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Osteochondritis Dissecans PDF Print E-mail
Stephen D. Heinrich, MS, MD
Clinical Professor and Surgeon
Department of Orthopedics
The Children's Hospital of New Orleans
New Orleans, Louisiana



Osteochondritis dissecans (OCD), first described by Konig1 in 1988, is an avascular necrosis involving a bone at the osteochondral junction in the epiphysis. The subchondral bone becomes avascular. The overlying cartilage may remain intact or may split, allowing the osteochondral fragment to become partly or completely detached from the joint surface.


OCD of the knee can be divided into a juvenile and an adult form. The prognosis of the former is better than the latter. This lesion is more common in males than females with a 3 to 1 ratio, peaking during the second decade of life. It occurs in 15 to 30 people per 100,000. Bilateral lesions are uncommon (20% to 30%).

The three joints at the most risk for an osteochondral lesion are the knee, the ankle and the elbow. Osteochondral lesions can also occur in the patella, the proximal femur, the carpal bones and the metatarsals. The knee is, by far, the most common site for OCD (75%). The medial femoral condyle is affected approximately 85% of the time. The classic OCD lesion is located in the lateral aspect of the medial femoral condyle within the intercondylar notch (incidence between 62% and 70%).

Differential Diagnosis

Acute osteochondral fractures, chondral delamination, multiple epiphyseal dysplasia and osteonecrosis may mimic OCD. It is important to distinguish these disorders from OCD because each results from its own distinct pathologic process and has a different response to treatment. Acute osteochondral fractures have a vascular base and are more likely to heal than are OCD lesions. The fragment in OCD lesions is avascular and fibrotic with radiographic features similar to a nonunion. Multiple epiphyseal irregularities and abnormal centers of ossification in young patients increase the possibility of multiple epiphyseal dysplasia. Osteonecrosis differs from OCD by its age of onset (50 to 60 years of age), a higher incidence in females than males and its larger lesions that progress over time.


Repetitive microtrauma with altered mechanical stresses, acute trauma, altered vascularity and a genetic predisposition have all been implicated in the pathogenesis of OCD. No one theory clearly explains the origin of all OCD lesions. Some authors believe that OCD results from multiple localized traumatic events (e.g., tibial spine abutting the medial femoral condyle). Airchroth and colleagues2 found that 61% of the patients with osteochondritis dissecans had been involved in sporting activities with repetitive motions. Increased pressure on the lateral aspect on the medial femoral condyle by the patella with knee flexion has also been implicated in the development of OCD lesions. Repeated vigorous exercise, including extreme knee flexion, may produce a rapid increase in the pressure over the medial femoral condyle. This causes an increased risk of subchondral fracture and collapse.

An acute traumatic event may also play a role in the pathogenesis of OCD. Konig was the first to discuss trauma as an etiology for OCD in 1988. A single direct traumatic episode has been found in 46% of patients with OCD lesions in the knee. The higher incidence of OCD in males than females also suggest a traumatic etiology. Other investigations dispute claims of trauma being associated with OCD. Mubarak and Carroll3,4 found no relationship between osteochondritis dissecans and trauma, patella dislocations and hypertrophic tibial spines.

Enniking5 suggested that compromise of the blood supply to the subchondral bone and a poor anastomosis with neighboring vascular systems may play a role in development of OCD. The vascular supply to femoral condyle lacks collateral circulation and has end arterials which makes this area prone to embolic events. The vascular supply is also susceptible to disruption from repetitive trauma.

Genetics may also have a role, although unclear, in the etiology of some OCD lesions. Multiple epiphyseal dysplasia has a genetic basis and should be ruled out in all young patients with OCD. Bilaterality of 20% to 30% suggests either a genetic etiology or predisposed areas that are susceptible the interruption of the blood supply or to mechanical stresses by repetitive trauma.

Natural History

There have been several long-term studies on OCD lesions. Linden6 followed 76 knee joints in patients with OCD for an average of 33 years. He and other authors note that skeletally immature patients with OCD did not develop premature osteoarthritis. Papas7 found that girls younger than age 11 and boys younger than age 13 (classified as Stage I) have an excellent prognosis. Stage II patients were skeletally immature, but had a skeletal age above 11 in females and age 14 in boys. Patients in this group had a guarded prognosis. Patients over the age of 20 years old had a poor prognosis and often needed intervention. Skeletally mature patients with OCD lesions have an increased risk of developing osteoarthritis of the knee joint.

Clinical Presentation

Patients with OCD can be asymptomatic, can have knee pain and swelling or can have locking of the joint when loose bodies develop in the later stages. Pain, if present, is diffuse over the affected joint and worsens with activities. Patients may also have complaints of knee swelling.

Tenderness to palpation can be identified over the affected area. A joint effusion may also be noted. Crepitus may be present with range of motion activities, and quadriceps atrophy is common. Wilson8 described a test for OCD of the knee. With the knee flexed at 90° and the tibia internally rotated, the knee is brought into full extension. Pain elicited at 30° of flexion is suggestive of OCD. Pain is usually relieved with external tibial rotation.

Radiographic modalities used to identify OCD lesions include plain radiography, technetium bone scans, computerized tomography and magnetic resonance imaging (MRI). Plain radiographs should include an anterior-posterior, lateral and tunnel view (knee flexed 20° to 30°). The tunnel view is excellent for delineating the classic lesion on the lateral aspect of the medial femoral condyle. Plain radiographs may also identify loose bodies in the joint. Plain radiographs do not, however, delineate whether or not the overlying cartilage is intact, or the degree of fibrous attachment of osteochondritis fragments to bone.

Technetium bone scans have been used in the past to help make decisions about treatment. There may be increased isotope uptake in OCD lesions that are healing. Four stages for isotope uptake were noted by Cahill and Berg9 using technetium-99 phosphate studies in younger patients with OCD of the knee.

Computer tomography accurately defines the extent of the osseous lesion and the presence of an ossified loose body. Tomographic arthrography can identify disruption of the cartilage overlying the bony lesion. Tomographic arthrography has excellent resolution, comparable to that of MRI. Disadvantages include its high radiation exposure and invasiveness.

MRI is another modality that can be used to assess the integrity of the cartilage overlying OCD lesions. It provides excellent anatomical detail. DeSmet and colleagues10 published several studies detailing the use of MRI for differentiating stable from unstable lesions.

Four MRI signs suggest instability. Dipaolo and colleagues11 characterize four MRI stages)

  • The presence of a high, single intensity line at the interface between the lesion and the underlying bone;
  • Cartilage fractures;
  • Focal cartilage defects; and
  • Underlying cysts.

Stage I is a thickening of the articular cartilage, with low signal changes. In Stage II, the articular cartilage is breached with a low signal intensity rim behind the fragment, indicating synovial fluid between the fragment and the underlying subchondral bone in Stage III. The OCD lesion is detached from its bed in Stage IV. Contrast enhanced MRI has recently been used to distinguish the viability of OCD lesions and to differentiate osteonecrosis from OCD.

Non-invasive techniques have improved our ability to accurately define the extent of OCD lesions without arthroscopy. Despite this, arthroscopy remains the most accurate tool in the evaluation of osteochondritis dissecans.

There are four arthroscopic stages of osteochondral lesions:

  • Stage I: Irregularity and softening of the articular cartilage without fissure of the cartilage.
  • Stage II: The articular cartilage is breached, but the fragment is not displaced.
  • Stage III: The fragment is displaced, but remains attached by an intact remnant of cartilage.
  • Stage IV: There is a loose body in this stage.


Treatment protocols for OCD range from no treatment with periodic observation to surgical intervention. Many factors affect the treatment algorithm, including the size of the lesion, involvement of the weight-bearing surface, location, stage and age at presentation.

The juvenile form of OCD presents before skeletal maturity and has a high rate of healing by conservative measures. Silent lesions noted incidentally on radiographs in the asymptomatic patient do not require treatment. The patient can remain involved in sporting activities as long as he/she remains asymptomatic. Parents and patients should be instructed to return if symptoms are noted. Follow-up radiographs are typically not needed, but can be taken at 6 to 12 months to demonstrate healing.

Conservative measures are used to treat the symptomatic, skeletally immature patient with a non-displaced lesion. These include limitation of sporting activities, protected weightbearing exercises, isometric quadriceps strengthening exercises and symptomatic use of a knee immobilizer. Conservative care should continue for 3 to 6 months or until symptoms resolve. Success of conservative treatment, which occurs in 57% to 91% of cases, is judged by radiographic healing of the lesion in juvenile OCD. Further evaluation may be needed, including a bone scan or MRI, to define the healing and stability of the lesion in refractory cases. If it appears that the lesion has the capacity to heal, further observation and continuation of nonoperative treatment may be warranted. If the lesion is displaced or has shown no capacity to heal, surgical intervention may be needed. Bradley and Dandy12 describe an arthroscopic drilling technique for treatment of refractory OCD lesions. This retrograde drilling resulted in pain relief in all patients and radiographic healing in 9 of 11 knees over the 12 month follow-up period. Children with completely separated and displaced fragments should be treated the same as adults with OCD.

OCD in the skeletally mature patient has a poorer prognosis than in the juvenile. It is, therefore, treated more aggressively. Conservative therapy may be indicated for young adults with stable lesions. The same protocol as described for the juvenile form may be implemented. The exception is the OCD lesion in the classic position on the medial femoral condyle in the knee. These should be treated operatively.

Operative indications include:

  • Failed nonoperative treatment in the juvenile and/or adult;
  • Unstable lesions with the evidence of detachment of the osteochondral fragment;
  • Confirmed avascularity of the subchondral fragment with diagnostic evidence of nonunion; and
  • Symptomatic loose bodies;

Treatment goals include the relief of pain, improved function, healing of lesions and the prevention of long-term sequelae such as osteoarthritis. Operative techniques include: drilling (retrograde or antegrade); curettage and drilling, with and without bone grafting; fixation of unstable fragments (K-wires, cannulated screws, bioabsorbable pins, Herbert screws, bone peg fixation); osteochondral allografts; and osteochondral autografts. All these procedures may be performed arthroscopically or with arthrotomy as indicated.

Stable lesions that have failed conservative therapy can be treated with an arthroscopic retrograde drilling. If an unstable lesion is present, curettage and drilling of the base of the lesion should be undertaken, followed by fixation with a compression screw, a bone peg or pins. In a review of literature, no clear benefit has been noted between different modes of fixation. The critical factor is the stability of the osteochondral fragment in its bony bed after the bed is debrided. If the loose body is removed, curette and drilling of the area may stimulate fibro-cartilage production and improve the prognosis.

Convery and colleagues13 performed osteochondral allografting of the femoral condyle in four patients with OCD. All had good-to-excellent results. One required a repeat allograft secondary to a size mismatch. A perfect press fit osteochondral allograft and a competent ACL are necessary for this procedure to be successful. This technique provides promise for OCD lesions that previously failed operative care, as well as for young patients with large lesions on the weightbearing articular surface. Garrett14 used osteochondral allografts to treat large OCD lesions in the lateral femoral condyle with success. Sixteen of seventeen grafts were viable 2 to 9 years after surgery, and provided the patients excellent relief from their symptoms.

Several authors have recently used autologous grafting from non-weight-bearing articular surfaces to repair osteochondral defects in the knee. No long-term studies have been reported using these techniques. Mueller had good results in a small number of patients in 2- and 4-year follow-ups. The role of autologous grafts in treatment of OCD lesions has not been established.


OCD is an uncommon clinical entity. It is a disease of unknown etiology that involves subchondral fracture. The overlying cartilage may fissure and, in some cases, allow displacement of the OCD lesion, which produces a loose body. OCD lesions, if left untreated, can lead to osteoarthritis. Conservative therapy is the treatment choice for stable OCD lesions. Operative treatment is indicated for unstable lesions, large lesions involving a significant portion of the weight-bearing articular surface, lesions that have shown avascularity and have the appearance of a nonunion by diagnostic testing, and lesions that have failed conservative therapy. Most displaced lesions should be treated with curettage and drilling of the base with or without bone grafting. The osteochondral fragment then should be fixed in stable position wherever possible. Osteochondral allografts offer an alternative in patients with previous failed surgeries for OCD and young patients with large defects in the weight-bearing articular surface. The role of autologous grafting in the OCD is still unclear (Slide 1, Slide 2A and Slide 2B).



  1. Konig F. Veber freie kurper in den Gelenken. Deutsche Zeitschr Chir. 1988; 27:90-109.

  2. Aichroth P. Osteochondritis dissecans of the knee. A clinical survey. J Bone Joint Surg Br. 1971; 53:440-447.

  3. Murbarak SJ, Carroll NC. Familial osteochondritis dissecans of the knee. Clin Orthop Rel Res. 1979; 140:131-136.

  4. Murbarak SJ, Carroll NC. Juvenile osteochondritis dissecans of the knee: Etiology. Clin Orthop Rel Res. 1981; 157:200-211.

  5. Enniking WF, ed. Clinical Musculoskeletal Pathology. Gainesville, Fla: University of Florida Press; 1990:166-170.

  6. Linden B. Osteochondritis dissecans of the femoral condyles. A long-term follow-up study. J Bone Joint Surg Am. 1977; 59:769-776.

  7. Pappas AM. Osteochondritis dissecans. Clin Orthop Rel Res. 1981; 158:59-69.

  8. Wilson JN. A diagnostic sign in osteochondritis dissecans of the knee. J Bone Joint Surg Am. 1967; 49:477-480.

  9. Cahill B. Treatment of osteochondritis dissecans and osteochondritis dissecans of the knee. Clin Sports Med. 1985; 4:367-384.

  10. DeSmet AA, Fisher DR, Burnstein MI, Graf BK, Lange RH. Value of MR imaging in staging osteochondral lesions of the talus (osteochondritis dissecans): Results in 14 patients. Am J Roentgeno. 1990;154:555-558.

  11. Dipaola JD, Nelson DW, Colville MR. Characterizing osteochondral lesions by magnetic resonance imaging. Arthroscopy. 1991; 7:101-104.

  12. Bradley J, Dandy DJ. Results of drilling osteochondritis dissecans before skeletal maturity. J Bone Joint Surg Br. 1989; 71:642-644.

  13. Convery FR, Meyers MY, Akeson WH. Fresh osteochondral allografting of the femoral condyle. Clin Orthop Rel Res. 1991; 273:139-145.

  14. Garrett JC. Osteochondritis dissecans. Clin Sports Med. 1991; 10:569-593.

  15. Garrett JC. Treatment of osteochondral defects of the distal femur with fresh osteochondral allografts: A preliminary report. Arthroscopy. 1986; 2:222-226.

  16. Garrett JC. Fresh osteochondral allografts for treatment of articular defects in osteochondritis dissecans of the lateral femoral condyle in adults. Clin Orthop Rel Res. 1994; 303:33-37.


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