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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 . 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.

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.

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.

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 . 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 . 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.

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.

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