Articular cartilage is a thin layer of specialized, connective tissue lining the articulations of diarthrodial joints. Properties that are unique to this tissue enable an almost frictionless joint movement and afford protection to the underlying bone from excessive load and trauma by dissipating the forces that are produced during movement.

The structural organization of articular cartilage can be divided into four major zones: (a) superficial, (b) middle, (c) deep, and (d) calcified (1,2). Each zone is distinctly structured, with cells and extracellular matrix (ECM) organized in specific patterns. The cells, known as chondrocytes, make up 1% to 2% of the total weight of the articular cartilage. On the other hand, the ECM, which makes up the rest of the cartilage, generally is composed of type II collagen, glycosaminoglycans, and proteoglycans.

Within joints and, in particular, the knee, are two types of cartilage: fibrocartilage and hyaline cartilage. Fibrocartilage is an elastic or “fibrous” cartilage, of which the menisci are composed, whereas hyaline cartilage is the tissue covering the extremities of the bones that make up the joint. Hyaline cartilage has extremely important biomechanical functions,
serving as a shock absorber as well as providing frictionless movement to the joint. Even though this layer of cartilage is only a few millimeters thick, it has a significant capacity for absorbing forces and for distributing loads to reduce stress on subchondral bone.

Chondral defects of the knee commonly affect the medial femoral condyle; once this protective layer of articular cartilage is compromised, subsequent trauma and excessive loading can accelerate the progression of the “wear and tear.” Moreover, significant functional properties are lost, leading to further pathologic changes that can involve the surrounding cartilage and subchondral bone (2,3).

As early as 1743, Hunter (4) recognized that “articular cartilage lesions don’t heal”; the limited intrinsic healing potential of articular cartilage is attributed to the presence of few and specialized cells with low mitotic activity. As the human body matures, the cell density, which influences the amount of ECM that is produced, declines further, limiting the capacity of articular cartilage to regenerate. Another property of articular cartilage that limits its reparative ability is that cartilage is avascular, and the absence of a vascular network prevents access by mesenchymal stem cells and macrophages, which normally would help in repairing tissues. Stem cells are responsible for the formation of new chondrocytes, whereas macrophages remove debris associated with damaged cartilage. Therefore, once injury occurs, surgical intervention may be necessary to repair of the resulting focal chondral defects and obtain good functional outcome.

Patients suffering from chondral injuries often find it difficult to recall a specific incident that triggered their symptoms. Swelling usually is present in the affected knee but sometimes can be accompanied by mechanical symptoms, such as catching and clicking. A high index of suspicion for chondral injuries should be considered in patients who present with episodes of recurrent swelling in a knee that has effusion at the time of examination (5). In addition, Mandelbaum (6) emphasized that chondropenia (i.e., a process involving loss of cartilage volume and elevation of contact pressures over time, resulting in downward progression on the dose–response curve and eventual osteoarthritis formation) is a possible causative factor and should not be overlooked when encountering patients who present with these particular knee symptoms.

Specific symptoms that are synonymous with chondral defects have been reported by several authors. Brittberg et al. (7) and Ochi et al. (8) stressed that knee pain, locking, retropatellar crepitus, and swelling are among the prominent findings. Other authors, including Hangody et al. (9), mentioned that instability also could be present. Because signs and symptoms elicited during physical examination can mimic the presentation of other knee pathologies, the authors agree that correlation with other diagnostic modalities should be routine to increase the accuracy of diagnosis.

Imaging modalities remain an essential part of the diagnosis, evaluation, and monitoring of articular chondral lesions. Advancements in this field have paralleled an increase in the accuracy of detecting lesions; however, a standard weight-bearing radiograph in full extension, a posteroanterior view at 45 degree flexion, and Merchant views remain the basics for diagnostics. Detection of malalignment requires a full-length standing film.

Among the diagnostic imaging modalities currently used, magnetic resonance (MR) imaging is the most accurate, with a reported sensitivity of 95% or greater (10,11,12). Aside from delineating the extent of the articular cartilage lesions, subchondral bone and associated ligament or meniscal injuries also can be assessed. The use of fast spin-echo (with or without fat suppression) and/or fat-suppressed (or water-selective excitation) spoiled-gradient echo images for better resolution has been recommended. Signal properties of articular cartilage are dependent on the following: (a) the MR pulse sequence used; (b) the cellular composition of collagen, proteoglycans, and water; (c) the orientation of collagen in different laminae of cartilage; and (d) an effective cartilage pulse sequencing (Potter).

Today, surgeons are using arthroscopy more extensively as a diagnostic tool. The benefit afforded by direct visualization of the extent of the defect (together with the information provided by MR imaging) significantly enhances the surgeon’s capacity to plan the treatment necessary for addressing the pathology.

The Outerbridge classification has been the traditional system, but recently, a more comprehensive system, the ICRS classification, has been adapted (13). In the ICRS system, normal cartilage is classified as ICRS 0 (normal). When visible fibrillation and/or slight softening on a rather intact surface is observed, the defect is classified as ICRS 1a, whereas with the presence of additional fissures/lacerations, the classification is ICRS 1b (nearly normal). Deeper defects that involve less than 50% of the cartilage thickness are classified as ICRS 2 (abnormal), and defects affecting more than 50% of the cartilage thickness are ICRS 3 (severely abnormal). Subgroupings in this class include the following: ICRS 3a, for defects that do not involve the calcified layer; ICRS 3b, for when the calcified layer is involved; ICRS 3c, for defects that extend down to, but not through,
the subchondral bone plate; and ICRS 3d, for blisters. Defects involving the subchondral bone are considered to be full-thickness lesions and are classified as ICRS 4.

Several options exist in the treatment of cartilage lesions; however, integrating these options into a comprehensive algorithm has not been easy. Any form of planned treatment should be based on patient characteristics and expectations, clinical symptoms, and type of lesions.

One algorithm proposed by Cole and Farr (14) and by Miller and Cole (15) presents an overview of a surgical
decision scheme. In this algorithm, multiple options are presented for similar lesions without endorsing one specific treatment over the others.

In general, surgeons agree that parameters such as lesion size, depth, and associated issues (e.g., alignment as well as ligament and meniscal integrity) should be considered when planning the treatment of chondral defects. Furthermore, other factors related to the patient (e.g., age, genetic predisposition, level of activity, associated pathologies, and expectations) should not be overlooked.

To facilitate decision making when confronted with a particular case, a summary of cases and treatment options that can be encountered in practice is provided in Tables 43.3.1 and 43.3.2.

Symptomatic chondral lesions are not likely to revert to a previous subclinical state without an appropriate form of intervention or some degree of modification in activity level. It should be emphasized that these lesions commonly are associated with other knee pathologies; therefore, managing the problem nonoperatively, with activity modification, weight loss, physiotherapy, and pain medications, can provide symptomatic relief only for a limited period, and if pain relief is provided, how long the patient will remain symptom-free is not known. To compound the situation, most patients are relatively young and active; therefore, prescribing activity modification does not always sound appealing. Because outcome data regarding the natural course of these lesions are either incomplete or inconclusive, determining the appropriate treatment option is always a challenge.

Traditional techniques in the categories of palliative or reparative treatment options have demonstrated variable results. Lavage and chondroplasty can provide symptomatic pain relief with no actual formation of hyaline tissue; however, these techniques remove superficial cartilage layers, which include collagen fibers that are responsible for tensile strength, thus creating a cartilage tissue that is functionally inferior (16). Marrow-stimulation techniques, such as subchondral plate drilling or microfracture, have been reported to stimulate production of hyalinelike tissue with variable properties and durability compared to normal cartilage, but in many cases, these techniques tend to produce fibrocartilaginous tissue that will degenerate with time (17,18). Although osteochondral autologous transplantation and mosaicplasty can restore normal cartilage tissue, application is restricted to small defects, and some concerns exist regarding donor-site morbidity (18,19). On the other hand, autologous chondrocyte implantation, also known as the Peterson technique, is capable of restoring normal cartilage tissue but requires two surgical procedures (12,20).