An osteochondral ankle defect (OCD) is a lesion of the talar cartilage and subchondral bone mostly caused by a single or multiple traumatic events, leading to partial or complete detachment of the fragment (Figs. 11.1 and 11.2) [1].

The defects cause deep ankle pain associated with weight bearing. Impaired function, limited range of motion, stiffness, catching, locking, and swelling may be present [2]. These symptoms place the ability to walk, work, and perform sports at risk.

Symptomatic osteochondral ankle defects often require surgical treatment [3].

A traumatic insult is widely accepted as the most important etiologic factor of an OD of the talus [1].

The injury was classified by Berndt and Harty in 1959 [4].

Ankle sprains cause intra-articular pressure impact and have a prominent role in the development of traumatic OCD. For lateral talar defects, trauma has been described in 93–98% and for medial defects in 61–70% [1].

The trauma causing the lesion can be a single event or a series of less intense (micro) traumas, which may remain unrecognized in some cases.

As not all patients report a history of ankle injury, a subdivision can be made in the etiology of nontraumatic and traumatic defects [2]. Ischemia, subsequent necrosis, and possibly genetics are etiologic factors in nontraumatic OCD [2].

Symptomatic OCDs of the talus usually appear in the second or third decade of life. Men are affected more often than women.

Approximately 1 in 10,000 people per day suffers an ankle injury [2]. Talar OCDs occur in 15–25% of these injuries. These data suggest that OCDs are common but not always cause symptoms [5].

In the acute situation, an OCD of the talus often remains unrecognized since the swelling and pain from the lateral ligament lesion prevail.

When the symptoms of the ligament injury have resolved after some weeks, symptoms of persistent swelling, limited range of motion, and pain on weight bearing may continue. If symptoms have not resolved within 4–6 weeks, an osteochondral defect should be suspected. Locking and catching are symptoms of a displaced fragment [2].

Chronic lesions typically present as persistent or intermittent deep ankle pain during or after activity. Most patients demonstrate a normal range of motion with the absence of recognizable tenderness on palpation and absence of swelling. However, reactive swelling or stiffness may be present [6].

Several factors can play a role in the cause of pain in ODs.

A rise in intra-articular pressure can be a cause of pain in degenerative joint disease [7]. However, it is unlikely that in a localized osteochondral talar defect, a raise in intra-articular pressure plays a role [8]. These patients typically do not demonstrate relevant joint effusion.

Nerve endings can be found in the synovium and joint capsule. Patients with an OD of the ankle, however, generally do not show much synovitis. The synovium of the anterior ankle joint can be palpated since it lies directly under the skin. These patients usually can differentiate this secondary synovial pain from the deep ankle pain caused by the OD. The disabling deep ankle pain on weight bearing cannot be reproduced during physical examination.

The most probable cause of this pain is the nerve endings in the subchondral bone that have been firstly detected in the early 1990s [5, 9] [3].

Pain probably develops as a rise in fluid pressure, and a decrease in pH excitates nerve fibers present in bone [4].

The lesions can either heal and remain asymptomatic or progress to deep ankle pain on weight bearing and formation of subchondral bone cysts [10].

The natural history of osteochondral lesions of the talus whether treated or not is benign [3]. Reports of ankle arthrodesis following ODs of the talus are rare [5].

The cartilage of the talar dome is thin in comparison with the cartilage of other articulating surfaces. The average cartilage thickness of the talar dome is 1.11 (±0.28 mm) in women and 1.35 (±0.22 mm) in men [5].

Braune and Fischer proposed that articular cartilage is thicker in regions of low congruence. Simon et al. related joint congruence to cartilage thickness [11].

Shepherd and Seedhom hypothesized that congruent joint surfaces, such as those in the ankle and elbow, are covered only by thin articular cartilage because the compressive loads are spread over a wide area, decreasing local joint stresses and eliminating the necessity for large cartilaginous deformations. Incongruent joints are covered by thicker cartilage which more easily deforms, thereby increasing the load-bearing area and decreasing the stress per unit area [12].

Ramsey and Hamilton found that a 1-mm lateral talar shift, as occurs after an ankle fracture malunion, reduces the contact area by 42% and a 2-mm lateral shift reduces the contact area by 58% [13]. A 1-mm shift generally is considered acceptable, while a 2-mm shift should be surgically corrected because of the high risk of degenerative changes [13].

Apparently, the talar cartilage can adapt to an increase in contact stress as great as 42%.

Christensen et al. evaluated the effect of talar OCDs graduated in size. Significant changes in contact stresses were demonstrated only for larger lesions (diameter, ≥15 mm) [14].

It has been postulated by van Dijk that the increase in load caused by a small OCD probably is not large enough to cause damage to the remaining cartilage in a normally aligned ankle [5]. However, any varus or valgus malalignment increases the likelihood of cartilage damage by high contact stresses [14].

The consecutive stages of local ODs may help us to understand the development of the defects. Superficial lesions consist of sheared off flakes with an intact subchondral bone plate. In a more severe defect, the subchondral bone is damaged, as with microfractures and bone bruises [9]. The reticular type bone bruise is not continuous with the adjacent articular surface. In general, this type heals normally, and the healing occurs from the periphery to the center.

Subchondral cyst formation (Fig. 11.1) has been hypothesized to be caused by the damaged cartilage functioning as a valve [10, 15]. This valve mechanism would allow intrusion of fluid from the joint space into the subchondral bone, but not in the opposite direction [5].