Until then, what doctors would like to have is some kind of test that will identify people in the earliest stages of osteoarthritis, before too much damage has occurred. That way their treatments might stand a better chance of arresting the degenerative process before disability sets in. Unfortunately, conventional X rays, which give very detailed pictures of bone, don't provide very good images of cartilage. And researchers haven't yet discovered any biological markers in the blood that reliably tell them, "Hey, this person's cartilage is starting to fall apart. Do something!"

To understand the latest insights and where they might be leading, it helps to know a little bit about how a joint is put together, and there's no better place to start than with the cartilage. Like so many tissues in the body, cartilage is composed mostly of water. Indeed, you can think of it as a damp sponge. The spongy part contains several important components, including the chondrocytes—cells that generate new bits of cartilage—and various molecules that give the "sponge" its structure and help hold it together.

With every step we take, our moving body puts pressure roughly equal to three times our weight on the knees and hips. As that pressure is distributed across those joints, cartilage is compressed, absorbing most of the load. And, as you might expect with something that resembles a damp sponge, water is squeezed out of the cartilage into the space between the bones. Once the pressure is released, the water flows back into the cartilage, carrying with it nutrients that were picked up from the synovial fluid, which fills the joint. This constant fluid exchange is critical to maintaining healthy, pliable cartilage and explains why joint-moving exercises, like walking, help delay the progress of osteoarthritis.

Sometime between ages 40 and 55, the activity of the chondrocytes starts slowing down and the cartilage takes longer and longer to replenish itself. As the cushion of cartilage grows progressively thinner, the bones begin to grind against one another. This is a normal consequence of aging, but aging isn't the only culprit. Something as simple as falling on an icy sidewalk or putting on some extra pounds can increase your risk of osteoarthritis. Anything that puts extra stress on the joints will wear out the cartilage that much faster.

That's simple enough. Now for the first wrinkle. "It appears that not all cartilage is created equal," says Dr. Roland Moskowitz, president of the Osteoarthritis Research Society International. Ankles, for example, bear the same heavy loads as knees and hips. Yet most people, unless they're ballet dancers, don't get osteoarthritis of the ankle. Similar discrepancies show up in non-weight-bearing joints as well. The wrist, for example, is much less prone to osteoarthritis than the joint at the base of the thumb. It could be that ankles and wrists have some mechanical advantage that protects them from osteoarthritis. But preliminary evidence suggests that the real advantage, at least for ankles, is biochemical; that there's something in their composition that allows them to bear greater loads and respond to changes in the joint without breaking down.

Some of the evidence for this comes from related research on bones. Most people think of bones as inert objects whose only job is to keep our bodies from collapsing into a puddle of flesh. But bones are actually quite active tissues, constantly building and rebuilding themselves from the inside out. Anytime you break a bone, the body produces repair proteins that direct cellular activities as the bone knits itself together. When investigators take these so-called osteogenic proteins and sprinkle them on laboratory samples of damaged cartilage, the cartilage begins to repair itself.

"Now here comes the interesting part," says Dr. Klaus Kuettner, professor of biochemistry at Rush­Presbyterian­St. Luke's. "The ankle joint responds better than the knee joint to osteogenic proteins." Is that why the ankle rarely gets osteoarthritis? "We don't know," says Kuettner, "but it's a hint in that direction."

Another hint comes from the observation that women with strong, healthy bones—the kind that are least susceptible to the brittleness of osteoporosis—are at greater risk of developing osteoarthritis. (Nature is often just not fair.) Once again, doctors suspect that a complex interplay of mechanical and biochemical factors is at work. Strong, healthy bones can support a heavier load. They also tend to replace old bone cells with new bone cells at a pretty fast clip. But somehow the biochemical signals that are responsible for the bone's increasing turnover rate trigger even greater damage to the cartilage.

Or is it the other way around? Is it the damaged cartilage that gets the degenerative process started by sending aberrant signals to the bone? "At this point, it would be a mistake to fight bitterly over whether osteoarthritis starts in the bones or cartilage, because in the end there may be different forms of the disease," says Dr. Bjorn Olsen, a cell biologist at Harvard University. "In some cases, it may start in the bone. In others, it might start in the cartilage."

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