Patellofemoral Pain: An Enigma Explained by Homeostasis and Common Sense

Chondromalacia Patella—Not the Problem

If chondromalacia is the source of AKP, what is it about conservative treatment that “cures” or even improves structurally softened articular cartilage? How can mere activity modification and exercise result in symptom resolution secondary to improvement in cartilage structure? There is no evidence of this occurring. Nevertheless, patients with this “diagnosis” commonly respond to nonoperative treatment.

Dr. Dye has had personal experience in the possible genesis of AKP in CMP. When he was 46 years old, he allowed his asymptomatic knees to be arthroscopically inspected, without intra-articular anesthesia, so that a neurosensory map of their internal components could be drawn (Figure 2).³

Surprisingly, the examination revealed grade 3+ CMP in both knees. During probing of the “pathologic” surfaces, he reported no sensation at all (Figure 3).⁴

Given that articular cartilage is aneural, this was no surprise. CMP alone cannot act as a nociceptive trigger. Although a deficient articular surface may transmit excess load to highly innervated subchondral bone, when excess load fails to cause a loss of homeostasis, symptoms are unlikely. Consistent and concurrent with this finding, each knee appeared normal on technetium 99m–methyl diphosphonate bone scan.

More than 18 years after this neurosensory mapping study, both knees are still asymptomatic, despite substantially reduced proteoglycan content of patellar articular cartilage bilaterally, recently detected with T1-ρ magnetic resonance imaging (MRI), the current favorite of many who use MRI to track early osteoarthritis (Figure 4).

Remarkably, the musculoskeletal system can painlessly deliver millions of load transfer cycles during overt structural failure of one of its main components.⁴ We think Dr. Dye’s experience is not an isolated case and that asymptomatic CMP is common. Research data and clinical experience confirm that CMP does not in and of itself play a significant role in the genesis or resolution of symptoms in the typical patient with AKP.

Conversely, during the arthroscopy without intra-articular anesthesia, Dr. Dye discovered quickly and dramatically that the synovium and the fat pad were the most sensitive tissues. Light touch on unanesthetized synovial and fat-pad tissues evoked “involuntary verbal exclamations” (Figure 5).³

Since then, it has been personally and professionally apparent to him that synovial and fat-pad tissues are potent sources of AKP.

Recurrent impingement of the synovium can result in hypertrophy producing thousands of cells instead of the normal few (Figures 6, 7).

This hypertrophied tissue can impinge between the patella and trochlea as well as around the fat pad. This is a very common cause of persistent AKP in our experience most commonly independent of alignment and chondromalacia.

When MRI of a patient with AKP shows CMP be cautious not to conclude this structural condition is the direct cause of pain. When overload results in loss of homeostasis, breakdown products of damaged articular cartilage can contribute to symptomatic synovial inflammation. In addition, the damaged articular surfaces may fail to efficiently minimize joint friction and load transmission to subchondral bone. Chondromalacia alone, however, cannot be linked to pain.

Malalignment—Not Often the Problem

That brings us to the historically popular concept of patellofemoral “malalignment/maltracking” as a primary cause for AKP. Although this etiology appeals to many in the orthopedic and physical therapy community,^5,6 we and others^7-10 reject the notion that it is common. What objective malalignment changes occur when a patient becomes asymptomatic without operative treatment? Imaging measures of malalignment do not change significantly after effective treatment. In studying patients with AKP in the mid 1980’s, Dr. Dye found no difference between 104 adults with PFP and 79 age- and activity-matched controls with respect to 9 objective indicators of malalignment, including quadriceps (Q) angle, congruence angle, sulcus angle, and subchondral sclerosis of the lateral patellar facet.

The clinical success of McConnell taping, which often produces instant pain relief by using tape to apply loads to the patella and peripatellar soft tissues, is sometimes cited as evidence that maltracking or malalignment is the cause of the pain. We disagree with that conclusion. This pain relief more likely results from relieving pressure and tension on sensitive soft tissues, including synovial, fat-pad, and retinacular tissues—equivalent to, say, using a finger to pull inflamed and swollen bitten cheek tissues away from the teeth, which might repetitively traumatize them. In both cases, healing is not spontaneous; but relieving the sensitive tissue of the exacerbating load is the common principle. We think subtle changes in the tension and impingement of synovial and fat-pad tissues can have profound effects on AKP. Pain relief with McConnell taping no more proves that the source of the pain is malalignment or maltracking than a finger pulling away inflamed and swollen cheek tissues proves that cheek pain is caused by malocclusion.