title: Synovial immunopathology in haemochromatosis arthropathy.
abstract: BACKGROUND
  Hereditary haemochromatosis (HH) is a common autosomal recessive inherited disorder that frequently causes arthritis. The pathophysiology of musculoskeletal involvement is, however, unclear.
  
  
  OBJECTIVE
  To analyse synovial tissue obtained at surgery from patients with HH arthropathy and compare it qualitatively and quantitatively with specimens from patients with rheumatoid arthritis (RA) and osteoarthritis (OA).
  
  
  METHODS
  Synovial tissue from 15 patients with HH, 20 with RA and 39 with OA was obtained during surgery. A synovitis grading system was used to determine the severity of synovial inflammation. Using immunohistochemistry, synovial neovascularisation and infiltration of macrophages, neutrophils and lymphocytes were quantitatively assessed.
  
  
  RESULTS
  Synovitis in HH arthropathy largely resembles OA with mild infiltration of mononuclear cells and lymphocytes, formation of synovial microvessels and a low degree of synovial hyperplasia. While many features of HH arthropathy are reminiscent of OA, macrophage and especially neutrophil invasion is clearly more prominent in HH arthropathy than in primary OA and mimics features of RA. This finding was observed particularly in synovial tissue of HH samples with marked haemosiderin deposition.
  
  
  CONCLUSIONS
  The histological picture of the synovium in HH arthropathy largely resembles a process reminiscent of OA. Neutrophil invasion is, however, markedly increased in HH arthropathy, especially in joints with iron deposition. Accumulation of neutrophils may be crucial for the production of matrix enzymes, which enables cartilage degradation and more rapidly progressive articular damage.
authors.affiliation: Department of Internal Medicine 3 and Institute for Clinical Immunology, University of Erlangen-Nuremberg, Krankenhausstrasse 12, 91054 Erlangen, Germany.
authors.forename: Gisela Ruiz
authors.initials: GR
authors.lastname: Heiland
authors.forename: Elmar
authors.initials: E
authors.lastname: Aigner
authors.forename: Tomás
authors.initials: T
authors.lastname: Dallos
authors.forename: Enijad
authors.initials: E
authors.lastname: Sahinbegovic
authors.forename: Veit
authors.initials: V
authors.lastname: Krenn
authors.forename: Christoph
authors.initials: C
authors.lastname: Thaler
authors.forename: Günter
authors.initials: G
authors.lastname: Weiss
authors.forename: Jörg H
authors.initials: JH
authors.lastname: Distler
authors.forename: Christian
authors.initials: C
authors.lastname: Datz
authors.forename: Georg
authors.initials: G
authors.lastname: Schett
authors.forename: Jochen
authors.initials: J
authors.lastname: Zwerina
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001168:Arthritis / Q000209:etiology / Q000276:immunology / Q000473:pathology; D001172:Arthritis, Rheumatoid / Q000276:immunology / Q000473:pathology; D005260:Female; D006432:Hemochromatosis / Q000150:complications* / Q000276:immunology / Q000473:pathology; D006801:Humans; D016131:Lymphocyte Subsets / Q000276:immunology; D008264:Macrophages / Q000276:immunology; D008297:Male; D008875:Middle Aged; D009389:Neovascularization, Pathologic / Q000473:pathology; D020556:Neutrophil Infiltration; D010003:Osteoarthritis / Q000276:immunology / Q000473:pathology; D013583:Synovial Membrane / Q000098:blood supply / Q000276:immunology*; D013585:Synovitis / Q000209:etiology* / Q000276:immunology* / Q000473:pathology