Reactive Arthritis is an inflammatory form of arthritis that develops after an infection elsewhere in the body. It is classified as an autoimmune response where the body’s defense system mistakenly targets its own healthy tissues, causing joint inflammation and pain. The reaction is a consequence of the immune system’s response to a prior trigger, not the presence of active bacteria within the joint; while ReA often resolves on its own, it can sometimes become a long-term issue.
Understanding Reactive Arthritis
Reactive Arthritis (ReA) is triggered by an antecedent bacterial infection, typically occurring one to four weeks before joint symptoms begin. Common triggers include gastrointestinal bacteria (Salmonella, Shigella, Campylobacter) and the sexually transmitted bacterium Chlamydia trachomatis. The body mounts an immune response to eliminate the infection, which then appears to cross-react with the body’s own joint tissues.
The condition is characterized by the “classic triad” of symptoms: arthritis, urethritis, and conjunctivitis. The arthritis usually affects the lower limbs, often appearing asymmetrically in the knees, ankles, or feet. Urethritis involves inflammation of the urinary tract, while conjunctivitis causes redness and irritation of the eyes. Note that most patients do not experience all three symptoms simultaneously.
The inflamed joints are “sterile,” meaning no living bacteria are found in the fluid aspirated from the joint, distinguishing ReA from septic arthritis. Joint inflammation is caused by bacterial antigens and the body’s overactive immune components. The arthritis typically appears after the initial infection has already cleared.
The Role of HLA-B27 in Susceptibility
The Human Leukocyte Antigen B27 (HLA-B27) is a protein on the surface of white blood cells that helps the immune system distinguish between self and non-self cells. Its presence is strongly associated with an increased risk of developing ReA. While only 6 to 8 percent of the general population carries the HLA-B27 gene, the protein is present in 60 to 70 percent of individuals who develop Reactive Arthritis.
The HLA-B27 protein does not directly cause the condition, but it contributes significantly to susceptibility after infection. The “arthritogenic peptide hypothesis” suggests that HLA-B27 improperly binds and presents microbial protein fragments (peptides) to T-cells. This faulty presentation causes T-cells to mistakenly recognize similar peptides in the body’s own tissues as foreign threats.
Molecular mimicry leads to the autoimmune inflammation seen in the joints. The presence of HLA-B27 suggests a more severe or chronic course of the disease, including a higher risk of developing persistent arthritis or inflammation of the spine and sacroiliac joints. However, most people who possess the HLA-B27 gene never develop Reactive Arthritis or any related inflammatory condition.
Diagnostic Process and Confirmation
Diagnosing Reactive Arthritis is primarily a clinical process, as no single laboratory test can definitively confirm its presence. Patient history focuses on recent infections, such as diarrhea or urethritis, that occurred one to four weeks before joint pain began. The physical examination looks for characteristic asymmetric swelling of joints, especially in the lower extremities, and signs of inflammation in the eyes or genitourinary tract.
Lab tests support the clinical diagnosis and rule out other conditions. Blood tests often show elevated inflammatory markers, such as the Erythrocyte Sedimentation Rate (ESR) and C-reactive protein (CRP), confirming systemic inflammation. Joint fluid may be analyzed to ensure the arthritis is sterile, distinguishing ReA from a direct bacterial joint infection.
Testing for the HLA-B27 marker is part of the diagnostic workup. A positive HLA-B27 test strengthens the suspicion of ReA, especially with characteristic symptoms and a preceding infection. Conversely, a negative result does not exclude the diagnosis, as many ReA patients do not carry the gene. Diagnosis is established by combining the patient’s symptoms, infection history, and the results of laboratory and imaging tests.
Managing Symptoms and Long-Term Outlook
The goal of treatment for Reactive Arthritis is to manage inflammation and pain, allowing the condition to run its course. Initial management involves Nonsteroidal Anti-inflammatory Drugs (NSAIDs), such as indomethacin or naproxen, which reduce joint swelling and discomfort. For large or severely inflamed joints, a healthcare provider may recommend a corticosteroid injection directly into the affected joint for localized relief.
If the arthritis is persistent or severe, and NSAIDs alone are not sufficient, other treatments may be introduced. Disease-Modifying Antirheumatic Drugs (DMARDs), such as sulfasalazine or methotrexate, suppress the immune response and control chronic inflammation. These medications are reserved for cases lasting longer than six months or those that are aggressive. Physical therapy helps maintain joint flexibility and muscle strength during the active phase of the disease.
The long-term outlook for Reactive Arthritis is favorable, as the condition is self-limiting. Most patients experience a full remission of symptoms within three to twelve months. However, approximately 15 to 30 percent may develop chronic arthritis or experience recurrent episodes. The presence of the HLA-B27 gene, hip involvement, or high inflammatory markers like an elevated ESR can suggest a greater risk for a chronic or recurring course.