Microfracture

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  Ideal for symptomatic, focal, Outerbridge grade III or IV chondral lesions of the weight-bearing femoral condyles, tibial plateau, trochlea, and patella.

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  Best suited for well-contained chondral defects less than 4 cm ² .

  
  
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  Best results seen in young, active patients, ideally less than 45 years old, who are aware of and capable of following postoperative rehabilitation regimen.

  
  
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  Inexpensive procedure with minimal required equipment.

Autologous Chondrocyte Implantation

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  Second-line treatment for large or irregularly shaped Outerbridge grade III-IV lesions of the femoral condyles, trochlear, or patella.

  
  
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  Most appropriate in high-demand patients less than 40 years old who will be dedicated to and compliant with a lengthy rehabilitation program.

  
  
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  Two-stage procedure, separated by at least 6 weeks.

  
  
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  Resource-intense and technically demanding, less frequently recommended for first-line treatment.

Osteochondral Autograft Transfer

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  Ideal for symptomatic, focal, Outerbridge grade III or IV chondral lesions of the weight-bearing femoral condyles.

  
  
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  Suited for well-contained chondral defects less than 4 cm ² .

  
  
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  Best results seen in less active patients less than 50 years of age with stable ligaments and normal alignment.

  
  
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  Histologic analysis of repair tissue shows greatest content of hyaline-like cartilage of any repair technique.

  
  
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  Technically demanding and commercially available instrumentation required.

  
  
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  Donor site morbidity may be an issue.

Osteochondral Allograft Transplant

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  Generally reserved for large lesions (greater than 2 cm ² ), associated with cavitary defects and bone loss.

  
  
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  Good choice in patients with symptomatic osteochondritis dissecans lesions (especially of the lateral aspect of the medial femoral condyle) for which failed prior attempts at native fragment fixation have failed.

  
  
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  Suitable for the revision of failed cartilage repair strategies.

  
  
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  No donor site morbidity.

  
  
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  Radiographs of the knee with a radiographic sizing marker are necessary for the allograft company provider to provide a size-matched hemicondyle.

  
  
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  Increased expense for the fresh osteochondral allograft and technical difficulty compared with other techniques.

  
  
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  Possible risk of disease transmission or immunologic reaction.

Anatomy and Function of Articular Cartilage

The composition of articular cartilage has important implications for its function. Water makes up 65% to 80% of the wet weight, with the majority distributed in the superficial layers. Its primary function is to lubricate and provide nutrition for the joint. The only cell present is the chondrocyte, whose primary function is to produce the abundant extracellular matrix. This matrix is composed of mainly collagen (of which 90% to 95% is type II collagen), proteoglycans, and other proteins. The collagen provides the cartilaginous framework as well as the tensile strength of the articular cartilage. The proteoglycans are mainly responsible for the compressive strength of the cartilage.

The thickness of the cartilage layer in joints is between 2 and 5 mm. It is organized into three distinct layers ( Fig. 2-1 ). The superficial zone is the thinnest zone, has the least metabolic activity, and has collagen fibers oriented parallel to the joint surface. It is strongest in shear due to its high concentration of collagen fibers. The transitional zone is several times thicker than the superficial zone. Collagen fibers are oriented more obliquely here than in the superficial zone, and this region has a higher concentration of proteoglycans. The radial (or deep) zone contains the largest-diameter collagen fibers organized perpendicular to the joint surface and has the highest concentration of proteoglycans. It is strongest in compression. The tidemark can be found deep to this last layer.

Schematic representation of articular cartilage

The tidemark is a thin basophilic line seen on light microscopy of decalcified cartilage. It corresponds to the boundary between calcified and uncalcified cartilage. Underlying the tidemark is a thin zone of calcified cartilage, deep to which can be found the subchondral and cancellous bone. It is believed that in order for healing of cartilage lesions to occur, the tidemark must be crossed so as to allow the underlying mesenchymal stem cell to access the zone of injury. This will allow these cells to differentiate and produce fibrocartilage. This has important implications in various methods of cartilage repair, such as abrasion chondroplasty and microfracture.

Cartilage Response to Injury

Articular cartilage has no blood supply, lymphatic drainage, or innervation. As a result, chondral injuries that do not cross the tidemark cannot generate an inflammatory response. This generates two types of responses from the resident chondrocytes. Apoptosis of the cells surrounding the edge of the injury has been demonstrated with subsequent proliferation of the remaining cell. This creates an incomplete healing response due to the limited ability of these terminally differentiated chondrocytes to proliferate and initiate repair. While many of the surviving cells may undergo proliferation in an attempt to repair the tissue, this increase in metabolic activity is brief. As a result, chondrocytes do not migrate into the defect and the edges of the injury do not fuse. If these lesions are unstable, they may easily progress to larger sizes and cause significant symptoms such as pain or mechanical symptoms.

Injuries that penetrate the subchondral bone may result in a more extensive healing response. Disruption of the underlying blood vessels may result in the formation of a fibrin clot at the site of the defect. As long as this surface is protected from excessive stress, undifferentiated mesenchymal stem cells will migrate and differentiate into cells with features of chondrocytes. This will result in formation of a fibrocartilagenous articular surface, with a higher ratio of type I to type II cartilage compared with normal articular cartilage. Depending on the size of the defect and the amount of disruption of the repair matrix, the defect may fill. In most cases, however, degenerative changes begin and they may eventually progress to large cavitary defects.

When considering repair or reconstruction of cartilage defects, it is important to consider these cited mechanisms. Techniques that repair the articular defect (e.g., microfracture) rely on the mesenchymal stem cells in the subchondral bone for the formation of the fibrocartilagenous surface. This, in combination with a protective rehabilitation program, may relieve symptoms in a majority of patients.

Overall Treatment Algorithm and Approach to Chondral Injuries

There are a variety of surgical options available for nonarthroplasty treatment of symptomatic, high-grade chondral defects. While patient age, activity level, occupation, and comorbidities are important factors to consider when choosing a suitable treatment, characteristics of the lesion itself can also suggest the optimal surgical technique. Surgical decision-making begins with a characterization of the cartilage defect. In the case of asymptomatic lesions found incidentally at the time of surgery, palliative treatment such as arthroscopic debridement may be performed; however, the clinical significance of these lesions is questionable. If the lesion is small (<2 to 3 cm ² ) and does not involve the subchondral bone, surgical options include microfracture, autologous chondrocyte implantation (ACI), and osteochondral autograft transfer (OAT). Failure of any of these procedures is often remedied by an osteochondral allograft transplant. Depending on availability, some surgeons choose transplantation as a primary option in this setting as well. In the setting of larger defects, especially when associated with involvement of the subchondral bone, surgeons should choose restorative options including osteochondral allografts. Larger cartilaginous lesions (≥2 to 3 cm ² ) may be restored with autologous chondrocyte implantation or reconstructed with bulk osteochondral allografting. The overall treatment algorithm for approaching chondral defects is presented in Figure 2-2 .

The overall treatment algorithm for the approach to chondral defects of the knee.

(Courtesy Adam Yanke.)

In all chondral repair procedures, the recognition of associated conditions such as axial malalignment, ligamentous instability, and meniscal deficiency is critical for success. These conditions must be addressed prior to or concurrent with the surgical treatment of cartilage lesions. Cartilage restoration surgery is often performed at the same time or in a staged fashion with ligament reconstruction, meniscal transplantation, and/or corrective osteotomies about the knee.

Patient evaluation is performed similarly independent of which cartilage procedure is determined to be most appropriate. Symptomatic chondral lesions should be suspected in patients with recurrent activity-related effusions and compartment-specific pain. The physical examination of patients with chondral lesions is often nonfocal with occasional defect-specific tenderness. Lesions of the patellofemoral joint may be identified with use of a patellar grind test or reproduction of symptoms during open chain knee extension. The surgeon should carefully assess ligamentous laxity and limb alignment. If a subtle acquired axial malalignment or dynamic thrust is suspected, long limb alignment radiographs should be reviewed. Standard weight-bearing radiographs should be scrutinized for evidence of generalized degenerative changes. Specifically, a bilateral posterior-to-anterior 45-degree flexion weight-bearing radiograph, a bilateral anterior-to-posterior extension weight-bearing radiograph, a 45-degree flexion non–weight-bearing lateral radiograph, and a patellofemoral view (i.e., Merchant) will demonstrate joint space abnormalities as well as evidence of overt osteoarthritis. Although magnetic resonance imaging (MRI) is not essential, careful review of cartilage-sensitive sequences has been shown to be highly sensitive and specific for determining exact location, size, and grade of chondral lesions.

Overview of the Surgical Options for Cartilage Treatment

Chondral repair techniques include reparative (microfracture), restorative (osteochondral autograft plug transfer and autologous chondrocyte transplantation), and reconstructive (bulk osteochondral allograft) methods. Through an improved understanding of cartilage biology, marrow stimulation techniques, such as microfracture, allow the delivery of stem cells and growth factors to the otherwise avascular tissue superficial to the subchondral plate. Careful anatomical and histologic studies have made the use of osteochondral allografts and autografts possible, delivering viable, metabolically active cartilage atop a supporting bone plug. Advances in the science of cell culture and delivery have made techniques such as ACI possible, where harvested autologous chondrocytes are expanded in culture and replaced into the defect under a periosteal patch. With careful attention to indications and surgical technique, these strategies have yielded good to excellent outcomes in 80% to 95% of patients in medium- and long-term studies.

Microfracture

The principles of marrow stimulation technique were developed by Pridie in the 1950s, who attempted to introduce a vascular-mediated healing response to cartilage lesions by drilling denuded bone via direct arthrotomy. Subsequent studies showed unpredictable results due to heat necrosis during drilling. With the advent of arthroscopy, researchers sought innovative approaches to cartilage repair, including abrasion chondroplasty, but were still unable to achieve predictable results. In 1994, Rodrigo et al. published details of their microfracture technique, which used angled arthroscopic awls to penetrate the subchondral bone in a controlled fashion, delivering pluripotent stem cells, cytokines, and growth factors to yield a stable fibrocartilage repair. The success of microfracture hinges on careful attention to operative indications, meticulous surgical technique, and strict adherence to postoperative rehabilitation. Microfracture has been shown to yield good to excellent functional results in medium- to long-term follow-up and represents a viable first-line treatment for symptomatic chondral defects.

Autologous Chondrocyte Implantation

ACI was developed in Sweden in the mid 1990s, and the first published large series of patients showed good to excellent results in over 90% of cases at mid-term follow-up. In broad terms, ACI is largely a second-line treatment for Outerbridge grade III-IV lesions of the femoral condyles, trochlear, or patella. This technique is most appropriate in high-demand patients younger than 50 years who will be dedicated and compliant with the lengthy rehabilitation. While debridement or microfracture may suffice in low-demand patients, multiple or irregularly shaped lesions (2 to 10 cm ² ) and lesions of the patellofemoral joint in demanding patients are more amenable to ACI. For others, chronicity is an important element, as “virgin” acute lesions are potentially treatable with other modalities. If an ACI fails, revision options are limited to a repeat ACI, osteochondral allograft, or arthroplasty. The need for additional procedures is an important consideration in planning for the ACI. Many surgeons will not perform the cartilage implantation in a meniscus-deficient or malaligned knee; thus, concurrent realignment procedures and meniscus transplantation are increasingly common. However, due to the propensity to cause stiffness, ligament reconstruction is often staged prior to the ACI, possibly at the time of biopsy.

Osteochondral Autograft Transfer

The mosaicplasty technique of OAT in the treatment of focal high-grade cartilage defects of the knee was popularized in the mid-1990s by L. Hangody. Several preclinical investigations in animal models have supported this technique, and a similar technique (involving solitary, not multiple, plugs) has been described. Subsequently, the OAT procedure has become widely accepted as an effective treatment of high-grade cartilage defects of the knee and talus.

The use of an osteochondral allograft in a primary cartilage surgery is becoming increasingly popular; because there is no concern for donor site morbidity, it can be performed in a single-stage and offers a fresh osteoarticular construct. However, this technique is not without limitations, including the potential for disease transmission, graft acquisition and storage, concerns regarding the amount of graft chondrocyte viability at the time of transplantation, and immunologic considerations.

The graft must be obtained from a suitable host with viable cartilage. Typically, the host will be between 15 and 40 years old. The grafts are used while fresh to maximize chondrocyte viability. It is also important to ensure that the cartilage is of good quality. In addition, the graft must be size matched to the recipient. This is accomplished by obtaining an anteroposterior radiograph of the patient’s knee with a magnification marker. The tissue bank may then make a correlation with the tibial plateau or femoral condyle of the donor. While these measurements may provide an estimate as to the correct size, the patient’s pathology must be carefully assessed to ensure proper sizing of the allograft.

The storage of the graft raises several important concerns. Fresh-frozen allograft has been shown to improve incorporation by increasing availability and reducing the immune response. However, freezing chondrocytes within their extracellular matrix may eliminate more than 95% of chondrocytes within the graft. Several studies have demonstrated maintenance of mechanical properties as well as viable chondrocytes with fresh allograft. Czitrom et al. demonstrated 69% to 78% viable chondrocytes in a femoral condyle allograft 24 months after transplantation.

An additional concern raised by the use of allograft is the risk of disease transmission and that of immune reaction. The risk of disease transmission is relatively low but not nonexistent. Proper screening techniques have been quoted to have reduced the risk of transmission of human immunodeficiency virus (HIV) to 1:1,667,600, and one case of hepatitis B and three cases of hepatitis C virus infection have been quoted in the literature. It is important for the surgeon to discuss these risks with the patient prior to proceeding with an allograft transfer.

Finally, there is very little doubt that the host immune reaction may have a serious impact on the eventual outcome of articular allograft. Currently, small fragment allografts are not human leukocyte antigen (HLA) or blood type matched between donor and recipient. Animal studies have demonstrated that fresh unmatched osteochondral allografts elicit a variable immune response. While most studies have shown that patients generally tolerate articular allograft immunologically, one particular study demonstrated that 50% of patients generated serum anti-HLA antibodies. While the relevance of these findings remains unknown, they may have serious implications on the long-term outcome of these allografts.

Microfracture

The technique for microfracture has been previously described by Steadman et al. The cartilage defect is first debrided of flaps and the calcified layer as described earlier. Violating and excising the calcified layer require special attention as insufficient debridement of this layer may lead to poor adherence of the fibrocartilage repair tissue, while thinning of the subchondral plate by aggressive debridement may lead to excessive bony proliferation during remodeling. Either phenomenon may jeopardize the biomechanical properties of the fibrocartilage repair tissue. After debridement, the arc of motion is recorded to quantify the position of contact that the lesion makes with the joint surface. This aids in planning for postoperative rehabilitation and restrictions.

Multiple small holes are made in the subchondral bone using a commercially available awl or another sharp device ( Fig. 2-4 ). It is critical that the awl penetrates the subchondral plate in a perpendicular fashion to prevent skiving and creating troughs that could compromise the integrity of the plate or otherwise lead to confluence of the microfractured holes. Selecting appropriately angled awls and positioning the knee in an optimally flexed position will ensure this perpendicular penetration. The awl tip is advanced with careful, controlled mallet taps ( Fig. 2-5 ). The depth of the holes is typically about 4 mm with adequate depth confirmed by the appearance of fatty marrow droplets or bleeding. Microfracture holes are created at the periphery of the lesion at 3- to 4-mm intervals and then continued in a spiral pattern to the center. The distance of 3 to 4 mm allows for adequate penetration and coverage of the defect while limiting the possibility of fracture of the bone between the holes. The shaver is again introduced and run over the newly created defects to debride any loose bone fragments that were created from the microfracture. The tourniquet, if used, should be deflated to evaluate the appearance of blood and/or fat droplets and final images of the lesion obtained prior to closure ( Fig. 2-6 ). The instruments are removed, the portals are closed, and a sterile dressing is applied. No drains should be placed, so as to not disturb the clot formed over the defect.

Microfracture of a defect on the femoral condyle. Note the spacing of the microfractures.

Microfracture awls penetrate the subchondral plate to stimulate the marrow elements and to allow access of the marrow elements to the bony surface.

Bleeding is visualized from the subchondral awl holes once the arthroscopic pump pressure is decreased.

Autologous Chondrocyte Implantation

ACI is a two-step procedure with an initial diagnostic arthroscopy at which time the chondrocytes are harvested, followed by a second procedure to reimplant the chondrocytes. In cases of axial malalignment, meniscal deficiency, or ligamentous instability, many surgeons recommend addressing this concomitant pathology at the time of the first stage of the procedure.

Arthroscopic biopsy is performed with a gouge or ring curette at the lateral intercondylar ridge (the region that is commonly removed when performing notchplasty during anterior cruciate ligament reconstruction). If pathology is present in this region, the biopsy specimen can be taken from the superolateral edge or from the lateral edge of the intercondylar notch. The biopsy specimen must be full thickness and should measure 5 to 10 mm, which has been shown to weigh 200 to 300 mg and contain between 200,000 and 300,000 cells. The biopsy specimen is transferred via sterile technique into a commercially provided cell culture vial and shipped next-day service in a controlled environment package at 4 °C for cell culture and expansion (Genzyme Biosurgery Corporation, Cambridge, MA). Once the specimen is received, the cellular expansion process is completed in approximately 1 month, yielding a suspension of 12 million cells per 0.4 mL culture medium, or approximately 20 to 50 times the initial cell number.

Implantation is performed through a carefully planned peripatellar arthrotomy that allows sufficient, direct access to the lesion. For larger lesions, this may involve an osteotomy of the femoral epicondyle or tibial tubercle to provide sufficient access, although most femoral condyle lesions can be addressed through mini-arthrotomies. Posterior lesions may require hyperflexion as well as subperiosteal mobilization of the meniscus, which may be repaired later. The defect is prepared by using a ring curette to sharply remove diseased cartilage at the periphery back to stable, vertical walls. Subchondral penetration is avoided, so that bleeding is minimized. This prevents a mixed cell population of undifferentiated stem cells with the end-differentiated chondrocytes. If the lesion extends to synovium, it may be beneficial to leave a rim of less healthy cartilage to keep the lesion contained and prevent having to suture the periosteal layer to synovium only. Hemostasis is achieved with pledgets of diluted epinephrine and saline solution applied with direct pressure. The lesion is then carefully measured, and a template can be made using sterile paper to assist in sizing the periosteal patch.

Periosteal harvest is preferentially performed from the ipsilateral proximal medial tibia, 2 cm distal to the pes anserine. Alternative sites include the distal anterior femur and the contralateral tibia or femur. The plane between the subcutaneous tissues and the periosteum is developed with blunt dissection and the periosteum is scored with a No. 15 blade knife, at least 2 mm larger in each dimension than the template to accommodate postharvest shrinking. The dissection should not be performed with electrocautery so as to avoid damage to the cambium layer of periosteum. The periosteum is gently lifted with the use of a sharp, curved periosteal elevator from distal to proximal ( Fig. 2-7 A ). Small tears can be later repaired with suture if necessary. The outer surface is marked with a sterile marking pen to distinguish it from the inner layer, and the graft should be kept moist at all times during the harvest to minimize the amount of cell death in the sensitive cambium layer.

(A) For autologous chondrocyte implantation, the periosteal patch is harvested and any remaining fat is removed gently to preserve the periosteum integrity. The outer layer should face the joint space. (B) The periosteum is sutured with 6-0 absorbable Vicryl lubricated with mineral oil at 2- to 3-mm intervals to ensure a solid seal and patch adherence. A 5- to 8-mm opening is left at the superior aspect of the patch to accommodate an 18-gauge angiocatheter.

The patch is placed over the defect and trimmed to size if necessary; no overlap on the healthy cartilage rim is desired, but some tenting should be created to accommodate the suspension to be injected. The outer layer of the periosteum should face toward the joint space, inverting its natural orientation. Suturing is accomplished with a 6-0 absorbable Vicryl on a small P-1 cutting needle, lubricated with mineral oil in multiple simple stitches placed approximately 2 mm apart ( Fig. 2-7 B ). The patch is tacked in four corners, initially, with sutures passed first through the periosteum from outside to inside and then through the cartilage from deep to superficial, 3 mm from the periphery of the defect. Sutures are tied directly over the junction of the periosteum and native cartilage, spaced 3 to 4 mm apart to ensure a watertight seal. Fibrin glue is used to seal the edges of the patch and the sutures except for a 5-mm opening at the superior aspect of the defect that is left for the final delivery of the cells. This fibrin sealant may be obtained either by having the patient donate a unit of autologous blood 14 days before surgery to be processed into fibrin glue or by using commercially available fibrin glue from pooled donors. Mini anchors or bone tunnels may be used if the cartilage rim is failing to hold the suture or if the patch needs to be sutured near the femoral notch. The seal is tested with a saline load delivered through an 18-gauge angiocatheter. After removal of all injected saline, the suture line is resealed with fibrin glue and tested again.

Chondrocyte injection begins with careful sterile preparation of the suspension. The top of the nonsterile vial is prepped with alcohol, and while maintaining the vial in an upright position, a sterile 18-gauge angiocatheter is inserted into the vial and the needle is removed. The fluid overlying the cellular sediment is gently aspirated and reinjected several times to agitate the suspension completely. The contents of the vial are then completely withdrawn into the syringe and transferred into the lesion from distal to proximal, with a gentle side-to-side motion ( Fig. 2-8 ). The remaining opening is then sutured and sealed with fibrin glue. The knee is then extended and layered closure of the incisions is performed. Drains are avoided, due to risk of patch disruption.

An 18-gauge angiocatheter is inserted into the opening of the patch, and the autologous cell transplant suspension is inserted.

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