chapter 11: Articular Cartilage Lesions in Patellofemoral Pain Patients


There is a lesion essentially the reverse of chondromalacia, but much less common. The cartilage becomes extraordinarily firm under the effect of mechanical pressure. Therefore, this sclerosis may represent one route of progression instead of the more common route of fissuring, fragmentation, and ulceration. The electron microscope shows that the surface is intact and, in general, is covered by a thin amorphous or microfibril electron dense material. The network of parallel fibers in C1 is very tight and very dense (Fig. 11.36). Ground substance is scarce, and there is no trace of edema. The collagen fibers form a dense network intermingled but frequently with a general preferential direction (Figs. 11.37, 11.38). The lesion is, with regard to the relative distributions of collagen and proteoglycan, not fibrocartilage.

The chondrocytes in all cases of chondrosclerosis have certain characteristics in common. They take on an aspect of storage cells with an excess of microfibrils (Fig. 11.39) and diverse vacuoles, some containing dense black globules (Fig. 11.40) and others, myelin‑like bodies. Frequently, glycogen‑forming granules are heaped up in thick layers spread throughout the whole cytoplasm (Fig. 11.41). These cells often have an aspect of hyperactive secretory activity and secrete quantities of proteoglycan, which is found as a crown surrounding the cell. This crown is itself limited by dense thick microfibrillar or amorphous layer (Fig. 11.42). Finally, there is a great deal of cellular multiplication with double cells and grouping of more numerous cells that show the same characteristic of excess secretory activity (Fig. 11.43). On the other hand, there is little evidence of necrosis. Chondrosclerosis seems to be very different from chondromalacia, not only as to the anatomical and clinical appearance, but also at the ultramicroscopic level.



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