Rheumatoid arthritis (RA) is a chronic autoimmune inflammatory disease in which the immune system mistakenly attacks tissues associated with the body's own joints. It principally affects the synovium, the specialised lining of synovial joints, producing persistent inflammation, pain, swelling and stiffness. Unlike osteoarthritis, which is strongly associated with mechanical and degenerative changes, RA is fundamentally an immune-mediated inflammatory disorder. It can affect multiple joints and commonly involves the hands, feet and wrists.
Disease activity can fluctuate, producing periods called flares in which symptoms become more pronounced. RA is systemic as well as articular: inflammatory activity can affect tissues outside the joints, including the eyes, lungs, heart and blood vessels, and can produce general symptoms such as fatigue and weight loss.
The central pathological process begins in the synovium. In RA, immune cells and inflammatory mediators accumulate in the synovial tissue, causing it to become thickened and inflamed. The inflamed synovium produces substances that can damage cartilage, bone, tendons and ligaments surrounding the joint. Persistent inflammation can therefore change the structure and alignment of joints rather than merely causing temporary discomfort. Over time, untreated disease can produce erosions of bone and irreversible loss of joint function. NHS information explains that antibodies generated by the abnormal immune response target the joint lining and that inflammatory chemicals can damage nearby bone, cartilage, tendons and ligaments.
RA commonly affects joints symmetrically, meaning that corresponding joints on both sides of the body may become affected, although symmetry is not universal and early disease can be less stereotyped. Small joints of the hands and feet are often among the first sites involved, although RA can affect almost any synovial joint. The wrists, elbows, shoulders, knees and ankles can also be affected.
The pattern helps clinicians distinguish RA from some other arthritides, but no single joint distribution is sufficient to diagnose it. Disease activity can change over time, and a person can experience periods of remission or low activity interrupted by flares. Early recognition matters because effective treatment can reduce inflammatory activity and help prevent permanent structural damage.
A defining feature of RA is prolonged inflammatory stiffness, particularly after waking or after inactivity. Joint pain is often described as aching or throbbing and can be accompanied by warmth, swelling and tenderness. Morning stiffness in RA often lasts substantially longer than the brief stiffness that is typical of uncomplicated osteoarthritis. Hand involvement can make it difficult to bend the fingers fully or form a fist.
Because inflammation affects the synovial tissue, the affected joints can feel swollen and hot rather than simply painful during movement. These symptoms can develop gradually over several weeks, although some cases progress more rapidly. The fluctuating course means that symptoms may improve temporarily without indicating that the underlying disease has disappeared.
RA is not confined to the joints. Systemic inflammatory effects can cause fatigue, reduced energy, fever, sweating, poor appetite and unintended weight loss. Extra-articular disease can affect several organ systems. Some people develop dry eyes, while inflammation can affect the lungs and heart and contribute to chest symptoms. Rheumatoid nodules are firm lumps that can form under the skin, often around pressure points near affected joints. RA is also associated with an increased risk of cardiovascular disease, including heart attack and stroke, partly reflecting the effects of chronic systemic inflammation and associated risk factors. NHS guidance notes that controlling RA can help reduce the risk of complications.
Diagnosis is clinical and cannot be established by one definitive test. A clinician assesses the pattern and duration of symptoms, examines joints for swelling and restricted movement, and uses blood tests and imaging when appropriate. Tests can include erythrocyte sedimentation rate and C-reactive protein to assess inflammation, a full blood count to look for associated abnormalities such as anaemia, rheumatoid factor and anti-cyclic citrullinated peptide antibodies.
Rheumatoid factor is not specific to RA, and some people with RA are rheumatoid-factor negative. Anti-CCP antibodies can provide additional diagnostic information. NHS guidance emphasises that no blood test can definitively prove or rule out RA, which is why clinical assessment and, when appropriate, specialist rheumatological evaluation remain essential.
Treatment aims not merely to reduce pain but to suppress the underlying inflammatory disease, prevent or minimise joint damage, preserve function and reduce systemic complications. Disease-modifying antirheumatic drugs, commonly called DMARDs, form the foundation of long-term treatment. Conventional synthetic DMARDs include medicines such as methotrexate, sulfasalazine, leflunomide and hydroxychloroquine; biological and targeted synthetic DMARDs may be used when conventional treatment is insufficient or according to disease characteristics.
Corticosteroids can sometimes be used for rapid control of inflammation, but long-term use is limited by significant adverse effects. Physiotherapy and occupational therapy can support mobility, strength and adaptation of daily activities, while surgery may be necessary for severe structural damage. NHS guidance states that early diagnosis and appropriate treatment can reduce progression and joint damage.
RA differs from osteoarthritis, gout and other forms of arthritis in cause and typical clinical pattern. OA primarily involves degenerative and biomechanical changes; gout results from deposition of monosodium urate crystals; RA results from autoimmune inflammation. OA often produces activity-related pain and relatively brief stiffness after inactivity, whereas RA commonly produces prolonged morning stiffness and warm, swollen joints. Gout typically produces abrupt, very severe attacks involving one or a few joints.
These distinctions are useful but not absolute, and an individual can have more than one form of arthritis. The term “arthritis” therefore describes a broad family of joint disorders rather than a single disease, and identifying the specific type matters because the underlying mechanisms and treatments are different.
