Osteochondral Lesion of the Talus

An osteochondral lesion of the talus (OLT) is a defect of the talar dome involving both the articular cartilage, the smooth bearing surface, and the subchondral bone beneath it, which can develop oedema, cysts or a detached fragment.

Terminology. Osteochondral lesion, osteochondral defect, osteochondritis dissecans and transchondral fracture overlap and are often used interchangeably. "Osteochondral lesion of the talus" is the preferred modern umbrella term because it does not assume a single cause.

Neighbouring topics. The same lesion in the knee is treated by different size thresholds and a different evidence base; see osteochondral defects of the knee. The mechanism that produces most lateral talar lesions is the inversion injury covered in lateral ankle sprains, with the chronic form in lateral ankle instability, which must be corrected or the lesion recurs.

Cause. Most lesions are post-traumatic: they typically follow a traumatic injury, classically an inversion ankle sprain or an ankle fracture (Anastasio 2024). A minority are atraumatic (idiopathic), where repetitive microtrauma with local vascular impairment is thought to play a role.

Who. The lesion is common in young, active patients, the same population that sustains ankle sprains and sports injuries. It is associated with chronic ankle instability, because recurrent inversion injuries expose the talar dome to repeated shear.

The talus. It is largely covered by articular cartilage and has no muscular attachments, so it relies on a precarious blood supply that enters around its neck. The talar dome articulates with the tibial plafond and the medial and lateral malleoli to form the ankle (tibiotalar) joint.

The cartilage. Talar dome cartilage is relatively thin and, like all hyaline cartilage, has poor intrinsic healing capacity because it is avascular. Once the cartilage and subchondral plate are breached, repair depends on cells reaching the defect.

Why the biology shapes treatment. A tenuous blood supply and cartilage that cannot heal itself explain why lesions persist. They also explain why treatments aim either to recruit marrow cells into the defect, the rationale behind bone marrow stimulation (microfracture), or to physically replace the osteochondral unit (OAT and grafting).

Where lesions sit. Medial lesions are the more common and lie posteromedially; lateral lesions lie anterolaterally. The two sides differ in shape, in how clearly they follow trauma and in the position of the foot at injury.

How a lesion evolves. Shear or compression across the talar dome during a sprain or fracture damages the cartilage and the subchondral plate. The lesion then evolves:

1. Subchondral response - oedema develops, and the fragment may stay in place (stable) or partially separate
2. Cyst formation - synovial fluid is driven into the subchondral bone through the cartilage breach, forming subchondral cysts over time
3. Progression - a stable lesion may remain quiet, while an unstable or cystic lesion causes mechanical symptoms and, if untreated, can lead to ankle osteoarthritis

Two classifications must be kept separate: Berndt-Harty, the original radiographic staging (I-IV), and Hepple, the MRI-based staging (1-5) that reflects modern practice. In a viva, lead with size and stability. How big the lesion is, and whether the fragment or cartilage is stable, matter more for the treatment decision than the stage number, so quote Hepple alongside the size and stability concept to show you understand the modern algorithm.

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History. The pain is deep and poorly localised, typically worse with weight-bearing and activity. Most patients give a history of a previous ankle sprain or fracture; ask specifically about a sprain that never fully recovered. Then ask about:

• Mechanical symptoms - catching, locking, clicking or a sense of giving way, suggesting an unstable fragment or loose body
• Recurrent swelling after activity
• Chronic ankle instability - recurrent inversion injuries point to both the cause and a target for treatment

The dome. Tenderness lies over the anteromedial or anterolateral talar dome, palpated with the ankle plantarflexed or dorsiflexed to bring the dome forward. Look for an ankle effusion or swelling. Range of motion is often preserved, with pain at the extremes.

The rest of the ankle. A complete assessment includes ligamentous stability and hindfoot alignment, not just dome tenderness. Test for lateral ligament laxity (anterior drawer, talar tilt), because instability frequently coexists and may need addressing, and assess hindfoot and ankle alignment (varus or valgus) standing, because malalignment changes management. Coexisting instability or malalignment must be treated to protect any cartilage procedure.

Plain radiographs. Weight-bearing AP, lateral and mortise ankle views are the first investigation but frequently miss or underestimate the lesion. A subtle flattening or lucency of the talar dome may be the only clue, and a normal film does not exclude an OLT. The films remain valuable for assessing overall alignment and joint space.

MRI is the best single test and the recommended way to diagnose an OLT, because it shows the cartilage, the subchondral bone, oedema, fragment stability and cysts in one study. On the scan, look for:

• Bone marrow oedema beneath the lesion, a marker of an active, often symptomatic lesion
• Cartilage integrity - an intact cap versus fissured or detached cartilage
• Fragment stability - a high-signal (fluid) line completely encircling a fragment suggests instability
• Subchondral cysts, Hepple stage 5

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CT. CT is superior to MRI for bony anatomy. It accurately maps the size, depth and cysts of the lesion and is useful for surgical planning, especially before grafting. CT arthrography adds contrast within the joint to reveal whether the cartilage cap communicates with the subchondral bone.

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Leave the incidental lesion alone. Incidental or asymptomatic lesions are best treated non-operatively, with reassurance, activity modification and monitoring. Not every talar dome lesion needs surgery.

A non-operative trial first. For many stable symptomatic lesions a trial of conservative care is reasonable before surgery:

• Activity modification and relative rest
• Protected weight-bearing for a period, especially in juvenile or stable lesions
• Physiotherapy to restore range, strength and proprioception, and to address ankle instability
• Analgesia and anti-inflammatories for symptom control

The juvenile lesion. Juvenile patients have greater healing potential, and stable lesions in this group may settle with conservative care or respond well to retrograde drilling.

Small and stable, failed conservative care. Arthroscopic debridement with microfracture or drilling (bone marrow stimulation) gives reliable short-term improvement for small lesions, and it is cheap and one-step.

Large or cystic, or failed marrow stimulation. Osteochondral autograft transfer (OAT, mosaicplasty) replaces the whole osteochondral unit with hyaline cartilage. The alternatives are ACI or MACI, in which cultured chondrocytes restore a cartilage surface over a large cartilage lesion, and osteochondral allograft, a donor osteochondral plug that avoids donor-site morbidity, for very large defects not suited to autograft.

Preserve native cartilage where you can. A stable in-situ fragment with an intact cartilage cap, often over a subchondral cyst, or a juvenile lesion, is treated first by retrograde drilling or fragment fixation (e.g. a bone peg), both of which preserve the native cartilage.

Realign, whatever the size. Uncorrected hindfoot or ankle malalignment overloads the lesion. A varus or valgus ankle must be corrected with a supramalleolar or hindfoot (e.g. calcaneal) osteotomy so the repaired surface is not overloaded, or any repair or graft will fail and the symptoms recur. This is the classic "what else would you do?" viva point.

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The classic critical size. Choi (2009) studied 120 ankles after arthroscopic bone marrow stimulation and found a sharp threshold at a defect area of about 150mm2. Only around 10 percent of lesions smaller than 150mm2 failed, against roughly 80 percent of those of 150mm2 or larger. Patient age, symptom duration, trauma and lesion location did not predict outcome; size did.

The refined figure, and how to read it. Ramponi (2017, PMID 27852595) systematically reviewed 25 studies (1,868 ankles) and is usually quoted as refining the threshold to an area under about 107mm2 and/or a diameter under about 10mm. But 107.4mm2 is the mean lesion area of the three studies that reported a significant size-outcome correlation, against 85.3mm2 in the eight studies that reported none. It is not a cutoff calculated from pooled patient data, and the review's own background notes that recent investigations have failed to detect any size-outcome correlation. Eighty-eight percent of included studies were level 3 or 4, and 96% were not of good quality.

Graft failure follows the same rule. Dekker (2018) similarly found that cartilage-graft failure rose sharply once lesion area exceeded 125mm2.

Why area, not a single diameter. A lesion is rarely a perfect circle, and a single "widest diameter" can badly under- or over-state the true defect. Measuring the area on MRI or CT, and ideally the volume including depth and any cyst, captures how much bearing surface is actually lost, which is why the area thresholds correlate with outcome more reliably than a lone diameter. In practice, measure the lesion on cross-sectional imaging, and if it is around 1 cm2 or larger, or deep or cystic, lean toward grafting rather than microfracture.

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Why augment. Standard microfracture heals a defect with mechanically inferior fibrocartilage, and its results deteriorate over time and with larger lesions. That has driven interest in augmenting bone marrow stimulation rather than abandoning it, a strategy the complication data point to: the Hollander meta-analysis found matrix-assisted bone marrow stimulation carried the lowest complication rate of any technique, about 3 percent.

The options.

• Platelet-rich plasma (PRP) - concentrated autologous platelets deliver growth factors to the microfractured base. In a Level I randomised trial of talar lesions, a single postoperative PRP injection after arthroscopic microfracture gave significantly better pain and function than hyaluronic acid or saline (Görmeli 2015)
• Concentrated bone marrow aspirate (cBMAC) - supplements the marrow released by the microfracture channels with additional mesenchymal stromal cells and growth factors
• Matrix-assisted bone marrow stimulation (AMIC, autologous matrix-induced chondrogenesis) - a collagen or hyaluronan membrane is laid over the microfractured base to stabilise the marrow clot and support a more organised repair, extending the technique to slightly larger lesions where bare microfracture would fail
• Hyaluronic acid - a viscosupplement adjunct; in the same randomised trial it outperformed saline but was inferior to PRP

What matters at the talus. The general cartilage-repair biology and the science of PRP and scaffolds belong to the dedicated cartilage topics. For the talus, these adjuncts are used to stretch the size ceiling of a one-step marrow-stimulation procedure and to make the fibrocartilage repair more durable before committing the patient to grafting.

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How safe is surgery. Generally safe: across 6,962 lesions in the Hollander/Dahmen meta-analysis, no life-threatening complications were reported. The complications to know are these:

• Persistent or recurrent pain - the commonest reason for revision; often due to an undersized procedure, a large or cystic lesion, or uncorrected malalignment
• Nerve injury - for example to cutaneous nerves around portals or approaches
• Failure or need for revision surgery - higher with larger lesions, and with biologics added to bone marrow stimulation in some series
• Donor-site morbidity - knee pain after harvesting OAT plugs
• Malleolar osteotomy problems - nonunion, malunion or hardware irritation when an osteotomy is used for access
• Subchondral cyst formation or progression - especially if the lesion is incompletely treated
• Ankle osteoarthritis - the long-term consequence of an untreated or failed lesion

Protect, then reload. A period of non- or partial weight-bearing protects the repair while it matures, and its duration depends on the procedure: longer for grafting or osteotomy than for simple debridement. Controlled early ankle motion encourages cartilage health and prevents stiffness, and loading then advances gradually to full weight-bearing as pain and healing allow.

Rehabilitate, and fix the cause. Physiotherapy regains strength, proprioception and balance and addresses any ankle instability that contributed to the lesion. The underlying instability or malalignment has to be fixed so the lesion does not recur.

Return to sport. Return is graded, typically over several months, and guided by symptoms, strength and imaging when needed.

Bone marrow stimulation gives good short-term results for small, stable lesions, but outcomes are strongly size-dependent: smaller lesions, around under 10mm, do significantly better than larger ones (Guo 2010).

Osteochondral autograft produces good long-term clinical and MRI outcomes, with significant improvements in pain and function maintained at long follow-up. Results are worse when OAT is used as a salvage after previous failed surgery (Imhoff 2011).

Patient and lesion factors also count. Higher age, BMI and larger lesion size are associated with poorer results and higher failure rates (Anastasio 2024; Dekker 2018).

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Global epidemiology. Osteochondral lesions of the talus are most common in young, active patients and are usually post-traumatic, classically following an inversion ankle sprain or an ankle fracture. They are a leading cause of persistent ankle pain after a sprain worldwide. There is no implant registry for OLT - the evidence is pooled case series, systematic reviews and consensus statements, so practice is consensus-driven globally.

Side-by-side guidance

High- vs limited-resource practice

Related pages: Osteochondral Defects of the Knee for the same techniques where the evidence base actually sits — note that the knee trials (SUMMIT, Knutsen) do not transfer to the talus, which has thinner, stiffer cartilage and a different loading pattern; Articular Cartilage Injuries and Cartilage Healing and Repair for the underlying biology and why marrow stimulation yields fibrocartilage; Lateral Ankle Instability and Chronic Ankle Instability for the mechanism behind most anterolateral lesions and the instability that must be corrected alongside them; Lateral Ankle Sprains for the injury in which these lesions are most often missed; Chronic Lateral Ankle Pain for the differential when a lesion is an incidental finding; and Ankle Arthritis for the endpoint that untreated or failed lesions progress toward.