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chapter 11: Articular Cartilage Lesions in Patellofemoral Pain Patients

Initiation of Arthrosis

The evolution of cartilage breakdown demonstrates two distinct phases. The primary lesion is often in cartilage (chondrosis) without any radiologic evidence of bone reaction. The patella occupies a unique position in presenting us the opportunity to investigate fully joint breakdown from its inception. For all practical purposes, this phase passes undetected at the level of other joints, because the clinician normally waits for the second phase (arthrosis) before making the diagnosis. The second phase, arthrosis, is characterized by the appearance of bone remodeling with a triad of reaction: osteophytosis, cyst formation, and sclerosis. These are finally associated with "joint space narrowing" (articular cartilage loss). Even minimal "joint space narrowing" takes on added significance because there may be fissures and even ulcerations with a normal joint space on radiograph.

If we return to the very beginning of articular cartilage breakdown and to the true initiating lesion of the process, two questions should be asked: (1) Does the beginning involve the surface layer or the deep layer of cartilage?, and (2) Which of the three substances of cartilage is first affected, ground substance, collagen, or chondrocytes? We do not intend to carry out a general review of these questions, but limit ourselves to pointing out the contribution that this study of patellar pathology has brought to these problems.

SURFACE OR DEEP LAYER?

The deep layer of cartilage (C3) has consistently appeared normal. The intermediate zone is the site of a focal lesion where the surgeon sees evidence of abnormalities in all three of the cartilage constituents. At the cellular level there is a mixture of cellular hyperactivity and necrosis. The more advanced the lesion the more numerous the number of necrotic cells. On the other hand, degenerative type cells with overloading of the cytoplasmic matrix appear frequently. The fibers are of unequal diameter and, occasionally, lose their striation. They become fragmented and separated by amorphous lakes. They sometimes appear tortuous and disorganized. The ground substance appears increased in volume by homogeneous material, which shows little electron density. This disruption of the equilibrium between fibrillar material and ground substance, which predominates, recalls the concept of cartilage edema.

The C1 layer is macroscopically intact but, as Meachim (51) has pointed out, that which is intact to the naked eye may be fissured under the light microscope. It remains that we can see some cases in which the integrity of the superficial layer has been verified by both transmission and scanning electron microscopy. However, this integrity may be purely morphologic, and the several layers of fibrillar material that appear normal may be functionally quite different. The cells of the superficial layer may appear to be involuting and take on a fibroblastic appearance. The fibers may be separated by lacunar zones or micro‑fibrillar lakes of osmiophilic material, having a fibrinoid appearance. Any of these alterations could cause this layer to lose its mechanical role of containment, which may explain the blister or nodule formation at the surface in the early stage.

These observations make an answer to the question concerning the initial lesion, surface or deep layer, particularly difficult. It is possible that the first manifestations of cartilage alterations apply to both the superficial and intermediate layers (C1 and C2) at the contact zone of excessive pressure. It may be that the C1 lesion is more subtle and more difficult to substantiate.

WHICH IS THE FIRST ELEMENT AFFECTED?

Ficat (53) obtained cartilage biopsy specimens as early as possible in the disease process in order to approach the initial lesion of the disease. He always found abnormalities in collagen fibers, chondrocytes, and ground substance and felt that the surgeon should not separate one of these elements from the whole and hold it responsible for everything that followed. Anything that affects one of these elements inevitably affects the others. One can say the same for the relationship between matrix and chondrocyte. What affects the matrix must affect the cell and vice versa. The fact that there is evidence of abnormality in all three elements of articular cartilage at the very earliest stage argues for simultaneous involvement from the beginning. No one of these elements appears to be more affected than the other. The failure of any one can, in fact, lead to the eventual degradation of cartilage as a whole. Rupture of the collagen network allows abnormal compression of the cartilage and chondrocytes. This facilitates loss of ground substance and depletion of glycosaminoglycan, which, in turn, weakens support for the collagen fiber network. Disturbance of function of chondrocytes leads to diminution or complete cessation of production of both collagen and proteoglycans matrix, weakening each in its turn and leading to destruction of the whole. The whole process revolves around three fundamental interdependent poles; depletion of proteoglycans, rupture of the collagen network, and disturbance or suppression of chondrocyte function. It is likely that excessive pressure reacts in each of these spheres, upsetting the tissue as a whole and unleashing a vicious cycle that ultimately leads to diffuse cartilage destruction. Chrisman et al (60) hypothesized that initial release of arachidonic acid in traumatized articular cartilage might initiate a series of events leading to catheptic enzyme release and subsequent progressive articular cartilage degradation, presumably mediated by prostaglandins (61, 62).

Subchondral bone undoubtedly plays an important, and early, role in the production of patellofemoral arthrosis. Radin's work (63‑65) points out the importance of this layer in understanding patellar cartilage breakdown. Microfractures in subchondral bone lead to increased stiffness of this layer after healing and, therefore, the surgeon might expect diminished resiliency of this subchondral support layer. Stiffening of subchondral bone may lead ultimately to overloading of articular cartilage because of inadequate subchondral impact resistance.

The diarthrodial joint is a functional entity (30), comprised of articular cartilage, subchondral bone, and synovium held together by ligaments and capsule. What affects any of these components usually affects all.

 

        

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