Articular cartilage is vulnerable to traumatic injury and subsequent degeneration. These changes are likely related to the limited capacity for cartilage repair, poor vascular supply, and deficiency in terms of the ability of an undifferentiated cell population to respond to the insult. While the natural history of isolated chondral and osteochondral defects is not predictable, clinical experience suggests that, when left untreated, these lesions do not heal and may progress to symptomatic degeneration of the joint1. Therefore, early surgical intervention for symptomatic lesions is often suggested in an effort to restore normal joint congruity and pressure distribution and prevent further injury. Treatment recommendations are made after an evaluation of symptomatic lesions and should be tailored to the specifics of each case.
The goals of surgical treatment are to provide pain relief and improve joint function, thus allowing patients to comfortably perform activities of daily living and potentially maintain or return to higher levels of activity. Multiple algorithms have been described in an effort to simplify the treatment of cartilage lesions. These are useful tools with which to organize thoughts. In general, surgical options can be grouped into three categories: palliative (arthroscopic débridement and lavage), reparative (marrow stimulation techniques), and restorative (osteochondral grafting and autologous chondrocyte implantation). All of these techniques have been reported to improve the clinical status as compared with the preoperative state. Thus, the appropriate treatment for any given cartilage lesion is patient-specific. The size and location of the lesion, the physical demands of the patient, and the treatment history all are important preoperative considerations. In addition, the surgeon must consider what subsequent treatment options are available if the current treatment fails to relieve the symptoms. A realistic and comprehensive understanding of the patient's goals is critical to any decision regarding how to treat a symptomatic chondral defect. In keeping with these principles, the treatment algorithm consists of a graduated surgical plan. The least destructive and least invasive treatment option necessary to alleviate the symptoms and restore joint function is performed first. The more extensive treatments are reserved for potential salvage operations later. If the symptoms persist despite conservative treatment, subsequent treatments are not impeded by previous management.
When treating articular cartilage lesions in the knee, the surgeon should focus on patient-specific and defect-specific variables and avoid "linear thinking." The clinical presentation should correlate with the underlying pathoanatomy. For example, a patient with known classic osteochondritis dissecans of the medial femoral condyle who reports bilateral anterior knee pain with stair-climbing should be evaluated initially with a presumptive diagnosis of patellofemoral pain before ascribing the symptoms to the osteochondritis dissecans lesion. Because the natural history of cartilage lesions is not known and the surgical treatments are neither benign nor associated with a predictable outcome (particularly with regard to the prevention of arthritis), surgical decision-making must be taken quite seriously.
Understanding and addressing the patient's specific concerns and goals are critical to achieving a successful outcome from the patient's perspective. More specifically, patients often express concerns about whether it is safe to remain active despite symptoms and whether a delay in surgical intervention precludes certain treatment options because of disease progression. In addition, knowledge of the specific marginal improvements that a procedure should provide gives the patient a reasonable expectation regarding the outcome. Unfortunately, the lack of understanding of the natural history of these defects makes it difficult to advise patients, and it is best to carry out careful discussions on a case-by-case basis.
Patient age, body mass index, symptom type (weight-bearing pain, non-weight-bearing pain, swelling, mechanical symptoms, giving-way, and aggravation of symptoms related to walking on level ground as opposed to stair-climbing), occupation and/or family commitments, risk-aversion (desire to avoid subsequent surgical procedures), responsiveness and rehabilitation after previous surgical treatments, and the patient's specific concerns related to his or her problem are all important preoperative considerations. While chronologic age is often cited as a relative indication or contraindication to cartilage repair, it is really physiologic age that determines the patient's eligibility for a non-arthroplasty solution. Typically, patients who become symptomatic in the fourth or fifth decade of life have concomitant chondral and subchondral disease involving apposing articular surfaces that precludes a biologic treatment option. In addition, the results of partial and total knee arthroplasty are predictably gratifying and satisfy most patients, even those who are relatively young. Finally, one must carefully search for associated pathological conditions, such as malalignment, ligament insufficiency, and concomitant meniscal deficiency, that may contribute to treatment failure and should be corrected before or during the surgery to treat the chondral lesion.
Defect-specific variables include defect location, number, size, depth, and geometry; the condition of the subchondral bone and surrounding cartilage; and the degree of containment. The condition of the apposing surface, which is often overlooked, is also an important variable. Even minor areas of early degeneration make achieving a satisfactory clinical outcome challenging. Specific management of each of these defect-specific variables increases the likelihood of a good clinical outcome.
Malalignment, ligament insufficiency, and concomitant meniscal deficiency are assessed and, when necessary, are treated with a concomitant or staged osteotomy (high tibial, distal femoral, or tibial tuberosity), ligament reconstruction, and perhaps a meniscal allograft transplantation2. Patellofemoral lesions are often treated with a simultaneous realignment procedure such as anteromedialization of the tibial tuberosity. Anteromedialization is more successful for lateral patellofemoral lesions than it is for lesions located along the medial aspect of the patellofemoral joint3. Medial patellofemoral lesions are treated with a more vertically oriented anteromedialization2. The treatment algorithm for chondral lesions is guided by the lesion size and location and the patient activity level (Fig. 1).
Primary repair is done for any chondral injury that is amenable to fixation. Any acute osteochondral fragment or in situ and unstable osteochondritis dissecans lesion is repaired primarily. It is particularly critical to fix large fragments (>1 cm2) from the weight-bearing portion of the femoral condyles. The basic principles for primary repair include elevation of the unstable fragment, débridement of the fibrous base, microfracture if necessary to gain access to the subchondral blood supply to promote healing, bone-grafting of areas of cystic changes or bone loss, and rigid fixation of the fragment under compression. Headless-compression-screw fixation, with subsequent screw removal in younger patients after eight weeks of non-weight-bearing, is often used. Continuous passive motion for up to six hours each day is recommended. Because fragments can settle over time, even headless screws can become prominent and damage the apposing surface. In addition, performing a second-look arthroscopy to evaluate the defect helps the surgeon to judge the success of the procedure and to provide accurate advice to the patient.
Patients with lesions that cannot be repaired primarily may benefit from another type of treatment (palliative, reparative, or regenerative). Marrow stimulation techniques are typically a first-line treatment. These techniques are often used for smaller lesions (<2 cm2), or in patients with larger lesions (>3 cm2) and modest physical or physiologic demand levels. Small lesions in high-demand patients or those for whom marrow stimulation has failed can be treated with one or two 10-mm osteochondral autografts harvested from the lateral femoral trochlea just proximal to the sulcus terminalis. Larger lesions (>2.5 cm2) are typically more amenable to osteochondral allografting or autologous chondrocyte implantation. Autologous chondrocyte implantation is advised for younger patients with shallow lesions, especially of the patellofemoral joint. This method does not violate the subchondral bone and minimizes the impact on future treatment such as osteochondral allograft transplantation. Larger, deeper lesions with bone loss typically require an osteochondral allograft.
Treatment is also guided by the location of the lesion. For example, osteochondral allografts are used for femoral condyle lesions because they allow accurate anatomic reconstruction. Lesions of the patellofemoral joint are often treated with autologous chondrocyte implantation because the lesions are small and the varying anatomic concavity and convexity make structural grafts too difficult to fit in place. The tibia remains a difficult articular surface to treat. Small tibial lesions that are found when the femoral articular cartilage is being restored are commonly treated with marrow stimulation techniques. Other options include the utilization of osteochondral autografts placed in a retrograde manner with use of a cannulated reamer system (Arthrex, Naples, Florida). The use of osteochondral allografts with an intact meniscus and concomitant realignment has been reported for the treatment of larger lesions of the tibial plateau, especially after fracture and the development of secondary arthritis, with graft survival rates of up to 65% at fifteen years4.
Marrow Stimulation Technique (Microfracture)
The microfracture marrow stimulation technique is carried out with a surgical awl to penetrate the subchondral bone. The violation of the subchondral plate promotes bleeding and the local migration of stem cells and other anabolic factors that support the formation of a "superclot." It is believed that the pluripotent nature of these stem cells allows the formation of reparative fibrocartilage tissue5 (Fig. 2).
Critical to the success of this technique is the creation of vertical walls of stable articular cartilage to create a "well-shouldered" lesion. This improves the local mechanical environment during healing by reducing shear and compression. All unstable cartilage is removed when the lesion site is prepared. The calcified cartilage layer is carefully débrided, and surgical awls are used to penetrate the subchondral bone (Fig. 3). The holes are placed perpendicular to the bone surface, 2 to 3 mm apart, and confluence is avoided. Postoperative rehabilitation is guided by the location of the lesion, but typically it involves up to six weeks of non-weight-bearing and the use of a continuous-passive-motion machine for six hours per day. Patients with a lesion in the patellofemoral joint wear a brace with a flexion stop of 30° to limit patellofemoral contact; weight-bearing is permitted.
The best outcomes of this technique are seen in younger patients with small traumatic lesions6. After two and five years of follow-up, Knutsen et al.7 found no difference between the outcomes of microfracture and those of autologous chondrocyte implantation for femoral condyle lesions, but patients with smaller lesions treated with microfracture did better than those with larger lesions. Similarly, Gudas et al. observed that, among patients with lesions exceeding 2 cm2 in the central part of the medial femoral condyle, those treated with microfracture had lower clinical outcome scores than did those treated with an osteochondral autograft transplantation (Table I)8. Location also plays a role in the success of marrow stimulation techniques, with better results seen after the treatment of femoral condyle lesions9.
Osteochondral Autograft Transplantation
Osteochondral autograft transplantation is the transfer of one or more cylindrical osteochondral autografts into the cartilage defect, providing a congruent hyaline-cartilage-covered surface (Fig. 4). The autografts are harvested from the non-weight-bearing periphery of the femoral trochlea or the margin of the intercondylar notch. With a combination of different graft sizes, 90% to 100% of the defect can be filled10. This technique is limited by the amount of donor tissue available in the knee, and donor site morbidity increases as more tissue is harvested. Osteochondral autograft transplantation is best for small lesions (<2 cm2), but good clinical results have been reported11 with lesions between 2 and 4 cm2. The use of "mega" osteochondral autograft transplants ("megaOATS") from the posterior part of the femoral condyle for large osteochondral lesions (>4 cm2) has had good clinical results at 5.5 years postoperatively12.
Osteochondral autograft transplantation can be done through a small arthrotomy or entirely arthroscopically. To harvest donor grafts perpendicular to the surface, we prefer to obtain the donor plugs through a small lateral arthrotomy because the lateral edge of the patella can interfere with an arthroscopic harvest. The plugs are then implanted arthroscopically. There are many available commercial systems that provide a series of donor and recipient harvesting tubes to create a press-fit implant of up to 10 mm in diameter. A sizing guide is used to determine the number and size of grafts that are needed. A properly sized graft harvester with a collared pin is introduced perpendicular to the donor site (Fig. 5) to a depth of approximately 12 to 15 mm. The recipient socket is created to a depth that is 2 mm less than the length of the donor graft. It is important to maintain a perpendicular relationship between the donor graft and the articular surface to create well-defined vertical walls in the recipient socket, as this facilitates congruent plug placement (Fig. 5, C). The donor plug is placed over the recipient site and gently advanced into the defect, where it is often left slightly proud. The chondrocytes can be damaged during impaction; therefore, it is critical to avoid high loads when inserting the graft13. The final plug position should be flush with the surrounding articular cartilage (Fig. 5, D). Postoperatively, patients are protected from weight-bearing for six weeks and use a continuous-passive-motion machine six hours per day.
Hangody and Kárpáti14 evaluated the survival of the transplanted hyaline cartilage. The graft undergoes osseous incorporation to the subchondral bone while the transplanted cartilage integrates with the adjacent host articular cartilage with fibrocartilage. Recently, Hangody et al.11 evaluated clinical outcomes at a mean of fourteen years after 1097 osteochondral autograft transplantation procedures. Encouraging results in this large multicenter series support the use of this technique for the treatment of small and medium focal chondral and osteochondral defects of the knee. The osteochondral autograft transplantation procedure has been compared with other cartilage restoration procedures (Table II).
Osteochondral Allograft Transplantation
Osteochondral allograft transplantation provides an option for treatment of larger lesions (>2.5 cm2) or those with substantial bone loss. It is normally a second-line treatment option, but can be a first-line treatment for high-demand patients with large lesions.
Osteochondral allograft transplantation can be used to resurface large, deep defects with mature hyaline articular cartilage while also filling any underlying osseous defect. Tissue matching and immunosuppression are not necessary because the transplanted chondrocytes are isolated by the cartilage matrix and not exposed to the host immune surveillance15. The allografts can be "fresh" or frozen. Fresh grafts are normally maintained at 4°C in standard or enriched culture medium for no more than twenty-eight days, which allows chondrocytes to survive after transplantation. Frozen allografts are maintained at -40°C for years. The fresh allografts elicit a minimal immune response, the chondrocytes survive, and the bone is successfully revascularized16-18.
Allograft transplantation can be done arthroscopically; however, it is more often performed through a small arthrotomy. The allograft is slowly warmed from 4°C to 37°C by placing it in normal saline solution at room temperature. The slow warming minimizes damage to the graft19. The lesion is sized with a template, and a correspondingly sized reamer is used to convert the defect to a circular recipient socket with a uniform depth of 6 to 8 mm (Fig. 6). This bone depth facilitates graft implantation and limits the amount of immunogenic donor bone that is implanted. A sterile marking pen is used to mark the 12 o'clock position of the lesion to orient the donor plug appropriately. An instrumentation system is used to size and harvest a cylindrical plug from the allograft (Fig. 7). The donor graft is drilled through its entire depth with a harvester under irrigation with normal saline solution. The graft is extracted, and a ruler is used to measure and mark the four quadrants of the graft at the depth of the previously measured recipient sites. Before insertion, pulsatile lavage (approximately 2 L) is used to remove the residual blood and bone-marrow elements from the allograft to reduce the risk of disease transmission and graft immunogenicity. The graft is then press-fit into the socket by hand after careful alignment of the four quadrants to the recipient site (Fig. 8). If the implanted allograft is particularly large, fixation may be augmented with bioabsorbable or metal compression screws.
Postoperatively, weight-bearing is limited to toe-touch for the first six weeks. Patients with a patellofemoral graft are allowed to bear weight as tolerated in extension and generally are limited to 45° of flexion during the first four weeks. Continuous passive motion is used immediately after the surgery. A return to normal activities of daily living and light sports activity is considered at eight to twelve months.
Subjective improvement can be expected in 75% to 85% of patients after osteochondral allograft implantation for properly selected chondral lesions4,20 (Table III).
Autologous Chondrocyte Implantation
Autologous chondrocyte implantation is ideal for symptomatic, unipolar, well-contained chondral or osteochondral defects measuring between 2 and 10 cm2 with bone loss of less than 6 to 8 mm. It is typically a second-line treatment after at least arthroscopic débridement has been performed.
The first stage of autologous chondrocyte implantation is an arthroscopic evaluation of the size and depth of the focal chondral lesion and a cartilage biopsy. The total volume of the biopsied material should be approximately 200 to 300 mg. The second stage is implantation of the cells. This is done usually no sooner than six weeks after the biopsy. At the time of implantation, the defect is prepared by removing any existing fibrocartilage down to the underlying calcified layer. Vertical walls are created at the periphery of the lesion with use of a combination of a number-15 blade and sharp ring curets. After débridement, the tourniquet, if used, should be deflated, and complete hemostasis should be obtained. The use of cotton pledgets soaked with epinephrine may help to obtain hemostasis (Fig. 9).
Next, a periosteal patch is harvested from the proximal-medial part of the tibia, just distal to the pes anserinus insertion, through a separate incision. The patch should be at least 2 mm larger than the defect. The patch edges are detached with a number-15 scalpel blade and elevated with a sharp, curved periosteal elevator, beginning distally. Synthetic collagen-membrane substitutes are commercially available (Chondro-Gide; Geistlich Biomaterials, Wolhusen, Switzerland) and can be used as a substitute for the periosteal patch. The use of these scaffolds not only reduces operating time but also has been shown to avoid typical problems related to the periosteum21.
The patch or scaffold is then sewn to the cartilage. When periosteum is used, the cambium layer is placed toward the lesion. With the Chondro-Gide scaffold, the porous surface should be placed toward the lesion with the smooth side facing out. Sutures (6-0 Vicryl [polyglactin]) are first passed into the patch approximately 2 mm from the edge and then passed through the cartilage at a depth of 2 to 3 mm below the cartilage surface. Sutures should be placed approximately 4 mm apart, and a gap should be maintained in the upper edge to allow chondrocyte implantation (Fig. 10). The edges of the patch are sealed with fibrin glue, and a water-tightness test is performed with an 18-gauge angiocatheter. The chondrocytes are then delivered through the opening with use of an angiocatheter. After the cells have been implanted, the opening gap is closed with suture and fibrin glue (Fig. 9, C).
Postoperatively, patients with a femoral condyle lesion are kept non-weight-bearing and use a continuous-passive-motion machine. Patients with a patellofemoral lesion are permitted full weight-bearing with the knee in extension. Continuous passive motion for six to eight hours per day at one cycle per minute is used for six weeks after the surgery. A return to normal activities of daily living and sports activities is allowed six months after the surgery.
It is estimated that autologous chondrocyte implantation has been performed in >10,000 patients worldwide. The procedure has better results when it is done for lesions in the femoral condyle or in patients with a patellofemoral lesion who are undergoing a concomitant realignment procedure22-24. There have been several studies comparing autologous chondrocyte implantation with other biologic reconstructive procedures (Table IV).
Articular cartilage defects of the knee are common. Treatment options range from palliative (débridement) to reparative (marrow stimulation) to restorative (osteochondral grafting and autologous chondrocyte implantation). All of these techniques improve the clinical status compared with the preoperative state. Decision-making is done case by case and is guided by the patient's physical and physiologic demand level, previous failed treatment, and the location and size of the defect. It is critical that the surgeon also consider what subsequent treatment options might be necessary should the first-line treatment fail to relieve the symptoms.
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