chapter 11: Articular Cartilage Lesions in Patellofemoral Pain Patients

Patellar Articular Cartilage Healing

A healing response occurs after articular cartilage injury (66). In the case of superficial injury, the initial death of chondrocytes at the margin of injury is followed by increased metabolic activity of surrounding chondrocytes, but no significant change in appearance of the superficial injury (67).

Once full‑thickness loss of articular cartilage occurs, a more dramatic response occurs. There is predominantly Type I collagen formed initially, followed by a predominance of Type II (articular cartilage) collagen formation at 6 to 8 weeks (68) in rabbit knees. By 1 year, however, the defects in articular cartilage are comprised of fibrocartilage because of collagen predominance and loss of proteoglycan.

The patella will respond in a similar fashion. Once an Outerbridge Grade 3 to 4 lesion occurs, the defect will never fill again with the true articular cartilage. Therefore, the smart clinician will recognize that isolated shaving of an area of patellar articular cartilage, which is chronically overloaded, will not stop the progression of surface degradation. The concept in patient treatment, therefore, is to remove loose flakes of cartilage and perform abrasion of exposed subchondral bone after adequate relief of focal articular loading. In the case of chronic patellar tilt, lateral release alone may be sufficient to alter patellar tracking, but more extensive alteration of patellar alignment may be necessary to provide adequate relief of articular overload when there is widespread patellar articular cartilage loss. Anteromedial tibial tubercle transfer (69) is the procedure of choice to unload areas of excessive lateral patellar overload and cartilage destruction, thereby providing an environment for resulting fibrocartilage healing that will not necessarily lead to further erosion.

It is possible that relieving intraosseous hypertension may facilitate articular healing. Intraosseous pressure, as measured in the metaphysis, has been shown to be in direct correlation to rest pain in arthrosis of the knee (70). Intraosseous hypertension has been demonstrated in both osteonecrosis of bone (71, 72) and reflex sympathetic dystrophy of bone (73). Drilling or abrasion of an Outerbridge Grade 3 to 4 defect may both relieve pain and enhance the healing response by reducing intraosseous hypertension as in osteoarthritis.

Osteotomy of the proximal femur causes an immediate fall in intraosseous pressure (74) as well as relief of rest pain in patients with arthrosis of the hip (74‑77). It may be that biomechanical failure of articular cartilage results in alteration of load transfer to subchondral bone and secondary intraosseous hypertension. It is certainly possible that articular cartilage degeneration may lead to pain in this way. Pressure on softened, but intact, articular cartilage can cause pain in some patients, whereas pressure on normal articular cartilage will not. On the other hand, many patients with focal articular cartilage degradation and fibrillation (noted incidentally at the time of arthroscopy for another problem) have little or no pain referable to the anterior knee.

In clinical practice, it is most important to determine where pain is coming from, and then try to identify and modify the pathomechanics leading to the painful disorder. It is clear that softened articular cartilage alone does not always cause pain.




Inside Chapter 11: