Autologous Chondrocyte Implantation

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Chapter 35 Autologous Chondrocyte Implantation

INTRODUCTION

The ancient Greeks acknowledged ulcerated cartilage as troublesome to treat, with little to no natural healing capacity. Articular cartilage lesions have for a long time been undiagnosed and their severity underestimated. The increased surgical approach to ligament injuries, along with the introduction of arthroscopy and magnetic resonance imaging (MRI), has increased the diagnostic possibilities for articular cartilage lesions and activated the search for an improved treatment. Articular cartilage lesions are much more common than earlier recognized.

Anterior cruciate ligament (ACL) and meniscus injuries are often combined with articular cartilage injuries, in which the cartilage injury is the most serious and most difficult to treat in the end. Noyes and coworkers18,19 and Shelbourne and associates24 found that acute and chronic ACL injuries were associated with articular cartilage injuries in 40% to 70% of knees. There are reports that in cases of meniscus injury, 40% to 50% of patients also have cartilage damage.25 Hjelle and colleagues11 reported on 1000 consecutive patients with symptoms requiring arthroscopy. Chondral or osteochondral lesions of any type were found in 61% of the patients. Curl and coworkers5 found that in 31,516 patients who underwent arthroscopy, 63% had a cartilage lesion and 19% had an Outerbridge grade IV cartilage lesion. Bone bruises have been reported in acute knee injuries12 and in combination with ACL injuries in 80%.17 The damage to the trabecular bone may heal, but the overlying cartilage may degrade over time.

Since the early 1980s different treatments for full-thickness cartilage lesions have been developed that show promise. Some treatments have been discarded whereas others have been further developed. However, no “gold standard” is currently established and injuries to articular cartilage are still difficult to treat. Without proper management, articular cartilage injuries may degrade through enzymatic and mechanical breakdown into post-traumatic osteoarthritis.

Autologous chondrocyte implantation (ACI) has been in clinical practice since 1987, with over 25,000 patients treated worldwide. ACI was approved by the U.S. Food and Drug Administration in 1997.

INDICATIONS

ACI is indicated for full-thickness cartilage lesions or osteochondral lesions, including osteochondritis dissecans (OCD) in the knee (International Cartilage Repair Society [ICRS] or Outerbridge classification grade III or IV). The size of the lesion should be between 2 and 16 cm2, but larger lesions and multiple lesions can be treated in the same joint. The lesions should be situated on either the patella, the femur, or the tibia, and the opposing articular surface should be undamaged or have only superficial cartilage damage. Bone-to-bone conditions between the tibia and the femur or between the trochlea and the patella can be tried as a salvage procedure in young patients. The age recommendation is between 15 and 55 years, but there is no definite limit. Ligamentous instability, varus or valgus deformities, patella malalignment or instability, meniscus deficiency, and bone pathology or defect are not contraindications, but these must be addressed in the treatment.

The recognition of serious articular cartilage injuries, including bipolar lesions in young and middle-aged individuals, has along with increased experience widened the indications for ACI (Fig. 35-1).

CLINICAL EVALUATION

INTRAOPERATIVE EVALUATION

During the first-stage arthroscopy, knee stability is reassessed under anesthesia. The lesion is examined to decide whether it meets the indications for ACI. The lesion should be surrounded by healthy cartilage (but uncontainment is not a contraindication) and the opposing articular surface should be undamaged or have only minor superficial cartilage injury (Fig. 35-2). All intra-articular structures should be examined. The location, size, and depth should be noted using, for instance, the ICRS Knee Evaluation Package. Slices of cartilage with subchondral bone are harvested with a curet. The recommended harvest sites are the medial and lateral proximal rim of the femoral trochlea and the lateral aspect of the intercondylar notch in the knee joint. In more than 1400 patients who have had cartilage removed from the proximal medial trochlea for cell culturing, no complications or late symptoms have occurred from the donor site area. An optimal harvesting of cartilage is of great importance for the success of the cell culturing. Optimal cell quality is necessary for a successful result of this procedure and should be performed according to good laboratory practice or national regulations if present.

Other pathology within the knee should also be noted. If present, loose bodies are removed before the cartilage harvest. Meniscal tears are treated after the cartilage biopsy has been harvested. Always consider the possibility of meniscus repair, especially in young patients.

OPERATIVE TECHNIQUE

Either general or spinal anesthesia is used, and a tourniquet-controlled blood field is optional. A central straight skin incision is used. If previous incisions are present, these are used if possible to avoid further scar formation. The cartilage injury is approached through either a medial or a lateral arthrotomy depending on the location of the lesion and concomitant procedures, and the arthrotomy is adjusted for adequate access to the lesion. When the lesion is difficult to reach, the patella may have to be dislocated. In posterior femoral and tibial lesions, the anterior meniscus attachment has to be released or the medial or lateral collateral ligament femoral insertion detached with a bone block. The injured area is excised with vertical edges including all damaged cartilage and débrided without causing any bleeding from the subchondral bone. This avoids possible contamination with fibroblasts and undifferentiated stem cells from the bone marrow. Intralesional osteophytes may be present as a result of an intrinsic healing attempt or a previous microfracture or drilling procedure. Smaller osteophytes are carefully tapped down to the level of the subchondral bone plate, whereas larger and prominent osteophytes may be carefully curetted down to the bone plate. Surprisingly, there is very little bleeding from the curettage. If bleeding is present, use an epinephrine sponge or a drop of fibrin glue to stop the bleeding. Avoid electrocautery to prevent any necrosis in the bone.

The length and width of the defect is measured, and a template of the lesion is made with sterile paper or aluminum foil. Through a separate incision on the upper medial tibia, below the pes anserinus and the medial collateral ligament insertion, the periosteum is dissected free from overlying fascia, fat, fibrous tissue, and crossing vessels. A periosteal flap of the correct size and form is excised using a template, but because of shrinkage and room for suturing, the flap is oversized with 1 to 2 mm in the periphery. The flap with intact cambium layer is gently dissected from the cortical bone with a periosteal elevator. The periosteal flap should be as thin as possible and transparent, which will give more volume in the defect, allowing diffusion of synovial fluid and the cells to spread and expand and produce hyaline matrix. A thin flap also reduces the risk of periosteal complications. With increased age and inactivity, the periosteum atrophies and can become so thin that it is impossible to harvest. In smokers and obese patients, the quality of the periosteum is also decreased. The periosteum is thicker and more fibrous on the medial and lateral femoral condyle, proximal to the articular surface, and covered with a rich vascular network with risk for bleeding. This can lead to postoperative hematoma with swelling, adhesions, and arthrofibrosis. Therefore, the distal shaft of the femur is a better option as a second region for periosteal flap harvesting.

The flap is sutured to the cartilage rim of the defect at the level of the surrounding cartilage and the periosteum-cartilage border is sealed with fibrin glue. A gentle saline injection under the flap reveals any leakage along the cartilage rim, which must be sealed. After aspiration of the saline, the cultured chondrocytes are injected underneath the periosteal cover and the injection site is sutured and sealed (Fig. 35-3). The arthrotomy is closed in separate layers. Bandaging including the foot, lower leg, and knee is applied.

Concomitant Stabilizing Procedures

For an optimal environment for the repair tissue, any instability must be corrected. In the tibiofemoral joint, an ACL or posterior cruciate ligament reconstruction or a medial or lateral collateral ligament shortening may be prepared before ACI. These procedures are usually done concomitantly with ACI. The aim is to avoid a second arthrotomy when staging. When performed concomitantly with ACI, a ligament reconstruction or shortening is done after the cartilage lesion is débrided and covered with periosteum but before the chondrocytes are injected.

Patellofemoral lesions are often related to an unstable patella, and the patella must thus be stabilized for good healing. Stabilizing procedures may include anteromedialization of the tibial tuberosity and sometimes slight distalization owing to patella alta, lateral release, proximal medial soft tissue (medial patellofemoral ligament and vastus medialis obliquus) shortening, and trochlear groove plasty21 (if the patella is dysplastic) (Fig. 35-4).

Patellofemoral (trochlear) lesions are often related to patellar instability. If a 6-month training program does not restore functional stability, the background factors present must be corrected. These factors are increased Q-angle (>15°–20°), patella alta, ligament instability (medial patellofemoral ligament [MPFL]), muscular imbalance (musculus vastus medialis obliquus [VMO] weakness) and trochlear dysplasia (flat, convex, and extended in a proximal direction or a flat articulating lateral trochlea) (Fig. 35-5).

Tibial tuberosity transfer is used to correct the Q-angle by approximately 8 to 12 mm of medialization. Tibial tuberosity ventralization unloads the patella-trochlear joint (used in bipolar and large, uncontained lesions). To distalize a patella alta, the tibial tuberosity is moved distally 3 to 5 mm to secure so that the apex of the patellae will articulate on the trochlea. This can be achieved by a tibial tuberosity oblique osteotomy. Stabilizing and unloading procedures may include anteromedialization when needed.

The trochlea groove plasty is performed to establish the skeletal stability of the patella in the trochlea groove in the first 0° to 30° of flexion when the patella is skeletally unstable. Release the synovial membrane from the proximal attachment to the trochlear articular cartilage with a knife. Dissect the membrane free from the femur. Take a curved osteotome and remove the cartilage and bone starting in the center, aiming to the top of the intercondylar notch. Extend 8 to 10 mm distal to the horizontal of the trochlear articular cartilage and widen the groove 15 mm medial and lateral to the center, for a total of approximately 30 mm. If the cortical femoral bone is flat or convex, continue the removal of the bone proximally. Reattach the synovial membrane to the articular cartilage using mattress sutures starting in the synovial edge, cutting through the edge surface 5 to 6 mm into the cartilage. Then, proceed transversely and return the suture through the articular cartilage and the synovial membrane. Adapt the synovial membrane to the cut edge of the articular surface. A maximum of three to five sutures should be used. Inject a layer of fibrin glue under the membrane and compress with a dry sponge for 60 to 120 seconds. Check the sliding of the patella in the new groove and adjust the edges when necessary. This technique preserves the congruity between the trochlea and the patella during the remaining flexion. The author does not address the patella dysplastic forms at any time (Fig. 35-6).

When a stabilization procedure is required, a midline incision is used, starting 3 cm proximal to the base of the patella and ending 4 to 5 cm distal to the patellar tendon insertion. Dissect medially and laterally and perform a lateral release and a medial arthrotomy 3 to 5 mm medial to patella in the VMO tendon. Divide the VMO proximal from the rectus femoris 1 to 2 cm proximal to the base of the patella. Distally, open the infrapatellar bursa medially and laterally. Predrill the tibial tuberosity for later fixation and perform the necessary osteotomy. Perform the ACI on the patella and/or trochlea defects and inject the cells. Fix the tibial tuberosity with one or two screws. Roughen the bone between the VMO and MPFL insertions and the articular cartilage. Suture the VMO and MPFL medial end to the roughened bony surface of the patella. Implicate the lateral flap by suturing it to the VMO tendon. Complete the closure distally. Round the sharp edges of the tibial tuberosity medially and distally. Leave an extra-articular drainage for 12 to 24 hours lateral to the tibial tuberosity. After each step of the procedure, check the range of motion (ROM) and the adequate correction of the Q-angle. Use a brace to limit the ROM to 0° to 60° for the first 3 weeks and then from 0° to 90° or 110° the following 3 weeks.

Concomitant Bone Grafting

When treating osteochondral lesions with bone defects and pathologic bone deeper than 6 to 7 mm, ACI is not enough and staged or concomitant autologous bone grafting is required. A staged procedure is preferable when both bone grafting and high tibial osteotomy are required. This can then be done concomitantly with the cartilage harvesting. Start by abrading away the sclerotic bottom of the defect and all pathologic bone down to spongy bone and undercut the subchondral bone plate. Use a 2-mm burr and drill holes into the spongy bone. Débride the cartilage to healthy cartilage with vertical edges. Then, harvest the cancellous bone used for grafting the bony defect. If the bony defect is small, use bone from the tibia or femoral condyle; if the defect is larger, harvest the bone from the iliac crest. Pack the bone from the bottom up and contour the bone graft just below the subchondral bone plate. Harvest a periosteal flap to cover the bone graft at the level of the subchondral bone plate, the cambium layer facing the joint. Anchor the graft with horizontal sutures into the cartilage and inject fibrin glue under the flap for fixation to the bone graft. Use a dry sponge to compress the area for 2 to 3 minutes. This will avoid bleeding into the cartilage defect. When required, use bone sutures through small 1.2-mm drill holes or resorbable microanchors (Mitec). Harvest another periosteal flap and suture to the cartilage edges, with the cambium layer facing the defect. Use fibrin glue to seal off the intervals between the sutures. Test the watertightness with a gentle saline injection. If there is no leakage, aspirate the saline and inject the chondrocytes. Close the last opening and seal with fibrin glue (Fig. 35-7).

REHABILITATION

Six to 8 hours after surgery, the patient begins passive motion training using a continuous passive motion machine in a pain-free ROM, usually 0° to 30° or 40°. The day after surgery, quadriceps activation, active ROM training, and gait training are the important parts of the rehabilitation, in addition to controlling swelling.

To avoid overloading, but still stimulate the chondrocytes and increase the exchange of fluids and nutrients in the cartilage, weight-bearing on the operated leg is kept partial for the first weeks. The amount of weight allowed depends on the size, location, and number of transplanted defects and possible concomitant procedures. After ACI to a small, contained lesion on the femoral condyle, weight-bearing to the pain threshold is allowed for the first 6 weeks. For large lesions or multiple lesions with concomitant procedures, weight-bearing is limited to 30 to 40 pounds for 6 to 8 weeks, and is then gradually increased up to full after the following 6 to 8 weeks. For patellar and trochlear contained lesions, weight-bearing to the pain threshold for the first 6 weeks is used, but stair climbing is not permitted.

Training on a stationary bike can be done when the wound is healed and knee flexion permits; low resistance is used. Encourage bicycling during the entire rehabilitation program. Training in water may be initiated when the wound is healed. Gradually increased functional and proprioceptive training is important during the entire course of rehabilitation.

When full weight-bearing is achieved, increase distances of walking. If possible, use skating, inline skating, or cross-country skiing on even surfaces as intermediate training before returning to running. Running should be postponed at least 6 to 9 months for small, contained, shouldered femoral condyle defects and begun on an individual basis. For larger or unshouldered femoral condyle defects or defects on patella, trochlea, tibia, or bipolar defects, running should be postponed longer, possibly for up to 12 to 18 months after ACI.

Return to professional athletic training and competition should be judged on an individual basis, including assessment of ROM, muscle strength and endurance, and arthroscopic evaluation and probing/indentation test of the repair area (Fig. 35-8).

AUTHOR’S EVIDENCE-BASED CLINICAL OUTCOMES

Subjective

A clinical evaluation at an intermediate to long-term follow-up of the first 101 patients showed that overall, 77% were considered a good or excellent result.22 The patients were divided into groups according to the location and type of the lesion as well as concomitant ACL reconstruction. In the isolated femoral condyle group, 92% were clinically graded as good or excellent; in the OCD group, 89% were in this category; and in the femoral condyle with ACL reconstruction, 75% were in this category. Patients with multiple lesions had a 67% good or excellent rate. The patellar lesions were often treated with concomitant transfer of the tibial tubercle, medial patellofemoral ligament and VMO shortening, and trochlea groove plasty. At follow-up, 65% had a good or excellent result22 compared with 28% in the initial follow-up study.2

An early consecutive cohort of 61 patients were followed for a mean of 7.4 years (range, 5–11 years).20 At the 2-year follow-up, 50 patients had a good or excellent clinical result; at the 5-to 11-year follow-up, 51 patients were considered good or excellent.

In a study published in 2003,23 58 patients with OCD were treated with ACI and followed an average of 5.6 years. The average age was 26.4 years, and the average defect size was 5.7 cm2, with a maximum defect of 12 cm2. Forty-eight patients had had a mean of 2.1 previous operations because of the injury. The modified Cincinnati clinical rating score was 2.0 points preoperatively and 9.8 points at follow-up. The overall clinical grading was excellent in 53%, good in 38%, fair in 7%, and poor in 2%. Self-assessed improvement was 93%23 (Figs. 35-9 to 35-12). At the ICRS meeting in Toronto in 2002,3 results were presented for patients treated with ACI for cartilage lesions on tibia and trochlea as well as tibiofemoral kissing lesions and multiple lesions (Fig. 35-13).

image

Figure 35-13 Good or excellent results for patients treated with ACI to the tibia (n = 8; mean size, 4.5 cm2) and trochlea (n = 15; mean size, 5.2 cm2) as well as tibiofemoral kissing lesion (n = 14, mean size, 11.8 cm2) and multiple lesions (n = 43; mean size, 10.8 cm2).

(From Brittberg, M.; Peterson, L.; Björnum, S.; Lindahl, A.: Multiple lesions in the knee treated with autologous chondrocyte implantation. Read at the meeting of the International Cartilage Repair Society, June 14-18, 2002, Toronto, Canada.)

Objective

Different objective tools have been used to evaluate the repair after ACI of chondral and osteochondral lesions including arthroscopic macroscopic assessment and indentation tests as well as repair tissue biopsy for histology and histochemistry. In the first 101 patients, 37 biopsies from the repair tissue were assessed for collagen type II.22 There was correlation between hyaline-like repair tissue and good or excellent clinical outcomes.

In the 61-patient cohort, biopsies from the repair tissue were obtained in 12 patients.20 Eight of the biopsies were characterized as hyaline-like by Safranin O staining and homogeneous appearance under polarized light. Eight hyaline-like and 3 fibrous biopsies stained positive to aggrecan and cartilage oligomeric matrix protein. Hyaline-like biopsies stained positive for collagen type II and fibrous biopsies stained positive for collagen type I. All histologic evaluations were performed by independent scientists.20

An arthroscopic indentation probe was used to measure the stiffness of the repair tissue in 11 of the 61 patients at a mean of 54.3 months (range, 33–84 mo).20 The mean stiffness of repair tissue characterized as hyaline-like by histologic evaluation was 3.0 ± 1.1 N, compared with 1.5 ± 0.35 N of fibrous repair tissue. Good and excellent clinical results correlated with hyaline-like repair tissue, whereas fair or poor clinical results correlated with fibrous repair tissue.20

Vasara and associates26 arthroscopically measured the stiffness of the repair tissue 8 to 18 months after ACI using an indentation probe, and compared it with the stiffness of normal surrounding cartilage. The mean stiffness of the repair tissue was 2.04 ± 0.83 N, and the mean stiffness of the surrounding cartilage was 3.58 ± 1.04 N. Non-OCD repair tissue was stiffer (2.37 ± 0.72 N) than the repair tissue of OCD defects (1.45 ± 0.46 N).26

Functional

In the study of the first 101 consecutive patients with chondral or osteochondral lesions of the knee treated with ACI, the activity levels of the patients were evaluated.22 According to the Tegner/Wallgren score, the patients were able to resume an active lifestyle that included sports with high demands on the knee (e.g., soccer). The modified Cincinnati score was an average 9 out of 10, indicating the patients returned to high-level sports.22

In one study, 45 soccer players treated with ACI were followed for a mean of 40 months.16 Eighty-three percent of the young players below 26 years of age, high–skill-level players, and players operated within 12 months after trauma returned to preinjury levels. The time to return from surgery to soccer was 12 to 18 months.16

Twenty adolescent athletes were followed for a mean of 47 months after ACI.15 At follow-up, the 0 to 10 Tegner activity score had increased from 4 to 8 points, and 96% of patients had returned to impact sports, 60% at the same or higher level than before the injury. Treatment with ACI within 12 months from injury lead to 100% return to preinjury sport, whereas 42% of the chronic cases returned to preinjury sport.15

OUTCOMES FROM OTHER AUTHORS

Gillogly68 evaluated 112 patients 2 to 5 years after ACI. The locations of the lesions were diverse and included 15 lesions on the patella, 27 on the trochlea, and multiple lesions in 22. When using the clinician evaluation portion of the modified Cincinnati scale, 93% were considered good or excellent. Using the patient evaluation portion, 89% considered themselves good or excellent.

Minas14 reported on 130 patients treated with ACI in the patellofemoral joint with a follow-up of 2 to 9 years. In a patient satisfaction survey, 80% rated themselves as good or excellent.

Bentley and colleagues1 compared ACI and mosaicplasty in a randomized, prospective study of 100 consecutive patients (58 ACI and 42 mosaicplasty) with a follow-up mean of 19 months. Functional assessment using the modified Cincinnati and Stanmore rating systems as well as clinical assessment showed good or excellent results in 88% after ACI and 69% after mosaicplasty. Arthroscopic assessment 1 year after treatment showed good or excellent repair in 82% after ACI and 34% after mosaicplasty.

In another study, Knutsen and coworkers13 reported on 80 patients with single symptomatic cartilage defects on the femoral condyle treated with either ACI (N = 40) or microfracture (N = 40). Ten patients in each group were treated at four different hospitals. At the 2-year follow-up, both groups had significant clinical improvement. However, according to the Short-Form 36-item questionnaire (SF-36) physical component score, the improvement in the patients treated with microfracture was significantly better than in the ACI group. Three failures were reported, 2 in the ACI group and 1 in the microfracture group. Biopsies from the repair tissue were taken arthroscopically in 67 patients. In the ACI group, 72% of the biopsies showed hyaline-like tissue and 25% showed a mix of hyaline and fibrocartilage. Only 3% showed fibrocartilage. In the biopsies from the microfracture group, 40% were identified as hyaline-like, 29% were a mix of hyaline and fibrocartilage, and 31% contained fibrocartilage.13

Henderson and associates9,10 evaluated 53 patients (72 lesions) with MRI 3 months, 12 months, and 2 years after ACI. The 3-month MRI demonstrated a filling of the defect of at least 50% in 75.3% of the lesions, 46.3% had a near-normal signal, 68.1% had mild or no effusion, and 66.7% had mild or no underlying bone marrow edema. At 12 months, 94.2% had at least 50% defect fill with 86.9% demonstrating a near-normal signal. By 2 years, 97% had at least 50% defect fill with 97% had a near-normal signal. The values for mild or no effusion and mild or no bone marrow edema increased to 91.3% and 88.4%, respectively, at 12 months and 95.6% and 92.6%, respectively, at 2 years. A clinical evaluation of the patients and results from second-look arthroscopy and repair tissue biopsy correlated well with the 12-month MRI.9,10

Brown and colleagues4 evaluated 180 MRIs of 112 patients treated with cartilage resurfacing techniques, including microfracture (MRI done a mean of 15 mo) and ACI (MRI done a mean of 13 mo). Lesions treated with ACI showed better filling of the defect, but graft hypertrophy was present in 63%. The repair tissue after microfracture was depressed compared with the native cartilage and had a propensity for bone development and loss of adjacent cartilage.4

PREVENTION AND MANAGEMENT OF COMPLICATIONS

Local Complications: Periosteal

Superficial fibrillation of the periosteal surface that causes crepitus has occurred (Fig. 35-14). Periosteal hypertrophy overlapping the surrounding normal cartilage may cause symptoms of clicking, catching, or crepitus (Fig. 35-15). This complication may appear between 3 and 9 months postoperatively and, in most patients, disappears spontaneously during continued rehabilitation. When this problem interferes with the rehabilitation, it is first handled with change and modification of the rehabilitation program and then with gentle arthroscopic resection. The frequency of periosteal complications was initially reported to be about 25%. By improved surgical technique and adapted rehabilitation, the incidence of this problem has been reduced to 5% to 8%. Other authors have reported frequencies between 5% and 65%.

Periosteal delamination has occurred in a few cases (Fig. 35-16). The delamination can be marginal, partial, or total. In a marginal delamination, the periosteal flap is avulsed from the surrounding cartilage up to 10 mm and should be excised or gently débrided. In a partial delamination, the periosteal flap is partly separated from the underlying repair tissue and can be removed by shaving or excising the superficial periosteal delamination. A total periosteal delamination can either be detached or appear as a loose body. It should be removed from the joint or the transplanted area. Usually, the repair tissue will continue filling the defect and motion will stimulate it to produce a new sliding surface. During the 6 to 8 weeks after periosteum removal, ROM training and bicycling with low resistance should be performed, but no running is permitted. Periosteal complications are benign and, when adequately addressed, will have no impact on the end result.

Local Complications: Graft Delamination

Separation and delamination of the total repair tissue down to the subchondral bone is a rare complication (Fig. 35-17). In a marginal graft delamination of less than 10 mm, the area is débrided and left alone. If any bone is visible, the bone is microfractured to create a fibrous repair filling, which will stabilize the area. In a partial graft delamination, the defect is excised and new cartilage is harvested for retransplantation of chondrocytes. In smaller defects up to 1.5 cm2, osteochondral cylinders or microfracture may be first options. In a total graft delamination, it either is detached in a small area or appears as a loose body. A loose body is removed and a delaminated graft excised. New cartilage is harvested for reoperation with ACI. Good results can be achieved after a second ACI procedure.

REFERENCES

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2 Brittberg M., Lindahl A., Nilsson A., et al. Treatment of deep cartilage defects in the knee with autologous chondrocyte transplantation. N Engl J Med. 1994;331:889-895.

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18 Noyes F.R., Bassett R.W., Grood E.S., Butler D.L. Arthroscopy in acute traumatic hemarthrosis of the knee: incidence of anterior cruciate tears and other injuries. J Bone Joint Surg Am. 1980;62:687-695.

19 Noyes F.R., Mooar P.A., Matthews D.S., Butler D.L. The symptomatic anterior cruciate–deficient knee: part I. The long-term functional disability in athletically active individuals. J Bone Joint Surg Am. 1983;65:154-162.

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21 Peterson L., Karlsson J., Brittberg M. Patellar instability with recurrent dislocation due to patellofemoral dysplasia. Results after surgical treatment. Bull Hosp Jt Dis Orthop Inst. 1988;48:130-139.

22 Peterson L., Minas T., Brittberg M., et al. Two- to 9-year outcome after autologous chondrocyte transplantation of the knee. Clin Orthop Relat Res. 2000;374:212-234.

23 Peterson L., Minas T., Brittberg M., Lindahl A. Treatment of osteochondritis dissecans of the knee with autologous chondrocyte transplantation: results at two to ten years. J Bone Joint Surg Am. 2003;85(suppl 2):17-25.

24 Shelbourne K.D., Jari S., Gray T. Outcome of untreated traumatic articular cartilage defects of the knee. J Bone Joint Surg Am. 2003;85(suppl 2):8-16.

25 Schimmer R.C., Brülhart K.B., Duff C., Glinz W. Arthroscopic partial meniscectomy: a 12-year follow-up and two-step evaluation of the long-term course. Arthroscopy. 1998;14:136-142.

26 Vasara A.I., Nieminen M.T., Jurvelin J.S., et al. Indentation stiffness of repair tissue after autologous chondrocyte transplantation. Clin Orthop Relat Res. 2005;433:233-242.