Arthritis has no single cause. It’s an umbrella term covering more than 100 conditions that produce joint pain and inflammation, and the triggers range from normal aging and genetics to infections, immune system misfires, and physical trauma. Roughly 67 million U.S. adults, about 28% of the population aged 20 and older, have some form of diagnosed arthritis. Understanding what drives each type can help you recognize your own risk factors and take steps to protect your joints.
Wear and Tear: How Osteoarthritis Develops
Osteoarthritis is the most common form, and it starts with the gradual breakdown of cartilage, the smooth, rubbery tissue that cushions the ends of your bones. Over time, the cells that maintain cartilage begin to age and malfunction. As they deteriorate, they release inflammatory signals into the surrounding joint tissue. That inflammation ramps up the production of enzymes that actively dissolve the cartilage matrix, turning a slow process into a destructive cycle: less cartilage leads to more inflammation, which leads to even faster cartilage loss.
Aging also weakens the energy-producing machinery inside cartilage cells. When those internal power plants falter, harmful molecules called free radicals accumulate, poisoning the cells and accelerating cartilage destruction. This is why osteoarthritis becomes dramatically more common after age 50, even in people who haven’t had obvious joint injuries.
Excess body weight amplifies the problem. For every additional pound of body weight, the compressive force on your knees increases roughly fourfold. A person who gains 10 pounds is effectively loading an extra 40 pounds of force onto each knee with every step. That persistent overload grinds down cartilage faster than the body can repair it, which is why obesity is one of the strongest modifiable risk factors for knee and hip osteoarthritis.
When the Immune System Attacks Joints
Rheumatoid arthritis (RA) works through a completely different mechanism. Instead of mechanical wear, the immune system mistakenly targets the lining of the joints, treating healthy tissue as a threat. The resulting chronic inflammation thickens the joint lining, erodes cartilage, and can eventually damage bone. Why the immune system turns on itself isn’t fully understood, but a combination of genetics and environmental exposures seems to prime the system for attack.
Genetics plays a measurable role. Most RA patients carry a specific set of gene variants on their immune cells. People who inherit one copy of these variants have about 2.4 times the odds of developing joint damage compared to those without them. Carrying two copies raises the odds to nearly 4 times. RA is also more common in people of European descent than in African populations, though the genetic risk markers appear in both groups.
Among environmental triggers, smoking stands out. It is the single strongest known environmental risk factor for RA. Smokers face roughly double the risk of developing RA compared to nonsmokers, and the risk climbs with the number of years and cigarettes smoked. Heavy smokers with more than 40 pack-years of use have about a twofold increase in risk. When smoking combines with high-risk genetics, the effect multiplies: a smoker who also carries two copies of the relevant gene variants faces a 21-fold higher risk than a nonsmoker without those genes.
Other environmental factors associated with RA risk include lower socioeconomic status (people with the least education face roughly double the risk of those with the most), geographic location (living in the northeastern United States is linked to about 45% higher risk compared to the West), and even birth weight. Babies born weighing more than about 10 pounds have roughly twice the risk of eventually developing RA. On the protective side, long-term breastfeeding of 13 months or more appears to lower risk in women.
Uric Acid Crystals and Gout
Gout is a form of arthritis caused by a metabolic problem rather than wear or autoimmunity. The body produces uric acid as it breaks down certain compounds found in food and in your own cells. Normally, the kidneys filter out uric acid efficiently. But when the body produces too much, excretes too little, or both, uric acid levels in the blood rise until sharp, needle-like crystals begin forming inside joint spaces.
Those crystals trigger an intense inflammatory reaction, often striking the big toe first. The pain typically comes on fast, peaking within hours, and the joint becomes red, hot, and swollen. Foods rich in compounds the body converts to uric acid (organ meats, shellfish, certain fish) and heavy alcohol consumption are well-known dietary triggers. Kidney disease, certain medications, and genetic tendencies to under-excrete uric acid all raise risk as well.
Infections That Inflame Joints
Bacteria, viruses, and fungi can all invade a joint and cause septic arthritis. Staphylococcus aureus is the most common culprit in both children and adults. In sexually active young adults, gonorrhea is the leading cause of sudden, nontraumatic joint infection. In newborns, a different set of bacteria dominates, including Group B Streptococcus and certain gram-negative organisms.
Septic arthritis usually affects a single joint and develops quickly, with severe pain, swelling, warmth, and fever. Puncture wounds and injection drug use are associated with Pseudomonas infections in joints, and people with sickle cell disease face elevated risk from Salmonella. Fungal joint infections tend to develop more slowly and are harder to diagnose, sometimes occurring in people who have been on long courses of antibiotics.
Joint Injuries and Post-Traumatic Arthritis
A significant joint injury, such as a torn ligament, fractured bone extending into the joint surface, or a dislocated joint, can set the stage for arthritis years later. Between 20% and 50% of people who experience a serious joint injury eventually develop osteoarthritis in that joint, and these cases account for about 12% of all osteoarthritis diagnoses.
The timeline varies enormously. Some people develop symptoms within a year of their injury. Others remain pain-free for 10 to 20 years before the damaged joint begins to break down. The initial trauma disrupts the smooth cartilage surface and alters the joint’s mechanics, creating uneven loading patterns that accelerate wear even after the original injury heals.
Repetitive Motion and Occupational Stress
You don’t need a single dramatic injury to damage a joint. Decades of repetitive motion can produce the same result. Farmers face some of the highest occupational risks, with hand and wrist arthritis rates nearly three times higher than in the general population. Dairy farmers, who spend hours milking and driving tractors, have significantly elevated rates of hip and knee osteoarthritis. One study of Swedish farmers found that those milking the most cows or working more than five hours a day had dramatically higher odds of hip or knee disease.
The key risk factors in any occupation include repetitive motion, awkward postures, forceful movements, vibration, and insufficient recovery time between tasks. Frequent knee bending shows a particularly strong association with knee osteoarthritis. Manual harvesting of fruits and vegetables, meat processing, and any job requiring sustained kneeling or squatting all carry elevated risk.
Genetics and the Spine: Ankylosing Spondylitis
Ankylosing spondylitis is a type of inflammatory arthritis that primarily targets the spine and the joints where the spine meets the pelvis. It causes pain and stiffness that typically start in the lower back and can, over years, cause vertebrae to fuse together. More than 8 out of 10 people with ankylosing spondylitis carry a gene variant called HLA-B27. Having this gene doesn’t guarantee you’ll develop the condition (most carriers never do), but it dramatically increases susceptibility, especially when combined with other genetic or environmental factors.
Skin Disease and Psoriatic Arthritis
About 30% of people with the skin condition psoriasis eventually develop psoriatic arthritis. The same overactive immune pathways that cause scaly, inflamed skin patches also attack the joints, tendons, and the places where ligaments attach to bone. Psoriatic arthritis can affect any joint but commonly targets the fingers and toes, sometimes causing them to swell into a sausage-like shape. In most cases, skin symptoms appear years before joint symptoms, though some people develop joint inflammation first or experience both simultaneously.
Risk Factors You Can and Can’t Control
Some causes of arthritis are fixed. Your genetics, sex (women develop RA more often; men develop gout more often), and age are beyond your control. But several major risk factors respond to lifestyle changes:
- Body weight: Losing even a modest amount reduces knee forces substantially, given the 4-to-1 force multiplier.
- Smoking: Quitting lowers RA risk, especially for people who know they carry genetic risk factors.
- Joint protection: Using proper ergonomics, varying tasks, and allowing recovery time between repetitive activities can slow occupational wear.
- Diet: Managing uric acid through dietary choices helps prevent gout flares.
- Injury prevention: Proper training, strengthening muscles around vulnerable joints, and wearing appropriate protective equipment reduce the chance of post-traumatic arthritis.