Knee Osteonecrosis

Updated: Jun 29, 2021
  • Author: Amar Rajadhyaksha, MD; Chief Editor: Thomas M DeBerardino, MD, FAAOS, FAOA  more...
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Practice Essentials

Osteonecrosis is a disease characterized by a derangement of local blood supply that leads to necrosis of osseous tissue. Osteonecrosis of the knee has been divided into two separate entities: spontaneous osteonecrosis of the knee (SPONK) and secondary osteonecrosis. [1, 2]  A rare form that is sometimes considered a separate entity is postarthroscopy osteonecrosis, which affects patients who have undergone arthroscopic knee surgery, most commonly meniscectomy. [3]

For patient education information, see Knee Pain, Knee Injury, and Knee Joint Replacement.


History of the Procedure

Ahlback et al first reported on osteonecrosis of the knee in 1968. [4] The osteonecrosis that Ahlback described now is referred to as spontaneous osteonecrosis of the knee (SPONK).



In osteonecrosis, the lesion can extend to the subchondral plate and result in collapse of the necrotic segment. This can lead to disruption of the joint line, resulting in painful secondary arthritis.




The knee is the second most common site for osteonecrosis, but it is affected much less often than the hip. The true incidence of the disease is unknown, but osteonecrosis of the knee is believed to account for approximately 10% of cases of osteonecrosis.

A study using data from the UK-based IQVIA Medical Research Data (IMRD) and US Medicare beneficiaries reported the following incidence rates [5] :

  • Knee osteonecrosis among adults diagnosed with osteoarthritis (OA): 0.006-0.10% 
  • Knee osteonecrosis in the year prior to knee replacement: 0.004–0.06%
  • Knee osteonecrosis after knee replacement: 0.24–0.7%.




The etiologies of both spontaneous osteonecrosis of the knee (SPONK) and secondary osteonecrosis are poorly understood. A systematic review by Hussain et al concluded that the meniscus plays a central role in the development of the disorder. They hypothesize that meniscectomy and meniscal tears, particularly of the medial meniscus posterior root, increase contact pressures and create an environment conducive to insufficiency fractures. These authors suggest that SPONK would be more accurately described as subchondral insufficiency fractures of the knee. [6]

Trauma may be a causative factor in SPONK. SPONK commonly is seen in elderly women with osteoporosis and may be associated with insufficiency fracture secondary to low bone mineral density in women over 60. [7, 8] See the Fracture Index WITH known Bone Mineral Density (BMD) calculator. Osteoporotic bone is more susceptible to microfracture with minor trauma, which leads to fluid accumulation in the marrow space. The intraosseous edema causes increased pressure within the marrow cavity, which may, in turn, lead to ischemia and necrosis.

Another possible cause may be vascular compromise to subchondral bone, resulting in osseous ischemia and subsequent edema. Again, edema leads to a rise in intraosseous pressure that further compromises blood flow, thus worsening ischemia and necrosis.

Although the etiology of secondary osteonecrosis is unknown, several risk factors are associated with the disease. Corticosteroid use is the most significant risk factor; other risk factors include the following [9] :

The pathogenesis of this condition is poorly understood. One possible mechanism is microvascular disruption in the subchondral bone that causes infarction. This circulatory compromise leads to bone marrow edema, with resultant ischemia and necrosis.

The mechanism by which corticosteroids contribute to osteonecrosis also is unclear. One hypothesis is that an increase in the size of the marrow fat cells decreases circulation and leads to ischemia. Other possible contributors to the etiopathogenesis are coagulopathies, fat emboli, and thrombus formation.



Clinical presentation of spontaneous osteonecrosis of the knee (SPONK) and secondary osteonecrosis is summarized in the following table.

Table. Clinical Presentation of SPONK and Secondary Osteonecrosis (Open Table in a new window)

Physical Characteristic


Secondary Osteonecrosis


Typically >55 y

Typically < 55 y

Sex (male-to-female ratio)



Associated risk factors


Corticosteroids, alcohol, SLE, sickle cell disease, caisson disease, Gaucher disease, fat emboli, thrombus formation

Other joint involvement


Approximately 75%


99% unilateral

Approximately 80% bilateral

Condylar involvement

One (usually medial femoral condyle or either tibial plateau)



Epiphyseal to the subchondral surface

Diaphyseal, metaphyseal, epiphyseal


Commonly, sudden onset of pain and increased pain with weightbearing, stair climbing, and at night

Usually long-standing insidious pain; patient may have symptoms and signs of an underlying disorder, such as SLE


Pain localized to affected area; small synovitis or effusion may occur; ligaments are stable; range of motion may be limited by pain or effusion

Pain is difficult to localize; ligaments are stable; range of motion is grossly intact but may be limited by pain

Differential diagnosis

Osteonecrosis of the knee is commonly mistaken for osteochondritis dissecans, primary osteoarthritis, meniscal tears, bone bruises, transient osteopenia of the knee, and pes anserine bursitis. [10, 11] Therefore, it is important to identify osteonecrosis correctly and to differentiate between SPONK and secondary osteonecrosis, so as to treat each patient appropriately. Spatiotemporal gait analysis has been advocated as a means of distinguishing osteonecrosis of the knee from other knee disorders and determining its functional severity. [12, 13]



Indications for intervention are guided by the clinical signs and symptoms of osteonecrosis combined with radiographic or magnetic resonance imaging findings. A thorough history and physical examination are necessary to recognize associated risk factors and to differentiate spontaneous osteonecrosis of the knee (SPONK) from secondary osteonecrosis. 


Relevant Anatomy

The blood supply to the knee joint comes from two major sources: the descending genicular artery (from the femoral artery) and the popliteal artery. Major branches of the descending genicular artery include the saphenous, deep oblique, and articular branches.

The popliteal artery gives off numerous muscular branches and five major articular branches. These articular arteries anastomose to form extensive collateral circulation around the knee joint.



There are few contraindications to surgical intervention. Cardiovascular or respiratory disease that would compromise the patient's ability to cope with anesthesia must be recognized. Obvious disorders aside (ie, severe systemic disease, sepsis), patients with osteonecrosis of the knee (especially secondary) often are young and have few surgical contraindications.



The prognosis in patients with spontaneous osteonecrosis of the knee (SPONK) relates directly to the size of the lesion. [14]  Aglietti et al reported that lesions greater than 5 cm2 had a worse prognosis than lesions with areas less than 3.5 cm2. [15] Juréus et al reported that six of seven patients with lesions greater than 40% of the anteroposterior radiographic view of the condyle at the time of diagnosis underwent major knee surgery, whereas none of 10 patients with a lesion of less than 20% ever underwent surgery. [16]

The prognosis in patients with secondary osteonecrosis depends on 2 factors: stage and location. In one study, stage I lesions had successful outcomes in 83% of lesions, whereas only 33% of stage IV lesions at presentation had successful outcomes. Lesions that involved the epiphysis of the distal femur fared better than lesions that affected the metaphyseal and/or diaphyseal region. In contrast with SPONK, the size of the lesion has not been a valuable prognosticator. Knees with osteonecrosis in the distal femur and proximal tibia do not do worse than knees with lesions isolated to the distal femur or proximal tibia.