Freiberg Disease (Freiberg Infraction)

Freiberg disease is an osteochondrosis of the metatarsal head, most commonly the second: an osteonecrosis that goes on to collapse and articular damage. The alternative name, Freiberg infraction, refers to the subchondral insufficiency fracture with which the process begins.

Who. An adolescent female. Females outnumber males 4:1, the peak age is 13-18 years, and the disease is bilateral in approximately 10% of cases.

Where. The second metatarsal in 68% of cases and the third in 27%.

The cause is debated and probably multifactorial, combining vascular insufficiency, repetitive microtrauma with a subchondral stress fracture, and a biomechanical or genetic predisposition.

The vascular argument. The developing metatarsal head epiphysis has a relatively tenuous blood supply and is vulnerable to ischaemia during adolescent growth.

The mechanical argument. A long second metatarsal (Morton foot) increases peak pressure on the second head, a 20-30% increase in loading, and may be a risk factor. High heels and tight footwear concentrate forefoot load, and tight footwear compresses the forefoot and restricts blood flow. The disease may be related to increased activity: repetitive activity such as ballet, especially en pointe, supplies the microtrauma.

The final common pathway. Whichever starts it, a subchondral insufficiency fracture leads to osteonecrosis, collapse and progressive articular destruction, which is the sequence Smillie staged.

Smillie's five stages follow the head from an ischaemic fissure to an arthritic joint, and each stage maps to a treatment.

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What actually does the guiding is the plantar articular surface. Freiberg destroys the head from dorsal to plantar, so through the earlier stages the plantar cartilage and its subchondral bone remain intact while the dorsal surface collapses. That single fact is what makes the classification operative rather than descriptive.

Stages 1-3: plantar surface intact. There is healthy cartilage available to be brought into load, which is exactly what the Gauthier dorsal closing wedge osteotomy does: it excises the damaged dorsal segment and rotates the preserved plantar cartilage up into the weight-bearing position. Stage 3 is the last stage at which that cartilage is reliably present, hence "good for Smillie 3".

Stage 4: the plantar hinge fails. The central fragment separates as a loose body and the peripheral rim fragments, so there is no longer an intact plantar surface to rotate up. Treatment shifts towards debridement and loose body removal, or to procedures that restore or resurface the head rather than reorient it.

Stage 5: established arthrosis. Reorientation is no longer the question; this is salvage.

History. An adolescent female with forefoot pain at the affected metatarsal head, worse with activity and weight-bearing. The onset may be insidious, and symptoms are sometimes minimal at first.

Examination. There may be swelling over the affected MTP joint, and the metatarsal head is tender dorsally and plantarly. MTP motion is reduced, dorsiflexion most of all because it loads the damaged articular surface, and the gait is modified to offload the forefoot. The signs are subtle: mild shortening of the involved toe and a broadened head are easier to see against the other foot than in isolation.

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Radiographs. Anteroposterior, oblique and lateral views. Early disease may look normal or show subtle flattening; as it progresses the head becomes sclerotic and flattened, then centrally collapsed, then accompanied by loose bodies. More than one view matters, because head changes subtle on a single projection show on another: the oblique shows a flattened head and subchondral cysts that an AP view can hide.

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MRI. Sensitive for early disease before any radiographic change: it shows bone marrow oedema and subchondral change. It also shows how much of the head is still viable and the state of the plantar cartilage, which is what decides whether a joint-preserving osteotomy is possible; the sagittal plane shows the dorsal collapse and the plantar cartilage together.

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CT. Detail of the collapse pattern for surgical planning: it quantifies the deformity.

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Differential diagnosis. Forefoot pain has several other causes, and marrow oedema on MRI is not specific to Freiberg:

Of the disease. Left untreated, the joint progresses through:

• Collapse and secondary osteoarthritis of the MTP joint (Smillie 5)
• Loose bodies and mechanical locking
• Stiffness and dorsal impingement limiting push-off
• Transfer metatarsalgia to adjacent rays from altered loading

Of treatment. Each operation has its own signature:

• After osteotomy: shortening, transfer metatarsalgia, stiffness, nonunion or malunion, recurrence
• After head resection: floating or dorsiflexed toe, instability, marked shortening, transfer metatarsalgia
• After arthrodesis: nonunion (10-15 percent), malunion, hardware irritation, loss of MTP motion
• After silicone implant: implant fracture or migration and silicone synovitis (high mid-term failure, especially in the young)

Freiberg disease is too uncommon to feature in formal national arthroplasty registries or major society guidelines; management is driven by case series and consensus rather than guideline statements. The principles below are consistent in practice worldwide.

Global Epidemiology

• Fourth most common osteochondrosis (after Köhler, Panner and Sever disease).
• Strong female predominance and adolescent onset, though adults present later; second metatarsal head is most often affected, then the third.
• Long second metatarsal (Morton foot) and high-impact forefoot loading (dance, running) are recurrent risk factors across populations.

Consensus Practice (Side by Side)

High- vs Limited-Resource Variation

• Well-resourced settings: early MRI, arthroscopic debridement and head-restoration/osteochondral techniques are increasingly used.
• Limited-resource settings: diagnosis relies more on plain radiographs and clinical staging; prolonged conservative care and simpler open procedures (debridement, dorsal wedge osteotomy, head resection) predominate. Outcomes for these established operations remain good, which is reassuring where advanced techniques are unavailable.

The entire surgical literature for Freiberg disease is Level III-IV, small retrospective series and one small randomised trial. There are no large randomised comparisons, so most "best operation" claims rest on low-grade evidence and surgeon preference.

Aetiology. None of the three mechanisms in the pathophysiology section is proven, and the likeliest answer is that all of them contribute.

Core decompression. Extrapolated from femoral-head AVN. For Smillie 1-2 it has only small case series, no controlled comparison with conservative care, and a real risk of iatrogenic fracture, so many surgeons reserve it for failed conservative treatment.

Which osteotomy. Dorsal closing wedge (Gauthier), shortening (Weil) and head restoration all report good results. The comparative data (Mutlu, Özkul 2016) favour preservation or restoration over excision, but the series are single-centre.

Salvage in the young. For end-stage disease, arthrodesis gives the most reliable pain relief but sacrifices motion; resection preserves motion but risks transfer metatarsalgia and a floating toe; silicone implants have high mid-term failure and are generally avoided in young patients.