How AS Progresses

vertebra-sketch-3The 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 vertebrae on up the spinal column.

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

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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.

Upon physical examination, the earliest abnormality is usually tenderness in the joints where the spine joins the pelvis (the sacroilliac joints). Over time, pain and stiffness may progress along the spine up to the neck region. Ultimately, the sacroiliac joints can fuse, causing various degrees of immobility as the normal flexibility of the spine is diminished. As AS progresses, the length of the spinal column can become fused and rigid. Often, scoliosis, when the spine assumes an abnormal curvature, affects how the spine gives the body its posture. It’s common that the neck is stooped in a forward position. These manifestations are common though are not present in everyone with AS. (Fortunately, my vertebras have fused in a fashion that gives a typical curvature to my spine. My neck though does have moderate stoop and the joints where my head join my neck (the atlanto-occipital joints) are almost entirely fused, allowing very little mobility at that joint.)

The fusion can also cause joints associated with the spine, such as the rib cage, to suffer a loss of some mobility. As the joints that connect the ribs to the spine (the vertebrocostral joints) fuse, full chest expansion is compromised to the degree of the bones’ fusions. The lungs are restrained in their ability to fully expand during inhalation. This lessened ability for lung expansion can bring less oxygen to the blood as it passes through the lungs when the body demands more oxygen. This can cause shortness of breath and increased fatigue during times of physical exertion.

The typical vertebral joint consists of two vertebrae, one above and one below, a disk between them made of fibrocartilage that provides tensile strength and absorbs compression shock throughout the spine, ligaments that configure the joint, and muscles that maintain the structure of the joint. Normally, the ligaments retain their connective tissue composition, and the bone remains simply as one of the chief structural component of the joint.

However, in the AS condition, the ligaments and bone of the vertebral joint lose their defined purpose. Chemical changes at the rim of the vertebra that sandwich the disk cause ossification beyond the edge of the vertebra. That is, bone growth begins to re-occur at the rim of the vertebra where it had stopped growing years before when the vertebra had finished developing. This abnormal bone growth slowly builds bony protrusions along some of the ligaments that connect the vertebras. Ossification, the growth of bone, follows the ligaments at the rim of the upper and lower vertebra and can eventually encapsulate the disk.

The growth of these bony protrusions may fully bridge the vertebras where ligament once was along side the disk. This advanced condition is termed “bamboo spine,” as an x-ray displays this vertebral column as a continuous structure of bone shaped like bamboo with vertebra and bulbous growth of bone between them. Other lesser developed ossification is termed “postage stamp” because of the x-ray visible bony protrusions that follow the ligament’s fibrous strands that run between the vertebra. This abnormal ossification is what fuses the vertebral column and gives it its rigid nature.

The typical vertebral joint consists of the vertebras, the disk, the ligaments, and muscle. Among the ligaments necessary are those associated with the outer portion of the vertebral disk that are called the anulus fibrosi. This ligament is vital in the disk’s attachment to the vertebrae and spans every intradisk space.

Prior to ossification, the ligament’s attachment at the rim of the vertebra becomes inflamed. Lesions form on the vertebra rim at the sites of this inflammation, a deteriating process known as enthesopathy. The reason for this inflammation is unknown. This inflammatory condition exists sporadically for many years, causing pain and some stiffness. This enthesopathy is known to occur along the anterior rim of the vertebra rim (the side facing the abdomen). The inflammation eventually causes bone to erode at the rim where the inflamed ligament is attached.

Findings indicate that bone cells fill in the fibrous tissue of the ligament to repair the defect caused by the eroded bone. This new bone is woven into the inflammed fibrous ligament tissue, joining the underlying bone of the vertebra with the fibrous tissue of the ligament, thus causing the bone surface to protrude outside the original vertebral surface. The result of the inflammation’s healing process are bony protrusions at the vertebra’s original ligament attachment. Over time, these protrusions grow and tend to fuse with one another along the length of the spine. This process usually occurs at several places on the vertebra and may also develop some distance away from the ligament’s attachment at the vertebra rim.

Typical 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 one 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 form new bone structures. The osteblasts are deposited in the body’s attempt to repair the damage to the bone caused by 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 new 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.

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