Immunohistochemistry of soft tissues surrounding late failures of Brånemark implants
Identifieur interne : 006F64 ( Istex/Corpus ); précédent : 006F63; suivant : 006F65Immunohistochemistry of soft tissues surrounding late failures of Brånemark implants
Auteurs : Marco Esposito ; Peter Thomsen ; Johan Mölne ; Christiana Gretzer ; Lars E. Ericson ; Ulf LekholmSource :
- Clinical Oral Implants Research [ 0905-7161 ] ; 1997-10.
Abstract
The objective of the present investigation was to characterize the cellular composition of the soft tissues surrounding consecutively retrieved late failures of Brånemark implants. Criteria for implant failure were signs of loss of osseointegration (radiographic peri‐fixtural radiolucency and mobility). The clinical history of the implants did not include adverse symptoms. At the time of retrieval, percussion‐induced pain was experienced at 4/S implants, but no macroscopical signs of inflammation or infection was observed. Immunohistochemistry was applied on 6 marginal peri‐implant specimens and on specimens of deeper tissues associated with the previously load‐bearing implant surface from 8 failed implants, whereas 6 clinically healthy mucosal specimens and 4 hyperplastic biopsies from stable implants served as controls. The immunohistochemical evaluation showed that the soft tissues surrounding failed implants contained a large number of macrophages (CD68), HLA‐DR positive cells, lymphocytes and plasma cells preferentially accumulated towards the removed implant surface. PMNs were a rare finding. Downgrowth of epithelium, in some cases encapsulating the whole fixture, was observed in sections where an intact implant/soft tissue interface was preserved. Healthy control mucosal specimens always contained labelled cells, albeit in a low amount, whereas hyperplastic control samples displayed an intense inflammatory and immunological response with numerous positive cells and PMNs scattered throughout the biopsy. In conclusion, failed implants were characterized by a chronic inflammatory response of the surrounding tissues with macrophages as the predominant labelled cell type, while hyperplastic tissues around stable implants were distinguished by an acute inflammatory process. These findings suggest that an on‐going infection is unlikely to be the etiological factor for the late failures of dental implants examined in this study.
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DOI: 10.1034/j.1600-0501.1997.080502.x
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Ericson</name><affiliation><mods:affiliation>Institute of Anatomy and Cell Biology, Faculty of Medicine and</mods:affiliation></affiliation></author><author><name sortKey="Lekholm, Ulf" sort="Lekholm, Ulf" uniqKey="Lekholm U" first="Ulf" last="Lekholm">Ulf Lekholm</name><affiliation><mods:affiliation>The Brånemark Clinic, Faculty of Odontology, Göteborg University, Sweden</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j" type="main">Clinical Oral Implants Research</title><title level="j" type="alt">CLINICAL ORAL IMPLANTS RESEARCH</title><idno type="ISSN">0905-7161</idno><idno type="eISSN">1600-0501</idno><imprint><biblScope unit="vol">8</biblScope><biblScope unit="issue">5</biblScope><biblScope unit="page" from="352">352</biblScope><biblScope unit="page" to="366">366</biblScope><publisher>Munksgaard International Publishers</publisher><pubPlace>Copenhagen</pubPlace><date type="published" when="1997-10">1997-10</date></imprint><idno type="ISSN">0905-7161</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0905-7161</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The objective of the present investigation was to characterize the cellular composition of the soft tissues surrounding consecutively retrieved late failures of Brånemark implants. Criteria for implant failure were signs of loss of osseointegration (radiographic peri‐fixtural radiolucency and mobility). The clinical history of the implants did not include adverse symptoms. At the time of retrieval, percussion‐induced pain was experienced at 4/S implants, but no macroscopical signs of inflammation or infection was observed. Immunohistochemistry was applied on 6 marginal peri‐implant specimens and on specimens of deeper tissues associated with the previously load‐bearing implant surface from 8 failed implants, whereas 6 clinically healthy mucosal specimens and 4 hyperplastic biopsies from stable implants served as controls. The immunohistochemical evaluation showed that the soft tissues surrounding failed implants contained a large number of macrophages (CD68), HLA‐DR positive cells, lymphocytes and plasma cells preferentially accumulated towards the removed implant surface. PMNs were a rare finding. Downgrowth of epithelium, in some cases encapsulating the whole fixture, was observed in sections where an intact implant/soft tissue interface was preserved. Healthy control mucosal specimens always contained labelled cells, albeit in a low amount, whereas hyperplastic control samples displayed an intense inflammatory and immunological response with numerous positive cells and PMNs scattered throughout the biopsy. In conclusion, failed implants were characterized by a chronic inflammatory response of the surrounding tissues with macrophages as the predominant labelled cell type, while hyperplastic tissues around stable implants were distinguished by an acute inflammatory process. These findings suggest that an on‐going infection is unlikely to be the etiological factor for the late failures of dental implants examined in this study.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Marco Esposito</name><affiliations><json:string>Institute of Anatomy and Cell Biology, Faculty of Medicine and</json:string></affiliations></json:item><json:item><name>Peter Thomsen</name><affiliations><json:string>Institute of Anatomy and Cell Biology, Faculty of Medicine and</json:string></affiliations></json:item><json:item><name>Johan Mölne</name><affiliations><json:string>Institute of Anatomy and Cell Biology, Faculty of Medicine and</json:string></affiliations></json:item><json:item><name>Christiana Gretzer</name><affiliations><json:string>Institute of Anatomy and Cell Biology, Faculty of Medicine and</json:string></affiliations></json:item><json:item><name>Lars E. 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tissues surrounding late failures of Brånemark implants</title><title level="a" type="short">Immunohistochemistry of late osseointegrated implant failures</title><author xml:id="author-0000"><persName><forename type="first">Marco</forename><surname>Esposito</surname></persName><affiliation>Institute of Anatomy and Cell Biology, Faculty of Medicine and</affiliation></author><author xml:id="author-0001"><persName><forename type="first">Peter</forename><surname>Thomsen</surname></persName><affiliation>Institute of Anatomy and Cell Biology, Faculty of Medicine and</affiliation></author><author xml:id="author-0002"><persName><forename type="first">Johan</forename><surname>Mölne</surname></persName><affiliation>Institute of Anatomy and Cell Biology, Faculty of Medicine and</affiliation></author><author xml:id="author-0003"><persName><forename type="first">Christiana</forename><surname>Gretzer</surname></persName><affiliation>Institute of Anatomy and Cell Biology, Faculty of Medicine and</affiliation></author><author xml:id="author-0004"><persName><forename type="first">Lars E.</forename><surname>Ericson</surname></persName><affiliation>Institute of Anatomy and Cell Biology, Faculty of Medicine and</affiliation></author><author xml:id="author-0005"><persName><forename type="first">Ulf</forename><surname>Lekholm</surname></persName><affiliation>The Brånemark Clinic, Faculty of Odontology, Göteborg University, Sweden<address><country key="SE"></country></address></affiliation></author><idno type="istex">E0C1DF1894531E075050A59D6625C2AFE8463694</idno><idno type="ark">ark:/67375/WNG-M2JH2RTC-Q</idno><idno type="DOI">10.1034/j.1600-0501.1997.080502.x</idno><idno type="unit">CLR080502</idno><idno type="supplier"></idno><idno type="toTypesetVersion">file:CLR.CLR080502.pdf</idno></analytic><monogr><title level="j" type="main">Clinical Oral Implants Research</title><title level="j" type="alt">CLINICAL ORAL IMPLANTS RESEARCH</title><idno type="pISSN">0905-7161</idno><idno type="eISSN">1600-0501</idno><idno type="book-DOI">10.1111/(ISSN)1600-0501</idno><idno type="book-part-DOI">10.1111/clr.1997.8.issue-5</idno><idno type="product">CLR</idno><idno type="publisherDivision">ST</idno><imprint><biblScope unit="vol">8</biblScope><biblScope unit="issue">5</biblScope><biblScope unit="page" from="352">352</biblScope><biblScope unit="page" to="366">366</biblScope><publisher>Munksgaard International Publishers</publisher><pubPlace>Copenhagen</pubPlace><date type="published" when="1997-10"></date></imprint></monogr></biblStruct></sourceDesc></fileDesc><profileDesc><abstract xml:lang="en" style="main"><p>The objective of the present investigation was to characterize the cellular composition of the soft tissues surrounding consecutively retrieved late failures of Brånemark implants. Criteria for implant failure were signs of loss of osseointegration (radiographic peri‐fixtural radiolucency and mobility). The clinical history of the implants did not include adverse symptoms. At the time of retrieval, percussion‐induced pain was experienced at 4/S implants, but no macroscopical signs of inflammation or infection was observed. Immunohistochemistry was applied on 6 marginal peri‐implant specimens and on specimens of deeper tissues associated with the previously load‐bearing implant surface from 8 failed implants, whereas 6 clinically healthy mucosal specimens and 4 hyperplastic biopsies from stable implants served as controls. The immunohistochemical evaluation showed that the soft tissues surrounding failed implants contained a large number of macrophages (CD68), HLA‐DR positive cells, lymphocytes and plasma cells preferentially accumulated towards the removed implant surface. PMNs were a rare finding. Downgrowth of epithelium, in some cases encapsulating the whole fixture, was observed in sections where an intact implant/soft tissue interface was preserved. Healthy control mucosal specimens always contained labelled cells, albeit in a low amount, whereas hyperplastic control samples displayed an intense inflammatory and immunological response with numerous positive cells and PMNs scattered throughout the biopsy. In conclusion, failed implants were characterized by a chronic inflammatory response of the surrounding tissues with macrophages as the predominant labelled cell type, while hyperplastic tissues around stable implants were distinguished by an acute inflammatory process. These findings suggest that an on‐going infection is unlikely to be the etiological factor for the late failures of dental implants examined in this study.</p></abstract><textClass><keywords xml:lang="en"><term xml:id="k1">dental implant‐titanium</term><term xml:id="k2">implant failure</term><term xml:id="k3">macrophages</term><term xml:id="k4">immune cells</term><term xml:id="k5">immunohistochemistry</term></keywords><keywords rend="tocHeading1"><term>Original Articles</term></keywords></textClass><langUsage><language ident="en"></language></langUsage></profileDesc><revisionDesc><change>undefined</change><change>[object Object]</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/document/E0C1DF1894531E075050A59D6625C2AFE8463694/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley component 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number="366">366</numbering></numberingGroup><correspondenceTo>Marco Esposito, Institute of Anatomy and Cell Biology, Goteborg University, Medicinaregatan 3, S‐41 3 90 Göteborg, Sweden</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:CLR.CLR080502.pdf"></link></linkGroup></publicationMeta><contentMeta><unparsedEditorialHistory>Accepted for publication 6 February 1997</unparsedEditorialHistory><countGroup><count type="linksPubMed" number="0"></count><count type="linksCrossRef" number="0"></count></countGroup><titleGroup><title type="main">Immunohistochemistry of soft tissues surrounding late failures of Brånemark implants</title><title type="shortAuthors">Esposito et al.</title><title type="short">Immunohistochemistry of late osseointegrated implant failures</title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#a1"><personName><givenNames>Marco</givenNames><familyName>Esposito</familyName></personName></creator><creator 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countryCode="SE"><unparsedAffiliation>The Brånemark Clinic, Faculty of Odontology, Göteborg University, Sweden</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en"><keyword xml:id="k1">dental implant‐titanium</keyword><keyword xml:id="k2">implant failure</keyword><keyword xml:id="k3">macrophages</keyword><keyword xml:id="k4">immune cells</keyword><keyword xml:id="k5">immunohistochemistry</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><p>The objective of the present investigation was to characterize the cellular composition of the soft tissues surrounding consecutively retrieved late failures of Brånemark implants. Criteria for implant failure were signs of loss of osseointegration (radiographic peri‐fixtural radiolucency and mobility). The clinical history of the implants did not include adverse symptoms. At the time of retrieval, percussion‐induced pain was experienced at 4/S implants, but no macroscopical signs of inflammation or infection was observed. Immunohistochemistry was applied on 6 marginal peri‐implant specimens and on specimens of deeper tissues associated with the previously load‐bearing implant surface from 8 failed implants, whereas 6 clinically healthy mucosal specimens and 4 hyperplastic biopsies from stable implants served as controls. The immunohistochemical evaluation showed that the soft tissues surrounding failed implants contained a large number of macrophages (CD68), HLA‐DR positive cells, lymphocytes and plasma cells preferentially accumulated towards the removed implant surface. PMNs were a rare finding. Downgrowth of epithelium, in some cases encapsulating the whole fixture, was observed in sections where an intact implant/soft tissue interface was preserved. Healthy control mucosal specimens always contained labelled cells, albeit in a low amount, whereas hyperplastic control samples displayed an intense inflammatory and immunological response with numerous positive cells and PMNs scattered throughout the biopsy. In conclusion, failed implants were characterized by a chronic inflammatory response of the surrounding tissues with macrophages as the predominant labelled cell type, while hyperplastic tissues around stable implants were distinguished by an acute inflammatory process. These findings suggest that an on‐going infection is unlikely to be the etiological factor for the late failures of dental implants examined in this study.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Immunohistochemistry of soft tissues surrounding late failures of Brånemark implants</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Immunohistochemistry of late osseointegrated implant failures</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Immunohistochemistry of soft tissues surrounding late failures of Brånemark implants</title></titleInfo><name type="personal"><namePart type="given">Marco</namePart><namePart type="family">Esposito</namePart><affiliation>Institute of Anatomy and Cell Biology, Faculty of Medicine and</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Peter</namePart><namePart type="family">Thomsen</namePart><affiliation>Institute of Anatomy and Cell Biology, Faculty of Medicine and</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Johan</namePart><namePart type="family">Mölne</namePart><affiliation>Institute of Anatomy and Cell Biology, Faculty of Medicine and</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Christiana</namePart><namePart type="family">Gretzer</namePart><affiliation>Institute of Anatomy and Cell Biology, Faculty of Medicine and</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Lars E.</namePart><namePart type="family">Ericson</namePart><affiliation>Institute of Anatomy and Cell Biology, Faculty of Medicine and</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Ulf</namePart><namePart type="family">Lekholm</namePart><affiliation>The Brånemark Clinic, Faculty of Odontology, Göteborg University, Sweden</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-6N5SZHKN-D">article</genre><originInfo><publisher>Munksgaard International Publishers</publisher><place><placeTerm type="text">Copenhagen</placeTerm></place><dateIssued encoding="w3cdtf">1997-10</dateIssued><edition>Accepted for publication 6 February 1997</edition><copyrightDate encoding="w3cdtf">1997</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><extent unit="linksCrossRef">0</extent></physicalDescription><abstract lang="en">The objective of the present investigation was to characterize the cellular composition of the soft tissues surrounding consecutively retrieved late failures of Brånemark implants. Criteria for implant failure were signs of loss of osseointegration (radiographic peri‐fixtural radiolucency and mobility). The clinical history of the implants did not include adverse symptoms. At the time of retrieval, percussion‐induced pain was experienced at 4/S implants, but no macroscopical signs of inflammation or infection was observed. Immunohistochemistry was applied on 6 marginal peri‐implant specimens and on specimens of deeper tissues associated with the previously load‐bearing implant surface from 8 failed implants, whereas 6 clinically healthy mucosal specimens and 4 hyperplastic biopsies from stable implants served as controls. The immunohistochemical evaluation showed that the soft tissues surrounding failed implants contained a large number of macrophages (CD68), HLA‐DR positive cells, lymphocytes and plasma cells preferentially accumulated towards the removed implant surface. PMNs were a rare finding. Downgrowth of epithelium, in some cases encapsulating the whole fixture, was observed in sections where an intact implant/soft tissue interface was preserved. Healthy control mucosal specimens always contained labelled cells, albeit in a low amount, whereas hyperplastic control samples displayed an intense inflammatory and immunological response with numerous positive cells and PMNs scattered throughout the biopsy. In conclusion, failed implants were characterized by a chronic inflammatory response of the surrounding tissues with macrophages as the predominant labelled cell type, while hyperplastic tissues around stable implants were distinguished by an acute inflammatory process. These findings suggest that an on‐going infection is unlikely to be the etiological factor for the late failures of dental implants examined in this study.</abstract><subject lang="en"><genre>keywords</genre><topic>dental implant‐titanium</topic><topic>implant failure</topic><topic>macrophages</topic><topic>immune cells</topic><topic>immunohistochemistry</topic></subject><relatedItem type="host"><titleInfo><title>Clinical Oral Implants Research</title></titleInfo><genre type="journal" authority="ISTEX" authorityURI="https://publication-type.data.istex.fr" valueURI="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</genre><identifier type="ISSN">0905-7161</identifier><identifier type="eISSN">1600-0501</identifier><identifier type="DOI">10.1111/(ISSN)1600-0501</identifier><identifier type="PublisherID">CLR</identifier><part><date>1997</date><detail type="volume"><caption>vol.</caption><number>8</number></detail><detail type="issue"><caption>no.</caption><number>5</number></detail><extent unit="pages"><start>352</start><end>366</end></extent></part></relatedItem><identifier type="istex">E0C1DF1894531E075050A59D6625C2AFE8463694</identifier><identifier type="ark">ark:/67375/WNG-M2JH2RTC-Q</identifier><identifier type="DOI">10.1034/j.1600-0501.1997.080502.x</identifier><identifier type="ArticleID">CLR080502</identifier><recordInfo><recordContentSource authority="ISTEX" authorityURI="https://loaded-corpus.data.istex.fr" valueURI="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-L0C46X92-X">wiley</recordContentSource><recordOrigin>Munksgaard International Publishers</recordOrigin></recordInfo></mods><json:item><extension>json</extension><original>false</original><mimetype>application/json</mimetype><uri>https://api.istex.fr/document/E0C1DF1894531E075050A59D6625C2AFE8463694/metadata/json</uri></json:item></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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