Read more about this disease, some with Classification – Types – Signs and symptoms – Genetics – Pathophysiology – Diagnosis – Screening – Prevention – Treatment and management – Cures and much more, some including pictures and video when available.
Ankylosing spondylitis (AS; previously known as Bechterew’s disease, Bechterew syndrome, Marie Strümpell disease), a form of Spondyloarthritis is a chronic, painful, inflammatory arthritis primarily affecting spine and sacroiliac joints, causing eventual fusion of the spine; it is a member of the group of the spondyloarthropathies with a strong genetic predisposition. Complete fusion results in a complete rigidity of the spine, a condition known as bamboo spine.[1]
The typical patient is young, aged 18-30, with chronic pain and stiffness in the lower part of the spine, often with pain referred to one or other buttock or back of thigh from the sacroiliac joint early on. Pain is often severe on rest, and improves with physical activity. Men are affected more than women by a ratio about of 3:1.[2] In 40% of cases, ankylosing spondylitis is associated with iridocyclitis causing eye pain and photophobia. Another common symptom is generalised fatigue. Less commonly aortitis, apical lung fibrosis and ectasia of the sacral nerve root sheaths may occur. As with all the seronegative spondarthropathies, lifting of the nails (onycholysis) may occur.
When the condition presents before the age of 18 it is relatively likely to cause pain and swelling of large limb joints, particularly the knee. The spine may be affected on later.
AS is one of a cluster of conditions known as seronegative spondarthropathies in which the characteristic pathological lesion is an inflammation of the enthesis (the insertion of tensile connective tissue into bone). Other forms of spondarthropathy area associated with ulcerative colitis, Crohn’s disease, psoriasis, and Reiter’s syndrome.
AS is a systemic rheumatic disease and is one of the seronegative spondyloarthropathies. About 90% of the patients express the HLA-B27 genotype. Tumor necrosis factor-alpha (TNF a) and IL-1 are also implicated in ankylosing spondylitis. Specific autoantibodies have not been detected and it is therefore probably not appropriate to consider it an autoimmune disease.
The association of AS with HLA-B27 and the absence of any autoantibodies suggests that the condition is due to overactivity of CD8 T cells, which interact with HLA-B. There is no evidence that this interaction involves a self antigen and at least in the related Reiter’s syndrome, which follows infections, the antigens involved are likely to be derived from intracellular microorganisms. There is, however, a possibility that CD4 T cells are involved in an aberrant way, since HA-B27 appears to have a number of unusual properties, including possibly an ability to interact with T cell receptors in association with CD4.
There has been a longstanding claim that AS arises from a cross-reaction between HLA-B27 and antigens of the Klebsiella bacterial strain (Tiwana et al. 2001).[3]The problem with this idea is that no such cross reactivity with B27 has been found (I.e. although antibody responses to klebsiella may be increased there is no antibody response to B27, so there seems to be no cross reactivity.) Particular authorities argue that elimination of the prime nutrients of Klebsiella (starches) would decrease antigenemia and improve the musculoskeletal symptoms. However, as Khan (2002) argues, evidence for a correlation between Klebsiella and AS is circumstantial so far, and that the efficacy of low-starch diets has not yet been scientifically evaluated.[4] Similarly, Toivanen (1999) found no support for the role of klebsiella in the etiology of primary AS.[5]
[tubepress mode=’tag’, tagValue=’Ankylosing spondylitis’]