Porter & Schon: Baxter's The Foot and Ankle in Sport, 2nd ed.

Section 3 - Anatomic Disorders in Sports

Chapter 14 - Osteochondral lesions of the talus and occult fractures of the foot and ankle

Michael Bowman




Occult fractures of the hindfoot



Talonavicular avulsion injuries



Cuboid fractures



Fractures of the anterolateral process of the calcaneus



Occult fractures of the talus



Osteochondral lesions of the talus




Occult Fractures of the Hindfoot

Occult fractures of the hindfoot represent a common source of prolonged pain and disability after athletic injuries. Increased knowledge about the existence and mechanisms of such injuries and a healthy suspicion about “soft-tissue injuries” that do not get better allow the health care provider to make a prompt diagnosis of occult foot and ankle fractures. Through history, physical examination, and proper use of diagnostic tests one can confirm the diagnosis and select the proper treatment.

Pertinent anatomy

With 28 bones, multiple joints, and connecting ligaments, the foot and ankle are vulnerable to compression and avulsion injuries with many complex movements during competitive sports. The bones comprising the hindfoot are the tibia, fibula, talus, calcaneus, navicular, and cuboid. The talus is especially prone to injury because it is involved in both dorsiflexion/plantarflexion and inversion/eversion motions. The talus is connected at the ankle joint to the tibia medially through the deltoid ligament ( Fig. 14-1, A ) and to the fibula laterally through the anterior talofibular ligament and posterior talofibular ligament ( Fig. 14-1, B ). The talus is connected to the calcaneus by the talocalcaneal interosseous ligament and the cervical ligament ( Fig. 14-2, A ). Thedorsal (see Fig. 14-2, A ) and plantar ( Fig. 14-2, B ) talonavicular ligaments connect the talus and navicular.



Figure 14-1  Hindfoot anatomy of the ankle. Note the (A) medial attachment of the talus the tibia with the deltoid and (B) laterally to the fibula with the anterior and posterior talofibular ligaments.





Figure 14-2  Hindfoot anatomy of the subtalar joint. Note the attachment of the talus to the calcaneus via the (A) talocalcaneal and cervical ligaments and the talus to the navicular via the (A) dorsal and (B) plantar talonavicular ligaments.



The talus is unique in that it has no direct muscular attachments. Approximately 60% to 70% of the talar surface is articular [0010] [0020] with the ankle joint superiorly, the talonavicular joint anteriorly, and the subtalar joint inferiorly. Blood supply to the talus therefore is limited, [0010] [0030] coming from its ligamentous attachments and a leash of vessels surrounding the talar neck that receive contributions from the artery to the tarsal canal medially, the dorsalis pedis artery anteriorly, and the artery to the sinus tarsi laterally ( Fig. 14-3, A through C ). The internal vasculature of the talus varies considerably[4] (Fig. 14-4 ). External athletic injuries to the talus that involve disruption of the vascular leash or the ligamentous attachments often produce vascular insult to the talar body or talar neck and may produce talar fractures or compression injuries that heal slowly or do not heal.


Figure 14-3  Vasculature supply anatomy for the talus. Note contributions from the (A-C) dorsal pedis artery, (A-C) peroneal (artery to the sinus tarsi), (A) artery to the tarsal canal, and (A and C) posterior tibial artery.




Figure 14-4  Internal vasculature anatomy of the talus.



The lateral process of the talus is a wide, triangular-shaped process that slopes down to meet the lateral calcaneus (see Fig. 14-5, A ). On the lateral view it is wedge-shaped and articulates superiorly with the fibular surface and inferiorly with the calcaneus (see Fig. 14-5, A ). The lateral talocalcaneal ligament attaches to the lateral process ( Fig. 14-5, B ).



Figure 14-5  Anatomy of the talus. Note the (A) predominance of articular surface and (B) laterally the attachment of the talocalcaneal ligament to the lateral process.



The posterior process of the talus originates from the convex-curved posterior half of the talar dome and slopes down and back to form the posterior talar “beak.” Inferiorly, it is concave and articulates with the posterior subtalar facet of the calcaneus. The posterior process has both a posteromedial tubercle and posterolateral tubercle. In between lies the flexor hallucis longus, which is commonly involved in posterior talar injuries ( Fig. 14-6 ). This posterior process is widely variable in shape, from a short, rounded end to a long “beak” that is prone to injury.


Figure 14-6  Posterior anatomy of the talus. Note the (A) posterior process of the talus, the (B) flexor hallucis longus between the two tubercles of the posterior talus, and (C) the posterior ligamentous anatomy.



The posterolateral tubercle (Stieda's process) is larger than the posteromedial tubercle. In approximately 7% to 10% of humans a separate os trigonum may exist—connected to the posterolateral tubercle by a fibrous cartilaginous synchondrosis ( Fig. 14-7, A and B ). The posterior talofibular ligament attaches the fibula to the posterolateral tubercle or the os trigonum (see Fig. 14-7, B ). The posterior deltoid or posterior talotibial ligament attaches the posterior tibia to the posteromedial tubercle of the talus. The Y-shaped transverse or bifurcate ligament is a thickening in the posterior ankle capsule that holds the two tubercles together and restrains the flexor hallucis longus. A meniscus-like “marsupial meniscus” also often exists in the posterior ankle superior to the posterior process of the talus ( Fig. 14-8 ).



Figure 14-7  (A) Lateral view. Anatomy of the os trigonum. Note that the os trigonum is the posterior process that is attached to the talus via a synchondrosis and (B) is attached to the posterior talofibular ligament (axial view).




Figure 14-8  A meniscus-like “marsupial meniscus” often noted in the posterior ankle superior to the posterior process of the talus.



The calcaneus is a complex, bony structure providing attachment for the Achilles posteriorly and the plantar fascia and plantar intrinsic muscles of the foot inferiorly. It articulates with the talus superiorly, as well as with the cuboid and navicular anteriorly. The anterolateral process of the calcaneus extends forward to form the calcaneocuboid joint. The saddle-shaped anterior surface articulates with the cuboid anteriorly, and the superior tip articulates to a varying degree with the lateral navicular. The extensor digitorum brevis also originates from this calcaneal process.

The blood supply to the calcaneus is quite robust, and fractures of the calcaneus tend to heal more easily. The ligamentous attachments at the calcaneus are the talocalcaneal interosseous ligament, lateral talocalcaneal ligament and cervical ligament to the talus and the calcaneofibular ligament laterally ( Fig. 14-9 ). The posterior, lateral, and anterior calcaneocuboid ligaments and the plantar calcaneonavicular (spring ligament) and lateral calcaneonavicular ligaments connect the calcaneus anteriorly to the cuboid and navicular, respectively.


Figure 14-9  Calcaneal ligaments. Note laterally the calcaneofibular, cervical, and lateral talocalcaneal ligaments.



The strong plantar calcaneonavicular or “spring” ligaments acts as a “sling” to hold the talar head in place. The bifurcate ligament (Y-ligament) is composed of the anterior and lateral calcaneocuboid ligament ( Fig. 14-10, A and B ) and is commonly injured during “sprain-type” inversion injuries, producing an avulsion fracture at the anterolateral process of the calcaneus. Inversion/adduction injuries of the midfoot also may produce avulsion fractures at the base of the cuboid.



Figure 14-10  Lateral plantar transverse tarsal ligaments.



The saddle-shaped cuboid articulates with the anterior process of the calcaneus and may be involved in either compression or avulsion tension-type injuries. The tarsal navicular is a “C” or saucer-shaped bone articulating with the talus posteriorly and the cuboid laterally. The dorsal talonavicular ligament and capsule may produce avulsion injuries of the navicular from plantarflexion-type injuries. Compression-type injuries also may be produced by the impact of the talar head on the navicular. The blood supply to the midportion of the navicular is poor ( Fig. 14-11 ) and may contribute to delayed healing or nonunion of such fractures. The articulation between the cuboid and the navicular varies from a true articulating joint to a fibrous connection to a bony bridge (tarsal coalition).


Figure 14-11  Vasculature anatomy of the tarsal navicular. Note the central area of decreased blood supply corresponding to areas of navicular stress fractures.



Various important and powerful tendons attach to the hindfoot; these produce considerable forces during athletic activities and can create injuries. The posterior tibial tendon attaches to the navicular ( Fig. 14-12, A and B ), producing inversion/supination and adduction while elevating the arch. It fires twice during each gait cycle or step—both eccentrically as a shock absorber and concentrically during push-off. The anterior tibial tendon, with attachments to the cuneiform and first metatarsal, is the primary dorsiflexor for the ankle and also inverts the foot. It also fires eccentrically during heel strike to decelerate and cushion the landing foot. The peroneus brevis and longus tendons ( Fig. 14-13 ) both evert the foot and ankle and resist inversion injuries. The peroneus brevis attaches to the base of the fifth metatarsal. The peroneus longus wraps around the cuboid at the trochlea to insert broadly underneath the foot near the base of the first metatarsal, which allows the longus also to help plantarflex and stabilize the medial foot.



Figure 14-12  Posterior tibial tendon anatomy. Note the attachment to the medial navicular, medial cuneiform, and lateral cuneiform that produces inversion, supination, and adduction.




Figure 14-13  Anatomy lateral ankle depicting peroneus longus and brevis tendons.




Talonavicular Avulsion Injuries

Incidence and mechanism

Avulsion fractures involving the tarsal navicular or talar head are not unusual after a plantarflexion injury of the ankle ( Fig. 14-14 ). The dorsal talonavicular capsule or ligament pulls off a small fragment with this injury (see Fig. 14-14 ). This injury is more common than thought, because many occur and are not treated immediately. They are seen in practices such as mine years later, asymptomatic with x-ray findings on films taken for an unrelated injury. Many of these minor fractures heal untreated by either painless bony or fibrous nonunion. However, a painful nonunion also may occur. Bony union of the fracture can result in the athlete's having pain from a bony prominence over the joint ( Fig. 14-15 ) or painful arthritis of the talonavicular joint.


Figure 14-14  Fracture of navicular caused by plantarflexion of foot and ankle with avulsion of dorsal fragment.




Figure 14-15  Nonunion of dorsal navicular avulsion fracture. This can cause a dorsal prominence and pain in the athlete.



An avulsion fracture from the medial or proximal end of the tarsal navicular at the distal insertion of the posterior tibial tendon is less common in athletics. This injury occurs in running sports in which a sudden change of direction is common. The athlete plants the foot, decelerates, and twists a plantarflexed foot to reaccelerate and push off. The force of the posterior tibial tendon on the navicular may produce an avulsion at its insertion. In cases in which the athlete has a congenital accessory navicular, the injury may occur through the cartilaginous synchondrosis between the main and “extra” (or accessory) bone ( Fig. 14-16 ).


Figure 14-16  Anterior-posterior radiograph of athlete's foot depicting painful medial accessory navicular attached by synchondrosis.




With dorsal navicular avulsion fractures, the athlete complains of anterior “ankle” pain after a sprain-type injury. In acute cases, ecchymosis may exist over the anterior ankle. Point tenderness will be noted over the dorsum of the navicular ( Fig. 14-17 ) or the talar head. Inversion or eversion may produce pain and plantarflexion of the foot. In chronic cases, a firm, bony “lump” (tender or nontender) will be noted over the dorsal navicular or talar head.


Figure 14-17  Clinical examination of athlete's foot depicting area of pain noted on foot with dorsal avulsion fracture of navicular.



In medial navicular avulsion injuries, the athlete will have ecchymosis, swelling, and tenderness over the medial and plantar navicular. Posterior tibial tendon function usually is still intact but may be painful against resistance to plantarflexion and inversion.


X-rays usually will show a wafer-like avulsion fracture on the dorsum of the navicular or talar head ( Fig. 14-18 ). In chronic cases, x-ray may show a rounded-off nonunion of the fragment or a healed, bony, beak-like projection, often with some arthritic changes in the dorsal talonavicular joint ( Fig. 14-19 ). More involved navicular body fractures also occur in the athlete but are not common. These larger body fractures require a computed tomography (CT) scan with axial and lateral views (Figs. 14-20 and 14-21 [0200] [0210]) to assess joint alignment and fracture orientation for surgical decision making. A CT scan also is helpful in chronic cases for assessment of joint irregularities and arthritis and to rule out a navicular stress fracture. In medial navicular avulsion fractures, x-rays will show calcified flecks or fragments on the medial navicular ( Fig. 14-22 ). Additional supination oblique views ( Fig. 14-23 ) sometimes are helpful, especially when an accessory navicular is present. Widening of the synchondrosis may or may not be seen.


Figure 14-18  Radiographic findings of dorsal, wafer-like fracture with acute injury.




Figure 14-19  Radiographic findings of chronic, dorsal, navicular nonunion. Note rounded edges and smooth contour in distinction from acute fracture in Fig 14-18 .




Figure 14-20  Computed tomography (coronal view) demonstrating more involved navicular body fracture with comminution.




Figure 14-21  Computed tomography (axial view) demonstrating navicular body fracture with displacement.




Figure 14-22  Anterior-posterior radiograph of foot demonstrating comminute medial navicular avulsion fracture.




Figure 14-23  Supination oblique (10 to 15 degrees of supination) demonstrating clear view of accessory navicular. This view also can give a clearer view of a navicular stress fracture.




For acute, minimally displaced (less than 1mm) fractures, boot immobilization for 6 to 8 weeks usually will result in healing, either a bony union or a painless, fibrous nonunion. The unusual large fragment (greater than 5mm) fracture may require internal fixation if displaced. The athlete is protected in a boot postoperatively, and nonweight bearing for approximately 6 weeks until the fracture is healed.

When a painful nonunion develops, an injection of corticosteroid sometimes will relieve the symptoms. Alternative shoe lacing ( Fig. 14-24 ), or a donut-type pad may reduce pressure in the area. If conservative treatment fails, the usual surgical treatment is excision of the fragment through a small dorsal longitudinal incision. Postoperatively the patient is nonweight bearing in a boot for approximately 2 weeks, followed by progressive weight bearing and active range of motion (AROM).


Figure 14-24  Lacing pattern on athlete's shoe to decrease pressure on a painful dorsal prominence of the foot such as a dorsal navicular avulsion nonunion.



In chronic cases in which a bony union has resulted in a painful bony prominence or dorsal talonavicular joint arthritis, conservative treatment is nonsteroidal anti-inflammatory drugs (NSAIDs), alternative shoe lacing or a donut-type pad dorsally, and molded foot orthoses with good arch support. A cortisone injection also may be helpful. If nonsurgical care is unsuccessful, the prominent and arthritic portion of the talus or navicular may be resected in a V-shaped fashion ( Fig. 14-25 ), leaving healthy joint behind. In severe cases of posttraumatic talonavicular arthritis, fusion may be needed.


Figure 14-25  V-shaped excision of dorsal prominence and portion of joint that has become arthritic.



Treatment of acute medial navicular fractures usually is conservative. Protection in a nonweight-bearing boot for 6 weeks until nontender followed by appropriate therapy for the posterior tibial tendon, usually will produce good results. The avulsion fragments may or may not demonstrate bony union on follow-up x-rays in successful cases. The rare large displaced fragment may require open reduction internal fixation (ORIF) ( Fig. 14-26, A and B ). The conservative treatment may be tried for nondisplaced accessory navicular injuries but in my experience is less successful. Excision of the accessory navicular and repair of the posterior tibial tendon to the navicular with bony anchors ( Fig. 14-27, A through G , followed by protection in a nonweight-bearing boot for 6 weeks, may be needed.



Figure 14-26  Fixation of large accessory navicular with two screws. (A) Anterior-posterior and (B) lateral radiographs depicting placement of screws.




Figure 14-27  Radiographs (A and B) of displaced accessory navicular requiring (C-F) excision of fragment, repair of posterior tibial tendon to medial navicular, and (G) postoperative anterior-posterior radiograph noting excision of accessory bone.



Rehabilitation and return to sports

Postoperative care of the previously described injuries involve nonweight-bearing protection in a boot until the fracture and associated ligament/tendon injury are healed (usually 6 weeks), followed by an ankle rehabilitation program working on edema control, range of motion (ROM), proprioception, and progressive resisted exercises (PREs) (especially the posterior tibial tendon). Running is added first and jumping activities are added next, followed by sports-specific exercises. The athlete may return to practice/play on successful completion of the program (6 to 10 weeks postinjury).


Cuboid Fractures

Incidence and mechanism

Cuboid fractures are much more rare in an athletic foot and ankle practice but tend to be overlooked and dismissed as a foot sprain. Two basic types are seen as athletic injuries: ( 1 ) an avulsion injury, caused by an inversion/adduction injury while landing (basketball, volleyball, and so forth) or rapid direction change (soccer, rugby, football) and ( 2 ) a compression injury, caused by forced eversion while plantarflexed or dorsiflexed in a pileup (e.g., football, rugby). In the avulsion cuboid injury, the calcaneocuboid capsule and plantar C-C ligament are torn, producing a usually small avulsion fragment off the plantar posterior cuboid. In the compression injury, the cuboid is crushed between the calcaneus and fifth metatarsal.


The athlete will complain of lateral foot pain, swelling, and difficulty walking, especially during push-off. Examination will show swelling and possible ecchymosis of the lateral foot, just proximal to the insertion of the peroneus brevis. There will be tenderness to palpation over the cuboid and possible pain with manipulation of the calcaneocuboid joint.


The small avulsion fractures may be seen with careful inspection of lateral or oblique x-rays ( Fig. 14-28 ). Compression injuries of the cuboid often do not show on standard x-rays. Posthealing x-rays may show increased radiodensity ( Fig. 14-29 ). A magnetic resonance imaging (MRI) ( Fig. 14-30, A and B ) or bone scan ( Fig. 14-31 ) can be used to confirm the fracture. Healing then must be followed by either routine radiographs or CT.


Figure 14-28  Oblique radiograph of foot demonstrating small fracture of cuboid.




Figure 14-29  Lateral radiograph of foot depicting increased density of cuboid indicating healing of prior occult cuboid fracture.





Figure 14-30  (A) Sagittal and (B) axial magnetic resonance imaging (MRI) demonstrating increased bone edema with occult compression fracture of cuboid.




Figure 14-31  Bone scan of athlete with occult cuboid fracture. Note increased signal center over area of cuboid.




Usually conservative treatment is used to successfully treat both types of cuboid injuries. Avulsion-type cuboid fractures are treated with a protective boot and allowed weight bearing as tolerated (WBAT). Ice and edema control are started immediately. Running and return to sports exercises are initiated when weight bearing is comfortable in a shoe. Usually a painless, fibrous nonunion of the fragment will result. In the rare case of a painful fragment, excision is performed. Compression cuboid injuries also are treated with edema control and WBAT in the boot. When the athlete is pain free, walking in the boot, and nontender to palpation, weight bearing in the shoe and progressive activities are allowed.


Fractures of the Anterolateral Process of the Calcaneus

Incidence and mechanism

The anterolateral process fracture represents up to 23% of all calcaneus fractures.[5] Two mechanisms of injury to the anterolateral process of the calcaneus have been noted. [0060] [0070] An inversion injury to a plantarflexed foot (much like the mechanism for a common ankle sprain) will produce an avulsion fracture of the tip of the anterolateral process through tension on the bifurcate ligament ( Fig. 14-32 ).


Figure 14-32  Diagram of right foot demonstrating supination and inversion of hindfoot causing avulsion of anterior process of calcaneus with tension on bifurcate ligament.



The second mechanism of injury to the anterolateral process is an eversion abduction injury ( Fig. 14-33 ) that produces a compression-type horizontal fracture through the calcaneus. [0050] [0070] Degan et al.[7] proposed the following classification for fractures of the anterior lateral process of the calcaneus: type I—nondisplaced tip avulsion, type 2—displaced avulsion fracture not involving the calcaneocuboid joint, and type 3—displaced larger fragments involving the calcaneocuboid joint.


Figure 14-33  Diagram of right foot demonstrating dorsiflexion and compression of calcaneocuboid joint with fracture of anterior process of calcaneus.




Athletes with a fracture of the anterolateral process will complain of lateral ankle and foot pain, increased by weight-bearing activity, push-off, or a change in direction. A history of an “inversion sprain” may be obtained. Often the diagnosis is delayed, and the athlete will give a history of an ankle sprain treated by the normal rest, ice, compression, and elevation (RICE) mechanism and physical therapy regimen that do not lead to improvement. Initial x-rays may have been taken and interpreted as negative.

Examination will show point tenderness over the bifurcate ligament and the anterolateral process of the calcaneus ( Fig. 14-34 ). Lateral ankle instability tests (drawer test, talar tilt test, and flexion rotation drawer test) often are negative. Often pain may be produced by inversion stress through the subtalar joint (distracting the fragment). There may be instability of the transverse tarsal joint, which is tested by holding the heel stable with one hand and pronating and supinating the midfoot with the other hand ( Fig. 14-35, A and B ).


Figure 14-34  Clinical photograph of right foot demonstrating area of hindfoot that is tender with underlying anterior process fracture of calcaneus.





Figure 14-35  Clinical photograph of right foot demonstrating assessment of transverse tarsal instability by stressing the hindfoot in (A) supination and (B) pronation.




As stated previously, initial x-rays may be interpreted as negative if the fracture is nondisplaced. However, review of the old x-rays or new anterior-posterior (AP), lateral, and oblique x-rays of the foot may show a displaced fracture through the tip of the anterolateral process of the calcaneus ( Fig. 14-36 ). Alternatively, a large, blunted, irregular and indistinct process may be visualized ( Fig. 14-37 ). In cases in which point tenderness exists over the anterolateral process but x-rays are not conclusive, a CT scan ( Fig. 14-38, A through C ) often will show the fracture and help in assessing the amount of healing. The CT also is helpful in surgical planning (ORIF vs. excision). A bone scan is used as a screening tool to distinguish this injury from other soft-tissue types of lateral ankle injuries.


Figure 14-36  Lateral radiograph of hindfoot demonstrating small anterior process fracture (arrows) of calcaneus.




Figure 14-37  Lateral radiograph of hindfoot demonstrating healed fracture of anterior lateral process (ALP) of calcaneus.




Figure 14-38  (A) Sagittal reconstruction, (B) coronal, and (C) axial computed tomography view of occult anterior process fracture (arrows) of calcaneus. Plain radiographs did not reveal fracture but athlete had tenderness over anterior process.




For acute, nondisplaced fractures (less than 8 weeks) and small fractures less than 2mm, cast or boot immobilization and nonweight bearing for approximately 6 weeks is used until the fracture is healed. For acute or semiacute fractures that are displaced (more than 5mm in diameter), either excision or open reduction internal fixation is suggested. If any instability of the transverse tarsal joint exists on testing, the bifurcate ligament may be repaired back to the remaining process of the calcaneus with a suture anchor or with internal fixation of the fragment.

In cases of chronic nonunion of the anterolateral process of the calcaneus, asymptomatic athletes are treated with observation only. For large fragments greater than 1cm or involving a significant portion of the articular surface, the fracture site is debrided and internal fixation is applied. For smaller fragments, the fragment is excised. The calcaneocuboid joint is inspected and debrided if necessary. The bifurcate ligament may be repaired back to the calcaneal process if any instability of the transverse tarsal joint exists.

For cases of malunited fractures of the anterolateral process of the calcaneus, arthritic changes in the superior portion of the calcaneocuboid joint and/or the junction between the process of the calcaneus and navicular may exist. In these cases, a trial injection of cortisone in the calcaneocuboid joint and calcaneonavicular space may provide relief or help to establish the diagnosis of arthritic changes. A CT scan or MRI with magnified views will help to provide information about the joints. Surgical treatment involves open resection of a portion of the anterolateral process of the calcaneus, trimming it back to a point at which a healthy calcaneocuboid joint is present. Recently, arthroscopic resection through a subtalar approach has been described.[8]

Rehabilitation and return to sports

In cases in which excision is required, boot immobilization and nonweight bearing are used for 2 weeks, followed by gentle AROM of the foot and protected weight bearing in the boot for an additional 4 weeks. General ankle rehabilitation then is begun, followed by sports-specific exercises.

Athletes with anterolateral process fractures treated by ORIF or excision and ligament repair are placed in a non-weight-bearing boot for 6 weeks until healed. General ankle rehabilitation followed by sports-specific exercises then is started. Return to sports usually is within 8 to 12 weeks.


Occult fractures of the talus

Occult fractures of the talus fall into several categories: posterior process fractures, lateral process fractures, global compression injuries of the talus (GCTs), and osteochondral lesions of the talus (OLTs).

Posterior talus fractures/posterior impingement syndrome (See Also Chapter 2 )

Incidence and mechanism

As noted previously, athletes with a long, slender, posterior talar “beak” may be more prone to posterior talar injuries. Two major athletic mechanisms exist that produce posterior process fractures. [0060] [0090] [0100] A forced ankle dorsiflexion and pronation injury such as forced planting of the foot backward with force applied ( Fig. 14-39, A ) or weight applied to the back of a dorsiflexed ankle at the bottom of a scrum or pileup ( Fig. 14-40 ) may produce an avulsion fracture of the posteromedial tubercle by traction on the posterior deltoid ligament (see Fig. 14-39, B ). [0060] [0110] [0120] [0130] A similar forced dorsiflexion/inversion injury also may produce injury to the posterolateral tubercle or os trigonum by traction on the posterior talofibular ligament. [0020] [0090] [0130]



Figure 14-39  (A) Lateral view of posterior talus process fracture caused by forced dorsiflexion of the ankle against a planted foot. (B) Posterior view, showing avulsion forces produced by the posterior deltoid ligament on the posterior medial tubercle of the talus.




Figure 14-40  Posterior talus process fracture caused by force on the back of the ankle, causing avulsion of the posterior talar process through tension on the posterior deltoid ligament.



Another and more common mechanism for producing posterior talar process fractures/os trigonum injuries is forceful plantarflexion. [0130] [0140] [0150] Repetitive plantarflexion and push-off activities (ballet, running, soccer), jumping and landing activities (gymnastics, basketball, volleyball, football), or twisting the ankle in a plantarflexion/inversion “sprain” position [0160] [0170] force the long talar beak/os trigonum against the posterior tibia and produce a fracture ( Fig. 14-41 ). Injuries to the posterior talus may result in chronic posterior impingement syndrome, [0060] [0090] in which athletes complain of posterior ankle pain, or pain with push-off, jumping, and landing.


Figure 14-41  Common mechanism for posterior process fracture with compression of posterior process between calcaneus and posterior tibia in severe plantarflexion of ankle.




The diagnosis of posterior process fracture often is delayed. In one study, five to eight physician visits were necessary until the diagnosis was made.[18] The posterior “ankle sprain” that does not get better should alert the physician to the possible presence of this fracture. The athlete often will give a history of posterior ankle pain worse with planting the foot back (tennis, football, racquetball), jumping and landing (basketball, volleyball), kicking (swimming), or tiptoe position (ballet). They may give a history of an ankle sprain or “Achilles pain.”


Ankle ROM may be normal or painful posteriorly with limits at both dorsiflexion (traction) and plantar fraction (compression). Passive subtalar joint motion, producing inversion and eversion with the ankle slightly plantarflexed, also may produce posterior ankle pain because the subtalar joint also may be affected. The “pinch test” posteromedially or posterolaterally just posterior to the ankle ( Fig. 14-42) will produce pain. The posterior impingement test ( Fig. 14-43, A and B ) will produce pain and possibly clicking. Manipulation of the great toe, producing stretch on the flexor hallucis longus, also may produce posterior ankle pain. Acutely, there also may be ecchymosis in the posterolateral or posteromedial ankle region.


Figure 14-42  Clinical demonstration of “pinch test.” Compression of posterior process fracture of talus (os trigonum) in athlete just behind ankle from medial and lateral sides cause pain.





Figure 14-43  Clinical demonstration of “posterior compression test.” Forced maximal plantarflexion (A and B) of ankle produces pain in athlete with posterior process fracture (os trigonum).




AP, lateral, and oblique x-rays may be negative if the fracture is nondisplaced or at a slight angle ( Fig. 14-44, A ). An os trigonum may appear normal. Repeat x-rays (especially lateral views) later may show the fracture ( Fig. 14-44, B ). A CT scan or MRI ( Fig. 14-44, C ) can be the standard for establishing the diagnosis, showing presence of the fracture, location, and size.[19] An MRI also will show compression injuries of the posterior talus ( Fig. 14-45 ) that did not exhibit a discreet fracture line, as well as surrounding edema. A bone scan ( Fig. 14-46 ) is useful to confirm a symptomatic os trigonum injury. [0190] [0200] [0210] An injection of cortisone into the os trigonum synchondrosis may provide temporary relief and help with the diagnosis.


Figure 14-44  Lateral radiograph and magnetic resonance imaging (MRI) ankle demonstrating os trigonum. Lateral x-ray shows (A) intact posterior process but repeat lateral radiograph demonstrated os trigonum with mild displacement. MRI clearly demonstrates the os trigonum as a separate fragment and area of chronic fracture.




Figure 14-45  Sagittal magnetic resonance imaging of talus demonstrating occult fracture of posterior facet, which causes posterior ankle pain in athlete and can be similar in presentation to posterior ankle impingement. Note edema in posterior talus and fluid posterior ankle.




Figure 14-46  Lateral bone scan image of ankle demonstrating increased uptake in posterior ankle consistent with posterior ankle impingement and painful os trigonum.




For acute nondisplaced fractures/os trigonum injury, immobilization in a boot/cast and limited weight bearing may lead to healing in 4 to 6 weeks. A repeat CT scan may be needed in subtle fractures to demonstrate healing.

For large displaced fractures (especially ones that extend into the weight-bearing talar body region), internal fixation through a posterolateral or posteromedial approach with cannulated 4.5 screws or headless screws is indicated. [0220] [0230] [0240] [0250] The flexor hallucis longus and medial neurovascular bundle must be protected with this approach. The head of the screws should be countersunk.

For smaller fractures/symptomatic os trigonum that do not heal or chronic fracture cases, excision of the posterior tubercle ( Fig. 14-47, A through D ) and debridement of the adjacent ankle and subtalar joint is the method of treatment. [0160] [0170] Although Marumoto and Ferkel[26] and others [0050] [0270] have advocated arthroscopic resection of the os trigonum, most surgeons still prefer resection through a small posteromedial [0090] [0280] or posterolateral[16] approach for medial process/lateral process fractures, respectively.


Figure 14-47  Symptomatic os trigonum. (A) Lateral radiograph and (B) sagittal magnetic resonance imaging confirm os trigonum. (C) Clinical appearance of os trigonum removed through lateral incision and (D) lateral radiograph demonstrating excision.



Rehabilitation and return to sports

Postoperatively, in cases in which internal fixation is required, the athlete is placed in a protective boot, nonweight bearing for 6 weeks with early AROM out of the boot to prevent stiffness. When the fracture is healed, progressive weight bearing and ankle rehabilitation is begun, followed by sports-specific exercises. ROM and strengthening of the flexor hallucis longus (FHL) is emphasized.

After excision of the fracture fragment or os trigonum, the athlete is protected nonweight bearing in a boot for 2 weeks with gentle AROM of the ankle and subtalar joint allowed out of the boot. At 2 weeks, progressive WBAT in the boot is allowed, and the athlete is weaned back into a shoe as tolerated. At 4 to 6 weeks postoperatively (depending on comfort), general ankle rehabilitation is permitted, followed by sports-specific exercises.

Athletes may return to sports on successful rehab completion, ranging from 4 to 8 weeks postinjury.

Lateral process fractures of the talus

Incidence and mechanism

Lateral process fractures of the talus are another commonly missed hindfoot injury in athletes. They represent the second-most common talar body fracture (almost 25%). [0020] [0130] It is estimated that they are present in 0.86% of all lateral ankle sprains.[28] Although more commonly seen in motor vehicle accidents and high-energy traumatic injuries to the ankle, athletically produced lateral process fractures of the talus have increased to an estimated 2000 per year in the U.S.[29] because of the recent popularity of snowboarding. They account for 2.5% of all snowboarding injuries.[30] In “snow boarder's ankle,” dorsiflexion and inversion applied to the ankle and talus are the most accepted mechanism for production of athletic lateral process fractures of the talus. [0130] [0280] [0290] [0310] [0320] However, experimental studies suggest that external rotation applied to a dorsiflexed inverted foot ( Fig. 14-48 ) may produce a force to the lateral process and result in a fracture. [0060] [0320] Both the body and the snowboard act as a lever arm on the ankle and talus. The leading leg is injured twice as often. [0290] [0300]


Figure 14-48  Diagram noting mechanism for lateral process fractures of talus. Forced external rotation with the ankle in dorsiflexion and inversion results in a lateral process fracture.




The athlete may give a history of a twisting injury to the ankle and complain of lateral ankle pain increased with weight bearing.


Athletes may exhibit ecchymosis on the lateral ankle. Tenderness is present inferior to the lateral malleolus, and pain may be produced with dorsiflexion and plantarflexion and/or inversion.


An AP, lateral, and oblique ankle x-rays may show an avulsion-type fragment laterally ( Fig. 14-49, A ) or be negative if the fracture is nondisplaced ( Fig. 14-49, B and C ). The mortise view is felt to be best to visualize these fractures.[32] A CT scan is the gold standard for identification of lateral talar process fractures, aiding in sizing and surgical planning ( Fig. 14-50 ). MRIs also may show associated talar cartilage and/or bony injuries.[33] A bone scan may be useful as a screening tool in cases of chronic lateral pain in which the fracture was undetected.


Figure 14-49  (A) Anterior-posterior (AP) radiograph of ankle demonstrating lateral process fracture of talus (arrows) noted just inferior to the tip of fibula. (B) Lateral and AP radiographs of athlete with lateral process fracture not able to be visualized on x-rays.




Figure 14-50  Axial computed tomography scan of talus demonstrating lateral process fracture that was not identified on ankle radiographs in athlete.




Two commonly used classifications for lateral talus process fracture exist: the Hawkins classification[13]: type1—simple two-part fracture, type 2—comminuted fracture, and type 3—avulsion fracture of the anterior inferior process and the Funk classification[29] ( Fig. 14-51 ): type A—small, minimally displaced, extra-articular avulsion fracture, type B—a medium-sized fracture involving only the talocalcaneal joint surface, and type C—a larger fracture involving both the talocalcaneal and talofibular joint articulations.


Figure 14-51  Funk classification for lateral process fracture talus. Type A involves only a small avulsion fragment, type B involves only the talocalcaneal joint, and type C involves both the talocalcaneal and talofibular articulations.




For acute, nondisplaced lateral process fractures, immobilization in a boot and nonweight bearing for 4 to 6 weeks is indicated. Repeat CT scan may be necessary to document healing. For small, displaced fractures (less than 5mm) conservative treatment with boot or cast immobilization and nonweight bearing also is indicated. Early excision of displaced small fragments and progressive weight bearing also has been proposed.[30] For larger displaced fractures (>1cm) and/or with joint surface irregularity greater than 2mm, open reduction internal fixation [0050] [0060] [0130] [0190] [0280] [0300] with headless or countersunk screws through a subfibular approach with sectioning of the calcaneofibular ligament for exposure is indicated. Postoperative, nonweight-bearing boot immobilization is used, with immediate, gentle AROM until healing is accomplished.

For chronic cases (previously undetected) or cases of nonunion after immobilization, treatment of large fragments (greater than 1cm) or fragments involving the articular surfaces require debridement and/or internal fixation. Small fragments (less than 1cm) may be excised.[13]

Rehabilitation and return to sports

Postinjury, athletes are treated in a nonweight-bearing boot until the fracture is healed. In most cases a repeat CT scan is needed to assess healing. Athletes with intra-articular lateral talus fractures requiring internal fixation are allowed to start gentle AROM exercises of the ankle and subtalar joints during this healing and nonweight-bearing phase to maintain joint mobility. When all fractures are healed, progressive weight bearing and ankle rehabilitation are begun, followed by sports-specific exercises and return to sports. In cases involving the subtalar joint, this may be up to 3 months.


Osteochondral Lesions of the Talus

Intra-articular ankle injuries to the talar body are a common source of athletic disability. Cartilage injuries to the talus may be partial thickness or full thickness, or may involve bone (OLTs).


Historically, various origins for OLT have been presented. König[34] coined the term “osteochondritis desiccans” to describe loose osteochondral fragments in the knee, and the theory of spontaneous necrosis for these lesions in the knee and ankle was postulated. Various theories concerning vascular insult to the talus have been described. [0020] [0270] [0340] [0350] [0360] The body of the talus has a generally poor blood supply because of its large articular surface, as noted earlier. There also is considerable variation in the intra-articular blood supply of the talar body. Embolic phenomena, sickle cell anemia, and corticosteroid use have been noted as causes for bony infarcts in the talar body. [0010] [0360] Inflammatory conditions such as rheumatoid arthritis, systemic lupus erythematosus, psoriatic arthritis, and ankylosing spondylitis, as well as genetic predisposition, parathyroid disease, and osteoarthritis have been associated with OLTs. [0010] [0360] However, these cases of nontraumatic talar body osteochondral lesions generally are more diffusely involved than the discrete OLT seen with sports injuries that we will discuss in this chapter.

The more well-defined and distinct OLTs seen in the athletic population usually result from an acute traumatic injury or chronic lateral ligament instability of the ankle. Most OLTs are located in the anterolateral ( Fig. 14-52, C and D ) or posteromedial corner (see Fig. 14-52, C and D ). Bruns and Behrens[37] postulated that an inversion injury to a plantarflexed foot ( Fig. 14-52 , A and B), similar to a common ankle sprain, would produce shear forces on the lateral talus and compression forces in the medial talus.[13] The posteromedial lesions likely occur with more concomitant ankle plantarflexion, and anterolateral lesions occur with more ankle dorsiflexion with inversion. Such forces could produce a compressive injury to the subchondral bone posteromedially and lead to shear forces with avulsion on the lateral talus. Berndt and Harty[35] experimentally produced lateral OLTs with application of inversion to a dorsiflexed foot while the tibia is internally rotated. Medial OLTs were produced by applying inversion force to a plantarflexed foot with tibial external rotation. Yao and Weiss[38] postulated that eversion of dorsiflexed ankles with the tibia internally rotated produces lateral OLTs.



Figure 14-52  Osteochondral lesions of the talus. Mechanism is (A) inversion of the ankle causing a (B) shear force on the lateral dome and compression force on medial talus. (C and D) Location of resultant lesions are anterolateral and posteromedial in the talus.



The overlying articular cartilage coverage still may be intact or partially intact while producing an injury to the underlying bone. The subchondral fracture fragment has no direct blood supply. Left unrecognized, with continued weight bearing, the bony defect may not heal, leading to a fibrous nonunion or collapse, and result in a cartilage defect, loose osteochondral fragment, and cystic changes. Scranton and McDermott[39] and Ferkel[40] have postulated that an articular cartilage defect produced by such an injury may lead to cystic changes in the subchondral bone when joint fluid is forced repetitively into the defect under pressure. Chronic lateral ankle instability after an ankle sprain also may produce repetitive forces on the talus resulting in an OLT. [0010] [0160]

GCTs represent a small minority of athletic injury to the talus. Usually the results of massive trauma, they can cause significant ankle pain and synovitis and inability to bear weight, and their diagnosis may be delayed because of lack of initial findings on routine radiographs ( Fig. 14-53, A and B ). An MRI best defines the lesion, with significant signal changes indicating edema and bony injury in the talar neck and/or body ( Fig. 14-53, C and D ). Because of the poor blood supply of the of the talar body, these lesions are slow to heal, if they heal at all. Literature reports of the natural history and my anecdotal experience show that talar collapse, chondrolysis, and gross ankle arthritis may be the result of such injuries.


Figure 14-53  Global talar compression injury. Routine radiographs (a and b) fail to demonstrate talus injury. Magnetic resonance imaging notes edema and “fracture” line (arrows) on (c) coronal and (d) sagittal images.




Ankle sprains occur at the rate of approximately 27,000,000 per year. OLTs have been estimated to occur in approximately 6.5% of these injuries. [0160] [0410] [0420] [0430] Thirty-eight percent of supination and external rotation-4 type ankle injures are felt to produce an OLT.[16] Sixteen percent to 23% of cases treated surgically for chronic instability of the ankle are found to have an OLT. [0130] [0160]Posteromedial lesions are more common than anterolateral and tend to be deeper in thickness. The average patient is 25 to 35 years of age, male (70%), [0130] [0160] with 10% to 25% incidence of bilaterality.[16] OLT is most commonly seen in sports in which running, jumping, or change of direction are common, all factors that typically lead to the production of ankle sprain injuries.

Diagnosis and evaluation


The diagnosis of OLT often is delayed. In several studies and in my own practice, there often are 5 to 9 months between the initial injury and the definitive diagnosis. [0370] [0440] [0450] The diagnostic tools have improved, but a high index of suspicion on the part of the surgeon for “ankle sprains that do not get better” is essential. The history of an “ankle sprain” is common. The athlete may give a history of continued anterior ankle pain and swelling despite initial radiographs that were read as negative and appropriate conservative treatment for an ankle sprain. A history of “catching” or “locking” may suggest a loose osteochondral fragment.

Another common scenario is that of an “old ankle sprain” months or years before presentation in which the initial symptoms seemed to improve and then recur without addition injury. These cases most likely represent progression of the disease process. A third presentation is one in which an initial ankle sprain results in chronic lateral ankle instability, producing painful “giving way” episodes and further talar injury.


Physical examination in acute OLT cases may closely resemble that of an acute ankle sprain with ecchymosis and tenderness in the anterior ankle or posteromedial ankle. There also may be swelling or an ankle effusion and synovitis. A drawer or talar tilt test (see Chapters 12 and 13 [] [] ) may be positive. There may be crepitus or “catching” with ankle ROM when a displaced OLT exists.

In cases associated with chronic ankle instability, the anterior drawer test, talar tilt test, and/or flexion/rotation drawer test will be positive. In chronic cases, only swelling and joint tenderness may be present.


Initial radiographs often are negative unless the fracture is displaced.[46] Serial or subsequent x-rays may show a subchondral fracture line, displacement of a fragment, or an area of radiolucency on the anterolateral or posteromedial talus ( Fig. 14-54, A ). A mortise view taken with a 4-cm heel rise may increase detection with conventional radiographs ( Fig. 14-54, B ). A bone scan, CT scan, or MRI may be used as a screening tool for chronic ankle pain. A CT scan with 1-mm overlapping cuts, axial, coronal, and sagittal views is the gold standard for lesion location, sizing, and surgical planning.[16] Similar views on MRI are helpful in evaluating early or compression injuries, demonstrating the amount of edema associated with the injury and assessing cartilage injuries. Arthroscopic evaluation [0470] [0480] has been proven to be essential for demonstrating the viability and stability of the overlying cartilage and whether the cartilage surface is still intact. At arthroscopic evaluation, the underlying subchondral bone can also be probed to determine its structural integrity. CT and MRI, however, have been shown to allow better assessment of the size of the OLT.[49]



Figure 14-54  Anterior-posterior radiograph of ankle (A) demonstrating radiolucency in talus (arrows) suggesting medial dome osteochondral lesion of talus. Oblique radiograph of ankle (B) showing clear evidence of large medial dome cyst and osteochondral lesion of talus.



Although Verhagen et al.[46] found that CT and MRI evaluation were equally valuable in assessing OLTs, my experience has shown that MRI tends to show a much larger lesion because of the bony edema surrounding the fracture ( Fig. 14-55, A through E ). An MRI usually is much better in assessing early-stage lesions and as a screening tool. When an OLT is present with a more global compression injury, CT scan is helpful to accurately localize the specific osteochondral fracture.


Figure 14-55  Osteochondral lesion of lateral dome of talus. (A) Anterior-posterior radiograph of ankle demonstrating lateral dome of talus osteochondral lesion. Coronal and sagittal (B and C) computed tomography images and (D and E) magnetic resonance imaging delineates more clearly chronic and cystic nature of lesion.



The history, physical examination, and these diagnostic tests all are helpful together to detect an OLT, to determine its size and location and to help with staging. However, the surgeon should be cautioned to determine that the presence of an osteochondral lesion is in fact the lesion producing the athlete's symptoms. I personally have seen several cases in which a chronic asymptomatic OLT was detected on evaluation or was sent to me on discovery, and, in fact, another condition was causing the patient's symptoms. We discuss treatment of asymptomatic OLTs later. However, the lesson here is to treat the patient not the imaging study.

Finally, intra-articular ankle injection with Xylocaine and Marcaine is helpful in cases in which there is doubt about whether the osteochondral lesion is producing the patient's symptoms.

I use MRI as a screening tool to detect OLTs when routine radiographs are negative, to localize and size osteochondral lesions preoperatively, and to assess and confirm healing of osteochondral lesions. However, as discussed later, actual treatment often depends on arthroscopic evaluation and determination of the intactness and viability of the cartilage.


Several classification and staging systems for OLTs have been devised as diagnostic capabilities have developed. The Berndt and Harty[35] radiograph-based classification introduced in 1959 is still the most widely used classification ( Fig. 14-56 ). Stage I represents an area of osteochondral compression. Stage II is a partially loose fragment. Stage III is a completely detached fragment without displacement. Stage IV represents a completely detached and displaced fragment. This has been appended to include Stage 0, which is an x-ray-negative but MRI-positive lesion. Scranton and others have added stage V [0390] [0500] to describe lesions with deep cystic changes ( Fig. 14-57 ). Ferkel[51] advanced a classification system based on CT in 1996 ( Fig. 14-58 ). Hepple et al.[43] presented an MRI-based classification system in 1999. Pritsch et al.,[52] Ferkel,[40] Mintz et al.,[47] and Taranow et al.[53] have all noted that arthroscopic evaluation of these lesions is essential to assess the overlying cartilage. An arthroscopic classification system was proposed by Ferkel.[51]


Figure 14-56  Berndt and Hardy classification for osteochondral lesions of talus. Stage I represents an area of osteochondral compression. Stage II is a partially loose fragment. Stage III is a completely detached fragment without displacement. Stage IV represents a completely detached and displaced fragment.




Figure 14-57  Classification of osteochondral lesions with addition of stage V [0390] [0500] to describe lesions with deep cystic changes.




Figure 14-58  Classification of osteochondral lesions as described by Ferkel[51] based on computerized tomography.



OLT Treatment

Treatment of acute injuries

Nonoperative treatment commonly is used for acute OLTs. [0030] [0130] [0350] [0400] [0410] [0540] Immobilization, nonweight bearing and crutches are used until healing is complete. Follow-up routine x-rays, CT scan, or MRI may be used to fully evaluate healing. Cases that are not healed may be treat-ed as chronic cases. There is some controversy whether immobilization and/or nonweight bearing are critical to the success rate of nonoperative treatment. [0010] [0400]

Acute OLTs that are displaced have been treated most commonly by arthroscopy and excision (if less than 1cm) or by arthroscopy/arthrotomy and ORIF.[40] Bioabsorbable pins or headless screws also may be used. For posterior medial lesions, transmalleolar pinning through a drill hole ( Fig. 14-59 ) or a medial malleolar osteotomy have been used. Anterolateral lesions often can be approached through an arthroscopic approach or by a small arthrotomy and/or excision of a small anterolateral edge of the distal tibia. [0500] [0550] In the case of a nonunion, the patient is then treated as a chronic case.


Figure 14-59  Diagram demonstrating transmalleolar pinning of medial dome osteochondral lesion through drill hole in medial malleolus.



Treatment of chronic injuries

Nonoperative treatment with or without immobilization has been shown to produce only approximately 50% good to excellent results [0010] [0030] [0380] [0420] and less than 33% good to excellent results in younger patients. Arthroscopic evaluation is essential in selecting the proper operative treatment of symptomatic patients with OLTs. A combination of x-ray, CT scan, and/or MRI evaluation along with arthroscopic assessment of the cartilage surface allows accurate staging. Most cases of chronic OLT involve partially or totally displaced cartilage and bony fragments. Excision of the OLT alone yields approximately 38% good to excellent results.[3] Excision and curettage ( Fig. 14-60, A through C ) yields 78% good to excellent results, whereas excision, curettage and drilling, or microfracture ( Fig. 14-61, A and B ) have produced 86% good to excellent results. [0010] [0180] [0560] For deep cystic lesions (stage V), excision, curettage, and bone grafting have yielded reasonable results.[6] “Second look” procedures have shown the fibrocartilage tissue[39] that forms in the lesions treated by excision and drilling or when microfracture is present ( Fig. 14-61, C ). The thickness and biomechanics of this fibrocartilaginous tissue is not identical to normal articular cartilage[11] but often can produce a good functional result.


Figure 14-60  Arthroscopic views of (A) osteochondral lesion (OCL), (B) curettage, and (C) postexcision and curettage. Note bloody base and stable rim (arrows) at donor site for OCL.




Figure 14-61  Osteochondral lesion treated with (A) K-wire drilling or (B) microfracture results in (C) replacement with fibrocartilage noted at second-look arthroscopy.



For OLTs in which the articular cartilage is found to be intact on arthroscopy, retrograde drilling of the talus and bone grafting has been suggested ( Fig. 14-62, A through I ). [0530] [0570] Under simultaneous arthroscopic and fluoroscopic control, a Micro Vector drill guide is used to place a guidepin from a lateral incision across the talus to just underneath the posteromedial lesion ( Fig. 14-62, F and G ). A cannulated drill bit then is used to drill a 4.5-mm “tunnel” just up to the lesion. Any necrotic bone in the lesion is removed with small ring curette ( Fig. 14-62, F and G ). Four-millimeter bone plugs are taken from the lateral calcaneus ( Fig. 14-62, H ) and tamped into place until the articular cartilage surface “tents up” a millimeter while visualized through the arthroscope ( Fig. 14-62, I ).


Figure 14-62  Medial dome osteochondral lesion (OCL) treated with retrograde drilling and bone graft. (A and B) Anterior-posterior and lateral radiographs noting only mild medial dome radiolucency, whereas (C and D) coronal and sagittal magnetic resonance imaging clearly demonstrate medial lesion. (E-G) Micro Vector drill guide is used to place a guidepin from a lateral incision across the talus to just underneath the posteromedial lesion. (H) Bone graft taken from calcaneus is (I) tamped into area curetted out under OCL causing mild tenting up of cartilage surface.



When excision, curettage and drilling, or microfracture do not produce a satisfactory result in treating an OLT ( Fig. 14-63, A ), osteochondral transfer or osteochondral autograft transfer system (OATS) procedures have proven useful ( Fig. 14-63, B through F ). Introduced by Hangody in 1997[58] and supported by several other studies, [0590] [0600] [0610] [0620] [0630] cartilage and bone “plugs” are harvested from nonweight-bearing portions of the femoral condyle arthroscopically ( Fig. 14-63, C and D ) or through a knee arthrotomy. Various-size plugs then are implanted into a similarly sized hole drilled into the OLT ( Fig. 14-63, E ). The plugs may be single or “nested” for larger lesions. For osteochondral lesions on the flatter part of the talus, the intercondylar notch of the knee is preferable as a donor site, where the lateral femoral ridge is used for OLTs located in the “corner” region of the talus. [0640] [0650] Despite the thicker articular cartilage of the knee as compared with the talus, good results have been achieved. Sammarco and Makwana[66] described using the nonweight-bearing articular surface of the talus as an ipsilateral donor site. Most cartilage/bone plugs used in OATS procedures are approximately 1cm in depth. Deeper plugs have been used for treating cystic, type-V lesions.[39]


Figure 14-63  (A) Osteochondral lesion (OCL) treated with microfracture with continued pain and poor cartilage production. This lesion required (B-F) osteochondral grafting by taking (C and D) 10-mm autograft plug from medial femoral condyle of knee and (E)placement into the OCL site of talus via a (F) medial malleolar osteotomy fixed with two cannulated screws.



All of the previously mentioned procedures have been used to treat focal, reasonably well-circumscribed lesions of the talus. Their success rates fall when matched against more diffuse areas of articular cartilage damage.

Autologous chondrocyte implantation (ACI) has been one of the newer methods to help treat larger (>1.5cm) talar chondral lesions. Brittberg et al.[67] described treatment for articular lesions of the knee in 1994, using cultured chondrocytes implanted under a periosteal blanket. The OLT is debrided back to stable cartilage borders and down to subchondral bone. Chondrocytes obtained from an initial cartilage biopsy are cultured and grown for later implantation. Fibrin “glue is used to secure and seal the periosteal cover. Giannini in 2001[68] reported use of this technique for resurfacing talar lesions. OLTs up to 3.3cm were treated with improvement to an American Orthopaedic Foot and Ankle Society (AOFAS) ankle score of 91. Patients were begun on continuous passive ROM and kept nonweight bearing for 12 weeks. Kouvalis et al.[69] described a series of patients treated with ACI that had failed previous surgery. Good results were achieved with ACI and weight bearing after 6 to 7 weeks. Schafer[1] and Ferkel[0010] [0700] suggested that this method could be used to treat patients up to 55 years of age with unipolar lesions that were constrained and with a history of previous failed surgery. Results treating “shoulder” lesions have not been as good.[70] “Sandwich” procedures with cultured chondrocytes between two periosteal layers have been used to cover deeper, cystic, type-V lesions filled with cancellous bone graft.

Recently, various commercially prepared collagen-based “scaffolds” or matrices that can be impregnated with cultured chondrocytes have been introduced to replace periosteum as the “blanket” holding the chondrocytes. This Matrix-induced Autologous Chondrocyte Implantation (MACI) offers to eliminate harvesting of periosteum. These methods are an exciting new opportunity to treat larger OLTs that previously had been left untreated or treated with fusion or total ankle replacement. The technique is expensive, demanding, and often considered “experimental” by many health insurers but likely will be more widely available in the future as more good long-term results are reported. Recently, Bently et al.[65] reported 89% good results with ACI in the knee versus 69% using mosaicplasty, although other studies show equivalent results.[71]

Talar body partial or total allografts recently have been reported for use in the treatment of more global talar cartilage damage. In 2001, Gross et al.[72] noted using matched allograft talar replacements (Fig. 14-64 ). Meehan et al.[73] have presented initial good results with this technique. However, long-term follow-up has shown complications of resorption, graft fracture, and failure. Tissue matching is not required for this procedure. Access to a large tissue bank where size-matched allograft can be obtained is essential for this new procedure, thereby limiting availability. The technical and immunologic complexity of this technique must be weighed against the alternatives of ankle fusion or replacement.


Figure 14-64  Anterior-posterior radiograph after allograft total ankle. Note two screws in tibia to hold graft in place and increased density of allograft in tibia and talus.



Review of the literature shows very little detailed, evidence-based information about the role of weight bearing or nonweight bearing in the treatment of these lesions. The literature also is scarce on surgical treatment options on GCTs other than to recognize that they exist and that fusion or total ankle replacement is difficult when such a lesion is present. Mont[74] has written about drilling these talar lesions if conservative measures fail. Methyl methacrylate or talar body prosthetic replacements[75] have been proposed in isolated cases. A talar body allograft may be used. [0720] [0730] Tibiocalcaneal fusion or ankle replacement also have been described as treatment.

My suggested treatment

Acute injuries (less than 4 to 6 weeks)

For acute lesions I prefer to use the Berndt and Harty classification but I often obtain a CT scan to further evaluate the size and position of the lesion. For stage 0 and 1 lesions, the athlete is treated nonweight bearing with active ankle ROM. Salter[76] reported that ROM is helpful in cartilage nutrition and healing. When swelling is down and tenderness of the talus to palpation is gone, a progressive weight-bearing program is begun, followed by general ankle rehabilitation focusing on edema control, ROM, PREs (especially the posterior tibial tendon and peroneal tendons), and proprioception. If the talus remains painful to palpation, a repeat CT scan may be performed to evaluate healing. After successfully completing sports-specific exercises, the athlete may return to sports.

Stage 2 lesions with a fracture line present are treated by nonweight bearing in a boot without AROM until radiographic evidence of healing. A CT scan may be needed to document healing. Return to sports comes after successful completion of ankle rehabilitation and sports-specific exercises. In some cases involving professional players and large fragments, arthroscopy and pinning with bioabsorbable pins or headless screws may allow earlier ROM, healing, and return to sports.

Stage 3 and stage 4 lesions are treated with excision and either drilling or microfracture if less than 1cm. ORIF is performed, either arthroscopically or through a malleolar osteotomy, if the OLT is more than 1cm. Choice of fixation is either bioabsorbable pins or headless screws, depending on the size of the fragment. Any fibrous tissue under the fragment is curetted. These patients are treated postoperatively nonweight bearing in a boot with gentle AROM until routine radiographs or a repeat CT scan reveal healing, General ankle rehabilitation is then initiated, followed by sports-specific exercises.

Chronic OLT lesions (more than 6 weeks old or failed previous treatment)

It is important to assess the patient's symptoms and the imaging study when caring for these athletes. As noted previously, the presence of an OLT on x-ray, CT scan, or MRI does not make it the source of the patient's current symptoms. It is critical to properly assess the athlete and his or her complaints to make sure the symptoms or disability are indeed from the OLT. This evaluation is sometimes difficult.

Treatment of asymptomatic OLTs visualized on incidental radiographs, CT scan, or MRI presents a treatment and ethical dilemma for the sports physician. Several of my colleagues and I have been consulted when an athlete has a totally asymptomatic OLT found on imaging studies of the ankle obtained for unrelated problems. In such situations, the OLT is almost always chronic. In these situations the best option is complete education of the patient. I explain to the athlete that the lesion may become partially or totally loose and symptomatic in the future, with the possibility of ankle arthritis. The nature of surgical treatment with accompanied risks, such as becoming symptomatic, is also discussed. The patient is presented with two general options: first is serial evaluation at yearly intervals with a repeat x-ray and/or MRI. The patient is told to call or report immediately if he or she has any ankle discomfort or swelling. I have followed several patients with large OLTs for several years that are completely asymptomatic and continue to run and engage in recreational athletics without pain or discomfort. Patients with asymptomatic stage 1 lesions are encouraged to take this option.

The other option is prophylactic surgical treatment, often at the end of the current athletic season. In the case of cystic lesions without an overlying osteochondral fragment, it is not unreasonable to offer the athlete retrograde drilling and bone grafting during the off season. Patients are nonweight bearing with AROM for approximately 6 weeks until healing is confirmed by repeat radiographs or CT scan. Rehabilitation then is begun. For asymptomatic stage 2 or 3 lesions, arthroscopy, excision, curettage and drilling with microfracture, or osteochondral transfer is selected. Athletes must understand that this treatment may result in increased symptoms and therefore must be approached with caution.

In treating symptomatic chronic OLTs, ankle radiographs are obtained for baseline evaluation and to help with serial examinations. MRI is used as a screening tool and to evaluate the extent of bony edema. Often a CT scan may be used to clearly define the location and size of the OLT before surgery. Patients are advised that the exact treatment depends on the findings noted at the time of arthroscopy.

If the articular cartilage surface of the talus is intact with either a stage 1 or stage 5 lesion, the preferred treatment is retrograde drilling of the talus, with bone grafting for stage 5 lesions. Postoperatively, athletes begin early AROM and are in a boot nonweight bearing until an x-ray or CT scan demonstrates bone healing. General ankle rehabilitation followed by sports-specific exercises then is started.

For lesions at stage 2, 3, or 4 that are shallow (less than 2mm deep) and less than 1cm in diameter, excision of the lesion and drilling or microfracture (depending on the location of the lesion) are performed. Athletes are nonweight bearing with AROM, as described previously, for 6 to 8 weeks until swelling and tenderness are gone. Rehabilitation and weight bearing then are started as discussed previously.

When treating stage 2, 3, and 4 OLT lesions in which the surface area is more than 1cm I prefer osteochondral transfer from the knee (OATS procedure). As long as the lesion appears to be located on the edge or medial or lateral surface of the talus and can be reached by a malleolar osteotomy or arthroscopy, single or nested matched osteochondral plugs provide very good results. Careful orientation of the drill holes perpendicular to the articular surface is critical. Proper matching of the plug contour to the natural contour of the talus also is important. As other authors have described,[64] the plug or plugs are left very slightly “proud” at the time of surgery. The postoperative regimen is the same as described previously.

For cystic lesions at stage 2, 3, or 5 (in which the cartilage surface is disrupted) less than 1cm, excision, curettage, and placement of cancellous bone graft as suggested by Lanny Johnson have proven successful. The same nonweight bearing and early AROM postoperative protocol is prescribed. On occasions in which I have had the opportunity to do a “second look” procedure on these patients, the fibrocartilage healing is similar to those with more shallow lesions treated by excision and drilling/microfracture. For larger cystic lesions at stage 2, 3, or 4, an osteochondral transfer with a deeper plug may be used, or cancellous bone graft may be inserted[39] before placing the plug.

In cases in which initial surgical treatment for OLT has failed, medial malleolar osteotomy and the OATS procedure seem to be the procedure of choice for lesions less than 3cm. Larger lesions (>1.5cm diameter) may be treated with ACI or MACI. I do not have any experience with this technique, although increasingly reports seem to indicate this is the procedure of choice for these large lesions. Expense and insurance approval are major hurdles to its use. Larger lesions or bipolar lesions involving both talar and tibial surfaces lend to treatment with talar allografts.[16] Immunologic difficulties, limited access to a large, talar bone bank, and lack of long-term experience have limited the use of this salvage procedure.

Treatment of GCTs

As noted previously, these injuries are commonly missed, both in the acute or chronic setting after a significant compression and/or twisting injury to the ankle. The initial radiographs usually are negative and the diagnosis rests with initial suspicion, talar tenderness on palpation, and MRI confirmation. Acute or chronic GCT is treated with protection in a boot, nonweight bearing with early AROM. I place the patients on calcium and vitamin D supplementation and use a bone stimulator. Weight bearing is permitted when the talus is nontender to palpation and swelling is diminished. Healing often is prolonged because of the poor blood supply of the talus and may take several months. If healing of the fracture or progress is in doubt, a repeat MRI is obtained at 3-month intervals. Usually I allow weight bearing in the boot first, followed by weight bearing in shoes. Appropriate therapy then is started followed by sports-specific exercises.

For GCT lesions in which the talus remains painful and healing is delayed (>6 months of treatment), I prefer arthroscopic and fluoroscopic-directed drilling of the talus in a retrograde fashion (see Fig. 14-65, A through F ). Multiple passes are made with a 2-mm drill bit into the area indicated on the recent MRI. When the talus is nontender and/or the MRI shows resolution, weight bearing and therapy are initiated. I have obtained roughly 50% good results with this approach. Failure of CGT treatment may lead to progressive ankle arthritis or talar avascular necrosis and collapse. Both ankle fusion and arthroplasty are difficult salvage procedures because of poor bone quality and obviously preclude competitive sports participation.


Figure 14-65  Global compression injury of talus treated with drilling as preferred by me. (A) Sagittal magnetic resonance imaging denoting global talar edema, with (B) normal cartilage noted on arthroscopy. (C-F) Fluoroscopically guided drilling of talus with multiple passes to improve blood supply and encourage healing.





  1. Schafer DB: Cartilage repair of the talus.  Foot Ankle Clin2003; 8:739.
  2. Higgins TF, Baumgaertner MR: Diagnosis and treatment of fractures of the talus: a comprehensive review of the literature.  Foot Ankle Int1999; 20:595.
  3. Tol JL, et al: Treatment strategies in osteochondral defects of the talar dome: a systematic review.  Foot Ankle Int2000; 21:119.
  4. Mulfinger GL, Trueta J: The blood supply of the talus.  J Bone Joint Surg Am1970; 52B:160.
  5. Frey C: Injuries to the subtalar joint.   In: Pfefer G, ed. Chronic ankle pain in the athlete,  Rosemont, IL: American Academy of Orthopedic Surgeons (AAOS) monograph series; 2000.
  6. Berkowitz M, Kim D: Process and tubercle fractures of the hindfoot.  J Am Acad Orthop Surg2005; 13:492.
  7. Degan T, Morrey B, Braun D: Surgical excision for anterior-process fractures of the calcaneus.  J Bone Joint Surg Am1982; 64:519.
  8. Frey C, et al: Arthroscopic resection of an anterior calcaneal fracture: a case report.  Foot Ankle Int2005; 26:409.
  9. Hedrick MR, McBryde AM: Posterior ankle impingement.  Foot Ankle1994; 15:2.
  10. Nasser S, Manoli A: Fracture of the entire posterior process of the talus: a case report.  Foot Ankle Int1990; 10:235.
  11. Kim D, Berkowitz M, Pressman D: Avulsion fractures of the medial tubercle of the posterior process of the talus.  Foot Ankle Int2003; 24:172.
  12. Wolf RS, Heckman JD: Case report: fracture of the posterior medial tubercle of the talus secondary to direct trauma.  Foot Ankle Int1998; 19:255.
  13. Ahmad J, Raikin S: Current concepts review: talar fractures.  Foot Ankle Int2006; 27:475.
  14. Hamilton WG: Stenosing tenosynovitis of the flexor hallucis longus tendon and posterior impingement upon the os trigonum in ballet dancers.  Foot Ankle Int1982; 3:74.
  15. McDougal A: The os trigonum.  J Bone Joint Surg Am1955; 37B:257.
  16. Abramowitz Y, et al: Outcome of resection of a symptomatic os trigonum.  J Bone Joint Surg Am2003; 85A:1051.
  17. Veazy BL, et al: Excision of ununited fractures of the posterior process of the talus: a treatment for chronic posterior ankle pain.  Foot Ankle Int1992; 13:453.
  18. Paulos LE, Johnson CL, Noyes FR: Posterior compartment fractures of the ankle: a commonly missed athletic injury.  Am J Sport Med1983; 11:439.
  19. Karasck D, Schweitzer M: The os trigonum syndrome: imaging features.  AJR1996; 166:125.
  20. Johnson RP, Collier BD, Carrera GF: The os trigonum syndrome: use of bone scan in the diagnosis.  J Trauma1984; 24:761.
  21. Sopov J, Liberson A, Grosher D: Bone scintigraphic findings of os trigonum: a prospective study of 100 soldiers on active duty.  Foot Ankle Int2000; 21:822.
  22. Ebraheim NA, Padanilam TG, Wong FY: Posterior process fractures of the talus.  Foot Ankle Int1995; 16:734.
  23. Nadim Y, Tosic A, Ebraheim N: Open reduction and internal fixation of fracture of the posterior process of the talus: a case report and review of the literature.  Foot Ankle Int1999; 20:50.
  24. Kanbe K, et al: Fracture of the posterior medial tubercle of the talus treated by internal fixation; a report of two cases.  Foot Ankle Int1995; 16:164.
  25. Giuffrida AY, et al: Pseudo os trigonum sign: missed posteromedial talar facet fracture.  Foot Ankle Int2003; 24:642.
  26. Marumoto JM, Ferkel RD: Arthroscopic excision of the os trigonum: a new technique with preliminary clinical results.  Foot Ankle Int1997; 18:777.
  27. Lombardi CM, Silhanek AD, Connolly FG: Modified arthroscopic excision of the flexor hallucis longus tendon: operative techniques and case study.  J Foot Ankle Surg1999; 38:347.
  28. Tucker DJ, Feder JM, Boylan JP: Fractures of the lateral process of the talus: two case reports and a comprehensive literature review.  Foot Ankle Int1998; 19:641.
  29. Funk JR, Srinivasan SCM, Crandall JR: Snowboarder's talus fractures experimentally produced by eversion and dorsiflexion.  Am J Sport Med2003; 31:921.
  30. Kirkpatrick DP, et al: The snowboarder's foot and ankle.  Am J Sport Med1998; 26:271.
  31. Heckman JD, McLean MR: Fractures of the lateral process of the talus.  Clin Orthop1985; 199:108.
  32. Valderrabano V, et al: Snowboarder's talus fracture: treatment outcome of 20 cases after 2.5 years.  Am J Sport Med2005; 33:871.
  33. Sanders TG, Ptaszek AJ, Morrison WB: Fracture of the lateral process of the talus: appearance at MR imaging and clinical significance.  Skeletal Radiol1999; 28:236.
  34. König F: Ueber freie korper in den celeken.  Deutsch Z Chir1888; 27:90.
  35. Berndt AL, Harty M: Transchondral fractures (osteochondritis dissecans) of the talus.  J Bone Joint Surg Am1959; 41A:988.
  36. Nunley J: Allograft placement for osteochondral lesions of the talus.   In: Easley ME, et al ed. Osteochrondral lesions of the talus: current therapeutic dilemmas,  2005.
  37. Brunes J, Behrens P: Etiological and pathophysiologic aspects of osteochondrosis dissecans.  Arthroskopie1998; 11:166.
  38. Yao J, Weiss Jr E: Osteochondritis dissecans.  Orthop Rev1985; 14:190.
  39. Scranton PE, McDermott JE: Treatment of type V osteochondral lesion of the talus with ipsilateral knee osteochondral autografts.  Foot Ankle Int2001; 22:380.
  40. Ferkel RD: Arthroscopic treatment of osteochondral lesions, soft-tissue impingement and loose bodies.   In: Pfefer G, ed. Arthroscopic treatment of osteochondral lesions, soft-tissue impingement and loose bodies,  Rosemont, IL: American Academy or Orthopedic Surgeons (AAOS) monograph series; 2000.
  41. Giannini S, Vannini F: Operative treatment of osteochondral lesions of the talar dome: current concepts review.  Foot Ankle Int2004; 25:168.
  42. Schachter AK, et al: Osteochondral lesions of the talus.  J Am Acad Orthop Surg2005; 13:152.
  43. Hepple S, Winson IG, Glew D: Osteochondral lesions of the talus: a revised classification.  Foot Ankle Int1999; 20:789.
  44. Angermann P, Jensen P: Osteochondritis dissecans of the talus: long term results of surgical treatment.  Foot Ankle Int1989; 10:161.
  45. Kumsi T, et al: Arthroscopic drilling for the treatment of osteochondral lesions of the talus.  J bone and Joint Surg1999; 81A:1229.
  46. Verhagen RAW, et al: Prospective study on diagnostic strategies in osteochondral lesions of the talus is MRI superior to helical CT?.  J Bone Joint Surg2003; 87B:41.
  47. Mintz DN, et al: Osteochondral lesions of the talus: a new magnetic resonance grading system with arthroscopic correlation.  Arthroscopy2003; 19:353.
  48. Schimmer RC, Dick W, Hintermann B: The role of ankle arthroscopy in the treatment strategies of osteochondritis dissecans lesions of the talus.  Foot Ankle Int2001; 22:895.
  49. Schafer D, Boss A, Hintermann B: Accuracy of arthroscopic assessment of anterior ankle cartilage lesions.  Foot Ankle Int2003; 24:317.
  50. Muir D, et al: Talar dome access for osteochondral lesions.  Am J Sport Med2006; 34:1457.
  51. Ferkel RD: Arthroscopic surgery the foot and ankle,  Philadelphia, Lippincott-Raven., 1996.
  52. Pritsch M, Horoshuski H, Farine I: Arthroscopic treatment of osteochondral lesions of the talus.  J Bone Joint Surg1986; 68A:862.
  53. Taranow WS, et al: Retrograde drilling of osteochondral lesions of the medial talar dome.  Foot Ankle Int1999; 20:474.
  54. Nam EK, Ferkel RD: Ankle and subtalar arthroscopy.   In: Thordarson DB, ed. Foot & ankle,  Philadelphia: Lippincott Williams & Wilkins; 2004.
  55. Tochigi Y, et al: Technique tip; surgical approach for centrolateral talar osteochondral lesions with anterolateral osteotomy.  Foot Ankle Int2002; 23:1038.
  56. Scranton Jr PE: An overview of strategies for resurfacing lower extremity osteochondral defects.   In: Easley ME, et al ed. Osteochrondral lesions of the talus: current therapeutic dilemmas,  2005.
  57. Kono M, et al: Retrograde drilling for osteochondral lesions of the talar dome.  Am J Sport Med2006; 34:1450.
  58. Hangody L, et al: Treatment of osteochondritis dissecans of the talus: use of the mosaicplasty technique—a preliminary report.  Foot Ankle Int1997; 18:628.
  59. Hangody L, et al: Mosaicplasty for the treatment of osteochondritis dissecans of the talus: two to seven year results in 36 patients.  Foot Ankle Int2001; 22:552.
  60. Al-Shaikh RA, et al: Autologous osteochondral grafting for talar cartilage defects.  Foot Ankle Int2002; 23:381.
  61. Assenmacher JA, et al: Arthroscopically assisted autologous osteochondral transplantation for osteochondral lesions of the talar dome: an MRI and clinical follow-up study.  Foot Ankle Int2001; 22:544.
  62. Lee CH, et al: Osteochondral autografts for osteochondritis dissecans of the talus.  Foot Ankle Int2003; 24:815.
  63. Kreuz PC, et al: Mosaicplasty with autogenous talar autograft for osteochondral lesions of the talus after failed primary arthroscopic management.  Am J Sport Med2006; 34:55.
  64. Marymont JV, et al: Computerized matching of autologous femoral grafts for the treatment of medial talar osteochondral defects.  Foot Ankle Int2005; 26:708.
  65. Bently G, et al: A prospective, randomized comparison of autologous chondrocyte implantation versus mosaicplasty for osteochondral defects in the knee.  J Bone Joint Surg2003; 85B:223.
  66. Sammarco GJ, Makwana NK: Treatment of talar osteochondral lesions using local osteochondral graft.  Foot Ankle Int2002; 22:693.
  67. Brittberg M, et al: Treatment of deep cartilage defects in the knee with autologous chondrocyte transplantation.  N Engl J Med1994; 331:889.
  68. Giannini S, et al: Autologous chondrocyte transplantation in osteochondral lesions of the ankle joint.  Foot Ankle Int2001; 22:513.
  69. Kouvalis D, Shultz W, Heyden M: Autologous chondrocyte transplantation for osteochondritis dissecans of the talus.  Clin Orthop2002; 395:186.
  70. Ferkel RD: Autologous chondrocyte implantation.   In: Easley ME, et al ed. Osteochrondral lesions of the talus: current therapeutic dilemmas,  2005.
  71. Smith GD, Knutsen G, Richardson JB: A clinical review of cartilage repair techniques.  J Bone Joint Surg2005; 87B:445.
  72. Gross AE, Zgnidis Z, Hutchinson CR: Osteochondral defects of the talus treated with fresh osteochondral allograft transplant.  Foot Ankle Int2001; 22:385.
  73. Meehan R, et al: Fresh ankle osteochondral allograft transplant for tibiotalar joint arthritis.  Foot Ankle Int2005; 26:793.
  74. Mont MA, et al: Avascular necrosis of the talus treated by core decompression.  J Bone Joint Surg1996; 78B:827.
  75. Harnroongroj T, Vanadurongwan V: The talar body prosthesis.  J Bone Joint Surg1997; 79A:1313.
  76. Salter RB: The biologic concept of continuous passive motion of synovial joints the first 18 years of basic research and its clinical application.  Clin Orthop1989; 242:12.