Ankylosing Spondylitis

Ankylosing spondylitis facts

  • Ankylosing spondylitis is a form of arthritis featuring chronic inflammation of the spine and the sacroiliac joints.
  • Ankylosing spondylitis belongs to a group of arthritis conditions that tend to cause chronic inflammation of the spine (spondyloarthropathies).
  • Ankylosing spondylitis affects males two to three times more commonly than females.
  • Ankylosing spondylitis is a cause of back pain in adolescents and young adults.
  • The tendency to develop ankylosing spondylitis is genetically inherited.
  • The HLA-B27 gene can be detected in the blood of most patients with ankylosing spondylitis.
  • Ankylosing spondylitis can also affect the eyes, heart, lungs, and occasionally the kidneys.
  • The optimal treatment of ankylosing spondylitis involves medications that reduce inflammation or suppress immunity, physical therapy, and exercise.

What is ankylosing spondylitis?

Ankylosing spondylitis is a form of chronic inflammation of the spine and the sacroiliac joints. The sacroiliac joints are located at the base of the low back where the sacrum (the bone directly above the tailbone) meets the iliac bones (bones on either side of the upper buttocks) of the pelvis. Chronic inflammation in these areas causes pain and stiffness in and around the spine, including the neck, middle back, lower back, and buttocks. Over time, chronic inflammation of the spine (spondylitis) can lead to a complete cementing together (fusion) of the vertebrae, a process referred to as ankylosis. Ankylosis causes loss of mobility of the spine.

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 individuals whose HLA-B27 blood test is positive, 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).

Other genes have been identified that are associated with ankylosing spondylitis, including 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 gene risk factors medical 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 health 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.

SOURCE:https://www.medicinenet.com

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