Sacroiliitis is the earliest radiographic finding of ankylosing spondylitis. Initial change is blurring of the subchondral cortex on the iliac side of the sacroiliac joints. The erosions usually develop earlier on the iliac side due to thinner iliac cartilage. After then, both sides of the sacroiliac joints are involved generally bilaterally and symmetrically (Bennett et al. 2004). Haziness of the subchondral bone on the radiography is an important finding of sacroiliitis that is not observed in degenerative joint disease. This finding is followed by the erosive changes of the joint and mild subchondral sclerosis. The erosions become larger with widening of the joint space (pseudo-widening), and the subchondral sclerosis (reactive bone proliferation) becomes more prominent. The destruction of cartilage progresses with narrowing of the joint space. The SI joints come to be fused with ossification of the capsuloligamentous structures. In advanced stage, the joint shows complete ankylosis with decreased periarticular sclerosis. The modified New York criteria grades the sacroiliitis as follows: grade 0 indicates normal findings; grade 1, suspicious changes; grade 2, minimum abnormality, defined as small localized areas with erosion or sclerosis without change in the joint width; grade 3, obvious abnormality with widening of the joint space; and grade 4, total ankylosis. Based on the modified New York clinical criteria, grades 0 or 1 are not sufficient for the diagnosis of definite ankylosing spondylitis.

CT is more sensitive than plain radiography in detecting subtle cortical erosions of the sacroiliac joints. MR imaging can detect the sacroiliitis earliest and evaluate the disease activity. Postcontrast T1 fat-saturated images improve the delineation of activity signs.

Bilateral and symmetrical sacroiliac joint abnormalities in ankylosing spondylitis must be differentiated from hyperparathyroidism and osteitis condensans ilii. In hyperparathyroidism, subchondral bone resorption in the ilium and subsequent joint space widening can be seen. In osteitis condensans ilii, a triangular segment of bony sclerosis is noted in the inferior aspect of the ilium. The joint surface is not affected, and the joint space is maintained. Osteitis condensans ilii results from chronic stress on the sacroiliac joints and occurs almost exclusively in women.

Spinal changes in ankylosing spondylitis can be seen in the diskovertebral junction, facet joints, costovertebral joints, posterior ligamentous attachments, and atlantoaxial joints. Ankylosing spondylitis predominantly involves the diskovertebral junction, including osteitis, erosions, syndesmophytes, and osteoporosis with diskal ballooning.

Osteitis causes cortical erosions along the anterior corners of the diskovertebral junction, typically seen at the thoracolumbar junction (Romanus lesions). These corner erosions and bony proliferation along the anterior aspect of the vertebral bodies result in loss of the normal concavity of the anterior vertebral surfaces and squaring of the vertebral bodies. Reactive subcortical scleroses frequently occur at the anterior corner of vertebral bodies (shiny corner sign). Romanus lesions show inflammatory and edematous changes at the anterior corners of the vertebral bodies on MRI (Jevtic et al. 2000). Fatty marrow change at vertebral corners on MR images is suggestive of chronic stage of the disease. Ossification of anterior and lateral paraspinal ligaments and the outer annulus of the disk results in thin vertical syndesmophytes. In later phase, ankylosis with diffuse syndesmophytes leads to the undulating vertebral contour (bamboo spine).

Ankylosing spondylitis may manifest as destructive diskovertebral lesions (Andersson lesions). Two types of Andersson lesions have been described. The type-A Andersson lesion is an inflammatory change in the central subchondral portions of the diskovertebral junction and reveals as Schmorl’s node, irregularity of vertebral endplate, and disk space narrowing. The type-B Andersson lesion is a pseudoarthrosis following a diskovertebral fracture in the frangible ankylosed spine. The type-B Andersson lesion is usually located at the thoracolumbar or cervicothoracic junction, around skip area of ankylosed segments.

The facet joints may exhibit cortical erosions, sclerosis, capsular calcifications, and fusion. The ankylosis of the facet joints is the main cause of the rigidity of the spine. Ossification of the facet joint capsules makes two vertical radiodense lines (the tram-track sign or trolley sign) on anteroposterior (AP) radiograph. Ossification of the posterior interspinous and supraspinous ligaments of the lumbar spine is seen as a single central radiodense line (the dagger sign) on AP radiographs.

Osteoporosis and spinal rigidity of advanced ankylosing spondylitis can cause spinal fractures (Wang et al. 2005). Fractures in ankylosing spondylitis are likely to be transverse and may spread through the vertebral body or intervertebral disk. The adjacent anterior and posterior paraspinal ligaments are frequently disrupted, and spinal cord compression or contusion may occur.

Severe osteoporosis may result in smooth biconcave endplate depressions of the vertebral body (fish vertebrae) and biconvex disk (diskal ballooning). Dural ectasia and associated widening of the spinal canal may develop particularly in the lumbar region.