What is Ankylosing Spondylitis?

Ankylosing spondylitis is a type of chronic inflammation of the spine and the sacroiliac joints. The sacroiliac joints are situated in the low back where the sacrum (the bone directly above the tailbone) joins the iliac bones (bones on either side of the upper buttocks). Chronic inflammation in these spots triggers stiffness and pain in and around the spine. Eventually, chronic spinal inflammation (spondylitis) can lead to a total bonding together (fusion) of the vertebrae, a progression called ankylosis. Ankylosis leads to loss of mobility of the spine.

Ankylosing spondylitis is furthermore a systemic rheumatic disease, indicating it can influence other tissues all through the body. For that reason, it can produce inflammation in or damage to other joints away from the spine, including other organs, for example the heart, eyes, kidneys, and lungs. Ankylosing spondylitis shares a lot of characteristics with a number of other arthritis forms, such as reactive arthritis, psoriatic arthritis and arthritis associated with Crohns disease and ulcerative colitis. Each of these arthritic forms can produce inflammation and disease in the spine, eyes, other joints, mouth, skin, and various organs. In view of their parallels and propensity to bring about inflammation of the spine, these conditions are as a group referred to as "spondyloarthropathies."

Ankylosing spondylitis is 2 to 3 times more widespread in males than in females. In women, joints away from the spine are more often affected than in men. Ankylosing spondylitis affects all age groups, counting children. The most usual age of onset of symptoms is in the second and third decades of life.

What causes ankylosing spondylitis?

The propensity to acquire ankylosing spondylitis is thought to be genetically inherited, and the preponderance (nearly 90%) of patients with ankylosing spondylitis are born with the HLA-B27 gene. Blood tests have been designed to detect the HLA-B27 gene marker and have furthered our knowledge of the relationship between HLA-B27 and ankylosing spondylitis. The HLA-B27 gene appears only to intensify the propensity of developing ankylosing spondylitis, while a few additional factor(s), possibly environmental, are needed for the disease to appear or become expressed. For instance, while 7% of the United States population have the HLA-B27 gene, only 1% of the population actually have the disease ankylosing spondylitis. In Northern Scandinavia (Lapland), 1.8% of the population have ankylosing spondylitis while 24% of the general population have the HLA-B27 gene. Even among HLA-B27 positive individuals, the danger of developing ankylosing spondylitis appears to be more related to heredity. In HLA-B27-positive persons who have relatives with the disease, their risk of developing ankylosing spondylitis is 12% (6 times more than for those whose relatives don’t have ankylosing spondylitis).

Lately, 2 more genes have been recognized that are associated with ankylosing spondylitis. These genes are called ARTS1 and IL23R. These genes appear to play a role in manipulating immune function. It is projected that by comprehending the effects of each of these known genes, researchers will make major progress in finding a cure for ankylosing spondylitis.