U.C.L.A. Rheumatology Pathophysiology of Disease Course Lecture,
Second Year Medical School 1997

  
 
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Ankylosing Spondylitis     Page 19
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      peptides may be molecularly similar to self antigens in the joint so that the presentation of these bacterial peptides by HLA-B27 to T cells will result in the disease process of Reiter's Syndrome or AS. Since there is a cross-reactivity to self peptides, the autoimmune inflammatory process will perpetuate itself. Bacterial fragments have been found to persist in the synovium of patients with Reiter's Syndrome. CD8+ T lymphocytes that are restricted in their ability to kill yersinia-infected B27 target cells and salmonella-infected target cells have recently been identified in the synovial fluid of patients with AS and Reiter's Syndrome. Long term treatment of Chlamydia-induced Reiter's Syndrome with an antibiotic, tetracycline, has been shown to be beneficial. It may work by killing the chlamydial organisms and thereby reducing the bacterial antigenic load.
      Unlike RA, the principal target of inflammation in both AS and Reiter's Syndrome is the enthesis. This is the site of attachment of strong ligaments to bone. There is a mononuclear inflammation at this site which results in pain and spasm of the surrounding ligaments and muscles. Movement around the area is reduced. The typical patient with AS presents with pain in the low back extending up to the thoracic spine and neck (figure 1). The sacroiliac joints are inflamed since these joints are the site of strong ligaments attached to bone and fibrocartilage. As the inflammation progresses, new bone is laid down which 		   
 
Figure 1. A patient with AS is examined for sacroiliac tenderness. Click thumbnail figure to view full graphic. jpeg 219 x 164 pixels 12kbs freehand 3dstudio max
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