chapter 11: Articular Cartilage Lesions in Patellofemoral Pain Patients

Open Chondromalacia

FISSURES

Fissures may be multiple or single, relatively superficial or extending down to sub­chondral bone (Fig. 11.3). They are nearly always associated with adjacent softening and represent the second stage in the evolution of chondrosis. Once the surface layer has been interrupted, the cartilage lesion would appear to be irreversible as surface le­sions do not heal. The clinician must recall, however, the teachings of Goodfellow et al. (20) that "surface degeneration changes do not cause patellofemoral pain until they have progressed to exposure of bone upon an area of habitual patellofemoral contact."

Fibrillation of articular cartilage usually follows fissuring with progression to ulcer­ation in some cases. When fibrillation progresses to a larger area of the patella (greater than 1/2 inch in diameter), bone may begin to experience abnormal pressure increases or irritation from flaps of cartilage that are placed under pressure, much as a flap of meniscus can cause pain.

ULCERATION

By this stage, there is localized loss of cartilage substance, more or less extensive, which eventually exposes the dense subchondral bone. When it is extensive, the bone has a polished appearance and is said to be eburnated. This is the final stage in cartilage de­struction.

Chondrosclerosis

Here the process seems reversed. Instead of finding softened cartilage, the surgeon finds cartilage that appears to be abnormally hard, not depressible, and presenting a translu­cent, yellowish, glazed appearance. We believe that the term chondrosclerosis is ap­plicable to this condition as it seems to be the opposite of chondromalacia. At the same time, the histology would seem to support this definition. Even though this abnormality appears to be the opposite of chondromalacia, it has similar significance in that it rep­resents a complete loss of the normal qualities of articular cartilage, which implies a con­siderable diminution in its functional capacity in transferring load to subchondral bone.

        

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