Articular cartilage is a highly specialized tissue with complex ultrastructure and unique biomechanical properties providing for load distribution and a low-friction weight-bearing surface essential for normal pain-free movement of synovial joints. Traumatic articular cartilage injuries are well-recognized sequelae of acute or repetitive impact or twisting injuries to a joint. The incidence and prevalence of traumatic cartilage injuries have not been fully delineated and are somewhat difficult to gauge clinically. However, arthroscopic studies have highlighted that such injuries are common. In a retrospective study of surgical reports from 19,827 patients undergoing knee arthroscopy, chondral lesions were documented in 63% of cases, with an average of 2.7 lesions per knee. Similar results have been more recently described in a prospective review of 993 knee arthroscopies illustrating cartilage abnormalities in 66% of patients, with full-thickness cartilage lesions ( Fig. 4-1 ) seen in 11% of cases.
Traumatic injuries may manifest as cartilage matrix and cellular injury with morphologically intact articular cartilage surface cover; mechanical disruption of articular cartilage in the forms of partial- or full-thickness cartilage fissures, flap tears, and segmental cartilage defects; or osteochondral injuries involving both articular cartilage and underlying subchondral bone. Injuries involving articular cartilage have a limited capacity for intrinsic repair secondary to insufficient vascularity of the cartilage and the chondrocytes’ inability to divide and migrate to repair significant tissue defects. Full-thickness injuries of articular cartilage that extend to involve subchondral bone do cause hemorrhage and fibrin clot formation and initiate an inflammatory response stimulating osseous and articular cover repair. However, although this repair tissue may anatomically fill an osteochondral defect and alleviate symptoms temporarily, this repair tissue rarely replicates the mechanical and biologic properties of normal native articular cartilage. Such repair tissue typically illustrates evidence of degeneration, fragmentation, fibrillation, and tissue depletion within 1 year or less after injury.
The majority of cartilage injuries may not result in clinical symptoms or disability; however, some patients may present with complaints of swelling, pain with movement, or mechanical symptoms of catching, locking, or giving way. Additionally, although the determinant of the true natural history of an articular cartilage lesion is likely multifactorial and somewhat poorly delineated at present, there is evidence to support the concept of lesional progression, degeneration, and, ultimately, the development of osteoarthritic disease.
Increased awareness of the prevalence and significance of articular cartilage lesions coupled with the limited natural capacity of cartilage for effective intrinsic repair have contributed to growing interest in surgical techniques for the treatment of articular cartilage lesions. Such operative techniques have advanced considerably over the past decade, paralleling advances in biologic science and results of experimental models of cartilage regeneration and repair. The most widely employed surgical treatment options for repair of cartilage lesions currently include marrow stimulation, osteochondral transplantation, and chondrocyte transplantation techniques. Success rates for these surgical options vary depending on defect location, size, and depth; status of underlying subchondral bone and adjacent surrounding cartilage; joint stability; biomechanical joint alignment; and clinical factors including patient age, weight, and general health status.
MAGNETIC RESONANCE IMAGING
MRI has been well established as an accurate noninvasive means of assessing articular cartilage, enabling accurate assessment of cartilage morphology and volume and providing insight into its constituent biochemical composition. MRI has similarly been well described as a valuable technique in the postoperative evaluation of cartilage repair procedures. As in the preoperative setting, critical user-dependent image acquisition factors that affect the MRI assessment of cartilage repair techniques include acquisition pulse sequences that determine image contrast, image spatial resolution, and overall image signal-to-noise ratio.
Although multiple existing and developing MRI pulse sequences have been evaluated in the assessment of articular cartilage, two classes of pulse sequence acquisitions have been found to be most accurate in this regard: 3D spoiled gradient-echo (SPGR) or fast low-angle shot (FLASH) sequences and intermediate-weighted or T2-weighted fast spin-echo (FSE) techniques.
Fat-suppressed 3D SPGR and FLASH acquisitions provide high-resolution contiguous thin-slice images with high contrast between bright cartilage and dark fluid, bone, fat, and muscle. However, such sequences may be limited in their assessment of internal cartilage pathology and small intrasubstance fissures or defects. An additional potential limitation of SPGR and FLASH acquisitions is their relative sensitivity to susceptibility and intravoxel dephasing artifacts, which may be important image quality considerations in a patient after cartilage repair. FSE acquisitions are less prone to postoperative metal-related artifacts originating from metallic debris from prior surgical instrumentation and possible stabilization hardware in the vicinity of the joint. Such metal-related artifacts may compromise image quality, particularly in the setting of prior osteochondral allograft transplants and autologous chondrocyte implantation.
Intermediate- and T2-weighted FSE acquisitions can provide high-resolution, high-contrast imaging of articular cartilage and repair tissue in postoperative patients, with excellent depiction of surface morphology as well as intrinsic signal changes potentially reflective of intrasubstance pathologic processes.
Intra-articular contrast material, either through direct or indirect MR arthrographic techniques, may offer advantages of improved definition of the integrity and integration of repair tissue. Investigators have advocated the use of indirect MR arthrography in the MR evaluation of surface morphology and potential delamination of repair tissue after autologous chondrocyte implantation. In contrast, other investigators have concluded that nonenhanced high-resolution fluid-sensitive imaging acquisitions are sufficient for accurate assessment of tissue integration and delamination without the need for contrast agent administration.
Because of the high image spatial resolution and signal-to-noise requisites of MRI assessment of postoperative cartilage repair procedures, imaging studies in such patients should ideally be performed on high field (1.0T or higher) MR scanners. Imaging at 3.0T provides the potential advantage of imaging with relative increased image signal to noise ratio or higher spatial resolution at similar imaging acquisition times, compared with 1.0T or 1.5T imaging (albeit with somewhat increased sensitivity to postoperative metal-related artifacts). In contrast, imaging at low field strength (0.18-0.2T) should generally be avoided in the evaluation of cartilage repair procedures and has been shown to have substantial limitations in visualizing cartilage pathology compared with imaging at 1.5T.
In addition to a routine assessment of joint anatomy, a complete MRI evaluation of cartilage repair procedures should include specific assessments of (1) repair tissue: defect fill, surface morphology, and MR signal characteristics; (2) adjacent cartilage and bone: repair tissue integration to native cartilage and subchondral bone and MR signal characteristics of subchondral bone; and (3) the articulation: joint effusion, synovitis, adhesions, and loose bodies.
SURGICAL CARTILAGE REPAIR PROCEDURES
Marrow Stimulation
Marrow stimulation techniques for cartilage repair include subchondral drilling, abrasion arthroplasty, and microfracture. The surgical objectives of marrow stimulation techniques are the introduction of pluripotent repair cells into the site of a cartilage defect via the induction of hemorrhage, facilitated through surgical penetration of the subchondral bone plate. Penetration of subchondral blood vessels and underlying subchondral bone marrow leads to filling of the chondral defect with a fibrin clot, with subsequent migration of undifferentiated mesenchymal cells into the clot. Proliferation and differentiation of these mesenchymal cells result in partial or complete filling of a defect with subchondral new bone formation and overlying fibrocartilaginous repair tissue.
Microfracture
Of the marrow stimulation methods described in the literature, the most widely employed surgical technique is microfracture. The technique is a commonly employed treatment option for the surgical management of full-thickness defects in the knee and other articulations. Developed and elaborated on by Steadman and coworkers, microfracture is a minimally invasive one-stage arthroscopic procedure that is relatively easy to technically perform, is cost effective, and does not preclude repeat surgical intervention if clinically warranted. Ideal candidates for microfracture cartilage repair include patients younger than 45 years of age, with isolated well-contained lesions of less than 4 cm 2 involving the weight-bearing femoral condyles, trochlea, or patella, without concomitant meniscal or ligamentous insufficiency.
Technically, the procedure involves débridement of a cartilage lesion to stable articular cartilage margins, curettage and removal of the calcified cartilage layer, and creation of multiple perpendicular microperforations of the subchondral bone with arthroscopic awls or picks at 3- to 4-mm intervals throughout the defect ( Fig. 4-2 ). Postoperatively, weight bearing is generally avoided for at least 6 weeks, with gradually advanced weight bearing, physiotherapy, and return to full activity (including high impact sports or professional activities) usually by 6 to 8 months postoperatively.
Histologic evaluation of repair tissue formed after microfracture or other marrow stimulation techniques in experimental and clinical models typically illustrates partial or complete filling of an articular defect primarily with fibrocartilaginous repair tissue, composed mostly of type I collagen. This is in contrast to the composition of native hyaline articular cartilage, which is composed primarily of type II collagen produced by chondrocytes.
Clinical results of microfracture surgical repair of focal articular cartilage lesions in the knee have shown the most substantial functional improvements within the first 2 years postoperatively. Optimal outcomes in these investigations were generally observed in younger active patients with a short duration of symptoms, low body mass index, and lesions involving the femoral condyles. However, despite initial improvements in clinical function, some clinical studies have shown a subsequent deterioration in clinical results beginning at 18 to 24 months postoperatively. These observations have been hypothesized to correlate to the histologic and biomechanical properties of fibrocartilage (type I collagen) observed in experimental animal models. In such models, fibrocartilaginous repair tissue illustrates degeneration, reduced stiffness, and a predilection for degradation after an initial period of fibrocartilage repair tissue formation and healing.
MRI of Microfracture
The MRI appearance of areas of microfracture repair varies over time postoperatively. Within the first few months after surgery, MRI illustrates repair tissue partially or fully filling the articular defect ( Fig. 4-3 ). This repair tissue typically shows increased signal on intermediate or T2-weighted imaging compared with native articular cartilage. Over time, within the first year postoperatively, the volume of repair tissue may increase with progressive defect fill ( Fig. 4-4 ). Despite good defect fill, some MRI investigations have described varying degrees of persistent depression of the repair cartilage’s surface morphology, mild persistent increased signal intensity on FSE imaging relative to adjacent native hyaline cartilage, and fissures or gaps between native and repair cartilage in the majority of microfracture cases imaged.
Subchondral bone subjacent to sites of microfracture repair may illustrate a less distinct, thin, and irregular appearance relative to adjacent subchondral bone. Subchondral marrow edema is also frequently seen in the initial postoperative period. Typically, this marrow edema progressively decreases over time, although mild degrees of persistent marrow edema-like signal may be observed in asymptomatic patients at varying time points postoperatively. Subchondral osseous overgrowth may also be observed at the microfracture repair site, possibly related to enchondral ossification of repair tissue or hypertrophic osseous healing of the multiple perforations of the subchondral bone plate. Such osseous overgrowth may contribute to overall defect volume fill, with relative thinning of overlying repair tissue, with potential implications on function and durability of the repair cartilage over time.
Clinical function after microfracture treatment has been correlated to postoperative MRI findings of defect fill. In this study, investigators found a correlation between good repair tissue defect fill and improved clinical knee function postoperatively and an association of limited/poor fill grade (<33% defect fill) and decreasing functional scores 24 months postoperatively.
MRI features of other potential complications or failure of microfracture cartilage repair may include visualization of chondral flaps and fissures, progressive tissue thinning, and defect enlargement suggestive of repair tissue breakdown and degeneration.
Osteochondral Transplantation
Osteochondral transplantation techniques of cartilage repair involve the use of autograft or allograft constructs of bone and overlying articular cartilage for restoration of an articular surface. Such repair techniques provide the theoretical advantage of implanting an articular surface composed of fully formed hyaline articular matrix with viable intrinsic chondrocytes.
OSTEOCHONDRAL AUTOGRAFTS
Autologous osteochondral transplantation (AOT) techniques include a series of similar procedures with varying names based on surgical instrumentation manufacturers: MosaicPlasty (Acuflex, Smith and Nephew), OATS (Osteochondral autograft transfer system, Arthrex), SDS (Soft delivery system, Sulzer Medica), and COR (Mitek). These techniques all involve the transplantation of one or more cylindrical plugs of autologous bone with overlying hyaline cartilage harvested from normal relatively non–weight-bearing aspects of the joint. These plugs are then transplanted into similarly sized holes created within the defect site to restore chondral and subchondral defects of the joint ( Fig. 4-5 ). Graft plugs utilized may vary in overall dimensions from 2.7 to 8.5 mm in diameter and 10 to 25 mm in length.
AOT procedures can be performed arthroscopically or utilizing a small arthrotomy, which may be of added benefit when treating large defects or defects posteriorly located within the joint. AOT procedures are usually done in one stage with multiple transplant plugs used to graft large defects and one or two plugs used to treat small articular defects.
Optimal candidates for osteochondral autograft transplantation are symptomatic young patients younger than 50 years of age with focal chondral or osteochondral defects 1 to 4 cm 2 in size. Although larger lesions of up to 8 cm 2 have been treated, donor site graft availability, operative morbidity, and other technical issues limit the absolute size of lesions that can be effectively treated with AOT techniques. AOT is used most commonly in the knee and ankle joints but has also been utilized in the repair of articular defects of other diarthrodial surfaces, including the tibia, humeral capitellum, and femoral head. As with other cartilage reparative procedures, malalignment and ligamentous or meniscal insufficiency are relative contraindications and are typically treated simultaneously or as a staged procedure with AOT repair.
Technically, AOT procedures involve débridement of a defect’s margins back to healthy hyaline cartilage and the base of a defect down to viable subchondral bone. The defect recipient site is then measured to determine the number and size of grafts required for reconstruction of the articular surface. Recipient tunnels are then cut with coring instruments, removing evenly spaced, properly sized bone plugs oriented perpendicular to the articular surface at the defect site. After preparation of the recipient site, an appropriate number of correspondingly sized osteochondral plugs are harvested, perpendicular to the articular surface, using tubular harvesting instruments. Harvested plugs are obtained from relatively non–weight-bearing donor aspects of the joint. Typical donor sites in the knee include the margins of the inferior lateral trochlear ridge, intercondylar notch, or supracondylar ridge. The harvested osteochondral graft plug(s) are then transplanted atraumatically into the recipient tunnel(s) using press-fit fixation. The surgical goal of the transplantation is reconstruction of the contour of the articulation, with positioning and orientation of the transplantation plugs flush with the surface of adjacent native cartilage. Graft plug positioning proud or recessed relative to the native articular surface of the joint, either secondary to technical difficulties at surgery or graft subsidence and motion, is associated with worse clinical outcomes likely secondary to excess mechanical stress on the transplant plugs or subjacent cartilage.
After AOT, patients are initially kept non–weight bearing postoperatively and then advanced to partial protective weight bearing with weight-bearing exercises and subsequent progressive advancement to full weight bearing, This phased and conservative approach to weight bearing postoperatively is employed to avoid early graft damage and to promote early graft osseous incorporation and healing. Timing of the progress of postoperative rehabilitation is dependent on the size of the treated defect, patient age, patient body mass index, and level of anticipated postoperative patient activity.
Second-look arthroscopic and histologic evaluations of autologous osteochondral transplants have shown consistent survival of transplanted hyaline cartilage overlying the osseous transplantation plugs. Fibrocartilaginous repair tissue has also been documented between transplant graft plug interstices and their junction with native articular cartilage of the joint.
Clinically, postoperative follow-up studies have reported high rates of symptomatic relief and functional improvement up to 7 years postoperatively. However, less favorable outcomes have been reported when defects greater than 4 cm 2 are repaired and for repair of defects utilizing a larger number of transplant graft plugs.
Few comparative investigations of AOT relative to other cartilage repair procedures are available in the literature. However, one such study of 413 arthroscopic resurfacing procedures (mosaicplasty, subchondral drilling, abrasion arthroplasty, and microfracture) showed superior long-term clinical outcome results for mosaicplasty relative to the other techniques evaluated. Other randomized clinical trials have shown outcomes after mosaicplasty to be superior to microfracture and comparable with outcome results after autologous chondrocyte implantation for repair of small- to medium-sized defects.
MRI after Autologous Osteochondral Transplantation
MRI after AOT procedures can provide information regarding congruity of repair articular surface, graft incorporation, as well as status of the donor site. At the donor sites, tubular regions of low T1 and increased T2 signal intensity are normally seen within the harvest marrow space, with corresponding defects seen in the overlying articular cartilage. These observed subchondral signal changes at the donor sites progressively resolve, returning to normal fatty marrow signal ( Fig. 4-6 ), while the associated articular defects may become less apparent as they progressively fill-in with fibrocartilaginous repair tissue.
