Sean M. Jones-Quaidoo and Eric W. Carson
DEFINITION
Articular cartilage of joints such as the knee is essential to the joint's normal function, in which it acts as a load-bearing structure and provides a nearly friction-free surface. Unfortunately, articular cartilage is particularly suspectible to traumatic injury or pathologic conditions such as osteochondritis dissecans, which can, over time, be significantly disabling in the young athlete and have the potential of degenerating over time.
The natural history of articular cartilage injuries currently is poorly understood.
The treatment of focal chondral lesions remains a significant challenge for the sports medicine orthopedic surgeon.
A retrospective review of 31,516 knee arthroscopies examined the prevalence of chondral injuries. This review reported 41% Outerbridge III chondral injuries and 19.2% Outerbridge IV chondral injuries, with an estimated 3% to 4% isolated chondral lesions that were larger than 2 cm2.13
The orthopedic surgeon is armed with a variety of surgical treatments for pathologic problems in articular cartilage. Numerous surgical techniques have been proposed to address this difficult and often disabling condition in a young patient population.
Current articular cartilage resurfacing procedures can be divided into three categories:
Bone marrow stimulation
Implantation of autologous articular cartilage
Transplantation of osteochondral allograft
The clinical results of all of these surgical procedures have generally good shortand long-term clinical results.2–5,14,19 All have specific drawbacks: for example, marrow stimulation produces fibrocartilage; the autogenous osteochondral autograft transfer system (OATS) has an issue with donor site morbidity; and allograft OATS has a significant risk of disease transmission along with a possible immune response to the allograft tissue.
In 1994, Brittberg et al7 proposed an innovative surgical treatment for articular cartilage injuries, autologous cartilage implantation (ACI).
ACI is performed in two stages.
The initial procedure is a comprehensive arthroscopic evaluation of the articular cartilage defect covering size, location, and depth of lesion (FIG 1).
At the same time, if the surgical indications are favorable, the orthopedic surgeon can harvest autologous articular cartilage cells. These articular cartilage cells are then digested enzymatically, with the ultimate isolation of mature chondrocytes.
The second stage involves implantation of these autologous chondrocyte cells into the defect through a small knee arthrotomy with a periosteal graft sutured over the defect. The cultured chondrocytes are then injected into the defect beneath the periosteal graft.
This once-experimental procedure, initially directed toward articular cartilage and used for broad-based indications, has become an important procedure for a specific subset of patients. More than 5000 ACI procedures have been performed in the United States by more than 600 orthopedic surgeons.
Second-look arthroscopy and biopsy of surgically implanted chondrocytes have documented a reconstitution of the articular surface with similar mechanical properties to the surrounding “hyaline-like articular cartilage,” with documented durability of clinical results.
ANATOMY
Articular cartilage consists of four distinct histologic zones: superficial, middle, deep, and calcified (FIG 2A).
The chondrocyte is the cell responsible for the growth of cartilage.
The metabolic balance of the protein macromolecular complex of articular cartilage is maintained by chondrocytes, which constitute about 5% of the weight of cartilage.
Water makes up about 75% of the weight of articular cartilage. Water's role as a cation makes it one of the most important elements.
Glycosaminoglycans provide the compressive strength of articular cartilage and account for about 10% of cartilage weight. These function to trap and hold water with the articular cartilage.
Collagen, predominantly type II, provides the form and tensile strength of articular cartilage. It makes up about 10% of the weight of cartilage.
FIG 1 • Overview of the autogenous cartilage implantation (ACI) technique. Step 1: articular cells are harvested. Step 2: cells are grown in culture for 4 to 6 weeks. Step 3: the lesion is débrided. Step 4: harvested periosteum is sutured onto the defect. Step 5: cultured chondrocyte cells are implanted.
FIG 2 • A. Histology of articular cartilage. B. Chondrocyte and matrix with labels.
The chondrocyte is the major producer of collagen, proteoglycans, and noncollagenous proteoglycans, as well as enzymes (FIG 2B).
Articular cartilage receives its nutritional supply from the synovial fluid in which it is bathed; it does not have a true blood supply.9
PATHOGENESIS
Injuries of the articular cartilage can result from either trauma, as in the case of a partialor full-thickness chondral or osteochondral injury, or a pathologic process such as osteochondritis dissecans or local osteonecrosis.
Shallow or partial articular cartilage lesions have limited ability to heal, related primarily to the lack of a blood supply.
An inflammatory response cannot occur, leading to a defect within the articular cartilage.11
In full-thickness chondral lesions, in contrast, there is penetration of the subchondral plate, leading to the migration of progenitor cells from the vasculature in the subchondral bone marrow meschencymal cells to the surface, an inflammatory response, and an attempted healing response.
The mescenchymal progenitor cells differentiate into fibrocartilage.
This tissue is a weak substitute for hyaline articular cartilage and lacks its resilient mechanical properties.11,20
NATURAL HISTORY
The natural history of articular cartilage injury is poorly understood. It is well recognized, however, that the human body has a limited capacity—or no capacity—to repair articular cartilage injuries.11,20
Limited studies have demostrated progressive and variable degenerative changes equivalent to those of osteoarthritis.
The repair tissue often succumbs to mechanical stresses with premature degeneration, delamination, interarticular osteophyte formation, and eventual breakdown and joint destruction over time.
Some limited studies have been published with long-term follow-up of untreated osteochondritis dissecans that progressed on to osteoarthritis in adulthood.13
PATIENT HISTORY AND PHYSICAL FINDINGS
Articular cartilage injury can present after a trauma sustained during an athletic event or as a slow progression of symptoms, as in osteochondritis dissecans.
Patients may present with what intially is believed to be meniscal pathology, with swelling, pain, palpable tenderness, and locking of the knee.
Articular cartilage chondral flap or more significant osteochondral injury must be part of the differential diagnosis in evaluating the young patient with knee pain.
Those patients with a more insidious onset and no trauma tend to fit more into the category of osteochondritis dissecans. The findings are more consistent with chronic or recurrent effusion, pain, and mechanical symptoms similar to those of meniscus pathology.
IMAGING AND OTHER DIAGNOSTIC STUDIES
The following plain radiographs are obtained in weightbearing knee flexion: anteroposterior view; notch view; sunrise view of the patella and trochlea; and lateral views (FIG 3A,B). Although the articular cartilage itself cannot be appreciated, joint space narrowing and other bony defects will be apparent.
Full-length lower-extremity radiographs are indicated for most patients to assess overall alignment and in consideration of the possibility of performing a realignment procedure concomitantly at the time of the ACI procedure in those patients with malalignment problems.
MRI can more clearly demonstrate articular lesions. As the technology advances, better imaging quality is becoming available.
MRI can assess the size of the lesion, location, involvement of subchondral bone, and number of lesions (FIG 3C).
After ACI, MRI also is being used to assess the degree of defect fill, the integration of the repair cartilage to the subchondral bone plate, and the status of the subchondral bone plate and bone marrow.
Recently, the development of MRI cartilage sequencing has better defined articular cartilage injuries and postoperative osteochondral fill.
T2-weighted MRI mapping techniques give remarkable detail at the proteoglycan level (FIG 3D,E).
Optical coherence tomography (OCT)12 involves crosssectional imaging technology using near-infrared light technology. The high-resolution images provide a noninvasive look at the microstructural level of articular cartilage.
DIFFERENTIAL DIAGNOSIS
Osteoarthritis
Osteochondritis dissecans
FIG 3 • Lateral (A) and AP (B) radiographs of osteochondritis dissecans. C. MRI of articular cartilage lesion (circled) of the medial femoral condyle. D,E. T2-weighted MRI mapping of articular cartilage, showing normal articular cartilage and degenerated articular cartilage. (D,E: Courtesy of Hollis Potter and Riley Williams, Hospital for Special Surgery, New York, NY.)
Osteonecrosis
Meniscus injury
Loose body
Chondral flap
Osteochondral injury
NONOPERATIVE MANAGEMENT
Nonoperative treament is controversial. Patients without symptoms can be treated nonoperatively, with modification of activity level. This may be effective for a period of time; however, with age there is the potential of developing degenerative arthritis, particularly in those younger patients with large lesions. The true natural history of articular cartilage injuries is not known.
Some surgeons have proposed aggressive surgical treatment in the hope of preventing degenerative arthritis. Few clinical data are available to support such a treatment algorithim, however.
SURGICAL MANAGEMENT
Patients who fail conservative treatment for chondral injury must be evaluated for surgical treatment.
The patient must have a full understanding of the surgical procedure and the extensive rehabilitation it requires.
The indications for ACI are as follows:
Symptomatic weight bearing, unipolar, focal fullthickness chondral injury
Cartilage lesions of grade III or IV in the Outerbridge classification16
Unstable osteochondritis dissecans fragment
There is no size restriction on the lesion treated, although lesions typically are larger than 1.5 to 2.0 cm2.
Physiologic young, active patients who will be compliant with the rehabilitation protocol
Contraindications
Osteoarthritis or bipolar lesions with characteristic radiographic Fairbanks changes:
Joint space narrowing
Osteophyte formation
Subchondral bony sclerosis or cyst formation
Comorbidities such as ligamentous instability or meniscal pathology, unless they are addressed either concomitantly with the ACI or in a staged fashion
Coexisting inflammatory arthritis or active infections
Preoperative Planning
The size of the lesion and the availability of adequate cartilage cells for ACI are assessed.
Any bony deficit is assessed for possible bone grafting at the same time as the ACI. This is especially important for those patients with traumatic osteochondral fractures and large osteochondritis dissecans lesions. These lesions are best evaluated with MRI or at the time of the intial knee arthroscopy and direct examination of the lesion.
Staged bone grafting can be done at the time of arthroscopic evaluation. In general, 6 months are required between bone grafting and ACI, to allow time for the bone graft to consolidate and recreate a new subchondral plate.
Alignment of the entire extremity and the status of ligaments and meniscus must be taken into consideration. Biomechanical malalignment, maltracking of the patella, lack of meniscus, and ligament insufficiency are examples of an altered intra-articular environment that can lead to shear stresses, excessive friction, and abnormal compressive loads across the autogenous chondrocyte implantation and thence potentially to failure.
Improvement in ACI results is directly related to recognizing coexisting knee pathology and addressing it, either in a staged procedure or concomitantly at the time of the ACI.
For patients with limb malalignment, the surgeon must consider either proximal tibia osteotomies (opening or closing) for varus alignment or, for those with valgus alignment, a distal femoral osteotomy.
Most lesions of the patellofemoral joint require distal patella realignment procedures.
Ligamentous insufficiency, whether of the ACL, which is most common, or medial or lateral collateral laxity, even the most subtle, may produce excessive shear forces in the knee, which may irreversibly damage the maturing repair tissue produced by ACI. These ligament injuries must be addressed at the time of the ACI.
Patients with significant loss of meniscus tissue, through either subtotal or total menisectomy, must be considered candidates for allograft meniscus transplantation.
Positioning
The patient is placed on the operating table in the supine position, and the entire lower extremity is sterily prepared and draped so that the knee may be placed in extreme flexion if necessary.
A tourniquet is applied to the upper thigh.
Approach
The first stage of a standard arthroscopy is performed for the harvest of articular cartilage followed by implantation of cells into the chondral defect.
A midline incision usually is recommended, followed by a medial or lateral parapatellar arthrotomy to expose the corresponding site of the chondral defect.
A separate incision is made or the proximal incision is continued along its distal extent to harvest the periosteal patch on the proximal medial tibia.
TECHNIQUES
ARTHROSCOPIC ASSESSMENT
Prior to the arthroscopic evaluation, 15 a comprehensive knee examination is performed, with close detail to the ligament stability of the knee and overall alignment.
Any ligament instability or malalignment must be addressed either concomitantly or in a staged procedure.
Taking into account all factors, including the preoperative evaluation, the arthroscopic evaluation of the osteochondral lesion or defect provides the ultimate determination as to whether a patient is a candidate for ACI. Strict attention is paid to the condition of the intra-articular structures, such as integrity of the ligaments and meniscus.
Undiagnosed pathology may be critical to the outcome of ACI surgery.
TECH FIG 1 • Arthroscopic view of a full-thickness medial femoral condyle lesion.
Complete arthroscopic evaluation of the articular surfaces, both visual and probing (TECH FIG 1), is undertaken.
Accurate assessment of the osteochondral lesion, including size (anteroposterior and medial–lateral dimensions), is best obtained with a graduated probe. The estimation of size is of the utmost importance with regard to the number of chondrocytes that must be grown in culture to provide optimal fill for the defects.
The cartilage injury area is probed for depth, size, number, and location of lesions. Additional assessment determines whether the lesion is a contained or uncontained defect, referring to the borders of the lesion.
The Outerbridge system (Table 1) is a practical working approach to arthroscopic grading of articular cartilage defects.16
A newer, more functional classification has been proposed by the International Cartilage Repair Society (Table 2).6
CARTILAGE BIOPSY FOR AUTOLOGOUS CARTILAGE IMPLANTATION
A biopsy specimen of cartilage can be obtained at the time of the diagnostic arthroscopy.
Articular cartilage biopsy sites include the superior medial and lateral femoral condyle, as well as the intercondylar notch.
The best instrument for harvesting is either a ring curette or a curved notchplasty gauge (TECH FIG 2A).
The two biopsies should be full-thickness cartilage measuring 5 × 8 mm, with a total weight of 200 to 300 mg (TECH FIG 2B).
The biopsy specimens are placed in a vial of media in the prepackaged biopsy transport kit from Carticel. This articular cartilage biopsy contains about 200,000 to 300,000 cells, which will be enzymatically digested and grown to approximately 12 million cells per 0.4 mL of culture medium per implanted vial after 4 to 6 weeks, to be used for the implantation procedure.
TECH FIG 2 • A. Use of a curette for articular cartilage biopsy. B. Arthroscopic biopsy of articular cartilage for ACI.
DEFECT PREPARATION
After the diagnostic arthroscopy, a medial or lateral parapatellar mini-arthrotomy is performed to provide adequate exposure to the osteochondral defect. If a lesion of the patella or trochlea is present, a formal medial parapatellar arthrotomy with eversion of the patella is done for complete exposure.
Defect preparation is crucial to the outcome of ACI. All of the unhealthy cartilage surrounding and remaining in the lesion must be débrided completely using a curette and a no. 15 scalpel blade.
Healthy vertical cartilage borders are necessary for optimal suturing of the periosteum graft (TECH FIG 3A–E).
The bed of the defect is débrided of fibrous tissue and calcified cartilage, but the subchondral plate must not be violated in the débridement process.
TECH FIG 3 • The ragged edges of unhealthy cartilage forming the articular cartilage defect (A) are excised with a curette (B,C) to create stable vertical borders (D,E). F. Measuring the medial femoral condyle lesion. (A,B,D,F: Courtesy of Genzyme, Inc.)
Bleeding at the cartilage defect must be controlled.
Three means of controlling bleeding from the subchondral plate are available:
Application of sponges soaked in a 1:1000 solution of epinephrine and saline
Application of fibrin glue on sites of bleeding on the subchondral bone
Use of a needle-point electrocautery with a needletip Bovie set on low.
Defect dimensions can be measured with a sterile ruler to determine the size of the periosteal patch.
The longest anterior to posterior and medial to lateral dimensions should be measured, after which 2 to 3 mm are added to each dimension to obtain the appropriate dimensions for the periosteal graft (TECH FIG 3F).
Another method is to make a template from sterile paper from the surgical gloves. A template is placed on the lesion and the defect is outlined with a permanent marking pen, oversizing by 1 to 2 mm. This template is then placed on the proximal tibia as a guide for the periosteal graft.
PERIOSTEAL GRAFT HARVEST
The osteochondral defect is measured with a disposable ruler at its widest mediolateral and superoinferior dimensions.
An alternative method is to create a template of the lesion with sterile paper, as just described above. The lesion is traced on the paper.
The proximal medial tibia provides the best site for harvesting periosteum. An alternative site for periosteal tissue is the distal femur.
The incision is placed 2.5 cm below the pes anserinus (TECH FIG 4A).
The dissection is carried out down to the periosteum with complete removal of the subcutaneous tissue and fascia. A sharp dissection is recommended to remove this fascia layer.
With a permanent marker, the template of the lesion is used to outline the periosteum with 2 to 3 mm added to the measured dimensions of the defect to take into account shrinkage of the periosteal graft after removal from the bone.
The cambium layer is marked to avoid confusion when suturing the periosteum onto the graft with the cambium layer closest to the defect.
With a no. 15 knife blade cutting sharply down to bone circumferentially, a sharp periosteal elevator is used to elevate the periosteum from the proximal tibia (TECH FIG 4B). It is lifted off the proximal tibia with a smooth pair of pick-ups so as to not damage the cells of the periosteum.
The periosteum is kept moist with saline.
TECH FIG 4 • A. The incision for periosteum harvest is located 2.5 cm below the insertion of the pes anserinus. B. A small periosteal elevator is used to create an edge around the border of the periosteum graft to be harvested from the proximal tibia. (Courtesy of Genzyme, Inc.)
PERIOSTEUM GRAFT FIXATION
If a tourniquet has been used, it is deflated at this point, and meticulous hemostatsis of the defect bed is undertaken with the techniques described earlier.
Any bleeding can affect the viability of the implanted chondrocytes. Use of thrombin-soaked pledgets in diluted epinephrine along with the use of a needle-point Bovie can help control any bleeding.
The orientation of moist periosteal graft on the defect is determined, with the cambium layer closet to the defect. Keeping the periosteum moist is of the utmost importance to preserve the viability of the cambium layer.
Any excess periosteum overlying the borders of the defect must be trimmed to provide an exact fit of the defect.
Once the appropriate orientation and size of the graft are established, the periosteum graft is secured in place with a 6.0 Vicryl suture on a P1 cutting needle using simple interrupted suture technique.
To facilitate easy passage of the suture through the cartilage and thin periosteum, mineral oil or glycerin is applied to the suture.
The four corners of the periosteal graft are first secured and tensioned, followed by sequential sutures about 3 to 4 mm apart from each other (TECH FIG 5A).
This will ensure a watertight seal for the implanted chondrocytes beneath the periosteum graft.
It is critical for the knots of the suture to be placed on the periosteum side to prevent shearing off of the knot and failure of the periosteal graft as the graft is maturing during early rehabilitation.
The suture needle should be passed through the periosteum from outside to inside, approximaely 2 mm from the edge of the periosteum.
The needle then is passed though the cartilage using the curvature of the needle, from inside to the outside of the cartilage with the needle entering the cartilage perpendicular to the inside wall of the defect and exiting the articular surface 2 to 3 mm from the débrided defect (TECH FIG 5B,C).
The sutures are placed alternately around the defect, spaced about 3 mm apart, leaving a 5- to 6-mm opening to accommodate an angiocatheter for injection of the chondrocyte cells.
A watertight integrity test is performed with the placement of the 18-gauge catheter into the superior aspect, and saline is slowly infused to assess the graft suturing (TECH FIG 5D).
Areas with of saline leakage are reinforced with additional sutures. The area then is retested until the graft is watertight.
Once a watertight seal is obtained, the excess saline is aspirated from the defect.
Commercially prepared fibrin glue, available in most operating rooms, is then passed circumferentially over the periosteum graft–cartilage interface suture line as an additional sealant to prevent leakage of the injected chondrocytes (TECH FIG 5E,F).
TECH FIG 5 • A. The four corners of the periosteum graft are secured first. B. The suture needle is angled toward the surface to obtain a bite in the cartilage. C. The knot is placed on the periosteum side, not the cartilage rim, to prevent shearing. D. Final suturing of the periosteum graft leaves an opening at the most superior point for insertion of an 18-gauge catheter for saline injection to test for a watertight seal. E,F. Fibrin glue is applied one drop at a time around the periphery of the defect. (Courtesy of Genzyme, Inc.)
SPECIAL SITUATIONS
Uncontained defects without vertical cartilage borders on the periphery or encroaching on the intercondylar notch require the use of mini-anchors or suturing into the synovial layer to secure the periosteal graft.
Those osteochondral defects may require bone grafts. Bone graft can be obtained from the proximal tibia or iliac crest in the standard fashion.
This can be done either in a staged fashion or concomitantly at the time of the ACI. Those procedures that are staged can have the bone graft packed into the defect with the plan of returning in 3 months after consolidation. If done concomitantly with ACI, the “periosteal graft sandwich” technique is used. Bone graft is placed in the defect, followed by a periosteal patch. Another periosteal graft is then sutured into place as described previously. The chondrocyte cells are then slowly injected between the two periosteum layers.
IMPLANTATION OF AUTOGENOUS CHONDROCYTES
The chondrocyte cells are delivered into the culture medium inside a Carticel vial (Genzyme Biosurgery, Cambridge, MA; TECH FIG 6A).
The cells require resuspension in the medium.
A sterile 18-gauge catheter is then inserted into the Carticel vial to mix and resuspend the chondrocytes, which settle to the bottom during shipping. This is repeated until the cells are completely resuspended in the medium.
The cells then are slowly injected under the periosteal patch into the defect.
After injection of the cells is completed, the needle is withdrawn, and the small opening for the angiocatheter is then sutured with 6.0 Vicryl and sealed with fibrin glue (TECH FIG 6B,C).
The arthrotomy wound is copiously irrigated, and the retractors are removed slowly. The arthrotomy is then closed in the standard, layered fashion.
A sterile dressing is applied. No drain is placed in the joint, because the ACI graft may be damaged by the suction of the drain.
TECH FIG 6 • A. Vial of chondrocyte for injection. B. Injection of cells. C. Periosteum graft post injection of cells. (B: Courtesy of Genzyme, Inc.)
POSTOPERATIVE CARE
The concept of a slow, gradual time course for healing is critical to understand in post-ACI rehabilitation. The foundation principles of a successful ACI rehabilitation program center on protection of the graft, mobility and motion exercises, muscle strengthening, progressive weight bearing, and patient education.
Protection of the repaired tissue from execessive intra-articular joint forces is critical during the early postoperative period, although early motion aids in cell orientation of the repaired tissue and prevents arthrofibrosis.
If the graft is overloaded with friction and delamination of the ACI tissue, or potential hypertrophy of the ACI tissue occurs, potential complications must be understood.
The intra-articular microenvironment must be protective of this complicated interaction of the implantated chondrocytes and the stimulutory aspects of the rehabilitation, such as early motion to allow for the remodeling and maturation of these chondrocytes into a hyaline-like cartilage phenotype.
During the early phase (day 1 through week 12), the patient is permitted non–weight bearing during weeks 0 to 2, toetouch weight bearing until weeks 8 to 9, and full weight bearing at 9 weeks.
The patient begins continuous passive motion (CPM) 6 to 24 hours after surgery.
CPM is performed 6 to 8 hours a day for 6 weeks.
The patient should obtain full range of motion.
The patient gradually returns to activities of daily living.
The transition phase is from week 13 through month 6.
The patient has increased activities of daily living and increased standing and walking.
The patient should have quadricep and hamstring strength greater than 80%.
The mid-phase is from month 7 through month 9.
The patient advances to strength training involving nonpivoting activities.
The final phase is month 10 through month 18.
The patient can perform low-impact activities, such as skating and cycling, during months 9 through 12; repetitive impact activities such as jogging and aerobic classes during months 13 through 15; and high-level pivoting activities such as tennis and basketball during months 16 through 18.
Rehabilitation of patellar and trochlear lesions requires special consideration. The contact pressure of the patellofemoral articulation is maximal between 40 and 70 degree of knee flexion; therefore, flexion of this magnitude should be avoided during active knee flexion until the graft is mature and can withstand these shear stresses.
Early, gentle patella mobility exercises also are important to prevent adhesions and decreased patella mobility.
Avoidance of active knee extension during the first 10 to 12 weeks and the use of continuous passive motion is encouraged to give the best clinical results.
The gradual progression of active extension exercises also depends on the size and location of the patellar or trochlear lesion as observed in the operating room.
OUTCOMES
Brittberg et al7 published their intial results with ACI in The New England Journal of Medicine, a study that revealed impressive intial results. Fouteen of 16 patients (87%) with isolated femoral condyle lesions treated with ACI had good to excellent results with 2-year follow-up. Subsequent follow-up of these patients at 11 years revealed the durability of and patient satisfaction with the ACI procedure.8,17,18
A more recent multicenter study assessed the clinical outcome of lesions of the distal femur treated with ACI in 100 patients.9 Eighty-seven percent of the patients completed a 5-year follow-up assessment. Patients were, on average, 37 years of age and had a mean total defect size of 4.9 cm2; and 70% of the patients had underogne at least one previous articular cartilage procedure. Seventy-three percent showed significant improvement, with an increase of 4.1 points on the Cincinnati knee rating system, substantiating ACI as a viable option for the treatment of chondral injuries.
Even though ACI is highly successful, new treatment modalities continue to be developed, including an arthroscopic approach and possibly a one-stage procedure.
Matrix-induced autologous chondrocyte transplantation (MACI) is one such treatment modality that is conducted arthroscopically (FIG 4). Similar to ACI, autologous chondrocytes are used but are placed into a collagen scaffold for implantation. This constrution can be used instead of a periosteal graft, with stabilization still provided with fibrin glue.
The scaffold has a porous surface that can embody the repairing tissue. Different scaffolds are under development. Each scaffold must fulfill specific requirements in regard to biocompatibility, endurance, and structural stability. The scaffold should induce maturation and differentiation of the cellular structures that it supports.
About 3200 surgical procedures using this technique have been performed in Europe, with excellent early clinical results.1
FIG 4 • Overview of the matrix-induced autologous chondrocyte transplantation (MACI) technique. Step 1: the defect is assessed and damaged cartilage débrided. Step 2: MACI membrane is cut according to the template, matching defect size and shape. Step 3: proper membrane orientation, in which cells face the bone bed. Step 4: fibrin sealant is applied to the defect and to the bone bed. Step 5: MACI is held in place with light pressure and fixed by fibrin glue, with no suturing required.
COMPLICATIONS
Hypertrophy or overgrowth of the periosteum graft
Delamination of the periosteum graft
Postoperative stiffness, arthrofibrosis
Infection
Donor site morbidity
Partial or full graft detatchment
REFERENCES
1. Bachmann G, et al. [MRI in the follow-up of matrix-supported autologous chondrocyte transplantation (MACI) and microfracture]. Radiology 2004;44:773–782.
2. Beris AE et al. Advances in articular cartilage repair. Injury 2005;36: Suppl 4:S14–23.
3. Blevins F, Steadman R, Rodrigo J, et al. Treatment of articular cartilage defects in athletes: an analysis of functional outcome and lesion appearance. Orthopedics 1998:21:761–768.
4. Bobic V, Morgan C, Carter T. Osteochondral autologous graft transfer. Oper Tech Sports Med 2000;8:168–178.
5. Borazjani BH et al. Effect of impact on chondrocyte viability during insertion of human osteochondral grafts. J Bone Joint Surg Am 2006;88A:1934–1943.
6. Brittberg M. ICRS: Clinical Cartilage Injury Evaluation System. Third ICRS Symposium, Gothenburg, Sweden, April 28, 2000.
7. Brittberg M, Lindahl A, Ohlsson C, et al. Treatment of deep cartilage defects in the knee with autologous chondrocyte transplantation. N Engl J Med 1994;331:889–895.
8. Brittberg M, Lindahl A, Ohlsson C, et al. Articular cartilage engineering with autologous chondrocyte transplantation: a review of recent developments. J Bone Joint Surg Am 2003:85A:109–115.
9. Browne J, Anderson A, Arciero R, et al. Clinical outcome of autologous chondrocyte implantation at 5 years in US subjects. Clin Orthop 2005;436:237–245.
10. Browne JE, Branchm TP. Surgical alternatives for treatment of articular cartilage lesions. J Am Acad Orthop Surg 2000;8:180–189.
11. Buckwalter JA. Articular cartilage: injuries and potential for healing. J Orthop Sports Phys Ther 1998;28:192–202.
12. Chu C, Lin D, Geisler J, et al. Arthroscopic microscopy of articular cartilage using optical coherence tomography. Am J Sports Med 2004;32:699–709.
13. Curl W, Krome J, Gordan E, et al. Cartilage injuries: a review of 31,516 knee arthroscopies. Arthroscopy 1997;13:456–460.
14. Jackson RW, Marans HJ, Silver RS. Arthroscopic treatment of degenerative arthritis of the knee. J Bone Joint Surg Am 1988;70A:332–336.
15. Minas T. Surgical manual defect assessment and biopsy procurement and cell implantation procedure. Carticel. Boston: Genzyme Biosurgery, 2004.
16. Outerbridge RE. The etiology of chondromalacia patellae. J Bone Joint Surg Br 1961;43B:752–757.
17. Peterson L, Brittberg M, Kiviranta I, et al. Autologous chondrocyte transplantation: biomechanics and long term durability. Am J Sports Med 2002;30:2–12.
18. Peterson L, Minas T, Brittberg M, et al. Two to 9 year outcome after autologous chondrocyte transplantation of the knee. Clin Orthop 2000;374:212–234.
19. Scopp JM, Mandelbaum BR. A treatment algorithm for the management of articular cartilage defects. Orthop Clin North Am 2005;36:419–426.
20. Shapiro F, Koide S, Glimcher MJ. Cell origin and differentiation in the repair of full-thickness defects of articular cartilage. J Bone Joint Surg Am 1993;75:532–553.