Background The pathophysiology of psoriatic arthritis (PsA) has still not been examined in minute detail as has rheumatoid arthritis (RA). As it is often difficult to differentiate between both diseases and there are numerous publications that synovial inflammation and cytokine pattern are different in PsA and RA, we analysed the synovial histological differences with respect to immunomodulatory adipokines resistin, visfatin and adiponectin.
Methods First, synovial tissues from affected joints with PsA were stained with hematoxylin/eosin to visualise the histology of the synovial membrane. Thereafter, macrophages were detected by immunohistochemistry using an anti-CD16 antibody, fibroblasts using an anti-vimentin antibody. Collagen type IV-antibodies were used to visualise vascular endothelial cells and anti-CD20 antibodies to identify B-lymphocytes. In addition, serial tissue sections were stained for resistin-, visfatin, and adiponectin.
Results In the majority of patients, the synovial tissue from PsA showed no hyperplasia of the lining layer in comparison to RA (lining thickness in % of PsA patients: 1 cell layer, 64%; 2–3 cell layers, 21%; >4 cell layers, 24%. Vice versa, an increased cellularity in the sublining could be detected. In PsA, a lower number of immune-cell follicles were observed although the number of synovial vessels was increased. In all samples, cellular adipokine signals were detectable. Adiponectin was mainly located in vessels showing a strong expression of this molecule. In contrast to RA, the expression of adiponectin in the lining layer was completely absent in most PsA patients. Resistin was detectable in the sublining but also in the lining layer. A strong expression of visfatin could be found in the sublining, and to a lower extent in the lining layer. There was no association between the localisation of the adipokines and the quantity or of compact inflammatory infiltrates.
Conclusions The synovial membranes from PsA show clear differences to those of RA-affected joints. Adipokine expression is -in part- also different between RA and PsA patients. Here, specifically adiponectin is more prominent in the RA than in the PsA lining layer. Adipokines may therefore play different roles in inflammatory processes operative in these chronic rheumatic diseases.