DEFINITION, STAGING, CLINICS

OCLs are articular injuries of the subchondral bone and the overlaying cartilage. Because of the still unclear natural history of OCLs, several terms can be found for this entity to date in the literature, for example, osteochondritis dissecans, osteochondral fracture, flake fracture, and others. Because currently there is no proof for an underlying inflammation, the traditional term osteochondritis dissecans introduced by König¹ in 1888 should be abandoned. Furthermore, the term transchondral/osteochondral/flake fracture may be meaningful only in traumatic cases. To include all these causes and others, for example, idiopathic osteonecrosis, the term osteochondral lesions (OCLs) provides the most cautious terminology.

The traditional staging system for OCLs of the talus is the Berndt and Harty² classification based on radiographic findings. This classification consists of the following stages of an osteochondral talus fragment: stage I, small compression area; stage II, incomplete avulsion of a fragment; stage III, complete avulsion without displacement; and stage IV, avulsed fragment displaced within the joint. The Berndt and Harty classification has the advantage of being popular, but it does not accurately reflect the integrity of the articular cartilage. The Ferkel and Sgaglione³ classification is a CT-based classification describing fragmentation, osteonecrosis, and cyst formations (stage I-IV). Anderson and colleagues⁴ described an MRI-based classification including the bone marrow edema. Last, a commonly used arthroscopic classification is the OCL classification of the International Cartilage Repair Society.⁵

Epidemiologically, the ankle registers 4% of all the human osteochondral defects.⁶ The cause of OCLs of the talus has multiple facets. However, it can be subdivided into a traumatic and nontraumatic cause. Trauma plays the most important role in the pathomechanism of talus OCLs. Overall, more than 80% of the talus OCLs are of traumatic origin.^7,8 In such traumatic cases, the acute OCLs are frequently located on the lateral dome of the talus (anterolateral) (Table 71-1). Hereby, the most common reasons are a severe inversion ankle sprain, chronic ankle instability (CAI; causing in 5–9% of the cases a lateral talar OCL),^9,10 or a fracture mechanism. However, medial lesions are more common than lateral OCLs. In these cases, the most affected area is the posteromedial talar dome (see Table 71-1). On the basis of repetitive microtraumas, avascular necrosis, genetics, endocrinic reasons, or systemic reasons, the nontraumatic causative agent with osteonecrosis represents to date still an unclear pathomechanism of chronic OCLs (longer than 2 months). Here, one should be alert on not missing a radiologically correlating hindfoot malalignment (hindfoot varus or valgus) that could explain the overload on the painful OCL joint region. In many cases, a causative agent cannot be traced and remains “idiopathic.”

An untreated OCL represents a local osteoarthritis model because of the altered joint biomechanics. Hereby, a traumatic osteochondral defect (flake fracture) or pathologic chronic shear forces (CAI¹¹) cause damage of the superficial layer of the cartilage, and with time deep cracks and degeneration of the cartilage. Subsequently, joint fluid pumps into the subchondral bone and creates painful cysts and large-area cartilage lifting. At the end, OCL fragments can break off and dislocate all over the joint.

Patients with OCLs of the talus typically report chronic ankle pain, joint stiffness, ankle swelling, snapping, giving way, and weakness. The patients, usually of young age (mean age in a meta-analysis on 734 patients, 26.9 years),¹² are substantially limited in their daily life, in their sports activities, and have a reduced sports level. Many of them lose their sports career or even jobs by disability.

Clinical examination should document patient history and include physical examination. Patients may report ankle sprain or CAI. Other predisposing factors may be a periarticular fracture or severe ankle trauma. Patient history should further include systemic risk factors, as causative factors of avascular necrosis, systemic diseases, and others. Clinically, OCL ankle joints show, in almost all cases, a swelling and effusion. Tenderness may be triggered on the affected ankle side (lateral, medial) or periarticular. Regarding the ligament instability, one may find pathologic signs for lateral ankle instability (anterior drawer test, inversion tilt test), medial ankle instability (eversion tilt test), or a combination of both (rotational ankle instability). Furthermore, hindfoot malalignment (hindfoot varus or valgus) and foot deformity (pes planovalgus, cavovarus, etc.) should be checked.

The diagnostics of OCLs of the talus include first conventional weight-bearing radiographs of the ankle joint, anteroposteriorly and laterally. Radiographs provide information on the OCL location and stage only if the x-rays hit the OCL perpendicular, that is, if the OCL lies on the highest point of the talar dome. Radiographs further provide information on possible osseous predisposition for CAI, which represents a possible causative factor of OCL in the ankle joint.

With CT, the stages described by Berndt and Harty can be better defined, OCL cysts and fragments better visualized, and the integrity of the subchondral bone better analyzed. The CT scan is therefore a valuable diagnostic for preoperative planning. MRI provides complementary information, for example, the status of the OCL overlaying cartilage, information on bony edema, and the situation of the ligaments. Scintigraphy showed to be useful in evaluating OCLs when radiographs appear to be normal.^4,13 Addressing the lack of anatomic accuracy of the classic scintigraphy, a new diagnostic tool for OCLs emerged: the SPECT-CT. The SPECT-CT combines data of the scintigraphy and CT scan and fuses it to one picture: SPECT providing the activity and metabolic rate of the OCL surrounding bone, and the CT the precise anatomic localization (Fig. 71-1). Lastly, diagnostic ankle arthroscopy remains a reliable diagnostic tool, allowing direct and dynamic examination of the talus OCLs and the ankle-stabilizing ligaments.¹⁴

FIGURE 71-1 Osteochondral lesion of the talus. Series shows the case of a 25-years-old man, a sports and physically active patient, with chronic ankle pain, a lateral talus osteochondral lesion (OCL), and chronic ankle instability. Radiographs (A, B) showed a suspicious area on the lateral talar dome. Further diagnostic was performed using the single-photon emission computed tomography-computed tomography (SPECT-CT; combination of scintigraphy and CT) (C–E). The SPECT-CT and diagnostic arthroscopy confirmed a lateral talus OCL stage III-IV with cystic lesions (C–F). (C–F, if in color, the SPECT-CT would have a red spot over the OCL) Therapy consisted of debridement, microfracturing (G), autologous bone transplantation (H), and treatment by “autologous matrix-induced chondrogenesis” (AMIC; bilayer collagen membrane; Geistlich Pharma AG, Wolhusen, Switzerland) (I, J). Further surgical treatment included the elimination of the OCL risk factor, chronic ankle instability, by lateral and medial ligament repair. About 6 months after osteochondral reconstruction, the patient is pain free, has an excellent function, and is back to daily life (job, sports).

TREATMENT OPTIONS

The conservative treatment of OCLs of the talus is limited for stages I and II only. Success rates for nonoperative treatment with sports restriction and nonsteroidal anti-inflammatory drug or cast immobilization differ from 0% to 100% (review article¹²). A meta-analysis on 201 patients proved a 45% success rate of conservative treatment for stages I and II, as well as medial stage III talus OCLs.¹⁵ Whereas acute lesions seem to do worse (0% success rates in acute transchondral fractures¹⁶), chronic lesions show different success rates between 41% (cast immobilization¹²) and 59% for restriction of activities, but free range of motion.^17,18 Young patients seem to do better with conservative treatment than aged patients. Bruns and Rosenbach¹⁹ showed 85% excellent and good results in patients 16 years and younger in comparison with 65% in adults, with 8% failure in each group only (Level IV evidence).¹⁹ These results are also confirmed by Higuera and coworkers (Level IV).²⁰ In long-term, persistent, radiologic irregularities were found in 38% (Level IV).²¹ Shearer and coworkers²² managed even high-grade cystic lesions nonsurgically (Level IV).²² However, after 38 months of follow-up, 18% of patients had to be transferred to ankle arthrodesis.

In most of the conservatively treated OCL cases, the pain remains untreated and the disease advances to further stages. Berndt and Harty² reported in 1959 that nonoperatively treated patients obtained poor results, and that good results were registered in 84% of the cases after surgical treatment (Level IV). Surgical treatment of OCLs traditionally includes excision of loose bodies, debridement of the area, and drilling or microfracturing. This surgery may be performed open or arthroscopically. The arthrotomy may sometimes require a medial or lateral malleolar osteotomy, grooving of the anteromedial distal tibia, or an osteotomy of the anterolateral tibia to reach the involved OCL talus region. As an alternative or as an addition to the open technique, ankle arthroscopy allows, beside a good diagnostic visualization of the OCLs, a minimal invasive therapy avoiding the high morbidity of an extensive arthrotomy or malleolar osteotomy. The treatment of OCLs of the talus includes a primary (as fixation of a flake fracture in traumatic cases) or a secondary repair (surgical treatment of chronic OCLs). The different options for secondary repairs depend on whether the OCL is predominantly a problem of the chondral layer, the osseous part, or a combination of both, on the age of the patient and the size of the OCL (Tables 71-2 and 71-3).

TABLE 71-3 Surgical Principles of Osteochondral Lesions of the Talus