Osteoarthritis develops when the cartilage cushioning your joints breaks down faster than your body can repair it. Over 450 million adults over 55 worldwide live with the condition, and its causes extend well beyond simple “wear and tear.” A combination of mechanical stress, inflammatory signals, genetics, hormones, and metabolic health all play a role in whether and how quickly joints deteriorate.
What Actually Happens Inside the Joint
Cartilage is a firm, slippery tissue that caps the ends of bones where they meet. In a healthy joint, cartilage absorbs shock and allows smooth, painless movement. In osteoarthritis, the cells that maintain cartilage (chondrocytes) begin producing inflammatory molecules and enzymes that chew through the surrounding tissue. These enzymes break down the two main structural components of cartilage: collagen fibers that give it strength and proteoglycans that help it absorb water and resist compression.
This isn’t just cartilage wearing thin like a brake pad. The entire joint becomes inflamed. The synovium, the membrane lining the inside of the joint, swells and produces its own wave of inflammatory signals. The bone underneath the cartilage thickens and stiffens. The body tries to stabilize the joint by growing bony spurs (osteophytes) around the edges, which can limit range of motion and press on nearby tissues. Ligaments, tendons, and even the fat pads within the joint all participate in a feedback loop of damage and inflammation that makes the condition progressive.
Genetics Set the Baseline
Your genes influence your risk more than most people realize. Known genetic variants account for over 20% of osteoarthritis heritability, and researchers suspect additional variants remain undiscovered. Genes involved in cartilage structure, bone development, and growth factor signaling have all been linked to higher risk. Some affect how your body builds collagen. Others influence how cartilage cells respond to stress.
This genetic component helps explain why osteoarthritis sometimes runs in families and why two people with similar lifestyles can have very different joint health. It also means that some people’s cartilage is inherently less resilient, making them more vulnerable to the other causes on this list.
Joint Injuries and Post-Traumatic Arthritis
A significant joint injury dramatically raises your risk, even if it’s surgically repaired. Among people who tear the ACL in their knee and undergo reconstructive surgery, about 25% show osteoarthritis symptoms within 10 years. By 15 years, that number climbs to roughly 50%. Dislocations, fractures that extend into a joint, and meniscus tears carry similar risks.
The more unstable a joint becomes after injury, the more likely it is to develop arthritis down the road. Recurrent ankle sprains, shoulder dislocations, and kneecap dislocations all increase lifetime risk. The initial trauma triggers inflammation and can subtly alter the mechanics of how the joint moves, concentrating force on areas of cartilage that weren’t designed for it.
Obesity Does More Than Add Weight
Carrying excess weight increases mechanical load on weight-bearing joints like the knees and hips, but the connection between obesity and osteoarthritis goes deeper. Fat tissue, particularly visceral fat around the organs, is an active endocrine organ that releases a large family of signaling molecules called adipokines. Around 100 different adipokines have been identified, and many of them directly promote inflammation in cartilage, the joint lining, and bone.
This explains a finding that purely mechanical theories can’t: obesity also raises the risk of osteoarthritis in non-weight-bearing joints like the hands. In people with obesity, fat tissue attracts immune cells that shift toward a pro-inflammatory state, creating low-grade, chronic, body-wide inflammation. One key hormone released by fat cells circulates at levels roughly 7 to 17 times higher in people with obesity compared to lean individuals, and it stimulates immune responses that accelerate joint damage. The metabolic environment of obesity, not just the extra pounds, actively degrades cartilage.
Occupational and Repetitive Stress
The work you do five days a week for decades shapes your joint health. A meta-analysis of 71 studies found that people in physically demanding jobs had 52% higher odds of developing knee osteoarthritis compared to those in sedentary roles. Specific activities that raised risk included heavy lifting (over 10 kg per day), squatting or kneeling for more than 30 minutes daily, climbing more than 15 flights of stairs a day, and standing for over two hours.
Certain occupations carry particularly elevated risk. Floor layers and bricklayers had roughly 2.5 times the odds of knee osteoarthritis compared to sedentary workers. Carpenters faced similarly high odds. Farmers, construction workers, metal workers, miners, cleaners, and service workers all showed significantly increased risk. Even routine housework was associated with nearly double the odds. The common thread is repetitive loading of the same joints in the same patterns, day after day, without adequate recovery.
Estrogen Loss After Menopause
Women develop osteoarthritis at higher rates than men, and the gap widens sharply after menopause. Postmenopausal women have nearly twice the prevalence of osteoarthritis compared to men of the same age. Radiographic knee osteoarthritis is three times more common in women aged 45 to 64 than in men of the same age group.
Estrogen appears to directly protect cartilage. It suppresses inflammation within joints, encourages cartilage cells to produce collagen and proteoglycans, and helps maintain the expression of genes critical for cartilage health. When estrogen levels drop at menopause, cartilage cells lose these protective signals. Research on cartilage cells shows that a specific estrogen receptor becomes less active in damaged osteoarthritic tissue compared to preserved cartilage, and when researchers restore that receptor’s activity in lab settings, markers of aging and degeneration in cartilage cells decrease. Clinical studies show that postmenopausal women receiving estrogen supplementation report modestly less joint pain than those on placebo.
Estrogen loss also alters the communication between the bone underneath cartilage and the cartilage itself. When researchers co-cultured cartilage cells with bone cells from estrogen-deficient mice, the cartilage cells ramped up tissue-destroying enzymes and dialed down protective ones. This crosstalk between bone and cartilage is one way menopause accelerates joint breakdown.
Diabetes and High Blood Sugar
Diabetes is an independent risk factor for osteoarthritis, separate from its association with obesity. Chronically elevated blood sugar promotes the formation of compounds called advanced glycation end products, which are essentially sugar molecules that permanently attach to proteins like collagen. In cartilage, this cross-linking makes the tissue stiffer and more brittle, impairing its ability to absorb shock. These sugar-modified proteins also block the normal turnover and repair of the cartilage matrix.
Beyond structural damage, these compounds bind to receptors on cartilage cells and trigger inflammation, increasing the production of the same tissue-destroying enzymes seen in other forms of osteoarthritis. Studies in diabetic mice show that elevated glycation products ramp up cartilage-degrading enzyme expression while simultaneously reducing the output of key structural proteins that cartilage needs to maintain itself. The result is a joint environment where damage accelerates and repair slows, creating a faster path to osteoarthritis regardless of body weight or joint injury history.
Age and the Accumulation of Risk
Age is the single strongest risk factor, but not because joints simply “wear out.” Over time, cartilage cells become less efficient at repairing damage and more prone to producing inflammatory signals. The cumulative effect of decades of mechanical loading, combined with age-related changes in metabolism, hormone levels, and immune function, tips the balance from maintenance to breakdown. Global projections estimate that age-adjusted osteoarthritis rates will rise another 14% by 2050, driven largely by aging populations worldwide.
What makes osteoarthritis so common is that its causes compound. A person with a genetic predisposition who also works a physically demanding job, carries extra weight, and enters menopause faces converging risks that each amplify the others. Understanding which factors apply to you can help clarify which ones you have the ability to modify, whether through weight management, protecting joints from repetitive strain, or managing blood sugar levels.