The most common cause of osteoarthritis is not simple “wear and tear,” as was long believed. It’s a complex breakdown in how your body maintains cartilage, driven by a combination of genetic susceptibility, excess body weight, and cumulative joint stress. Around 528 million people worldwide live with osteoarthritis, and the knee is the most frequently affected joint, accounting for roughly 365 million of those cases.
No single factor causes osteoarthritis on its own. Instead, several forces converge to tip the balance inside your joints from healthy cartilage maintenance toward progressive cartilage loss. Understanding which of these factors matter most can help you make sense of your own risk.
How Cartilage Breaks Down
Healthy cartilage is in a constant state of renovation. Your cartilage cells build new structural proteins while enzymes clear away old or damaged material. In osteoarthritis, that balance shifts decisively toward destruction. The enzymes that break down cartilage become overproduced, and the natural inhibitors that keep them in check get overwhelmed. The result is a net loss of the proteins that give cartilage its strength and cushioning ability.
Early on, your cartilage cells actually try to compensate. They multiply and ramp up production of new structural material. But as the disease progresses, these repair efforts fall behind. Inflammatory signaling molecules accelerate the damage by suppressing the production of new cartilage proteins, triggering cartilage cell death, and promoting further inflammation. In simple terms, osteoarthritis is a repair process that can’t keep up with an accelerating demolition.
Researchers have also discovered that specific cartilage cells reactivate a program from early development. During childhood bone growth, certain cells are supposed to break down cartilage and replace it with bone. In osteoarthritis, these cells switch on again at the wrong time and in the wrong place, creating the hallmark features of the disease: disappearing cartilage, abnormal bone growth at joint edges, and new blood vessels forming where they shouldn’t.
Genetics Account for Half Your Risk
Studies in twins have shown that roughly 50% or more of your susceptibility to osteoarthritis comes from your genes. The heritability varies by joint. For hand and knee osteoarthritis in women, genetic factors explain between 39% and 65% of the variation in risk. For hip osteoarthritis, that figure is about 60%. The spine shows the strongest genetic influence, with heritability estimates around 70% to 74%.
Researchers have identified linkages on multiple chromosomes and implicated genes involved in cartilage structure, growth factor signaling, and collagen production. You can’t change your genetic makeup, but knowing that a parent or sibling has osteoarthritis is a meaningful signal that your own joints may be more vulnerable to the other risk factors on this list.
Why Excess Weight Does More Than Stress Joints
Obesity is one of the strongest modifiable risk factors for osteoarthritis, and it works through two separate pathways. The obvious one is mechanical: extra body weight puts more force through your knees and hips with every step. But the less obvious pathway may be just as damaging.
Fat tissue is not passive storage. It actively releases inflammatory signaling molecules called adipokines into the bloodstream. These chemicals travel throughout the body and can trigger inflammation inside joints, stimulate the overproduction of cartilage-degrading enzymes, and suppress the repair processes that keep cartilage healthy. This helps explain why obesity increases the risk of osteoarthritis even in non-weight-bearing joints like the hands.
The connection runs both ways. Weight loss is associated with meaningful reductions in systemic inflammatory markers in people with osteoarthritis, and it can both prevent onset and relieve existing symptoms. The metabolic component of obesity, including abnormal blood lipids and elevated blood sugar, creates what researchers describe as a “toxic internal environment” that accelerates cartilage deterioration from the inside out.
Joint Injuries and Repetitive Stress
A significant joint injury earlier in life is one of the clearest paths to osteoarthritis. Fractures, dislocations, and severe sprains from car accidents, sports injuries, or falls can all set the stage for cartilage breakdown years or even decades later. This form, sometimes called post-traumatic osteoarthritis, develops because the injury disrupts the joint’s normal mechanics and can trigger low-grade inflammation that never fully resolves.
You don’t need a single dramatic injury, though. Repetitive occupational stress is a well-documented risk factor, particularly for the knee. A large review from Oxford’s Nuffield Department of Orthopaedics found that floor layers, bricklayers, and carpenters face about 2.5 times the odds of knee osteoarthritis compared to sedentary workers. Agricultural workers had up to 64% increased odds, and construction workers 63%. Unpaid houseworkers had up to 93% increased odds. The specific activities driving risk include excessive kneeling, squatting, prolonged standing, heavy lifting, and frequent stair climbing.
Age Is a Risk Factor, Not a Cause
Osteoarthritis becomes far more common with age, but aging alone doesn’t cause it. The old framing of joints “wearing out” like machine parts has been replaced by a more nuanced understanding. What aging does is reduce the cartilage cells’ ability to repair damage, thin the cartilage slightly, and make joints more susceptible to the inflammatory and mechanical forces described above.
One protective factor that works against age-related changes is regular physical activity. Exercise prompts your cartilage to release a signaling molecule that suppresses inflammation and keeps the problematic cartilage cells in check. This is part of why moderate exercise protects against osteoarthritis rather than accelerating it, a finding that contradicts the outdated wear-and-tear model.
How These Factors Work Together
Osteoarthritis rarely comes from one cause acting alone. A person with a strong genetic predisposition might develop it in their hands without any obvious trigger. Someone else might develop it in one knee decades after tearing a ligament playing sports, especially if they also carry extra weight. The combination of genetic vulnerability, metabolic inflammation from excess fat tissue, and mechanical stress on the joint is what pushes most people across the threshold from healthy cartilage maintenance into progressive joint disease.
Systemic low-grade inflammation ties many of these risk factors together. Obesity, metabolic conditions, and aging all contribute to a baseline level of inflammation that circulates through the body and settles in joints. This chronic, simmering inflammation promotes cartilage degradation even in the absence of a clear injury. It’s the reason osteoarthritis is increasingly understood as a whole-body condition with local consequences in the joints, not simply a mechanical problem of bones grinding together.