Osteoarthritis develops when the cartilage cushioning your joints breaks down faster than your body can repair it. About 528 million people worldwide live with the condition, and while aging is the most familiar risk factor, the actual causes involve a complex mix of mechanical wear, metabolic dysfunction, hormonal shifts, and inflammatory processes that can start years before you feel any pain.
How Cartilage Breaks Down
Healthy cartilage is maintained by specialized cells called chondrocytes, which constantly build new cartilage matrix and clear away damaged tissue. In osteoarthritis, these cells stop functioning properly. When the joint environment becomes inflamed or stressed, chondrocytes shift from their normal energy-producing pathway to a less efficient one. This metabolic switch involves mitochondrial dysfunction and disrupted fat and protein processing within the cells, essentially starving them of the resources they need to maintain cartilage.
At the same time, inflammatory signaling molecules ramp up production of enzymes that actively dissolve the cartilage matrix. These enzymes chew through the collagen and protein scaffolding that gives cartilage its structure and shock-absorbing ability. The result is a vicious cycle: inflammation triggers enzyme release, enzymes destroy cartilage, cartilage debris fuels more inflammation, and the chondrocytes caught in the middle lose their ability to keep up with repairs. Over time, cartilage thins, roughens, and eventually wears away entirely, leaving bone grinding against bone.
Age and Wear Over Time
About 73% of people with osteoarthritis are older than 55. This isn’t simply because joints “wear out” like machine parts. Aging changes the biology of the joint itself. Chondrocytes become less responsive to repair signals, the cartilage loses water content and becomes stiffer, and the low-grade inflammation that accumulates with age creates a more hostile environment for joint tissues. Decades of loading also cause microscopic damage that healthy young cartilage repairs easily but aging cartilage cannot.
The knee is the most commonly affected joint, with 365 million people affected globally, followed by the hip and hand. These are the joints that bear the most weight or perform the most repetitive movements over a lifetime.
Obesity: More Than Extra Weight
Carrying excess body weight increases the mechanical load on your knees and hips with every step. But obesity drives osteoarthritis through a second, less obvious pathway. Fat tissue is metabolically active, releasing hormones and signaling molecules that promote inflammation throughout the body. These fat-derived substances trigger the same inflammatory cascades and cartilage-destroying enzymes found in osteoarthritic joints, leading to cartilage breakdown and changes in the bone beneath it.
This explains something that puzzled researchers for years: why obese individuals develop osteoarthritis in their hands, joints that don’t bear any extra weight. The metabolic inflammation from excess fat tissue reaches every joint, not just the load-bearing ones. Losing weight reduces both the mechanical stress and the inflammatory burden, which is why even modest weight loss can significantly slow disease progression.
Joint Injuries and Post-Traumatic Arthritis
A major knee injury, such as a torn ACL or damaged meniscus, leads to osteoarthritis in 25 to 50% of patients. The initial trauma causes bleeding and inflammation inside the joint, and this inflammatory surge can damage cartilage cells even in areas far from the original injury. The joint’s biomechanics also change after an injury. A repaired ligament may restore stability, but subtle shifts in how forces distribute across the joint surface can accelerate cartilage wear in specific spots.
Post-traumatic osteoarthritis develops gradually, often progressing over many years before symptoms appear. This means someone who tears their ACL at 20 may not feel the consequences until their 30s or 40s, well before the age when osteoarthritis typically shows up. Athletes, military personnel, and anyone with a history of significant joint trauma carry elevated long-term risk.
Why Women Are Affected More Often
Women make up 60% of osteoarthritis cases worldwide, and the gender gap widens sharply after menopause. Estrogen plays a protective role in joint health that goes well beyond what most people realize. It suppresses inflammatory molecules that damage cartilage, promotes chondrocyte survival and reproduction, reduces oxidative stress within joint tissues, and helps maintain the balance between bone building and bone breakdown in the layer just beneath the cartilage.
When estrogen levels drop during menopause, all of these protective effects diminish at once. The rate of bone remodeling beneath the cartilage increases significantly, the subchondral bone becomes stiffer and more sclerotic, and the biomechanical environment of the joint shifts in ways that accelerate cartilage loss. Women also tend to develop knee osteoarthritis at a younger average age than men, and their disease tends to be more severe. Estrogen’s influence extends even to pain perception: it modulates neurotransmitter activity in brain regions that process pain signals, which may partly explain why osteoarthritis pain often intensifies around menopause.
Occupational and Repetitive Stress
Your job can be a significant risk factor. A WHO/ILO systematic review found that workers exposed to ergonomic risk factors for two or more hours per day, including kneeling, squatting, heavy lifting, repetitive movements, and forceful exertion, had roughly 2.2 times the risk of developing knee or hip osteoarthritis compared to workers with low exposure.
This means construction workers, farmers, floor layers, warehouse workers, and others whose jobs demand sustained physical loading on specific joints face meaningfully higher risk. The damage accumulates over years and decades. Unlike a single traumatic injury, occupational wear produces chronic low-level damage that overwhelms the cartilage’s repair capacity gradually. The pattern of arthritis often reflects the specific demands of the job: knee osteoarthritis in workers who kneel or squat, hip osteoarthritis in those who climb or lift heavy loads repeatedly.
Genetics and Joint Alignment
Osteoarthritis runs in families, particularly for hand and hip involvement. Genetic factors influence the thickness and resilience of your cartilage, the shape and alignment of your joints, and how aggressively your immune system responds to joint damage. If your parents or siblings developed osteoarthritis, your own cartilage may be inherently less durable or your inflammatory responses more pronounced.
Joint alignment matters independently of genetics. Bow-legged or knock-kneed alignment concentrates force on one side of the knee, accelerating wear in that compartment. Previous fractures that healed with even slight misalignment change the distribution of forces across the joint surface, creating focal points of stress where cartilage deteriorates faster. These structural factors interact with every other risk factor: an overweight person with slight knee malalignment faces compounding risk that neither factor alone would produce.
How Multiple Causes Interact
Osteoarthritis rarely has a single cause. In most cases, several risk factors converge. A postmenopausal woman with a history of knee injury and a physically demanding job is experiencing hormonal, traumatic, and mechanical drivers simultaneously. An overweight man with a family history of arthritis faces metabolic inflammation layered on top of genetic susceptibility. The 113% increase in global osteoarthritis cases since 1990 reflects population aging, rising obesity rates, and longer working lives all pushing in the same direction.
Understanding which factors apply to you matters because some are modifiable. You can’t change your age, sex, or genetics, but maintaining a healthy weight, protecting joints from injury, strengthening the muscles that support vulnerable joints, and modifying repetitive occupational exposures can all slow the process that leads from early cartilage changes to symptomatic disease. Currently, 344 million people live with osteoarthritis severe enough to benefit from rehabilitation, a number that underscores how much room exists for earlier intervention.