What Causes Patellofemoral Pain Syndrome and Chondromalacia, Part II

Last week I shared a “unified theory of chronic knee pain” -- basically, that bad cartilage was involved much of the time.

Let me be clear what we’re talking about: diffuse, achy pain generally. There are other, more specific pains when a doctor pokes something and you go “ouch.” Different structures are probably involved there (e.g., I wouldn’t consider “patellar tendinitis” to be PFPS -- I could be wrong here -- because patellar tendinitis diagnoses a clear, identifiable problem).

Now what are some objections to this “unified theory”?

An MRI shows that my cartilage is fine but I have knee pain! So how can the source of pain be the cartilage?

Remember, a typical MRI takes a picture that is imperfect. (Two wood-frame houses may look identical in a photograph, but if the beams of one have been hollowed out by termites, they will not perform the same structurally.)

Initial cartilage damage associated with chondromalacia starts deep within the tissue -- and so, it appears, would not be detectable by a standard MRI.

In chondromalacia of the patella, the initial lesion is a change in the ground substance and collagen fibers at the deep levels of the cartilage. It is a disorder of the deep layers of the cartilage that involves the surface layer only late in its development. (Weinstein, Stuart L. and Buckwalter, Joseph A., eds. Turek’s Orthopaedics: Principles and Their Application.)

Some people with cartilage lesions have no pain, and others with lesions have pain -- if that’s the case, how can bad cartilage be to blame?

Partly the answer appears to be that thin cartilage becomes a problem at some point, despite a knee pain sufferer having a number of initially non-painful lesions:

A recent study proved that one can have as much as Grade III wearing without pain. So, pain is variable. The source of chondromalacia pain is not the articular cartilage itself, but the thinning of it, which transfers loads onto the underlying subchondral bone, which is pain-sensitive. (UCSF School of Medicine, Physical Therapy and Rehabilitation, on patellofemoral pain)

Another important thing to consider here, it seems, is the quality of the remaining cartilage. Recall that chondromalacia literally is an abnormal softening of cartilage. It may have minor wear and be soft (and hurt more), or may have more wear but be fairly stiff (in a good way) and resilient (and hurt less).

Still, if you have a lot of deep lesions, chances are good you have more pain than someone with less damage.

The severity of cartilage lesions detected at arthroscopy highly correlates with incident pain (Aaron, Roy K. and Ciombor, Deborah M. “Pain in Osteoarthritis.” Medicine and Health Rhode Island, July 2004) 

How can damaged cartilage cause pain if the tissue has no nerves?

The key thing to remember here: the source of the pain sensation isn’t the cartilage itself.

Because there are no nerves in cartilage itself, the pain must emanate from subchondral bone, which is experiencing deficient conduction of stress through mechanically inadequate cartilage. ... Fibrillation of articular cartilage usually follows fissuring with progression to ulceration in some cases. When fibrillation progresses to a larger area of the patella, bone may begin to experience abnormal pressure increases or irritation from flaps of cartilage that are placed under pressure. (Fulkerson, John Pryor. Disorders of the Patellofemoral Joint.)

Or, here are some other ways bad cartilage triggers pain sensations:

The articular cartilage is not sensitive to stimulation, but ... the adjacent synovium is the primary pain source [fragments of cartilage can migrate through the synovial fluid to the synovium, irritating it]. The subchondral bone ... is another likely source of pain from excessive load on an unprotected bone surface. Finally, the resulting effusion [swelling] caused by articular breakdown may itself be a source of pain. (Johnson, Donald H. and Pedowitz, Robert A., eds. Practical Orthopaedic Sports Medicine and Arthroscopy)

And as for inflammation:

... Cartilage debris and sulfated polysaccharides liberated from cartilage breakdown have been shown to be inflammatory in joints and to stimulate the release of proinflammatory cytokines. (Aaron, Roy K. et al. “Pain in Osteoarthritis.” Medicine and Health Rhode Island, July 2004)

Then, if you happen to believe that where there’s smoke there’s fire, well, osteoarthritis and cartilage damage go hand in hand:

This loss or damage of articular cartilage is an early finding in osteoarthritis. Chondromacia patella is thus an arthritis involvement of the patella. (MDGuidelines, entry on patella chondromalacia)

But there are other things going on inside bad knees. How can you blame poor cartilage for everything? For example:

The association of bone marrow edema with pain in osteoarthritis of the knee has recently been emphasized. Bone marrow edema was found in 78% of patients with pain compared to 30% of patients without knee pain. The presence of bone marrow edema is associated with progression of cartilage degradation. (Aaron, Roy K. et al. “Pain in Osteoarthritis.” Medicine and Health Rhode Island, July 2004)

Here’s where a careful person has to admit, “Yeah, there's plenty going on that we don’t fully comprehend.”

But consider for a moment swelling of the bone marrow. The first matter to ponder: Does this contribute to cartilage degeneration or is this caused by cartilage degeneration? To me, the latter sounds more plausible. Still, let’s posit the former: that the bone marrow swelling is responsible for cartilage damage -- or that a third, even larger unknown force causes both the cartilage degeneration and the bone marrow swelling.

Okay then, where does that leave us, in terms of finding a path toward healing?

If your main problem is bone marrow swelling (or intraosseous hypertension, or focal osteonecrosis, or bone marrow lesions), then it seems you’d want a more bone-oriented treatment regimen. Now, I am way out on a limb here (I’ve done very little reading on this subject), but bone resembles cartilage a lot more than muscle. So I would think a gentle, joint-friendly program of high-repetition movement would be a smarter way to go than a “strengthen your quads” approach.

So even if the “unified theory” is wrong -- even if cartilage isn’t involved in much of all chronic knee pain -- I think the same activities that would strengthen and help repair this tissue would probably also benefit the joint overall.