History

Articular cartilage injuries may be caused by a direct trauma associated with impact or an indirect injury usually involving a twisting or shearing movement associated with an axial load. Patients with a history of a previous cartilage repair procedure may not describe their additional symptoms as a new injury to the knee. However, a thorough discussion about the patient’s additional symptoms such as mechanical clicking, locking, or instability may help discern whether an associated pathology may have contributed to cartilage failure.

Similar to patients with a primary focal cartilage defect, pain is most often the patient’s chief complaint, which is aggravated by certain positions or activities. Pain at the ipsilateral joint line is often associated with a condylar injury and can be aggravated by weight-bearing activities. Joint line pain caused by meniscal deficiency may be difficult to discern from a focal cartilage defect. However, a previous history of meniscectomy may heighten the surgeon’s awareness to the possibility of meniscal deficiency causing or contributing to continued symptoms. Patients presenting with pain in the anterior compartment of the knee may be suffering from a trochlear or patellar lesion, which can be aggravated by activities that increase patellofemoral contact pressure, such as stair climbing or squatting. In addition to pain, patients may also report activity-related effusions in the knee.

Prior attempts at treatment should be reviewed with the patient. If prior surgeries have been performed, the timing and type of surgery, type of rehabilitation that followed, and whether the patient experienced a period of symptomatic relief postoperatively should be thoroughly discussed preoperatively. In addition, nonsurgical management such as oral medications, injections, bracing, physical therapy, and lifestyle modification should also be discussed as an important part of the patient’s prior treatment.

Physical Examination

The physical examination of a patient with a symptomatic cartilage lesion begins with observation of the patient’s gait and body habitus. Gait evaluation may reveal any antalgia caused by pain or weakness, malalignment or a varus or valgus thrust associated with ligament insufficiency or clinical malalignment. The physician should also observe and measure any associated quadriceps atrophy and effusions, and determine the location of any previous surgical incisions.

Palpation of bony and soft tissue structures about the knee may provide some insight into the location of the patient’s symptoms, associated conditions such as meniscal deficiency, or presence of a subtle effusion. Patients with chondral injuries of the condyle typically present with ipsilateral joint line tenderness. Meniscal injury or deficiency may also present similarly to condylar pain with joint line tenderness; however, the pain is usually appreciated more posteriorly. Patellofemoral lesions may have pain and crepitus in the anterior compartment. Patellar tilt and glide should be evaluated for tightness of the lateral retinaculum and potential patellar instability. Finally, range of motion should be assessed in both knees, noting limitation in range and/or flexion contractures.

Identification of associated pathology is critical to the successful outcome of revision and complex articular cartilage restoration. As noted, persistent instability, malalignment, or meniscal deficiency is often a cause of premature failure of articular cartilage repairs and poor outcomes. Stability of the anterior cruciate ligament (ACL), posterior cruciate ligament (PCL), medial collateral ligament (MCL), as well as the lateral collateral ligament (LCL) and posterolateral complex, should be a routine part of any knee examination.

Imaging

Standard radiographs for cartilage injury should include bilateral knees in at least three views: anteroposterior (AP) weight-bearing view; non–weight-bearing, 45-degree flexion lateral view; and axial (Merchant) view of the patellofemoral joint. Additional views include a 45-degree flexion posteroanterior (PA) view, which may be useful to identify subtle joint space narrowing. A full-length alignment view of the affected and unaffected limb may help evaluate the mechanical axis and associated varus or valgus malalignment (Fig. 27-1). A computed tomography (CT) scan may be useful to assess the patellofemoral joint and the associated tibial tubercle–trochlear groove (TT-TG) distance.^1,13 This measurement is particularly useful in patients with patellar instability when associated with chondrosis. Magnetic resonance imaging (MRI) scans are often used in the preoperative assessment of previously failed cartilage repair procedure. They provide a detailed assessment of lesion size, depth, quality of subchondral bone, and presence or absence of bony fractures. MRI may also confirm the presence of associated ligamentous, meniscal, or other soft tissue pathology.

Figure 27-1 Standing long-leg alignment x-rays. The mechanical axis of the extremity is represented by the red line from the center of the femoral head to the center of the talus. This patient has an obvious varus deformity to the lower extremity. The desired correction for this patient is just beyond neutral. This angle is calculated by a line drawn from the center of the femoral head to the desired correction level at the joint line and a second line from the center of the talus to the same correction point at the joint line (yellow).

Nonoperative Treatment

Nonoperative therapies play a role for patients with previous cartilage repair surgery. Patients with unreasonable expectations or goals, failed multiple procedures, advanced physiologic age with low demand, or unwilling to have further surgery may be amenable to these conservative modalities. These therapies include oral medications, physical therapy, weight loss, and injections (cortisone and hyaluronic acid derivatives). Oral medications such as nonsteroidal anti-inflammatory drugs and oral chondroprotective agents (e.g., glucosamine, chondroitin sulfate) are commonly used in symptomatic patients. Although the precise mechanism of action of these medications has not been elucidated, it has been hypothesized that glucosamine stimulates chondrocytes and synoviocytes to increase production of extracellular matrix, whereas chondroitin manages to inhibit fibrin clot formation and degradative enzymes.²

Cortisone injections are commonly used in practice for short-term pain relief because of the anti-inflammatory action of the steroids. Similarly, intra-articular injections containing hyaluronic acid provides viscosupplementation, resulting in significant pain reduction and improved function.^5,7,12,14

Operative Treatment

Surgical managements of articular cartilage lesions can be grouped into three categories:

The appropriate treatment for any given cartilage lesion is patient- and defect-specific. Lesion-specific variables include lesion size, location, depth, geometry, and bone quality; patient-specific variables include the patient’s physiologic age, activity level, goals and expectations, and previous surgeries. Consideration of these variables and the associated comorbid conditions allow the management of cartilage lesions to be considered as part of an algorithm from the least invasive to the most invasive intervention (Fig. 27-2). The overall goal is to restore the patient’s function and ameliorate symptoms using the least invasive technique. In the setting of a revision procedure, the least invasive procedure can often be exhausted, with undesirable outcomes requiring the surgeon to consider more invasive techniques for cartilage restoration while also addressing the reasons for primary failure, as noted earlier.

Figure 27-2 Algorithm used to guide decision making for primary and revision articular cartilage repair.

Reparative Procedure

Small- to medium-sized (2 to 3 cm²), full-thickness chondral defects can be managed using marrow stimulation techniques, such as microfracture, subchondral drilling, and abrasion arthroplasty. Microfracture involves the use of a surgical awl on the subchondral bone to allow migration of marrow elements (mesenchymal cells). This migration results in the formation of a surgically induced fibrin clot at the defect site and the production of fibrocartilage. The newly formed repair tissue possesses a preponderance of types I and II collagen,¹¹ rendering it biologically and mechanically inferior to hyaline cartilage. This is especially helpful when prior procedures have been only partially successful in creating a complete defect repair (Fig. 27-3).

Figure 27-3 Second-look arthroscopy of a trochlear defect previously treated by ACI, with partial delamination of the repair site being prepared for microfracture.

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