Format

Send to

Choose Destination
Nat Rev Rheumatol. 2010 Jul;6(7):399-405. doi: 10.1038/nrrheum.2010.79. Epub 2010 Jun 1.

Pathogenesis of ankylosing spondylitis.

Author information

1
Department of Medicine and Therapeutics, 9/F Clinical Science Building, Chinese University of Hong Kong, Prince of Wales Hospital, Shatin, Hong Kong, China.

Abstract

Ankylosing spondylitis (AS) is a potentially disabling form of seronegative spondyloarthritis. The main symptom of AS is inflammatory spinal pain; with time, some patients develop ankylosis and spinal immobility. The pathology mainly affects the entheses, where ligaments, tendons and capsules are attached to the bone. Three processes are observed at the entheses: inflammation, bone erosion and syndesmophyte (spur) formation. Tumor necrosis factor is an important mediator of the inflammatory processes, but this proinflammatory cytokine is not closely involved in bone erosion or syndesmophyte formation. The major causative factors of AS are genetic, with the gene encoding HLA-B27 being the most important genetic factor. Several other susceptibility genes have also been identified. An enormous number of papers have been published and many diverse hypotheses have been generated regarding the pathogenesis of AS. This Review outlines the key areas of current research in this field, describes several hypotheses regarding the pathogenesis of AS, which are under intense investigation, and concludes with a dissection of the processes involved in bone erosion and syndesmophyte formation.

PMID:
20517295
DOI:
10.1038/nrrheum.2010.79
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Nature Publishing Group
Loading ...
Support Center