Cartilage is the thin, slippery tissue that caps the ends of bones wherever they meet, and it does more for your joints than any other single structure. It absorbs shock, distributes your body weight, and creates a surface so smooth that your bones glide against each other with less friction than ice on ice. When cartilage is healthy, you never think about it. When it starts to wear down, every step can remind you it’s there.
What Makes Cartilage So Slippery
The cartilage lining your joints, called hyaline cartilage, produces one of the lowest-friction surfaces found anywhere in nature. The coefficient of friction inside a healthy synovial joint is roughly 0.001 to 0.01. For comparison, Teflon on Teflon sits around 0.04. Your knee joint is, by that measure, several times slipperier than a nonstick pan.
This near-frictionless performance comes from the cartilage surface working together with synovial fluid, the thick liquid that fills the joint capsule. Synovial fluid acts as both a lubricant and a nutrient delivery system. When you bend your knee or rotate your shoulder, the fluid spreads across the cartilage surface and gets pressed into its pores, maintaining a thin protective film that keeps bone ends from ever touching each other directly.
How Cartilage Absorbs Impact
Cartilage is 70% to 80% water by weight. That’s not a design flaw. It’s the central feature of how cartilage protects your bones from impact. The water is trapped within a mesh of collagen fibers and large molecules called proteoglycans, which carry a strong negative electrical charge. Those negative charges repel each other, causing the proteoglycans to spread out and hold water like a sponge.
When you land from a jump or take a step, the compressive force pushes those negatively charged molecules closer together. Their mutual repulsion increases, pushing back against the load and adding stiffness exactly when the joint needs it most. At the same time, pressurized fluid within the cartilage bears a significant portion of the total load, reducing stress on the solid framework of the tissue. The result is a material that gets stiffer under pressure and then rebounds when the load is removed. It distributes force across the underlying bone rather than concentrating it in one spot.
Cartilage Thickness Varies by Joint
Not all joints carry the same load, and cartilage thickness reflects that. In the knee, the thickest cartilage in the body, maximum thickness averages about 3.8 mm with a mean of 1.9 mm across the joint surface. Hip cartilage peaks at around 2.6 mm and averages 1.3 mm. The ankle, despite bearing your full body weight, has the thinnest cartilage of the three major lower-limb joints: a maximum of about 1.7 mm and a mean of just 1.0 mm.
The ankle compensates with a much more congruent joint surface, meaning the bones fit together more precisely, so load is spread more evenly across a thinner layer. The knee, with its flatter and less congruent surfaces, needs thicker cartilage and the help of menisci (wedge-shaped pads of fibrocartilage) to handle the same forces.
Why Cartilage Can’t Heal Itself
Cartilage has three features that make it uniquely bad at self-repair. It has no blood supply, no nerve connections, and a very low density of living cells. Bone, skin, and muscle all rely on blood flow to deliver the immune cells and growth factors that drive healing. Cartilage cells, called chondrocytes, get their oxygen and nutrients solely through diffusion from the surrounding synovial fluid, a much slower and less efficient process.
The lack of blood vessels also means that when cartilage is damaged, stem cells and repair cells from elsewhere in the body can’t easily migrate to the injury site. The dense matrix of the tissue itself acts as a physical barrier. Once the collagen network within cartilage is broken down, it cannot be rebuilt to its original architecture. This is a one-way street: small defects tend to stay or grow rather than fill in.
Movement Keeps Cartilage Nourished
Because cartilage has no blood supply, joint movement plays a role in keeping the tissue alive. Nutrients like glucose and oxygen are small enough to reach chondrocytes primarily through passive diffusion from synovial fluid. The cyclic loading that happens when you walk, bend, or shift your weight helps circulate synovial fluid across the cartilage surface, refreshing the supply of dissolved nutrients at the tissue boundary.
Interestingly, the physical “pumping” of fluid in and out of cartilage during loading doesn’t significantly speed up nutrient transport for small molecules like glucose and oxygen. Diffusion handles that on its own. But movement still matters because it keeps synovial fluid well-mixed and in contact with all cartilage surfaces, rather than allowing nutrients to deplete in stagnant pockets. Prolonged immobility, whether from a cast, bed rest, or a sedentary lifestyle, reduces this circulation and can compromise cartilage health over time.
Exercise Can Thicken Cartilage
A common concern is whether high-impact activities like running wear cartilage down. Recent evidence suggests the opposite for healthy joints. A cross-sectional study comparing recreational runners to sedentary individuals found that runners had significantly greater cartilage thickness and volume in several regions of the knee, including the medial femoral and tibial surfaces, which bear the most load during running.
The researchers attributed this to long-term mechanical stress stimulating cartilage metabolism and enhancing functional adaptability. While a single run temporarily compresses cartilage and reduces its thickness (the tissue rebounds within hours), years of regular running appear to build thicker, more robust cartilage. This fits a broader principle in biology: tissues that experience regular, moderate loading tend to strengthen, while tissues that are underloaded tend to weaken.
What Happens When Cartilage Breaks Down
Osteoarthritis is what develops when cartilage degradation outpaces whatever limited repair the tissue can manage. The process typically starts with surface-level fraying, called fibrillation, where the smooth top layer of cartilage becomes rough and irregular. The normally quiet chondrocytes become activated and shift their behavior, producing enzymes that break down the surrounding matrix rather than maintaining it. This creates a destructive feedback loop: as collagen fragments accumulate, they trigger receptors on the chondrocytes that stimulate even more enzyme production and inflammation.
Over time, the cartilage thins, the joint space narrows, and the underlying bone begins to change. It may harden (sclerosis), develop bony spurs (osteophytes) at the joint margins, and eventually deform. Doctors grade this progression on a 0-to-4 scale using X-rays. Grade 1 shows only questionable narrowing with possible early spurs. By Grade 4, there is severe joint space narrowing, large osteophytes, pronounced bone hardening, and visible deformity of the bone ends. The transition from Grade 1 to Grade 4 can take decades or, in some cases following injury, just a few years.
Different Cartilage Types for Different Jobs
Hyaline cartilage, the type that coats joint surfaces, is the most abundant cartilage in the body. It’s smooth, pale, and built primarily from type II collagen and water-trapping proteoglycans. Its job is minimizing friction and resisting compression.
Fibrocartilage shows up where joints need to handle both compression and tension. It’s rich in type I collagen, the same tough protein found in tendons and ligaments, which makes it better at resisting pulling forces. The menisci in your knees, the discs between your vertebrae, and the labrum in your hip and shoulder are all fibrocartilage. These structures act as gaskets and shock distributors, deepening joint sockets and spreading load across a wider area.
Elastic cartilage, found in the ear and parts of the throat, plays almost no role in joint function. It’s flexible and pressure-resistant, but its job is maintaining the shape of soft structures rather than bearing weight.
Why Aging Changes the Equation
Cartilage changes with age in ways that make it more vulnerable. The tissue becomes drier, thinner, and more yellow over time. The total collagen content doesn’t drop dramatically, but the organization and integrity of the collagen network weakens, and the tissue’s ability to retain water diminishes. Since water content is central to cartilage’s shock-absorbing ability, even modest changes in hydration alter how the tissue performs under load.
Aging chondrocytes also become less metabolically active and less responsive to the signals that normally maintain tissue balance. They produce matrix components more slowly while degradation continues at its usual pace. This gradual imbalance is why osteoarthritis becomes increasingly common after age 50, even in people who have never had a joint injury. The tissue simply loses its ability to keep up with normal wear.