Articular Cartilage Defects of the Ankle

Articular Cartilage Defects of the Ankle




Articular cartilage lesions continue to be a challenging problem for the orthopedic community. The growth of athletic participation and an increase in active individuals across all age groups have necessitated the development of improved strategies to treat symptomatic osteochondral defects. Despite significant advances in cartilage restoration over the previous decade, we still have not discovered the “gold standard” to repair damaged cartilage back to its native form. Current treatment options have yielded inconsistent results secondary to the inferior biomechanical properties that result from a variable healing response. However, with improved technology and the advancement of surgical techniques, we are now, more than ever, able to treat these lesions effectively. This chapter will focus on the basic science, etiology, diagnosis, and treatment of osteochondral lesions of the talus (OLT) and tibia.


A distinct knowledge of the unique and complex structure of articular cartilage is essential in order to understand the various treatment options. Articular cartilage possesses a unique biphasic viscoelastic property that provides a smooth, low-friction surface that transmits variable loads across the joint and minimizes the peak stress on the underlying subchondral bone. Although many subtypes of collagen exist in small amounts, hyaline cartilage is predominately comprised of type II collagen. Negatively charged side chains, such as keratin and chondroitin sulfate, result in a high affinity for water. This property helps resist compressive loads and makes articular cartilage particularly biomechanically efficient in compression.

The zonal organization of hyaline cartilage creates its unique and complex biomechanical profile. The superficial zone provides resistance to shear forces and protects deeper layers. Hyaline cartilage in this zone consists of flattened chondrocytes and tightly packed type II collagen fibers that are oriented parallel to the surface. The intermediate or transitional zone not only resists compressive forces but also provides a transition between the shear forces and compressive forces that are transmitted to the superficial and deep layers, respectively. The deep zone or layer of hyaline cartilage primarily resists compressive forces as collagen fibers are oriented perpendicular to the surface. A calcified area called the tidemark is a basophilic line, which straddles the boundary between the calcified and uncalcified cartilage (Fig. 9-1).

Despite hyaline cartilage’s exquisite ultrastructure, it’s avascularity and limited access to the underlying subchondral bone result in the inability to repair or regenerate after injury. Partial-thickness injuries that do not penetrate the subchondral bone have a limited vascular response and, thus, possess a minimal healing response to injury. The vascular access to bone marrow that occurs with osteochondral lesions provides cellular migration of progenitor cells, growth factors, and cytokines, resulting in a reparative fibrous, fibrocartilage mosaic. Despite a more “normal” response to injury, the resulting repair tissue has inferior biomechanical properties and poorer wear characteristics than native hyaline cartilage.11

FIGURE 9-1. Cross-sectional, schematic diagram of the cellular organization of healthy articular cartilage.

Although the ultrastructure of hyaline cartilage is universal, properties unique to the talus and tibia result in different biomechanical properties compared to other major joints in the body. In a recent study, Sugimoto et al. studied cartilage thickness of the talar dome. The average thickness of articular cartilage was 1.35 mm in men and 1.11 mm in women. The thickest area was the medial corner of the talus, while the thinnest was the lateral gutter.12 Several investigators compared human cartilages of the ankle and knee. Interestingly, the ankle cartilage was more resistant to osteoarthritis than cartilage in the knee. It is theorized that this is a result of the thinner, stiffer, and less permeable properties of ankle cartilage. In addition, ankle chondrocytes possess the ability to up-regulate matrix synthesis and produce more glycosaminoglycans and protein than those in the knee joint. These inherent properties create a unique environment within the ankle joint and contribute to the specific injury patterns seen as will be discussed later in the chapter.13


Injuries to the talar dome include a wide array of pathologic conditions.14 Lesions involving the articular cartilage of the ankle can range from small defects to more severe injuries, such as large cysts or fractures of the underlying subchondral bone. Multiple terms have been used to describe similar problems, including transchondral fracture, osteochondral fracture, osteochondritis dissecans, talar dome fractures, and flake fractures. Perhaps the most widely used and most descriptive term for these injuries is osteochondral lesions of the talus (OLT).


The etiology of osteochondral lesions remains controversial in some cases. Although trauma plays a major role in most patients, idiopathic osteonecrosis may be the cause in those patients that present without a history of a traumatic event. Several reports have cited a 10% incidence of bilateral osteochondral lesions without a history of trauma.14, 15 Furthermore, these lesions have been associated with alcohol abuse, emboli, and some endocrinopathies. The trauma theory continues to be the most plausible and suggests that a distinct traumatic event, or repetitive microtrauma, initiates the osteochondral lesion. A subsequent osteonecrotic process may ensue and result in a subchondral fracture and eventual collapse. Resulting symptoms leads to altered biomechanics, which forces synovial fluid beneath the fractured talus and prevent healing of the fragment.

Subchondral cyst formation is often visualized on MRI or CT and is believed to be caused by damaged
cartilage functioning as a one-way valve. The valve allows the flow of fluid from the joint space into the subchondral bone but not in the opposite direction. During weight bearing, similar contact pressures in the talus and tibial cartilage forces fluid into the damaged subchondral bone, which is the path of least resistance. Unloading of the joint allows fluid to re-enter the articular cartilage, but as the cycle of fluid shift continues, cyst formation slowly ensues16 (Fig. 9-2A-D).

FIGURE 9-2. (A) Coronal CT scan showing an oval-shaped subchondral cystic lesion in the talar body. Note communication from cyst within the joint (B). Corresponding diagram indicating the supposed mechanism of cyst formation with synovial fluid leaking through a crack in the articular cartilage (black arrow) to form a cyst in the bone. (C) Coronal MRI scan showing an elongated subchondral cyst.

Although the exact incidence of OLT is unknown, the reported incidence ranges from 0.09% of talar fractures to 6.5% of ankle sprains. However, their exact incidence is probably underestimated because they may occur more commonly than clinically seen. Moreover, minor trauma or minimal symptomatology may preclude x-ray examination of the ankle and delay the diagnosis. OLT comprise 4% of all osteochondritis dissecans.17 The average age of patients with OLT appears to be between 20 and 30 years old, with
males slightly predominant and medial dome lesions more common than lateral. A recent report by Hermanson and Ferkel15 found the incidence of bilateral lesions to be 10% in a population of 526 patients with OLT.

FIGURE 9-2. (Continued) (D) Corresponding schematic of elongated cyst. With joint compression (white arrow), fluid (black arrow) is forced through the crack in the articular cartilage to create the cyst. (B, D redrawn by Susan Brust with permission, van Dijk et al. AAOS Instructional Course Lecture, Vol 59, 2010.)


Medial osteochondral lesions occur more commonly than lateral lesions in most series. They occur primarily in the mid to posterior third of the talus dome and tend to be nondisplaced, cup shaped, and deeper than lateral lesions. Posteromedial lesions are generally chronic in nature and tend to be associated with cystic degeneration of the subchondral bone. Lateral lesions are more commonly a result of trauma, which is reported in 90% to 98% of cases.18 They are typically located in the mid or anterior portion of the talus and are generally displaced, shallow, and wafer shaped (Figs. 9-3 and 9-4). In addition, lateral lesions tend to occur due to shear forces, while medial lesions are the result of compression forces. It is important to note that there are exceptions and a careful evaluation is essential before determining a treatment plan.

Raikin et al. evaluated the true incidence of osteochondral lesions of the talar dome based on morphological characteristics on MRI. They established a nine-zone anatomic grid of the talus in order to accurately report the location of osteochondral lesions. They found medial lesions to be more common than lateral. In addition, zones 4 and 6 were the most frequently involved sites for OLT (Fig. 9-5).19


The mechanism of injury for OLTs appears to differ for medial, lateral, and central lesions. In addition, more than one mechanism is probably associated with similar-appearing lesions. Berndt and Harty5 used cadavers to try to reproduce the mechanisms of these lesions. Lateral talar dome lesions were reproduced by a strong inversion force to a dorsiflexed foot with the tibia internally rotated. Medial dome lesions were reproduced by a strong inversion force to a plantar flexed foot with lateral rotation of the tibia on the talus (external rotation). They thought that the principal force causing medial and lateral talar dome lesions was torsional
impaction. With the lateral lesions, as the foot is dorsiflexed and strongly inverted, the lateral talar margin is impacted and compressed against the medial articular surface of the fibula, causing a shearing and compressing component that could potentially displace the osteochondral fragment. Conversely, in medial talar dome lesions, when the foot was inverted and plantar flexed with the tibia in external rotation, the posteromedial edge of the talar dome impacted against the posteromedial tip of the tibia, causing increased shear stress.

FIGURE 9-3. Location of osteochondral lesions of the talus. Most lesions are central to posteromedial or anterior to midlateral, as seen on the axial view of the talus. (Illustration by Susan Brust.)

FIGURE 9-4. The size of the osteochondral lesion varies by location. Lateral lesions tend to be shallower and wafer shaped, and medial lesions deeper and cup shaped. (Illustration by Susan Brust.)

FIGURE 9-5. Topographic anatomic map of the nine zones of the talar dome. Zones 4 and 6 are most commonly affected. (Redrawn from Elias I, Zoga AC, Morrison WB, et al. Osteochondral lesions of the talus: localization and morphologic data from 424 patients using a novel anatomical grid scheme. Foot Ankle Int 2007;28:154-161.) (Illustration by Susan Brust.)

FIGURE 9-6. Inversion stress on the ankle joint creates a moment of force (M) that can be resolved along coordinate axes as a vertical (Fv) and a horizontal (FH) force. The result of these two forces is a shear force (Fs) along which the osteochondral lesion occurs. (Modified from Stauffer RN. Intraarticular ankle problems. In: Evarts CM. Surgery of the musculoskeletal system, vol 3. New York, NY: Churchill Livingstone, 1983. By permission of Mayo Foundation.) (Illustration by Susan Brust.)

The shear stress that is the inversion stress on the ankle joint creates a moment of force that can be resolved along coordinate axes (Fig. 9-6). A fracture may occur along the line of the shear force component (Fs). Whether the medial or lateral aspect of the dome is involved may depend on whether the ankle is in a dorsiflexed or plantar flexed position. The amount of displacement of the fragment that may occur depends on whether the shear stress is greater than the ultimate strength of the bone or cartilage. If the ultimate shear stress is greater than bone, articular cartilage may momentarily deform but will remain intact while the underlying bone fractures (Fig. 9-7A). However, if the magnitude of the resultant shear stress is greater than the ultimate strength of both articular cartilage and bone, a complete lesion is produced and displacement of the fragment from its bed may occur (see Fig. 9-7B).20

Yao and Weis21 reasoned that lateral lesions were caused by eversion of the foot with the ankle dorsiflexed and the tibia internally rotated on the talus. In addition, they thought medial lesions were produced by inversion of the foot with the ankle plantar flexed. Clearly, no single mechanism can explain each case because many lesions,
particularly on the medial side, occur without preceding known trauma.

FIGURE 9-7. Development of the osteochondral lesion. The articular cartilage may remain intact or may be injured along with the subchondral bone, depending on whether (A) the shear stress is greater than the ultimate strength of the bone, but less than that of the cartilage; or (B) the shear stress is greater than the ultimate strength of both cartilage and bone. (Modified from Stauffer RN. Intraarticular ankle problems. In: Evarts CM. Surgery of the musculoskeletal system, vol 3. New York, NY: Churchill Livingstone, 1983. By permission of Mayo Foundation.) (Illustration by Susan Brust.)

Patients may develop this injury from a fall from a height or associated fractures or crushing-type trauma. In some patients, no specific mechanism of injury or associated etiologic factor can be documented. In this group, idiopathic osteonecrotic processes versus repetitive microtrauma may be postulated.

Differences in material properties of tibial and talar cartilage may also contribute to the pattern of injuries appreciated. It has been postulated that a grinding mechanism between articulating surfaces may contribute to abrasive forces that lead to cartilage degeneration. Athanasiou et al. demonstrated differences in mechanical properties between contact points of the tibia and talus. More specifically, the softer posteromedial cartilage of the talus articulates with stiffer posteromedial cartilage of the talus. Chronic osteochondral lesions may be initiated by this disparity in mechanical properties of the two articulating surfaces. These disparities are not appreciated in other portions of ankle articulations.19


The diagnosis of an osteochondral lesion can be difficult and is often delayed. It has been reported that the incidence of delayed or misdiagnosis in patients with unexplained chronic ankle pain as high as 81%. A definitive diagnosis can range from 4 months to 2 years, suggested by several studies. Therefore, it is uncommon to diagnose this lesion acutely, which contributes to the difficult nature of this problem.

Patients can present acutely after a distinct injury, but often times present with persistent ankle pain, particularly after a trauma such as an inversion injury to the lateral ligamentous complex. Chronic lateral ankle pain is usually associated with a severe ankle sprain or a history of multiple, recurrent sprains. Symptoms may be vague and subtle, but may often include deep aching pain, stiffness and swelling, clicking, locking, and giving way.

The differential diagnosis of a patient with intermittent symptoms following an ankle sprain can be extensive, but must be considered. It includes OLT, calcific ossicles beneath the medial or lateral malleolus, peroneal subluxation, tarsal coalition, subtalar joint dysfunction, degenerative joint disease, soft tissue impingement, instability, infection, and reflex sympathetic dystrophy.


With recent advances in diagnostic imaging and operative arthroscopy, the diagnosis and evaluation of OLT have improved dramatically. As a result, several classification and staging systems exist based on plain x-ray, CT, MRI, or arthroscopic findings. It is essential to have a good understanding of these various systems in order to improve the ability to develop a well-informed treatment plan for a given lesion.

In 1959, Berndt and Harty5 were the first to develop a four-stage radiologic classification based on plain x-rays of the ankle. Their study used cadaveric specimens strapped to a wooden block with slanted grooves that made it possible to immobilize the foot in any position. As one held the foot in place, the other used his body weight and hands to apply a manual force to the ankle past its normal range of motion. X-ray analysis and specimen dissection was then used to develop their classification (Fig. 9-11). Stage I is a small compression fracture without displacement. Stage II is a partially detached osteochondral fracture that remains in its native bed. Stage III is completely detached, but nondisplaced. Stage IV is a completely detached and displaced fragment. As mentioned earlier, x-rays frequently do not reveal the osteochondral lesion and often do not correlate with arthroscopic findings. Loomer et al.17 modified this classification to include a fifth subtype of radiolucent, cystic lesions, as seen on CT scans.

More recently, Ferkel and Sgaglione developed a four-stage classification based on CT scans evaluated in two planes24 (Table 9-1, Fig. 9-12). They found this classification to correlate more accurately with arthroscopic findings and treatment outcome. Zinman et al. reported on

32 patients with osteochondritis dissecans of the talar dome and also found CT scans to be superior to x-rays for both diagnosis and follow-up.

FIGURE 9-9. MRI of osteochondral lesion of the talus. (A) Coronal T1- and T2-weighted images with the lesion well demonstrated. (B) Sagittal image demonstrating the large extent of the lesion in the anterior/posterior direction. (tb, tibia; tal, talus; cal, calcaneus; fb, fibula.)

FIGURE 9-10. A sagittal cropped and colored T2 map is depicted of the knee. Arrows mark the site of cartilage repair. The regions of interest (deep and superficial) of the T2 analysis are visualized for the area of cartilage repair (between the arrows) and the control cartilage (anterior to the repair tissue). The T2 values are relatively low in the control cartilage site; in the cartilage repair tissue, higher T2 values are visible. A slight zonal increase is visible for both the control cartilage (blue-green) and the repair tissue (blue/green-green/red). (From Welsch GH, Mamisch TC, Zak L, et al. Evaluation of cartilage repair tissue after matrix-associated autologous chondrocyte transplantation using a hyaluronic-based or a collagen-based scaffold with morphological MOCART scoring and biochemical T2 mapping: preliminary results. Am J Sports Med 2010;38:934-942, with permission.)

FIGURE 9-11. Drawings illustrating the methods of manipulation of amputation specimens. (A) The manipulation that produced fracture of the lateral border of the talus. (B) The method of producing fracture of the medial border. (Redrawn from Berndt AL, Harty M. Transchondral fractures (osteochondritis dissecans) of the talus. J Bone Joint Surg Am 1959;41:988, with permission.) (Illustration by Susan Brust.)

Table 9-1. CT Classification

Stage I

Cystic lesion within dome of the talus, intact roof on all views

Stage IIA

Cystic lesion with communication to talar dome surface

Stage IIB

Open articular surface lesion with overlying nondisplaced fragment

Stage III

Undisplaced lesion with lucency

Stage IV

Displaced fragment

From Ferkel RD, Sgaglione NA. Arthroscopic treatment of osteochondral lesions of the talus: long term results. Orthop Trans 1993-1994;17:1011.

MRI staging had been described by several authors. Anderson and colleagues modified the Berndt and Harty classification to consider fragment separation, underlying bone marrow edema and subchondral cyst formation (Table 9-2, Fig. 9-13). They compared CT and MRI findings in 24 patients and found good correlation between the studies in most cases. However, CT failed to make the diagnosis in four cases of stage I lesions.25

Pritsch et al. were the first to classify OLT based on the arthroscopic appearance of the overlying cartilage.
They classified lesions in three grades: intact, firm, and shiny articular cartilage; intact, but soft cartilage; and frayed cartilage (Fig. 9-14). Several lesions were noted to progress from grade 1 to grade 3 during the course of treatment. In addition, there was a poor correlation between x-ray appearance and arthroscopic findings. Therefore, they concluded that the arthroscopic appearance was considered the most important determinant of treatment.26

FIGURE 9-12. CT scan classification. See also Table 9-1. (Modified after J. Daugherty and Richard Ferkel.) (Illustration by Susan Brust.)

Cheng, Ferkel and Applegate studied 80 patients treated for OLT at the Southern California Orthopedic Institute between 1985 and 1994. They reviewed patients’ preoperative x-rays and CT or MRI with intraoperative findings. These were correlated with a new arthroscopic classification system based on the appearance of the articular cartilage 27 (Table 9-3, Fig. 9-15A, B). We believe this is the best way to stage osteochondral OLT and will be further discussed later in the chapter.

Table 9-2. MRI Classification

Stage I

Subchondral trabecular compression

Plain radiograph normal, positive bone scan

Marrow edema on MRI

Stage IIA

Formation of subchondral cyst

Stage II

Incomplete separation of fragment

Stage III

Unattached, undisplaced fragment with presence of synovial fluid around fragment

Stage IV

Displaced fragment

From Anderson IF, Crichton KJ, Grattan-Smith T, et al. Osteochondral fractures of the dome of the talus. J Bone Joint Surg Am 1987;71:1143.


The goals of initial treatment are pain reduction, functional improvement, and limiting the progression of arthritis and long-term disability. However, the long-term natural history of OLT is usually benign.29, 30 In one study, only 1 of 38 patients treated surgically for OLT developed radiologic progression of arthritis at long-term follow-up. In addition, ankle arthrodesis has been extraordinarily rare after treatment for OLT.29 If surgical treatment is considered for osteochondral lesions, the goal in the acute setting is to reduce the osteochondral fracture anatomically and stabilize it while it heals. If no bone is attached to the chondral fragment, then the goal is similar to chronic OLTs. In the chronic situation, the goal is to produce a more predictable repair tissue that closely resembles zonal hyaline cartilage and can integrate with native tissue that remains durable over time. Unfortunately, all of the current treatment options for chondral resurfacing have disadvantages,
and no one surgical technique reliably produces zonal hyaline cartilage. Although our current treatment options have produced encouraging results, not all patients will achieve a successful outcome. Therefore, it is essential to have an informed discussion with the patient to develop a treatment plan with realistic expectations.

FIGURE 9-14. Arthroscopic grade III lesion according to the Pritsch classification.

Table 9-3. Surgical Grade Based on Articular Cartilage

Grade A

Smooth, intact but soft or ballottable

Grade B

Rough surface

Grade C


Grade D

Flap present or bone exposed

Grade E

Loose, undisplaced fragment

Grade F

Displaced fragment

From Cheng MS, Ferkel RD, Applegate GR. Osteochondral lesions of the talus: a radiologic and surgical comparison. Presented at the Annual Meeting of the Academy of Orthopaedic Surgeons, New Orleans, FL, 1995; Ferkel RD, Zanotti RM, Komenda GA, et al. Arthroscopic treatment of chronic osteochondral lesions of the talus: long-term results. Am J Sports Med 2008;36:1750.

FIGURE 9-15. (A) and (B) Two arthroscopic images of an arthroscopic stage D according to the Cheng, Ferkel and Applegate arthroscopic classification system. Stage D lesions are the most commonly found.


Technique for Acute and Chronic OLT

The technique used to approach OLTs is the same as that described in Chapter 7. Small-joint 2.7-mm 30° and 70° arthroscopes and small-joint instrumentation are particularly useful in treating these lesions because they enable the arthroscopist to see a wide angle of vision with minimal distraction and to work in small spaces. Occasionally, a 1.9-mm 30° is necessary in tight joints.

Arthroscopic evaluation of osteochondral lesions starts with a complete 21-point examination. Care is taken to examine not only the talus but also the tibial articular surfaces, because some patients will either have isolated or associated tibial plafond lesions that are symptomatic and require treatment. The arthroscope must be placed in all three portals so that no area is left unvisualized.

Principles of Acute OLT

The principles of treating acute osteochondral lesions are different than those for chronic lesions. With acute OLT, the first priority is to identify the lesion. CT or MRI may be used if needed to further visualize and distinguish the exact appearance and radiologic stage. If the acute lesion is displaced, arthroscopy should be performed immediately, and the consent should read “arthroscopy with possible open pinning or removal of osteochondral lesion of the talus.”

In the acute situation, the lesion should be palpated with a small-joint probe. Subsequent assessment should be made as to whether the chondral fragment has enough bone to allow healing if it is reattached. If the lesion is primarily chondral in nature, excision is recommended, with subsequent debridement and drilling and/or microfracture of the base to stimulate new vascularity and the formation of fibrocartilage. If the chondral fragment has enough underlying bone, the piece should be reattached with absorbable pins, K-wires, or screws. If the lesion is severely displaced, reduction with a probe or grasper is done gently to reduce the fragment anatomically so it can be temporarily fixated with a K-wire. Then firm fixation can be accomplished with further K-wires, absorbable pins, or screws (Fig. 9-16A, B, Table 9-5).

FIGURE 9-16. Acute osteochondral lesion of the talus. (A) The acute lesion is stabilized so that absorbable pins can be inserted. (B) Insertion of absorbable pins is done arthroscopically using a plunger after measuring the appropriate length of the pin and predrilling the hole. (Illustration by Susan Brust.)

Table 9-5. Treatment of Acute OLT

1. Palpate the lesion with a small-joint probe.

2. Excise chondral fragments with little or no bone and drill/microfracture the base.

3. Reattach loose osteochondral fragments with absorbable pins, K-wire, or screws.

4. If lesion is displaced, reduce with probe or grasper gently and temporarily fixate with K-wire, then firmly fixate with absorbable pins, screws, or K-wire.

Principles of Chronic OLT

With chronic OLT, it is again critical to identify the lesion correctly. CT or MRI should be obtained when indicated, as described previously. Generally, arthroscopy is performed on all stage III and IV lesions and stage I and II lesions that fail conservative treatment.

There is controversy as to the best way to treat full-thickness loss of articular cartilage such as in OLT. Penetration of the subchondral bone disrupts subchondral
blood vessels. This leads to the formation of a fibrin clot, and a fibrocartilaginous repair tissue often forms over the surface if it is protected from excessive loading. It has been shown experimentally that the cells responsible for the new fibrocartilaginous articular surface enter the fibrin clot from the marrow. These cells start as undifferentiated mesenchymal cells and then differentiate into chondroblasts and chondrocytes.

Different methods have been developed for penetrating subchondral bone to perform cartilage repair, including resecting sclerotic subchondral bone, drilling through the subchondral bone, abrading the articular surface, and creating small-diameter defects with microfracture pics. Although it is unclear which of these methods produces the best new articular surface, we prefer a combination of drilling and microfracture through the subchondral plate. A recent comparison of abrasion with drilling for treatment of experimental chondral defects in rabbits demonstrated that the long-term results of drilling appear to be better than those of abrasion. These findings support other works that have shown that cartilage surface can be repaired by tissue that grows up through the drill holes and then spreads to cover the exposed subchondral bone between the holes.

In the chronic setting, the lesion should be carefully probed. If the lesion is posterior, visualization should be done through the posterolateral portal to facilitate complete assessment of the size, location, and looseness of the lesion. On occasion, a question still arises as to how loose the fragment is and its potential for healing. In this instance, a dilute methylene blue solution can be injected to detect staining around the lesion, which may suggest whether it is loose. If the lesion is not loose, transmalleolar or transtalar drilling can be done (Fig. 9-17). If the lesion is loose, fixation can be accomplished with absorbable pins, K-wires, or screws if the articular cartilage is healthy. Usually, chronic lesions must be excised, as they are found to be loose and occasionally displaced. After excision, curettage, transmalleolar or transtalar drilling, and microfracture are performed. For deeper lesions, only drilling is performed. However, in shallower lesions, we prefer to microfracture the rim and drill the center.

FIGURE 9-17. Transmalleolar and transtalar drilling, both laterally and medially. (Copyright, Richard D. Ferkel.)

Table 9-6. Treatment of Chronic OLT

1. Probe with small-joint probe.

2. Evaluate with palpation whether lesion is loose; if there is any question, use dilute methylene blue to detect staining around the lesion that would suggest whether it is loose or not.

3. Drill the lesion if it is not loose.

4. Fixate the lesion if loose and if articular cartilage and underlying bone are healthy, with or without inserting bone graft, using absorbable pins, K-wires, or screws.

5. Excise the lesion if loose or displaced, and then drill/microfracture the base.

6. Bone-graft large cystic areas if cartilage is intact; otherwise, curette the cyst out and drill or abrade the base. (Bone grafting of open defects can be considered.)

Rarely, a large cystic area is identified with an intact cartilage surface. If the cyst is symptomatic, it should be drilled and curetted out arthroscopically through a transtalar approach, and then bone graft inserted. However, if the large cystic area does not have an intact cartilage, the entire cystic region, including the deformed loose cartilage, should be curetted out and the area debrided, drilled, and microfractured. Some asymptomatic cystic lesions can be followed for years without adverse results. Cysts >7 mm should also be bone grafted, which can be obtained from either the proximal tibia or calcaneus. Demineralized bone matrix (DBM) allograft can also be used (Table 9-6).


Acute Anterolateral Lesions

Acute anterolateral lesions are usually displaced and may be upside down in the joint (Fig. 9-18). We have termed these lesions lateral inverted osteochondral fractures of the talus (LIFT).31, 32 Anterolateral lesions are best approached with the arthroscope in the anteromedial portal, inflow posterolaterally, and instrumentation anterolaterally. Loose lesions can be reduced and fixated or excised through the anterolateral portal (Fig. 9-19A, B). A small-joint cannula can then be used to stabilize the K-wire while drilling into the base of the lesion to assist in fixation of the fragment. Fixation can be maintained with K-wires, screws, or absorbable pins.
(Refer to Fig. 9-16.) The Orthosorb pin (Biomet, Warsaw, IN), an absorbable pin, is made of polyglycolic acid and takes 6 months to absorb. Usually two or three pins are necessary for stable fixation. If drilling is difficult from the anterolateral portal, the MicroVector drill guide can be inserted through the anterolateral portal, and drilling can be done from the medial portion of the talus across into the lateral talar dome lesion. Alternatively, the arthroscope can be inserted anterolaterally, and the MicroVector can be inserted anteromedially to drill into the anterolateral lesion. Postoperative x-rays at 4 months demonstrate excellent healing (Fig. 9-20A-F).

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