Predisposition to ankylosing spondylitis is largely genetic, and epidemiologic studies suggest that the environmental trigger is ubiquitous. HLA-B27 and -B60 predispose to ankylosing spondylitis, but in neither case is the mechanism of effect known. Other major histocompatibility complex and non-major histocompatibility complex genes are likely to influence susceptibility to spondyloarthritis as well as the disease pattern. Spondyloarthritis occurs in genetically predisposed inviduals exposed to certain as yet undefined environmental triggers. Although genes within the major histocompatibility complex are clearly major determinants of susceptibility to spondyloarthritis, epidemiologic evidence suggests that their contribution accounts for less than 50percnt; of the total. The mechanism of association of B27 with these diseases is unknown; we are currently unable to predict which B27 carriers will develop arthritis or which form of B27-associated spondyloarthritis they will develop. Lessons from transgenic animal experiments and technical and statistical advances in the field of genetics have greatly increased our ability to investigate these questions.
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