Arthritis in the knees develops when the cartilage that cushions the joint breaks down, the immune system attacks the joint lining, or a past injury sets off long-term degeneration. The knee is the most commonly affected joint worldwide, with roughly 365 million people living with knee osteoarthritis alone. Understanding what triggers that damage helps explain why some people develop it decades earlier than others.
How Cartilage Breaks Down
The most common form of knee arthritis is osteoarthritis, and it starts with a shift in how cartilage maintains itself. Healthy cartilage constantly rebuilds. Cells called chondrocytes break down small amounts of worn-out tissue and replace it with fresh material, keeping the cushion intact. In osteoarthritis, the enzymes that break tissue down become overactive, and this balance tips toward destruction. The cartilage cells try to compensate by producing more material, but over time the repair effort falls behind.
Damage appears first on the surface of the cartilage as tiny cracks and rough patches. Over months and years, those cracks deepen, exposing more of the joint’s underlying structure. Eventually, large areas of cartilage erode completely, leaving bone pressing against bone. This is when pain, stiffness, and swelling become hard to ignore. The process is gradual, which is why many people have significant cartilage loss on imaging before they ever feel symptoms.
The Bone Beneath the Cartilage
Cartilage loss is only part of the picture. The bone sitting directly underneath the cartilage, called subchondral bone, plays a surprisingly active role in how knee arthritis progresses. Computer modeling of the human shinbone has shown that even a 1 to 2 percent increase in the size of this bone layer can significantly raise the mechanical stress on the cartilage above it. As arthritis advances, that bone thickens and hardens, a process called sclerosis, and bony spurs (osteophytes) grow along the joint margins. These changes reshape the joint, limit its range of motion, and contribute to pain that cartilage loss alone doesn’t fully explain.
When the Immune System Attacks the Joint
Rheumatoid arthritis is a completely different disease that can also target the knees. Instead of wear-and-tear cartilage loss, the immune system mistakenly sends antibodies to the thin tissue lining the joint capsule, called the synovium. That lining normally produces fluid that keeps the joint lubricated. When it becomes inflamed, it swells, thickens, and gradually eats away at both the cartilage and the bone underneath. Left unchecked, rheumatoid arthritis can cause the knee to bend out of its normal alignment and shift out of place. It tends to affect joints symmetrically, so both knees are often involved.
Excess Weight and Joint Pressure
Body weight has an outsized effect on the knees because of simple physics. Every pound of body weight places four to six pounds of pressure on each knee joint. That means carrying just 10 extra pounds translates to 40 to 60 additional pounds of force with every step. Over thousands of steps a day, across years, that extra load accelerates cartilage breakdown considerably.
But the damage from excess weight isn’t purely mechanical. Fat tissue produces signaling molecules that drive inflammation throughout the body. One of these, leptin, has been directly linked to increased cartilage loss and greater joint pain in the knee. Others promote the same destructive enzymes that break cartilage down from the inside. This explains a pattern researchers have noticed: people with obesity develop arthritis not only in weight-bearing joints like knees but also in hands and fingers, where mechanical load isn’t a factor. The combination of excess force and chronic low-grade inflammation makes obesity one of the strongest modifiable risk factors for knee arthritis.
Past Injuries That Catch Up
A torn ACL, a meniscus tear, or a fracture that extends into the joint surface can set the stage for arthritis years or even decades later. This is called post-traumatic arthritis, and the timeline is well documented. Within 10 years of tearing an ACL and having it surgically reconstructed, about 25 percent of people show symptoms of osteoarthritis in that knee. By 15 years, the number climbs to roughly 50 percent.
The injury itself disrupts the smooth cartilage surface and changes the way forces travel through the joint. Even after surgical repair restores stability, the subtle mechanical changes remain. Inflammation from the original trauma can also linger in the joint environment, keeping destructive enzymes active long after the ligament or meniscus has healed. This is why younger athletes sometimes develop knee arthritis in their 30s or 40s, well before the age when age-related wear would normally cause problems.
Jobs That Wear the Joint Down
What you do for a living matters. A large analysis pooling 71 studies found that people in physically demanding occupations had about 52 percent higher odds of developing knee osteoarthritis compared to those in sedentary jobs. The specific movements that increase risk are lifting heavy loads, prolonged kneeling, frequent squatting, climbing, and extended standing. Agriculture workers, construction workers, floor layers, carpenters, cleaners, and metalworkers all showed elevated rates. The common thread is sustained or repetitive loading of the knee in positions that compress the cartilage unevenly, particularly deep flexion positions like kneeling and squatting.
Genetics and Family History
Some people inherit joints that are more vulnerable. You don’t inherit arthritis itself, but you can inherit a predisposition to it. Several genes are involved, including ones that influence collagen structure, bone development, and the body’s inflammatory responses. The inheritance pattern isn’t straightforward, though. It involves common variations across many genes, each contributing a small amount of risk. If your parents or siblings developed knee arthritis relatively early, your own risk is likely higher, but lifestyle factors like weight, activity level, and injury history still heavily influence whether that genetic tendency becomes actual disease.
Age and Sex
About 73 percent of people living with osteoarthritis are older than 55, and 60 percent are female. Age matters because cartilage loses its ability to repair itself over time. The chondrocytes that maintain the tissue become less responsive, the water content of cartilage decreases, and the cumulative effect of decades of use adds up. Women face higher rates partly due to hormonal changes after menopause, which appear to reduce the protective effects of estrogen on cartilage and bone, and partly due to differences in knee alignment and joint geometry that alter how forces distribute across the joint surface.
How These Causes Overlap
In most people, knee arthritis doesn’t have a single cause. It develops from a combination of factors reinforcing each other. A person with a genetic predisposition who works a physically demanding job and carries extra weight will face a very different trajectory than someone with the same genes who stays lean and works at a desk. A knee injury in your 20s may cause no problems for a decade, then progress rapidly if you gain significant weight in your 40s. The metabolic inflammation from excess fat tissue amplifies the mechanical damage, and both accelerate the cartilage breakdown that aging alone would produce slowly. Recognizing which factors apply to you is the first step in understanding what can still be changed and what needs to be managed.