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Noninfective inflammations of the vertebral spine can be caused by seronegative spondyloarthropathies or by seropositive rheumatoid arthritis. The seronegative spondyloarthropathies include ankylosing spondylitis, psoriatic arthritis, reactive arthritis, arthritis associated with inflammatory bowel diseases, and undifferentiated arthritis.
Ankylosing spondylitis is the most frequent seronegative inflammatory spinal disease in adults and the prototype for other members of the spondyloarthropathies. The prevalence of this disorder is estimated at 0.1% to 0.2% in the general population. Ankylosing spondylitis primarily affects young males, with a male-to-female ratio of 4 to 10:1. The peak age at onset is 15 to 35 years, with a mean age of 26 years. In 15% to 20% of patients, the disease begins in the second decade of life. In 10%, onset occurs after age 39 years.
Ankylosing spondylitis classically begins in the sacroiliac joints and then affects the thoracolumbar and lumbosacral spinal junctions. The disease typically ascends as it progresses, involving the mid lumbar, the upper thoracic, and then the cervical vertebrae. However, the disease does not always conform to this ascending pattern. In general, atypical patterns occur more frequently in women, but spinal disease without sacroiliac joint involvement is unusual in either sex. The cervical spine becomes ankylosed late in the course of the disease, leading to restriction in neck movement and head rotation. Eventually, the spine becomes completely rigid, with loss of its normal curvatures and movement.
Patients with ankylosing spondylitis test negative for rheumatoid factors. HLA-B27 is present in 95% of patients, but only a small percentage of all individuals positive for HLA-B27 actually develop the disorder. Therefore, this test cannot be used diagnostically.
Inflammatory spinal disease typically presents in patients younger than age 40 years with back pain that is insidious in onset, persists for at least 3 months, is associated with morning stiffness, and improves with exercise. Ankylosing spondylitis is the most common inflammatory spinal disease in adults and the prototype for all of the spondyloarthropathies. It usually starts in the sacroiliac joints early in the disease and progresses to involve other parts of the axial skeleton later. Inflammatory back pain is most frequently located at the lower part of the back, partly as alternating buttock pain. The pain may spread to multiple other locations in the spine, typically at night. The disorder tends to follow a more mild and benign course in females.
Ankylosing spondylitis is a distinct disease entity characterized by inflammation of multiple articular and para-articular structures. The inflammation frequently results in bony ankylosis of the joints. The term ankylosing derives from the Greek word ankylos , meaning “stiffening of a joint.” Spondylos means “vertebra”; spondylitis refers to inflammation of one or more vertebrae. Ankylosing spondylitis is usually classified as a chronic and progressive form of seronegative arthritis. It has a predilection for the axial skeleton (particularly the sacroiliac joints), the spinal facet joints, and the paravertebral soft tissues. Extraspinal manifestations of the disease include peripheral arthritis, iritis, pulmonary involvement, and systemic upset.
The basic pathologic lesion of ankylosing spondylitis occurs at the entheses. These are the sites at which the ligaments, tendons, and joint capsules attach to the bone. Cellular infiltration by lymphocytes, plasma cells, and polymorphonuclear leukocytes is associated with erosion and eburnation of the subligamentous bone. The inflammation forms new bone within the outer layers of the annulus fibrosus of the intervertebral discs. The margins of the disc are invaded by hyperemic granulation tissue arising from the subchondral bone. This tissue replaces the disc fibers with new bone. Insufficiency fractures and traumatic fractures of the affected vertebrae also occur. Another important sign of spondyloarthritis is enthesitis. This affects the interspinal and supraspinal ligaments of the vertebral spine and the interosseous ligaments in the retroarticular space of the sacroiliac joints.
CT is useful for documenting the presence of ankylosing spondylitis in patients whose initial sacroiliac joint radiographs are normal or equivocal. Features such as joint erosions, subchondral sclerosis, and bony ankylosis are visualized better on CT than on radiographs. However, normal variants of the sacroiliac joint may simulate the features of sacroiliitis. CT supplements bone scintigraphy in evaluating areas of increased radionuclide uptake, particularly in the spine. Bony lesions such as pseudarthroses, fractures, spinal canal stenosis, and facet inflammatory disease are well detected using CT, particularly with multiplanar reformatting into coronal, sagittal, or oblique images ( Fig. 20-1 ). Other useful applications of CT include the assessment of costovertebral disease, manubriosternal disease, dural ectasia, and paraspinal muscle atrophy. Multidetector CT (MDCT) is superior to radiographs and to MRI for showing the number of lesions and demonstrating fracture morphology. In patients with advanced disease, MDCT is the primary modality for evaluating cervical spine fractures ( Fig. 20-2 ). MDCT complements MRI, which better shows spinal cord and soft tissue injuries. CT is accurate for diagnosing complications of ankylosing spondylitis, such as spinal pseudarthrosis, fractures, and vertebral scalloping from dural ectasia.
MRI may contribute to the early diagnosis of sacroiliitis. MRI detection of synovial enhancement correlates with disease activity as measured by laboratory inflammatory markers. MRI is superior to CT for detecting abnormal cartilage, bone erosions, and subchondral bone changes. It is also sensitive for assessing disease activity early in the course of ankylosing spondylitis. Affected sites include the discovertebral junctions and peripheral joints. In general, areas of increased T2 signal intensity correlate with the presence of edema or vascularized fibrous tissue ( Fig. 20-3 ).
In established disease, MRI can assess the integrity of the intervertebral discs and spinal ligaments and display spinal fractures. MRI detects pseudarthroses, diverticula associated with cauda equina syndrome, and spinal canal stenosis. In patients with complications of fractures or pseudarthroses, MRI demonstrates any compromise of the spinal canal or spinal cord injury. MRI is very helpful in patients with neurologic symptoms, especially those with a symptom-free interval after initial diagnosis and those with neurologic deterioration after established spinal cord injury from trauma. Advantages of MRI include direct visualization of cartilage abnormalities, detection of bone marrow edema, improved detection of bone erosions, and lack of ionizing radiation.
Early in ankylosing spondylitis, the spinal lesions mainly involve the intervertebral discs, the adjacent edges of the vertebrae, and the rims. The cartilage and the subchondral bone are involved secondarily. Neither MRI nor CT is diagnostic of spondylitis/spondylodiscitis specifically early in the disease. However, it is possible to differentiate between the noninfective spinal inflammation of spondyloarthropathy and infectious spondylitis/spondylodiscitis if the bacterial infection has already spread to adjacent structures. Noninfectious spondyloarthropathy does not spread outside the bone and ligament, so evidence of such spread implicates infection. MRI is sensitive enough to detect early inflammation of the axial skeleton in both spondyloarthritis and rheumatoid arthritis.
Radiographs are the single most important imaging technique for detection, diagnosis, and follow-up of patients with ankylosing spondylitis. Bony morphology, subtle calcifications, and ossifications are well demonstrated radiographically. Early spondylitis manifests as small erosions at the corners of the vertebral bodies with surrounding reactive sclerosis, findings designated the “shiny corner sign” or “Romanus lesion.” Squaring of the vertebral bodies is another characteristic feature of ankylosing spondylitis and is caused by a combination of corner erosions and periosteal new bone formation along the anterior aspect of the vertebral body. Squaring is most easily appreciated in the lumbar spine, where the anterior border of the vertebral body is normally concave. Further inflammation is associated with formation of syndesmophytes: ossifications of the outer fibers of the annulus fibrosus that form bony bridges between the inflamed corners of adjacent vertebrae. Ossification also occurs within the fibers of the adjacent paravertebral connective tissue. Ossification of the posterior interspinous ligaments links sequential spinous processes into a solid vertical midline “bone,” which causes a dense line on frontal radiographs. In similar fashion, the apophyseal and costovertebral joints are frequently affected by erosions and then ossification and eventually fuse. Complete fusion of the vertebral bodies by syndesmophytes and related ossifications produces the “bamboo spine” ( Fig. 20-4 ). The intervertebral discs may calcify at single or multiple levels, usually in association with apophyseal joint ankylosis and adjacent syndesmophytes.
In established ankylosing spondylitis, fractures usually occur at the thoracolumbar and cervicothoracic junctions. Upper cervical spine fractures and atlantoaxial subluxations are rare. Spinal fractures are characteristically transverse (i.e., horizontal) rather than vertical or oblique and are called “chalk stick” fractures. They extend from anterior to posterior and frequently pass through the unossified disc.
Pseudarthroses are seen radiographically as areas of discovertebral destruction and adjacent sclerosis. These changes are referred to as the Anderson lesion and may resemble disc infection. Pseudarthrosis usually develops secondary to a previously undetected fracture or at an unfused segment. Therefore, an important imaging feature of ankylosing spondylitis is the involvement of the facet joints, which is seen as a linear hypodense area with sclerotic borders.
The spinal abnormalities found in ankylosing spondylitis may also be encountered in other diseases, such as enteropathic arthropathy, psoriasis, and Reiter syndrome. Careful analysis and classification of bony outgrowths in the vertebrae help to differentiate among these conditions. Flowing anterior ossification is a feature of diffuse idiopathic skeletal hyperostosis. Paravertebral ossification is present in both psoriasis and Reiter syndrome. Syndesmophytes are found in alkaptonuria as well as ankylosing spondylitis.
Spinal pseudarthrosis in ankylosing spondylitis may produce marked discovertebral destructive changes that resemble infective spondylodiscitis. The detection of posterior element fractures or defects is an important distinguishing clue in diagnosing these patients with ankylosing spondylitis. The spondyloarthritides often share common features of aggressive erosions, bone density preservation, and proliferative bony response to inflammation. These features along with asymmetric involvement of the appendicular skeleton, sacroiliitis, and spine abnormalities usually allow differentiation of ankylosing spondylitis from rheumatoid arthritis and other inflammatory arthritides based on imaging studies.
Psoriatic arthritis is a unique inflammatory arthritis associated with psoriasis. Its exact prevalence is unknown, but estimates vary from 0.3% to 1% of the population. The prevalence of psoriasis among patients with arthritis in the general population is 2% to 3%. Inflammatory arthritis occurs in 2% to 3% of the general population, but among patients with psoriasis the prevalence of inflammatory arthritis varies from 6% to 42%.
Typically, psoriatic arthritis initially presents as a mild oligoarticular disease. It becomes polyarticular and a severe disease in at least 20% of patients. Patients with psoriatic arthritis who present with polyarticular disease have an increased risk for disease progression. Health-related quality of life is reduced among patients with this disease.
The histopathologic correlate of MRI bone edema has not been defined in psoriatic arthritis.
Psoriatic arthritis shares MRI features with rheumatoid arthritis and spondyloarthropathy. On MRI, the synovitis of psoriatic arthritis appears indistinguishable from the synovitis of rheumatoid arthritis. Although in some patients the synovitis observed conforms to a typical rheumatoid pattern, in others the inflamed tissue extends far beyond the joint capsule and involves adjacent structures, such as thickened collateral ligaments and periarticular soft tissue. The erosions themselves consist of a break in the cortical bone overlying a region of altered signal intensity with definite margins. Psoriatic arthritic erosions can be large, ill-defined areas in the subcortical bone with increased signal on short tau inversion recovery (STIR) and T2-weighted (T2W) imaging with fat saturation. They may enhance on postcontrast T1-weighted (T1W) fat saturation sequences.
Radiographically, the spondylitis and reactive arthritis of psoriatic arthritis are chunky and asymmetric, as compared with the smooth, fine, symmetric changes of ankylosing spondylitis.
Reactive arthritis (Reiter syndrome) is an acute nonpurulent seronegative arthritis that complicates an infection elsewhere in the body.
Reactive arthritis is associated with HLA-B27, which is not always present in affected individuals, particularly in the presence of human immunodeficiency virus (HIV). When reactive arthritis occurs in African Americans, it is frequently HLA-B27 negative.
In the United States, the frequency of reactive arthritis is estimated at 3.5 cases per 100,000 individuals. It is reported most frequently in whites. The male-to-female ratio following venereal disease is 5 to 10:1. The peak onset is in persons aged 15 to 35 years. Reactive arthritis is rarely seen in children; if it does occur it almost always follows an enteric infection.
An estimated 1% to 3% of all patients with a nonspecific urethritis develop an episode of arthritis. Most patients have severe symptoms lasting weeks to 6 months. Fifteen to 50 percent have recurrent bouts of arthritis. Chronic arthritis or sacroiliitis occurs in 15% to 30% of patients. Symptoms generally appear within 1 to 3 weeks but can range from 4 to 35 days from the onset of the urethritis/cervicitis or diarrhea. Symptoms include fever (usually low grade), malaise, myalgias (early), low back pain with radiation to the buttocks or thighs, and asymmetric joint stiffness primarily involving the knees, ankles, and feet. Symptoms become worse with rest or inactivity.
Reactive arthritis is triggered by enteric or urogenital infections.
Paravertebral calcifications may be seen as the initial manifestation of reactive arthritis, in contrast to the syndesmophytes seen in early ankylosing spondylitis. Erosions of the anterior corners of the vertebral bodies are rare in reactive arthritis.
There is no specific role for MRI in the diagnosis of reactive arthritis.
In early reactive arthritis radiographs may show no abnormalities. Two typical findings are unilateral or bilateral sacroiliitis and asymmetric paravertebral comma-shaped ossification involving the lower thoracic and upper lumbar vertebrae.
The prevalence of rheumatoid arthritis is approximately 1% of the adult population in Europe and North America (range: 0.3%-2.1%). The prevalences are higher in some Native American groups and lower in the Caribbean. Worldwide, the incidence is about 3 cases per 10,000 population.
Severe rheumatoid arthritis occurs at approximately four times the expected rate in first-degree relatives of individuals with seropositive disease. Approximately 10% of patients with rheumatoid arthritis have an affected first-degree relative. Women are affected approximately three times more often than men. Disease onset is most frequent during the fourth and fifth decades of life, with 80% of patients developing disease between the ages of 35 and 50 years. The incidence of rheumatoid arthritis is more than six times greater in 60- to 64-year-old women compared with 29-year-old women. Older patients are more likely to have lesions in the lower spine.
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