Saving My Knees: How I Proved My Doctors Wrong and Beat Chronic Knee Pain (8 page)

The adults saw a similar breakdown, though skewed lower. The healing rate was three percent for those immobilized, five percent for the older rabbits that roamed their cages, and forty-four percent for those who underwent continuous passive motion.

The winner by a country mile: continuous passive motion. Anyone doubting the numbers only had to look at the photos included in the article. They made the point as dramatically as those anti-smoking ads that contrast a healthy, pink pair of lungs with a black, tarry set that belongs to a longtime smoker.

One photo shows a close-up of knee cartilage that seems magically restored to perfect health, no evidence of any drilled holes. That rabbit spent three weeks on the continuous passive motion machine. Above that is a startling image of a knee joint that has decayed horribly. The scar tissue resembles a glue-like jelly. It surrounds small islands of normal-looking cartilage. That rabbit spent ten weeks with its leg in a cast.

During the investigation, the authors of the report, led by Robert B. Salter, made a couple of curious observations about how cartilage healed. Initially the replacement tissue was immature, fibrous, and not as durable as the original. Over several weeks though, the newly formed tissue took on the characteristics of normal articular cartilage. Chondrocyte factories appeared, ready to start spewing out matrix.

Also the holes didn’t heal from the sides. In other words, the surrounding healthy tissue didn’t branch across the hole, plugging it. Rather, the defects seemed to heal from the underlying bone upwards. That turned out to have one not-so-good implication. Further research by Salter’s team didn’t find continuous passive motion to be effective for cartilage lesions that weren’t deep enough to reach the bone.

Salter’s rabbit study, though impressive, does warrant a few caveats. First, a one-millimeter hole is very small (though to be fair, for a 6-pound rabbit, it’s proportionately much bigger than for a 160-pound human). Also the rest of the rabbit’s joint is presumably in fine shape—he doesn’t have pre-existing bone spurs, bad synovial fluid, or cartilage lesions. And obviously this is a rabbit, not a person.

Still, other scientific trials have examined the effects of immobility on knee cartilage. Some looked at animals, others humans. They reached a similar conclusion: joints start to go bad when they don’t get any movement.

United States, 1981: An article in
Arthritis and Rheumatism
reviews what happened after seven mongrel dogs had their right rear limbs placed in casts for six weeks. None had any surgery beforehand. Conclusion: “Immobilization of the knee of a normal dog by casting results in rapid degeneration of articular cartilage.”

Finland, 2000: Researchers write that they observed “significant softening” of the cartilage of beagles that had their knees immobilized for eleven weeks. Conclusion: “Immobilization of the joint of a young individual may cause long-term, if not permanent, alterations of cartilage biomechanical properties. This may predispose the joint to degenerative changes later in life.”

Switzerland, 2003: A published study looks at changes that occurred in the knee cartilage of patients after they suffered traumatic accidents involving the spinal cord. Conclusion: “Human cartilage atrophies in the absence of normal joint loading and movement after spinal cord injuries.”

The Switzerland study shows that inactive knees actually suffer a couple of related problems. One, the cartilage is deprived of the movement needed to nourish itself. Two, it isn’t called upon to bear any weight, and so begins to thin out and get soft.

That would seem to argue against a sedentary lifestyle. After all, cartilage responds to expectations, as signaled by how active you are. If you want to be a couch potato, your cartilage gets the message and weakens. If being inactive is bad, might exercise have a salutary effect? Indeed, that appears to be true.

Healthy adults between twenty-one and seventy-nine years of age lost knee cartilage more slowly as they became more physically active, Australian researchers found. Beagles that ran regularly on an uphill treadmill boasted up to twenty-three percent thicker cartilage in their knees, a Finnish study claimed. Also the dogs’ glycosaminoglycans jumped by almost a third. Remember, those long, negatively charged sugar chains contribute a lot to the tissue’s strength and elasticity.

While exercise seems to benefit the cartilage of healthy people, what about those with damaged joints? Swedish researchers Ewa M. Roos and Leif Dahlberg assembled thirty people whose knees had already been operated on once. Members of this group stood a high chance of developing osteoarthritis. Most of the patients, ages thirty-five to fifty, complained of painful, stiff knees.

The participants were split up. Half received no special intervention. The others attended hour-long exercise sessions, three times a week. Under close supervision, they cycled on stationary bikes, jogged on trampolines, performed knee bends with light weights. An enhanced MRI test evaluated their knees at the beginning of the trial and four months later.

The results: exercisers saw a significant increase in glycosaminoglycan content in their knee cartilage, according to a 2005 medical journal article. The findings suggest, the authors wrote, that “human cartilage responds to physiologic loading in a way similar to that exhibited by muscle and bone.” What’s more, they went on, the improvement in the tissue may explain why osteoarthritis patients report benefits from exercise.

All these studies were eye-opening and exhilarating for me. For months, I had felt as if I was in the fight of my life with one arm tied behind my back. My doctors kept insisting I couldn’t get better. They were the experts. They went through medical school, served grueling residencies in their specialty, examined hundreds of problem knees every year.

Their pessimism left me wrestling with self-doubt. My family rallied to support me, but behind their expressions of sympathy, I sensed their doubt too. They assumed that the medical professionals must be right. To them, I was like the terminal cancer patient who stubbornly refuses to believe half a dozen doctors who make the same diagnosis.

Now I possessed evidence that exercise could improve the quality of cartilage. But what about the quantity? Does damaged tissue ever thicken on its own? Or does cartilage that is blistered, or pocked by a shallow hole or deep hole, just continue to wear away? The question has wide relevance beyond problem knees. A 2005 study found that three-fifths of healthy, middle-aged adults had defective cartilage on the inner half of their dominant knee alone.

My doctors gave me the impression that bad cartilage recovered rarely if ever. Fortunately, in 2000, researchers in the Australian state of Tasmania decided to look at how defects in the tissue changed over time. In all, 325 subjects completed a two-year study. An MRI exam was used to grade the quality of the cartilage at various locations in their knee joints.

The scoring system went like this: Zero represented normal, while four stood for the other extreme, worn to the bone. The other grades accounted for intermediate levels of cartilage damage and loss: one (blistering), two (irregularities and less than fifty percent loss of thickness), three (deep ulceration with at least half the tissue gone).

So for example, a subject might start out with good cartilage at a certain location, say under the patella. It would be scored a “zero.” Two years later, if almost half the tissue was found to be gone, it would be downgraded to a “two.” I expected to find evidence of good cartilage going bad. The more tantalizing question was, did bad cartilage ever become good—or at least better?

Surprisingly it did, and with an astounding frequency. The figures appeared in a March 2006 edition of
Archives of Internal Medicine
, in an article bearing the rather clunky title, “Natural History of Knee Cartilage Defects and Factors Affecting Change.”

A full thirty-seven percent of the subjects had a cartilage defect improve in one of their knee compartments! That even exceeded the thirty-three percent that were found to have a worsening somewhere. The report included an MRI image showing a case of clear thickening. A sizable hole had filled in, going from a “three” to a “one.” The researchers wrote, “The decrease in cartilage defects may represent cartilage repair and healing.”

Intrigued, I scanned the top of the article to learn more about the subject population. If perfectly healthy, perhaps these people just healed better. But it turned out that one-third suffered from chronic knee pain. Despite that, their defects improved at about the same rate as those of their pain-free counterparts.

The authors did identify factors that led to an increase in cartilage defects over time. Being overweight or female boosted your risk. Being over forty did too. But there was also good news buried in the age-related statistics. Subjects over forty and under shared roughly the same chance of having faulty cartilage improve somewhere in their knee. That suggests the ability of the tissue to heal doesn’t flip off, like a toggle switch, once you reach a certain age.

A huge risk factor for worsening cartilage was having bone spurs, outgrowths that form when the body tries to restore stability to a decaying joint. The bony protrusions often restrict normal leg movement and damage or interfere with the remaining cartilage. From that revelation, I took the message that knee pain sufferers should take early action, before the joint undergoes significant structural changes.

Overall, the study seemed to support much more hope than despair. Those subjects whose cartilage got better didn’t even follow any knee-friendly exercise regimen, as with the Swedish experiment.

At this point, a skeptical reader might protest. There’s an unacknowledged elephant in the room: measurement error. MRI technology isn’t perfectly accurate. Also the resulting images are literally black-and-white, but their interpretation isn’t. Opinions can vary among those reading the same MRI.

The Australian researchers took pains to address the potential for human error at least. The same person graded all the MRIs at the beginning and end of the study. Also he evaluated the final set of MRIs without knowing any of the initial scores, to avoid prejudicing him.

Even so, some errors probably crept in. Say the human grader initially scores a cartilage lesion a “three,” but it’s actually a “two.” Two years later, he rechecks it. The defect is still a “two.” He correctly marks it as such but incorrectly records the lesion as having improved. The problem lies with his early mismeasurement.

Of course committing such errors can skew the figures both ways. He also may incorrectly measure and fail to capture an improvement.

It’s unclear how eliminating measurement error would have affected the results. That’s not so for a related issue: the problem of how precise the measuring tool is. Once you factor this in, it becomes clear that the study probably
undercounted
the number of defects that improved—perhaps by a lot.

That’s because the precision of a measuring tool can matter a good deal when quantifying change. This is an important point to grasp. Here’s a simple illustration of what I mean:

Imagine you’re monitoring the growth of teenagers, year to year. There’s only one catch: you’re using a very crude ruler. Whereas normal rulers display not only inches, but also eighths or sixteenths of an inch, this ruler measures only in feet. So for example, anyone who is more than four feet tall, but no more than five, is considered five feet in height.

Say Carol is five-three, Bill five-eight, and Jim five-eleven. They’re all marked down as six feet tall (more than five feet, less than six). Now let’s suppose the purpose of this experiment is to quantify the percentage of teenagers that grow from year to year.

If, one year later, Carol has spurted three inches, Bill has gained two, and Jim one and a half, what will our statistics show, after we’ve measured everyone with our foot-long rulers? That’s right: only one-third of our subjects have grown. Carol and Bill are still six feet tall. Jim is now seven feet.

The problem: our measuring device lacks sufficient precision.

Now apply that idea to the cartilage defect study.

The researchers employed a commonly used zero-to-four scale to grade the quality and thickness of cartilage. What if they could have been more precise than that five “slice” measurement (zero, one, two, three, four)? Instead of rating a location a “three,” for instance, what if they could measure the equivalent of inches in our height example above?

If so, a 3.3 defect that changed to a 3.1 would count as an improvement, whereas under the old scale, both 3.3 and 3.1 were considered “3.” Simply because of this greater measurement precision, and for no other reason, the number of observed subjects whose cartilage got better somewhere in their knee joint will rise. (Of course we also must accept the corollary: more of them will be found to have a worsening at some area in the joint too.)

All this may seem a bit arcane or tangential. However, it’s very significant. A five-point scoring system isn’t that precise at all. Had the researchers possessed better technology and more confidence, they might have expanded their scale to accommodate fifteen different grades, fifty, or even one hundred.

The implication is worth pondering. Knee cartilage may conform to a very dynamic model, constantly changing both for worse and for better. I found that very heartening. It struck me as a cutting-edge view.

Advances in high-tech imaging will be critical to settling the matter. It’s risky and unethical to slice open living knees just to satisfy scientific curiosity, so we depend on machines to peer inside the joints. At this point, it appears the heavy lifting will fall to the MRI scanner, a relatively recent invention.