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Regarding Ankylosing Spondylitis (AS)
Basic bone growth and AS
More AS implications
AS pathological physiology
View animations of AS development



The progression of AS can be highlighted by:

The initial inflammation of the joint where the spine meets the pelvis.

The eventual fusion of the bones of that joint and subsequent fusion of the vertebras on up the spinal column.

The cause of this inflammation and fusion in unknown, though research continues.


Typical bone growth, ossification, occurs as cartilage cells that are determined to become bone, called chondracytes, develop into cells called osteoblasts, that in turn develop into bone tissue. This bone tissue is of two types, cancellous bone, the inner largely porous


bone where blood cells are stored, and cortical bone, which is the strong denser outer bone.

The AS condition provides for abnormal ossification in which the cartilage-to-bone process is bypassed and the osteoblasts that are intended for repair instead form new bone structures. The osteblasts are deposited in the body's attempt to repair the damage to the bone caused at the point of damage, the enthesopathy.

As the enthesopathy's inflammation cells are infused with blood vessels, osteoblasts assemble at the site of the enthesopathy, weaving into the existing bone's cellular matrix, producing small points


of cortical bone called syndamorphytes. These syndamorphytes comprise the bony protusions that ultimately replace the anulus fibrosus' fibrous tissue, thereby fusing the vertebrae as they grow across the intervertebral space.

AS is a chronic, systemic inflammatory disorder of the axial skeleton. In simpler terms, AS is a slowly developing disease that takes years to manifest itself on the spine and associated joints. Prior to advanced stages of AS, the course is highly variable and can be characterized by spontaneous remissions and exacerbation, that is, that there are episodes of moderate to high levels of pain and immobility between periods of time when no symptoms are present. The cause of the ascending spinal inflammation which characterizes AS is unknown. Though research continues, a number of studies seems to reveal potential enteric (intestinal) bacteria involvement.

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