chapter 11: Articular Cartilage Lesions in Patellofemoral Pain Patients
PATELLAR ARTICULAR CARTILAGE BREAKDOWN
Patellar articular cartilage does not appear, from an anatomic or functional point of view, to be different from articular cartilage found in any other diarthrodial joint. Its function, nourishment, gross and microscopic anatomy, and relationship to synovium and subchondral bone is typical of articular cartilage in general. With this background, it would seem that a detailed study of the various stages of patellar articular cartilage degeneration may lead to improved understanding of articular cartilage and arthrosis in general.
The terms chondrosis, to signify a disorder affecting only the articular cartilage, and arthrosis, a disorder affecting all three components of the patellofemoral joint (30) (cartilage, bone, and synovial membrane), may be helpful. For ease of understanding, we use the term arthrosis when there is exposed bone in the joint.
Patellar articular cartilage presents two principally different modes of degeneration. Cartilage softening (chondromalacia) of the lateral facet appears to be secondary in most cases to prolonged patellar tilt and secondary compression with eventual arthrosis. Seedholm et al (31) noted that this breakdown occurs on areas of the patella corresponding to what articulates in the 40‑ to 80‑degree knee flexion range. Increased density of subchondral bone appears early in the disorder, after the initial cartilage changes. Initial cartilage softening often progresses to fissure formation, ulceration, and arthrosis.
Chondromalacia of the medial facet appears to be somewhat different. It may be secondary to deficient contact or to a combination of compression and shearing forces particularly in knee flexion. Iatrogenic medial facet chondromalacia or arthrosis may be a consequence of overzealous medial imbrication (Figure B), or excessive medial transfer of the tibial tubercle. Müller (32) pointed out that relatively little is known about nutritional factors that might lead to medial facet articular cartilage breakdown. Goodfellow et al (20) differentiated between "age‑dependent surface degeneration" on the medial facet, and "basal degeneration" on the ridge separating the medial and odd facets. Radin (21), Abernathy et al (22), and others believe that central medial facet chondromalacia is not a significant entity causing pain in most patients. Nonetheless, a chronically unloaded medial facet will deny its articular cartilage an appropriate mechanism of synovial fluid nutrition (33) and in patients with malalignment or trauma, this may lead to eventual extension of medial facet degeneration and symptomatic arthrosis. If changes in bone are present, the radiograph more often shows decreased density rather than an increase in the subchondral bone of the region affected. The surgeon must consider the specific alignment pattern and how it might affect patellar (and trochlear) contact (Fig. 11.1) in different degrees of knee flexion.
A review of patellofemoral joint contact patterns reveals that the secondary ridge marks the medial edge of the contact zone from 20 to 90 degrees. Progression to full flexion involves sliding across the convex secondary ridge that may bring it briefly into high pressure contact with the convex femoral condyle. It is also likely that considerable shear forces are developed as the contact area traverses the ridge as suggested by Goodfellow et al (20).
Several authors (20, 34‑36) have pointed out the tendency for cartilage that is habitually out of contact with other articular cartilage to undergo surface fibrillation. This age‑dependent, nonprogressive, surface change does not usually tend to develop into an advanced cartilage lesion (21) with eventual full thickness cartilage loss and bony eburnation. Autopsy series have shown these lesions to increase in frequency with age. The odd facet represents an area of habitual noncontact. Akizuki et al (37) noted that cartilage from low weightbearing areas is stiffer than that from high weightbearing areas. It is, therefore, not surprising that the medial facet is also a site for nonprogressive age‑related surface changes. The lack of recognition of this form of cartilage abnormality may explain the predominance of medial facet chondromalacia described in many series. Of particular interest, along these lines, is the report of Marar and Pillay (38) on the low incidence of chondromalacia of the patella in a series of autopsies in Chinese people. In Oriental people, the odd facet is not a habitual noncontact area because of the frequent squatting, characteristic of this population. The observation of Hoaglund et al (39) on the low incidence of osteoarthritis of the hip in South Cantonese Chinese and its relation to movement and, therefore, also to decreasing habitual noncontact cartilage, may have some bearing on this subject. One must, however, consider other factors also, including the overall smaller stature of many Oriental people.
There would seem, under normal circumstances, to be a possible conflict between the secondary ridge and the femoral condyle. Because not everyone has chondromalacia of the medial facet, other factors must play an important role. There is considerable variation in the prominence of the secondary ridge. Several authors (40, 41) have called attention to a prominence of the medial ridge separating the medial trochlear facet from the femoral metaphysis. This has been called the Outerbridge ridge, after the surgeon who first drew attention to its significance. There is no clear evidence, however, that this ridge is important in patellofemoral pain patients.
Finally, it is important to remember that articular cartilage injury may occur at the time of arthroscopy (42) or other knee surgery. Anti‑inflammatory agents (43), hemarthrosis (44), immobilization (45‑47), irrigating solutions (48, 49), iatrogenic trauma, local anesthesia (49), and corticosteroids (50) can have profound effects on patellar articular cartilage. We have found evidence of considerable articular cartilage loss and subchondral bone damage (resulting in osteochondral loose body formation) after overzealous laser chondroplasty. After arthroscopic or open surgical intervention, a suitable period of time should be allowed before returning to vigorous athletics (42) so that articular cartilage metabolism and function can stabilize.
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