Rheumatoid arthritis (RA) is an autoimmune disease in which the body’s immune system – which normally protects its health by attacking foreign substances like bacteria and viruses – mistakenly attacks the joints. This creates inflammation that causes the tissue that lines the inside of joints (the synovium) to thicken, resulting in swelling and pain in and around the joints. The synovium makes a fluid that lubricates joints and helps them move smoothly.
If inflammation goes unchecked, it can damage cartilage, the elastic tissue that covers the ends of bones in a joint, as well as the bones themselves. Over time, there is loss of cartilage, and the joint spacing between bones can become smaller. Joints can become loose, unstable, painful and lose their mobility. Joint deformity also can occur. Joint damage cannot be reversed, and because it can occur early, doctors recommend early diagnosis and aggressive treatment to control RA.
Rheumatoid arthritis most commonly affects the joints of the hands, feet, wrists, elbows, knees and ankles. The joint effect is usually symmetrical. That means if one knee or hand if affected, usually the other one is, too. Because RA also can affect body systems, such as the cardiovascular or respiratory systems, it is called a systemic disease. Systemic means “entire body.”
The cause of RA is not yet fully understood, although doctors do know that an abnormal response of the immune system plays a leading role in the inflammation and joint damage that occurs. No one knows for sure why the immune system goes awry, but there is scientific evidence that genes, hormones and environmental factors are involved.
Researchers have shown that people with a specific genetic marker called the HLA shared epitope have a fivefold greater chance of developing rheumatoid arthritis than do people without the marker. The HLA genetic site controls immune responses. Other genes connected to RA include: STAT4, a gene that plays important roles in the regulation and activation of the immune system; TRAF1 and C5, two genes relevant to chronic inflammation; and PTPN22, a gene associated with both the development and progression of rheumatoid arthritis. Yet not all people with these genes develop RA and not all people with the condition have these genes.
Researchers continue to investigate other factors that may play a role. These factors include infectious agents such as bacteria or viruses, which may trigger development of the disease in a person whose genes make them more likely to get it; female hormones (70 percent of people with RA are women); obesity; and the body’s response to stressful events such as physical or emotional trauma. Research also has indicated that environmental factors may play a role in one's risk for rheumatoid arthritis. Some include exposure to cigarette smoke, air pollution, insecticides and occupational exposures to mineral oil and silica.
In the early stages, people with RA may not initially see redness or swelling in the joints, but they may experience tenderness and pain.
These following joint symptoms are clues to RA:
Along with pain, many people experience fatigue, loss of appetite and a low-grade fever.
The symptoms and effects of RA may come and go. A period of high disease activity (increases in inflammation and other symptoms) is called a flare. A flare can last for days or months.
Ongoing high levels of inflammation can cause problems throughout the body. Here of some ways RA can affect organs and body systems:
Factors that may increase your risk of rheumatoid arthritis include:
Rheumatoid arthritis increases your risk of developing:
A primary care physician may suspect RA based in part on a person's signs and symptoms. If so, the patient will be referred to a rheumatologist – a specialist with specific training and skills to diagnose and treat RA. In its early stages, RA may resemble other forms of inflammatory arthritis. No single test can confirm RA. To make a proper diagnosis, the rheumatologist will ask questions about personal and family medical history, perform a physical exam and order diagnostic tests.
The doctor will ask about personal and family medical history as well as recent and current symptoms (pain, tenderness, stiffness, difficulty moving).
The doctor will examine each joint, looking for tenderness, swelling, warmth and painful or limited movement. The number and pattern of joints affected can also indicate RA. For example, RA tends to affect joints on both sides of the body. The physical exam may reveal other signs, such as rheumatoid nodules or a low-grade fever.
The blood tests will measure inflammation levels and look for biomarkers such as antibodies (blood proteins) linked with RA.
Erythrocyte sedimentation rate (ESR, or “sed rate”) and C-reactive protein (CRP) level are markers of inflammation. A high ESR or CRP is not specific to RA, but when combined with other clues, such as antibodies, helps make the RA diagnosis.
Rheumatoid factor (RF) is an antibody found in about 80 percent of people with RA during the course of their disease. Because RF can occur in other inflammatory diseases, it’s not a sure sign of having RA. But a different antibody – anti-cyclic citrullinated peptide (anti-CCP) – occurs primarily in patients with RA. That makes a positive anti-CCP test a stronger clue to RA. But anti-CCP antibodies are found in only 60 to 70 percent of people with RA and can exist even before symptoms start.
An X-ray, ultrasound or magnetic resonance imaging scan may be done to look for joint damage, such as erosions – a loss of bone within the joint – and narrowing of joint space. But if the imaging tests don’t show joint damage that doesn’t rule out RA. It may mean that the disease is in an early stage and hasn’t yet damaged the joints.
The goals of rheumatoid arthritis (RA) treatment are to:
To meet these goals, the doctor will follow these strategies:
Early, aggressive treatment. The first strategy is to reduce or stop inflammation as quickly as possible – the earlier, the better.
Targeting remission. Doctors refer to inflammation in RA as disease activity. The ultimate goal is to stop it and achieve remission, meaning minimal or no signs or symptoms of active inflammation. One strategy to achieve this goal is called “treat to target.”
Tight control. Getting disease activity to a low level and keeping it there is what is called having “tight control of RA.” Research shows that tight control can prevent or slow the pace of joint damage.
There are different drugs used in the treatment of rheumatoid arthritis. Some are used primarily to ease the symptoms of RA; others are used to slow or stop the course of the disease and to inhibit structural damage.
Nonsteroidal anti-inflammatory drugs (NSAIDs) are available over-the-counter and by prescription. They are used to help ease arthritis pain and inflammation. NSAIDs include such drugs as ibuprofen, ketoprofen and naproxen sodium, among others. For people who have had or are at risk of stomach ulcers, the doctor may prescribe celecoxib, a type of NSAID called a COX-2 inhibitor, which is designed to be safer for the stomach. These medicines can be taken by mouth or applied to the skin (as a patch or cream) directly to a swollen joint.
Corticosteroids. Corticosteroid medications, including prednisone, prednisolone and methyprednisolone, are potent and quick-acting anti-inflammatory medications. They may be used in RA to get potentially damaging inflammation under control, while waiting for NSAIDs and DMARDs (below) to take effect. Because of the risk of side effects with these drugs, doctors prefer to use them for as short a time as possible and in doses as low as possible.
DMARDs. An acronym for disease-modifying antirheumatic drugs, DMARDs are drugs that work to modify the course of the disease. Traditional DMARDs include methotrexate, hydroxycholorquine, sulfasalazine, leflunomide, cyclophosphamide and azathioprine. These medicines can be taken by mouth, be self-injected or given as an infusion in a doctor’s office.
Biologics. These drugs are a subset of DMARDs. Biologics may work more quickly than traditional DMARDs, and are injected or given by infusion in a doctor’s office. These includes abatacept (Orencia), adalimumab (Humira), anakinra (Kineret), certolizumab (Cimzia), etanercept (Enbrel), golimumab (Simponi), infliximab (Remicade), rituximab (Rituxan), tocilizumab (Actemra), Benlysta, and Cosentyx. Because they target specific steps in theinflammatory process, they don’t wipe out the entire immune response as some other RA treatments do. In many people with RA, a biologic can slow, modify or stop the disease – even when other treatments haven’t helped much.
JAK inhibitors. A new subcategory of DMARDs known as “JAK inhibitors” block the Janus kinase, or JAK, pathways, which are involved in the body’s immune response. Tofacitinib belongs to this class. Unlike biologics, it can be taken by mouth.
If medications fail to prevent or slow joint damage, you and your doctor may consider surgery to repair damaged joints. Surgery may help restore your ability to use your joint. It can also reduce pain and correct deformities.
Rheumatoid arthritis surgery may involve one or more of the following procedures:
Surgery carries a risk of bleeding, infection and pain. Discuss the benefits and risks with your doctor.
While there is no specific “diet” for RA, researchers have identified certain foods that are rich in antioxidants and can help control and reduce inflammation. Many of them are part of the so-called Mediterranean diet, which emphasizes fish, vegetables, fruits and olive oil, among other healthy foods. It’s also important to eliminate or significantly reduce processed and fast foods that fuel inflammation.
Rest is important when RA is active and joints feel painful, swollen or stiff. Rest helps reduce inflammation and fatigue that can come with a flare. Taking breaks throughout the day conserves energy and protects joints.
For people with RA, exercise is so beneficial it’s considered a main part of RA treatment. The exercise program should emphasize low-impact aerobics, muscle strengthening and flexibility. The program should be tailored to fitness level and capabilities, and take into account any joint damage that exists. A physical therapist can help to design an exercise program.
Heat treatments, such as heat pads or warm baths, tend to work best for soothing stiff joints and tired muscles. Cold is best for acute pain. It can numb painful areas and reduce inflammation.
These treatments are applied directly to the skin over the painful muscle or joint. They may be creams or patches. Depending on the type used, it may contain nonsteroidal anti-inflammatory drugs (NSAIDs), salicylates or capsaicin, which help reduce pain.
Relaxation techniques, such as deep breathing, guided imagery and visualization can help train painful muscles to relax. Research shows massage can help reduce arthritis pain, improve joint function and ease stress and anxiety. Acupuncture may also be helpful. This involves inserting fine needles into the body along special points called “meridians” to relieve pain. Those who fear needles might consider acupressure, which involves applying pressure, instead of needles, at those points.
Many studies have demonstrated that resilience, an ability to “bounce back,“ encourages a positive outlook. Having a network of friends, family members and co-workers can help provide emotional support. It can help a patient with RA cope with life changes and pain.