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

Section 4 - Unique Problems in Sport and Dance

Chapter 25 - New advances in the foot and ankle

Gregory C. Berlet,Peter B. Maurus,
Terrence Philbin,
Thomas H. Lee







Osteochondral lesions of the talus



On the horizon



Chronic ankle instability



Foot and ankle arthroscopy





Orthopaedic surgery is a dynamic field of medicine with ever-changing advances in knowledge and techniques. As our patient populations continue to grow younger and more active, we search for more anatomic and less invasive methods of addressing pathology. The subspecialty of surgery of the foot and ankle likewise is participating in this exciting evolution of understanding and approaches to common acute and chronic conditions of the foot and ankle. In this chapter we discuss newer techniques and treatment options for foot and ankle disorders.


Osteochondral Lesions of the Talus

Osteochondral lesions of the talus (OLT) are rare, representing just 4% of all such lesions in the body.[1] The term OLT evolved from an 1888 report that described “osteochondritis dissecans” as a loose body associated with articular cartilage and subchondral bone fracture.[2] Because inflammation is not an important factor in the etiology of OLT, many authors do not use the term “osteochondritis dissecans.”

The two locations most often seen in which OLTs are involved are posteromedial and anterolateral. Trauma is cited as the etiology in more that 85% of patients. [0030] [0040] [0050] [0060] [0070] Although the etiology of nontraumatic OLT is unknown, some reports have cited a primary ischemic event or genetic predisposition (e.g., identical medial talar lesions in identical twins, multiple lesions occurring in the same patient) as a cause.[8]

Acute traumatic events are typically the cause of lateral lesions. Lesions on the anterolateral aspect of the talar dome are caused by inversion and dorsiflexion, resulting in the anterolateral aspect of the talar dome's impacting the fibula. These lesions usually more shallow and “wafer shaped” than medial lesions.[9]

Medial lesions usually are caused by repetitive overuse syndromes; ; only a small number of medial lesions can be attributed to trauma. Posteromedial lesions result from inversion, plantarflexion, and external rotational forces. The posteromedial talar dome impacts the tibial articular surface, leading to a deep, cup-shaped lesion in the talus.

The classic presentation for the OLT is characterized by chronic ankle pain with swelling. The pain usually is localized to the side of the ankle where the lesion is located. Other symptoms include weakness, stiffness, catching, and giving way with repeated inversion injuries. Initial physical examination signs include tenderness on palpation behind the medial malleolus with the ankle dorsiflexed (posteromedial lesions) and over the anterolateral ankle joint when in maximal plantarflexion (anterolateral lesions). A joint effusion is a clear sign of intra-articular involvement.

Weight-bearing plain radiographs should be used to evaluate the ankle (anterior-posterior, lateral, and mortise views). Posteromedial lesions are evaluated best by imaging the ankle in various degrees of plantarflexion. Anterolateral lesions are evaluated best by imaging the ankle in various degrees of dorsiflexion. In our experience, magnetic resonance imaging (MRI) is the most appropriate imaging modality to evaluate for OLT. Areas of low signal intensity on T1-weighted images indicate a chronic lesion resulting from sclerosis of the bed of the talus.[10] High signal rims on T2-weighted images indicate an unstable osteochondral fragment. [0110] [0120] Intra-articular, gadolinium-enhanced MRI can provide images of articular cartilage, assess stability, and detect intra-articular bodies.[13] Significant ankle effusions may provide a “physiologic arthrogram,” negating the need for gadolinium.

The OLT should be staged before treatment is determined. In 1959, Berndt and Harty[14] devised a system for staging OLT. Since that time, various researchers have revised and refined their original classification systems as newer technologies, such as arthroscopy, computed tomography (CT), and MRI became available. Table 25-1 is a staging classification developed by Hepple et al.[15] and is based on MRI imaging.

Table 25-1   -- Classification System for Staging Osteochondral Lesions of the Talus Using Magnetic Resonance Imaging

Stage I

Articular cartilage damage only

Stage IIa

Articular cartilage injury with underlying fracture and edema

Stage IIb

Stage II without edema

Stage III

Detached fragment (rim signal) but nondisplaced

Stage IV

Displaced fragment

Stage V

Subchondral cyst formation





Generally, conservative treatment should be attempted first. Two studies reviewed the long-term outcomes of patients with OLT and the possible development of osteoarthrosis. Conservative treatment consists of protected ambulation for pain relief and an appropriate sports brace during activity. Conservative treatment should be attempted for at least 6 months. McCullough and Venugopal[16] followed 10 patients for 15 years and found that although conservative treatment often does not lead to radiographic union, osteoarthrosis was uncommon unless the fragment was detached. They stated that patients with nondisplaced fragments could be treated conservatively but that acute displaced fractures should undergo immediate reduction and internal fixation. Bauer et al.[17] concurred that osteoarthrosis of the ankle is a rare occurrence and found that skeletally immature ankles have the best prognosis for healing with conservative treatment. In summary, asymptomatic and nondisplaced OLT should undergo conservative treatment, whereas displaced or continued symptomatic lesions should be treated surgically.


There are three surgical options for the displaced OLT. These are acute open reduction and internal fixation (ORIF), open or arthroscopic debridement and/or excision with drilling, and cartilage restoration procedures.

Internal fixation

ORIF is most appropriate for acute lesions with a significant osseous piece remaining attached to the chondral flap. Internal fixation historically has been accomplished with hardware (Kirschner wires, screws), although recent trends move toward biologic fixation. Biologic fixation can be accomplished using antegrade or retrograde bioabsorbable screws and/or antegrade biologic pins (SmartNail, Bionx Implants, Finland). An interesting recent advantage is the use of osteochondral plug transfer to internally fix an unstable osteochondritis dissecans (OCD) lesion. In two separate articles, Berlet and Yoshizumi reported on their technique for fixation and grafting of an OCD lesion about the knee. [0180] [0190] This technique (COR, Mitek Worldwide, Westwood, MA), which uses smaller diameter plugs, can function both to stabilize the lesion and graft across the lesion into healthy bone. It is the authors' experience that most acute lesions may be reduced and secured using antegrade biologic pins. Fibrin sealant may be an appropriate adjuvant to the internally stabilized OLT and has been shown to be effective in clinical studies.[20]

Debridement, microfracture, and drilling

If a lesion is detached or sufficiently fragmented such that it is not amenable to internal fixation, excision of the fragments, debridement, and drilling are warranted. The cartilage edges are trimmed and smoothed, and the bony base is debrided down to bleeding bone. Subchondral drilling provides vascular access channels. Mesenchymal stem cells released from the underlying bone proliferate and undergo chondrocyte differentiation to provide a fibrocartilage cap for the chondral defect. Studies have shown this method to be more effective than simple excision and curettage or simple excision alone. [0210] [0220] [0230]

Retrograde drilling is ideal for cystic subchondral lesions with intact articular cartilage. Using specialized systems, accurate drilling of the lesion is possible. This drill path provides revascularization, and the bone graft serves as osteoconductive and osteoinductive material. This technique has advantages over antegrade drilling in that it does not alter the actual articular surface integrity. Retrograde drilling of a talar OCD was first described in 1981 as an isolated case.[24] More recently, a modification of this technique with arthroscopic assistance was described. Clinical research has shown good clinical results with this technique.[23] A study by Taranow et al.[23] looked at 16 patients after retrograde drilling and grafting of OLTs. There were no complications and a significant increase in the American Orthopaedic Foot and Ankle Society (AOFAS) Ankle/Hindfoot score. This technique is recommended for the subchondral cyst on the basis of its early surgical success and the absence of complications associated with transmalleolar osteotomies, transmalleolar drilling, and chondrolytic debridement.

Cartilage Restoration Procedures

Although microfracture and drilling techniques produce a fibrocartilage tissue in the affected area, it does not produce normal hyaline cartilage. In efforts to restore a joint surface with more anatomic and favorable biomechanical properties, newer procedures have been developed to restore a hyaline cartilage surface. Lesions greater than 10mm in diameter may be best managed primarily with cartilage restoration procedures instead of excision and drilling. [25]

Autologous osteochondral grafting (osteoarticular transfer system, mosaicplasty)

The osteoarticular transfer system (OATS) and mosaicplasty transplant viable plugs of cartilage and subchondral bone from various donor sites into the talar dome.

Single-plug systems, such as OATS, harvest a single, large plug to match the size of the lesion. This method is postulated to reduce the fibrocartilage ingrowth seen in multiple-plug system. Donor site morbidity, however, is a bigger concern because of the size of the graft. Arthrex OATS procedures were used in nine patients in a study by Assenmacher et al.[26] At an average of 9.3 months, MRI revealed stable graft osteointegration by DeSmet criteria in all patients. Patients reported significant clinical improvement on the basis of visual analog pain scales and the AOFAS Ankle/Hindfoot scores (average 80.2).[4] Al-Shaikh et al.[27] reviewed the results of 19 patients who underwent the Arthrex OATS technique for lesions averaging 12 × 10mm in 19 patients. Sixty-eight percent of these patients had failed prior attempts at excision, curettage, and/or drilling. At an average of 16 months, patients reported improvement in AOFAS Ankle/Hindfoot scores (88 average) and reported no significant donor site morbidity. Eighty-nine percent of these patients stated that they would have this procedure done again. Al-Shaikh et al.[27] concluded that the OATS procedure is a viable salvage technique for patients who failed prior debridement procedures.

In multiple-plug systems (mosaicplasty), a number of osteochondral plugs are harvested to fill the defect. These plugs can recontour the surface of the talar dome, but critics have found that up to 20% to 40% of the defect is replaced by fibrocartilage.[27] Gautier et al.[28] showed good to excellent results in 11 patients at an average of 24 months, using Sulzermedica's SDS “Soft Delivery System.” The lesions in this study averaged 18 × 10mm, and the authors made no recommendations for absolute size limits. Previous studies, however, recommended a lower size limit of 10mm. Hangody et al.[25]looked at 36 patients treated with mosaicplasty at 2- to 7-year follow-up. All of these lesions were greater than 10mm in diameter. Ninety-four percent of these patients reported good to excellent results using the Hannover scoring system, with no long-term knee donor site morbidity.

Osteochondral plugs can also be harvested from the ipsilateral talus. Sammarco and Makwana[29] harvested osteochondral plugs form the medial and lateral talar facets in 12 patients. The authors reported significant improvement in the AOFAS Ankle/Hindfoot scores and found no structural failures in the donor site or graft site.

Autogenous chondrocyte implantation

If the osteochondral lesion is large (greater than 2 × 1cm), it is not amenable to OATS or mosaicplasty because of the expected size of the donor defect. Autogenous chondrocyte implantation (ACI) is a new technique that is showing promise for these larger lesions in the knee and ankle. In 1994, Swedish investigators first reported on this novel technique for large osteochondral lesions in the knee.[30] They looked at 23 patients over a 2- to 7-year follow-up period with lesions measuring from 1.5 to 6.5cm in diameter and in whom all prior treatments had failed. Eighty-eight percent of their patients had good or excellent results. Studies in the United States and further extensive studies in Sweden have validated these results at up to 10 years. [0310] [0320] [0330] [0340]

ACI is indicated in younger patient [0150] [0160] [0170] [0180] [0190] [0200] [0210] [0220] [0230] [0240] [0250] [0260] [0270] [0280] [0290] [0300] [0310] [0320] [0330] [0340] [0350] [0360] [0370] [0380] [0390] [0400] [0410] [0420] [0430] [0440] [0450] [0460] [0470] [0480] [0490] [0500] [0510] [0520] [0530] [0540] [0550] [0560] [0570] [0580] [0590] with focal osteochondral defects without diffuse arthritis. A “kissing lesion” on the tibial plafond is a contraindication to this procedure because results are very poor when this is present. Other patients who could benefit from this procedure are those with failed prior surgeries and those who have large lesions with extensive subchondral cystic changes. Multifocal lesions could be treated with ACI in some cases. Patients who should not undergo ACI are those who have not had an attempt at other forms of surgical treatment, those with early degenerative changes or osteoarthritis, or those with uncorrected malalignment or instability.

The basic principle is to harvest viable chondrocytes from the patient, culture the chondrocytes, and reimplant them into the patient. This technique requires a two-stage procedure. First, an arthroscopic evaluation of the lesion is undertaken. Arthroscopy allows a thorough evaluation of the size and shape of the lesion, as well as the overall integrity of the adjacent and opposite cartilage surfaces. A biopsy of healthy articular cartilage (approximately 200-300mg) then is taken from a nonweight-bearing area of articular cartilage (typically the intercondylar notch of the knee in a separate arthroscopic procedure). This biopsy is sent for laboratory culture and growth of additional chondrocytes. The process involves enzymatic digestion of the tissue and cultivation, which leads to a tenfold increase in chondrocytes. After 2 to 3 weeks in culture under the presence of antibiotics to ensure sterility, approximately 10 to 12 million cells will be available for transplantation. The second stage of this procedure is the implantation of the cultured cells. Postoperative care is essential in ensuring a good result.

Giannini et al.[35] reported excellent results at up to 26 months in eight patients who underwent ACI for OLT. They not only showed improved clinical scores (AOFAS Ankle/Hindfoot scores improving from 32 to 91/100) but also showed regenerated areas of cartilage on follow-up arthroscopy and normal type II hyaline cartilage by histology. Minas and Peterson published a study of 14 patients with ACI at an average follow-up of 28 months.[36] They reported an 11/14 good to excellent outcome, with two poor results and one lost to follow-up. In a recent study on the economics and quality of life profile of this procedure, Minas[37] showed significant improvement in quality of life at 2 years, and the technique was found to be cost effective in comparison with other treatment modalities.

Other new techniques

There is a new interest in bulk fresh osteochondral allografts for the replacement of large areas of focal cartilage damage. Candidates are matched to donors on the basis of joint size, and the surgery is performed within 5 days of tissue recovery to optimize the survival of the donor cartilage. Tontz et al. report on 12 patients at an average of 21-month follow-up who had bulk tibiotalar allografts.[38] They reported intraoperative fracture in one patient and graft collapse in another, but overall satisfaction and relief of pain in the other 10 patients. They concluded that this technique shows promise for the treatment of articular cartilage defects in young, active patients. Gross et al.[39] performed fresh osteochondral graft transplantation in nine patients for OLT (one case was for acute open fracture of the talus). Six of the nine grafts remained viable at an average of 11 years. Three cases went on to arthrodesis because of graft resorption. In a literature review on the treatment of OLT, Caylor and Pearsall[40]conclude that bulk fresh allografts can provide excellent results. The concern with these fresh bulk allografts is the host immune reaction to viable cells within the graft and the possibility of major infections. Also, graft collapse has been shown to occur in some cases.[41] More research in this area is needed to ensure the safety and efficacy of this procedure.


On The Horizon

Tissue engineering and gene therapy currently are being studied as a way to provide a growth mechanism for normal hyaline cartilage. This current technique already has shown early success in animal models but still remains in the early experimental stages. [0400] [0410] [0420] [0430] [0440] [0450] Filling cartilage defects with scaffolds of collagen or synthetic carbons promotes cell migration provides a template for matrix formation. The chondrocyte response may be amplified by embedding growth factors into the scaffold.[46] These newer modalities possibly will revolutionize our approach to cartilage lesions.


The time relationship between pain and instability is important. That is, pain followed by instability often is due to intra-articular pathology. Pain inhibition of normal neuromuscular pathways can mimic ligamentous instability. Therefore ankle instability episodes can originate from an OLT with ligamentous laxity.

A persistent ankle joint effusion points to an intra-articular pathology, and an articular cartilage lesion should be suspected.

ACI and OATS are salvage procedures to be used after debridement, microfracture, or drilling have failed.

Literature supports debridement, microfracture, or drilling as the first-line treatment when an OCD fragment cannot be stabilized.

Internal fixation of OLT provides the best prognosis because you are saving the patient's own cartilage.

Case Studies 1 and 2  

A 40-year-old, male physician presents to the office with severe pain and swelling in his right ankle after an eversion injury while playing basketball. He complains of pain along the anterolateral aspect of his ankle. He also has a great deal of crepitus, catching, and locking with any motion. On examination, the ankle is grossly swollen with lateral ecchymosis. Range-of-motion testing elicits severe pain and crepitus along the lateral aspect of the ankle. Ankle stability is grossly normal on examination. Plain radiographs of the ankle illustrate a lateral talar defect ( Fig. 25-1, A ). The ankle mortise is intact. MRI examination shows a 0.5- to 1.0-cm osteochondral defect with fluid surrounding the lesion ( Fig. 25-1, B ). This represents a detached osteochondral lesion of the talus. An ankle arthroscopy was performed that allowed the visualization of a large osteochondral fragment ( Fig. 25-1, C ). The talus then was approached through a lateral incision ( Fig. 25-1,D ). The fragment was reduced and fixed with bioabsorbable pins (SmartNail, Bionx Implants, Finland). The patient tolerated the procedure well and has returned to normal activities without pain at 8 months.

A 30-year-old woman presents with complaints of continued right ankle pain after an inversion injury 3 months prior. She has suffered from pain, swelling, locking, and catching since that time. She has no history of prior ankle injuries. On examination, she has an antalgic gait on the right. The foot and ankle are neurovascularly intact. There are no obvious deformities, and the ankle is stable on drawer testing. There is, however, an ankle effusion. Plain radiographs of the ankle do not show any abnormalities. An MRI showed an obvious osteochondral lesion off the posteromedial aspect of the talus. The lesion measured approximately 1cm[2], with clear fluid seen within the cavity. This represents a displaced osteochondral lesion ( Fig. 25-2, A ). For a lesion that cannot be fixed, first-line treatment is ankle arthroscopy with debridement and drilling. Only if this technique were to fail would we consider cartilage restoration procedures. She underwent the arthroscopy and followed a conservative rehabilitation protocol. After 8 months, she has continued pain and swelling in her right ankle. A repeat MRI shows edema and incongruity of the talus in the area of the OCD. Because of her continued symptoms, we decided to perform osteochondral autograft reconstruction of the defect (mosaicplasty) ( Fig. 25-2, B ). She is now 1 year out from surgery and has no pain or swelling and has returned to her normal activities.



Figure 25-1  A, Plain radiograph of an ankle illustrating an anterolateral osteochondral lesion of the talus (OLT). B, Magnetic resonance imaging (MRI) of the ankle from A illustrating a displaced OLT. C, Intraoperative arthroscopic image of a large displaced OLT.D, Intraoperative image of the OLT from C after open reduction and internal fixation with bioabsorbable pins.  Photographs courtesy Gregory C. Berlet, MD, Orthopedic Foot and Ankle Center, Columbus, Ohio.




Figure 25-2  A, Magnetic resonance imaging of an ankle illustrating a large, displaced posteromedial osteochondral lesion of the talus (OLT). B, Intraoperative image of the OLT from A after mosaicplasty reconstruction of the defect.  Photographs courtesy Gregory C. Berlet, MD, Orthopedic Foot and Ankle Center, Columbus, Ohio.



Chronic Ankle Instability

Lateral ankle sprains are one of the most common sports-related injuries, representing as many as 40% of presenting complaints.[47] Chronic lateral ankle instability has been estimated to occur in up to 42% of patients who sustain acute injuries. [0480] [0490] Functional lateral instability, as introduced by Freeman[50] describes a subjective complaint of giving way in the ankle joint. Work by Tropp et al.[51]further described this condition as motion beyond voluntary control but not exceeding the physiologic range of motion. Mechanical instability is motion beyond the normal physiologic limits of the ankle joint. This is manifested as excessive anterolateral ankle laxity. The lateral ankle ligaments (anterior talofibular ligament and calcaneofibular ligament) work to prevent inversion of the talus in the ankle mortise. Conservative treatment for chronic lateral ankle instability consists of rest, anti-inflammatories, and physical therapy. Persistent failure (repeated giving way) of this lateral ligament complex, however, is an indication for surgical stabilization of the ankle.

Surgical options

There are multiple surgical options for surgical stabilization of the chronically unstable ankle, both anatomic and nonanatomic. One should refer to Chapter 13 for a more exhaustive review of the traditional surgical approaches for ankle instability.

Nonanatomic lateral ligament stabilizations are characterized by extra-articular tendon weave techniques. These techniques risk overconstraining the ankle joint and are not isometric in their kinematic effect on the ankle joint. Thus they should be reserved for revisions or unique clinical situations.

Anatomic lateral ligament stabilizations accept the patient's natural ligament insertion points but adjust the tension on that ligament. Isometry is not disturbed, and overconstraint is rare. Anatomic reconstructions include the modified Brostrom lateral ligament reconstruction and thermal capsular modification. The Brostrom reconstruction is described in Chapter 13 .

Thermal capsular modification

Thermal capsular modification has been shown to be a new and effective treatment of lateral ankle laxity. A thermal probe applied to the anterior talofibular ligament and lateral capsule causes denaturing and “shrinkage” of the tissue by breaking the intramolecular bonds within the type I collagen. Thermal energy applied through a feedback-controlled probe at 65° to 70° C results in a 30% contracture of the tissue.[52] Through stabilization and immobilization, these ligaments can assume a new, shortened position on healing. Postoperative immobilization is mandatory for a 9-week period to prevent stretching of the treated tissue. This procedure is indicated for patients with moderate builds, nonavulsed ligaments, no prior stabilization procedures, and a commitment to the strict postoperative protocol. Moreover, with this technique, other intra-articular pathology can be identified and treated arthroscopically. Clinical results with thermal capsular modification have been encouraging.[53] Berlet et al. presented the largest series in the literature, reporting on 42 patients who underwent thermal capsular shrinkage for chronic lateral ankle instability.[54] At an average follow-up of 12 months, there was a significant increase in the AOFAS Ankle/Hindfoot scores and the SF-12 (SF-12 Health Survey, The Health Institute, New England


An anatomically based physical examination will guide the physician to the appropriate diagnosis in chronic ankle pain in the athlete.

Thermal capsular modification can be considered for patients with functional ankle instability and grade I/II ankle instability. Grade III and revision situations are addressed best with open techniques.

Medical Center, Boston, MA) physical and mental components. Patients' SF-12 scores returned to normal when compared with age and sex matched controls with no history of ankle pain.[54]

Case Study 3  

A 20-year-old, college cheerleader presents to the office with recurrent ankle sprains. An aggressive rehabilitation program with physical therapy has been performed for each significant injury (once a year for the last 3 years). Her recovery from the sprains is becoming more prolonged. Her last sprain resulted in the loss of a 3-month period of cheering. She has never felt that she has returned to her full strength. On physical examination, she has normal hindfoot alignment (no varus) and poor proprioception (could single balance for only 10 seconds). An anterior drawer examination showed redundancy compared with the contralateral uninjured side (translation of 3-mm side-to-side difference) and normal peroneal strength. X-rays were normal. MRI showed the anterior talofibular ligament to be in continuity but with evidence of previous injury. A thermal capsular modification was performed. Postoperative immobilization was 3 weeks nonweight bearing in a cast, 3 weeks in a weight-bearing cast, and 3 weeks in a boot walker. Physician-supervised physical therapy was initiated at 9 weeks and emphasized proprioception retraining and peroneal strengthening. This patient returned to competition at 16 weeks with no recurrent instability at 2-year follow-up.


Foot and Ankle Arthroscopy

The introduction of arthroscopy to the armamentarium of orthopaedic surgeons has revolutionized the treatment of many commonly seen injuries. In 1918, Dr. Takagi of Tokyo University first applied an endoscopic technique to the knee joint. [0010] [0020] [0030] [0040] Since that time, arthroscopy has grown to be a safe and successful treatment modality that has gained widespread acceptance in diagnosing and treating disorders of the foot and ankle. [0550] [0560] [0570] [0580] [0590] [0600] [0610] [0620] [0630] [0640] [0650] [0660] [0670] [0680] [0690] [0700] [0710] The advantages of arthroscopy are the ability to closely inspect the articular and synovial surfaces without the need for extensile surgical approaches. The typical arthroscopic portals used in the ankle are the anteromedial, anterolateral, and anterocentral portals. Chapter 16addresses ankle arthroscopy more extensively. In this chapter, we describe a newer approach to posterior ankle arthroscopy.

Posterior ankle arthroscopy

In certain circumstances, posterior portals are necessary. On the basis of studies in which patients were placed in the standard supine position, most investigators have commented that the anterior portals and the posterolateral portal are safe and so have recommended the use of those portals. The most common posterior portals are the posterolateral, the trans-Achilles, and the posteromedial portals.[72]Posterior access is beneficial in visualizing posteromedial and posterolateral talar lesions (OLT) and mandatory to address flexor hallucis longus (FHL) stenosing tenosynovitis, posterior ankle impingement, displaced fractures of the os trigonum, insertional Achilles tendinitis, and retrocalcaneal bursitis.

Of the three posterior portals, the posterolateral portal has been subjected to the most clinical research. With the patient in the prone position, this portal is made at the level or just slightly above the level of the tip of the lateral malleolus just lateral to the Achilles tendon. Typical scope placement technique is used, and a 30-degree, 4.5-mm arthroscope is used. A coaxial portal placed directly posterior to the peroneal tendons also can be used. Care must be taken not to injure the sural nerve or the small saphenous vein, which run within 3.2mm and 4.8mm of the portal, respectively.[73] Ferkel et al.[74] reports a neurologic complication of rate of 4.4% using both anterior and posterior portals.

A review by Drez et al.[75] of 56 ankle arthroscopies performed with a combination of anterior and posterior portals found that the posterolateral portal allowed for excellent access to the posterior recess and that the posteromedial portal was rarely needed. Ferkel et al.[74] confirmed this finding in their study and recommended posterolateral ankle arthroscopy to ensure a thorough visualization of the ankle joint.

The posteromedial portal is made in a para-Achilles location or in a truly posteromedial location, between the posterior tibial tendon and flexor digitorum tendons. [0760] [0770] [0780] The Achilles tendon posteromedial portal is made just medial to the Achilles tendon in the horizontal plane at the same level as the posterolateral portal. Typical scope placement technique is used, and a 30-degree, 4.5-mm arthroscope is used. Before placing the portal, position can be checked through the use of a needle and visualization through the posterolateral portal. Developing the interval between the posterior tibial tendon and the flexor digitorum longus behind the medial malleolus makes the alternative posteromedial portal. Structures at risk with the posteromedial portal include the FHL, tibial nerve, and tibial artery, which average 2.7mm, 6.4mm, and 9.6mm away from the portal, respectively.[73] Using a posteromedial portal directly behind the medial malleolus adjacent to the posterior tibial tendon, the average distance from the cannula to the posterior tibial nerve was 5.7mm and 6.4mm to the tibial artery. The para-Achilles posteromedial portal is best used with the patient in the prone position, whereas the posteromedial portal may be used with the patient in the standard supine position.

Ankle arthroscopy with the patient in the prone position has been discussed infrequently. Zimmer and Ferkel[79] discussed the use of posterior portals with the patient in the prone position but for endoscopy of the retrocalcaneal bursa only. In a cadaveric study Sitler et al.[73] demonstrated that, during posterior ankle arthroscopy with the limb in the prone position, the posteromedial and posterolateral portals could be used with a relatively small risk to the neurovascular structures. The prone posterior ankle arthroscopy approach allows for visualization and accessibility to the posterior half of the tibiotalar joint, subtalar joints, and the FHL tendon and its sheath. It is the authors' experience that 50% of the posterior ankle can be visualized from the posterior portals, although only 30% can be manipulated directly because of the curvature of the talus and tibia. Prone positioning for posterior ankle arthroscopy is most helpful for resection of pathologic os trigonum and retrocalcaneal bursitis, where the pathology is all in the posterior recesses of the ankle.

Arthroscopy of the great toe

Wantanabe[80] described the first arthroscopy of the first metatarsophalangeal (MTP) joint in 1972. This procedure is indicated for osteophytes, hallux rigidus, chondromalacia, osteochondral dissecans, loose bodies, arthrofibrosis, and synovitis. Dorsal osteophytes, hallux rigidus, and osteochondral lesions are common indications among athletes. Diagnostic first MTP arthroscopy may be indicated for patients who fail conservative treatment of recurrent edema, locking pain, and diminished range of motion.[81]

The dorsal medial, dorsal lateral, and straight medial portals are used most commonly for arthroscopic evaluation and treatment of the first MTP joint. van Dijk et al.[82] reported that two portals are needed to visualize and treat disorders of the lateral sesamoid—one in the first webspace and another 4cm proximal to the joint line between the short abductor and the flexor hallucis brevis muscle. When making portals, care must be taken to avoid injuring the branches of the deep peroneal nerve laterally, branches of the superficial nerve medially, and branches of the saphenous around the medial aspect of the first MTP joint ( Fig. 25-3 ).


Figure 25-3  Illustration of metatarsophalangeal joint scope placement.  Illustrated by Peter Maurus, MD.


There is a paucity of literature on the clinical results of first MTP arthroscopy. Ferkel and Van Buecken[83] reported the results of 22 patients whose ages ranged from 18 to 70 years (mean age, 40), with a mean follow-up of 54 months. They reported a good outcome in 73% of the cases, fair in 13.5%, and poor in 13.5%. All patients in the fair and poor categories had degenerative joint disease and required a fusion later. van Dijk et al.[82] reported on 23 patients who underwent first MTP arthroscopy. The patients averaged 33 years of age (range, 16-61 years), and the follow-up period averaged 2 years. They reported excellent or good results for 14 patients and fair or poor results for nine patients. One patient experienced transient loss of medial hallux sensation and another experienced loss of lateral hallux sensation. The authors advocate sesamoid removal laterally with the scope but state that removing the medial sesamoid arthroscopically has not proven promising.

Davies and Saxby[84] performed first MTP arthroscopy on 11 patients ranging from 15 to 58 years of age (mean, 30 years) with a mean follow-up of 19.3 months. At the final follow-up, all the patients exhibited minimal or no pain, decreased edema, and increased range of motion. One patient had a minor wound complication. Three patients required an arthrotomy during the surgery. In summary, first MTP arthroscopy is an evolving technique. The best indications are osteochondral lesions. Debridement of marked degenerative joint disease should be discouraged.

Endoscopic calcaneal prominence resection

In 1928, Haglund[85] described a clinical condition in which the retrocalcaneal bursa and Achilles tendon are compressed and irritated by a posterior-superior calcaneal prominence. When nonoperative treatment fails, the condition can be treated by open calcaneal resection, retrocalcaneal bursectomy, and Achilles debridement with repair, when necessary. Recently, endoscopic calcaneoplasty has been described. The procedure is performed with the patient in a prone position, and posteromedial and posterolateral portals are used. The portals are placed just medial and lateral to the Achilles tendon and just proximal to the superior aspect of the calcaneus. A 2.7-mm arthroscope and small joint equipment are recommended.

Extra-articular endoscopic decompression of the retrocalcaneal space can be useful for treating retrocalcaneal bursitis, Haglund's spur, and impingement. The arthroscopic approach may decrease postoperative recovery time and incisional complications. Using lateral and accessory medial portals, Leitze et al. showed at an average of 22 months postoperatively a comparable result to open retrocalcaneal decompression as measured by the AOFAS Ankle/Hindfoot scoring system. We believe that this technique is useful in minimizing wound complications and decreasing the postoperative recovery time. Leitze et al. studied this procedure in a prospective study in 2003. They performed endoscopic decompressions on 33 heels (30 patients) in which nonoperative treatments had failed. This group was compared with 17 heels (14 patients) treated with a traditional open technique. Postoperatively, the clinical scores were not significantly different on the basis of AOFAS Ankle/Hindfoot scales, but operative time was shorter, there were fewer complications, and cosmetic results were better.[86] It is our experience that endoscopic resection of the Haglund's process is rewarding when the pathology involves bursitis with a prominent Haglund's process. Intratendinous calcifications of the Achilles insertion are handled best with conventional open techniques.


The dorsal cutaneous branches of the superficial peroneal nerve are at the greatest risk with anterior ankle portal placement.

Endoscopic Haglund resection is best reserved for patients with a mild Haglund's deformity but marked retrocalcaneal bursitis ( Fig. 25-4 ). This may be a technique to help athletes return to play earlier.


Figure 25-4  Magnetic resonance imaging (MRI) of an ankle illustrating a mild Haglund's deformity and marked retrocalcaneal bursitis.  Courtesy Gregory C. Berlet, MD, Orthopedic Foot and Ankle Center, Columbus, Ohio.




  1. Alexander AH, Lichtman DM: Surgical treatment of transchondral talar-dome fractures (osteochondritis dissecans): long-term follow-up.  J Bone Joint Surg1980; 62A:646.
  2. Konig F: Uber freie korper in den gelenken.  Dtsch Z Chir1888; 27:90.
  3. Parisien JS: Arthroscopic treatment of osteochondral lesions of the talus.  Am J Sports Med1986; 14:211.
  4. Baker CL, Andrews JR, Ryan JB: Arthroscopic treatment of transchondral talar dome fractures.  Arthroscopy1986; 2:82.
  5. Pettine KA, Morrey BF: Osteochondral fractures of the talus: a long-term follow-up.  J Bone Joint Surg1987; 69B:89.
  6. Van Buecken K, et al: Arthroscopic treatment of transchondral talar dome fractures.  Am J Sports Med1989; 17:350.
  7. Anderson IF, et al: Osteochondral fractures of the dome of the talus.  J Bone Joint Surg1989; 71A:1143.
  8. Woods K, Harris I: Osteochondritis dissecans of the talus in identical twins.  J Bone Joint Surg1995; 77B:331.
  9. Bruns J, Rosenbach B, Kahrs J: Etiopathogenetic aspects of medial osteochondrosis dissecans tali.  Sportverletz Sportschaden1992; 6:43.
  10. Mesgarzadeh M, et al: Osteochondritis dissecans: analysis of mechanical stability with radiography, scintigraphy, and MR imaging.  Radiology1987; 165:775.
  11. Higashiyama I, et al: Follow-up study of MRI for osteochondral lesion of the talus.  Foot Ankle Int2000; 21:127.
  12. DeSmet AA, et al: Value of MI imaging in staging osteochondral lesions of the talus (osteochondritis dissecans): results in 14 patients.  AJR Am J Roentgenol1990; 154:555.
  13. Loredo R, Sanders TG: Imaging of osteochondral injuries.  Clin Sports Med2001; 20:249.
  14. Berndt AL, Harty M: Transchondral fractures (osteochondritis dissecans) of the talus.  J Bone Joint Surg1959; 41A:988.
  15. Hepple S, Winson IG, Glew D: Osteochondral lesions of the talus: a revised classification.  Foot Ankle Int1999; 20:789.
  16. McCullough CJ, Venugopal V: Osteochondritis dissecans of the talus: the natural history.  Clin Orthop1979; 144:264.
  17. Bauer M, Jonsson K, Lindén B: Osteochondritis dissecans of the ankle. A 20-year follow-up study.  J Bone Joint Surg1967; 69B:93.
  18. Berlet GC, Mascia A, Miniaci A: Treatment of unstable osteochondritis dissecans lesions of the knee using autogenous osteochondral grafts (mosaicplasty).  Arthroscopy1999; 15:312.
  19. Yoshizumi Y, et al: Cylindrical osteochondral graft for osteochondritis dissecans of the knee: a report of three cases.  Am J Sports Med2002; 30:441.
  20. Angermann P, Riegels-Nielsen P: Fibrin fixation of osteochondral talar fracture.  Acta Orthop Scand1990; 61:551.
  21. Tol JL, et al: Treatment strategies in osteochondral defects of the talar dome: a systematic review.  Foot Ankle Int2000; 21:119.
  22. Kumai T, et al: Arthroscopic drilling for the treatment of osteochondral lesions of the talus.  J Bone Joint Surg1999; 81A:1229.
  23. Taranow WS, et al: Retrograde drilling of osteochondral lesions of the medial talar dome.  Foot Ankle Int1999; 20:474.
  24. Lee CK, Mercurio C: Operative treatment of osteochondritis dissecans in situ by retrograde drilling and cancellous bone graft.  Clin Orthop1981; 158:129.
  25. Hangody L, Fules P: Autologous osteochondral mosaicplasty for the treatment of full-thickness defects of weight-bearing joints: ten years of experimental and clinical experience.  J Bone Joint Surg Am2003; 85A(suppl 2):25.
  26. Assenmacher JA, Kelikian AS, Gottlob C, Kodros S: Arthroscopically assisted autologous osteochondral transplantation for osteochondral lesions of the talar dome: an MRI and clinical follow-up study.  Foot Ankle Int2001; 22(7):544-551.
  27. Al-Shaikh RA, et al: Autologous osteochondral grafting for talar cartilage defects.  Foot Ankle Int2002; 23:381.
  28. Gautier E, Kolker D, Jakob RP: Treatment of cartilage defects of the talus by autologous osteochondral grafts.  J Bone Joint Surg2002; 84B:237.
  29. Sammarco GJ, Makwana NK: Treatment of talar osteochondral lesions using local osteochondral graft.  Foot Ankle Int2002; 22:693.
  30. Brittberg M, et al: Treatment of deep cartilage defects in the knee with autologous chondrocyte transplantation.  N Engl J Med1994; 331:889.
  31. Gillogly SD, Voight M, Blackburn T: Treatment of articular cartilage defects of the knee with autologous chondrocyte implantation.  J Orthop Sports Phys Ther1998; 28:241.
  32. Farnworth L: Osteochondral defects of the knee.  Orthopedics2000; 23:146.
  33. Minas T, Peterson L: Advanced techniques in autologous chondrocyte transplantation.  Clin Sports Med1999; 18:13.v
  34. Minas T: The role of cartilage repair techniques, including chondrocyte transplantation, in focal chondral knee damage.  Instr Course Lect1999; 48:629.
  35. Giannini S, et al: Autologous chondrocyte transplantation in osteochondral lesions of the ankle joint.  Foot Ankle Int2001; 22:513.
  36. Minas T, Peterson L: Advanced techniques in autologous chondrocyte transplantation.  Clin Sports Med1999; 18(1):13-44.
  37. Minas T: Implantation in the repair of chondral lesions of the knee: economics and quality of life.  Am J Orthop1998; 27:739.
  38. Tontz Jr WL, Bugbee WD, Brage ME: Use of allografts in the management of ankle arthritis.  Foot Ankle Clin2003; 8(2):361-373.
  39. Gross AE, Agnidis Z, Hutchison CR: Osteochondral defects of the talus treated with fresh osteochondral allograft transplantation.  Foot Ankle Int2001; 22:385.
  40. Caylor MT, Pearsall 4th AW, et al: Fresh osteochondral grafting in the treatment of osteochondritis dissecans of the talus.  J South Orthop Assoc2002; 11:33.
  41. Hsieh PC, et al: Repair of full-thickness cartilage defects in rabbit knees with free periosteal graft preincubated with transforming growth factor.  Orthopedics2003; 26:393.
  42. Guo X, et al: Expression of transforming growth factor—beta 1 in mesenchymal stem cells: potential utility in molecular tissue engineering for osteochondral repair.  J Huazhong Univ Sci Technolog Med Sci2002; 22:112.
  43. Siebert CH, et al: Healing of osteochondral grafts in an ovine model under the influence of bFGF.  Arthroscopy2003; 19:182.
  44. Mierisch CM, et al: Transforming growth factor—beta in calcium alginate beads for the treatment of articular cartilage defects in the rabbit.  Arthroscopy2002; 18:892.
  45. Martinek V, et al: Treatment of osteochondral injuries. Genetic engineering.  Clin Sports Med2001; 20:403.viii
  46. Lohmann CH, et al: Pretreatment with platelet derived growth factor-BB modulates the ability of costochondral resting zone chondrocytes incorporated into PLA/PGA scaffolds to form new cartilage in vivo.  Biomaterials2000; 21:49.
  47. Holmer P, et al: Epidemiology of sprains in the lateral ankle and foot.  Foot Ankle Int1994; 15:72.
  48. Gerber JP, et al: Persistent disability associated with ankle sprains: a prospective examination of an athletic population.  Foot Ankle Int1998; 19:653.
  49. Balduini FC, et al: Management and rehabilitation of ligamentous injuries to the ankle.  Sports Med1987; 4:364.
  50. Freeman MAR: Instability of the foot after injuries to the lateral ligament of the ankle.  J Bone Joint Surg1965; 47B:669.
  51. Tropp H, Ekstrand J, Gillquist J: Stabilometry in functional instability of the ankle and its value in predicting injury.  Med Sci Sports Exerc1984; 16:64.
  52. Hyashi T, Curran-Patel S, Prockop DJ: Thermal stability of the triple helix of type I procollagen and collagen. Precautions for minimizing ultraviolet damage to proteins during circular dichroism studies.  Biochemistry1979; 18:4182.
  53. Cline S, Wolin P: The use of thermal energy in ankle instability.  Clin Sports Med2002; 21:713.
  54. Berlet GC, Raissi A, Lee TH: Thermal capsular modification for chronic lateral ankle instability.  2002.
  55. Andrews FR, Previte WJ, Carson WG: Arthroscopy of the ankle: technique and normal anatomy.  Foot Ankle1985; 6:29.
  56. Chen YC: Clinical and cadaver studies on the ankle joint arthroscopy.  J Jpn Orthop Assoc1976; 50:631.
  57. Drez D, Guhl JF, Gollehon DL: Ankle arthroscopy: technique and indications.  Clin Sports Med1982; 1:35.
  58. Drez D, Guhl JF, Gollehon DL: Ankle arthroscopy: technique and indications.  Foot Ankle1981; 2:138.
  59. Ewing JW: Ankle arthroscopy.  Arthroscopy surgery update,  Ariz: Scottsdale; 1989.
  60. Ferkel RD: Arthroscopy of the foot and ankle,  New York: Lippincott-Raven; 1996.
  61. Ferkel RD, Fischer SP: Progress in ankle arthroscopy.  Clin Orthop1989; 240:210.
  62. Ferkel RD, Scranton Jr PE: Current concepts review: arthroscopy of the ankle and foot.  J Bone Joint Surg1993; 75A:1233.
  63. Gollehon DL, Drez D: Ankle arthroscopy: approaches and technique.  Orthopedics1983; 6:1150.
  64. Gollehon DL, Drez D: Arthroscopy of the ankle.   In: McGinty J, ed. Arthroscopic surgery update,  Rockville, MD: Aspen; 1985.
  65. Harrington KD: Degenerative arthritis of the ankle secondary to long-standing lateral ligament instability.  J Bone Joint Surg1979; 61A:354.
  66. Johnson LL: Diagnostic and surgical arthroscopy,  ed 2. St Louis, Mosby, 1981.
  67. Parisien JS: Arthroscopy of the posterior subtalar joint: a preliminary report.  Foot Ankle1986; 6:219.
  68. Parisien JS: Arthroscopy of the ankle: state of the art.  Contemp Orthop1982; 5:21.
  69. Parisien JS, Shereff MJ: The role of arthroscopy in the diagnosis and treatment of disorders of the ankle.  Foot Ankle1981; 2:144.
  70. Parisien JS, Vangsness T: Operative arthroscopy of the ankle: three years' experience.  Clin Orthop1985; 199:46.
  71. Stetson WB, Ferkel RD: Ankle arthroscopy. I. Technique and complications. II. Indications and results.  J Am Acad Orthop Surg1996; 4:17.
  72. Voto SJ, et al: Ankle arthroscopy: neurovascular and arthroscopic anatomy of standard and trans-Achilles tendon portal placement.  Arthroscopy1989; 5:41.
  73. Sitler DF, et al: Posterior ankle arthroscopy. An anatomic study.  J Bone Joint Surg2002; 84A:763.
  74. Ferkel RD, Heath DD, Guhl JF: Neurological complications of ankle arthroscopy.  Arthroscopy1996; 12:200.
  75. Drez Jr D,, Guhl JF, Gollehon DL: Ankle arthroscopy: technique and indications.  Foot Ankle1981; 2:138.
  76. van Dijk CN, Scholten PE, Krips R: A 2-portal endoscopic approach for diagnosis and treatment of posterior ankle pathology.  Arthroscopy2000; 16:871.
  77. Berlet GC, Lee TH, Puri DR: The posteromedial portal for ankle arthroscopy,  Buenos Aires: Argentina; 2000.
  78. Acevedo JI, et al: Coaxial portals for posterior ankle arthroscopy: an anatomic study with clinical correlation on 29 patients.  Arthroscopy2000; 16:836.
  79. Zimmer T, Ferkel RD: Future developments. B. Endoscopic procedures for the retrocalcaneal bursa, plantar fascia, and Achilles tendon.   In: Ferkel RD, Whipple TL, ed. Arthroscopic surgery: the foot and ankle,  Philadelphia: Lippincott-Raven; 1996.
  80. Watanabe M: Selfox-Arthroscope (Wantantabe No. 24 arthroscope),  Tokyo, Japan, Teishin Hospital, 1972.
  81. Frey C, van Dijk CN: Arthroscopy of the great toe.  AAOS Instruct Course Lect1999; 48:343.
  82. van Dijk CN, Veenstra KR, Neusch BC: Arthroscopic surgery of the metatarsophalangeal first joint.  Arthroscopy1998; 14:851.
  83. Ferkel RD, Van Buecken K: Great toe arthroscopy: indications, technique and results,  1991.
  84. Davies MS, Saxby TS: Arthroscopy of the first metatarsophalangeal joint.  J Bone Joint Surg1999; 81B:203.
  85. Haglund P: Contribution to the diseased conditions of the tendo-Achilles.  Acta Chir Scand1928; 63:292.
  86. Leitze Z, Sella E, Aversa JM: Endoscopic decompression of the retrocalcaneal space.  J Bone Joint Surg2003; 85A:1488.