Ankylosing Spondylitis Flashcards
Definition/Description
Ankylosing spondylitis (also called Bechterew’s disease or Marie- Strumpell disease) is a spondyloarthritis of the spine and pelvis. It is a chronic inflammatory rheumatic disease with unknown etiology. AS is associated with the HLA-B27 antigen and also with other chronic inflammatory diseases.
AS affects the axial skeleton usually involving the sacroiliac joints, apophyseal joints, costovertebral joints, and intervertebral disc articulations
AS causes characteristic inflammatory back pain, which can lead to structural and functional impairments and a decrease in quality of life.
Affected joints progressively become stiff and sensitive due to a bone formation at the level of the joint capsule and cartilage. It causes a decreased range of motion and gives the spine an appearance similar to bamboo, hence the alternative name “bamboo spine”.
Although not often recognised, ankylosing spondylitis can also cause peripheral joint pain, particularly in the hips, knees, ankles, and shoulders and neck.It involves synovial and cartilaginous joints, as well as sites of tendon and ligamentous attachment.Early diagnosis and treatment helps to control the pain and stiffness and may reduce or prevent significant deformity.
Clinically Relevant Anatomy
Pain in AS can be caused by sacroiliitis, enthesitis and spondylitis.
Initially the sacroiliac joints, situated in the lumbar part of the back, which connect the spine and the pelvis, are damaged. Subsequently the inflammation moves to entheses, where ligaments and tendons integrate into bone.
Eventually, the spine is affected by this inflammation. The vertebral column normally exists of 24 vertebrae, joined together by ligaments and separated by intervertebral discs.
Patients diagnosed with AS form calcium deposits in the ligaments between and around the intervertebral discs. An accumulation of the deposits leads to ossification, starting from the vertebral rim towards the annulus fibrosis and characterised by syndesmophytes.
In highly advanced cases, the spine can fuse together as a result of the bone formation.
Epidemiology /Etiology
AS Affects 0.1 to 0.2% of the population andis predominantly seen in males in a 3:1 ratio. The onset of symptoms generally occurs in late adolescent years to early adulthood. The peak age in which AS manifests varies from the teens to the fourth decade of life.
Its prevalence is highest among white people (0.1-0.2%), less common in American blacks and rare among Japanese, so there is both a familial and a racial predisposition to this disease
The etiology of AS is not fully understood, although a strong genetic link has been determinedIn addition, a direct relationship between AS and the major histocompatibility human leukocyte antigen (HLA)-B27 has also been determine] The exact role of this antigen is unknown, but is believed to act as a receptor for an inciting antigen leading to AS. HLA-B27 occurs in 90-95% of patients with ankylosing spondylitis, compared to a 6 to 9% incidence in the normal population.
The majority of patients are HLA-B27 positive and the risk passing the same antigen onto a child is 1 in 2, so ankylosing spondylitis is a common, highly heritable inflammatory arthritis. Environmental or bacterial factors can also be a trigger.
Initially, there is an infiltration of the subchondral bone by granulation tissue which causes small lesions, ultimately leading to joint erosion (the adjacent cartilage is distorted which produces a very irregular surface).
These lesions in the annulus eventually undergo ossification, leading to a fusion effect of the spinal segments and the similarity in appearance to bamboo. In the spine this occurs at the junction of the vertebrae and the annular fibres of the intervertebral disc.
When synovium is the affected tissue, there is an infiltration by macrophages and lymphocytes. This is followed by replacement of the cartilage or fibrous tissue by a scar like fibroblast invasion which rapidly ossifies. The inflammatory response in the bone adjacent to the involved fibrocartilage, ligament or periosteum is frequently quite severe. As of the spine can resemble an infectious discitis when the spine is initially involved and can be an additional source of confusion for the treating therapist.
Characteristics/Clinical Presentation
The clinical presentation is usually an insidious onset of back pain in the sacroiliac (SI) joints and gluteal regions and progresses to involve the entire spine. Morning stiffness lasting greater than 30 minutes is a common subjective complaint, as well as waking up in the second half of the night.
Pain and stiffness increase with inactivity and improve with exercise.[6] It may also variably involve peripheral joints, eyes, skin, and the cardiac and intestinal systems. Eye disease occurs in about 25% of the patients as either iridocyclitis or conjunctivitis.
Joints other than those of the axial skeleton can be involved with an inflammatory arthritis and synovitis which is seldom as destructive as that of rheumatoid arthritis. The hips, shoulder and knees are the most commonly and most severely affected of the extremity joints.
Complaints of intermittent breathing difficulties may also be a common complaint because AS may cause a decrease in chest expansion. In advanced stages the spine can become fused and a loss of normal lordosis with accompanying increased kyphosis of the thoracic spine, painful limitations of cervical joint motion, and loss of spine flexibility in all planes of motion.
A decrease in chest wall excursion less than 2 cm could be an indicator of AS because chest wall excursion is an indicator of decreased axial skeleton mobility. Since AS is a systemic disease an intermittent low grade fever, fatigue, or weight loss can occur.
Diagnostic Procedures
Lab tests:
Erythrocyte sedimentation rate (ESR): This is a blood test for inflammation, in approximately one third of the SA patients there is a raised ESR observable in exacerbations of the disease, but other conditions can also cause a high ESR.
C-reactive proteins (CRP): This is also a marker of inflammation and is found in 50-70% [12] of people with AS.[12] However, this test is discouraged because it is associated with a high rate of false positives due to the fact that high CRP occurs in 10% of the Caucasian population.
HLA-B27 antigen: HLA B27 is positive in 80-90% of AS patients, more so in the white population and than in some other ethnic groups, especially African Americans. The presence of this hereditary factor is not required for a diagnosis of AS and it does not absolutely confirm or exclude the presence of this disease. The HLA-B27 antigen also occurs in other inflammatory conditions of the joints or intestines.
Tests ?
A thorough physical examination, particularly of the musculoskeletal system, is needed. Clinical signs are sometimes minimal in the early stages of the disease. Examination of the sacroiliac joints and the spine (including the neck), measurement of chest expansion and range of motion of the hip and shoulder joints, and a search for signs of enthesitis are critical in making an early diagnosis of AS.
Schober test is to assess the mobility of the lumbar spine, which can be abnormal even when it is not obvious to the individual.
The lumbar spine side flexion test is another test to measure the lumbar spine mobility.
When ankylosing spondylitis affects the mid-back region, normal chest expansion may be compromised. The aim of the chest expansion test is to assess the thoracic mobility.
The tragus to wall test is a test to measure the cervical mobility.
