Saving My Knees: How I Proved My Doctors Wrong and Beat Chronic Knee Pain (7 page)

When I moved on to his writings on bad knees, my jaw dropped. He perfectly described my failed experience in physical therapy. It was uncanny.

The problem, he said, is that standard physical therapy targets quadriceps muscles, but the force required to strengthen the muscle often exceeds what the joint can tolerate. That results in aching and swelling. The missing ingredient: an exercise program aimed at improving the soft joint surface. Weak muscles are not the main problem.

It seemed like a stunningly obvious application of common sense. Why not direct your energy toward fixing the part of your body that actually hurts? Once you accept this, you start to see why regular physical therapy often fails in treating bad knees.

A
muscle-first
approach generally emphasizes lower repetitions, higher loads. Tim prescribed many quadriceps exercises for me that included sets of ten—a good number of repetitions for bulking up a muscle. The trouble was, the force needed to strengthen my quads overwhelmed my weak joints.

A
joint-first
approach emphasizes higher repetitions, lower loads. Cartilage, the soft tissue in need of attention, requires a lot of repetitions (Kelsey says in the thousands) with a much gentler load in order to biologically adapt.

Kelsey believed bad knees could get better, when you undertake a program that subjects them to the proper amounts of load and motion. That lifted my spirits. Here at last someone was offering to restore the hope that my doctors had snatched away.

I badly wanted to seize that hope, but I wasn’t convinced yet. It was time to put on my geek hat and dive into the mystery of knee cartilage and what the latest scientific research revealed about its inner workings.

One popular line of thinking maintains that God was asleep at the switch when it came time to design the human knee.

Just look at how it’s rather exposed; no big muscles protect the knee as with the shoulder and hip. Or consider how the simple act of descending a staircase appears to court disaster. Our body weight shifts from bending leg to bending leg. View this process through an X-ray machine and you’ll be left marvelling that, with each step, the thighbone doesn’t thrust over the top of the shinbone, causing the limb to collapse in two pieces.

I first heard a version of the “crummy design” view of knees while in college. A Tufts University freshman who had a car (unlike me) gave me a ride home from the Boston area to Maine for Christmas vacation. She was studying anatomy and went off on a long rant about how poorly engineered knees are. I pretty much accepted this at face value for the next two decades.

When I hurt my own knees, I found myself thinking again about whether the joints were intrinsically, and hopelessly, flawed. This was now more than a matter of passing interest. I wanted to understand what my chances of recovery were. If the pessimists were right, and knees were the anatomical equivalent of an April Fool’s joke, my prospects didn’t look good. 

I soon learned that, contrary to what an X-ray may suggest, bent knees are fairly stable. They’re held together by a nest of tissues, most prominently ligaments, which connect bone to bone and act as stabilizers. The hamstrings, quadriceps, and large calf muscle all cross the joint too. These muscles and ligaments help preserve the integrity of your skeleton, so you don’t have to reassemble your legs like a cartoon character after you go down a couple of stairs.

If the design of knees had stopped after throwing in a bunch of supporting tissues to stabilize the area, we would be in very bad shape indeed. Any time we tried to walk, the end of the femur would grind into the end of the tibia, or shinbone. Bones are well-supplied with nerves, so the end result would probably involve a lot of screaming.

Understanding why this doesn’t occur requires a journey inside the joint itself, where things get really rough, where heavy loads must be withstood daily without structural damage occurring. This is where the fascinating story lies.

Bones don’t clumsily crunch into each other because a special tissue known as
hyaline articular cartilage
pads their endings. This cartilage—normally pearly white, smooth and spongy—measures about one-tenth of an inch thick (almost the height of a couple of stacked quarters).

Articular cartilage lives in an unusual environment. Prick your finger with a needle and out comes blood. Prick a joint capsule (the fibrous sac that encloses the knee joint) and out comes
synovial fluid
. The thick, straw-yellow liquid has a consistency similar to that of egg whites. Its viscosity keeps our constantly moving knees well-lubricated. It bathes the cartilage in the absence of blood.

In the absence of blood
.

That simple phrase turned out to be a revelation of the first order for me.

It deserves special attention, like words on a banner trailing a prop plane in the sky.

THIS CARTILAGE HAS NO BLOOD SUPPLY.

This matters hugely when you’re trying to heal aching knees. Remember how the blood rushes in troops to tidy up and repair damaged tissue, such as with a sprained ligament. When you hurt your articular cartilage, all these MASH units are effectively sidelined, impotent. They can’t get to the accident site.

Unfortunately, it gets worse.

THIS CARTILAGE HAS NO NERVE SUPPLY EITHER.

Predictably, this creates the makings of a real mess. If the tissue had nerves, you could immediately sense damage being done. You’d no doubt respond by modifying your activity, knowing the cartilage can’t heal the same way as muscles and ligaments.

The lack of both blood and nerves seems like powerful support for the “knees suffer from lousy design” argument. My investigation had just begun though. As I delved deeper, a very different picture emerged.

It turns out that knees have adapted beautifully to what’s demanded of them. Their job isn’t easy. We sporting types in particular put them through a hellish obstacle course over a lifetime: jumping, stop-and-go sprinting, squatting while balancing heavy weights, running 26.2 miles straight in a marathon. In fact, the environment inside the joint capsule might be thought of as “Mechano World,” a harsh place of constant mechanical stresses.

Knees successfully handle a lot of abuse, and articular cartilage deserves a lot of the credit. It may not heal well, but its other qualities happen to be outstanding. It’s a Superman among our various body tissues.  

Cartilage’s amazing properties begin with its crazy slipperiness. Two wet ice cubes rub together with practically no friction. Cartilage would be incredible if it were two or three times as slippery as ice, but actually, it’s up to eight times more. When healthy, it glides freely. All the hard surfaces that meet in the knee joint that could become irritated by rubbing together—the underside of the knee cap, the ends of the thighbone and shinbone—are capped with this slick tissue.

It’s also a super-resilient cushion that spreads load. Without this property the sport of running wouldn’t exist. A runner’s knees absorb force equal to up to six times his body weight. That’s like a 150-pound person supporting a 750-pound friend on his back.

How cartilage absorbs shock is quite ingenious. It’s not a dry cushion, like the one on the couch. It’s wet, like a sponge. When your knees don’t have to support any load, such as when you lie down, cartilage fills with synovial fluid and water. When you stand up, the pressure of your weight squeezes out the fluids. So when you go for a walk, fluid is constantly being pressed out and absorbed back into the tissue.

If you’re worried that when the water and synovial fluid are pushed out, the cartilage might collapse too much, don’t be. Another design trick prevents it from deflating like a beach ball someone just sat on. To see why, you first need to appreciate how cartilage is structured. You need to understand the “
matrix
.”

Cartilage is as much as four-fifths water—about what you’d expect for a really wet sponge—but the other chief ingredients are pretty important. It also consists of a tough, ropy protein called
collagen
. On the surface, knee cartilage has a higher proportion of collagen than in the middle, keeping the tissue tear-resistant where it most matters.

The other big element in the matrix is—big word alert—
proteoglycans
. They weave all around the collagen skeleton. They give it body and form cartilage’s spongy scaffolding.

A proteoglycan is a large molecule that combines a protein core with many long-chain sugar molecules. Easy visualization: a bottle brush. The spine of the brush represents the protein; the individual bristles the sugar chains called—bigger word alert—
glycosaminoglycans
.

(Does that word look familiar? That’s no coincidence. Glucosamine is one of the sugars that link together to form a single glycosaminoglycan. When my doctor advised me to take glucosamine tablets, he was hoping the amino sugar would wind up in my knees after its voyage through my body.)

Now it’s time to answer that “beach ball” question: why doesn’t this watery, tenth-of-an-inch thick layer of cartilage go flat when you step down hard and it must support your entire body weight?

Thank the glycosaminoglycans. On the atomic level, they carry a negative charge. That means they repel each other, in the same manner that the like poles of two magnets resist being pushed together. So your cartilage does begin to compress when the water and synovial fluid are expelled, but the glycosaminoglycans in the tissue push back. The closer they are squeezed toward each other, the more they resist.

All these properties of articular cartilage combine to make for an impressive substance well-suited to surviving the rigors of Mechano World. It excels at absorbing shock and minimizing friction. However, it’s still living tissue. It needs to be nourished. It needs to dispose of waste. That’s a problem without a blood supply.

How the cartilage meets this challenge is enormously significant. In Mechano World, logically enough, it resorts to a mechanical solution. Its answer to the basic problem of eating and excreting, if you will, is wonderfully simple and elegant: motion.

Yes, take a walk and feed your knees! When your foot lifts, pressure comes off the knee and synovial fluid hurries into the cartilage, bearing nutrients. When your foot strikes the ground, the fluid is pressed out, bearing waste products.

As living tissue though, cartilage requires more than the ability to obtain nutrients. It would wear down pretty quickly without some capacity to rebuild over time. So there are special cells scattered throughout the articular cartilage in our knees. These tiny factories churn out more matrix. They’re called
chondrocytes
.

Remember from biology class that cells are fairly sophisticated. They are the smallest structural units of any organism capable of independent functioning. So chondrocytes are like the smart guys in the control room. They have to figure out how much new matrix to make. They take their cues from the daily forces they must withstand.

Not surprisingly, chondrocytes figure heavily into theories of why good knees go bad. Sometimes it all starts with an initial trauma, such as from repeated high loads. Maybe that paunchy, out-of-shape cubicle dweller starts playing pickup basketball during lunch breaks. He leaps and lands on hard pavement, again and again. After a while, the high compressive forces damage the structure of his knee cartilage and kill chondrocytes too.

A common view of osteoarthritis is that chondrocytes can’t pump out enough matrix as cartilage deteriorates and thins. The delicate balance between removing old tissue and making new is upset. Inflammation of the joint worsens the situation. A pro-inflammatory protein called interleukin-1 delivers a double whammy. It stimulates the production of enzymes that strip away cartilage. At the same time it inhibits chondrocytes from making replacement tissue.

Most people with achy knees don’t realize what’s happening on a cellular level. They just know their knees hurt worse and worse. They fall into what I call the death spiral. It happened to me and I fought to escape it.

The death spiral is simple yet deadly. Because your knees hurt, you move them less. Inactivity weakens the joints and supporting muscles, leading to even less movement and more pain. Then repeat the cycle: Because your knees hurt, you move them less. Inactivity weakens the joints and supporting muscles . . . and on and on, until climbing one flight of stairs becomes an ordeal.

What you’re doing to protect your grumbling knees makes sense intuitively. Rest them so they’ll get better. That’s what I thought initially. But too much inactivity is poison for joints; they need movement. The cartilage starves without it. From my research, I knew this in an academic sense. Now I sought concrete proof.

I began spelunking through medical journals. The publications sported unsexy names like
Arthritis Care and Research
and
Archives of Internal Medicine
. The dry, technical articles inside contained phrases like “the volumes of individual cartilage plates (medial tibial, lateral tibial and patella) were isolated from the total volume by manually drawing disarticulation contours.”

It wasn’t exactly beach reading. Yet my fascination with the subject matter propelled me through the statistical and clinical jargon. What I ended up discovering was incredible.

For example, in a 1980 article in the
Journal of Bone and Joint Surgery
, researchers described how they operated on 147 New Zealand White rabbits and created small holes in their knee cartilage. They wanted to see whether the rabbits’ limbs healed best when put in a cast or when moved freely soon after surgery, either actively or passively.

The procedure went like this: The sedated rabbits had the knees of their right hind limbs shaved, then cut open. A dentist drill was used to sink four holes in the cartilage. Each hole spanned one millimeter in diameter (the thickness of eight sheets of copier paper) and penetrated to the bone.

After surgery, the rabbits were split into three groups. One group was set loose to move about a large cage as they wished (and they did so, gingerly at first). The second bunch had their knees immobilized in a plaster-of-Paris cast. The rest found themselves hooked up to a strange-looking apparatus.

As their bodies rested comfortably in a padded half-shell, their operated-on knees continuously flexed back and forth. The rabbits didn’t do anything; a small electric motor powered the contraption. The motor drove a vertical rod attached to a plastic cup that securely held the animal’s foot. The rod moved up and down, straightening and bending the rabbit’s knee through continuous passive motion.

At selected weekly intervals, the 120 adolescent rabbits and 27 adults were killed. Their knees were sliced open for examination. What the researchers found was stunning.

It didn’t matter much whether the rabbits had their operated-on knee encased in a cast or whether they wandered freely about their cages. Among the younger animals who were immobile, only eight percent of the drilled holes healed. The rate barely improved to nine percent for those allowed to move about at will (they tended to be hopping around after one week). However, a whopping fifty-two percent of the defects mended among the rabbits hooked up to the device that repeatedly flexed their joints.