Osteochondral Lesions of the Talus 

  • Author: Gregory C Berlet, MD, FRCS(C); Chief Editor: Jason H Calhoun, MD, FACS   more...
 
Updated: Feb 26, 2009
 

History of the Procedure

The earliest report of osteochondritis dissecans (OCD) was published in 1888 by Konig, who characterized a loose-body formation associated with articular cartilage and subchondral bone fracture.[1] In 1922, Kappis described this process in the ankle joint.[2]

Osteochondral lesions of the talus. Osteochondral lesions of the talus.

On the basis of a review of all literature describing transchondral fractures of the talus, Berndt and Harty developed a classification system for radiographic staging of osteochondral lesions of the talus (OLTs).[3] Their classification system has been the foundation for other systems, yet it remains the most widely used system today (see Staging).

Berndt and Harty staging system for osteochondral Berndt and Harty staging system for osteochondral lesions of the talus, with grades 1-4.
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Epidemiology

Frequency

Osteochondral lesions are rare joint disorders. Most often, they affect the knee, followed by the elbow and the talus. Lesions of the talus account for 4% of all osteochondral lesions in the body.[4]

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Etiology

Both Konig and Kappis believed that lesions due to osteochondritis dissecans (OCD) were the result of ischemic necrosis of the underlying subchondral bone that eventually led to separation of the fragment and its overlying articular cartilage.[1, 2]

Inflammation has not been shown to be a significant factor in the etiology of OCD. Therefore, the term OCD may be misleading. Assenmacher proposed the term osteochondral lesions of the talus, or OLTs.[5]

A history of trauma is documented in more than 85% of patients.[6, 7, 8, 9, 10] Pritsch et al reported that a traumatic event preceded 75% of both medial and lateral lesions in 24 patients.[11] Trauma is implicated less often in posteromedial lesions.[4, 12, 13]

Although the etiology of nontraumatic OLTs is unknown, a primary ischemic event may cause this form of the disease. Nontraumatic OLTs can also be familial. Multiple lesions can occur in the same patient, and identical medial talar lesions have occurred in identical twins.[14]

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Pathophysiology

Anterolateral lesions on the talar dome result from inversion and dorsiflexion forces, which cause the anterolateral aspect of the talar dome to impact the fibula. These lesions are usually shallower and more wafer-shaped than medial lesions, possibly because of a more tangential force vector that results in shearing-type forces.[15]

Posttraumatic medial lesions are deeper and cup-shaped. They result from a combination of inversion, plantarflexion, and external rotation forces that cause the posteromedial talar dome to impact the tibial articular surface with a relatively more perpendicular force vector.

A study of the contact pressures on the talus with varying degrees of lateral ligament transections and ankle positions showed that the medial rim of the talus was subjected to high pressures, even without ligamentous transection.[15] Results of another study implicated the difference in cartilage stiffness; the tibial cartilage is 18-37% stiffer than the corresponding sites on the talus.[16]

The results of other studies indicated that the mean cartilage thickness is inversely related to the mean compressive modulus.[17, 18] These findings may lend credence to the clinically observed etiology of osteochondral lesions of the talus (OLTs) (ie, repetitive overuse syndrome in medial lesions and an acute traumatic event in lateral lesions).

Observations from biomechanical studies suggest that the size of the lesion may alter the contact stresses in the ankle. Statistically significant changes in contact characteristics occur with lesions larger than 7.5 mm × 15 mm; this finding indicates that lesion size may play a role in predicting long-term outcome.[19]

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Presentation

In most cases, the mechanism of injury is an inversion injury to the lateral ligamentous complex. Patients typically present with chronic ankle pain along with intermittent swelling and, possibly, weakness, stiffness, instability, and giving way.

Upon physical examination, assess joint laxity with the anterior drawer test and assess strength by comparison with the contralateral ankle. Physical examination findings of joint laxity are uncommon. Palpation may reveal tenderness behind the medial malleolus when the ankle is dorsiflexed, indicating a posteromedial lesion. Anterolateral lesions may be tender when the anterolateral ankle joint is palpated with the joint in maximal plantarflexion.

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Indications

Conservative treatment should be attempted first, whenever possible. Studies have shown that a trial of conservative treatment has no adverse effect on subsequent surgical intervention.[4, 13] One study demonstrated that nonoperative conservative treatment can sometimes result in healing of higher-stage lesions.[9]

After a period of immobilization followed by physical therapy, patients with continued symptoms should be evaluated with MRI and other imaging studies to assess the condition of the articular cartilage and stability, and to detect any intra-articular bodies.[20]

Symptoms of intra-articular derangement are indications for operative intervention. Such symptoms include effusion, catching or locking of the ankle, instability preceded by pain, and ankle pain relieved with diagnostic lidocaine.

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Relevant Anatomy

The dome of the talus is covered by the trochlear articular surface, which supports the weight of the body. The talar dome is trapezoidal in shape, and its anterior surface is on average 2.5 mm wider than the posterior surface. The medial and lateral articular facets of the talus articulate with the medial and lateral malleoli. The articular surface of these facets is contiguous with the superior articular surface of the talar dome.

Osteochondral lesions of the talus. Modified stagiOsteochondral lesions of the talus. Modified staging system by Loomer et al.

Approximately 60% of the talar surface is covered by articular cartilage. The talus has no muscular or tendinous attachments. Most of the blood supply of the talus enters through the neck via the sinus tarsi. The dorsalis pedis artery supplies the head and neck of the talus. The artery of the sinus tarsi is formed from branches of the peroneal and dorsalis pedis arteries. The artery of the tarsal canal branches from the posterior tibial artery. The sinus tarsi artery and the tarsal canal artery join to form an anastomotic sling inferior to the talus, from which branches enter the talar neck.

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Contraindications

Surgery to treat osteochondral lesions of the talus (OLTs) is contraindicated when the risks outweigh the perceived benefits. Risks include active infection in the operative area, patient noncompliance, and medical instability in patients. Relative contraindications include degenerative changes of the ankle involving more than an isolated OLT.

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Contributor Information and Disclosures
Author

Gregory C Berlet, MD, FRCS(C)  Clinical Assistant Professor of Orthopedics, Chief of Foot and Ankle Surgery, Department of Orthopedic Surgery, Ohio State University College of Medicine and Public Health

Gregory C Berlet, MD, FRCS(C) is a member of the following medical societies: American Medical Association, American Orthopaedic Foot and Ankle Society, Canadian Medical Association, Canadian Orthopaedic Association, College of Physicians and Surgeons of Ontario, Ontario Medical Association, and Royal College of Physicians and Surgeons of Canada

Disclosure: Nothing to disclose.

Coauthor(s)

Christopher F Hyer, DPM, FACFAS  Foot and Ankle Surgeon, Director, Advanced Foot and Ankle Surgery Fellowship, Orthopedic Foot and Ankle Center

Christopher F Hyer, DPM, FACFAS is a member of the following medical societies: American College of Foot and Ankle Surgeons and American Podiatric Medical Association

Disclosure: Nothing to disclose.

Robert D Santrock, MD  Consulting Surgeon, Orthopedic Associates of Meadville, PC

Disclosure: Nothing to disclose.

Specialty Editor Board

James K DeOrio, MD  Director of Foot and Ankle Fellowship Program, Assistant Professor of Orthopedic Surgery, Orthopedic Surgery, St Lukes Hospital, Jacksonville, Florida

James K DeOrio, MD is a member of the following medical societies: American Academy of Orthopaedic Surgeons, American Orthopaedic Foot and Ankle Society, Florida Medical Association, and German Society of Neurology

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Senior Pharmacy Editor, eMedicine

Disclosure: eMedicine Salary Employment

Shepard R Hurwitz, MD  Executive Director, American Board of Orthopaedic Surgery

Shepard R Hurwitz, MD is a member of the following medical societies: American Academy of Orthopaedic Surgeons, American Association for the Advancement of Science, American College of Rheumatology, American College of Sports Medicine, American College of Surgeons, American Diabetes Association, American Orthopaedic Association, American Orthopaedic Foot and Ankle Society, Association for the Advancement of Automotive Medicine, Eastern Orthopaedic Association, Orthopaedic Research Society, Orthopaedic Trauma Association, and Southern Orthopaedic Association

Disclosure: Nothing to disclose.

Dinesh Patel, MD, FACS  Associate Clinical Professor of Orthopedic Surgery, Harvard Medical School; Chief of Arthroscopic Surgery, Department of Orthopedic Surgery, Massachusetts General Hospital

Dinesh Patel, MD, FACS is a member of the following medical societies: American Academy of Orthopaedic Surgeons, American Association of Physicians of Indian Origin, American College of International Physicians, and American College of Surgeons

Disclosure: Nothing to disclose.

Chief Editor

Jason H Calhoun, MD, FACS  Frank J Kloenne Chair in Orthopedic Surgery, Professor and Chair, Department of Orthopedics, The Ohio State University Medical Center

Jason H Calhoun, MD, FACS is a member of the following medical societies: American Academy of Orthopaedic Surgeons, American College of Surgeons, American Diabetes Association, American Medical Association, American Orthopaedic Association, American Orthopaedic Foot and Ankle Society, Missouri State Medical Association, Musculoskeletal Infection Society, Southern Medical Association, Southern Orthopaedic Association, Texas Medical Association, and Texas Orthopaedic Association

Disclosure: Nothing to disclose.

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Berndt and Harty staging system for osteochondral lesions of the talus, with grades 1-4.
Osteochondral lesions of the talus. Modified staging system by Loomer et al.
Osteochondral lesions of the talus. Classification system based on CT.
Osteochondral lesions of the talus.
Osteochondral lesions of the talus. Illustration of percutaneous transmalleolar drilling.
Osteochondral lesions of the talus. Cannulated drill placed over a guidewire.
 
 
 
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