Arthritis is inflammation in one or more joints that causes pain, stiffness, and swelling. It’s not a single disease. The term covers more than 100 conditions, from the gradual cartilage breakdown of osteoarthritis to the immune system attacks of rheumatoid arthritis to the crystal deposits of gout. Globally, osteoarthritis alone affects roughly 24 out of every 100 people when adjusted for age, a rate that climbed about 9% between 1990 and 2021.
What Happens Inside an Arthritic Joint
Healthy joints are lined with a thin membrane called the synovium, which produces fluid that lubricates cartilage and allows bones to glide smoothly. In arthritis, that system breaks down. The specifics depend on the type, but the result is the same: the protective cartilage wears away, the joint lining becomes inflamed, and eventually the underlying bone itself can be damaged.
In osteoarthritis, the cartilage cells (chondrocytes) lose their normal balance between building new tissue and breaking old tissue down. Stress and low-grade inflammation flip a switch that causes these cells to release enzymes that chew through the cartilage matrix. Once fragments of broken-down cartilage float into the joint fluid, they trigger more inflammation, which releases more enzymes. This feedback loop is why osteoarthritis tends to accelerate over time rather than stay stable.
In rheumatoid arthritis, the immune system drives the process. White blood cells flood the synovial membrane and new blood vessels form there, thickening the lining into an aggressive tissue called pannus. This overgrown tissue is rich in bone-destroying cells called osteoclasts, which erode bone directly. Meanwhile, inflammatory signaling molecules like TNF-alpha and interleukin-6 stimulate the release of cartilage-degrading enzymes. The destruction happens from two directions at once: bone eaten from the outside and cartilage dissolved from within.
Osteoarthritis: Wear, Load, and Biology
Osteoarthritis is by far the most common form. It most frequently strikes the knees, hips, and hands. The knee accounts for the largest share of cases worldwide, followed by the hand and then the hip. The United States has among the highest rates of hip osteoarthritis of any country.
The old explanation was simple mechanical wear and tear, but the reality is more nuanced. Osteoarthritis develops when normal forces act on weakened cartilage, or when excessive forces act on healthy cartilage. Both paths lead to the same destination: the cartilage cells can’t keep up with the damage.
Several factors push the process along:
- Obesity. Joints absorb forces up to 10 times your body weight during activities like walking. People with a BMI above 30 have nearly seven times the risk of developing knee osteoarthritis compared to those at a healthy weight. For every 5-unit increase in BMI, knee osteoarthritis risk rises by 35% and hip osteoarthritis risk by 11%. Excess body fat also releases inflammatory compounds that damage cartilage independent of joint loading, which is why obesity raises the risk of hand osteoarthritis too.
- Joint injury. A torn ligament, meniscus injury, or fracture that runs through a joint surface can alter how force distributes across the cartilage, accelerating breakdown years or even decades later.
- Age. Cartilage gradually loses its ability to repair itself. Aging chondrocytes become less responsive to growth signals and more susceptible to inflammatory ones.
- Genetics. Some people inherit cartilage that is structurally weaker or joints that are slightly misaligned. Animal models with genetic defects in cartilage composition develop spontaneous osteoarthritis even without excessive loading.
Rheumatoid Arthritis: The Immune System Turns Inward
Rheumatoid arthritis is an autoimmune disease. The immune system, which normally targets bacteria and viruses, mistakenly attacks the joint lining. The synovium fills with a mix of immune cells: T cells that coordinate the attack, B cells that produce antibodies, macrophages that amplify inflammation, and dendritic cells that recruit still more immune cells to the site. The result is a hot, swollen, painful joint that progressively loses function.
Genetics play a major role. The strongest known genetic risk factor involves a group of immune system genes called HLA-DRB1. Certain versions of this gene contain a shared sequence of five amino acids that makes the immune system more likely to misfire against joint tissue. The specific versions vary by ancestry. In people of European descent, a few variants of the DR4 and DR1 types dominate. In East Asian populations, a different DR4 variant is most common. Among some Native American groups, yet another variant carries significant risk for severe disease. Beyond this single gene, large genetic studies have identified over 100 locations in the genome that contribute to rheumatoid arthritis risk, including genes involved in immune cell signaling and the process of protein modification that may trigger the autoimmune response in the first place.
But genetics alone aren’t enough. Environmental triggers matter too. Smoking is the best-established one, particularly in people who already carry the high-risk gene variants. Hormonal factors likely play a role as well, since rheumatoid arthritis is two to three times more common in women than men.
Gout: A Crystal Problem
Gout is caused by a completely different mechanism. When uric acid levels in the blood exceed 6.8 mg/dL, the acid begins crystallizing in and around joints. These needle-shaped crystals trigger an intense inflammatory response, typically striking the base of the big toe first but capable of affecting ankles, knees, wrists, and fingers.
Uric acid is a normal byproduct of breaking down compounds called purines, found in certain foods (red meat, organ meats, shellfish, beer) and produced by your own cells. Most people clear enough uric acid through their kidneys to stay below the crystallization threshold. Gout develops when either production rises too high or the kidneys don’t excrete enough, or both. The long-term treatment target is keeping blood uric acid below 6 mg/dL, safely under the point where new crystals form and low enough to gradually dissolve existing ones.
Risk factors include a diet high in purine-rich foods and alcohol, obesity, kidney disease that reduces uric acid clearance, and certain medications (particularly some diuretics used for blood pressure).
Infectious Arthritis
Bacteria, viruses, or fungi can also infect a joint directly. This is called septic arthritis, and it’s a medical emergency. Staphylococcus aureus (staph) is the most common bacterial cause. The infection usually reaches the joint through the bloodstream from a wound, surgery, or infection elsewhere in the body. Unlike other forms of arthritis that develop over months or years, septic arthritis comes on within hours to days, with rapid-onset pain, swelling, warmth, and often fever. Left untreated, it can permanently destroy a joint.
How to Tell the Types Apart
The pattern of symptoms often points toward the type. Osteoarthritis tends to affect joints asymmetrically, worsens with activity, and improves with rest. Morning stiffness typically lasts less than 30 minutes. Rheumatoid arthritis, by contrast, usually affects joints symmetrically (both wrists, both knees) and causes morning stiffness lasting longer than 30 minutes, often an hour or more. Gout announces itself with sudden, excruciating flares, frequently starting overnight, with the affected joint turning red and becoming extremely tender to the touch.
Joint location helps as well. Osteoarthritis commonly targets the knees, hips, spine, and the joints at the tips of the fingers. Rheumatoid arthritis favors the small joints of the hands and feet, particularly the knuckles and the middle joints of the fingers, while typically sparing the fingertips. Gout has a well-known preference for the big toe, though it can appear in many joints as it progresses.
These patterns aren’t absolute. People can have more than one type of arthritis simultaneously, and early symptoms sometimes overlap. Blood tests for inflammation markers, autoantibodies, and uric acid levels, along with imaging, help clarify the picture when symptoms alone aren’t definitive.