Introduction
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 2 separate entities: spontaneous osteonecrosis of the knee (SPONK) and secondary osteonecrosis.
Related Medscape topics:
Specialty site Orthopaedics
Orthopaedics News
History of the Procedure
Ahlback et al first reported on osteonecrosis of the knee in 1968.1 The osteonecrosis that Ahlback described now is referred to as spontaneous osteonecrosis of the knee (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.
Related Medscape topics:
Resource Center Arthritis
Resource Center Joint Disorders
Related eMedicine topics:
Lateral Compartment Arthritis
Medial Compartment Arthritis
Frequency
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.
Related eMedicine topic:
Osteonecrosis, Hip
Etiology
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. 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.2 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.
Related eMedicine topics:
Osteoporosis
Alcoholism
Sickle Cell Anemia
Systemic Lupus Erythematosus
Barotrauma
Gaucher Disease
Presentation
Clinical presentation of spontaneous osteonecrosis of the knee (SPONK) and secondary osteonecrosis is summarized in the following table.
Table 1. Clinical Presentation of SPONK and Secondary Osteonecrosis
Open table in new window
Table
| 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 |
| 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 |
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.3,4 Therefore, it is important to identify osteonecrosis correctly and to differentiate between SPONK and secondary osteonecrosis, so as to treat each patient appropriately.
Related eMedicine topics:
Osteochondritis Dissecans
Osteoarthritis
Indications
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 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 branches. 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), patients with osteonecrosis of the knee (especially secondary) often are young and have few surgical contraindications.
More on Osteonecrosis, Knee |
 Overview: Osteonecrosis, Knee |
| Workup: Osteonecrosis, Knee |
| Treatment: Osteonecrosis, Knee |
| Follow-up: Osteonecrosis, Knee |
| Multimedia: Osteonecrosis, Knee |
| References |
| Next Page » |
References
Ahlback S, Bauer GC, Bohne WH. Spontaneous osteonecrosis of the knee. Arthritis Rheum. Dec 1968;11(6):705-33. [Medline].
Zizic TM, Marcoux C, Hungerford DS. Corticosteroid therapy associated with ischemic necrosis of bone in systemic lupus erythematosus. Am J Med. Nov 1985;79(5):596-604. [Medline].
Soucacos PN, Beris AE, Xenakis TH, et al. Knee osteonecrosis: Distinguishing features and differential diagnosis. In: Urbaniak JR, Jones JP, eds. Osteonecrosis: Etiology, Diagnosis, and Treatment. Rosemont, IL: The American Academy of Orthopaedic Surgeons;1997: 413-24.
Williams JS Jr, Bush-Joseph CA, Bach BR Jr. Osteochondritis dissecans of the knee. Am J Knee Surg. Fall 1998;11(4):221-32. [Medline].
Ohdera T, Miyagi S, Tokunaga M, Yoshimoto E, Matsuda S, Ikari H. Spontaneous osteonecrosis of the lateral femoral condyle of the knee: a report of 11 cases. Arch Orthop Trauma Surg. Jul 1 2008;[Medline].
Sakai T, Sugano N, Nishii T, Haraguchi K, Yoshikawa H, Ohzono K. Bone scintigraphy for osteonecrosis of the knee in patients with non-traumatic osteonecrosis of the femoral head: comparison with magnetic resonance imaging. Ann Rheum Dis. Jan 2001;60(1):14-20. [Medline].
Takeda M, Higuchi H, Kimura M, Kobayashi Y, Terauchi M, Takagishi K. Spontaneous osteonecrosis of the knee: histopathological differences between early and progressive cases. J Bone Joint Surg Br. Mar 2008;90(3):324-9. [Medline].
Aglietti P, Insall JN, Buzzi R. Idiopathic osteonecrosis of the knee. Aetiology, prognosis and treatment. J Bone Joint Surg Br. Nov 1983;65(5):588-97. [Medline].
Mont MA, Hungerford DS. Osteonecrosis of the shoulder, knee, and ankle. In JR Urbaniak and JP Jones, eds. Osteonecrosis: Etiology, Diagnosis, and Treatment. Rosemont, IL: The American Academy of Orthopaedic Surgeons;1997: 429-436.
Ficat RP, Arlet J. Necrosis of the femoral head. In: Hungerford DS, ed. Ischemia and Necrosis of Bone. Baltimore: Williams and Wilkins;1980: 171-82.
Ficat RP. Idiopathic bone necrosis of the femoral head. Early diagnosis and treatment. J Bone Joint Surg Br. Jan 1985;67(1):3-9. [Medline].
Ficat RP. [Aseptic necrosis of the femur head. Pathogenesis: the theory of circulation]. Acta Orthop Belg. Mar-Apr 1981;47(2):198-9. [Medline].
Mont MA, Hungerford DS. Non-traumatic avascular necrosis of the femoral head. J Bone Joint Surg Am. Mar 1995;77(3):459-74. [Medline].
Mont MA, Rifai A, Baumgarten K. Osteonecrosis of the Knee, Insall and Scott. Surgery of the knee. 2001;438-456.
Ficat RP, Arlet J. Functional investigation of bone under normal conditions. In: Hungerford DS, ed. Ischemia and Necrosis of Bone. Baltimore: Williams and Wilkins;1980: 29-52.
Ecker ML, Lotke PA. Osteonecrosis of the medial part of the tibial plateau. J Bone Joint Surg Am. Apr 1995;77(4):596-601. [Medline].
Lotke PA, Ecker ML. Osteonecrosis of the knee. J Bone Joint Surg [Am]. Mar 1988;70(3):470-3. [Medline].
Lotke PA, Ecker ML. Osteonecrosis-like syndrome of the medial tibial plateau. Clin Orthop. Jun 1983;(176):148-53. [Medline].
Bayne O, Langer F, Pritzker KP. Osteochondral allografts in the treatment of osteonecrosis of the knee. Orthop Clin North Am. Oct 1985;16(4):727-40. [Medline].
Matsusue Y, Yamamo T, Hama H. Arthroscopic multiple osteochondral transplantation to the chondral defect in the knee associated with anterior cruciate ligament rupture. Arthroscopy. 1993;9:318.
Hangody L, Kish G, Karpatiz. Osteochondral plugs: Autogenous osteochondral mosaicplasty for the treatment of focal chondral and osteochondral articular defects. Operative Techniques Orthop. 1997;7:12.
Koshino T. The treatment of spontaneous osteonecrosis of the knee by high tibial osteotomy with and without bone-grafting or drilling of the lesion. J Bone Joint Surg [Am]. Jan 1982;64(1):47-58. [Medline].
Forst J, Forst R, Heller KD, Adam G. Spontaneous osteonecrosis of the femoral condyle: causal treatment by early core decompression. Arch Orthop Trauma Surg. 1998;117(1-2):18-22. [Medline].
Mont MA, Tomek IM, Hungerford DS. Core decompression for avascular necrosis of the distal femur: long term followup. Clin Orthop. Jan 1997;(334):124-30. [Medline].
Parratte S, Argenson JN, Dumas J, Aubaniac JM. Unicompartmental knee arthroplasty for avascular osteonecrosis. Clin Orthop Relat Res. Nov 2007;464:37-42. [Medline].
Myers TG, Cui Q, Kuskowski M, Mihalko WM, Saleh KJ. Outcomes of total and unicompartmental knee arthroplasty for secondary and spontaneous osteonecrosis of the knee. J Bone Joint Surg Am. Nov 2006;88 Suppl 3:76-82. [Medline].
Marmor L. Unicompartmental arthroplasty for osteonecrosis of the knee joint. Clin Orthop. Sep 1993;(294):247-53. [Medline].
Bergman NR, Rand JA. Total knee arthroplasty in osteonecrosis. Clin Orthop. Dec 1991;(273):77-82. [Medline].
Ritter MA, Eizember LE, Keating EM, Faris PM. The survival of total knee arthroplasty in patients with osteonecrosis of the medial condyle. Clin Orthop Relat Res. Jun 1991;108-14. [Medline].
Mont MA, Myers TH, Krackow KA. Total knee arthroplasty for corticosteroid associated avascular necrosis of the knee. Clin Orthop. May 1997;(338):124-30. [Medline].
Yates PJ, Calder JD, Stranks GJ, Conn KS, Peppercorn D, Thomas NP. Early MRI diagnosis and non-surgical management of spontaneous osteonecrosis of the knee. Knee. Mar 2007;14(2):112-6. [Medline].
Lotke PA, Abend JA, Ecker ML. The treatment of osteonecrosis of the medial femoral condyle. Clin Orthop Relat Res. Nov-Dec 1982;109-16. [Medline].
Banzer W, Hübscher M, Schikora D. Laser-Needle Therapy for Spontaneous Osteonecrosis of the Knee. Photomed Laser Surg. Jul 22 2008;[Medline].
Deie M, Ochi M, Adachi N, Nishimori M, Yokota K. Artificial bone grafting [calcium hydroxyapatite ceramic with an interconnected porous structure (IP-CHA)] and core decompression for spontaneous osteonecrosis of the femoral condyle in the knee. Knee Surg Sports Traumatol Arthrosc. Aug 2008;16(8):753-8. [Medline].
Koshino T, Okamoto R, Takamura K. Arthroscopy in spontaneous osteonecrosis of the knee. Orthop Clin North Am. Jul 1979;10(3):609-18. [Medline].
Miller GK, Maylahn DS, Drennan DB. The treatment of idiopathic osteonecrosis of the femoral condyle with Arthroscopic Debridement. Arthroscopy. 1986;2:21.
Soucacos PN, Xenakis TH, Beris AE. Idiopathic osteonecrosis of the medial femoral condyle. Classification and treatment. Clin Orthop. Aug 1997;(341):82-9. [Medline].
Zizic TM, Hungerford DS. Avascular necrosis of bone. In: Kelley WN, Harris ED, Ruddy S, Sledge CB, eds. Textbook of Rheumatology. Vol 2. Philadelphia: WB Saunders;1985: 1689-1710.
Further Reading
Keywords
osteonecrosis, knee osteonecrosis, osteonecrosis of knee, spontaneous osteonecrosis of the knee, SPONK, secondary osteonecrosis, avascular necrosis, AVN, aseptic necrosis, ischemic necrosis, idiopathic necrosis, knee pain, knee arthritis, bone death, mass bone death, bone disease, necrosis
