Spontaneous Osteonecrosis of the Knee

Etiology

Spontaneous osteonecrosis of the knee can be distinguished from secondary osteonecrosis of the knee by its insidious onset and lack of identifiable cause.[5] Previous authors have proposed that the primary etiology for SONK is a subchondral insufficiency fracture resulting in localized osteonecrosis based on both histopathologic analysis and marked similarities to subchondral insufficiency fractures of the femoral head.[6] Other investigators have corroborated these findings through small case-series, adding additional evidence in favor of a traumatic etiology.[7] The thinking is that these insufficiency fractures lead to the accumulation of fluid in the bone marrow, resulting in focal ischemia and subsequent necrosis.[8]  This concept is in contrast to earlier theories that suggested a vascular etiology of the condition.[9] Further evidence is needed to pinpoint the exact pathogenesis of the disease, as it remains a source of controversy.  

In 2019, Hussain et al. published a systematic review re-examining the proposed etiologies of spontaneous osteonecrosis of the knee to understand the pathogenesis of the disease better. Here, the investigators noted a strong association between meniscal tears and spontaneous osteonecrosis of the knee.  Meniscal tears were found to occur in 50 to 100% of patients with spontaneous osteonecrosis of the knee in the included studies, with the extent of medial meniscus extrusion correlating to the stage and volume of SONK lesions.[10]  The investigators hypothesized that disruption of the posterior medial meniscus root increases tibiofemoral contact pressures, altering normal knee biomechanics, which in turn leads to the subchondral insufficiency fractures seen in SONK.[8]  Additionally, the authors recommended a change in nomenclature, as they believed that abandoning the term SONK in favor of subchondral insufficiency fractures of the knee (SIFK) would better reflect the disease pathogenesis.[8]

Epidemiology

Spontaneous osteonecrosis of the knee is the most common form of knee osteonecrosis.[11] The condition typically affects patients fifty to sixty years or older.[3] The classic patient is active, exercises regularly, and may have a history of osteoporosis or osteopenia.[3] Women are more affected than men. A correlation appears to exist between decreased bone mineral density and the incidence of SONK in women over 60 years of age as well as with medial meniscus posterior root tears.[12][8] The true prevalence may be greater than currently reported, as many patients who present with end-stage osteoarthritis may have had SONK that went unrecognized.[2]

History and Physical

Typically, the patient presents with acute onset, unilateral knee pain. The pain is severe and often localizes to the medial side of the joint, with lesions of the medial femoral condyle being most common. Notable history of trauma is usually absent; however, patients can sometimes recall precisely when the symptoms began.[7] Pain both at rest and night, as well as pain with weight-bearing, is common and can be quite debilitating. Localized tenderness to palpation over the area affected is the most common physical exam finding. Patients will usually have mild synovitis, a small effusion, ligamentous stability, and range of motion only minimally limited by pain.[5]

Evaluation

Evaluation of patients with suspected spontaneous osteonecrosis of the knee begins with obtaining a comprehensive history and performing a physical exam. After this initial evaluation, further imaging is the next step. Anteroposterior (AP), oblique, and lateral plain films of the knee should be obtained and can demonstrate flattening of the involved condyles in later stages of the disease. It is important to note that plain radiographs are often negative early on in the course of the disease.

 Magnetic resonance imaging (MRI) is especially useful in the early stages of the disease, given its high sensitivity to detect bone edema.[11] MRI findings usually include bone marrow edema localized to the medial femoral condyle, with extension into the inter-condylar notch. Additionally, a subchondral crescent of a linear focus of low signal intensity can be seen on the T1-, and frequently on the T2-weighted sequences.[13] Concurrent meniscal tears are common and can be diagnosed accurately on MRI as well. Bone scintigraphy may show increased uptake in the affected area. However, the sensitivity and specificity of this test are lower than MRI, limiting its utility if MRI is readily available.[11]

Spontaneous osteonecrosis of the knee can be staged to assess the severity and to guide treatment. The Koshino classification, described in 1979, consists of four stages. Stage I is a patient with knee symptoms but normal x-ray findings. Stage II consists of patients with flattening and subchondral radiolucencies without collapse. Stage III shows an extension of these radiolucencies with subchondral collapse. Stage IV consists of further degenerative changes with osteosclerosis and osteophyte formation.[11] 

Treatment / Management

Treatment of spontaneous osteonecrosis of the knee is guided based on the extent and severity of the disease. In the initial stages of the disease, non-operative treatment is an option, especially if the lesion is small (less than 3.5 centimeters squared).[11] Non-operative treatment consists of lateral wedge insoles, non-steroidal anti-inflammatory medications (NSAIDs), multimodal analgesia, protected weight-bearing, and bisphosphonates.[14] Yates et al. observed a complete resolution of symptoms in all 20 observed patients with stage I SONK treated non-operatively.[15](B2)

Prior to subchondral collapse, joint-preserving surgical techniques can be employed, including diagnostic and therapeutic arthroscopy, core decompression, and osteochondral autologous transplants. Duany et al. reported an 87% success rate in preserving the native knee joint using such joint preserving surgical techniques in patients with pre-collapse SONK at a mean follow-up of 40 months.[16]

 Advanced stages of the disease can have treatment with a high tibial osteotomy (HTO) and unicompartmental knee arthroplasty (UKA) or total knee arthroplasty (TKA). HTO is usually the choice for younger, more active patients. Depending on lesion characteristics and the condition of the overall joint, UKA can be an attempt to maintain bone stock and native knee kinematics.[14] Both UKA and TKA have shown favorable results comparable to those seen after total knee arthroplasty for osteoarthritis, so long as surgical indications are followed.[17](B2)

Differential Diagnosis

The diagnosis of spontaneous osteonecrosis of the knee can be challenging due to the insidious onset of disease and nonspecific symptoms. Care is necessary to rule out both referred pain from concurrent hip disease as well as intra-articular pathology.[18] A careful history and physical can help differentiate between SONK and similar clinical entities, including osteochondritis dissecans, transient osteoporosis, shifting bone marrow edema, secondary osteonecrosis, or bone contusion, and occult fractures.

Prognosis

Few studies exist which examine the natural course and downstream consequences of spontaneous osteonecrosis of the knee. Previous work has suggested that the prognosis for the condition does indeed depend on the size of the lesion, with larger lesions portending an increased risk of osteoarthritis.[19] Jureus et al. reported on SONK patients with a mean follow up of 15 years, confirming these findings and indicating that the development of osteoarthritis was likely when 40% or more of the joint surface was affected.[4] If diagnosed in its early stages, non-operative measures for treating SONK can be effective. If undiagnosed, patients will likely go on to develop end-stage osteoarthritis.

Complications

Spontaneous osteonecrosis of the knee is a progressive disease, and the patient’s condition will continue to deteriorate if not diagnosed and treated promptly. If diagnosed and treated conservatively in the early stages of the disease, patients can avoid risks and subsequent complications inherent in surgery.