The pathogenetic mechanisms in the development of
spondyloarthropathies are multifactorial. These include the possible role of infective micro-organisms which can by direct invasion lead to persistence of microbial
antigens and thus trigger
arthritis or by cross-reactions with the host tissue lead to inflammatory symptoms or by cross-reactions with
HLA-B27 trigger cytotoxic T-cell response. After the primary event, exaggerated inflammatory response can lead to amplification of
inflammation. The components in the amplification of
inflammation include hyperreactive neutrophils and serum factors such as enhanced production of activation products of
complement in subjects with
HLA-B27. The enhanced neutrophil function seems to persist in patients with previous severe inflammatory symptoms during acute
reactive arthritis or in those with late inflammatory complications. The enhancement is probably caused by priming effect by
lipopolysaccharide, which seems to persist for a long period in patients with acute
reactive arthritis. Enhanced production of
monokines can contribute to the enhanced
inflammation in patients with
spondyloarthropathies. The primed phagocytes can respond vigorously when rechallenged with antigenic load during a new
infection, thus leading in some patients to recurrent or chronic inflammatory symptoms. Antimicrobial
therapy or
sulphasalazine by modifying
antigen elimination or absorption can diminish inflammatory response during acute
arthritis and in chronic
spondyloarthropathies. Long-term follow-up studies are needed to find out whether prolonged
therapies with these agents affect the prognosis of
spondyloarthropathies.