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Osteochondral lesions of the talus - OLT

Osteochondral lesions of the talus as such were first described in 1856 Monro (36) but Konnig (37) coined the term ‘osteochondritis’ when he found similar pathology elsewhere in the body and thought the aetiology was osteonecrosis. Kappis (38) in 1922 first applied the term osteochondritis to the ankle joint.

Berndt and Harty (39) in 1959 postulated a traumatic aetiology and used the term transchondral fracture of the talus. O’Donoghue (40) said the lesions were intra-articular fractures and Campbell and Ranawat (41) felt the cause was ischaemia in 1966. Alexander and Lichtman (42) + Canale and Belding (43) have subsequently lent support to the traumatic aetiology in 1980. However the exact aetiology remains uncertain.

It is certainly a condition which tends to be under diagnosed bearing in mind that talar osteochondritis accounts for 4 -10% of all the osteochondritides. It affects males more commonly than females and a peak incidence at 20-30 yrs of age (44).

The lesions are either posteromedial or anterolateral. If they are posteromedial - 70% are traumatic - are deep and not usually displaced. They are usually caused by inversion of the dorsiflexed foot (torsional impaction) (45). Of the anterolateral lesions, 90% are traumatic - they are usually thinner and are more commonly displaced. They are typically caused by inversion of the plantar flexed foot (45).

Clinically, patients present with a history of trauma, pain, swelling, catching, giving-way or locking. On examination one may find swelling and tenderness.

The diagnosis is best made by CT or MRI according to Verhagen in 2005 (46). A classification based on CT correlates better with the arthroscopic findings than the original classification of Berndt and Harty (45, 47). Zinman (48, 49) and his colleagues found CT to be superior to XR’s in diagnosis, but MRI also has been advocated (50, 51) particularly by Dipaoala. Anderson has developed an MRI based classification and found CT to be as good as MRI except in diagnosing Grade 1 lesions (52).

Cheng and Ferkel (53) went on to show CT to be the scan of choice if the diagnosis is known but MRI if it is not. They have also developed an arthroscopic classification.

Treatment of the stages 1 & 2 lesions is 6-12 weeks in a cast, but arthroscopy if conservative treatment fails. Stages 3 & 4 lesions are treated arthroscopically immediately.

Results of treatment are good with Loomer (54) showing 80% good or excellent results. Of those patients who don’t do well, Takao M et al in 2004 (55) showed that debriding and re-drilling partially healed lesions produced improved outcomes in 93%.

The surgical approach is as follows for acute OLT. They are palpated with hook. Loose chondral fragments alone are excised but osteochondral fragments are pinned or screwed into the base of the defect whether displaced or undisplaced .

For chronic OLT, again palpate with a hook; see if it is loose. Fix it if it is loose and the underlying bone is healthy; if the underlying bone is unhealthy, you need to excise the loose fragment and drill the base of the defect. Large areas can be treated by osteochondral graft large.

It has been shown by Buckwalter that penetration of subchondral bone disrupts subchondral vessels (56-59), this produces bleeding , a clot and fibrocartilagenous repair (60, 51). The cells responsible for this enter from the marrow (62, 63). Significant cartilage defects can be repaired by tissue which grows up drill holes to cover exposed subchondral bone (64).

The results of arthroscopic treatment of OLT are as good if not better than open surgery (65-71) ie 80% plus.

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