Common causes of lower back pain include strain injury from athletics or overuse, disc herniation, kidney infection, pinched nerve in the spine, and pregnancy. Less common causes of back pain include infection of the spine, ankylosing spondylitis with lumbosacral and sacroiliac joint disease, compression fracture of a spinal vertebra, disc ligament tear (annular tear), and spinal tumor or cancer in the bone of the spine.
Symptoms that can be associated with low back pain include
- dull ache,
- numbness,
- tingling,
- sharp pain,
- pulsating pain,
- pain with movement of the spine,
- pins and needles sensation,
- muscle spasm,
- tenderness
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 factors, 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). This means that not everyone who has the gene will develop 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.
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