NB This page is from the 2005 Hyperbook.
Last evidence check February 2007 but no substantial revision since Feb 2005.
Chondral and osteochondral lesions or defects (OCD) are an important source of pain after ankle injuries. The advent of CT and MR scanning has shown that they are commoner and more complex than was thought.
Although the majority of osteochondral lesions occur after a definite injury, some have no clear history of injury. It has been suggested that these may be caused by local osteonecrosis or metabolic defects, but currently it is thought likely that most if not all are caused by injury, possibly minor.
Most OCDs occur on the talus, but about 10% occur on the tibial plafond, often as “kissing lesions” with a talar defect. Talar lesions usually occur in two distinct regions:
The standard classification is that of Berndt and Hardy (1959), which was derived from plain radiographs and surgical exploration.
|
|
|
|
| Stage 1 - impaction fracture (invisible on Xray) | Stage 3 - undisplaced fragment | Stage 4 - displaced fragment |
The appearance of arthroscopy and CT and MR imaging has shown that only about 50% of OCDs are visible on plain radiographs, and that their natural history is more complex and not yet fully understood. New classifications have appeared using the information from these investigative techniques, but no consensus has yet emerged as to which classification will replace that of Berndt and Hardy. For the FRCST+O it would be best to know the Berndt and Hardy classification and to be aware of at least one of the newer classifications – we suggest the Bristol system. There is little data on the reproducibility of these classifications. The Bristol classification gives some prognostic information in that stage 2b and 5 lesions are probably more chronic and do worse.
 |
 |
 |
| Stage 1 - chondral lesion only | Stage 2a - subchondral fracture with surrounding oedema | Stage 2b - subchondral fracture without surrounding oedema |
 |
 |
 |
| Stage 3 - undisplaced fragment | Stage 4 - displaced fragment | Stage 5 - subchondral cystic lesion |
The main presenting symptom is pain, which may be quite diffuse or localised to the region of the lesion. There is usually a history of injury to the ankle, which may have been considered a sprain that failed to resolve. Sometimes the presentation is quite acute, with severe pain and swelling in the ankle after injury and difficulty weightbearing.
Some patients complain of locking or catching - which may be due to a loose body or to synovitis – or of instability.
Examination may show an antalgic gait. There is usually tenderness in the joint which may be localised, giving a clue to the site of the lesion, or diffuse. There may be swelling or synovitis, and 30-50% of patients have ligament injuries.
Occasionally other diagnoses such as inflammatory arthritis will be suggested by the clinical picture and require appropriate investigation. However, the main investigation is imaging:
Plain films will show about half of all lesions and will also show other fractures, spurs and joint narrowing. Our radiology colleagues prefer to obtain plain radiographs before MR.
Isotope bone scanning will show an area of increased activity at the site of an OCD, but has been largely superseded by MR and CT.
CT shows bony fragments and cysts well, but does not show bone oedema or cartilage defects. CT arthrography, however, shows cartilage lesions at least as well as MR arthrography (Scmid et al 2003)
MR is probably the imaging modality of choice, showing cartilage and bone lesions well, including bone oedema. The significance of oedema is not yet clear; it can be seen even after normal exercise and does not always reflect clinical problems or prognosis. Robinson et al (2003) recommend MR in any ankle injury which is failing to settle after 3 months, and we generally follow this.
 |
 |
 |
| Large lateral OCD visible on plain film | Complex cystic medial OCD | "Kissing" OCDs on tibia and talus |
As the natural history is not known for all OCD types, there is some controversy about whether any can be managed symptomatically, perhaps with rehabilitation to improve muscle strength, range of movement and proprioception, or with protection in a cast or brace. Some authors recommend non-surgical treatment for surface injuries only – Berndt + Hardy stage 1/Bristol stage 1. However, Shearer (2002) reported satisfactory results in half of 35 ankles with chronic “stage 5” cystic lesions (Bristol stage 5), with few developing OA. Follow-up ranged from 4 months to 20 years, and only six patients opted for surgery, all within 2 years.
There have been no RCTs comparing surgical to non-surgical treatment for any grade of OCD.
Older series described the open surgical treatment of OCDs, but recent series have concentrated on arthroscopic treatment. Generally, debridement of flaps of cartilage and removal of loose bodies are recommended. Most ankles will require some degree of synovectomy for access and this may help joint pain. Undisplaced fragments can be fixed with bone pegs, non-protruding screws or absorbable pins.
Several methods have been proposed to stimulate the growth of fibrocartilage:
There have been no RCTs of different techniques. Tol et al (2000) reviewed studies up to 1998 and found that both curettage and curettage and drilling had success rates of around 80%, with the addition of drilling slightly better. However, the quality of reporting made it difficult to draw conclusions. Subsequent reports have not clarified this. We debride and curette all lesions. Drilling is used when curettage does not reach fresh bone.
Even large, deep lesions sometimes settle clinically with arthroscopic surgery. However, lesions which fail to settle or recur may be considered for further reconstructive surgery by bone and/or cartilage grafting.
Osteochondral plug grafting has been extensively used in the knee. For the talus graft may be harvested from the intercondylar notch of the femur (Mendicino 2001, Hangody 2001, al-Shaikh 2002, Scranton 2006) or the non-weightbearing surface of the talus (Sammarco 2002). Access to the talus may require a medial malleolar osteotomy. The longest follow-up is from Hangody (2001), who reported 34/36 excellent or good results according to the Hannover score at 2-7 years (mean 4.2 years). Clinical details were not reported. Follow-up MR scans and arthroscopy showed congruent joint surface and incorporation of graft in unspecified numbers of patients.
An alternative is the use of autologous cultured chondrocyte grafts applied under a periosteal flap (Giannini 2001). Bone graft may be used to fill underlying voids. Giannini reported improvement from a mean AOFAS ankle-hindfoot score of 32 pre-operatively to 91 at 24 months. Defect sizes ranged from 2.2-4.3cm 2 and arthroscopic biopsies in 5 patients showed healthy cartilage. Whittaker (2005) reported success in 9/10 patients at follow-up averaging 2 years; the Mazur ankle score increased from 51/90-74/90. Nine had arthroscopic confirmation of graft incorporation.
Whittaker J-P et al. Early results of autologous chondrocyte implantation in the talus. JBJS 2005;87B:179-83