chapter 11: Articular Cartilage Lesions in Patellofemoral Pain Patients
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.CHONDROCYTES
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:
At the level of the nucleus, important changes are evident, which include:
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.
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.
Inside Chapter 11: