Ankylosing spondylitis is characterized by a persistent inflammation of the spine and the sacroiliac joints. The chronic inflammation in the spine eventually leads to a cementing of the vertebrae. This process is known as ankylosis. Ankylosis results in the loss of mobility of the spine. The usual symptoms of the disease include fatigue associated with irritation of the spine, lower back, upper buttock, and the neck. The onset of pain and a rigor mortis kind of stiffness is gradual and worsens with time. The inclination to develop this form of spondylitis is a genetic feature. It has been observed in 90% of the patients suffering from ankylosing spondylitis are born with the HLA-B27 gene making them vulnerable to this disease.
The presence of the HLA-27 gene in 90% of the patients suggests that the vulnerability to this disease is indeed an inherent trait. Tests have been specially developed to spot the presence of the HLA-B27 gene marker which will help in furthering the studies of the connection between ankylosing spondylitis and HLA-B27. The HLA-B27 gene only seems to increase the inclination of developing the disease. Some additional factors like environmental anomalies are essential for the disease to set in. Amongst people who test positive for HLA-B27, the chances of contracting ankylosing spondylitis is further related to inheritance causes. In the HLA-B27-positive people who have relatives suffering from the disease, the probability of developing ankylosing spondylitis is nearly 12 percent. The figure is six times greater than the risk faced by the HLA-27 positive individuals who do not have any relative suffering from this disease.
In recent times, two other genes have been acknowledged for their association with this disease. IL23R and ARTS1 are these genes and they have been found to influence the immune system. The onset of inflammation in different organs is a subject matter of research and an exact idea of the same is not known. The initial swelling of bodily organs may be due to an activation of the body’s immune system by a bacterial infection or a group of infectious microorganisms. Once triggered, the body’s immune system reaches a state where it is unable to control the rapid developments happening in the body although the initial bacterial infection may have died down. This chronic tissue tenderness as a result of continued activation of the immune system is the trademark feature of such inflammatory autoimmune diseases.
