency stress fractures of the subchondral bone rather than true vascular occlusion, though the end result — bone death and potential collapse — is the same.
Secondary Osteonecrosis: Occurs as a consequence of an identifiable underlying condition or exposure (see Causes below). Secondary AVN tends to affect younger patients, is more likely to be bilateral or multi-focal, and often involves multiple joints throughout the body simultaneously.
Causes
1. Corticosteroid Use: Long-term or high-dose corticosteroid therapy (oral or intravenous) is the most common cause of secondary AVN. Steroids are thought to cause fat accumulation within bone and increased intraosseous pressure, impairing blood flow to the subchondral bone. This is seen in patients treated for conditions such as asthma, lupus, inflammatory bowel disease, and organ transplant recipients.
2. Alcohol Abuse: Excessive alcohol consumption is the second most common cause of secondary osteonecrosis. Similar to steroids, alcohol promotes fat accumulation in blood vessels and bone marrow, reducing blood supply to the bone.
3. Trauma: Fractures around the knee or significant ligamentous injuries can directly disrupt the vascular supply to the bone. Post-traumatic AVN is most commonly seen following fractures of the tibial plateau or femoral condyle, as well as after knee dislocation.
4. Subchondral Insufficiency Fracture: Particularly in osteoporotic patients, repetitive mechanical loading can produce a stress fracture just beneath the articular cartilage (subchondral bone). This fracture disrupts the local blood supply and can progress to osteonecrosis if unrecognized or untreated — this is now believed to be the underlying mechanism in many SONK cases.
5. Sickle Cell Disease: Sickling of red blood cells causes vascular occlusion throughout the body, including within bone. Patients with sickle cell disease have a significantly elevated lifetime risk of AVN at multiple sites, including the knee.
6. Systemic Lupus Erythematosus (SLE): AVN is a well-recognized complication of lupus, arising both from the disease itself (vasculitis, hypercoagulability) and from the high-dose corticosteroids commonly used to treat it.
7. Coagulation Disorders: Conditions that promote abnormal blood clotting — including antiphospholipid syndrome, protein C or S deficiency, and factor V Leiden mutation — can cause thrombosis of the small vessels supplying bone, leading to osteonecrosis.
8. Dysbaric Osteonecrosis: Seen in divers and compressed air workers, rapid decompression causes nitrogen gas bubbles to form within blood vessels, obstructing bone blood flow. The knee is a less common site than the hip or shoulder but can be affected.
9. Radiation Therapy: Radiation to or near the knee can damage the vascular supply to the bone and impair the bone's capacity for repair, eventually leading to osteonecrosis — sometimes years after treatment.
10. Idiopathic: In some cases, no clear cause can be identified. These cases are classified as idiopathic osteonecrosis.
Symptoms
- Pain: Knee pain is the primary symptom. In SONK, pain is often sudden in onset — patients frequently recall the exact moment it began — and is typically located over the medial aspect of the knee. Pain is worsened by weight-bearing and activity and may be present at rest in more advanced cases.
- Swelling: Joint effusion (fluid accumulation within the knee) is common, particularly in the early stages. Swelling may be intermittent and tends to worsen with activity.
- Tenderness: Direct tenderness over the affected condyle — most often the medial femoral condyle — is a characteristic finding on physical examination.
- Stiffness: Limited range of motion and joint stiffness, especially after periods of rest, may develop as the condition progresses.
- Mechanical Symptoms: As the subchondral bone collapses and the joint surface becomes irregular, patients may experience catching, clicking, or giving-way of the knee.
- Progressive Deformity: In advanced or neglected cases, collapse of the femoral condyle can lead to visible deformity, varus (bow-legged) or valgus (knock-kneed) malalignment, and the development of severe osteoarthritis.
Diagnosis
Medical History and Physical Examination:
- A thorough history is critical. Your provider will ask about the onset and character of pain, associated risk factors (steroid use, alcohol, prior trauma, systemic illness), and any history of similar problems in other joints.
- Physical examination will assess knee tenderness, effusion, range of motion, and alignment. Tenderness localized to the medial femoral condyle in an older patient with sudden-onset knee pain is a classic presentation of SONK.
X-rays:
X-rays are the first imaging study obtained. In early AVN, X-rays are often normal — this is an important limitation. As the condition progresses, X-rays may show subchondral lucency (a crescent sign indicating bone collapse), flattening or irregularity of the condylar surface, and joint space narrowing in later stages.
MRI (Magnetic Resonance Imaging):
MRI is the gold standard for diagnosing AVN of the knee and is far more sensitive than X-ray, particularly in the early stages before bony collapse has occurred. MRI findings include a characteristic low signal intensity band on T1-weighted images that outlines the necrotic segment, bone marrow edema surrounding the lesion, subchondral fracture lines, and articular cartilage changes. MRI is essential not only for confirming the diagnosis but for assessing lesion size, location, and stability — all of which determine the appropriate treatment strategy. It is also the best tool for monitoring progression or healing over time.
If AVN is suspected, a knee MRI should be obtained promptly — early detection before subchondral collapse occurs is the single most important factor in preserving the joint and avoiding knee replacement.
Bone Scan:
A nuclear medicine bone scan can detect increased bone turnover at the site of osteonecrosis before X-ray changes appear. While less specific than MRI, it can be useful when MRI is contraindicated.
CT Scan:
CT provides detailed imaging of bony architecture and is useful for evaluating the degree of subchondral collapse in surgical planning, particularly when assessing whether the articular surface has fractured or deformed.
Classification (Ficat & Arlet / ARCO Staging)
AVN of the knee is staged based on radiographic and MRI findings. The most widely used system is adapted from the ARCO (Association Research Circulation Osseous) classification:
- Stage I: Normal X-rays; MRI shows bone marrow edema and early necrotic changes. The patient is symptomatic but imaging findings are subtle. This stage is only detectable on MRI.
- Stage II: X-rays show sclerosis or cystic changes in the condyle, but the articular surface remains intact with no collapse. MRI clearly delineates the necrotic zone.
- Stage III: Subchondral collapse has occurred — the crescent sign is visible on X-ray, indicating a fracture beneath the cartilage. The articular surface may begin to flatten. This is a critical transition point.
- Stage IV: Collapse of the articular surface with flattening of the condyle and joint space narrowing. Secondary osteoarthritis is developing.
- Stage V: Severe joint destruction with marked joint space loss, deformity, and end-stage osteoarthritis of the knee.
Treatments
Treatment is guided by the stage of disease, lesion size, patient age, and underlying cause. The primary goals are to relieve pain, prevent progression to collapse, preserve the joint, and address any modifiable risk factors.
Addressing Underlying Risk Factors:
Whenever possible, the causative factor should be eliminated or reduced. This includes tapering corticosteroid doses to the lowest effective level, eliminating alcohol use, and optimizing management of systemic conditions such as lupus or sickle cell disease. These measures will not reverse established necrosis but may slow progression and reduce the risk of involvement at other sites.
Non-surgical Treatment:
- Protected Weight-Bearing: Reducing load across the knee with crutches or a walker is recommended in early-stage disease to minimize the risk of subchondral collapse. The duration depends on lesion size and stage.
- Physical Therapy: Strengthening exercises for the quadriceps and surrounding musculature help maintain joint stability and function while protecting the articular surface.
- Medications: NSAIDs are used to manage pain and inflammation. Bisphosphonates (such as alendronate) have been studied as a means of reducing bone resorption and preventing collapse in early-stage AVN, with some evidence of benefit in SONK cases.
Core Decompression:
In early-stage AVN (Stages I and II) before collapse has occurred, core decompression involves drilling one or more small tunnels through the femoral condyle into the necrotic zone to relieve intraosseous pressure and stimulate revascularization. This procedure is most effective when the necrotic lesion is small and the articular surface is intact. It is often combined with bone grafting or biologic augmentation (such as concentrated bone marrow aspirate) to enhance healing.
Biological and Regenerative Treatments:
- Platelet-Rich Plasma (PRP) and Stem Cell Therapy: These emerging treatments may be used in conjunction with core decompression or as standalone interventions in early disease to promote bone and cartilage healing.
- Bone Grafting: Structural bone grafting through the decompression channel provides mechanical support to the collapsing subchondral bone while stimulating new vascular ingrowth.
Osteochondral Procedures:
In cases where the articular surface has collapsed but the overall joint is still relatively preserved (Stage III to early Stage IV), cartilage restoration procedures such as osteochondral allograft transplantation may be considered to resurface the affected condyle and delay or avoid total knee replacement.
Unloading Osteotomy:
A high tibial osteotomy (HTO) or distal femoral osteotomy can realign the knee to shift mechanical load away from the necrotic condyle. This is particularly useful in younger patients with Stage III to IV disease and associated malalignment, as it can slow progression and extend the life of the native joint.
Knee Replacement Surgery:
For advanced disease (Stage IV to V) with significant joint destruction, pain, and loss of function that has not responded to other treatments, knee replacement is often the most reliable option. Depending on whether one or both compartments are affected, either a unicompartmental (partial) knee replacement or a total knee replacement may be recommended. Outcomes after knee replacement for osteonecrosis are generally good, though younger patients face the likelihood of eventual implant revision.
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