Introduction

Osteochondral defects of the talar dome have been documented in the literature under various names since first being described by Alexander Monro in 1738.¹ Perhaps the name we are most familiar with, osteochondritis dissecans (OCD), coined in 1888 by Konig, is an inappropriate term nowadays given the lack of scientific support for inflammation as the causative factor in cartilage separation of talar dome lesions (TDL).² In addition, medical documentation of OCD is often misconstrued as the abbreviation for the mental condition of obsessive compulsive disorder, which can result in medical legal issues if misinterpreted by a third party. The term flake fracture is true in Berndt-Harty stage II, III, and IV lesions, but would be inaccurate as terminology in stage I lesions or subchondral cyst. Osteochondral lesion of the talus (OLT) is perhaps more accurate; however, it fails to address which of the 3 joints of the talus is being referred to. Regardless of antiquated or misleading nomenclature, TDL have increasingly been the focus of interest and training of many foot and ankle surgeons over the past decade.

Why the increased interest in TDL, if statistical literature indicates TDL only accounts for 0.09% of all fractures and only 1% of talus fractures?³ The answer, simply put, is more than 1 in 20 ankle sprains and more than 1 in 4 ankle fractures will develop a TDL, which is a large volume of patients in a foot and ankle specialty practice.² Statistics are based on properly diagnosed cases, and fail to take into account undiagnosed incidence. Hence, the most important treatment aspect of TDL is diagnosis, so that appropriate treatment protocols can be enacted in a timely and stepwise manner. Once diagnosis is made, appropriate treatment with either conservative or surgical management can begin. By being aware of all practical treatment options and their indications, success rates, benefits, risks, and alternative options, foot and ankle specialists will be able to make an informed decision on appropriate care selection after perusing this article.

Anatomy of the talus

It is commonly stated that the talus has poor vascularity, which is not necessarily correct. The vascularity throughout the talus is quite good, but is fragile and compromised easily with trauma, leading to poor healing potential after certain injuries. Arterial supply of the talus is via a combination of small branches from the anterior tibial artery, peroneal artery, and posterior tibial artery. The talus has no muscular coverage and therefore does not receive any indirect arterial supplementation from musculature. Given that the talus is 60% articular cartilage, the remaining surface is covered by less than 40% blood-rich periosteum. Arterial components may be compromised by traumatic events that lacerate, compress, or occlude vessels, which may occur in talar or ankle fracture or subluxation, or be disrupted in surgical incisions and fixation. Such compromise can lead to poor healing of talar bone and cartilage defects, and progress to avascular necrosis.

The talus is the key component of connection of the leg to the foot. The talus is shaped similar to the head of a dog with a long snout. The body of the talus is covered dorsally by a dome covered with cartilage, which articulates primarily with the distal tibia plafond dorsally and medially at the medial malleoli, and to a much lesser degree laterally with the fibula at the lateral malleoli to create the saddle hinge ankle joint. The inferior body of the talus articulates with the calcaneus at the subtalar joint with a combination of cartilage interfaces, the interosseus ligament, and adipose tissue of the Hoke tonsil. Distally the talar head articulates with the navicular in a modified ball-and-socket type joint. Between the talar body at the ankle and the articular head at the talonavicular joint transverses the talar neck. The talus has no muscular or tendinous attachments, but has all pedal extrinsic flexor and extrinsic extensor tendons, and both peroneal tendons passing in close proximity.

The ankle is predominately limited to motion in the sagittal plane only, but under excessive stress or compromise of ligamentous integrity the talus can also experience frontal-plane motion, which can lead to injury of the talus and ankle.

The articular surface of the talar dome is covered with a thin layer of avascular hyaline cartilage that receives nourishment from the articular fluid. Cartilage thickness ranges from 1.11 (±0.28 mm) in women and 1.35 (±0.22 mm) in men on the talar dome.⁴ The hyaline cartilage consist of chondrocytes that lie in groupwise lacunae of the extracellular matrix it produces, composed of collagen, hyaluronic acid, proteoglycans, and a small amount of glycoproteins.⁵

Etiology of osteochondral talar lesions and defects

The proposed causes of TDL have included ischemia, genetics, and infection; however, it is generally believed that trauma is the causative factor in the vast majority of lesions. If trauma is the primary cause of Talar Dome Lesions (TDL), then perhaps TDL can also stand for Traumatic Dome Lesion when appropriate. Ankle fractures have been identified as the primary cause of TDL, followed secondarily by ankle sprains. Ankle instability caused by posttraumatic causes or ligamentous laxity owing to genetic causes may lead to repetitive microtrauma due to ankle joint misalignment, and lead further to TDL development.

Berndt and Harty,⁶ using cadaveric models, were able to recreate TDL and correlate lesion location with causative forces. By dorsiflexing the foot at the ankle and placing the talus in complete contact with the medial and lateral malleoli and tibial plafond followed by applying an inversion force to the foot, they were able to force the talus against its fibular articulation and create lateral TDL. In addition, by plantarflexing the foot at the ankle and placing the posterior aspect of the medial axilla of the talus in direct contact with the tibia by relaxing the collateral ligaments and placing the narrow aspect of the talar dome in the ankle joint by applying an inversion force, they were able to reproduce medial lesions. As a general rule, lateral lesions are located anteriorly and are small, shallow, and wafer-shaped because of shearing force, whereas medial lesions are located posteriorly or centrally and are larger, cup-shaped, and deep, caused by torsional impact.⁷ Because of their shape, lateral lesions are more likely than medial lesions to displace.⁸ Lesions may also be iatrogenically induced during surgical intervention by inappropriately inserted or manipulated arthroscopic equipment, or with internal or external fixation of ankle fractures from malpositioned drills, screws, or pins.

Classification of talar dome lesions

Classically lesions have been classified as 1 of 4 types for the past 50 years, using the Berndt and Hardy classification system based on radiographic findings.⁶ In 2001, Scranton and McDermott⁹ proposed their addition of a stage V lesion to the Berndt and Hardy classification system to describe a cystic lesion. Anderson and colleagues and Ferkel and colleagues^10,¹¹ both developed classification systems using magnetic resonance imaging (MRI). Loomer and colleagues¹² developed a classification system using computed tomography (CT) imaging. Pritsch and colleagues¹³ developed a classification system based on arthroscopic appearance of articular ankle cartilage.

Clinical Examination

The reason TDL are missed in some patients is perhaps because the subjective complaints of pain or ankle limitations expressed by the patient are not matched by significant objective findings recognized by the physician. Clinical examination should follow the key podiatric components of a foot and ankle examination with special care to a few details. In reviewing the vascularity, attention should be directed to identifying excessive edema, particularly when compared with the contralateral uninvolved extremity in both acute and chronic conditions. In acute conditions, bruising and formation of fracture blisters may be present, indicating additional injury such as ankle sprain or fracture. Dermatologic conditions are generally limited or nonexistent except for acute fracture blisters, or skin irritation from shoe gear or bracing owing to ankle instability. Atypical skin presentations may represent either comorbid skin issues, or differential diagnosis such as psoriatic arthritis. Neurologic findings include pain out of proportion for palpation, ambulation, and range of motion. The majority of notable issues will be related to the musculoskeletal examination. Pain with palpation of the anteromedial and anterolateral margins of the ankle joint, and possibly at the posteromedial aspect, are generally found with TDL; however, lack of pain in these areas does not exclude a TDL.² Range of motion actively and passively may have a clicking sound with popping sensation with or without severe pain to the patient, as the fragment or defect catches in the joint, affecting smooth normal motion. Gait analysis may demonstrate limping, guarding, and instability of the affected limb in symptomatic patients. TDL may be asymptomatic or limited in severity, with no clinical manifestations.

Imaging for Talar Dome Lesions

Plain radiography

As with most musculoskeletal injuries or complaints of pain, the initial imaging begins with standard radiographs of the involved area. Scout films should include the standard 3-view ankle and foot. Foot radiographs are used not to evaluate TDL, but rather to evaluate additional injuries or rule out other causative factors, such as fractures of the fifth metatarsal base that may be causing ankle pain. Ankle films may be shot weight bearing or non–weight bearing, depending on patient’s ability to bear weight.

Additional beneficial ankle views may include a 4-cm heel lift, which plantarflexes the foot, allowing for some posterior TDL to be better visualized.¹⁴ Stress inversion and anterior drawer may indicate ligamentous injury and can help confirm the probability of ankle sprain leading to TDL.

Radiographs, however, are limited in their ability to readily identify TDL and may not visualize 30% to 43% of lesions.^3,^14,¹⁵ Plain radiographs are limited by their ability to predominately only visualize osseous bone structures and are not able to visual noncalcified cartilage structures. As a result, TDL that only involve cartilage surfaces may not readily be identified until they progress with time to cause cystic bone lesions to appear as radiopaque lesions. Serial radiographs may be needed with several weeks to months between series before a TDL is evident.