Arthritis isn’t a single disease with a single cause. It’s an umbrella term for more than 100 conditions that damage your joints, and each type has its own triggers. You can get arthritis from wear and tear on your cartilage, from your immune system attacking your own joints, from infections, from a buildup of crystal deposits, or from a past injury that never fully healed. Nearly 19% of U.S. adults have been diagnosed with some form of arthritis, and by age 75, more than half of all adults have it.
Wear and Tear on Cartilage
Osteoarthritis is the most common form, and it develops when the smooth cartilage cushioning your joints gradually breaks down. Cartilage doesn’t have its own blood supply, so once it’s damaged, it has very limited ability to repair itself. Over time, the erosion progresses until the underlying bone is exposed. When bone grinds against bone, your body responds by thickening and hardening the bone surface at pressure points. The stressed bone can also develop fluid-filled cysts from chronic impact or from joint fluid seeping into tiny cracks.
This process unfolds over years or decades, which is why osteoarthritis is strongly linked to aging. Only about 3.6% of adults aged 18 to 34 have diagnosed arthritis, compared with nearly 54% of adults 75 and older. But age alone doesn’t cause it. The joints you’ve used hardest, injured, or overloaded are the ones most likely to develop osteoarthritis. Knees, hips, hands, and the spine are the most common sites.
Your Immune System Turning on Your Joints
Rheumatoid arthritis works completely differently from osteoarthritis. Instead of cartilage wearing down mechanically, your immune system mistakenly identifies the tissue lining your joints as a threat and attacks it. This causes chronic inflammation that can erode cartilage and bone from the inside, often affecting the same joints on both sides of your body.
Genetics play a significant role in who develops rheumatoid arthritis. Variations in a gene called HLA-DRB1 are the strongest known genetic risk factor, with two specific versions of the gene strongly linked to higher risk. But carrying the gene doesn’t guarantee you’ll get the disease. Environmental triggers appear to set the process in motion.
Smoking is one of the clearest triggers. Long-term cigarette use raises the risk of developing rheumatoid arthritis and makes the disease worse in people who continue smoking. Severe gum disease (periodontal disease) is another established risk factor. The bacteria that damage gum tissue appear to provoke immune responses that can extend to the joints. Researchers also suspect that imbalances in gut bacteria play a role, since the trillions of microbes in your digestive system help regulate immune function, and disruptions to that microbial community may push the immune system toward attacking healthy tissue.
Crystal Deposits From High Uric Acid
Gout is a form of arthritis caused by a metabolic problem rather than wear or autoimmunity. Your body naturally produces uric acid when it breaks down compounds called purines. Normally, uric acid dissolves in your blood and gets filtered out by your kidneys. But when your body produces too much or your kidneys don’t excrete enough, uric acid builds up and forms sharp, needle-like crystals inside a joint. The result is sudden, intense pain, usually striking the big toe first.
Several dietary factors push uric acid levels higher. Red meat, organ meats like liver, and certain seafood (anchovies, sardines, mussels, scallops, trout, and tuna) are all rich in purines. Beer is particularly linked to gout risk, and drinks sweetened with fructose also raise uric acid. Being overweight compounds the problem: your body produces more uric acid when you carry extra weight, and your kidneys have a harder time clearing it. Chronic conditions like high blood pressure, diabetes, metabolic syndrome, and kidney disease all increase your risk further.
Infections That Reach the Joint
Bacteria, viruses, and other pathogens can invade a joint directly, causing what’s called septic arthritis. The most common culprit across all age groups is Staphylococcus aureus, the same bacterium responsible for staph infections elsewhere in the body. In sexually active younger adults, gonorrhea is a leading cause, responsible for roughly 75% of septic arthritis cases in that group. Streptococcal species account for about 20% of cases overall.
The bacterium that causes Lyme disease can also produce arthritis. Weeks to months after a tick bite, the infection can settle into the joints, particularly the knee, causing swelling and pain that comes and goes. Several viruses, including hepatitis B, rubella, and parvovirus B19, can trigger joint inflammation as well, either by directly invading joint tissue or by prompting immune complexes that irritate the joint lining.
There’s also a category called reactive arthritis, where your joints flare up not from a direct infection inside the joint but as an immune reaction to an infection somewhere else in your body. Gastrointestinal infections from bacteria like Salmonella, Campylobacter, and Shigella can trigger it, as can urinary tract infections caused by Chlamydia.
Joint Injuries That Lead to Arthritis Later
A major joint injury doesn’t just heal and disappear from the story. Post-traumatic arthritis can develop years after the original injury, with first symptoms typically appearing about a decade later. The numbers are striking: the reported incidence of osteoarthritis after an ACL tear reaches as high as 87% when the meniscus (the rubbery shock absorber inside the knee) is removed during surgery. When the meniscus is preserved, that rate drops to around 26%, which underscores how much the meniscus matters for long-term joint health.
Meniscus tears on their own also carry significant risk. After a total meniscectomy, arthritis rates range from 24% within four years to 71% within 20 years. Even without surgery, a meniscal tear raises your risk of developing knee arthritis by roughly 10 percentage points compared to people with uninjured knees over a 19-year follow-up. Fractures that extend into the joint surface, dislocations, and other structural injuries similarly alter the joint’s mechanics in ways that accelerate cartilage breakdown.
How Excess Weight Affects Your Joints
Carrying extra weight increases arthritis risk through two separate mechanisms. The obvious one is mechanical: more body weight means more force pressing down on your knees, hips, and ankles with every step. But obesity also drives arthritis in joints that don’t bear weight at all, like the hands, which points to a second, less obvious pathway.
Fat tissue is metabolically active. It releases inflammatory signaling molecules that circulate throughout your body. One of these, leptin, stimulates the production of other inflammatory compounds and reactive oxygen species, creating a persistent low-grade inflammatory state. Even a molecule traditionally considered anti-inflammatory, adiponectin, appears to have the opposite effect inside joints, where it stimulates the release of inflammatory mediators. This means excess body fat doesn’t just load your joints mechanically. It bathes them in a chemical environment that promotes inflammation and cartilage breakdown, increasing the risk of both osteoarthritis and rheumatoid arthritis.
Multiple Factors Usually Combine
Most people who develop arthritis don’t have just one risk factor. A person might carry a genetic predisposition, smoke for 15 years, and carry 30 extra pounds. Someone else might tear their ACL at 25, gain weight during recovery, and develop knee arthritis by 40. The combination of mechanical stress, metabolic inflammation, immune dysfunction, and genetic vulnerability determines not just whether you get arthritis, but which type, how early, and how severe it becomes.
The factors you can’t control, like your genes and your age, set the baseline. The factors you can influence, like body weight, smoking, diet, joint protection after injuries, and treatment of infections, determine how much of that baseline risk actually turns into disease.