Disclosure Osteonecrosis is a disease characterized by a derangement of osseous circulation leading to actual necrosis of osseous tissue. Osteonecrosis of the knee has been divided into 2 separate entities, spontaneous osteonecrosis of the knee (SPONK) and secondary osteonecrosis. 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 SPONK. Problem: 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. Frequency: The knee is the second most common site for osteonecrosis, and it is affected much less often than the hip. True incidence of the disease is unknown, but osteonecrosis of the knee is believed to account for approximately 10% of cases of osteonecrosis. Etiology: The etiology of SPONK is poorly understood. A possible causative factor may be trauma. SPONK commonly is seen in elderly women with osteoporotic bone. Osteoporotic bone is more susceptible to microfracture with minor trauma, which leads to fluid accumulation in the marrow space. The intraosseous edema leads to increased pressure within the marrow cavity and may lead to subsequent ischemia and necrosis. Another possible cause may be vascular compromise to the 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. The etiology of secondary osteonecrosis is unknown. However, several risk factors are associated with this disease. Corticosteroid use is the most significant risk factor. Other risk factors include alcohol consumption, sickle-cell disease, systemic lupus erythematosus (SLE), caisson disease, and Gaucher disease. The pathogenesis for this condition is poorly understood. A possible mechanism is microvascular disruption in the subchondral bone, which causes infarction. This compromise of circulation leads to bone marrow edema and resultant ischemia and necrosis. The mechanism by which corticosteroids contribute to osteonecrosis also is unclear. A possible hypothesis is an increase in size of the marrow fat cells, which leads to decreased circulation and ischemia. Other possible contributors to the etiopathogenesis are coagulopathies, fat emboli, and thrombi formation. Clinical: Clinical presentation is summarized in the following table. Table 1. Clinical Presentation of SPONK and Secondary Osteonecrosis
Differential diagnosis Osteonecrosis of the knee commonly has been mistaken for osteochondritis dissecans, primary osteoarthritis, meniscal tears, bone bruises, transient osteopenia of the knee, and pes anserine bursitis. Therefore, it is important to identify osteonecrosis, to differentiate between SPONK and secondary osteonecrosis, and to treat each disease appropriately.
Clinical signs and symptoms of osteonecrosis combined with radiographic or magnetic resonance imaging examination findings of osteonecrosis lesions indicate the need for intervention. A thorough history and physical examination are necessary to recognize associated risk factors and to aid in differentiating SPONK from secondary osteonecrosis.
Relevant Anatomy: Blood supply to the knee joint comes from 2 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 branch. The popliteal artery gives off numerous muscular branches and 5 major articular branches. These articular arteries anastomose to form extensive collateral circulation around the knee joint. Contraindications: 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), those afflicted with osteonecrosis of the knee (especially secondary) often are young and have few surgical contraindications. |
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Lab Studies:
Imaging Studies:
Other Tests:
Diagnostic Procedures:
Macroscopic pathology Early in the disease, there may be slight discoloration and flattening of the articular cartilage. As the disease progresses, a line of demarcation becomes evident, and an osteochondral flap overlies the area of osteonecrosis. Late in the disease course, secondary arthritic changes occur, leading to a defect in the cartilage filled with necrotic debris and signs of osteoarthritis (eg, osteophyte formation, eburnated bone). Microscopic pathology On microscopic examination, a specimen of osteonecrotic bone shows empty lacunae and fatty degeneration within the center of the lesion. The surrounding area shows evidence of osseous healing, including osteoblastic activity, fibrovascular granulation tissue, and cartilage formation.
For secondary osteonecrosis, Mont and Hungerford developed a staging system that is a modification of the Ficat and Arlet staging of osteonecrosis of the hip.
Medical therapy: Several nonoperative and operative treatment options exist for osteonecrosis of the knee. SPONK and secondary osteonecrosis can be treated nonoperatively when the patient is asymptomatic. However, once the patient is symptomatic, treatment options for the 2 entities differ. Nonoperative treatment has shown to produce good results in patients with SPONK. This encompasses a conservative regimen of protected weightbearing with crutches, analgesics, nonsteroidal anti-inflammatory medications, and physical therapy focusing on strengthening the quadriceps and hamstrings. Lotke et al reported on 87 knees with SPONK. Thirty-six of these knees were treated nonoperatively, with only 1 progressing to arthroplasty. The 35 remaining knees did well. Outcomes of this nonoperative regimen in secondary osteonecrosis are relatively poor. One study of 51 knees with secondary osteonecrosis treated nonoperatively reported that eventually, 31 knees required arthroplasty. Nonoperative treatment has shown poor results in secondary osteonecrosis. Therefore, operative therapy usually is used once the patient is symptomatic. Pharmacotherapy has been attempted with mixed results. Medications are aimed at attacking the pathophysiology of the disease. Examples include nifedipine and lipid-lowering agents, such as Lopid. Surgical therapy: Arthroscopy Arthroscopic debridement for treatment of osteonecrosis of the knee has had mixed results. Arthroscopy may not alter the natural course of the disease. Patients with SPONK may have degenerative tears of the menisci. Debridement of these tears does not improve osteonecrosis of the bone. Partial meniscectomy actually has been hypothesized to possibly cause further degeneration of the knee joint. Arthroscopy is controversial, with questions arising about the possibility of increased interosseous pressure. Osteochondral grafts Reports regarding results with osteochondral allografts have been discouraging for both SPONK and secondary osteonecrosis. Bayne et al used fresh allografts in 6 knees with SPONK, resulting in only 1 good result. The authors suspect that these poor results were due to the poor compliance of elderly patients, resulting in fragmentation of the allograft. The 3 knees with steroid-induced secondary osteonecrosis also failed the grafting procedure. This may be due to continued use of corticosteroids, which may lead to poor vascularization of the graft and subsequent subsidence. Some surgeons have focused on using osteochondral autografts. This procedure, commonly referred to as an OATS (osteochondral autologous transfer system), was first introduced by Matsusue in 1993. Using this procedure, Hangody et al reported a 2-5 year follow-up with good or excellent results in up to 90% of cases. Use of other grafting methods may improve results, but further studies are required. High tibial osteotomy High tibial osteotomy (HTO) has been used in patients with SPONK with encouraging results. Aglietti et al described 31 patients treated with high tibial osteotomy, with 21 of these knees having ancillary bone grafting. Of the 31 knees, 87% had excellent to good results at a mean follow-up of 6.2 years, and only 2 knees progressed to arthroplasty. Use of high tibial osteotomy in secondary osteonecrosis is limited because most of these patients have bicondylar femoral involvement and also may have tibial involvement. Core decompression The principal behind core decompression is reduction of interosseous pressure, thereby restoring adequate circulation. This procedure has been used with some success in the earlier stages of osteonecrosis. Core decompression is a relatively lesser procedure than total knee arthroplasty, and it has been shown to delay the need for joint replacement. Core decompression has been used with some success in SPONK. Forst et al achieved successful outcomes with core decompression of the femoral condyle in precollapsed lesions in their study of 16 knees. Results have not been as encouraging with SPONK as in secondary osteonecrosis. Therefore, it should be reserved for refractory cases. Mont et al reported on 79 knees that were treated for secondary osteonecrosis. Forty-seven knees were treated with core decompression, and 32 were treated nonoperatively. For core decompression, clinical success was achieved in 73% (34 of 47) of knees (good to excellent Knee Society Scores) at a mean follow-up of 11 years (range of 4-16 y). Radiographically, seventeen of the 47 (36%) knees progressed to Ficat and Arlet stage III or IV, as opposed to 24 of 32 knees (75%) treated nonoperatively. Unicondylar (unicompartmental) knee arthroplasty Unicondylar arthroplasty has been used with success in SPONK, as the disease usually is confined to 1 condyle (see Image 3). This procedure is not, however, recommended for secondary osteonecrosis, as the disease can affect both condyles. Marmor reported an 89% success rate in a study of 34 knees with medial femoral condyle osteonecrosis treated with unicondylar replacement. Total knee arthroplasty Knee arthroplasty is indicated in the late stages of the disease, when patients have severe pain that does not respond to other treatments (see Image 4). Total knee arthroplasty is an appropriate intervention for late-stage secondary osteonecrosis with degenerative changes, for patients with severe pain, or for those with functional disability. It has had varying success with SPONK. Bergman and Rand reported that 87% of 38 knees treated with total knee arthroplasties had excellent or good results. Of those knees, 27 had SPONK, and 9 had secondary osteonecrosis. These results were inferior to those of total knee replacements performed for other diagnoses. Ritter et al compared 32 knees with SPONK to 63 osteoarthritic knees. The success rate was 82% in SPONK knees, and no statistical significance of success rates exists between the 2 groups. For secondary osteonecrosis, Mont et al reported on 31 knees treated with total knee arthroplasty; all of these patients had a history of corticosteroid use. After 8.2 years mean follow-up, results were 55% excellent to good. Preoperative details: Core decompression Determining areas of pain on the tibia and/or femur is essential. The lesion should be delineated carefully on MRI examination to determine which areas need to be cored and to determine extent of involvement. Intraoperative details: Core decompression Intraoperatively, when coring the knee, a tourniquet is applied but rarely is inflated. For femoral coring, a small incision is made on the lateral or medial side under fluoroscopic control, just above the flare of the condyle (see Image 5). Then, a 3- to 6-mm Michelle trephine is inserted through the metaphyseal flare into the lateral and medial condyles up to within a few millimeters of the subchondral plate. For tibial coring, the trephine is introduced through a small incision just medial to the tibial tubercle, being sure to avoid the medial saphenous nerve. The trephine then is guided into the medial and lateral plateaus. It is helpful to turn the trocar while advancing it within the bone to clear the teeth and obtain the best biopsy possible. Postoperative details: Core decompression Fifty percent weightbearing with a cane or crutch for 6 weeks is advised, after which the patient may return to full weightbearing. Follow-up care: For excellent patient education resources, visit eMedicine's Foot, Ankle, Knee, and Hip Center, Breaks, Fractures, and Dislocations Center, Arthritis Center, and Bone Health Center. Also, see eMedicine's patient education articles Knee Pain, Knee Injury, and Knee Joint Replacement.
Core decompression Complications are minimal when the surgeon is experienced. The operation causes minimal blood loss and is a quick procedure. Possible complications may include infection, fracture, and possible failure of the procedure to alleviate symptoms. Total knee arthroplasty Although more extensive compared to core decompression, this is a relatively safe and effective procedure. Possible problems include, but are not limited to, reactions to anesthesia, deep venous thrombosis (DVT), injury to a nerve or blood vessel (peroneal nerve palsy), fracture, infection, swelling, and dislocation of the patella.
Studies have shown the prognosis of SPONK to be directly related to the size of the lesion. Aglietti et al reported that lesions greater than 5 cm2 had a worse prognosis than lesions with areas less than 3.5 cm2. Lotke et al reported that lesions occupying greater than 50% of the femoral condyle have a worse prognosis. Prognosis also has been shown to be worse in advanced stage lesions. Prognosis of secondary osteonecrosis is dependent on 2 factors, stage and location. In 1 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. As opposed to SPONK, size of the lesion has not been a valuable prognosticator. Knees with osteonecrosis in the distal femur and proximal tibia did not do worse than those knees with lesions isolated to the distal femur or proximal tibia.
Atraumatic osteonecrosis is characterized by a poorly understood derangement of osseous circulation. There are no proven causes, only associated risk factors. Systemic corticosteroids and alcohol abuse continue to be the most common associated factors. Perhaps, future treatment modalities will reverse the pathophysiology of the disease, rather than merely stopping progression or palliating symptoms. The role of core decompression in atraumatic osteonecrosis has been questioned. However, many patients do feel immediate relief after the procedure, and it also may halt the progression of the disease. Core decompression is also a less invasive operative procedure than a total knee arthroplasty.
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