Osteochondral lesions of the talus (OLTs) are rare, representing approximately 4% of all such lesions in the body.¹ These lesions also have been termed osteochondritis dissecans, transchondral fracture, talar dome fracture, and osteochondral defect. OLTs consist of a focal cartilage deficit with associated reactive bone edema. Lesions may extend to subchondral bone, causing bone loss. Following traumatic injury to articular cartilage, the capacity for intrinsic repair is limited by chondrocyte encasement in a matrix, limited vascularity, and chondrocyte apoptosis. Full-thickness injuries that extend to subchondral bone allow recruitment of marrow elements, but injuries greater than 2 to 4 mm show a poor potential to heal with normal appearing cartilage.²

The talar dome is trapezoidal in shape, and its anterior surface averages 2.5 mm wider than the posterior surface. The medial and lateral articular facets of the talus articulate with the medial and lateral malleoli. The articular surface of these facets is contiguous with the superior articular surface of the talar dome. Approximately 60% of the dome of the talus is covered by the trochlear articular cartilage, which is incapable of supporting intrinsic repair. The cartilage is largely avascular and incapable of healing through the typical inflammatory phase.

The talus has no muscular or tendinous attachments, further limiting the healing potential of cartilage defects. Most of the blood supply of the talus enters through the neck via the sinus tarsi. The dorsalis pedis artery supplies the head and neck of the talus. The artery of the sinus tarsi is formed from branches of the peroneal and dorsalis pedis arteries. The artery of the tarsal canal arises from branches of the posterior tibial artery. The sinus tarsi artery and the tarsal canal artery join to form an anastomotic sling inferior to the talus, from which branches enter the talar neck.

The articular cartilage of the talus is inconsistent in thickness, with the posteromedial corner having a greater depth of cartilage than the anterolateral. This is manifest in geographic mechanical properties and may influence the rate and type of articular injury.^{3, 4, 5} Various mechanisms have been suggested by authors to describe the location of OLTs although there is no clear consensus. Raikin et al. examined 428 ankles by MRI and developed a nine-cell grid to describe the location of injuries in the talar dome (Fig. 15-1). They found that both medial (53%) and lateral (26%) defects were most common at the equator or mid talar dome.⁶

Patients with OLT typically present with chronic ankle pain along with variable amounts of swelling, catching, stiffness, and instability. Ligamentous instability may be a predisposing factor and should be assessed. Palpation may reveal tenderness behind the medial malleolus when the ankle is dorsiflexed, indicating a posteromedial lesion. Anterolateral lesions may be tender when the anterolateral ankle joint is palpated with the joint in maximal plantar flexion. An effusion in a chronically painful joint usually indicates intra-articular pathology, which could include an OLT.

A history of trauma is documented in more than 85% of patients.^{7, 8, 9, 10, 11} In most cases, the mechanism of injury is an inversion injury to the lateral ligamentous complex. Although the etiology of nontraumatic OLTs is unknown, a primary ischemic event may be responsible. Nontraumatic OLTs can also be familial, multiple lesions can occur in the same patient, and identical medial talar lesions have occurred in identical twins.¹²

Patients with an acute ankle injury with hemarthrosis or substantial tenderness should first undergo weight-bearing plain radiography in anteroposterior, lateral, and mortise views (Fig. 15-2). Radiographs in varying degrees of plantar flexion and dorsiflexion may help in diagnosing posteromedial and anterolateral lesions, respectively.¹³ Plain radiographs of the contralateral ankle should be obtained, as there is a 10% to 25% incidence of a contralateral lesion.¹⁴

Symptomatic patients with negative findings on plain radiographs should undergo an initial period of immobilization, followed by physical therapy. Patients whose plain images indicate OLTs and patients who remain symptomatic after 6 weeks should undergo additional evaluation with MRI.

Magnetic resonance imaging (MRI) can identify occult injuries of the subchondral bone and cartilage that may not be detected with routine radiographs.^{15, 16} Classic MRI findings include areas of low signal intensity on T1-weighted images, which suggests sclerosis of the bed of the lesion and that it is chronic (Fig. 15-3).^{17, 18} T2-weighted images reveal a rim that represents instability of the osteochondral fragment.^{17, 18, 19} Posttreatment
MRI should reveal a reduction or disappearance of the low signal intensity on T1-weighted images and the rim on T2-weighted images.

Conservative treatment for symptomatic OLTs may be attempted with smaller lesions in the absence of mechanical symptoms. A period of immobilization with weight-bearing restriction and progressive range of motion has been advocated. Studies have shown that a trial of conservative therapy does not adversely affect surgery performed after conservative therapy has failed.^{1, 20} Arthroscopy is indicated for unstable lesions and those that have failed conservative treatment with stable lesions. The initial surgical treatment for most OLTs involves curettage and microfracture using arthroscopic technique. Best results are seen in patients with small lesions (<1 cm²) and stable surrounding cartilage. The lesion is debrided to a stable articular rim with marrow stimulation techniques used to create the healing cartilage. This technique is described in detail later in this chapter.

Surgical repair of OLTs is contraindicated when the risks outweigh the perceived benefits. Patients with advanced osteoarthritis and deformity are poor candidates due to compromised healing potential. Risks include active infection in the operative area, the likelihood of patient noncompliance, and patients who are medically unstable. Relative contraindications include degenerative changes of the ankle involving more than an isolated OLT.

The goals of cartilage repair are to restore the articular cartilage surface, match the biochemical and biomechanical properties of normal hyaline cartilage, improve patient symptoms and function, and prevent or slow progression of focal chondral injury. O’Driscoll²¹ has posited that articular cartilage injury can be restored, replaced, relieved, or resected (the four r’s). Acute restoration is
performed on the rare lesion with a bony defined fragment that is technically repairable. Delamination must not be present and the best candidates are young athletes with good healing potential who are able to comply with weight-bearing restrictions. Techniques include open reduction and internal fixation with recessed transchondral screws, retrograde internal fixation, and biodegradable fixation devices. No large scale studies are available to evaluate these techniques.²² Open reduction, internal fixation (ORIF) is reserved for large acute OLTs and will not be covered here.

Replacing, relieving, or resecting the OLT can be facilitated through open or arthroscopic approaches. Prior to the advent of arthroscopic technology, namely, high-resolution, small-diameter scopes, the open approach was the standard treatment of OLT.²³ Arthrotomies and osteotomies allowed access to the tibiotalar articular surface.

Open treatment for OLT has been well described by Flick and generally requires extensive arthrotomy and dissection.²⁰ Morbidity with these open approaches is often severe, with reported atrophy and stiffness of the ankle, as well as malleolar malunion or nonunion from transmalleolar osteotomies.²⁴ Arthroscopy of the ankle has eliminated many of these complications associated with open approaches.