Ankylosing Spondylitis (AS) is classified as an autoimmune disease. This condition involves the immune system mistakenly targeting healthy tissues, leading to chronic inflammation and specific symptoms.
Defining Autoimmune Diseases
Autoimmune diseases arise when the body’s immune system, which is designed to protect against foreign invaders like bacteria and viruses, mistakenly attacks its own healthy cells and tissues. In an autoimmune response, this recognition system malfunctions, leading to a “friendly fire” scenario where the body turns against itself.
This misdirection causes the immune system to produce proteins called autoantibodies, or to activate specific immune cells, that target and damage healthy tissues. The resulting inflammation can affect various parts of the body, depending on the specific autoimmune condition. All share this underlying mechanism of immune system misdirection.
Ankylosing Spondylitis: An Autoimmune Perspective
Ankylosing Spondylitis manifests as an autoimmune disease by targeting the joints and surrounding structures, primarily in the spine and pelvis. The immune system mistakenly attacks the sacroiliac joints and the spinal vertebrae, leading to chronic inflammation.
The inflammation in AS particularly affects entheses, the sites where tendons and ligaments attach to bone. This chronic inflammation at the entheses can cause erosion of the bone at these attachment points. In an attempt to repair the damage, the body may form new bone, a process called calcification. Over time, this repeated cycle of inflammation, damage, and repair can lead to the fusion of spinal vertebrae, restricting movement and potentially causing a hunched posture. This pathological new bone formation is a hallmark feature distinguishing AS from other types of arthritis.
Genetic Predisposition and Triggers
A strong genetic link exists for the development of Ankylosing Spondylitis, with a particular gene playing a significant role. The human leukocyte antigen B27 (HLA-B27) gene is present in a large majority of individuals with AS. This gene produces a protein on cell surfaces that helps the immune system distinguish between the body’s own cells and foreign invaders.
Despite this strong association, inheriting the HLA-B27 gene does not guarantee that an individual will develop AS; only a small fraction of those with the gene will develop the condition. This indicates that other factors are involved in triggering the autoimmune response. Environmental triggers, while not fully understood, are thought to interact with genetic predisposition to initiate the disease. These potential triggers may include certain infections, exposure to toxins, or even changes in gut microbiota. For example, smoking has been implicated in worsening disease progression in individuals with AS. The development of AS is therefore a complex interplay between an individual’s genetic makeup and external influences.
Distinguishing AS from Other Conditions
Ankylosing Spondylitis differs significantly from other more common types of arthritis, such as osteoarthritis. Osteoarthritis is primarily a “wear and tear” condition resulting from the breakdown of cartilage in joints due to mechanical stress and aging. In contrast, AS is an inflammatory condition driven by the immune system mistakenly attacking healthy tissues.
The pain associated with AS often improves with physical activity and worsens with rest, particularly morning stiffness that can last for more than 30 minutes. This is distinct from osteoarthritis, where pain typically worsens with activity. While osteoarthritis usually affects older adults and common joints like knees and hips, AS often begins in late adolescence or early adulthood and primarily targets the spine and sacroiliac joints. These differences in cause, affected joints, and pain patterns help differentiate AS as a distinct autoimmune form of arthritis.