Osteochondral Lesions of the Talar Dome: Cartilage Replacement Using Autologous Chondrocyte Implantation and Allografts

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CHAPTER 14 Osteochondral Lesions of the Talar Dome

Cartilage Replacement Using Autologous Chondrocyte Implantation and Allografts

Gregory C. Berlet, Eric R. Giza

Osteochondral lesions of the talus (OLTs) are rare, representing only about 4% of all such lesions in the body.¹ This lesion also has been called osteochondritis dissecans, transchondral fracture, talar dome fracture, and osteochondral defect. OLTs consist of a focal cartilage deficit with associated reactive bone edema.

Several staging systems have evolved since Berndt and Harty proposed the first system based on radiographic imaging of the talus in 1959 (Table 14-1).² Loomer and colleagues³ reviewed computed tomographic (CT) data of 92 patients with OLTs and found a previously unclassified lesion—the radiolucent lesion—in 77% of the patients in their series. In 1999, Hepple and coworkers,⁴ using magnetic resonance imaging (MRI) added another characteristic to the original classification system—stage 5, subchondral cyst formation.

TABLE 14-1 Staging System Proposed by Berndt and Harty

Stage	Description
Stage 1	Compression of the border of the talus
Stage 2	Incomplete detachment of fragment
Stage 3	Complete detachment, no displacement
Stage 4	Displaced fragment or loose body

From Berndt AL, Harty M. Transchondral fractures (osteochondritis dissecans) of the talus. J Bone Joint Surg Am. 1959;41A:988-1020.

For clarity, most investigators prefer the simplicity of the Berndt and Harty classification system. However, MRI is the imaging modality of choice instead of the plain radiographs used in the original classification description.

NORMAL AND PATHOLOGIC ANATOMY

The talar dome is trapezoidal, 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. Because the chondrocytes are contained in a thick extracellular matrix, they are unable to migrate from uninjured matrix to the zone of injury.

The talus has no muscular or tendinous attachments. Most of the blood supply of the talus enters by the neck through 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 branches from 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 with the posteromedial corner, having a greater depth of cartilage than the anterolateral. This manifests in geographic mechanical properties and may influence the rate and type of articular injury.⁵^–⁷

PATIENT EVALUATION

History and Physical Examination

Patients typically present with chronic ankle pain and various degrees of swelling, catching, stiffness, and instability. Ligamentous instability may be a predisposing factor, and joint laxity should be assessed with the anterior drawer test and with varus and valgus stress. Strength should be assessed by comparison with the contralateral ankle. 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 can include an OLT.

A history of trauma is documented in more than 85% of patients.⁸^–¹² In most cases, the mechanism of injury is an inversion injury to the lateral ligamentous complex. Although the cause 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.¹³

Diagnostic Imaging

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

MRI can identify occult injuries of the subchondral bone and cartilage that may not be detected with routine radiographs.¹⁶^,¹⁷ Classic MRI findings include areas of low signal intensity on T1-weighted images, which suggests sclerosis of the bed of the talus and indicates a chronic lesion.¹⁸^,¹⁹ T2-weighted images reveal a rim that represents instability of the osteochondral fragment.¹⁸^,²⁰ After treatment, MRI should reveal a reduction or disappearance of the low signal intensity on T1-weighted images and the rim on T2-weighted images.

TREATMENT

Indications and Contraindications

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

Surgical repair of OLTs is contraindicated when the risks outweigh the perceived benefits. 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. Studies have shown that a trial of conservative therapy does not adversely affect surgery performed after conservative therapy has failed.¹^,²¹

Treatment Options

The goals of cartilage repair are to restore the articular cartilage surface, match the biochemical and biomechanical properties of normal hyaline cartilage, improve the patient’s symptoms and function, and prevent or slow progression of focal chondral injury.

The approach to the OLT can be facilitated through open or arthroscopic approaches. Most primary interventions are performed with the assist of the arthroscope (i.e., microfracture). Open approaches are indicated for lesions unable to be accessed through the arthroscope or when the selected therapy requires direct access to the lesion.

Arthroscopy of the Ankle

Anterior Ankle Arthroscopy.

Arthroscopic surgery of the anterior ankle allows the direct visualization of intra-articular structures of the anterior ankle joint without an arthrotomy or malleolar osteotomy. The congruency of the distal tibia and talar dome makes arthroscopic visualization difficult through a single portal. The distal tibia is concave in the sagittal plane and convex in the coronal plane. The anterior tibial plafond is slightly convex with a medial notch (i.e., notch of Harty) that recedes approximately 4 mm near the junction of the plafond with the medial malleolus. This is an ideal location for introduction of the arthroscopic instruments. The medial malleolus is approximately 2 cm anterior to the lateral malleolus. Anatomic studies have shown that the tibial plafond covers only two thirds of the talar dome in any position.

Anteromedial and anterolateral portals are the standard approach for anterior ankle arthroscopy. The anteromedial portal is located at the level of the joint line just medial to the anterior tibialis tendon. The notch of Harty allows passage of the arthroscope posteriorly. The saphenous vein and nerve run along the anterior border of the medial malleolus. The saphenous nerve and its branches are usually located lateral to the vein and are at risk with this approach. Staying close to the tibialis anterior tendon minimizes the risk of damage to the saphenous structures.

The anterolateral portal is found just lateral to the peroneus tertius, entering the joint between the fibula and the talus just distal to the joint line. In this location, the lateral and medial branches of the superficial peroneal nerve may be injured if their locations are not carefully identified before a skin incision is made.

Distraction techniques facilitate the placement of the arthroscope and instruments into the tightly configured ankle joint (Fig. 14-1). Noninvasive techniques involving straps, harnesses, and outriggers are distraction methods used most commonly. These techniques minimize the risk of neurovascular injury and other complications.²²

FIGURE 14-1 Ankle arthroscopic setup.

Posterior Ankle Arthroscopy.

Occasionally, posterior lesions are not accessible from the anterior ankle. In these cases, a posterior arthroscopic approach is favored. Through the posterior scope, 54% of the talar dome surface can be visualized and treated.²³

Arthroscopic Débridement with Microfracture.

Arthroscopic treatment of OLTs involves three principles: removing loose bod ies, securing the OLT to the talar dome (i.e., open reduction with internal fixation), and stimulating development of fibrocartilage. Open reduction with internal fixation is reserved for large, acute OLTs. More often, the lesion is débrided to a stable articular rim, and marrow stimulation techniques are used to create the healing cartilage.

The microfracture technique for OLTs is based on the success of similar techniques in the knee (Fig. 14-2).²⁴^,²⁵ Using awls, microfractures (i.e., perforations) are made approximately 3 to 4 mm apart in the subchondral bone while maintaining the integrity of the bone plate. The microfracture technique promotes new tissue formation by releasing substances such as mesenchymal stem cells, growth factors, and healing proteins.²⁴ Ultimately, cartilage-like cells (i.e., fibrocartilage) form and fill the original defect.

FIGURE 14-2 An osteochondral lesion of the talus was drilled to create a fibrocartilage cap.

Tol and associates ²⁶ reviewed 32 studies that reported the results of treatment for OTL. Nonoperative treatment had an average success rate of 45%, whereas the best success rate of 85% was achieved with excision, curettage, and drilling. Posteromedial lesions are difficult to access with this technique. The size of the lesion also plays a role in the success or failure of this procedure. In the meta-analysis by Tol and colleagues,²⁶ the lesion size averaged 0.7 cm; currently, lesions larger than 1 cm are thought to have a less predictable outcome with microfracture.

The limitation of microfracture is that fibrocartilage is created to fill the defect. This is predominantly type I cartilage, which lacks the organized structure of normal hyaline cartilage and therefore has inferior wear characteristics (Fig. 14-3).