Synovial immunopathology in haemochromatosis arthropathy
Identifieur interne : 001A52 ( Istex/Corpus ); précédent : 001A51; suivant : 001A53Synovial immunopathology in haemochromatosis arthropathy
Auteurs : Gisela Ruiz Heiland ; Elmar Aigner ; Tomáš Dallos ; Enijad Sahinbegovic ; Veit Krenn ; Christoph Thaler ; Günter Weiss ; Jörg H. Distler ; Christian Datz ; Georg Schett ; Jochen ZwerinaSource :
- Annals of the Rheumatic Diseases [ 0003-4967 ] ; 2010-06.
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. Discussion 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.
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DOI: 10.1136/ard.2009.120204
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Distler</name><affiliation><mods:affiliation>Department of Internal Medicine 3 and Institute for Clinical Immunology, University of Erlangen-Nuremberg, Erlangen, Germany</mods:affiliation></affiliation></author><author><name sortKey="Datz, Christian" sort="Datz, Christian" uniqKey="Datz C" first="Christian" last="Datz">Christian Datz</name><affiliation><mods:affiliation>Department of Internal Medicine, Hospital Oberndorf, Salzburg, Austria</mods:affiliation></affiliation></author><author><name sortKey="Schett, Georg" sort="Schett, Georg" uniqKey="Schett G" first="Georg" last="Schett">Georg Schett</name><affiliation><mods:affiliation>Department of Internal Medicine 3 and Institute for Clinical Immunology, University of Erlangen-Nuremberg, Erlangen, Germany</mods:affiliation></affiliation></author><author><name sortKey="Zwerina, Jochen" sort="Zwerina, Jochen" uniqKey="Zwerina J" first="Jochen" last="Zwerina">Jochen Zwerina</name><affiliation><mods:affiliation>Department of Internal Medicine 3 and Institute for Clinical Immunology, University of Erlangen-Nuremberg, Erlangen, Germany</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Annals of the Rheumatic Diseases</title><title level="j" type="abbrev">Ann Rheum Dis</title><idno type="ISSN">0003-4967</idno><idno type="eISSN">1468-2060</idno><imprint><publisher>BMJ Publishing Group Ltd and European League Against Rheumatism</publisher><date type="published" when="2010-06">2010-06</date><biblScope unit="volume">69</biblScope><biblScope unit="issue">6</biblScope><biblScope unit="page" from="1214">1214</biblScope></imprint><idno type="ISSN">0003-4967</idno></series><idno type="istex">C182C4ECA47D86A51F936CFE3979BC240A9B4845</idno><idno type="DOI">10.1136/ard.2009.120204</idno><idno type="href">annrheumdis-69-1214.pdf</idno><idno type="ArticleID">annrheumdis120204</idno><idno type="PMID">19933745</idno><idno type="local">annrheumdis;69/6/1214</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0003-4967</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="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. Discussion 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.</div></front></TEI><istex><corpusName>bmj</corpusName><author><json:item><name>Gisela Ruiz Heiland</name><affiliations><json:string>Department of Internal Medicine 3 and Institute for Clinical Immunology, University of Erlangen-Nuremberg, Erlangen, Germany</json:string></affiliations></json:item><json:item><name>Elmar Aigner</name><affiliations><json:string>Department of Internal Medicine, Hospital Oberndorf, Salzburg, Austria</json:string></affiliations></json:item><json:item><name>Tomáš Dallos</name><affiliations><json:string>Department of Internal Medicine 3 and Institute for Clinical Immunology, University of Erlangen-Nuremberg, Erlangen, Germany</json:string><json:string>2nd Department of Paediatrics, Medical Faculty, Comenius University in Bratislava, Bratislava, Slovakia</json:string></affiliations></json:item><json:item><name>Enijad Sahinbegovic</name><affiliations><json:string>Department of Internal Medicine 3 and Institute for Clinical Immunology, University of Erlangen-Nuremberg, Erlangen, Germany</json:string></affiliations></json:item><json:item><name>Veit Krenn</name><affiliations><json:string>Institute of Pathology, Trier, Germany</json:string></affiliations></json:item><json:item><name>Christoph Thaler</name><affiliations><json:string>Department of Orthopedic Surgery, Medical University of Salzburg, Austria</json:string></affiliations></json:item><json:item><name>Günter Weiss</name><affiliations><json:string>Department of Internal Medicine, Medical University of Innsbruck, Austria</json:string></affiliations></json:item><json:item><name>Jörg H Distler</name><affiliations><json:string>Department of Internal Medicine 3 and Institute for Clinical Immunology, University of Erlangen-Nuremberg, Erlangen, Germany</json:string></affiliations></json:item><json:item><name>Christian Datz</name><affiliations><json:string>Department of Internal Medicine, Hospital Oberndorf, Salzburg, Austria</json:string></affiliations></json:item><json:item><name>Georg Schett</name><affiliations><json:string>Department of Internal Medicine 3 and Institute for Clinical Immunology, University of Erlangen-Nuremberg, Erlangen, Germany</json:string></affiliations></json:item><json:item><name>Jochen Zwerina</name><affiliations><json:string>Department of Internal Medicine 3 and Institute for Clinical Immunology, University of Erlangen-Nuremberg, Erlangen, Germany</json:string></affiliations></json:item></author><articleId><json:string>annrheumdis120204</json:string></articleId><language><json:string>eng</json:string></language><originalGenre><json:string>research-article</json:string></originalGenre><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. Discussion 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.</abstract><qualityIndicators><score>8.045</score><pdfVersion>1.3</pdfVersion><pdfPageSize>595.277 x 793.702 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>0</keywordCount><abstractCharCount>1661</abstractCharCount><pdfWordCount>3333</pdfWordCount><pdfCharCount>22778</pdfCharCount><pdfPageCount>6</pdfPageCount><abstractWordCount>226</abstractWordCount></qualityIndicators><title>Synovial immunopathology in haemochromatosis arthropathy</title><pmid><json:string>19933745</json:string></pmid><refBibs><json:item><author><json:item><name>A Pietrangelo</name></json:item></author><host><volume>350</volume><author></author><title>N Engl J Med</title></host><title>Hereditary hemochromatosis – a new look at an old disease</title></json:item><json:item><author><json:item><name>HR Schumacher Jr</name></json:item></author><host><volume>7</volume><pages><last>50</last><first>41</first></pages><author></author><title>Arthritis Rheum</title></host><title>Hemochromatosis and arthritis</title></json:item><json:item><author><json:item><name>IW Dymock</name></json:item><json:item><name>EB Hamilton</name></json:item><json:item><name>JW Laws</name></json:item></author><host><volume>29</volume><author></author><title>Ann Rheum Dis</title></host><title>Arthropathy of haemochromatosis. 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For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions</p></availability><date>2009-11-23</date></publicationStmt><notesStmt><note>GRH and EA contributed equally.</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a">Synovial immunopathology in haemochromatosis arthropathy</title><author xml:id="author-1"><persName><forename type="first">Gisela Ruiz</forename><surname>Heiland</surname></persName><affiliation>Department of Internal Medicine 3 and Institute for Clinical Immunology, University of Erlangen-Nuremberg, Erlangen, Germany</affiliation></author><author xml:id="author-2"><persName><forename type="first">Elmar</forename><surname>Aigner</surname></persName><affiliation>Department of Internal Medicine, Hospital Oberndorf, Salzburg, Austria</affiliation></author><author xml:id="author-3"><persName><forename type="first">Tomáš</forename><surname>Dallos</surname></persName><affiliation>Department of Internal Medicine 3 and Institute for Clinical Immunology, University of Erlangen-Nuremberg, Erlangen, Germany</affiliation><affiliation>2nd Department of Paediatrics, Medical Faculty, Comenius University in Bratislava, Bratislava, Slovakia</affiliation></author><author xml:id="author-4"><persName><forename type="first">Enijad</forename><surname>Sahinbegovic</surname></persName><affiliation>Department of Internal Medicine 3 and Institute for Clinical Immunology, University of Erlangen-Nuremberg, Erlangen, Germany</affiliation></author><author xml:id="author-5"><persName><forename type="first">Veit</forename><surname>Krenn</surname></persName><affiliation>Institute of Pathology, Trier, Germany</affiliation></author><author xml:id="author-6"><persName><forename type="first">Christoph</forename><surname>Thaler</surname></persName><affiliation>Department of Orthopedic Surgery, Medical University of Salzburg, Austria</affiliation></author><author xml:id="author-7"><persName><forename type="first">Günter</forename><surname>Weiss</surname></persName><affiliation>Department of Internal Medicine, Medical University of Innsbruck, Austria</affiliation></author><author xml:id="author-8"><persName><forename type="first">Jörg H</forename><surname>Distler</surname></persName><affiliation>Department of Internal Medicine 3 and Institute for Clinical Immunology, University of Erlangen-Nuremberg, Erlangen, Germany</affiliation></author><author xml:id="author-9"><persName><forename type="first">Christian</forename><surname>Datz</surname></persName><affiliation>Department of Internal Medicine, Hospital Oberndorf, Salzburg, Austria</affiliation></author><author xml:id="author-10"><persName><forename type="first">Georg</forename><surname>Schett</surname></persName><affiliation>Department of Internal Medicine 3 and Institute for Clinical Immunology, University of Erlangen-Nuremberg, Erlangen, Germany</affiliation></author><author xml:id="author-11"><persName><forename type="first">Jochen</forename><surname>Zwerina</surname></persName><affiliation>Department of Internal Medicine 3 and Institute for Clinical Immunology, University of Erlangen-Nuremberg, Erlangen, Germany</affiliation></author></analytic><monogr><title level="j">Annals of the Rheumatic Diseases</title><title level="j" type="abbrev">Ann Rheum Dis</title><idno type="pISSN">0003-4967</idno><idno type="eISSN">1468-2060</idno><imprint><publisher>BMJ Publishing Group Ltd and European League Against Rheumatism</publisher><date type="published" when="2010-06"></date><biblScope unit="volume">69</biblScope><biblScope unit="issue">6</biblScope><biblScope unit="page" from="1214">1214</biblScope></imprint></monogr><idno type="istex">C182C4ECA47D86A51F936CFE3979BC240A9B4845</idno><idno type="DOI">10.1136/ard.2009.120204</idno><idno type="href">annrheumdis-69-1214.pdf</idno><idno type="ArticleID">annrheumdis120204</idno><idno type="PMID">19933745</idno><idno type="local">annrheumdis;69/6/1214</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2009-11-23</date></creation><langUsage><language ident="en">en</language></langUsage><abstract><p>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. Discussion 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.</p></abstract></profileDesc><revisionDesc><change when="2009-11-23">Created</change><change when="2010-06">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/document/C182C4ECA47D86A51F936CFE3979BC240A9B4845/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="corpus bmj" wicri:toSee="no header"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="no"</istex:xmlDeclaration><istex:docType PUBLIC="-//NLM//DTD Journal Archiving and Interchange DTD v2.3 20070202//EN" URI="archivearticle.dtd" name="istex:docType"></istex:docType><istex:document><article article-type="research-article"><front><journal-meta><journal-id journal-id-type="hwp">annrheumdis</journal-id><journal-id journal-id-type="nlm-ta">Ann Rheum Dis</journal-id><journal-id journal-id-type="publisher-id">ard</journal-id><journal-title>Annals of the Rheumatic Diseases</journal-title><abbrev-journal-title abbrev-type="publisher">Ann Rheum Dis</abbrev-journal-title><abbrev-journal-title>Ann Rheum Dis</abbrev-journal-title><issn pub-type="ppub">0003-4967</issn><issn pub-type="epub">1468-2060</issn><publisher><publisher-name>BMJ Publishing Group Ltd and European League Against Rheumatism</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="publisher-id">annrheumdis120204</article-id><article-id pub-id-type="doi">10.1136/ard.2009.120204</article-id><article-id pub-id-type="other">annrheumdis;69/6/1214</article-id><article-id pub-id-type="other">annrheumdis;ard.2009.120204</article-id><article-id pub-id-type="pmid">19933745</article-id><article-id pub-id-type="other">1214</article-id><article-id pub-id-type="other">ard.2009.120204</article-id><article-categories><subj-group subj-group-type="heading"><subject>Basic and translational research</subject></subj-group><series-title>Extended report</series-title></article-categories><title-group><article-title>Synovial immunopathology in haemochromatosis arthropathy</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Heiland</surname><given-names>Gisela Ruiz</given-names></name><xref ref-type="aff" rid="A1">1</xref></contrib><contrib contrib-type="author"><name><surname>Aigner</surname><given-names>Elmar</given-names></name><xref ref-type="aff" rid="A2">2</xref></contrib><contrib contrib-type="author"><name><surname>Dallos</surname><given-names>Tomáš</given-names></name><xref ref-type="aff" rid="A1">1</xref><xref ref-type="aff" rid="A3">3</xref></contrib><contrib contrib-type="author"><name><surname>Sahinbegovic</surname><given-names>Enijad</given-names></name><xref ref-type="aff" rid="A1">1</xref></contrib><contrib contrib-type="author"><name><surname>Krenn</surname><given-names>Veit</given-names></name><xref ref-type="aff" rid="A4">4</xref></contrib><contrib contrib-type="author"><name><surname>Thaler</surname><given-names>Christoph</given-names></name><xref ref-type="aff" rid="A5">5</xref></contrib><contrib contrib-type="author"><name><surname>Weiss</surname><given-names>Günter</given-names></name><xref ref-type="aff" rid="A6">6</xref></contrib><contrib contrib-type="author"><name><surname>Distler</surname><given-names>Jörg H</given-names></name><xref ref-type="aff" rid="A1">1</xref></contrib><contrib contrib-type="author"><name><surname>Datz</surname><given-names>Christian</given-names></name><xref ref-type="aff" rid="A2">2</xref></contrib><contrib contrib-type="author"><name><surname>Schett</surname><given-names>Georg</given-names></name><xref ref-type="aff" rid="A1">1</xref></contrib><contrib contrib-type="author"><name><surname>Zwerina</surname><given-names>Jochen</given-names></name><xref ref-type="aff" rid="A1">1</xref></contrib></contrib-group><aff id="A1"><label>1</label>Department of Internal Medicine 3 and Institute for Clinical Immunology, University of Erlangen-Nuremberg, Erlangen, Germany</aff><aff id="A2"><label>2</label>Department of Internal Medicine, Hospital Oberndorf, Salzburg, Austria</aff><aff id="A3"><label>3</label>2nd Department of Paediatrics, Medical Faculty, Comenius University in Bratislava, Bratislava, Slovakia</aff><aff id="A4"><label>4</label>Institute of Pathology, Trier, Germany</aff><aff id="A5"><label>5</label>Department of Orthopedic Surgery, Medical University of Salzburg, Austria</aff><aff id="A6"><label>6</label>Department of Internal Medicine, Medical University of Innsbruck, Austria</aff><author-notes><corresp><label>Correspondence to</label> Dr Jochen Zwerina, Department of Internal Medicine 3 and Institute for Clinical Immunology, University of Erlangen-Nuremberg, Krankenhausstrasse 12, 91054 Erlangen, Germany; <email xlink:type="simple">jochen.zwerina@uk-erlangen.de</email></corresp><fn><p>GRH and EA contributed equally.</p></fn></author-notes><pub-date pub-type="ppub"><month>6</month><year>2010</year></pub-date><pub-date pub-type="epub-original"><day>23</day><month>11</month><year>2009</year></pub-date><pub-date pub-type="epub"><day>23</day><month>11</month><year>2009</year></pub-date><volume>69</volume><volume-id pub-id-type="other">69</volume-id><volume-id pub-id-type="other">69</volume-id><issue>6</issue><issue-id pub-id-type="other">annrheumdis;69/6</issue-id><issue-id pub-id-type="other">6</issue-id><issue-id pub-id-type="other">69/6</issue-id><fpage>1214</fpage><history><date date-type="accepted"><day>1</day><month>11</month><year>2009</year></date></history><permissions><copyright-statement>Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions</copyright-statement><copyright-year>2010</copyright-year></permissions><self-uri content-type="pdf" xlink:role="full-text" xlink:href="annrheumdis-69-1214.pdf"></self-uri><abstract><sec><title>Background</title><p>Hereditary haemochromatosis (HH) is a common autosomal recessive inherited disorder that frequently causes arthritis. The pathophysiology of musculoskeletal involvement is, however, unclear.</p></sec><sec><title>Objective</title><p>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).</p></sec><sec><title>Methods</title><p>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.</p></sec><sec><title>Results</title><p>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.</p></sec><sec><title>Discussion</title><p>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.</p></sec></abstract></article-meta></front></article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo><title>Synovial immunopathology in haemochromatosis arthropathy</title><partName>Extended report</partName></titleInfo><titleInfo type="alternative" contentType="CDATA"><title>Synovial immunopathology in haemochromatosis arthropathy</title><partName>Extended report</partName></titleInfo><name type="personal"><namePart type="given">Gisela Ruiz</namePart><namePart type="family">Heiland</namePart><affiliation>Department of Internal Medicine 3 and Institute for Clinical Immunology, University of Erlangen-Nuremberg, Erlangen, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Elmar</namePart><namePart type="family">Aigner</namePart><affiliation>Department of Internal Medicine, Hospital Oberndorf, Salzburg, Austria</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Tomáš</namePart><namePart type="family">Dallos</namePart><affiliation>Department of Internal Medicine 3 and Institute for Clinical Immunology, University of Erlangen-Nuremberg, Erlangen, Germany</affiliation><affiliation>2nd Department of Paediatrics, Medical Faculty, Comenius University in Bratislava, Bratislava, Slovakia</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Enijad</namePart><namePart type="family">Sahinbegovic</namePart><affiliation>Department of Internal Medicine 3 and Institute for Clinical Immunology, University of Erlangen-Nuremberg, Erlangen, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Veit</namePart><namePart type="family">Krenn</namePart><affiliation>Institute of Pathology, Trier, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Christoph</namePart><namePart type="family">Thaler</namePart><affiliation>Department of Orthopedic Surgery, Medical University of Salzburg, Austria</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Günter</namePart><namePart type="family">Weiss</namePart><affiliation>Department of Internal Medicine, Medical University of Innsbruck, Austria</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jörg H</namePart><namePart type="family">Distler</namePart><affiliation>Department of Internal Medicine 3 and Institute for Clinical Immunology, University of Erlangen-Nuremberg, Erlangen, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Christian</namePart><namePart type="family">Datz</namePart><affiliation>Department of Internal Medicine, Hospital Oberndorf, Salzburg, Austria</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Georg</namePart><namePart type="family">Schett</namePart><affiliation>Department of Internal Medicine 3 and Institute for Clinical Immunology, University of Erlangen-Nuremberg, Erlangen, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jochen</namePart><namePart type="family">Zwerina</namePart><affiliation>Department of Internal Medicine 3 and Institute for Clinical Immunology, University of Erlangen-Nuremberg, Erlangen, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="research-article"></genre><originInfo><publisher>BMJ Publishing Group Ltd and European League Against Rheumatism</publisher><dateIssued encoding="w3cdtf">2010-06</dateIssued><dateCreated encoding="w3cdtf">2009-11-23</dateCreated><copyrightDate encoding="w3cdtf">2010</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><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. Discussion 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.</abstract><note type="footnotes">GRH and EA contributed equally.</note><relatedItem type="host"><titleInfo><title>Annals of the Rheumatic Diseases</title></titleInfo><titleInfo type="abbreviated"><title>Ann Rheum Dis</title></titleInfo><genre type="journal">journal</genre><identifier type="ISSN">0003-4967</identifier><identifier type="eISSN">1468-2060</identifier><identifier type="PublisherID">ard</identifier><identifier type="PublisherID-hwp">annrheumdis</identifier><identifier type="PublisherID-nlm-ta">Ann Rheum Dis</identifier><part><date>2010</date><detail type="volume"><caption>vol.</caption><number>69</number></detail><detail type="issue"><caption>no.</caption><number>6</number></detail><extent unit="pages"><start>1214</start></extent></part></relatedItem><identifier type="istex">C182C4ECA47D86A51F936CFE3979BC240A9B4845</identifier><identifier type="DOI">10.1136/ard.2009.120204</identifier><identifier type="href">annrheumdis-69-1214.pdf</identifier><identifier type="ArticleID">annrheumdis120204</identifier><identifier type="PMID">19933745</identifier><identifier type="local">annrheumdis;69/6/1214</identifier><accessCondition type="use and reproduction" contentType="copyright">Published by the BMJ Publishing Group Limited. 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