chapter 11: Articular Cartilage Lesions in Patellofemoral Pain Patients


Closed Chondromalacia

To better understand the degenerative process, it is necessary to approach, insofar as possible, the earliest lesion. In this case, the localized nodule with intact surface (Outerbridge Grade 1) characterizes the first phase of chondromalacia.


The surface of the cartilage, in general, shows regressive fibrous metaplasia (53‑55) of the surface cells that appear to be more flattened than normal. Some superficial fissures may be evident. The deeper layer of cartilage shows what can best be described as edema with apparent increase in the quantity of ground substance. There is an unmasking of collagen fibers and a diminution of ground substance staining with Alcian blue, toluidine blue, and safranin O. However, the ground substance remains PAS‑positive. The chondrocyte lacunae retain a normal appearance. Hirsch (14) has shown that these histochemical changes represent a diminution in the glycosaminoglycan content, which accounts for the softening of the cartilage and its decrease in resistance to compression.


The percentage of strictly intact surfaces steadily decreases as one progresses from naked eye appearance through optical, scanning electron, and transmission electron microscopy (Fig. 11.10). With this progression, the criteria for surface integrity become increasingly strict. With the light microscope, one is measuring defects in tens of microns, whereas with the electron microscope, defects of a few angstroms are apparent. The absence of fissures, however, does not exclude other alterations such as edema, in which the superficial fibers are separated. This might explain the decrease in tensile strength over the entire zone of softening. The superficial microfibrillar covering has frequently disappeared and collagen fibers running parallel to the surface are often separated by electron transparent lacuna zones. These zones are bordered by microfibrillar condensation, which may foreshadow fissures running parallel to the surface. At other times there may be areas of more or less irregular osmiophilic microfibrils.

The area of softening is situated between the superficial zone (C1), more or less normal but always macroscopically intact, and the deep layer (C3), which is also normal to electron microscopic examination. The area of abnormality then is localized in the intermediate zone (C2) and, at least in the beginning, in the superficial portion of this zone. Initially the lesion is relatively well defined. This localized focal picture appears to be consistent in degenerating cartilage. All three constituents of cartilage (chondrocytes, collagen fibers, and ground substance) demonstrate abnormalities.


In these earliest lesions, signs of cellular hyperactivity abound. These are expressed primarily at the cytoplasmic level. There are the following cytoplasmic alterations that may demonstrate increased cellular activity.

  1. Increase in pinocytosis (Fig. 11.11).
  2. Increase in the number of cytoplasmic villi and fine filaments (Fig. 11.12).
  3. An abundance of glycogen or ribosomal granulation (Fig. 11.13).
  4. Development of the Golgi apparatus (Fig. 11.13).
  5. Encirclement of the cell by proteoglycans, which in turn, are ringed by granular or amorphous microfibrillar material (Fig. 11.14).
  6. Cellular multiplication and cloning (Fig. 11.15).
  7. Increase in the number of dense bodies of all sizes and character (lipid, lysosomal) (Fig. 11.16).
  8. Dilatation of the endoplasmic reticulum (Fig. 11.17).
  9. Mitochondrial distention, with disappearance of cristae and, occasionally, rupture (Fig. 11.18).

The last four signs imply the tendency toward degeneration. However, cells that are typically degenerating or, more important, necrotic, occur infrequently in these earliest lesions. It would, therefore, appear that the initial phase of cartilage disorder is char­acterized by a proliferative reaction manifest by increased cellular activity. Stimulated by increased load, the chondrocytes lose their quiescent appearance, and increase me­tabolism and secretion, as if this defensive reaction would reinforce those structures that are endangered.


The collagen component of the cartilage matrix shows a variety of abnormalities. Those encountered in the earliest lesions include:

  1. Angulation and abrupt change of direction, sometimes more than 90 degrees, of a whole series of fibers, which suggests a process of compression and disorganization (Fig. 11.19).
  2. Inequality of fiber diameter (Fig. 11.20).
  3. Anomalies in both diameter and orientation of fibers that are involved in a disorga­nized process (Fig. 11.21).
  4. Loss of the usual functional orientation, loss of striation and fragmentation, and dis­sociation of fibers by edema (Fig. 11.22).
  5. Fiber disintegration (Fig. 11.23).


This seems to increase in volume and appears more abundant. Mankin and Thrasher (56) have noted a 9% increase in the water content of osteoarthritic articular cartilage, and this may constitute the basis for cartilage edema (Fig. 11.24), which is character­istic of chondromalacia. Occasionally, the surgeon can find crevices or small fissures, particularly in those cases that are clinically more developed. Some of these fissures may be interpreted as artifacts (Fig. 11.25), but others are lined by material that is elec­tron dense and amorphous (Fig. 11.26). Other fissures show margins that have a dif­ferent aspect, a fibrillar border with random orientation (Fig. 11.27). The authenticity of these fissures is without doubt, because some of them have a cystic appearance, even with parietal proliferation protruding into the cavity. All these matrix lesions are rela­tively discrete, particularly in the early cases. This must not be forgotten in the inter­pretation of the ultramicroscopic photographs. The clinician must not expect profound and spectacular changes in incipient lesions. These lesions are characterized more by their repetitive nature than their intensity, which makes interpretation potentially con­troversial.



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