Ankylosing spondylitis (AS) is an inflammatory disease of unknown cause that primarily affects the medial bones; peripheral joints and extra-articular structures may also be involved. It often begins in the late teens or early twenties; the ratio of men to women is 3:1. AS is closely related to the histocompatibility antigen HLA-B27, and its worldwide prevalence is probably proportional to the rate of positivity for this antigen. However, B27 is not associated with the severity of the disease. Pathology: The pelvic and peri-spinal ligamentous attachments are the main sites of AS pathogenesis, and attachment point inflammation is associated with edema of the adjacent bone marrow, culminating in an erosive lesion of ossification. (1) Sacroiliac arthritis is often one of the earliest manifestations of AS and includes both attachment point inflammation and synovitis. Early lesions of granulation tissue and inflammatory cells infiltrate the ligamentous and periosteal areas and edema of the subchondral bone marrow. This is followed by synovitis, which leads to the formation of vascular opacities and new bone islands. The eroded joint edges are gradually replaced by regenerated fibrocartilage ossification and, eventually, the joint space is completely lost. (ii) Early lesions of the spine are characterized by inflammatory granulation tissue infiltrating the fibrous rings of the disc cartilage and the vertebral rim junction. Progressive erosion of the fibrous ring results in the formation of osteophytes, persistent chondrogenic bone, and eventually bridges between adjacent vertebrae. The upward progression of this process results in a radiographic “bamboo-like spine”. Other lesions of the spine include extensive osteoporosis, erosion of the vertebral body at the disc margin, squared vertebral body changes, and inflammation and destruction of the disc-bone boundary. (iii) Peripheral arthritis in AS manifests as synovial hyperplasia, lymphatic-like infiltration, and vascular opacification formation, but the process does not present with synovial villous hyperplasia, fibrin deposition, ulceration, and plasma cell aggregation as seen in RA. Pathogenesis: The pathogenesis of AS is not fully understood, but is almost certainly immune-mediated. The dramatic response of all aspects of disease manifestations to tumor necrosis factor alpha (TNF-α) blocker therapy suggests a central role for this cytokine in the immunopathogenesis of AS. Inflamed sacroiliac joints infiltrated by CD4+ and CD8+ T cells and macrophages show high levels of TNF-α. Clinical manifestations: Symptoms of the disease begin to be noticed in late adolescence or early adulthood.1 The initial symptoms are insidiously appearing deep dull pain in the lower back or gluteal region, accompanied by half-hour morning stiffness in the lower back, improving with activity and worsening with rest. During the first few months of the disease, the pain is often bilateral and persistent. The pain increases at night and often forces the patient to get up and move around. Pain persists early in the disease and then occurs intermittently, alternating between periods of exacerbation and periods of quiescence. Peripheral arthritis is often asymmetric and can occur at any stage of the disease. Neck pain and stiffness due to cervical spine involvement is often a relatively advanced manifestation. The most common extra-articular manifestation is acute anterior uveitis, with the typical episode being unilateral with ocular pain, photosensitivity, and increased tear production. ② The initial physical examination responds to inflammatory lesions, including decreased spinal mobility, limited anterior, lateral, and lateral flexion and extension movements of the lumbar spine, and thoracic expansion. The limitation of motion is often disproportionate to the degree of bone strengthening and reflects muscle spasm secondary to pain and inflammation. Sacroiliac joint pain may be elicited by direct pressure on the joint or by manipulation of the joint by traction. It is important to note that in the early stages of mild cases, symptoms may be mild as well as nonspecific and the physical examination may be completely normal. Laboratory tests: No laboratory tests are available to confirm the diagnosis of AS. In most populations, about 90% of patients with AS have a positive B27 ESR, CRP is often, but not always, elevated. Mild anemia may be present; alkaline phosphatase may be elevated; IgA levels are often elevated. Rheumatoid factor and antinuclear antibodies are mostly negative unless there is a combination of other diseases. Imaging: Radiologically confirmed sacroiliac arthritis is common in AS. The earliest change is blurring of the subchondral cortical rim, followed by erosion and sclerosis. The progression of erosion leads to “pseudo-widening” of the joint space, followed by fibrosis with bony ankylosis and loss of the joint space. In the lumbar spine, disease progression leads to straightening of the lumbar spine due to loss of anterior spinal protrusion, osteitis of the anterior horn of the affected vertebrae and subsequent osteosclerosis due to bone erosion, resulting in a “squared off” vertebral body. Progressive ossification culminates in the formation of marginal ligamentous tuberosities, which can be seen on plain radiographs as bony bridges connecting the anterior and lateral sides of adjacent vertebrae. Diagnosis: New York criteria (1984): (i) history of inflammatory back pain (ii) restricted lumbar motion in both the sagittal and frontal planes (iii) restricted thoracic expansion compared to the same age and sex criteria (iv) radiologically definite sacroiliac arthritis. The diagnosis was made by meeting item ④ and one of the remaining three items.