Fresh Osteochondral Grafting in the Treatment of Osteochondritis Dissecans of the Talus

Mark T. Caylor, MD, Albert W. Pearsall IV, MD


J South Orthop Assoc. 2002;11(1) 

In This Article


In 1888, König[10] removed loose bodies from a patient's knee and subsequently theorized that the causative factor for the fragmentation of the underlying bone was spontaneous necrosis. He coined the term "osteochondritis dissecans" to describe his findings. In 1922, Kappis[11] became the first author to apply the term osteochondritis dissecans to lesions of the talus.

In 1959, Berndt and Harty[1] showed that trauma was the cause of many types of osteochondritis dissecans of the talus. The authors described a mechanism of talar injury and classified these osteochondral fractures into 4 stages: stage I -- a small area of compression of subchondral bone; stage II -- a partially detached osteochondral fragment; stage III -- a completely detached osteochondral fragment remaining in the crater; and stage IV -- a displaced osteochondral fragment. More recently, Canale and Belding[2] confirmed Berndt and Harty's findings that lateral talar lesions are predominantly traumatic in origin. However, Canale and Belding[2] noted that medial talar lesions were not universally associated with a traumatic event. Although various causes have been proposed for these injuries, currently no single theory is universally accepted. Indeed, the gross morphologic characteristics of the two lesions appear to be different.[2,4,5] Medial lesions are frequently dome-shaped, whereas lateral injuries have a wafer-like appearance.[2,4,5] Histologically, both medial and lateral talar osteochondritis dissecans lesions appear identical.[2]

Osteochondral lesions of the talus frequently occur in the second decade of life.[2,4,5] These lesions account for approximately 4% of all reported cases of osteochondritis, with a slight male predominance.[5] Patients are usually young, active adults who initially complain of an ankle sprain. However, after the acute symptoms subside, patients describe continued chronic ankle pain that does not improve. Osteochondral fractures have been reported to occur in approximately 2% to 6% of ankle sprains.[5]

The treatment of osteochondritis dissecans of the talus is based on the classification of the lesion and the degree of symptoms. Operative intervention is recommended for stage III anterolateral lesions and all stage IV lesions.[2] Operative treatment consists of removal of any loose or small fragments. Historically, large fragments have either been fixed with pins or screws or removed, with the base of the lesion curretted down to bleeding bone.[2,3,4] Arthroscopic drilling has also been shown to produce good results in carefully selected patients.[3] Kumai et al[3] evaluated 18 ankles treated by arthroscopic drilling for symptomatic grade II (Berndt and Harty classification) osteochondral lesions of the talus. They reported 72% good results at an average follow-up of 4.6 years; all patients noted improvement in their ankle. The authors concluded that young patients with an early osteochondral lesion, intact cartilaginous surface, and stable osteochondral fragment are excellent candidates for drilling. Older patients and those with longstanding lesions have less potential for healing with this technique even if the cartilage is intact and the fragment stable.[3] However, it has been well documented that osteochondral drilling results in type I fibrocartilage in the defect that is biomechanically inferior to normal type II articular cartilage. It is unclear whether the results observed by Kumai et al[3] will continue with longer follow-up.

In the current case, we used a fresh osteochondral allograft for an isolated Berndt and Harty grade II lesion of the talus. Recently, the use of autologous osteochondral grafting has been reported for osteochondral lesions of the talus.[4,7,8,9] Our technique was similar to that described by Hangody et al,[7] using a medial malleolar osteotomy for exposure of the talus. Care was taken to maintain an anatomic contour to the talus with the transplanted osteochondral plugs. The patient was maintained non-weight-bearing or partial weight-bearing for approximately 3 months and gradually returned to activities thereafter. Findings on postoperative CT and the patient's clinical results suggest complete incorporation of the graft. Although a postoperative biopsy of the recipient site was not done, it appears that the articular surface of the talus has been restored.

In conclusion, we believe that fresh allograft osteochondral grafting of the talus is an excellent technique for symptomatic Berndt and Harty grade II or higher lesion of the talus without significant tibiotalar arthritis. The procedure is technically demanding and should be done only by surgeons experienced in osteochondral transplant grafting. In selected patients, this procedure can provide excellent functional results.