Osteoarthritis sort of comes with the territory of aging. If you live long enough, you'll probably get it.
For those fortunate enough not to have a working acquaintance with the disease, I describe its onset in a just-published Stanford Medicine article, "When Bones Collide":
You start to feel some combination of pain, stiffness and tenderness in a thumb, a knee, a hip, a toe or perhaps your back or neck. It takes root, settles in and, probably, gets worse. And once you’ve got it, it never goes away. Eventually, it can get tough to twist off a bottle cap or to get around, depending on the joint or joints affected.
All too many of us, of course, are perfectly familiar with the symptoms of osteoarthritis. An estimated 27 million people in the United States have been diagnosed with it. By 2030, due mainly to the aging of the population, the number will be more like 50 million. Anything so common is all too easy to look at as inevitable: basically, the result of the same kind of wear and tear on your joints that causes the treads on a commuter car's set of tires to disappear eventually.
But Stanford rheumatologists Bill Robinson, MD, PhD, and Mark Genovese, MD, think that just may not be the way it works. Almost four years ago I wrote about Robinson's discovery that osteoarthritis is propelled by a sequence of inflammatory events similar to ones associated with Alzheimer's disease, cardiovascular disease, and type-2 diabetes. That discovery and a steady stream of follow-up work in his lab have spawned a clinical trial, now underway and led by Genovese, to see if a regimen of anti-inflammatory medicines that's been shown to roll back osteoarthritis's progression in mice can do the same thing in people.
That's the kind of progress most of us could live without.
Previously: New thinking about osteoarthritis, older people's nemesis and Inflammation, not just wear and tear, spawn arthritis
Illustration by Jeffrey Decoster
