CHAPTER 15 Osteochondral Lesions of the Talar Dome
New Horizons in Cartilage Replacement
Osteochondral lesions of the talar dome larger than 2.5 to 3.0 cm2 pose a special problem in the young and middle-aged population (Figs. 15-1 to 15-3). These lesions affect the articular cartilage of the talar dome and the underlying subchondral bone.1 If encountered acutely or if a large fragment exists, some of these lesions can be stabilized and internally fixed with metallic or bioabsorbable implants. Success rates of 78% (range, 40% to 100%) have been reported with reduction and fixation of the osteochondral fragments.2 Most of the acute lesions suitable for internal fixation are laterally located and are usually anterior on the talar dome, making them relatively easy to access using a small, anterolateral arthrotomy incision or arthroscopic techniques.
FIGURE 15-2 Anteroposterior magnetic resonance imaging shows an osteochondral lesion of the medial talus.
Unfortunately, patients with these lesions represent a small proportion of those who present for treatment of symptomatic osteochondral lesions of the talar dome. Most have chronic, medial lesions, which tend to occur more posteriorly on the talar dome. They are more difficult to access and usually require a medial malleolar osteotomy for open exposure. The posteromedial lesions more commonly manifest as chronic lesions that have greater depth than their lateral counterparts and that demonstrate degenerated articular cartilage with necrotic supporting subchondral bone.
Most chronic lesions of the posteromedial talar dome may be treated with conventional arthroscopic techniques, including débridement of the major fragments of bone and articular cartilage, establishment of a stable articular cartilage margin with perpendicular edges, and some type of marrow stimulation of the bony base, such as abrasion, drilling, or microfracture. This technique can produce good or excellent results in approximately 80% of patients.
Patients who fail conventional treatment or who have lesions known to have a poor prognosis with conventional treatment may be treated with some type of articular cartilage replacement technique. Large lesions (>1.5 to 2 cm in diameter) and lesions associated with large subchondral cysts (stage V lesions) are thought to have a poor prognosis with standard débridement procedures and may be considered for articular cartilage replacement. The indications for surgical cartilage replacement are symptomatic, deep lesions classified by the International Cartilage Repair Society (ICRS) as grade 3 (i.e., greater than 50% cartilage depth and down to but not through subchondral bone) or grade 4 (i.e., subchondral bone exposed, with lesions extending through the subchondral bone plate or deeper into the trabecular bone). There should be no uncorrected malalignment or instability and no significant osteoarthritis.
When considering the appropriate treatment for a talar dome lesion, it is important to separate the short-term from the long-term goals. In the short term, the goal is to eliminate or reduce pain to improve function. In the long term, the goal is to forestall the development of degenerative arthritis in the ankle joint while maintaining pain relief. In evaluating the various types of articular cartilage replacement techniques presented in this and previous chapters discussing autologous osteoarticular transplant techniques and autologous chondrocyte implantation (ACI) techniques, it is important to understand that there has been no level 1 study that has prospectively evaluated a randomized group of patients to compare techniques in the ankle.
Autologous osteochondral implantation techniques using plugs obtained from the knee joint or ACI using cultured chondrocytes implanted beneath a layer of periosteum using open techniques are approved for use in the United States. Orthopedic surgeons in other countries are using various types of articular cartilage implantation techniques that are potentially more amenable to arthroscopic surgery but are not approved for use in the United States. They represent a promising avenue of research for treatment of these lesions and are described in this chapter.
COLLAGEN-COVERED AUTOLOGOUS CHONDROCYTE IMPLANTATION
The technique of harvesting and suturing a periosteal patch in ACI is technically demanding and time consuming. Problems such as periosteal patch quality, symptomatic periosteal hypertrophy, and delamination have stimulated the development of biocompatible and bioabsorbable membranes to cover the chondral defect. A bilayer, absorbable, porcine collagen I/III membrane (Chondro-Gide, Geistlich Biomaterial, Wolhuser, Switzerland) has been used in European studies instead of a periosteal patch. The membrane is degraded by enzymatic division (i.e., collagenase), and the resultant collagen fragments denature at 37° C to gelatin.
In a prospective study presented at the ICRS meeting in 2004, Steinwachs17 described 163 patients treated for chondral defects in the knee with ACI using a periosteal flap or the Chondro-Gide membrane instead of the periosteal patch. At approximately 3 years of follow-up, 78% of patients in the periosteal group reported good or excellent results, and 88% of patients in the Chondro-Gide group reported good or excellent results. Statistical significance was not discussed by the investigator. There were no cases of membrane hypertrophy.17
MATRIX/MEMBRANE-INDUCED AUTOLOGOUS CHONDROCYTE IMPLANTATION
Matrix/membrane-induced autologous chondrocyte implantation (MACI) is a second-generation chondrocyte implantation process. MACI is a new biotechnology in which cultured autologous chondrocytes are impregnated onto a highly purified, porcine collagen I/III membrane (Verigen AG, Genzyme Corp., Cambridge, MA) (Fig. 15-4). The MACI implant can be fixed to the chondral defect by fibrin glue (with little or no suture necessary), suture, or bioabsorbable pins or tacks. The procedure can be performed arthroscopically or by mini- arthrotomy. No periosteal graft is needed.
Chondrocytes are harvested arthroscopically from a non–weight-bearing area of the ipsilateral knee (200 to 300 mg of healthy cartilage). The chondrocytes are then cultured and expanded in vitro (3 to 5 weeks) and then impregnated on an absorbable, three-dimensional, bilayered, purified, porcine collagen I/III membrane. The bilayer structure has a smooth side that acts as a natural barrier and faces the joint. Chondrocytes are seeded on the porous side of the matrix. The membrane is tear resistant and can be templated and cut to shape. The membrane is nonantigenic (i.e., telopeptides are split during the manufacturing process), and it is bioabsorbable. The bioabsorbable membrane can be fixed to the ankle cartilage defect with fibrin glue, pins, or suture.
The talar dome lesion may be approached using a simple arthrotomy for an anterior lesion, or a malleolar osteotomy may be required to expose a middle to posterior talar lesion. The osteochondral defect is débrided, and the base is curetted to remove the calcified cartilage layer (Fig. 15-5). A stable cartilage rim with sharp vertical walls of healthy cartilage is created, and the chondral defect is templated for size and shape (Fig. 15-6). The MACI membrane is cut to the proper shape with a scalpel or scissors (Fig. 15-7). The membrane is then fixed with fibrin glue (Tisucol, Baxter, Spain) (Fig. 15-8). Suture or bioabsorbable pins, or both, may be used, but fibrin glue by itself is usually all that is needed (Figs. 15-9 and 15-10).18,19
Postoperatively, the patient is placed into a soft dressing, and continuous passive motion is initiated for 8 weeks, during which time the patient does not bear weight on the extremity. Patients with larger and more central lesions are not allowed to bear weight for 12 weeks.
Chondrocytes for culture are obtained from the knee joint as described previously. After the chondrocyte population has been expanded in vitro and impregnated on the membrane, standard ankle arthroscopy is performed through a specially designed arthroscopic cannula, and the cartilage defect is curetted using sharp ring curettes to remove the calcified cartilage layer. The surgeon creates a stable articular cartilage rim with sharp vertical walls of healthy cartilage. Using a flexible ruler, a standard probe, and a specially designed arthroscopic caliper, the size of the lesion is calculated. A template is created using packaging from a suture pack or a rubber drain, and it is placed in the cartilage defect to test for size.
Placement of the graft is performed using a dry scope technique, which is done without fluid in the joint. Two small anchors with 5-0 absorbable sutures are then placed at opposite sides of the periphery of the cartilage lesion (i.e., 3 and 9 o’clock or 12 and 6 o’clock). The sutures are then passed through the MACI membrane outside the joint at points corresponding to the cartilage lesion (Figs. 15-11 to 15-13).
FIGURE 15-11 The lesion is curetted (A), and suture anchors are placed (B, C). The membrane is placed (D, lower right).
(From Chu C, ed. Articular cartilage surgery. Oper Tech Orthop. 2006;16:217-292.)