Ankylosing spondylitis (pronounced ank-kih-low-sing spon-dill-eye-tiss), or AS, is a form of arthritis that primarily affects the spine, although other joints can become involved. It causes inflammation of the spinal joints (vertebrae) that can lead to severe, chronic pain and discomfort. In the most advanced cases (but not in all cases), this inflammation can lead to new bone formation on the spine, causing the spine to fuse in a fixed, immobile position, sometimes creating a forward-stooped posture. This forward curvature of the spine is called kyphosis.
Although the exact cause of AS is unknown, we do know that genetics play a key role in AS. Most individuals who have AS also have a gene that produces a “genetic marker” – in this case, a protein – called HLA-B27. This marker is found in over 95% of people in the Caucasian population with AS (the association between ankylosing spondylitis and HLA-B27 varies greatly between ethnic and racial groups). It is important to note, however, that you do not have to be HLA-B27 positive to have AS. Also, a majority of the people with this marker never contract ankylosing spondylitis.
To further complicate matters, in blunt medical terminology, “spondylitis is an inflammation of the vertebra”, where “ankylosis” refers to joint fusion or immobility.
This group of diseases primarily affect the spine (spondylo) and other joints. The group includes: ankylosing spondylitis, reactive arthritis (formerly Reiter’s syndrome), psoriatic arthritis, Juvenile SpA, enteropathic arthritis (spondylitis/arthritis associated with inflammatory bowel disease), and undifferentiated SpA. All display a variety of symptoms and signs, but they also share many features in common, including:
The complete medical term for this group of diseases is the “seronegative” spondyloarthritides. “Sero” refers to blood (blood serum) and “negative” indicates that there is usually no rheumatoid factor present in the blood.