Ankylosing Spondylitis (cont.)
William C. Shiel Jr., MD, FACP, FACR
Dr. Shiel received a Bachelor of Science degree with honors from the University of Notre Dame. There he was involved in research in radiation biology and received the Huisking Scholarship. After graduating from St. Louis University School of Medicine, he completed his Internal Medicine residency and Rheumatology fellowship at the University of California, Irvine. He is board-certified in Internal Medicine and Rheumatology.
Catherine Burt Driver, MD
Catherine Burt Driver, MD, is board certified in internal medicine and rheumatology by the American Board of Internal Medicine. Dr. Driver is a member of the American College of Rheumatology. She currently is in active practice in the field of rheumatology in Mission Viejo, Calif., where she is a partner in Mission Internal Medical Group.
Melissa Conrad Stöppler, MD
Melissa Conrad Stöppler, MD, is a U.S. board-certified Anatomic Pathologist with subspecialty training in the fields of Experimental and Molecular Pathology. Dr. Stöppler's educational background includes a BA with Highest Distinction from the University of Virginia and an MD from the University of North Carolina. She completed residency training in Anatomic Pathology at Georgetown University followed by subspecialty fellowship training in molecular diagnostics and experimental pathology.
In this Article
- Ankylosing spondylitis facts
- What is ankylosing spondylitis?
- What causes ankylosing spondylitis?
- What are ankylosing spondylitis symptoms and signs?
- How is ankylosing spondylitis diagnosed?
- What are ankylosing spondylitis treatment options?
- Can ankylosing spondylitis be prevented?
- What is the prognosis (outlook) for patients with ankylosing spondylitis?
- What is in the future for patients with ankylosing spondylitis?
- Where can people find more information about ankylosing spondylitis and learn about support groups?
- Ankylosing Spondylitis FAQs
- Find a local Rheumatologist in your town
What causes ankylosing spondylitis?
The tendency to develop ankylosing spondylitis is believed to be genetically inherited, and a majority (nearly 90%) of people with ankylosing spondylitis are born with a gene known as the HLA-B27 gene. Blood tests have been developed to detect the HLA-B27 gene marker and have furthered our understanding of the relationship between HLA-B27 and ankylosing spondylitis. The HLA-B27 gene appears only to increase the tendency of developing ankylosing spondylitis, while some additional factor(s), perhaps environmental, are necessary for the disease to appear or become expressed. For example, while 7% of the United States population has the HLA-B27 gene, only 1% of the population actually has the disease ankylosing spondylitis. In northern Scandinavia (Lapland), 1.8% of the population has ankylosing spondylitis while 24% of the general population has the HLA-B27 gene. Even among HLA-B27-positive individuals, the risk of developing ankylosing spondylitis appears to be further related to heredity. In HLA-B27-positive individuals who have relatives with the disease, the risk of developing ankylosing spondylitis is 12% (six times greater than for those whose relatives do not have ankylosing spondylitis).
Recently, two more genes have been identified that are associated with ankylosing spondylitis. These genes are called ARTS1 and IL23R. These genes seem to play a role in influencing immune function. It is anticipated that by understanding the effects of each of these known genes researchers will make significant progress in discovering a cure for ankylosing spondylitis.
How inflammation occurs and persists in different organs and joints in ankylosing spondylitis is a subject of active research. Each individual tends to have their own unique pattern of presentation and activity of the illness. The initial inflammation may be a result of an activation of the body's immune system, perhaps by a preceding bacterial infection or a combination of infectious microbes. Once activated, the body's immune system becomes unable to turn itself off, even though the initial bacterial infection may have long subsided. Chronic tissue inflammation resulting from the continued activation of the body's own immune system in the absence of active infection is the hallmark of an inflammatory autoimmune disease.
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