Cartilage

Carlos A. Guanche MD

Key Points

Full-thickness articular cartilage defects have a limited capacity to heal. Thus, articular cartilage lesions and osteochondral defects in any joint present a challenging problem.
Cartilage lesions are less likely to be seen in the glenohumeral joint than in the knee, therefore there has not been extensive research on shoulder cartilage repair.
Making the diagnosis without the benefit of an arthroscopic visualization of the joint can be problematic.
Mechanical injuries include direct trauma to the cells and matrix, causing an acute disruption of the surface, or more subtle changes attributable to damage of the matrix macromolecules.
Biologic injuries include metabolic abnormalities, most commonly osteoarthritis, but also avascular necrosis and a variety of osteochondral injuries.
Although the use of gadolinium-enhanced arthrograms has improved diagnosis, a significant portion of lesions are not identified prospectively.
The goal of treatment is often to restore durable hyaline cartilage through a practical and minimally invasive approach (preferably arthroscopic), which is associated with minimal morbidity postoperatively and in the long term.
The end-stage management of many cartilage lesions is a replacement procedure. A titanium coated shaft portion with an articular bearing surface of cobalt-chrome alloy is implanted in the central articular defect and recreates the circumference of the humerus.
The goals of arthroscopic debridement are primarily to relieve pain and secondarily to improve function. The removal of loose tissues that cause pain and impingement helps to achieve these goals.
The decision making process for arthroscopic debridement is radiographic analysis. The proper views are critical to allow an appropriate diagnosis. These include an anteroposterior (AP) view in internal rotation, an AP view in the scapular plane with the arm in external rotation and slight abduction and an axillary view.

Articular cartilage lesions and osteochondral defects in any joint present a challenging problem to both patient and physician. The critical issue is that full-thickness articular cartilage defects have a limited capacity to heal at any age. Many procedures have been described to improve the joint alignment, induce reparative tissue proliferation or provide cartilage tissue that is more nearly normal. The bulk of this work has occurred in lesions about the knee, with very little research in any other joints. The use of autogenous and allograft reconstruction of focal defects has been extensively studied in the knee (1,2,3). Other techniques including abrasion arthroplasty, drilling, and microfracture have been described for smaller lesions (4,5,6). There is a paucity of research that discusses the problem of cartilage lesions about the glenohumeral joint and provides treatment recommendations, with the exception of a few case reports and small series of patients.

Certainly, the problem is less likely to be seen about the glenohumeral joint and therefore impacts the lack of need for extensive research. Complicating the problem is that unlike the knee, there is significant difficulty with access to the joint when a lesion is identified. Furthermore, the management options are not as obvious as a result of the lack of large-scale research.

There is a spectrum of pathology encountered with the lesions ranging from simple chondral delamination injuries to more extensive osteochondral injuries and culminating in arthritic degeneration of the glenohumeral joint. All of these lesions can be encountered in the typical active population commonly seen in the average sports medicine practice.

Making the diagnosis can also be problematic without the benefit of arthroscopic visualization of the joint. Several series point to the need for improved imaging techniques that allow better determination of the articular surfaces in a prospective fashion and this area also requires further study (7,8). In addition, the concurrent association of cartilage defects with the status of other areas of the joint, specifically, the rotator cuff and impingement is poorly understood both with respect to etiology and treatment (9,10).

After the diagnosis has been made, there are many options available for treatment if the management algorithms follow those historically applied to knee pathology. There are a variety of autogenous techniques including osteoarticular harvest with subsequent transplantation as well as the more complex technique of biologic regeneration of cartilage (2). Allograft applications are also available and those include fresh and preserved specimens. In addition to the biologic resurfacing techniques, there are also devices that allow for resurfacing using metallic and other materials. Finally, in cases of limited damage or sometimes in the face of extensive degeneration of the cartilage surfaces, arthroscopic techniques can be employed primarily for symptom amelioration (9,11,12,13).

Impact of Cartilage Lesions

The spectrum of pathology includes a gradation in the severity of cartilage damage beginning with simple delamination of a small area and ending with complete degeneration of the articular surfaces, i.e., osteoarthritis.

Although the glenohumeral joint surface geometry historically has been considered less of a stabilizing factor as a result of the smaller surface area of the glenoid in comparison with the humeral head and the apparent shallowness of the glenoid, technology has now given us a new perspective. Classically, most studies of the joint have analyzed congruency with radiographs, thus underestimating the degree of congruity afforded by the articular cartilage because only the bony surfaces were visualized and assessed (14). If only the subchondral bone is analyzed, there appears to be less conformity within the joint. With the addition of the articular cartilage, the effective congruence of the joint is much greater.

As an example, Kelkar et al. (14) analyzed a group of glenohumeral cadaveric joints. In their analysis, the average radii of the humeral head and glenoid articular surfaces were 25.5 and 27.2 mm, respectively. The average difference between the two radii was 1.7 ± 1.5 mm. When the same technique was employed to analyze the subchondral bone, the radii of curvature of the humeral heads and glenoids were 25.2 and 33.4 mm, respectively. These findings lend more importance to the articular cartilage, or more specifically the preservation of this tissue. It appears that the articular cartilage of the glenohumeral joint is a factor in the maintenance of stability in the joint. Given the inherently unstable nature of the joint with its small surface area, it is paramount to save as much cartilage as possible in order to preserve normal joint function.

Another consideration is the impact of associated coexistent disease processes in the shoulder. More importantly, focal articular lesions are often found incidentally at the time of arthroscopic evaluation of the joint for other presumptive diagnoses. This problem has been seen less frequently as a result of the improvements made in prospective diagnosis with the use of MRI techniques, particularly those employing gadolinium-enhanced arthrograms.

Several studies allude to the coexistence of other disease processes with cartilage lesions, however, especially more advanced lesions seen with osteoarthritis (8,9,10). In their study, Feeney and colleagues assessed 33 cadaveric shoulder joints and documented the incidence of rotator cuff tearing and cartilage lesions (10). Articular cartilage degeneration was almost twice as frequent in the group with rotator cuff tears as in those without tearing (10).

Another study revealed that in a series of 52 patients undergoing surgery for subacromial impingement syndrome, humeral cartilage lesions were found in 29%, of which four lesions were subtle and eleven were marked (9). In the glenoid, 15% were found to have lesions with three subtle and five marked. In essence, patients with clear surgical indications for impingement surgery may have coexistent cartilage lesions in up to one third of instances. This consideration should be taken into account at the time of preoperative discussion with the patient, as other procedures may be essential for complete treatment.

Types of Lesions

Cartilage repair response has been the focus of investigations for more than 250 years. In 1742 Hunter noted that “ulcerated cartilage is a troublesome thing … once destroyed it is not repaired (15). Since that time, the observations made by Hunter have been reiterated by nearly every scientific study on the topic. The lack of predictability of repair of cartilage is attributable to the many factors that often come together in a specific injury. Some of the factors include the precise injury, the age of the individual, the condition of the joint before injury, the quality, extent, and durability of the repair and the long-term function of the joint.

The types of injuries can be divided into mechanical and biologic. The mechanical types of injuries include direct trauma to the cells and matrix causing an acute disruption of the surface, or more subtle changes attributable to damage of the matrix macromolecules. This type of damage occurs with surgical disruption of the synovial membrane, infection
and other inflammatory diseases, immobilization and possibly joint irrigation (15).

In cases of blunt injury, the degree of disruption is often underestimated in the acute phases. The response of articular cartilage to penetrating injury depends on the depth of injury such that injuries limited to cartilage elicit a different repair response than injuries involving cartilage and subchondral bone. Likewise, blunt trauma can have much more significant impact than is acutely appreciated as a result of the consequent cell injury and effect on the cellular matrix, as well as any injury to the subchondral supporting bone (16).

The biologic injuries include metabolic abnormalities, most commonly osteoarthritis, but also avascular necrosis and a variety of osteochondral injuries that damage the articular layer indirectly as a result of the collapse of the supporting structures. For example, MRI analysis in degenerative joint disease, osteochondritis dissecans, and avascular necrosis has shown that the subchondral region shows reactive enhanced vascularization and heightened metabolism with insufficient repair (17).

One particular disease process that deserves further mention is that of avascular necrosis because the humeral head is the second most common site of nontraumatic osteonecrosis, after the head of the femur (18). In humeral head osteonecrosis, subchondral osteolysis occurs in the superior portion. When resorption of subchondral bone is extensive, it appears that even ordinary forces transmitted across the joint will lead to subchondral fracture and humeral head collapse (18). The likelihood of this collapse and the consequent degenerative changes that would occur make this disease process one that must be addressed more expediently than other cartilage lesions.

The treatment of specific injuries is impacted by the underlying nature of the cartilage injury. The best outcomes are obviously in isolated lesions that have a clear, mechanical etiology without any underlying metabolic abnormalities. The discussion of the factors involved is beyond the scope of this chapter, but the reader is directed to the appropriate references (14,19,20).

Separate consideration should be given to osteoarthritis, as there are clear surgical indications in the treatment of the disease in the glenohumeral joint (without prosthetic replacement). The arthroscopic management of this problem, if performed in the appropriate patient, has been shown to provide significant improvement in symptomatology (11,12,13,21).

Diagnosis of Cartilage Lesions

Much effort has been directed at the development of imaging techniques that effectively diagnose cartilage lesions in the shoulder. The thrust of the research has employed a variety of magnetic resonance imaging techniques to delineate not only the actual lesions, but also something about their physiology. It is well established that cartilage functions as the load-bearing surface in the joints of the musculoskeletal system. Major macromolecules in cartilage are collagen Type II and proteoglycans. Although proteoglycans provide much of the compressive stiffness through electrostatic repulsion, collagen provides tensile and shear strength. Several studies have shown that the earliest stages of cartilage degeneration are primarily associated with loss of proteoglycan and minor changes in collagen structure (22). In one study, bovine articular cartilage was analyzed with a variety of MR parameters including T2 relaxation rates and spine-lattice relaxation times in the rotating frame (T1ρ) mapping method (23). The findings included a significant correlation between the changes seen on T1ρ mapping and the sequential depletion of proteoglycan. Studies like these have served to expand the base of knowledge with regards to grading of articular lesions. Although arthroscopy is the so-called gold standard at this point for final determination of the management of these lesions, it would be ideal to have a noninvasive modality that fully assesses the lesions.

In the clinical setting, it is important to be able to delineate the presence of cartilage lesions with some certainty. There are several studies available in the literature that give some guidance (7,8,24). In one study, a double blind prospective study of 15 patients with anterior shoulder instability were analyzed with respect to the efficacy of MRI versus arthroscopy in the evaluation of chondral or osteochondral lesions of the humeral head (24). MR produced 6 true positives, 5 true negatives, and 4 false negatives for an accuracy and sensitivity of 60% and 87%, respectively. Arthroscopy gave 8 true positives, 5 true negatives, and 2 false negatives, with a sensitivity of 80% and an accuracy of 87%. All lesions diagnosed with either method were regarded as positive by definition, with the result that the specificity was always 100%. The differences in diagnosis sprang from the false negatives. As a result of the variable ability to identify the cartilage lesions prospectively, it was advised that both of these methods should be employed to ensure the correct diagnosis, and hence the correct choice of treatment.

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