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AB0038 Adipokine expression in synovial tissue from patients with psoriatic arthritis
  1. E. Schmitt1,
  2. J. Kriegsmann2,
  3. R. Straub3,
  4. U. Müller-Ladner4,
  5. E. Neumann4
  1. 1Justus-Liebig-University Of Giessen, Bad Nauheim
  2. 2Department of Molecular Pathology, Center for Histology, Cytology and Molecular Diagnostics, Trier
  3. 3Department of Internal Medicine I, University of Regensburg, Regensburg
  4. 4Department of Internal Medicine and Rheumatology, Justus-Liebig-University Of Giessen, Bad Nauheim, Germany

Abstract

Background The pathophysiology of psoriatic arthritis (PsA) is not as well understood as for rheumatoid arthritis (RA), and the distinction between both diseases is often difficult. However, both diseases are characterized by synovial alterations within the affected joints and the central involvement of pro-inflammatory factors. Adipokines such as adiponectin, visfatin/PBEF and resistin have recently been identified as signaling molecules with substantial immunomodulatory potential. These adipokines are increased in RA synovium and exert a pro-inflammatory impact on central cells of RA pathophysiology.

Objectives Therefore, the synovial adipokine expression of adiponectin, visfatin/PBEF and resistin was evaluated in PsA synovium.

Methods Synovial tissues from affected joints of PsA patients were stained with hematoxylin/eosin. Immunohistochemical staining against fibroblasts (vimentin), macrophages (CD16), T cells (CD3), B cells (CD20), vessels (collagen type IV) as well as against adiponectin, visfatin/PBEF and resistin were performed in serial sections. Additionally, adipokine expression was compared to the expression pattern of RA patients.

Results In the majority of patients, the synovial tissue from PsA showed no hyperplasia of the lining layer in comparison to RA. 71% of the synovial tissue showed a high expression of Visfatin/PBEF. However resistin was less detectable in PsA lining layer, 71% showed a low resistin secretion. In comparison to RA, resistin expression was lower in PsA whereas visfatin/PBEF was comparable. In contrast to RA, the expression of adiponectin in the lining layer was completely absent in most PsA patients. 86 % of the samples showed moderate adiponectin signals, which were mainly located in the sublining in vessels showing a strong expression in PsA. In RA, the sublining showed adiponectin expression in the vessels but also by connective tissue cells. Resistin and visfatin/PBEF were detectable in the sublining and comparable between RA and PsA tissues. Adiponectin was expressed in inflammatory infiltrates in RA. However, this pattern was not present in PsA tissue.

Conclusions The synovial membranes from PsA and RA show clear differences to those of RA-affected joints and are in part reflected by the adipokine expression. 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.

Disclosure of Interest None Declared

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