Arthroscopic Treatment of Osteochondral Lesions of the Talus

Arthroscopic Treatment of Osteochondral Lesions of the Talus

Steven M. Raikin, MD

John J. Mangan, MD

Dr. Raikin or an immediate family member has received research or institutional support from Zimmer. Neither Dr. Mangan nor any immediate family member has received anything of value from or has stock or stock options held in a commercial company or institution related directly or indirectly to the subject of this chapter.

This chapter is adapted from Raikin SM, Slenker NR: Arthroscopic Treatment of Osteochondral Lesions of the Talus, in Flatow E, Colvin AC, eds: Atlas of Essential Orthopaedic Procedures. Rosemont, IL, American Academy of Orthopaedic Surgeons, 2013, pp 491-497.


Osteochondral lesions of the talus (OLTs) are a common source of ankle pain and instability. They are defined as a defect in the articular hyaline cartilage, predominantly within the weight-bearing area of the talar dome, and with involvement of the underlying bone. Although trauma is implicated in many cases, it does not account for the etiology of every lesion. The etiology of OLTs has been debated since 1888, when König first described “osteochondritis dissecans” of the knee, which he suggested was the result of spontaneous necrosis.1 Talar involvement was then described in 1922 by Kappis,2 who identified a strong association with prior trauma. The initial classification of talar lesions was described in 1959 by Berndt and Harty,3 who proposed an anatomic rationale for the association of these “transchondral fractures of the talar dome” with intra-articular trauma. In their review that included 582 patients with OLTs, a history of ankle trauma was reported in 76% of patients.3 However, the etiology of OLTs in patients without a history of trauma remains unknown. Repetitive microtrauma, vascular abnormalities resulting in osteonecrosis, and congenital factors have been speculated to play a role.

Historically, most OLTs were described as occurring either posterior-medial or anterior-lateral, and there has been a stronger association between lateral lesions and a history of trauma. More recently, Raikin and Elias et al4 developed an anatomic grid that divides the talar dome into nine equal zones. They analyzed MRI examinations of 424 patients with OLTs using this grid and determined that 62% of the lesions were medial and 34% were lateral. More striking was that in the sagittal plane, most of the lesions (80%) were central. They also confirmed an earlier observation that medial lesions were wider and deeper than lateral lesions. This is consistent with the mechanism originally proposed by Berndt and Harty, in which lateral lesions are typically caused by shear between the talus and the fibula that causes shallow, displaced, “wafer-shaped” lesions on the lateral dome of the talus, whereas medial lesions result from torsion and impaction of the tibia on the talus, resulting in deeper, “cup-shaped” lesions.

Symptomatic OLTs typically present with pain, catching, instability, and/or swelling of the ankle. Lesions are commonly seen on radiographic studies but may be incidental findings. Although often nonspecific, a meticulous clinical evaluation is essential to differentiate among the many potential diagnoses, including ligamentous injury, fractures of the fibula, and fractures of the tibial plafond. The index of suspicion should be high in the setting of ankle pain without any recognized trauma or with persistent ankle pain after an acute injury has resolved.


Diagnostic imaging should begin with AP, lateral, and mortise weight-bearing radiographs of the ankle. However, after an acute injury with a nondisplaced lesion, plain radiographs may be unrevealing. A chronic lesion with displacement, osteonecrosis, or cystic change may be clearly evident on plain radiographs. The limitations of radiographs include a low sensitivity, inability to assess the articular cartilage, and an inability to assess the extent of the lesion. MRI has proven to be very sensitive and specific in the diagnosis of OLTs and allows good visualization of the articular surface.5 The benefits of MRI include an accurate assessment of the location and extent of the lesion and the presence of bone marrow edema, which is suggestive of an active lesion, and an evaluation of the vascular status of the fragment. However, excessive edema can sometimes obscure the bony extent of the lesion. Polyaxial CT scanning accurately delineates the bony defect (Figure 1). In clinical practice, MRI is typically obtained before CT to evaluate a patient with unexplained pain because MRI can detect
a variety of pathologic conditions. Frequently, a CT scan is then obtained to characterize bony lesions more fully when the MRI findings are inconclusive.

FIGURE 1 Coronal (A) and sagittal (B) CT scans demonstrate a stage III medial osteochondral lesion of the talus.


The classification system introduced by Berndt and Harty in 1959 remains the most widely used method of describing an OLT.3 It is based on the appearance of the lesion on plain radiographs and includes four stages. Since its introduction, several authors have revised the original classification to include findings on MRI, CT, and arthroscopy. In particular, a fifth and a sixth stage have been added to describe cystic changes and massive-volume lesions, respectively.6,7 The senior author (S.M.R.) has proposed a grading system that is a combination of the various modality-specific systems described previously (Figure 2).

Stage I lesions involve an isolated cartilaginous flap, without subchondral bony compromise. Radiographs and CT scans are usually negative. MRI demonstrates edema in the underlying bone without evidence of fracture. Symptoms are commonly mechanical and include painful catching and giving way of the ankle.

Stage II lesions involve an incomplete or completely nondisplaced fracture of the underlying bone (Berndt and Harty stage I and II). This is often not visible on plain radiographs, but it is clearly discernible on MRI or CT scans. These lesions are stable and unlikely to displace, and they may respond best to nonsurgical treatment.

Stage III lesions are unstable and displaced. The fragment usually remains in its bed or crater, covered by dysmorphic cartilage, and can be balloted arthroscopically. These lesions are clearly visible on plain radiographs, MRI, or CT. Large acute fragments may maintain their vascularity and can potentially be reduced and fixed with a bioabsorbable pin, particularly in the acute traumatic setting. If the fragment is avascular, treatment is by arthroscopic resection, débridement, and microfracture of the lesion base.

Stage IV lesions involve a defect devoid of any remaining bony fragments. The fragments may be free floating within the joint as loose bodies or crushed and no longer present. The lesion base may still be covered by damaged cartilage or unstable fibrocartilage that, in symptomatic cases, should be arthroscopically débrided and the base microfractured.

Stage V lesions are subchondral cysts, often with an intact cartilaginous cap. These have been shown to do poorly with arthroscopic débridement and microfracture.7 Treatment options include retrograde drilling and bone grafting of the lesion (arthroscopic confirmation of an intact and healthy cartilage cap is an essential part of the procedure) or osteochondral autologous transfer.

Stage VI lesions are very large and include either a large surface area of chondral damage and/or a large subchondral cyst communicating with the joint (ie, osteochondral cyst). These lesions are too large to treat arthroscopically or with an osteochondral autologous transfer procedure and require fresh osteochondral allograft transplantation.8,9,10

Feb 2, 2020 | Posted by in ORTHOPEDIC | Comments Off on Arthroscopic Treatment of Osteochondral Lesions of the Talus

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