chapter 11: Articular Cartilage Lesions in Patellofemoral Pain Patients

Open Chondromalacia


When the surgeon biopsies an area of malacic cartilage with the surface apparently in­tact just adjacent to chondromalacia with the surface fissured, he/she is struck by two facts. First, changes affecting each of the constituents of the articular cartilage are more exaggerated and second, the distribution of the kinds of lesions has shifted to a pre­dominance of degenerative lesions. This increase in severity of the abnormality affects each of the constituents of the cartilage.


Next to cells showing hyperactivity, as described in the previous section, there is an increase in degenerating and even necrotic cells. Degeneration now exceeds proliferation. At the cytoplasmic level there is:

  1. A tendency toward disappearance of organelles (Fig. 11.28).
  2. A granular microfibrillar or amorphous homogenization and dilatation of endoplasmic reticulum (Fig. 11.29).
  3. A more or less extensive degeneration of the cytoplasmic membrane (Fig. 11.30).
  4. At the extreme, a disintegration of the cytoplasm, with rupture and fragmentation (Fig. 11.31).

At the level of the nucleus, important changes are evident, which include:

  1. Alteration of the chromatin (Fig. 11.32).
  2. A thickened and greatly invaginated nuclear membrane (Fig. 11.33).
  3. Pyknosis.
  4. Disappearance of the nuclear membrane‑the principal sign that allows confirmation of necrosis.
  5. Finally, fragmentation and rupture of the nucleus, which may involve entire clones (Fig. 11.34).


In general, the clinician sees both a quantitative and qualitative increase in the early changes previously described. The collagen fibers are more dissociated and fragmented, the degree of severity paralleling the severity of edema. These changes are maximal in the exuberant lesion of the medial facet where the intermittent pressure and excessive shearing forces do not seem to exercise the same degree of restraint evoked by the more constant aggressive pressure on the lateral facet.


The edema is more marked, with its development paralleling the clinical importance. The change is one of degree rather than character. One exception should be noted. There are some cases of considerable edema involving the medial facet, particularly the region between the medial and odd facet. The cartilage remains closed and the ultramicroscopic examination shows little or no chondrocyte necrosis, even though the cells themselves show degenerative changes. It is probable that the chondrocytes are protected from necrosis because of the anatomical situation that prevents the excessive forces from being continuous.

As the cartilage lesion progresses from the incipient stage into the well‑developed stage, the distribution of changes of all three elements is modified. Early, the middle of the edematous nodule that is the site of our biopsy is characterized by a mixture of changes where proliferative lesions predominate. Cellular necrosis is very rare. Fibril separation by edematous ground substance remains discrete as long as the lesion is small and not particularly soft. By Stage II, and particularly where softening is important, the surgeon sees involvement of the entire intermediate zone with beginning of proliferative changes affecting the C3 layer as well. The necrotic and degenerative lesions become more apparent and affect more chondrocytes. These lesions are more concentrated in the center of the softened area where one might suppose the zone of compression is maximum. Surrounding this central zone of predominant degenerative lesions is a circle of proliferative abnormalities. Finally, all 'this reactional regenerative peripheral activity disappears and is replaced by a massive collar of cartilage necrosis surrounding the ulcerative lesion.

  1. Initially, the excessive pressure elicits a response on the part of the cartilage in the sense of increased chondrocyte activity that appears to be an attempt to counter the increase in mechanical load. This increase is manifested by increased metabolism, increased proteoglycan synthesis, accumulation of filaments, cellular multiplication (mitoses), and formation of clusters and clones. These lesions appear essentially pro­liferative and reconstructive. The quiescent cells are stimulated and resume activ­ity. This would correspond to an initial reactional and proliferative phase. It is even conceivable that this might be successful if the inciting cause is minimal or if the excessive pressure is terminated.
  2. Later, there will be failure of increasing numbers of chondrocytes and fatigue rupture of the fiber network of the matrix. Initially, the central, predominantly degenerative and necrotic zone is surrounded by a proliferative reaction that is progressively pushed toward the periphery and the depth of the articular cartilage. This is the phase of de­ generation and necrosis characterized by increasing numbers of cellular necroses, in­ crease in softening of the cartilage, and destruction of the collagen network. It is, of course, possible that this degenerative phase proceeds directly from a severe injury without passing through the initial proliferative phase. It might also be evident early in the disorder if the cause is overwhelming or the proliferative response insufficient.
  3. Finally, there is fragmentation of the matrix. Eventually, the subchondral bone be­comes exposed and eburnated. This is the terminal destructive phase of arthrosis.           Even the cartilage that borders the ulceration dies progressively, leading to expan­sion of the defect by means of mechanical pressure.

There is one additional observation that has some bearing on this process. The sur­geon can see dead yellow cartilage, with reduced elasticity but apparently preserved when it is situated in an area that is not submitted to mechanical constraint. We see this on the medial facet in patients with lateral subluxation and excessive lateral pressure as well as the superior third of the patella in patients who have limitation of flexion to less than 90 degrees, and therefore, this area does not come into contact (Fig. 11.35). This observation accents the necessity of the mechanical factor for the complete destruction of cartilage.


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