Osteonecrosis is a disease characterized by a derangement of osseous circulation 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]
History of the Procedure
Ahlback et al first reported on osteonecrosis of the knee in 1968.  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.
The etiologies of both spontaneous osteonecrosis of the knee (SPONK) and secondary osteonecrosis are poorly understood.
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. [4, 5] 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 alcohol abuse, sickle cell disease, systemic lupus erythematosus (SLE), caisson disease (barotrauma), and Gaucher disease.  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||SPONK||Secondary Osteonecrosis|
|Age||Typically >55 y||Typically < 55 y|
|Sex (male-to-female ratio)||1:3||1:3|
|Associated risk factors||None||Corticosteroids, alcohol, SLE, sickle cell disease, caisson disease, Gaucher disease, fat emboli, thrombus formation|
|Other joint involvement||Rare||Approximately 75%|
|Laterality||99% unilateral||Approximately 80% bilateral|
|Condylar involvement||One (usually medial femoral condyle or either tibial plateau)||Multiple|
|Location||Epiphyseal to the subchondral surface||Diaphyseal, metaphyseal, epiphyseal|
|Symptoms||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|
|Examination||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|
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. [7, 8] Therefore, it is important to identify osteonecrosis correctly and to differentiate between SPONK and secondary osteonecrosis, so as to treat each patient appropriately.
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.
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 an 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.
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