Clinical Immunology focuses on the immune system’s health. Learn about the diagnosis and treatment of allergies, autoimmune diseases, and immunodeficiencies.
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Rheumatoid arthritis is a chronic, systemic autoimmune disease that primarily affects the lining of the synovial joints. Unlike the mechanical wear and tear of osteoarthritis, this condition arises when the body’s immune system mistakenly attacks healthy tissue, specifically the synovium, which lines the joints. This immune response causes inflammation (synovitis) that thickens the synovium and can eventually destroy the cartilage and bone within the joint. While the joints are the primary target, the definition of rheumatoid arthritis extends to the entire body, as the systemic inflammation can damage other systems, including the skin, eyes, lungs, heart, and blood vessels.
Pathophysiology of Joint Destruction
The core of rheumatoid arthritis lies in the immune system’s failure to distinguish self from non-self. In a healthy immune system, white blood cells protect the body from invaders like bacteria and viruses. In this disease, the immune system sends antibodies to the lining of the joints, where they attack the tissue surrounding the joint.
Cellular Interaction
This attack causes the release of chemical signals called cytokines. These chemicals cause the blood vessels in the synovium to leak fluid into the joint tissues, resulting in swelling, warmth, and pain.
Pannus Formation
Over time, the inflamed synovium grows thicker and forms a rough, grainy tissue called pannus. This pannus releases enzymes that eat away at the bone and cartilage, leading to joint deformity and loss of function.
Rheumatoid arthritis affects a significant portion of the global population, generally estimated to be about one percent. It is more than just a joint disease; it is a major public health concern due to its potential for causing disability.
The condition can occur at any age, but the peak onset is typically between the ages of 30 and 50. It is significantly more common in women than in men, with women being two to three times more likely to develop the disease.
Prevalence rates can vary by geography and ethnicity, suggesting that while genetics play a role, environmental factors are also critical in the disease’s definition and onset.
This classification is defined by the presence of specific antibodies in the blood, namely rheumatoid factor (RF) or anti-cyclic citrullinated peptide (anti-CCP). Patients with these markers often have a more aggressive course of the disease.
Being seropositive often correlates with more severe joint deformities and extra-articular manifestations, requiring more aggressive early intervention.
In this variation, patients exhibit the clinical symptoms of the disease, such as joint pain and swelling, but their blood tests are negative for RF and anti-CCP antibodies.
Diagnosing seronegative arthritis can be more difficult as it relies heavily on physical observation and exclusion of other conditions. The treatment approach, however, remains similar to the seropositive form.
Research has identified specific genetic markers associated with a higher risk of developing rheumatoid arthritis. The most significant genetic risk factor is found in the HLA (human leukocyte antigen) complex, which helps the immune system distinguish the body’s own proteins from proteins made by foreign invaders.
While having a family member with the disease increases risk, it is not a direct inheritance pattern like some other genetic diseases. It implies a susceptibility that, when combined with environmental triggers, leads to disease onset.
Since genetics alone do not account for all cases, environmental factors are crucial in the overview of the disease. These factors are believed to trigger the immune system in genetically susceptible individuals.
Cigarette smoking is the most well-established environmental risk factor. It not only increases the risk of developing the disease but can also make the disease more severe and less responsive to treatment.
Recent studies suggest that changes in the bacteria that live in the gut or mouth (periodontal disease) might trigger the immune system dysfunction characteristic of rheumatoid arthritis.
A comprehensive overview must recognize that rheumatoid arthritis is a systemic inflammatory disease. The inflammation that damages joints can also damage blood vessels.
Chronic inflammation is a risk factor for cardiovascular disease. Patients with rheumatoid arthritis have a higher risk of heart attack and stroke, making cardiovascular health a central part of the disease definition and management.
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Rheumatoid arthritis is an autoimmune disease where the immune system attacks the joints, causing inflammation. Osteoarthritis is a degenerative condition caused by mechanical wear and tear on the cartilage over time.
While you cannot directly inherit the disease, you can inherit a genetic susceptibility. If a close relative has it, your risk is higher, but it does not guarantee you will develop the condition.
It is a chronic, lifelong condition. While symptoms can disappear during periods of remission, the underlying disease process usually remains and requires long-term management.
In the past, it could shorten life expectancy due to complications like heart disease. However, with modern treatments that control inflammation effectively, the life expectancy gap has significantly narrowed.
The exact cause is unknown. It is believed to be a combination of genetic factors, environmental triggers like smoking or infection, and hormonal changes that cause the immune system to malfunction.
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