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.
The ankle joint (or talocrural joint) is formed by the articular surfaces of the distal tibial and fibular epiphyses and the talus in its superior, lateral, and medial aspects. The morphology of these surfaces forms a hinge-type synovial joint with a single axis of movement that allows dorsiflexion (flexion) and plantar flexion (extension) of the ankle and foot in the sagittal plane. Because of this configuration and the fact that the ankle is a load-bearing joint, the interarticular space is narrow, and therefore the medial side of the talus is hard to reach. To expose the talus, a medial malleolar osteotomy is necessary.
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. A posteromedial or posterolateral defect may be revealed by a heelrise mortise view with the ankle in plantarflexion.
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.
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.
Conservative treatment and arthroscopic treatment options are described in arthroscopic treatment of osteochondral defect medial talar dome- microfracturing.
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.
Osteochondral autograft transfer (OATS)
OATS is a reconstructive bone grafting technique that use one (or more, i.e. mosaiplasty) cylindrical osteochondral grafts from the less weigthbearing periphery of the ipsilateral knee. This is transplanted into the prepared defect site on the talus. OATS is indicated by large lesions, in some cases as secondary treatment. The results of OATS are excellent in 87% of the cases, however morbidity of the donor knee joint was present in 0-37% of patients.
Autologous chondrocyte implantation (ACI)
Autologous chondrocyte implantation is a two-step procedure. First, by means of arthroscopy, a biopsy is taken from a region of healthy articular cartilage. Chondrocytes are separated by filtration and cultivated for 11-21 days. After removing a periosteal flap from the tibia, which is sutured to the surrounding rim of normal cartilage next to the lesion, the cultured chondrocytes are injected beneath the flap. ACI should be considered for focal lesions, preferably larger than 1,5 cm in diameter. Also for secondary defects, ACI is considered to be a valuable treatment option. Contraindications are bipolar lesions and diffuse degenerative joint changes.
A relatively new open procedure for osteochondral defects is a contoured articular inlay implant with a diameter of 15 mm. The procedure is performed with a medial malleolar osteotomy and has no disadvantages such as donor-site morbidity or two-stage surgery. Clinical goals of the implant are to offer relief of pain and swelling, return to activity and to prevent (further) cyst formation.
Sliding calcaneal osteotomy
A decrease in joint congruence and malalignment can increase contact pressure per area and therefore may lead to osteolysis and osteochondral defects. Other treatment options have good results; however the originally problem is not solved. A sliding calcaneal osteotomy is sometimes necessary to restore the natural congruency of the ankle joint.
Before starting the operation, make sure it is the right patient and that the right side is signed. Thirty minutes before incision 2 grams of Cefamandol i.v. is administered, which is continued onto one gift of 1 gram after 6 hours, 12 hours, 18 hours and 24 hours postoperative. Antithrombotics (fondaparinux, 2.5 mg subcutaneously) is started 6 hours postoperative until the day the plaster cast is removed and weight bearing is allowed.
Reilingh ML, van Bergen CJ, van Dijk CN. Diagnosis and treatment of osteochondral defects of the ankle. SA Orthopaedic Journal. 2009 winter; 44-50.
Verhagen RA, Maas M, Dijkgraaf MG, Tol JL, Krips R, van Dijk CN. Prospective study on diagnostic strategies in osteochondral lesions of the talus. Is MRI superior to helical CT? J Bone Joint Surg Br. 2005 Jan;87(1):41-6.
Van Bergen CJ, Reilingh ML, van Dijk CN. Tertiary osteochondral defect of the talus treated by a novel contoured metal implant. Knee Surg Sports Traumatol Arthrosc. 2011 Jun;19(6):999-1003.
Van Bergen CJ, de Leeuw PA, van Dijk CN. Treatment of osteochondral defects of the talus. Rev Chir Orthop Reparatrice Appar Mot. 2008 Dec;94(8 Suppl):398-408.
Van Bergen CJ, Zengerink M, Blankevoort L, van Sterkenburg MN, van Oldenrijk J, van Dijk CN. Novel implantation technique for osteochondral defects of the medial talar dome. A cadaver study. Acta Orthop 2010 Aug;81(4):495-502.
Van Bergen CJ, Tuijthof GJ, Siervelt IN, van Dijk CN. Direction of the oblique medial malleolar osteotomy for exposure of the talus. Arch Orthop Trauma Surg. 2011 Jul;131(7):893-901.
Van Dijk CN, Reilingh ML, Zengerink M, van Bergen CJ. Osteochondral defects in the ankle: why painful? Knee Surg Sports Traumatol Arthrosc. 2010 May;18(5):570-580.
Zengerink M, Szerb I, Hangody L, Dopirak RM, Ferkel RD, van Dijk CN. Current concepts: treatment of osteochondral ankle defects. Foot Ankle Clin. 2006 Jun;11(2):331-59, vi.
Zengerink M, Struijs PA, Tol JL, van Dijk CN. Treatment of osteochondral lesions of the talus: a systematic review. Knee Surg Sports Traumatol Arthrosc. 2010 Feb;18(2):238-46.