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Ankylosing spondylitis

Ankylosing spondylitis (AS) is a chronic, progressive inflammatory arthritis primarily affecting spine and sacroiliac joints, causing eventual fusion of the spine; it is a member of the group of the spondylarthropathies. Complete fusion results in a complete rigidity of the spine, a condition known as bamboo spine. more...

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Treatment is with physiotherapy and medication. Some cases remain mild, while other result in marked disability.

Signs and symptoms

The typical patient is a young man of 15-30 years old (although women are also affected) with pain and stiffness in the spine. It is also associated with iridocyclitis (anterior uveitis), ulcerative colitis, psoriasis and Reiter's disease, through HLA-B27 (see below).

Osteopenia or osteoporosis of AP spine, causing eventual compression fractures and a back "hump" if untreated.

Organs affected by AS, other than the axial spine, are the hips, heart, lungs, heels, and other areas (peripheral).

Ankylosing spondylitis affects the eyes in up to 40 percent of cases, leading to episodes of eye inflammation called acute iritis. Acute iritis causes eye pain and increased sensitivity to light (photophobia).

Diagnosis

The diagnosis is by X-ray studies of the spine, which show characteristic spinal changes and sacroiliitis. A normal X-ray does not exclude the disease.

Variations of the HLA-B gene increase the risk of developing ankylosing spondylitis, those with the HLA-B27 variant are at highest risk of developing the disorder. HLA-B27, demonstrated in a blood test, is occasionally used as a diagnostic, but does not distinguish AS from other diseases and is therefore not of real diagnostic value. Effective Diagnosis can also happen via MRI scans. Unattended cases normally lead to knee pain, resulting in a fair assumption of normal rheumatism.

Pathophysiology

AS is a systemic rheumatic disease, and about 90% of the patients are HLA-B27 positive. HLA-DR and IL1ra are also implicated in ankylosing spondylitis. Although specific autoantibodies cannot be detected, its response to immunosuppresive medication has prompted its classification as an autoimmune disease.

Hypotheses on its pathogenesis include a cross-reaction with antigens of the Klebsiella bacterial strain (Tiwana et al. 2001). Particular authorities argue that elimination of the prime nutrients of Klebsiella (starches) would decrease antigenemia and improve the musculoskeletal symptoms. On the other hand, Khan (2002) argues that the 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. Similarly, Toivanen (1999) found no support for the role of kebsiella in the etiology of primary AS.

Epidemiology

The sex ratio is 3:1 for men:women. In the USA, the prevalence is 0.25%, but as it is a chronic condition, the number of new cases (incidence) is fairly low.

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Ankylosing spondylitis
From American Family Physician, 7/1/90 by Gilda Cardenosa

Alkylosing spondylitis is an inflammatory disorder that affects synovial and cartilaginous joints, as well as entheses (sites of attachment of muscle or ligament to bone). The etiology is unknown. Characteristically, the axial skeleton is involved, although significant changes may also occur in the appendicular skeleton. (1,2)

Ankylosing spondylitis is most commonly seen in young men between 15 and 35 years of age. It is associated with the HLA-B27 antigen. The prevalence of the disorder, reflecting differences in the frequency of HLA-B27 antigen, varies in different populations. (3) In the United States, the prevalence is 0.1 percent. The prevalence in blacks is about one-fourth that in whites. (4)

Clinical Features

Typically, 70 to 80 percent of patients pix-sent with an insidious onset of low back pain and stiffness. Peripheral joint pain (10 to 20 percent) and sciatic pain (5 to 10 percent) are less frequent complaints. (2) Extraskeletal manifestations are variable. Chest pain (possibly related to costochondral junction inflammation or pleuritis) and pulmonary fibrosis that predominantly involves the upper lobes can occur. Acute and recurrent iritis affects as many as 25 percent of patients and may be the initial presenting symptom. Aortic insufficiency (the result of aortic valve inflammation) and conduction defects and pericarditis are common in patients with chronic disease and peripheral joint involvement. Ankylosing spondylitis is also associated with an increased incidence of inflammatory bowel disease and amyloidosis. (2,3)

Sacroiliac joint tenderness may be elicited in the acute phase of the disease. Normocytic anemia, elevated erythrocyte sedimentation rates and moderate elevation in alkaline phosphatase levels have been reported in patients with ankylosing spondylitis. (3)

Synovial biopsies and synovial fluid aspirates are nonspecific. Sites of erosion contain a nonspecific inflammatory cell infiltrate. Ligaments and involved bones are invaded by lymphocyte- and plasma cell-containing connective tissue. This process leads to the deposition of reactive bone and the proliferative bony changes that characterize the disease. (2,5)

Radiographic Findings

Bilaterally symmetric sacroiliitis is the hallmark of ankylosing spondylitis. Synovial and cartilaginous portions of the joint are affected. Changes predominate on the ileal side of the joint. In the early stages, asymmetric or unilateral involvement may be seen. Initial changes involving the synovial portion of the joint include loss of joint definition, patchy periarticular osteoporosis, superficial erosions and sclerosis of the subchondral bone. Progressive inflammation leads to continued erosion with fraying and widening of the joint space. Proliferative bony changes parallel the inflammatory erosions so that joint fusion leading to ankylosis slowly occurs.

Additional changes in the pelvis include ossification at ligamentous attachments, which gives a "whiskered" appearance to the iliac crest and ischial tuberosities. Involvement of the symphysis pubis is seen in up to 23 percent of patients. Initially, erosion and blurring of the subchondral bone occurs. The subsequent reparative bony proliferative process leads to ankylosis. (1,2)

Spinal involvement in ankylosing spondylitis occurs at the discovertebral, apophyseal, costovertebral and atlantoaxial joints. Ligamentous attachment sites are also involved along the spine posteriorly. Discovertebral joint involvement is characterized by a multitude of findings. Early in the disease, osteitis involving the superior and inferior comers of the vertebral bodies leads to loss of the normal anterior concavity of the vertebral bodies, resulting in the characteristic squared vertebral bodies. Concomitant ossification of the outer annulus fibrosus portion of the disc occurs. These syndesmophytes bridge the disc spaces, fusing the vertebral bodies. (2)

Discovertebral joint involvement can also include erosions of the vertebral body end plates, which may result in central or peripheral herniation of disc material. Spinal pseudarthrosis, the result of extensive central and peripheral destruction of the discovertebral joint, is seen only in patients with advanced disease. Associated fractures through the ankylosed articulations are possible. They are associated with epidural hematoma in 20 percent of patients. (1,2)

Apophyseal joint changes, initially hard to detect in the thoracic and lumbar spine, are more easily seen in the cervical spine. Costovertebral joint changes include erosion, sclerosis and eventual ankylosis. While pathologically apparent, these changes are typically not seen radiographically. (2)

Erosion of the dens with subsequent atlantoaxial subluxation can occur in ankylosing spondylitis, although less frequently than it occurs in patients with rheumatoid arthritis. Posteriorly, erosion of the spinous process tips takes place, particularly at the cervicothoracic junction. Additionally, the interspinous and supraspinous ligaments become calcified and ossified, which produces a central radiodense line on anteroposterior radiographs (2).

The frequency of peripheral joint involvement in ankylosing spondylitis increases with the duration of the disease. Eventually, 30 to 50 percent of patients manifest peripheral symptoms. The hips (50 percent) and shoulders (30 percent) are most commonly involved. Destructive changes in the hips are slowly progressive, usually unilateral and associated with marked deformity of the femoral head prior to the development of ankylosis. (8) More commonly, however, nondestructive symmetric loss of the hip joint space is associated with a fairly characteristic osteophytic collar that forms at the junction of the femoral head and neck. (1,8,9)

In the shoulders, joint space narrowing, osteoporosis and erosive changes in the superolateral aspect of the humeral head, with eventual ankylosis, usually occur. In some patients, destruction of the outer aspect of the proximal humerus and the humeral head leads to a "hatchet-like" deformity. Chronic rotator cuff tears are manifested by elevation of the humeral head with respect to the glenoid. Also seen are acromioclavicular joint erosions and resorption of the undersurface of the distal clavicle at the attachment of the coracoclavicular ligament.

Knees, hands and wrists are the most frequent sites of involvement distal to the hips and shoulders. The disease is asymmetric, with superficial erosive changes, characteristic periostitis around the erosions and classic ankylosis.

REFERENCES

1. Brower AC. Arthritis in black and white. Philadelphia: Saunders, 1988:197-212.

2. Resnick D, Niwayama G. Diagnosis of bone and joint disorders. 2d ed. Vol 2. Philadelphia: Saunders, 1988:1103-70.

3. Forouzesh S, Bluestone R. The clinical spectrum of ankylosing spondylitis. Clin Orthop 1979; (143):53-8.

4 .Masi AT, Medsger TA Jr. A new look at the epidemiology of ankylosing spondylitis and related syndromes. Clin Orthop 1979;(143):15-29,

5 .Ball J. Articular pathology of ankylosing spondylitis. Clin Orthop 1979; (143):30-7.

6 .Martel K Braunstein E. Spondyloarthritides. In: Taveras JM, Ferrucci JT, eds. Radiology: diagnosis, imaging, intervention. Vol 5. Chap. 46. Philadelphia: Lippincott, 1988:1-5.

7. Resnick D. Radiology of seronegative spondyloarthropathies. Clin Orthop 1979;(143): 38-45.

8. Dwosh IL, Resnick D, Becker MA. Hip involvement in ankylosing spondylitis. Arthritis Rheum 1976;19:683-92.

9. Resnick D. Patterns of peripheral joint disease in ankylosing spondylitis. Radiology 1974; 110:523-32.

COPYRIGHT 1990 American Academy of Family Physicians
COPYRIGHT 2004 Gale Group

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