Ankylosing Spondylitis is a chronic inflammatory condition that attacks young males. It may lead to the fusion of the spine (Sarker, 2016). The fusion can result in the spin being rigid thereby making the patient develop a hunched back. Subsequently, the patient may have breathing problems because of the posture. Other inflammatory signs may show up in other parts of the body such as the eyes (Sieper & Braun, 2010).
Etiology and Incidences
Ankylosing's etiology is still unknown but there are pointers to a genetic risk and component. Researchers have highlighted the association it has with the HLA B27 gene. They have proposed ineffective mechanisms but they are seen to be less apparent as is the case with reactive arthritis.
The prevalence of Ankylosing spondylitis in the general population is low (0.1% to 1.4%). It is more prevalent among Caucasians than in members of other races. Those suffering from chronic lower back pain are more vulnerable to the disease. Among North American Caucasians, the HLD B27 gene occurs in 7% of the normal population and greater than 90% for those with ankylosing sponylitis (Gaidukova & Rebrov, 2016). Those with HLA B27 have a greater chance of up to 6% of developing the condition. It had been previously perceived that the disease mainly affected males but studies done in the recent past indicate that...
The female to male ration stands at 1:3. The mean age of the onset of the condition is 23 years (Moon & Kim, 2014).
Pathophysiology
There are several difficulties faced in getting information about the condition and not so much knowledge is available. It is difficult to get tissues to be used for laboratory analysis as the condition is one that slowly progresses and manifests in the sacroiliac joints. The disease is characterized by inflammation, erosion of the cartilage and then repair of the cartilage. Axial skeleton inflammation among AS patients gets dominated by mononuclear cell infiltrates in the initial stages as osteoclasts increase. Bone resorption makers are higher among AS patients and are perceived to be the trigger for trabecular bone loss (Moon & Kim, 2014).
Studies indicate that inflammation starts at the bone cartilage interface. Macrophages and T-cells have been shown to be rampant in inflamed sacroiliac joints. Biopsies of sacroiliac joints of patients having active disease have a huge amount of mRNA and protein for tumor necrosis factor (TNF)-alpha. There is evidence of facet joints having ongoing inflammation which may lead to the inhibition of osteoroliferation, but which may also be the precursor for the formation of new bones.
As is the case with
Rheumatoid arthritis, peripheral joints' synovium may be inflamed. Nuclear factor kB, osteoprotegerin and Rank ligand may be affected by the receptor…
