Arthritis breaks down the structures inside your joints, causing pain, stiffness, and gradual loss of movement. But depending on the type, it can also affect your heart, lungs, eyes, and nervous system. About 21% of U.S. adults have been diagnosed with some form of arthritis, making it one of the most common chronic conditions in the country. What it does to your body depends heavily on which type you have and how far it has progressed.
How Arthritis Destroys Cartilage
The most common form, osteoarthritis, starts with a failure of the cells that maintain your cartilage. These cells, called chondrocytes, are responsible for keeping a balance between building up and breaking down the tough, slippery tissue that cushions your joints. In osteoarthritis, that balance tips toward destruction. Normal joint use creates tiny wear particles, and when the body can’t clear them fast enough, they trigger inflammation. That inflammation causes the cartilage cells to release enzymes that dissolve the very proteins holding the cartilage together.
Once this cycle starts, it accelerates. The cartilage cells begin dying off faster than they can be replaced, and the ones that survive lose their ability to make repairs. As people age, many of these cells become senescent, essentially entering a state of permanent retirement where they can no longer maintain the tissue around them. The cartilage thins, roughens, and eventually wears away entirely, leaving bone grinding against bone.
What Happens in Inflammatory Arthritis
Rheumatoid arthritis works through a completely different mechanism. Instead of wear and tear, your immune system attacks the thin membrane lining your joints. This membrane, called the synovium, becomes inflamed and swollen. Immune cells flood the area, releasing inflammatory signals that sustain and worsen the attack. Over time, a destructive tissue called pannus forms at the border between the synovium, cartilage, and bone. Pannus is packed with immune cells and produces enzymes that erode both cartilage and the bone underneath it.
Gout, another inflammatory form, works differently still. When uric acid levels in the blood get too high, needle-shaped crystals form inside the joint fluid. Immune cells rush in to engulf these crystals, but in doing so they trigger a massive inflammatory reaction. This is why gout attacks come on suddenly and intensely, often in the big toe, with severe swelling and pain that can peak within hours.
Why Arthritis Pain Gets Worse Over Time
Arthritis doesn’t just damage tissue. It rewires how your nervous system processes pain. Normally, the nerve endings in your joints are relatively quiet. But when cartilage breaks down or the joint lining becomes inflamed, chemical signals from the damaged tissue bind to nerve fibers and lower their activation threshold. This means nerves that previously required strong pressure to fire now respond to gentle touch or normal movement. This process, called peripheral sensitization, is why an arthritic joint can hurt during activities that never used to cause pain.
Over time, the nervous system itself changes. The spinal cord neurons that receive pain signals from the joint become hyperexcitable, firing more easily and responding to a wider area of the body. This central sensitization means the brain receives amplified pain signals even when the joint itself hasn’t gotten measurably worse. It also explains two hallmarks of advanced arthritis pain: hyperalgesia, where mildly painful things hurt much more than they should, and allodynia, where completely painless stimuli like a light touch or a change in temperature register as painful.
Bone Spurs and Joint Deformity
As cartilage wears away, the body tries to compensate by growing new bone at the edges of the joint. These bony outgrowths, known as bone spurs or osteophytes, start as cartilage-like tissue that gradually hardens into bone. They form in response to both abnormal mechanical stress and inflammatory signaling in the joint. While they increase the joint’s surface area (which may reduce pressure on any one spot), they also change the shape of the joint and physically block movement. Studies in both animals and humans show that larger bone spurs are associated with decreased range of motion and, somewhat paradoxically, increased joint stability because the protruding bone limits how far the joint can move in any direction.
In advanced osteoarthritis, X-rays reveal a predictable pattern of changes. Early on, there may be only tiny, questionable bone spurs. As the disease progresses, the space between bones narrows visibly as cartilage thins. In the most severe stage, large bone spurs are present, the joint space is markedly narrowed, the bone beneath has become dense and hardened, and the ends of the bones are visibly deformed. This progression can take years or decades, and the speed varies enormously from person to person.
How to Tell Osteoarthritis From Rheumatoid Arthritis
Morning stiffness is one of the simplest ways to distinguish the two most common forms. In osteoarthritis, stiffness after waking typically fades within a few minutes of moving around. In rheumatoid arthritis, morning stiffness lasts an hour or longer before it begins to improve. The pattern of affected joints also differs. Osteoarthritis tends to hit weight-bearing joints like knees and hips, or joints you’ve used heavily over your lifetime. Rheumatoid arthritis typically starts in smaller joints, often the knuckles and toes, and affects both sides of the body symmetrically.
Doctors diagnose rheumatoid arthritis using a scoring system that evaluates four factors: how many joints are involved and which ones, whether blood tests show specific immune markers, whether inflammation markers are elevated, and how long symptoms have lasted. A score of 6 out of 10 points, combined with confirmed joint swelling and no better explanation for the symptoms, leads to a formal diagnosis.
Effects Beyond the Joints
Rheumatoid arthritis is a systemic disease, meaning it can affect organs throughout the body. The same inflammatory process that attacks the joints can target the lining of the lungs, the sac around the heart, the blood vessels, and the eyes. These effects tend to be more common in people with more severe or longer-standing disease.
In the lungs, inflammation of the lining (pleuritis) affects roughly 5% to 10% of people with rheumatoid arthritis, though mild cases often go undetected. More seriously, 8% to 12% develop clinically significant interstitial lung disease, where inflammation scars the lung tissue and impairs breathing. Rheumatoid nodules can also form in the lungs, appearing as coin-shaped spots on imaging that can be difficult to distinguish from tumors.
The most common heart-related complication is pericarditis, inflammation of the membrane surrounding the heart. In some cases, this can be the very first sign of rheumatoid arthritis, appearing before significant joint symptoms. Heart failure is another underrecognized association. Nodules can form on heart valves, occasionally causing valve dysfunction.
Eye involvement most commonly appears as severe dryness, affecting at least 10% of patients. This dryness often comes alongside a dry mouth and swollen salivary glands. In more severe cases, inflammation can attack the white of the eye itself, causing a painful condition called scleritis that, if untreated, can thin and weaken the eye wall.
What Gout Does Beyond Flares
Gout is often thought of as a joint-only problem, but the uric acid crystals that cause it can deposit in other tissues too. When immune cells engulf these crystals, they activate a powerful inflammatory cascade that doesn’t stay confined to the joint. This same reaction contributes to blood vessel inflammation and has been linked to accelerated progression of atherosclerosis, the buildup of plaque in arteries. People with gout face a measurably higher risk of cardiovascular events as a result, making it important to manage uric acid levels even between flares.