Osteochondral Lesions of the Talar Dome: Anatomy, Etiology, and Evaluation

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CHAPTER 11 Osteochondral Lesions of the Talar Dome

Anatomy, Etiology, and Evaluation

Steven Mussett, W. Bryce Henderson, Mark Glazebrook, Johnny Tak-Choy Lau

TERMINOLOGY

Pathologic lesions involving the talar dome have been widely reported in the orthopedic literature, along with lesions of the cartilage and subchondral bone. Osteochondritis dissecans was historically described in 1887 as an inflammatory process of the bone cartilage interface that resulted in the loss of structural integrity.¹ This process has also been called osteochondrosis dissecans, and the pathogenesis was thought to be related to repeated trauma or spontaneous focal avascular osteonecrosis, resulting in the loss of structural support for the overlying articular cartilage.² Berndt and Harty³ described the occurrence of talar articular injury in 1959 and attributed the primary cause of the traumatic lesions to these osteochondral fractures. The term osteochondral defect has been loosely used in the literature to refer to defects of the talus with traumatic or atraumatic causes. To encompass all previous terminology, these lesions are referred to as osteochondral lesions in this chapter.

NORMAL AND PATHOLOGIC ANATOMY

Ankle Anatomy and Cartilage Biology

The ankle represents a ginglymus joint, with the saddle-shaped trochlea articulating with the distal tibia. A congruent mortise is formed with the distal tibia and its malleolus and with the lateral malleolus of the fibula. The dome of the talus is trapezoidal, and on average the anterior aspect is 2.5 mm wider than the posterior aspect. Approximately 60% of the talus is covered with articular cartilage, and the thickness varies with location. The thickest area is the medial corner, and the thinnest area is in the lateral gutter.⁴

Topographic studies have shown significant differences in the mechanical properties of human ankle cartilage. Tibial cartilage is significantly stiffer than the corresponding talar articulating cartilage, and the softest tissue is found in the posteromedial and posterolateral talus.⁵ Mean cartilage thickness is inversely related to the mean compressive modulus, with thicker cartilage found medially and thinner cartilage found laterally. These properties may explain the clinically observed findings of osteochondral lesions with repetitive overuse syndromes in medial lesions and acute traumatic events resulting in lateral lesions.

Pathology

Early reports on osteochondral lesions suggested a vascular insult as the primary cause. However, the current consensus supports a traumatic event or repeated insults as the inciting cause. In most cases, a history of trauma can be elicited from the patient. In their original work, Berndt and Harty ³ elicited a history of trauma in 90% of their patients studied. This finding has been reproduced by subsequent investigators.

There appears to be a discrepancy between lateral and medial lesions. Canale and Belding ⁶ retrospectively reviewed 31 osteochondral lesions and found that all of the lateral lesions were related to trauma, whereas only 64% of the medial lesions were related to a significant traumatic event. In a comprehensive review of the early literature, including more than 500 reported cases of osteochondral lesions, Flick and Gould⁷ found that 98% of lateral lesions and only 70% of medial lesions were associated with a traumatic event. These findings support the theory that almost all lateral lesions occur as a result of trauma, whereas most medial lesions are traumatic in origin. The findings also suggest that there is an atraumatic cause for certain patients. In a series of 50 patients, Bauer and Ochsner⁸ reported no history of trauma in 33 patients with deep medial lesions. They also demonstrated deep osteolysis close to the margin of the lesion, suggesting an atraumatic cause.⁸ Reports of medial lesions occurring in identical twins and siblings with no history of trauma and the occurrence of bilateral talar dome lesions in up to 10% of cases further suggest an atraumatic cause in some patients.⁹^,¹⁰

For osteochondral lesions with atraumatic causes, vascular ischemia is thought to be the precipitating factor, but other possible predisposing events may include vascular insufficiency, embolic phenomena, endocrine disorders, or genetic predisposition. It is unknown whether medial talar dome lesions due to acute or repetitive trauma have a natural history different from that of medial dome lesions of atraumatic origin.

INCIDENCE AND CLASSIFICATION

Epidemiology

The incidence of osteochondral lesions depends on the associated cause. Although early studies reported an incidence of osteochondral lesions of 6.5% with ankle sprains, improved imaging techniques and the use of arthroscopy have suggested that the incidence in cases of acute ankle injury is about 70%.¹¹^–¹⁴ The prevalence is increased with associated trauma. Hinterman and colleagues¹⁴ showed that 69.4% of 288 ankle fractures requiring open reduction and fixation had associated talar articular cartilage injury. Leontaritis and coworkers¹³ reported a similar arthroscopic finding; the incidence of chondral injury was 74% in a series of 84 acute ankle fracture patients. The average age of occurrence is usually between 20 and 30 years, with a slight preponderance in men.¹⁵

Frequency of Lesion Location

Lesions of the talus are commonly located in two main areas: anterolateral and posteromedial. Central and posterolateral lesions have been reported, but they remain uncommon.

The biomechanical forces responsible for producing medial or lateral osteochondral lesions were investigated by Berndt and Harty ³ on a small number of cadavers. They were able to replicate these lesions in the laboratory using various combinations of ankle dorsiflexion and plantar flexion combined with inversion of the ankle joint. Lateral osteochondral lesions are caused by inversion with ankle dorsiflexion and subsequent internal rotation of the tibia on the talus, resulting in impaction with the face of the fibula. These lesions are usually shallow and wafer shaped, and they are thought to be caused by a tangential force vector that results in shearing forces.¹⁶ Medial osteochondral lesions occur with inversion and plantar flexion of the foot. These lesions are deeper and cup shaped, factors that are related to impaction of the posteromedial talar dome on the tibial articular surface with a more perpendicular force vector. They tend to be more stable and have less of a tendency to displace compared with the shallower lateral osteochondral lesions.

Medial lesions occur more frequently than lateral lesions. It has been shown in cadaveric studies even without dissection of the lateral ligaments that peak pressures occur at the medial rim of the talus.¹⁷ A biomechanical topographic study has shown that the softest cartilage of the talar dome is found at the most medial and lateral edge of the talus.⁵ Lesions can involve the articular cartilage, underlying subchondral bone, and various depths of cancellous bone of the talus. Occasionally, a cystic component may develop beneath the articular cartilage, and this lesion may be overlooked by the inexperienced arthroscopist.

Classification

The most recognized classification system is that of Berndt and Harty.³ It is unclear from their original paper whether it was based on radiographic imaging or intra-operative findings. However, it has traditionally been adopted as a radiographic staging system (Table 11-1).

TABLE 11-1 Berndt and Harty Classification

Stage	Description
I	Small subchondral compression
II	Incomplete fragment avulsion
III	Complete fragment detachment undisplaced
IV	Complete fragment detachment displaced

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

With the advent of more advanced imaging, various investigators have introduced other classification systems. Ferkel and Scranton ¹⁸ developed a computed tomography (CT) classification system that corresponded with the original Berndt and Harty system and that included information on the amount of subchondral necrosis, cyst formation, and displacement of the fragment. A magnetic resonance imaging (MRI) classification has been introduced by Hepple and associates¹⁹. It includes information on the degree of bone and cartilage injury, amount of displacement, and subchondral cyst formation. The addition of more complicated imaging modalities has added to the description of the location of the lesion and degree of injury but has not changed operative management when the clinical course and chronicity of symptoms are included in the decision-making process. With remarkable foresight, Berndt and Harty³ referred to their classification system as arbitrary. Although it is still the most recognized classification and is useful for research purposes and preoperative planning, the staging of patients has not changed operative management based on intra-operative findings.

PATIENT EVALUATION

History

Patients with an osteochondral lesion usually present with persistent pain in the ankle, which frequently is localized to the side of the lesion. In acute cases, the pain is accompanied by swelling, ecchymosis, and decreased range of motion. In a more chronic presentation, the pain is usually a dull ache in the ankle joint with associated stiffness. Crepitation, tenderness with weight baring and range of motion, mechanical clicking, and recurrent swelling should raise the suspicion of an osteochondral lesion. Uncommonly, the ankle joint may lock because of a loose bony fragment or cartilaginous flap. A thorough history of a traumatic event or instability should be elicited, and if absent, the factors predisposing to possible vascular insufficiency should be sought, including endocrine abnormalities; vascular, hematologic, and coagulation disorders; and any relevant family history. These patients should be questioned about symptoms in the contralateral ankle.

Physical Examination

Results of the physical examination vary, and there is no specific test to diagnose an osteochondral lesion. Inspection of the ankle may demonstrate acute injury with swelling and ecchymosis, or it may appear completely normal, as is often the case with delayed presentations. An attempt to elicit tenderness with palpation should be made by focusing on the common sites of osteochondral lesions. Posteromedial lesions may produce tenderness on palpation when the ankle is dorsiflexed and the region posterior to the medial malleolus is palpated. Anterolateral lesions demonstrate tenderness on palpation when the joint is palpated laterally with the ankle in plantar flexion. These findings are nonspecific because the tenderness is likely related to joint synovitis rather than the lesion itself. The joint should be taken through a range of motion to assess stiffness and to feel for crepitus and mechanical signs of clicking or locking. Ligamentous stability should be assessed to ascertain evidence of laxity, specifically of the lateral complex. The examination is completed with a thorough neurovascular assessment and examination of the contralateral ankle for comparison.

Diagnostic Imaging

Plain radiographs are the initial investigation of choice for a suspected lesion. Anteroposterior, lateral, and mortise views should be obtained on presentation. Radiographs obtained with the ankle in various degrees of plantar flexion and dorsiflexion may help demonstrate posteromedial and anterolateral lesions, respectively (Fig. 11-1).²⁰ Plain radiographs of the other ankle should be obtained to exclude bilateral lesions. Although useful as a primary investigation, radiographs are limited in their ability to demonstrate subtle subchondral cyst formation, and they provide no information on the status of the soft tissue.

FIGURE 11-1 Lateral (A) and medial (B) radiographs show an osteochondral lesion.

CT provides valuable information on the involved bony architecture. Scans in the coronal and axial planes should be obtained for patients with persistent pain, even when initial radiographs appeared normal (Fig. 11-2). Baseline CT scans can accurately diagnose all lesions except for early (stage I) lesions. Information can be obtained on the size and location of bone fragments, the integrity of subchondral bone, and the presence or absence of cyst formation. Intra-articular injection of contrast can add to the diagnostic accuracy of cartilage lesions and provide information on the state of attachment of the osteochondral fragment to the talus.²¹^,²²

FIGURE 11-2 Coronal (A), sagittal (B), and axial (C) computed tomography views show a medial osteochondral lesion.

MRI affords an accurate assessment of the ankle’s soft tissue structures, including the articular cartilage and supporting ligaments. Multiplanar evaluation is possible with no radiation exposure to the patient. Sequences can identify the size and location, and they provide information on the stability of the lesion (Figs. 11-3 and 11-4). DeSmet and colleagues²³ prospectively showed an excellent correlation between staging in MRI and arthroscopy and correctly predicted stable and unstable lesions in 92% of cases. MR arthrography (MRA) has become a useful adjunct to routine MRI and may provide more detail about the osteochondral lesion and afford improved preoperative planning (Fig. 11-5).

FIGURE 11-3 Coronal (A) and axial (B) T2-weighted MRI scans shows a medial osteochondral lesion.

FIGURE 11-4 Coronal, T1-weighted (A) and sagittal, T2-weighted (B) MRI scans show a lateral osteochondral lesion.

FIGURE 11-5 Coronal magnetic resonance arthrography shows a lateral osteochondral lesion.

Bone scintigraphic results correlate with osteochondral injury and can be used to discern which joint is causing clinical discomfort if other imaging modalities have not been helpful in locating the lesion.²⁴ It may also have a role in localizing CT to the specific area of uptake. More advanced imaging has largely replaced scintigraphy, but it still provides a valuable tool in the workup of persistent ankle pain for the surgeon without immediate access to CT or MRI.

Verhagen and coworkers ²⁵ prospectively compared the patient’s history and physical examination, plain radiographs, CT, MRI, and arthroscopy for diagnosing an osteochondral fracture of the talus or tibial plafond in 104 painful ankles with 35 lesions. Plain radiographs had a sensitivity of 70% and a specificity of 94%. CT had a sensitivity of 81% and a specificity of 99%. MRI showed a sensitivity of 96% and a specificity of 99%, whereas arthroscopy showed a sensitivity of 100% and a specificity of 97%. There was no statistically significant difference found between CT, MRI, and arthroscopy. CT had a better positive predictive value than other modalities, and MRI had a better negative predictive value.²⁵ Arthroscopy tended to miss the lesions on the tibial side, so the specificity of this diagnostic modality would like trend closer to 100% if only talar lesions were studied.

TREATMENT

Natural History and Recommended Treatment

The natural history of osteochondral lesions remains controversial because most patients receive some form of nonoperative or operative treatment. In a small series of 10 ankles with osteochondral lesions followed for more than 15 years, 4 of 6 ankles treated nonoperatively failed to heal, but the ankles remained asymptomatic. Osteoarthritis developed in only 2 of 10 ankles and was reported as an uncommon complication.²⁷ Further study by Bruns²⁸ showed that development of osteoarthritis was uncommon and that it occurred only to a mild degree in adult patients with osteochondral lesions.

Most published sources recommend nonoperative treatment for Berndt and Harty stage I and II lesions. Controversy exists for stage III lesions and lesions in the skeletally immature patient. In a systematic review of 210 patients, Tol and associates ²⁹ found a success rate of 45% for nonoperative treatment of stage I and II lesions and medial stage III lesions. This nonoperative intervention included a period of immobilization and limited or no weight bearing.²⁹ Canale and Belding⁶ showed that nonoperative and operative treatment of stage III lesions was equivalent, but the results of operatively treated lateral lesions were superior. This finding likely reflects the fact that medial lesions are deeper and inherently more stable than lateral lesions.

Results of operative treatment are varied and depend on the lesion’s characteristics and the intervention provided. Tol and colleagues ²⁹ found that excision, curettage, and drilling had an 85% success rate, whereas excision and curettage without drilling had a success rate of 78%, a difference that was not statistically significant. Operative intervention is recommended for Berndt and Harty stage III and IV lesions and for smaller lesions with ongoing clinical symptoms. Stage V lesions (cystic) remain controversial, with evidence for and against operative intervention. Shearer and coworkers ³⁰ showed that 71% of these lesions had good or excellent results at an average follow-up of 38 months. They suggested that these lesions usually run a benign course and remain stable with time, and unless progressive enlargement occurs, they do not warrant operative management. In contrast, Scranton and associates⁴¹ suggested that type V cystic lesions have a poorer surgical prognosis, and they suggested that an aggressive surgical approach using osteochondral autografting was more appropriate for patients with large cystic lesions. Concern also exists about the urgency of intervening operatively if nonoperative management fails, but it is generally agreed that delaying operative intervention for a period of up to 12 months does not compromise the results of subsequent surgical treatment.³¹

For skeletally immature patients, most physicians have traditionally recommended a trial of nonoperative management for stage I, II, or III lesions because they retain the propensity to heal. This was disputed by Letts and colleagues ³², who reported a series of 26 lesions followed for a mean of 16 months. They reported good results for only 37.5% of all patients with stage I, II, or III lesions treated with immobilization and protected weight bearing.³² The trend will likely be toward treating skeletally immature patients with the same principles as applied to the adult population, with a trial of nonoperative treatment for stable stage I or II lesions and operative intervention for stages III and IV.

The indications for operative and nonoperative treatment of osteochondral lesions remain controversial because most published series do not provide an accurate description of the size and site of the involved lesions.²⁶ When making treatment decisions, it is important to consider patient characteristics (e.g., age, activity) and lesion characteristics (e.g., size, site, stability, chronicity). Based on these characteristics, a decision can be made to treat with nonoperative regimens or with surgical intervention.

Nonoperative Management

Nonoperative management is aimed at reducing the associated synovitis, relieving pain, and maintaining range of motion. Nonsteroidal anti-inflammatory drugs and physiotherapy together with a period of restricted weight bearing are indicated. During the acute presentation, cast or brace immobilization may be beneficial. The duration of weight-bearing restriction required is not clearly defined because this factor has been poorly controlled in most published series. An injection of local corticosteroid into the joint may help to reduce inflammation, but this effect is temporary and is not routinely recommended. Chondroprotective agents may have some role, but no objective evidence exists to support their use in osteochondral lesions.

Operative Treatment

Operative management of osteochondral lesions is indicated for lesions that have failed nonoperative intervention and for larger, inherently unstable lesions. Many methods of operative management are available, and recommended guidelines continue to be published and presented on a regular basis, although no firm evidence-based guideline exists to aid in the operative decision-making process for osteochondral lesions.

The principles of operative intervention are to relieve pain and restore joint function by the removal of loose bodies, stabilization of the adjacent interface of bone and articular cartilage, and removal of any necrotic subchondral bone at the base of the lesion. The cause of pain in patients with an osteochondral lesion of the talar dome is unclear but probably is related to the presence of loose bodies or to unstable bone margins, because the articular cartilage itself has no nerve innervation. The primary goal of pain relief may be achieved in most patients by débridement procedures combined with some form of treatment of the base to stimulate the formation of fibrocartilage, such as curettage, abrasion, drilling, or microfracture. The secondary goal of prevention of development of degenerative arthritis is more difficult to define because there are no long-term studies to document the prevention of degenerative changes by other forms of articular cartilage replacement or regeneration.

Treatment can be accomplished by open or arthroscopic means, depending on the location of the lesion and the expertise of the surgeon. Operative management includes primary fixation or intervention using techniques of nontissue transplantation or tissue transplantation for the treatment of an irreparable or chronic osteochondral lesion (Table 11-2). Many techniques have been described, and they often are based on the patient’s age and the stage and size of the osteochondral lesion. Am in-depth review of all techniques is beyond the scope of this chapter, but an overview of the available techniques follows.

TABLE 11-2 Surgical Intervention Options

We recommend arthroscopic débridement associated with any technique of subchondral bone penetration (i.e., curettage, drilling, or microfracture) for osteochondral lesion of the talus that is less than 15 mm in diameter (see Fig. 11-1). This approach aims at promoting revascularization of the lesion and creating stability with a healthy rim of attached cartilage and a base of bleeding subchondral bone. Thorough débridement of the degenerative cartilage together with a secondary intervention (e.g., drilling) does make a significant difference in lesion grade over time and is recommended.³³ These techniques are simple, are cost effective, and have shown good results, as reported in the literature for primary and revision procedures. However, the base of the lesion is filled with fibrocartilage, and although this is usually sufficient for smaller lesions, the inferior mechanical properties compared with hyaline cartilage may lead to earlier failure in larger lesions. Other techniques are recommended for larger lesions, but the exact size is controversial. Some surgeons suggests that lesions should be no larger than 1.5 cm² and 7 mm deep and lesions that fail to respond to arthroscopic débridement and subchondral bone penetration.³⁴

For larger lesions and lesions that fail to respond to arthroscopic débridement and subchondral bone penetration, management options include tissue transplantation with autograft tissue (i.e., osteochondral autologous transfer system [OATS] or mosaicplasty) or allograft tissue (i.e., fresh allograft or fresh-frozen allograft). Common guidelines suggest lesions with a diameter of more than 10 mm are best suited to tissue transplantation. OATS and mosaicplasty harvest full-thickness osteochondral plugs from a donor site and implant these plugs into the osteochondral lesion’s site using an interference fit. Donor site cartilage appears to remain as type II collagen with normal articular proteoglycans and microarchitecture. However, the border area of most grafts is filled in with fibrocartilage.³⁵^–³⁷ These techniques have shown good or excellent results (mostly level IV evidence) during short-term to intermediate-term follow-up. Results are less promising in older patients with larger lesions, and concern still exists about donor site morbidity and the considerable mechanical differences between knee and ankle cartilage. The use of osteochondral allografts negates the risk of donor site morbidity but comes with a low risk of disease transmission. Short-term and intermediate-term results with fresh and fresh-frozen allograft transplantation are promising, with most grafts incorporating and functioning reasonably well at long-term follow-up.³⁸

Autologous chondrocyte implantation has gained popularity based on its reported success in treating lesions of the knee. Koulalis and colleagues ³⁹ have reported good or excellent results with no complications for their small series of patients, and Whittaker and coworkers⁴⁰ reported a 90% rate of good or excellent results in their series; the defect was filled in all cases. This method can treat larger lesions and, with careful technique, can address shoulder lesions. However, it is costly, requires staged procedures, and is associated with a longer recovery period. Despite these factors, autologous chondrocyte implantation remains a favorable approach for certain osteochondral lesions involving the talus, such as large, noncystic lesions in younger patients. Autologous stem cells have also been implanted on acellular scaffolds or mixed within the implanted matrix. These pluripotential cells are thought to have the ability to organize and recreate structural tissue, including chondral and subchondral anatomy.

PEARLS& PITFALLS

• The primary cause of osteochondral lesions is trauma, and the incidence is high when associated with an ankle fracture.

• Patients with atraumatic osteochondral lesions warrant workup for secondary predisposing causes.

• Further imaging is recommended for patients with ongoing symptoms after adequate initial management of an ankle sprain.

• Definitive management is based on patient characteristics (e.g., age, activity) and characteristics of the osteochondral lesion (e.g., site, size, stability, chronicity).

• The natural history of these lesions is controversial, but it appears that late development of osteoarthritis is uncommon and, if present, remains mild.

• The incidental finding of an osteochondral lesion in an asymptomatic patient does not require surgical intervention.

• For patients requiring intervention, a thorough assessment of the lesion’s characteristics is required to determine the optimal technique to minimize complications and afford the best possible outcome.