ETIOLOGY AND PATHOGENESIS OF SPONDYLOARTHRITIDES

Authors:

Branimir Anić, Mislav Cerovec

Summary

Seronegative spondyloarthritides are inflammatory rheumatic diseases which are classified together because of numerous common and similar clinical, epidemiologic and genetic characteristics. Pathogenesis of seronegative spondyloarthritides is usually described as development of clinical characteristics of the disease in genetically susceptible person in the presence of favorable environmental factors. Development of seronegative spondyloarthritides, notably ankylosing spondylitis, is strongly connected with presence of the HLA-B27 gene. There are clear evidence that HLA-B27 positive individuals have significantly higher risk for disease development. The role of infection in occurence of seronegative spondyloarthritides is not completely understood – its role is better clarified in the case of reactive arthritis than in ankylosing spondylitis. The relation between HLA-B27 gene and infection is not clarified. Molecular mimicry theory is based on similarities between HLA-B27 molecule and microbial particle.

Sažetak
Seronegativne spondilartropatije su skupina upalnih reumatskih bolesti koje se zajednički klasificiraju zbog niza zajedničkih i sličnih kliničkih, epidemioloških i genetičkih obilježja. Patogeneza bolesti kod seronegativnih spondiloartropatija najčešće se opisuje kao razvoj kliničkih očitovanja bolesti u genetski predisponiranih osoba uz povoljne okolišne čimbenike. Razvoj seronegativnih spondiloartropatija, a osobito ankilozantnog spondilitisa povezuje se s prisutnošću gena HLAB27. Dokazano je da osobe s HLA-B27 imaju značajno viši rizik za razvoj SpA. Uloga infekcije u nastanku seronegativnih spondiloartropatija nije posve jasna; njezina je uloga najjasnija u nastanku reaktivnog artritisa, a evidentno je manje očita u ankilozantnom spondilitisu. Povezanost HLA-B27 i infekcije nije sasvim razjašnjena. Teorija o molekularnoj mimikriji temelji se na opažanju sličnosti između molekule HLA-B27 i dijelova mikroba.

Vol.: 58

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