Knee Avascular Necrosis (Osteonecrosis of the Knee)

Bone is living tissue that requires a continuous blood supply. The femoral condyles and tibial plateau of the knee receive their blood supply from a network of vessels that can be disrupted by vascular disease, trauma, medication effects, or systemic conditions. When this occurs, a zone of bone tissue loses its blood supply and begins to die. The process is initially invisible on X-ray, which is why MRI is essential for early diagnosis.

Spontaneous osteonecrosis of the knee (SONK) typically affects women over the age of 60 and involves the medial femoral condyle (the weight-bearing surface on the inner side of the knee). Despite its name, SONK is now understood to begin with subchondral bone stress injury, often following a minor meniscal event, rather than being truly spontaneous in origin. Small lesions may heal spontaneously; larger lesions progress to collapse without treatment.

Secondary AVN is caused by an identifiable systemic risk factor. Corticosteroid use is the most common cause worldwide, accounting for over a third of non-traumatic AVN cases. High-dose or prolonged steroid therapy (for example, for rheumatoid arthritis, inflammatory bowel disease, or organ transplantation) disrupts fat metabolism and microvascular bone circulation. Secondary AVN tends to affect younger patients, is often bilateral, and may affect multiple joints simultaneously.

Key risk factors:

• Age over 60 (SONK). The medial femoral condyle becomes progressively more vulnerable to subchondral bone stress injury with age, particularly in osteoporotic women. SONK is rare under the age of 55.
• Corticosteroid use. The most common identifiable cause of secondary AVN. High-dose or prolonged steroid therapy disrupts lipid metabolism, causing fat emboli in the subchondral bone vessels and leading to ischaemia. The risk is dose-dependent and remains elevated for years after steroid therapy.
• Alcohol excess. Chronic heavy alcohol consumption causes fat deposition in bone marrow vessels, increasing AVN risk. The mechanism is similar to steroid-induced AVN.
• Sickle cell disease. Sickling episodes cause direct vascular occlusion in the subchondral bone. Knee AVN is less common than hip AVN in sickle cell disease but occurs in the same pattern of multi-joint involvement.
• Post-meniscal surgery (SONK). Arthroscopic meniscal resection, particularly total or subtotal meniscectomy, increases the risk of subsequent SONK. Loss of the meniscal cushioning effect concentrates stress on the subchondral bone of the medial femoral condyle.
• Decompression sickness (diving). Nitrogen gas emboli from rapid decompression can occlude subchondral bone vessels, causing AVN in divers and caisson workers. Less common in the knee than in the hip and shoulder.

Non-surgical management is appropriate for early-stage SONK where the lesion is small and has not yet progressed to condylar collapse. Key elements include:

• Protected weight-bearing. Reducing load on the affected condyle with crutches for 6 to 12 weeks may allow small lesions to heal. The goal is to protect the necrotic bone from collapse before revascularisation can occur.
• Anti-inflammatory medication. NSAIDs reduce joint pain and swelling during the acute phase. They do not alter the natural history of the necrotic zone but improve patient comfort during the observation period.
• Bisphosphonates. Bone-protective agents (such as alendronate) have been used in small studies of SONK to reduce bone resorption in the necrotic zone and improve outcomes. Evidence remains limited, but Mr Hussain may discuss this option in selected patients with early-stage disease.
• Elimination of risk factors. For secondary AVN, addressing the underlying cause (reducing corticosteroid dose in consultation with the prescribing physician, cessation of alcohol, management of sickle cell disease) is an essential part of management alongside orthopaedic treatment.
• Monitoring with repeat MRI. Lesion size and progression are monitored with repeat MRI at 6 to 12 weeks. Small lesions (under 40 per cent of the condylar width on MRI) are more likely to heal; larger lesions have a high rate of progression to collapse and earlier surgical planning is indicated.

Outcomes of knee replacement for AVN are generally excellent when the disease is staged and treated appropriately. The main surgical challenge in AVN is managing the subchondral bone defect left by condylar collapse: in some cases, bone grafting is required to provide an adequate bed for the tibial component before fixation.

Mr Hussain's approach combines preoperative CT or MRI assessment of bone loss with intraoperative robotic planning, allowing the surgical bone cuts to be adjusted to account for the irregular condylar surface and ensure optimal implant positioning and fixation. This is particularly important in secondary AVN, where bone quality may be compromised by underlying disease or corticosteroid effects.

For patients with early-stage SONK who are managed non-surgically, the prognosis for small lesions (under 40 per cent condylar width) is good, with approximately 50 to 60 per cent resolving without surgery. Larger lesions carry a significantly higher risk of collapse and eventual joint replacement.