Jim was a 68-year-old retired executive, and I was his third opinion for knee pain many years ago. He used to play tennis and walk the golf course. After being told he had ‘moderate’ osteoarthritis of his hip and knee, he stopped playing tennis, thinking that was the right treatment. Without docs giving folks clear direction after that diagnosis, many will go off quite intuitively and stop many activities— they think they’re saving their knees.
Jim reminded me of our previous conversation where I said, you have some arthritis; activity in reason will not lead to progression, but doing nothing will; do whatever your knee tolerates and come see me if the pain ever worsens. Four years later, Jim still has his natural knees and hips; he’s back on the courts, and he’s back to walking the golf course. He has also lost 5 pounds and plans to lose more. Now his partial rotator cuff tear hasn’t kept him off the court either.
If you are new here, you may want to read through Healthy Knees Parts 1 & 2.
Healthy Knees: Part 1
Over the next several weeks, I want to explore a topic that has occupied much of my professional life. This will be a multi-part series on maintaining healthy knees. Why so many parts?!? You see, it’s a much more complicated topic than most of you would think. And the longer I practice, the more complicated it seems to get. Not the surgery part… but the basic principles governing the prevalence of issues, healing, and joint health.
I hear some version of Jim’s story in my office several times a week. I see many second- and third-opinion patients typically referred in by someone who has heard the talk and reclaimed the active part of their lives. You see, very often when someone hears the word arthritis, or worse, bone-on-bone, they then make what feels like the responsible decision… they slow down or stop. It seems intuitive if you believe the knee joint behaves like a mechanical hinge. They end up giving up tennis, hiking, running, and sometimes even long walks because they believe cartilage wears down like tire tread. I get that. If you picture your knee as a mechanical part, protecting it by using it less seems like the obvious answer. But your cartilage isn’t tire tread. It’s living tissue, and when we take movement away from it, we take away one of the main stimuli it needs to stay healthy.
In Part 2, we talked about the chemical environment inside your joint, and how chronic, low-grade inflammation from poor metabolic health nudges cartilage cells toward breaking tissue down rather than building it up. Today we’re going to look at the other half of that conversation, which is the mechanical signal. How does cartilage get nutrition when it has no blood supply? How do its cells decide whether to build or break down? And why does a knee that stops moving so often end up stiffer and more painful instead of more capable? Stay with me for a second, because once you understand how cartilage receives nourishment, the advice to “take it easy” starts to look less appealing.
Healthy Knees Part 2: When Metabolism, Genetics and Alignment Meet Cartilage
“It’s amazing… I’ve only lost three pounds, but my knees already feel better.”
Okay… Let’s do this…
A tissue with no blood supply
Almost every tissue in our body is fed by blood. Muscle, bone, skin, and even tendons have blood vessels that deliver oxygen and nutrients and carry waste away. Articular cartilage, the smooth, glistening layer covering the ends of the bones in your knee, is different. It’s only about 2 to 4 millimeters thick, and it has no blood vessels, no nerves, and no lymphatics, which are the drainage channels that clear fluid and waste from most other tissues. The absence of nerves is also why cartilage itself doesn’t hurt… the pain we feel with arthritis comes from surrounding structures, like the bone beneath it and the joint lining (synovium).
So how does it get fed? The answer is synovial fluid, the slippery, egg-white-like fluid that fills the joint space. It’s produced by the synovium, the thin lining of the joint we spent time on in Part 2, and it bathes the cartilage surface with nutrients. But cartilage is dense, and nutrients don’t drift into it very well on their own. Its matrix, the scaffold of collagen fibers and water-loving molecules called proteoglycans that gives cartilage its structure and springiness, is packed tightly, and the cells living inside it have no direct delivery system at all.
This is where movement comes in. When you put weight on your knee, the cartilage compresses and fluid is squeezed out of the matrix, and when the load comes off, fluid flows back in. Think of a sponge sitting in a bucket of water. If you squeeze and release it over and over, water moves through it constantly, but if you leave it on the bottom of the bucket, very little exchange happens. Each cycle of loading and unloading helps pull nutrients in and push waste out, so walking, cycling, climbing stairs, and swinging a tennis racket are a big part of how your cartilage gets fed. A knee that sits still for most of the day isn’t being spared, because the pump that nourishes its cartilage has slowed to a crawl. Pretty ironic, right? The very thing Jim did to protect his joints reduced the primary source of nourishment to the tissue he was trying to preserve.
Your cartilage cells are listening
The cells inside the cartilage are called chondrocytes, and they’re the cells that build and maintain cartilage. They make up only about 2% of the volume of your cartilage, yet they’re responsible for producing and repairing the entire ‘matrix’ around them… and they’re remarkably sensitive to what’s happening mechanically around them.
When cartilage is compressed, the chondrocytes feel it. They sense it. Their shape changes slightly, the fluid pressure around them rises, and fluid flows past them. Scientists call the process by which a cell converts a physical force into a chemical signal mechanotransduction. The concept is simple: sensors and channels on the chondrocyte surface detect the load and resultant deformation and relay that information into the cell, where it switches on the machinery that builds collagen and proteoglycans. Healthy, rhythmic, repeated loading signals that this tissue is needed and should be kept strong. When those signals fade, the cell gets a much weaker message about what to build, and when loading is abrupt and excessive, particularly after an injury, the message can shift toward breakdown.
This is where Part 3 connects directly to Part 2. Remember the idea that chondrocytes are constantly deciding whether to build matrix or break it down? In Part 2, we looked at the chemical inputs to that decision. Today’s point is that the chondrocyte is listening on a second set of channels at the same time, and those channels are stimulated mechanically.
Researchers who study cartilage biology describe a complex interplay among mechanical, inflammatory, and biochemical factors that can either support or undermine the health of the matrix. Your cartilage cells integrate your body's chemistry and how you move all day long, and both inputs are shaped by the choices we make. We have agency here… we can make a big difference to the health of the cartilage in our joints. Even after you’re told you have osteoarthritis.
For Members, I’ll show you how your cartilage cells sense every step you take and decide whether to build or break down, and what the studies show about cartilage that is loaded vs. unloaded. We’ll look at the randomized trial that showed adult cartilage getting healthier with exercise, what decades of running does to your knees, and why dose matters. And I’ll give you the simple next-morning check I use with my patients to know if you’ve done too much, along with my take-home list for loading a cranky knee… the same approach that got Jim back on the tennis court.