Knee arthritis most commonly results from gradual cartilage breakdown driven by a combination of aging, excess body weight, previous injuries, and genetics. More than 250 million people worldwide live with knee osteoarthritis, which accounts for roughly 80% of the global osteoarthritis burden. But “arthritis” isn’t a single disease. Several distinct conditions can damage the knee joint, each with its own underlying cause.
How Cartilage Breaks Down in the Knee
The most common form of knee arthritis, osteoarthritis, starts with changes in the cartilage cells that line the ends of your bones. Healthy cartilage is smooth, flexible, and rich in a specific type of collagen (type II) that cushions the joint. As osteoarthritis develops, those cartilage cells begin behaving abnormally. Some enlarge and start producing enzymes that actively digest the cartilage matrix around them. Others shift into a different cell type that produces an inferior form of collagen (type I), resulting in rough, stiff fibrocartilage instead of the smooth original surface.
At the same time, immune cells in the tissue surrounding the joint release inflammatory signals into the joint fluid. These signals reach the cartilage surface and trigger even more enzyme production, creating a cycle: inflammation drives cartilage damage, and fragments of damaged cartilage provoke further inflammation. Over time, cartilage cells begin dying off entirely, thinning the protective layer until bone grinds against bone.
Body Weight: More Than Just Extra Pressure
Carrying excess weight is one of the strongest risk factors for knee arthritis, and the reason goes beyond simple mechanics. Yes, every extra pound of body weight multiplies the force on your knees during walking. But fat tissue itself is metabolically active and releases signaling molecules that promote inflammation throughout the body.
As fat cells accumulate, they produce substances like leptin and resistin that act as pro-inflammatory triggers. Circulating leptin is directly associated with increased knee cartilage loss and greater joint pain. These fat-derived signals stimulate the same inflammatory pathways and cartilage-degrading enzymes that drive osteoarthritis from within the joint. This is why people with obesity develop arthritis not only in weight-bearing joints like the knee but also in the hands, where mechanical load isn’t a factor. The combination of increased joint stress and a body-wide inflammatory environment makes excess weight a particularly potent cause.
Past Knee Injuries Raise Long-Term Risk
A torn ligament, meniscus tear, or fracture involving the knee significantly increases your chances of developing arthritis later. A large population-based study published in the British Journal of Sports Medicine tracked young adults over 19 years and found that 11.3% of those who had sustained a knee injury were eventually diagnosed with knee osteoarthritis, compared to just 4% of those without injuries. Overall, a knee injury increases your risk of future osteoarthritis roughly sixfold.
What’s surprising is the timeline. Injured individuals developed osteoarthritis only about 7 to 9 months sooner than uninjured people who also developed it at a young age. This suggests that injury doesn’t simply accelerate an inevitable process by decades. Instead, it sets off a distinct biological cascade: damage to cartilage or the structures that stabilize the joint alters how forces distribute across the knee, creating zones of abnormal wear that accumulate over years.
Genetics Account for About 40% of Risk
The heritable component of knee osteoarthritis is estimated at approximately 40%, meaning your genes play a substantial role in determining whether your cartilage holds up over time. Researchers have identified specific gene variants linked to cartilage thickness and structure, including genes involved in bone growth signaling and the composition of the material between cartilage cells. Additional variants affect how cartilage genes are expressed, influencing the quality and resilience of the tissue you’re born with.
If your parents or siblings developed knee arthritis, your risk is meaningfully higher, independent of weight or activity level. Genetics likely influence cartilage composition, the strength of the inflammatory response in your joints, and even the alignment of your leg bones.
Why Women Are Affected More Often
Knee arthritis is not evenly distributed between sexes. Among people aged 40 to 49, about 10% of women and 7% of men have knee osteoarthritis. By ages 60 to 69, the gap widens dramatically: 35% of women versus 19% of men. After age 70, the rates converge again.
The sharp increase in women around age 50 points strongly to hormonal factors tied to menopause. Estrogen appears to play a role in cartilage cell metabolism and in regulating inflammation within the joint. During periods of higher estrogen, such as certain phases of the menstrual cycle or pregnancy, knee joints become looser, which may contribute to altered mechanics over time. Menopause also commonly brings weight gain, compounding the mechanical and metabolic stress on the knees.
Occupational Wear and Repetitive Stress
Certain jobs and activities place the knee under repeated strain that accelerates cartilage damage. Men whose occupations involve frequent squatting, kneeling, and heavy lifting have roughly 1.8 times the risk of worse cartilage damage at the front of the knee (the patellofemoral joint) compared to men without those exposures, even after accounting for age, weight, and prior injuries. Professions like flooring installation, plumbing, farming, and construction carry elevated risk for this reason.
Recreational activities matter too. Sports that involve sudden pivoting, jumping, or repeated impact contribute to cumulative cartilage stress. The effect is dose-dependent: occasional activity strengthens the joint, but years of high-volume, high-impact loading without adequate recovery can tip the balance toward breakdown.
Autoimmune Arthritis in the Knee
Rheumatoid arthritis is a fundamentally different disease from osteoarthritis. Instead of cartilage wearing down from use, the immune system attacks the joint lining directly. Specialized cells in the synovial membrane become abnormally aggressive, proliferating and forming a thick, invasive tissue called pannus. This tissue creeps over the cartilage surface and actively erodes both cartilage and bone.
The process is driven by inflammatory signals, particularly a molecule called TNF-alpha, along with others that activate bone-dissolving cells and suppress bone-building cells. The result is progressive joint destruction that can occur rapidly if untreated. Rheumatoid arthritis typically affects joints symmetrically (both knees, for instance) and often starts in smaller joints before progressing to larger ones. It can begin at any age, unlike osteoarthritis, which becomes increasingly common after 50.
Crystal Deposits in the Knee
Two types of crystal-related arthritis can affect the knee. Gout occurs when uric acid crystals accumulate in the joint, triggering intense, sudden inflammation. The knee is one of the most commonly affected joints after the big toe. Repeated gout flares can cause permanent cartilage and bone damage if uric acid levels remain elevated over time.
Pseudogout, which is caused by calcium pyrophosphate crystals, is especially common in the knee. These crystals deposit within the cartilage itself and can be released into the joint space, particularly after an injury. Once loose in the joint, they provoke an inflammatory reaction that mimics gout. Chronic or recurring pseudogout can lead to progressive joint degeneration that resembles osteoarthritis on imaging but follows a different underlying mechanism.
How Damage Progresses Over Time
Knee arthritis is graded on a five-point scale based on X-ray findings. At the earliest stage, there are no visible changes. The next stage shows only questionable narrowing of the joint space and possible small bone spurs. By the moderate stages, bone spurs are clearly visible, the space between bones has narrowed noticeably, and the bone beneath the cartilage begins to harden. At the most advanced stage, large bone spurs, severe joint space loss, dense bone hardening, and visible bone deformity are all present.
This progression is not inevitable or linear. Some people remain at mild stages for decades, while others progress rapidly over a few years. The speed depends on the interplay of all the factors above: weight, genetics, activity, injury history, hormonal status, and the type of arthritis involved. What every form shares is that once cartilage is lost, the body cannot regenerate it to its original quality, making early attention to modifiable risk factors, especially body weight and joint protection, particularly valuable.