Osteonecrosis of the Knee

Aetiology and Pathogenesis

Historically the disease was thought to be initiated by a vascular insult, resulting in diminished microcirculation and increased intraosseous pressures and ending with ischemia and necrosis of the subchondral bone. However, histopathological studies suggest an insufficiency fracture mechanism. Hatanaka et al. examined a surgically resected medial femoral condyle specimen from a patient with diagnosed SONK. Their analysis revealed a linear fracture line paralleling the subchondral endplate, callus formation with granulation tissue on both sides of the fracture and fracture-related bone debris at the osteochondral side of the fracture. The authors concluded that their findings suggested that SONK was the result of a subchondral fracture rather than primary osteonecrosis. Similarly, Yamamoto and Bullough described insufficiency fractures as the primary occurrences leading to osteonecrosis after their histopathologic evaluation of 14 patients with SONK.

As a result of the subchondral insufficiency fracture theory, a growing level of interest has developed to look at the potential role meniscus tears play in the advancement of this pathological process. The meniscus functions to maintain joint kinematics by dissipating joint reaction forces while protecting the articular cartilage and underlying subchondral bone. A disruption of the posterior medial meniscus root has been shown to result in a loss of hoop tension, increased contact pressures, and subsequent alteration of normal knee biomechanics, mimicking the biomechanics seen in total meniscectomy. Therefore, tears of the meniscus may increase joint reaction forces and lead to subchondral insufficiency fractures and subsequent bone marrow oedema of the knee. Patients with low bone mineral density and vitamin D deficiency are at high risk for this process. A comprehensive review found 21 of 26 articles (80.7%) connecting the meniscus in the development of SONK with the medial meniscus and posterior medial meniscus root tears more commonly involved ( Fig. 25.1 ). Five studies reported posterior medial meniscus root tears in association with the development of SONK. Yamagami et al. noted 62.2% of patients who underwent surgery for SONK had medial meniscus posterior root tears. Similarly, Robertson et al. observed these posterior medial meniscus root tears in 80% of patients with SONK and attributed the condition to femoral condyle overload due to the tear. As a result of this work in elucidating the true aetiology, there is a current trend towards replacing the term SONK with subchondral insufficiency fractures of the knee (SIFK).

Clinical Presentation and Diagnosis

Patients with SONK will typically present with a sudden onset of medial knee pain without a history of trauma. Pain with weightbearing and at night is common. Tenderness over the medial femoral condyle is often present on examination. Routine radiographic studies include a standing anteroposterior (AP), lateral, Merchant and 45-degree flexion posteroanterior (PA) view. The radiographs will be normal in the early course of the disease but may reveal subchondral radiolucencies or flattening of the femoral condyle in the later stages of disease. Magnetic resonance imaging (MRI) is the imaging modality of choice to detect early changes and to determine the extent of disease. The two key findings on MRI include oedema, which indicates stress, and insufficiency fracture with collapse of trabeculae ( Fig. 25.2 ). These findings often present as a subchondral area of low signal intensity on T2 weighted images, focal epiphyseal contour depressions and lines of low signal intensity deep in the affected condyle. The most common classification systems are the Ficat and Arlet, Aglietti and Koshino, which was the first classification for SONK described in 1979. There are four stages in the Koshino staging system, which are based on clinical and radiographic findings. A patient who has knee symptoms but normal radiographs is classified as stage I. Stage II includes flattening of the weightbearing area with subchondral radiolucencies surrounded by osteosclerosis. Stage III reveals extension of the radiolucencies around the affected area and subchondral collapse. Stage IV is the degenerative phase with osteosclerosis and osteophyte formation around the condyles. Prognostic value has been placed on the size of the lesion, with an increased risk of osteoarthritis with increasing size.

Treatment

The treatment options for patients with SONK include operative and nonoperative options and depend on the stage of the disease, associated structural abnormalities and symptoms. The size of the lesion, which is taken by measuring the greatest width in the AP radiograph and the greatest length in the lateral radiograph, can also help guide management. Small lesions (<3.5 cm ² ) have a high potential to respond well to nonoperative management and heal. On the other hand, larger lesions (>5 cm ² ) have a higher likelihood of failure with nonoperative treatment and tend to progress to advanced osteoarthritis. Another method to assess size involves calculating the width of the lesion in the AP radiograph as a percentage of the entire affected condyle width. With this method Lotke et al. determined that small lesions involving 32% of the condyle responded well to conservative treatment, whereas large lesions involving more than 50% of the condyle progressed rapidly to collapse and required arthroplasty.