chapter 11: Articular Cartilage Lesions in Patellofemoral Pain Patients

MECHANICAL PATHOGENESIS OF ARTHROSIS

There is generally a mechanical reason for patellar cartilage breakdown, as has been demonstrated in earlier chapters. This often consists of excessive pressure from trauma or abnormal alignment. Aging facilitates either of these processes. The initial lesion is perfectly isolated and localized in the superficial half of the intermediate zone. It is detectable both clinically and radiologically from its beginning and is accessible by biopsy. This cartilage lesion is characterized by nodular edema, which is the beginning of the degenerative process that leads to arthrosis. Microscopic studies have demonstrated that clinically apparent softening is due to a change in the ground substance and disorganization of the collagen network. The superficial layer (C1) is undergoing fibrous dedifferentiation. Even if the surface has a normal appearance, it is qualitatively not less changed than the deeper layer and participates in the softening effect, which explains the blister appearance. The intermediate zone (C2) shows alterations in collagen, cells, and ground substance, with perhaps some evidence of the chondrocytes themselves changing earliest.

Origin of Arthrosis: Its Mechanical Nature

It is likely that excessive pressure from tilt/compression bears the primary responsibility for the more severe lateral facet lesions encountered (57). Trauma, dysplasias with diminution of load‑bearing surfaces, incongruence of load‑bearing surfaces, and static disorders (genu varum, genu valgum, and so on) all enter into a group in which joint breakdown relates to excessive articular cartilage compression. Abnormal articular cartilage loading may eventually cross the threshold of cartilage resistance and lead to the failure of healthy cartilage under conditions of mechanical overload. Deficient medial cartilage contact pressure created by abnormal alignment also leads to cartilage breakdown. This is frequently less severe (although common) than the lateral facet lesions created by overload, and probably requires intermittent shear or compression to cause breakdown (57). Certain occupations and activities also increase the risk of patellofemoral degeneration. Kivimaki et al (58) found that kneeling activities (such as carpet and floor laying) increase the risk of patellar osteophytosis.

Breakdown of articular cartilage of the femoral trochlea occurs commonly as a result of direct trauma. Dislocation of the patella leads to an articular cartilage defect on the lateral trochlea, probably as a result of patella relocation in most cases. Trochlear degeneration can occur in other ways also. Butler‑Manuel et al (59) noted that there is increased scintigraphic uptake in the femoral trochlea of patients following patellectomy.

Lesions created in this manner often lead to arthrosis. This group of disorders symbolizes the pathologic action of excessive pressure on cartilage, whatever form that may take, whether a single severe traumatic overload, moderately excessive and repetitive microtraumatic episodes, continuous pressure of abnormal tilt, excessive pressure associated with facet incongruity, or the excessive pressure of high unit load on reduced surface area, as in a dysplasia. Areas of chronically deficient load (at the central and medial patella) may soften from cartilage malnutrition and eventually break down spontaneously in areas that experience only intermittent normal loads.

 

 

        

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