The incidence of (osteo)chondral defects of the talar dome in patients with acute lateral ankle ligament ruptures is 5-7%. The osteochondral defect leads to a prolonged swelling and synovitis, diminished range of motion and pain on weight bearing. A plain radiograph can disclose a lesion but is often negative.
As not all patients report a history of ankle injury. A subdivision can be made of non-traumatic and traumatic defects.
The non-traumatic etiology concerns idiopathic osteochondral defects. Ischemia, necrosis and possibly genetics play a role. Osteochondral defects in identical twins and in siblings have been described. In 10% to 25% of patients the occurrence of the defect is bilateral. Most of these lesions are asymptomatic. They can become symptomatic after a traumatic event. In lateral lesions trauma is described in 98% of cases, in medial lesions this is 70%.
Lateral osteochondral lesions are usually located in the anterior third of the talar dome. Medial lesions are mostly located in the posterior half. A lateral lesion is typically shallow and wafer-shaped, indicating a shear mechanism of injury. Medial lesions are most often deep and cup-shaped, indicating a mechanism of torsional impaction. Lateral lesions are more often displaced than medial lesions.
Repetitive loading of the damaged articular cartilage surface can lead to local cellular degeneration or death by the disruption of collagen fibril ultrastructure and thickening of the subchondral bone. Animal experiments have shown that oscillating fluid pressure can lead to osteolysis. Fluid pressure induced bone resorption seems to be a powerful bone resorptive stimulus. In situations with net bone loss, there is ongoing bone formation adjacent to bone resorption. This bone resorption due to hydrostatic pressure leads to subchondral cysts surrounded by a newly formed calcified zone.
Most osteochondral defects of the talar dome are caused by trauma, which may be a single event or repeated, less intense events (microtrauma). A defect may heal, remain asymptomatic, or progress to deep ankle pain on weight bearing, prolonged joint swelling and formation of subchondral bone cysts. During loading, compression of the cartilage forces water into the microfractured subchondral bone. The increased flow and pressure of fluid in the subchondral bone can cause osteolysis and the slow development of a subchondral cyst.
The pain does not arise from the cartilage defect but most likely is caused by repetitive high fluid pressure during walking, which results in stimulation of the highly innervated subchondral bone. Further degeneration depends on several factors, including the repair of subchondral bone plate and correct alignment of the ankle joint.
History & Physical Examination
Osteochondral defects (OD) typically cause deep pain. Sometimes there is recurrent swelling, synovitis, and sometimes locking complaints. A differentiation has to be made between the acute and chronic situation. In the acute situation symptoms of OD compared to those of acute ankle injuries, including lateral or medial ankle pain, swelling and limited range of motion. In patients with an isolated ligamentous ankle injury these acute symptoms usually resolve after functional treatment within two to three weeks. If symptoms do not resolve after three to six weeks there should be suspicion of an OD. These patients usually present with persisting symptoms and often a limited range of motion. Locking and catching are symptoms of a displaced fragment. In most patients with a nondisplaced lesion symptoms in the acute situation cannot be distinguished from the soft tissue damage.
Chronic lesions typically present as persistent or intermittent deep ankle pain, during or after activity. Reactive swelling and stiffness may be present, but absence of swelling, locking, or catching does not rule out an OD. There may be a normal range of motion, with the absence of both swelling and absence of recognizable tenderness on palpation.
Conventional radiographs of the ankle should be obtained after careful history taking and physical examination of the ankle. These consist of weightbearing anteroposterior (mortise) and lateral views of both ankles. The sensitivity and specificity of the combination of medical history, physical examination and radiography are 59% and 91%, respectively. The radiographs may not reveal any pathology, or show an area of radiolucency. Initially the damage may be too small to be visualized on a routine X-ray. The OD sometimes becomes apparent on radiographs at a later stage. A posteromedial or posterolateral defect may be revealed by a heelrise mortise view with the ankle in plantarflexion.
1. 2. 3.
1. Weight-bearing anteroposterior radiograph of the right ankle of a 31-year-old male patient showing a radiolucency in the medial talar dome (arrow), indicating an osteochondral defect. In case there is no clinical information or this diagnosis is not considered, it can easily be missed on this conventional radiograph.
2. Lateral weight-bearing radiograph of this same patient. The osteochondral defect is not visible.
3. A 4 cm heelrise view of the same ankle reveals the posteromedial osteochondral defect more clearly (arrow).
For further diagnostic evaluation magnetic resonance imaging (MRI) or computed tomography (CT) are often used, with similar accuracy. A multislice helical CT-scan is useful for defining the exact size and location of the lesion and is therefore preferred for pre-operative planning. The scanning protocol involves "ultra high resolution" axial slices with an increment of 0.3 mm and a thickness of 0.6 mm. Multi-planar coronal and sagittal reconstructions should be 1 mm.
1. 2. 3.
1. CT-scan of the right ankle of a 31-year-old female patient showing a cystic posteromedial osteochondral ankle defect. Axial slice.
2. Coronal reconstruction.
3. Sagittal reconstruction.
The choice of treatment depends on several factors, such as the patient's age, symptoms, duration of complaints, location and size of the defect, and whether it concerns a primary or secondary OD.
In spite of a variety of grading systems, none of them is sufficient to direct the choice of treatment. Therefore, as a guideline, we propose to use the location and size of the lesion as the main indicator for treatment. Other factors playing a role in the decision- making is the age of the patient and whether it concerns a primary or secondary procedure.
Asymptomatic or low-symptomatic lesions are treated nonoperatively by rest, ice, temporarily reduced weightbearing, and an orthosis in case of giving way for a trial period of six months. Although nonoperative therapy yields only 45% successful results, a trial period in general does not adversely affect the outcome of surgery. OCDs have demonstrated a tendency to only deteriorate slowly or not at all in the ankle joint.
Surgical treatment is considered in case of failure of nonoperative treatment or continuing symptoms after previous surgery (secondary OD). According to reviews of the literature the best currently available treatment for primary OD is the combination of excison, debridement and bone marrow stimulation. According to the ISAKOS - FIMS consensus debridement and drilling or microfracturing is the first step in the treatment of symptomatic osteochondral lesions that are too small to consider fixation. Hence, symptomatic lesions up to 15 mm are treated primarily by debridement and bone marrow stimulation. In case of a (cystic) defect sized 15 mm or larger this technique might also be considered as a primary treatment option. In these cases a cancellous bone graft may be placed in the defect after debridement.
A wide range of open procedures including medial malleolar osteotomy or ligament- detachment procedures is available for larger defects or when the defect is too far posterior in a very tight joint, but these are not considered in this chapter.
There are various published surgical techniques for treatment of symptomatic osteochondral lesions. Generally these are based on one of the following three principles:
1. Debridement and bone marrow stimulation (microfracture, abrasion arthroplasty, drilling)
2. Securing a lesion to the talar dome (retrograde drilling, fragment fixation)
3. Stimulating the development of hyaline cartilage (osteochondral autografts, allografts, autologous chondrocyte implantation)
The choice of the treatment for osteochondral lesions depends on the symptoms, the duration of complaints, the size of the defect and whether it concerns a primary or secondary osteochondral defect.
Asymptomatic or low symptomatic lesions are treated conservatively with rest, ice, temporarily reduced weightbearing and, in case of giving way, an orthosis.
Treatment of lesions smaller than 15 mm by means of excision, debridement and bone marrow stimulation (microfracturing/ drilling/ abrasion) is the first choice of treatment and results in 86% good/excellent results. All other therapeutic options clearly resulted in lower percentages of good/excellent results. There are currently not enough publications on osteochondral transplant or cartilage repair reported to determine their position. Concerning osteochondral transplants an ISAKOS expert panel stated that the technique looks simple but this is not the case. The technique of osteochondral transplant should be reserved for secondary cases. Often a medial malleolar osteotomy is needed in order to gain adequate access to the lesion.
For mechanically unstable lesions treatment options are fixation, debridement with bone marrow stimulation, retrograde drilling, osteochondral transfer or autologous chondrocyte transplantation.
Fixation is preferred in (semi)acute situations in which the fragment is 15 mm or larger. In adolescents refixation of an osteochondral defect should always be considered even with fragments smaller than 15 mm.
Large talar cystic lesions can be treated by retrograde drilling and filling the defect with a bone graft. In case of failed primary treatment an osteochondral transplant can be considered. The place of cultured chondrocyte transplant still needs to be determined.
The type of surgical treatment will influence the amount of exposure of the defect. The majority of primary lesions can be treated by means of arthroscopy. Many posteromedial lesions do not have to be treated by malleolar osteotomy, but can be treated arthroscopically by bringing the foot in hyperplantarflexion, although skill and experience are required.
Our research group is currently investigating the applicability of a novel resurfacing technique of the medial talar dome by means of a contoured metal implant when primary and secondary treatment failed in patients with defects of at least 12 mm in size.
In this chapter we present a patient with deep ankle pain due to an osteochondral defect of the talus smaller than 15 mm as measured on a pre-operative CT-scan. Therefore this patient is treated by means of artrhoscopic debridement and microfracturing.
The patient can be discharged the same day of surgery and partial weightbearing. The patient is instructed to perform active dorsiflexion of the ankle to the neutral position (knee slightly bent). This exercise should be performed 2 or 3 days times per hour for the first days after surgery. The patient is instructed to elevate the foot when not walking to prevent edema. The dressing is removed 3 days post-operative. The period of partial weightbearing varies between 10 days and 6 weeks. For defects up to 1 cm, 10-14 days partial weightbearing is enough. Larger defects can possibly benefit from a longer period of partial weightbearing since the filling of the defect gets a better chance of maturing without maximal loading. Patients with limited range of motion are directed to a physiotherapist. Running is best to be postponed untill 3 month postsurgery. Sport resumption can on average be expected at 4-5 month post surgery.
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