1. Genetic theory: AS has a strong genetic factor as a cause behind its development. About 90 % of patients with AS are born with HLA –B27 gene. There are blood tests to detect HLA-B27 gene marker. 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.
Interestingly, the presence of HLA-B27 alone does not make one prone to develop this disease. As per a study, about 7% of the United States populations have the HLA-B27 gene, only 1% of the population actually has 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 risk of developing Ankylosing spondylitis appears to be further related to heredity. In HLA-B27-positive individuals who have relatives with the disease, their risk of developing Ankylosing spondylitis is 12% (six times greater than for those whose relatives do not have Ankylosing spondylitis).

2. Autoimmune theory: Autoimmunity is considered significantly involved in the development of AS. Again, autoimmunity itself may be genetically oriented.

3. Prolonged stressful situation in one’s life could possibly trigger the unerlyingn genetic tendency for AS.

4. Bacterial infection triggering AS is one of the other theories.
 

Current research about 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 body's immune system by a 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.