Composition of plaque‐associated lesions in the gingiva and the peri‐implant mucosa in partially edentulous subjects
Identifieur interne : 007301 ( Istex/Corpus ); précédent : 007300; suivant : 007302Composition of plaque‐associated lesions in the gingiva and the peri‐implant mucosa in partially edentulous subjects
Auteurs : B. Liljenberg ; F. Gualini ; T. Berglundh ; M. Tonetti ; J. LindheSource :
- Journal of Clinical Periodontology [ 0303-6979 ] ; 1997-02.
English descriptors
- KwdEn :
- Adjacent periimplant mucosa, Biopsy, Cell markers, Cellules positives, Clinical periodontology, Connective, Connective tissue, Corresponding lesion, Crevicular fluid, Current study, Discrete infiltrates, Edentulous, Edentulous patients, Edentulous regions, Edentulous subjects, Epithelium, Gingiva, Gingival, Gingival tissue, Healthy gingiva, Heavy points, Image system, Implant, Implant site, Inflammatory, Inflammatory cell, Inflammatory cells, Interproximal surface, Junctional, Junctional epithelium, Larger numbers, Larger proportions, Leitz microscope, Lesion, Light points, Liljenberg, Liquid nitrogen, Lymphocyte, Monoclonal antibodies, Morphometric analyses, Morphometric measurements, Mucosa, Mucosa interface, Normal gingiva, Oral environment, Osseointegrated implants, Periimplant, Periimplant mucosa, Periodontal disease, Periodontal research, Plasma cells, Polymorphonuclear leukocytes, Positive cells, Present investigation, Quantitative changes, Restorative therapy, Similar volume, Site implantaire, Soft tissue, Soft tissue biopsy, Standard deviations, Tonetti, Tooth site, Various cells.
- Teeft :
- Adjacent periimplant mucosa, Biopsy, Cell markers, Cellules positives, Clinical periodontology, Connective, Connective tissue, Corresponding lesion, Crevicular fluid, Current study, Discrete infiltrates, Edentulous, Edentulous patients, Edentulous regions, Edentulous subjects, Epithelium, Gingiva, Gingival, Gingival tissue, Healthy gingiva, Heavy points, Image system, Implant, Implant site, Inflammatory, Inflammatory cell, Inflammatory cells, Interproximal surface, Junctional, Junctional epithelium, Larger numbers, Larger proportions, Leitz microscope, Lesion, Light points, Liljenberg, Liquid nitrogen, Lymphocyte, Monoclonal antibodies, Morphometric analyses, Morphometric measurements, Mucosa, Mucosa interface, Normal gingiva, Oral environment, Osseointegrated implants, Periimplant, Periimplant mucosa, Periodontal disease, Periodontal research, Plasma cells, Polymorphonuclear leukocytes, Positive cells, Present investigation, Quantitative changes, Restorative therapy, Similar volume, Site implantaire, Soft tissue, Soft tissue biopsy, Standard deviations, Tonetti, Tooth site, Various cells.
Abstract
Abstract The purpose of the present investigation was to study characteristics of the plaque associated lesions in the gingiva and the adjacent periimplant mucosa sampled from the same subjects. 20 partially edentulous patients (12 female and 8 male. 30–60 years of age) volunteered to participate in the study. They had all been treated for moderate to advanced periodontal disease. Edentulous regions had been restored with implants. The restorative therapy had been completed 6–24 months prior to soft tissue biopsy. Samples of gingival tissue (GM) and periimplant mucosa (PIM) from an “interproximal surface” of one tooth site and one implant site of the same jaw were harvested. One portion of the biopsy was embedded in EPON®. stained in PAS and toluidine blue and used for histometric and morphometric analyses. The 2nd portion of the biopsy was snap frozen in liquid nitrogen. 15 sections, about 5 μm thick, were prepared in a cryostat and used for immune histochemical staining. The analysis of the sections included determination of the size of the lesions as well as assessments of various cells and cell markers. In all samples of both PIM and GM discrete infiltrates of inflammatory cells (ICT) were found in the connective tissue lateral to the junctional epithelium. The ICT of PIM occupied on the average 0.17±0.14 mm2 of the soft tissue, while the corresponding lesion in GM occupied an area that was 0.25 mn2±0.21 mm2 large. The density of CD19 positive cells was 7 times higher in GM than in PIM (3.7 versus 0.5) while the densities of CD3 positive cells were 7.5 (GM) and 4.7 (PM> respectively. The density of PMN elastase positive cells was about 3 times higher in GM than in PIM (3.7 versus 1.2). Care must be exercised when these differences are interpreted. It is possible that a prolonged exposure of the implant site to the oral environment may induce both qualitative and quantitative changes of the infiltrate in PIM.
Url:
DOI: 10.1111/j.1600-051X.1997.tb00477.x
Links to Exploration step
ISTEX:E7ABEB667EEF0F98A99E194838522F21D9BA7EA9Le document en format XML
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Gothenburg University, Sweden</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j" type="main">Journal of Clinical Periodontology</title><title level="j" type="alt">JOURNAL OF CLINICAL PERIODONTOLOGY</title><idno type="ISSN">0303-6979</idno><idno type="eISSN">1600-051X</idno><imprint><biblScope unit="vol">24</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="119">119</biblScope><biblScope unit="page" to="123">123</biblScope><biblScope unit="page-count">5</biblScope><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="1997-02">1997-02</date></imprint><idno type="ISSN">0303-6979</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0303-6979</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adjacent periimplant mucosa</term><term>Biopsy</term><term>Cell markers</term><term>Cellules positives</term><term>Clinical periodontology</term><term>Connective</term><term>Connective tissue</term><term>Corresponding lesion</term><term>Crevicular fluid</term><term>Current study</term><term>Discrete infiltrates</term><term>Edentulous</term><term>Edentulous patients</term><term>Edentulous regions</term><term>Edentulous subjects</term><term>Epithelium</term><term>Gingiva</term><term>Gingival</term><term>Gingival tissue</term><term>Healthy gingiva</term><term>Heavy points</term><term>Image system</term><term>Implant</term><term>Implant site</term><term>Inflammatory</term><term>Inflammatory cell</term><term>Inflammatory cells</term><term>Interproximal surface</term><term>Junctional</term><term>Junctional epithelium</term><term>Larger numbers</term><term>Larger proportions</term><term>Leitz microscope</term><term>Lesion</term><term>Light points</term><term>Liljenberg</term><term>Liquid nitrogen</term><term>Lymphocyte</term><term>Monoclonal antibodies</term><term>Morphometric analyses</term><term>Morphometric measurements</term><term>Mucosa</term><term>Mucosa interface</term><term>Normal gingiva</term><term>Oral environment</term><term>Osseointegrated implants</term><term>Periimplant</term><term>Periimplant mucosa</term><term>Periodontal disease</term><term>Periodontal research</term><term>Plasma cells</term><term>Polymorphonuclear leukocytes</term><term>Positive cells</term><term>Present investigation</term><term>Quantitative changes</term><term>Restorative therapy</term><term>Similar volume</term><term>Site implantaire</term><term>Soft tissue</term><term>Soft tissue biopsy</term><term>Standard deviations</term><term>Tonetti</term><term>Tooth site</term><term>Various cells</term></keywords><keywords scheme="Teeft" xml:lang="en"><term>Adjacent periimplant mucosa</term><term>Biopsy</term><term>Cell markers</term><term>Cellules positives</term><term>Clinical periodontology</term><term>Connective</term><term>Connective tissue</term><term>Corresponding lesion</term><term>Crevicular fluid</term><term>Current study</term><term>Discrete infiltrates</term><term>Edentulous</term><term>Edentulous patients</term><term>Edentulous regions</term><term>Edentulous subjects</term><term>Epithelium</term><term>Gingiva</term><term>Gingival</term><term>Gingival tissue</term><term>Healthy gingiva</term><term>Heavy points</term><term>Image system</term><term>Implant</term><term>Implant site</term><term>Inflammatory</term><term>Inflammatory cell</term><term>Inflammatory cells</term><term>Interproximal surface</term><term>Junctional</term><term>Junctional epithelium</term><term>Larger numbers</term><term>Larger proportions</term><term>Leitz microscope</term><term>Lesion</term><term>Light points</term><term>Liljenberg</term><term>Liquid nitrogen</term><term>Lymphocyte</term><term>Monoclonal antibodies</term><term>Morphometric analyses</term><term>Morphometric measurements</term><term>Mucosa</term><term>Mucosa interface</term><term>Normal gingiva</term><term>Oral environment</term><term>Osseointegrated implants</term><term>Periimplant</term><term>Periimplant mucosa</term><term>Periodontal disease</term><term>Periodontal research</term><term>Plasma cells</term><term>Polymorphonuclear leukocytes</term><term>Positive cells</term><term>Present investigation</term><term>Quantitative changes</term><term>Restorative therapy</term><term>Similar volume</term><term>Site implantaire</term><term>Soft tissue</term><term>Soft tissue biopsy</term><term>Standard deviations</term><term>Tonetti</term><term>Tooth site</term><term>Various cells</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract">Abstract The purpose of the present investigation was to study characteristics of the plaque associated lesions in the gingiva and the adjacent periimplant mucosa sampled from the same subjects. 20 partially edentulous patients (12 female and 8 male. 30–60 years of age) volunteered to participate in the study. They had all been treated for moderate to advanced periodontal disease. Edentulous regions had been restored with implants. The restorative therapy had been completed 6–24 months prior to soft tissue biopsy. Samples of gingival tissue (GM) and periimplant mucosa (PIM) from an “interproximal surface” of one tooth site and one implant site of the same jaw were harvested. One portion of the biopsy was embedded in EPON®. stained in PAS and toluidine blue and used for histometric and morphometric analyses. The 2nd portion of the biopsy was snap frozen in liquid nitrogen. 15 sections, about 5 μm thick, were prepared in a cryostat and used for immune histochemical staining. The analysis of the sections included determination of the size of the lesions as well as assessments of various cells and cell markers. In all samples of both PIM and GM discrete infiltrates of inflammatory cells (ICT) were found in the connective tissue lateral to the junctional epithelium. The ICT of PIM occupied on the average 0.17±0.14 mm2 of the soft tissue, while the corresponding lesion in GM occupied an area that was 0.25 mn2±0.21 mm2 large. The density of CD19 positive cells was 7 times higher in GM than in PIM (3.7 versus 0.5) while the densities of CD3 positive cells were 7.5 (GM) and 4.7 (PM> respectively. The density of PMN elastase positive cells was about 3 times higher in GM than in PIM (3.7 versus 1.2). Care must be exercised when these differences are interpreted. It is possible that a prolonged exposure of the implant site to the oral environment may induce both qualitative and quantitative changes of the infiltrate in PIM.</div></front></TEI><istex><corpusName>wiley</corpusName><keywords><teeft><json:string>gingiva</json:string><json:string>positive cells</json:string><json:string>periimplant</json:string><json:string>gingival</json:string><json:string>epithelium</json:string><json:string>liljenberg</json:string><json:string>implant</json:string><json:string>junctional</json:string><json:string>periimplant mucosa</json:string><json:string>connective tissue</json:string><json:string>junctional epithelium</json:string><json:string>lymphocyte</json:string><json:string>tonetti</json:string><json:string>lesion</json:string><json:string>inflammatory</json:string><json:string>healthy gingiva</json:string><json:string>inflammatory cells</json:string><json:string>edentulous</json:string><json:string>clinical periodontology</json:string><json:string>implant site</json:string><json:string>gingival tissue</json:string><json:string>biopsy</json:string><json:string>plasma cells</json:string><json:string>edentulous subjects</json:string><json:string>soft tissue</json:string><json:string>mucosa</json:string><json:string>edentulous patients</json:string><json:string>discrete infiltrates</json:string><json:string>various cells</json:string><json:string>liquid nitrogen</json:string><json:string>morphometric analyses</json:string><json:string>tooth site</json:string><json:string>interproximal surface</json:string><json:string>corresponding lesion</json:string><json:string>soft tissue biopsy</json:string><json:string>oral environment</json:string><json:string>quantitative changes</json:string><json:string>inflammatory cell</json:string><json:string>periodontal disease</json:string><json:string>restorative therapy</json:string><json:string>edentulous regions</json:string><json:string>leitz microscope</json:string><json:string>image system</json:string><json:string>light points</json:string><json:string>cell markers</json:string><json:string>adjacent periimplant mucosa</json:string><json:string>monoclonal antibodies</json:string><json:string>polymorphonuclear leukocytes</json:string><json:string>morphometric measurements</json:string><json:string>heavy points</json:string><json:string>standard deviations</json:string><json:string>larger numbers</json:string><json:string>larger proportions</json:string><json:string>current study</json:string><json:string>present investigation</json:string><json:string>similar volume</json:string><json:string>normal gingiva</json:string><json:string>osseointegrated implants</json:string><json:string>mucosa interface</json:string><json:string>crevicular fluid</json:string><json:string>site implantaire</json:string><json:string>cellules positives</json:string><json:string>periodontal research</json:string><json:string>connective</json:string></teeft></keywords><author><json:item><name>B. Liljenberg</name><affiliations><json:string>Department of Periodontology. Gothenburg University, Sweden</json:string></affiliations></json:item><json:item><name>F. Gualini</name><affiliations><json:string>Department of Periodontology. Gothenburg University, Sweden</json:string></affiliations></json:item><json:item><name>T. Berglundh</name><affiliations><json:string>Department of Periodontology. Gothenburg University, Sweden</json:string><json:string>E-mail: Berglund@odontologi.gu.se</json:string></affiliations></json:item><json:item><name>M. Tonetti</name><affiliations><json:string>Department of Periodontology and Fixed Prostodontics, University of Berne, Switzerland</json:string></affiliations></json:item><json:item><name>J. Lindhe</name><affiliations><json:string>Department of Periodontology. Gothenburg University, Sweden</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>gingiva</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>periimplant mucosa</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>biopsy: immunohistochemistry</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>humans</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>histometry</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>implants: morphometry</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>titanium</value></json:item></subject><articleId><json:string>JCPE119</json:string></articleId><arkIstex>ark:/67375/WNG-5VC73FPG-V</arkIstex><language><json:string>eng</json:string></language><originalGenre><json:string>article</json:string></originalGenre><abstract>Abstract The purpose of the present investigation was to study characteristics of the plaque associated lesions in the gingiva and the adjacent periimplant mucosa sampled from the same subjects. 20 partially edentulous patients (12 female and 8 male. 30–60 years of age) volunteered to participate in the study. They had all been treated for moderate to advanced periodontal disease. Edentulous regions had been restored with implants. The restorative therapy had been completed 6–24 months prior to soft tissue biopsy. Samples of gingival tissue (GM) and periimplant mucosa (PIM) from an “interproximal surface” of one tooth site and one implant site of the same jaw were harvested. One portion of the biopsy was embedded in EPON®. stained in PAS and toluidine blue and used for histometric and morphometric analyses. The 2nd portion of the biopsy was snap frozen in liquid nitrogen. 15 sections, about 5 μm thick, were prepared in a cryostat and used for immune histochemical staining. The analysis of the sections included determination of the size of the lesions as well as assessments of various cells and cell markers. In all samples of both PIM and GM discrete infiltrates of inflammatory cells (ICT) were found in the connective tissue lateral to the junctional epithelium. The ICT of PIM occupied on the average 0.17±0.14 mm2 of the soft tissue, while the corresponding lesion in GM occupied an area that was 0.25 mn2±0.21 mm2 large. The density of CD19 positive cells was 7 times higher in GM than in PIM (3.7 versus 0.5) while the densities of CD3 positive cells were 7.5 (GM) and 4.7 (PM> respectively. The density of PMN elastase positive cells was about 3 times higher in GM than in PIM (3.7 versus 1.2). Care must be exercised when these differences are interpreted. It is possible that a prolonged exposure of the implant site to the oral environment may induce both qualitative and quantitative changes of the infiltrate in PIM.</abstract><qualityIndicators><score>8.366</score><pdfWordCount>3366</pdfWordCount><pdfCharCount>22094</pdfCharCount><pdfVersion>1.4</pdfVersion><pdfPageCount>6</pdfPageCount><pdfPageSize>477 x 664 pts</pdfPageSize><refBibsNative>true</refBibsNative><abstractWordCount>322</abstractWordCount><abstractCharCount>1945</abstractCharCount><keywordCount>7</keywordCount></qualityIndicators><title>Composition of plaque‐associated lesions in the gingiva and the peri‐implant mucosa in partially edentulous subjects</title><pmid><json:string>9062859</json:string></pmid><genre><json:string>article</json:string></genre><host><title>Journal of Clinical Periodontology</title><language><json:string>unknown</json:string></language><doi><json:string>10.1111/(ISSN)1600-051X</json:string></doi><issn><json:string>0303-6979</json:string></issn><eissn><json:string>1600-051X</json:string></eissn><publisherId><json:string>JCPE</json:string></publisherId><volume>24</volume><issue>2</issue><pages><first>119</first><last>123</last><total>5</total></pages><genre><json:string>journal</json:string></genre></host><namedEntities><unitex><date><json:string>1997</json:string></date><geogName></geogName><orgName><json:string>Lindhe Department of Pertodonto</json:string><json:string>Switzerland Liljenberg B, Gualini F, Berglundh T, Tonetti</json:string><json:string>Department of Periodontology</json:string><json:string>University of Beme</json:string><json:string>Sweden and Praktikertjanst AB, Sweden</json:string></orgName><orgName_funder></orgName_funder><orgName_provider></orgName_provider><persName><json:string>Our</json:string><json:string>F.Guaiini</json:string><json:string>M.Tonetti</json:string><json:string>I. Results</json:string></persName><placeName><json:string>Germany</json:string><json:string>Mannheim</json:string><json:string>Sweden</json:string></placeName><ref_url></ref_url><ref_bibl><json:string>Tonetti et al. 11995</json:string><json:string>Adonogianaki et al. (1995)</json:string><json:string>Seymour 1987</json:string><json:string>Liljenberg et al, (1994, 1996)</json:string><json:string>Tonetti et al. (1995)</json:string><json:string>Liljenberg et al. 1996</json:string><json:string>Tonetti et al.</json:string><json:string>Seymour et al. (1989)</json:string><json:string>1968, 1972</json:string><json:string>Okada et al. 1982, 1983</json:string><json:string>Karnowsky 1965</json:string><json:string>Liljenberg et al.</json:string><json:string>Liljenberg et al. 1994</json:string><json:string>Schroeder 1969</json:string><json:string>Hsu et al. 1981</json:string><json:string>Seymour et al. (1979, 1989)</json:string><json:string>Payne et al, (1975)</json:string></ref_bibl><bibl></bibl></unitex></namedEntities><ark><json:string>ark:/67375/WNG-5VC73FPG-V</json:string></ark><categories><wos><json:string>1 - science</json:string><json:string>2 - dentistry, oral surgery & medicine</json:string></wos><scienceMetrix><json:string>1 - health sciences</json:string><json:string>2 - clinical medicine</json:string><json:string>3 - dentistry</json:string></scienceMetrix><scopus><json:string>1 - Health Sciences</json:string><json:string>2 - Dentistry</json:string><json:string>3 - Periodontics</json:string></scopus></categories><publicationDate>1997</publicationDate><copyrightDate>1997</copyrightDate><doi><json:string>10.1111/j.1600-051X.1997.tb00477.x</json:string></doi><id>E7ABEB667EEF0F98A99E194838522F21D9BA7EA9</id><score>1</score><fulltext><json:item><extension>pdf</extension><original>true</original><mimetype>application/pdf</mimetype><uri>https://api.istex.fr/document/E7ABEB667EEF0F98A99E194838522F21D9BA7EA9/fulltext/pdf</uri></json:item><json:item><extension>zip</extension><original>false</original><mimetype>application/zip</mimetype><uri>https://api.istex.fr/document/E7ABEB667EEF0F98A99E194838522F21D9BA7EA9/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/E7ABEB667EEF0F98A99E194838522F21D9BA7EA9/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main">Composition of plaque‐associated lesions in the gingiva and the peri‐implant mucosa in partially edentulous subjects</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="1997-02"></date></publicationStmt><notesStmt><note type="content-type" subtype="article" source="article" scheme="https://content-type.data.istex.fr/ark:/67375/XTP-6N5SZHKN-D">article</note><note type="publication-type" subtype="journal" scheme="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</note></notesStmt><sourceDesc><biblStruct type="article"><analytic><title level="a" type="main">Composition of plaque‐associated lesions in the gingiva and the peri‐implant mucosa in partially edentulous subjects</title><author xml:id="author-0000"><persName><forename type="first">B.</forename><surname>Liljenberg</surname></persName><affiliation>Department of Periodontology. Gothenburg University, Sweden<address><country key="SE"></country></address></affiliation></author><author xml:id="author-0001"><persName><forename type="first">F.</forename><surname>Gualini</surname></persName><affiliation>Department of Periodontology. Gothenburg University, Sweden<address><country key="SE"></country></address></affiliation></author><author xml:id="author-0002" role="corresp"><persName><forename type="first">T.</forename><surname>Berglundh</surname></persName><affiliation>Department of Periodontology. Gothenburg University, Sweden<address><country key="SE"></country></address></affiliation><affiliation>Tord Berglundh, Department of Periodontology, Göteborg University, Medicinaregatan, S‐41390 Göteborg, Sweden, Tel.: +46 31 773 31 90, Fax: +46 31 773 37 91, e‐mail: Berglund@odontologi.gu.se</affiliation></author><author xml:id="author-0003"><persName><forename type="first">M.</forename><surname>Tonetti</surname></persName><affiliation>Department of Periodontology and Fixed Prostodontics, University of Berne, Switzerland<address><country key="CH"></country></address></affiliation></author><author xml:id="author-0004"><persName><forename type="first">J.</forename><surname>Lindhe</surname></persName><affiliation>Department of Periodontology. Gothenburg University, Sweden<address><country key="SE"></country></address></affiliation></author><idno type="istex">E7ABEB667EEF0F98A99E194838522F21D9BA7EA9</idno><idno type="ark">ark:/67375/WNG-5VC73FPG-V</idno><idno type="DOI">10.1111/j.1600-051X.1997.tb00477.x</idno><idno type="unit">JCPE119</idno><idno type="toTypesetVersion">file:JCPE.JCPE119.pdf</idno></analytic><monogr><title level="j" type="main">Journal of Clinical Periodontology</title><title level="j" type="alt">JOURNAL OF CLINICAL PERIODONTOLOGY</title><idno type="pISSN">0303-6979</idno><idno type="eISSN">1600-051X</idno><idno type="book-DOI">10.1111/(ISSN)1600-051X</idno><idno type="book-part-DOI">10.1111/cpe.1997.24.issue-2</idno><idno type="product">JCPE</idno><idno type="publisherDivision">ST</idno><imprint><biblScope unit="vol">24</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="119">119</biblScope><biblScope unit="page" to="123">123</biblScope><biblScope unit="page-count">5</biblScope><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="1997-02"></date></imprint></monogr></biblStruct></sourceDesc></fileDesc><profileDesc><abstract xml:lang="en" style="main"><p><hi rend="bold">Abstract</hi> The purpose of the present investigation was to study characteristics of the plaque associated lesions in the gingiva and the adjacent periimplant mucosa sampled from the same subjects. 20 partially edentulous patients (12 female and 8 male. 30–60 years of age) volunteered to participate in the study. They had all been treated for moderate to advanced periodontal disease. Edentulous regions had been restored with implants. The restorative therapy had been completed 6–24 months prior to soft tissue biopsy. Samples of gingival tissue (GM) and periimplant mucosa (PIM) from an “interproximal surface” of one tooth site and one implant site of the same jaw were harvested. One portion of the biopsy was embedded in EPON®. stained in PAS and toluidine blue and used for histometric and morphometric analyses. The 2nd portion of the biopsy was snap frozen in liquid nitrogen. 15 sections, about 5 μm thick, were prepared in a cryostat and used for immune histochemical staining. The analysis of the sections included determination of the size of the lesions as well as assessments of various cells and cell markers. In all samples of both PIM and GM discrete infiltrates of inflammatory cells (ICT) were found in the connective tissue lateral to the junctional epithelium. The ICT of PIM occupied on the average 0.17±0.14 mm<hi rend="superscript">2</hi> of the soft tissue, while the corresponding lesion in GM occupied an area that was 0.25 mn<hi rend="superscript">2</hi>±0.21 mm<hi rend="superscript">2</hi> large. The density of CD19 positive cells was 7 times higher in GM than in PIM (3.7 versus 0.5) while the densities of CD3 positive cells were 7.5 (GM) and 4.7 (PM> respectively. The density of PMN elastase positive cells was about 3 times higher in GM than in PIM (3.7 versus 1.2). Care must be exercised when these differences are interpreted. It is possible that a prolonged exposure of the implant site to the oral environment may induce both qualitative and quantitative changes of the infiltrate in PIM.</p></abstract><textClass><keywords xml:lang="en"><term xml:id="k1">gingiva</term><term xml:id="k2">periimplant mucosa</term><term xml:id="k3">biopsy: immunohistochemistry</term><term xml:id="k4">humans</term><term xml:id="k5">histometry</term><term xml:id="k6">implants: morphometry</term><term xml:id="k7">titanium</term></keywords><keywords rend="tocHeading1"><term>Original Article</term></keywords></textClass><langUsage><language ident="en"></language></langUsage></profileDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/document/E7ABEB667EEF0F98A99E194838522F21D9BA7EA9/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Blackwell Publishing Ltd</publisherName><publisherLoc>Oxford, UK</publisherLoc></publisherInfo><doi origin="wiley" registered="yes">10.1111/(ISSN)1600-051X</doi><issn type="print">0303-6979</issn><issn type="electronic">1600-051X</issn><idGroup><id type="product" value="JCPE"></id><id type="publisherDivision" value="ST"></id></idGroup><titleGroup><title type="main" sort="JOURNAL OF CLINICAL PERIODONTOLOGY">Journal of Clinical Periodontology</title></titleGroup></publicationMeta><publicationMeta level="part" position="02002"><doi origin="wiley">10.1111/cpe.1997.24.issue-2</doi><numberingGroup><numbering type="journalVolume" number="24">24</numbering><numbering type="journalIssue" number="2">2</numbering></numberingGroup><coverDate startDate="1997-02">February 1997</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="0011900" status="forIssue"><doi origin="wiley">10.1111/j.1600-051X.1997.tb00477.x</doi><idGroup><id type="unit" value="JCPE119"></id></idGroup><countGroup><count type="pageTotal" number="5"></count></countGroup><titleGroup><title type="tocHeading1">Original Article</title></titleGroup><eventGroup><event type="firstOnline" date="2005-12-13"></event><event type="publishedOnlineFinalForm" date="2005-12-13"></event><event type="xmlConverted" agent="Converter:BPG_TO_WML3G version:2.3.2 mode:FullText source:HeaderRef result:HeaderRef" date="2010-03-09"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:4.0.1" date="2014-03-19"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-24"></event></eventGroup><numberingGroup><numbering type="pageFirst" number="119">119</numbering><numbering type="pageLast" number="123">123</numbering></numberingGroup><correspondenceTo>Tord Berglundh, Department of Periodontology, Göteborg University, Medicinaregatan, S‐41390 Göteborg, Sweden, Tel.: +46 31 773 31 90, Fax: +46 31 773 37 91, e‐mail: <email>Berglund@odontologi.gu.se</email></correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:JCPE.JCPE119.pdf"></link></linkGroup></publicationMeta><contentMeta><unparsedEditorialHistory>Accepted for publication 11 April 1996</unparsedEditorialHistory><countGroup><count type="referenceTotal" number="17"></count><count type="linksCrossRef" number="6"></count></countGroup><titleGroup><title type="main">Composition of plaque‐associated lesions in the gingiva and the peri‐implant mucosa in partially edentulous subjects</title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#a1"><personName><givenNames>B.</givenNames><familyName>Liljenberg</familyName></personName></creator><creator creatorRole="author" xml:id="cr2" affiliationRef="#a1"><personName><givenNames>F.</givenNames><familyName>Gualini</familyName></personName></creator><creator creatorRole="author" xml:id="cr3" affiliationRef="#a1" corresponding="yes"><personName><givenNames>T.</givenNames><familyName>Berglundh</familyName></personName></creator><creator creatorRole="author" xml:id="cr4" affiliationRef="#a2"><personName><givenNames>M.</givenNames><familyName>Tonetti</familyName></personName></creator><creator creatorRole="author" xml:id="cr5" affiliationRef="#a1"><personName><givenNames>J.</givenNames><familyName>Lindhe</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="a1" countryCode="SE"><unparsedAffiliation>Department of Periodontology. Gothenburg University, Sweden</unparsedAffiliation></affiliation><affiliation xml:id="a2" countryCode="CH"><unparsedAffiliation>Department of Periodontology and Fixed Prostodontics, University of Berne, Switzerland</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en"><keyword xml:id="k1">gingiva</keyword><keyword xml:id="k2">periimplant mucosa</keyword><keyword xml:id="k3">biopsy: immunohistochemistry</keyword><keyword xml:id="k4">humans</keyword><keyword xml:id="k5">histometry</keyword><keyword xml:id="k6">implants: morphometry</keyword><keyword xml:id="k7">titanium</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><p><b>Abstract</b> The purpose of the present investigation was to study characteristics of the plaque associated lesions in the gingiva and the adjacent periimplant mucosa sampled from the same subjects. 20 partially edentulous patients (12 female and 8 male. 30–60 years of age) volunteered to participate in the study. They had all been treated for moderate to advanced periodontal disease. Edentulous regions had been restored with implants. The restorative therapy had been completed 6–24 months prior to soft tissue biopsy. Samples of gingival tissue (GM) and periimplant mucosa (PIM) from an “interproximal surface” of one tooth site and one implant site of the same jaw were harvested. One portion of the biopsy was embedded in EPON®. stained in PAS and toluidine blue and used for histometric and morphometric analyses. The 2nd portion of the biopsy was snap frozen in liquid nitrogen. 15 sections, about 5 μm thick, were prepared in a cryostat and used for immune histochemical staining. The analysis of the sections included determination of the size of the lesions as well as assessments of various cells and cell markers. In all samples of both PIM and GM discrete infiltrates of inflammatory cells (ICT) were found in the connective tissue lateral to the junctional epithelium. The ICT of PIM occupied on the average 0.17±0.14 mm<sup>2</sup> of the soft tissue, while the corresponding lesion in GM occupied an area that was 0.25 mn<sup>2</sup>±0.21 mm<sup>2</sup> large. The density of CD19 positive cells was 7 times higher in GM than in PIM (3.7 versus 0.5) while the densities of CD3 positive cells were 7.5 (GM) and 4.7 (PM> respectively. The density of PMN elastase positive cells was about 3 times higher in GM than in PIM (3.7 versus 1.2). Care must be exercised when these differences are interpreted. It is possible that a prolonged exposure of the implant site to the oral environment may induce both qualitative and quantitative changes of the infiltrate in PIM.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Composition of plaque‐associated lesions in the gingiva and the peri‐implant mucosa in partially edentulous subjects</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Composition of plaque‐associated lesions in the gingiva and the peri‐implant mucosa in partially edentulous subjects</title></titleInfo><name type="personal"><namePart type="given">B.</namePart><namePart type="family">Liljenberg</namePart><affiliation>Department of Periodontology. Gothenburg University, Sweden</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">F.</namePart><namePart type="family">Gualini</namePart><affiliation>Department of Periodontology. Gothenburg University, Sweden</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">T.</namePart><namePart type="family">Berglundh</namePart><affiliation>Department of Periodontology. Gothenburg University, Sweden</affiliation><affiliation>E-mail: Berglund@odontologi.gu.se</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M.</namePart><namePart type="family">Tonetti</namePart><affiliation>Department of Periodontology and Fixed Prostodontics, University of Berne, Switzerland</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">J.</namePart><namePart type="family">Lindhe</namePart><affiliation>Department of Periodontology. Gothenburg 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>Blackwell Publishing Ltd</publisher><place><placeTerm type="text">Oxford, UK</placeTerm></place><dateIssued encoding="w3cdtf">1997-02</dateIssued><edition>Accepted for publication 11 April 1996</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="references">17</extent><extent unit="linksCrossRef">6</extent></physicalDescription><abstract>Abstract The purpose of the present investigation was to study characteristics of the plaque associated lesions in the gingiva and the adjacent periimplant mucosa sampled from the same subjects. 20 partially edentulous patients (12 female and 8 male. 30–60 years of age) volunteered to participate in the study. They had all been treated for moderate to advanced periodontal disease. Edentulous regions had been restored with implants. The restorative therapy had been completed 6–24 months prior to soft tissue biopsy. Samples of gingival tissue (GM) and periimplant mucosa (PIM) from an “interproximal surface” of one tooth site and one implant site of the same jaw were harvested. One portion of the biopsy was embedded in EPON®. stained in PAS and toluidine blue and used for histometric and morphometric analyses. The 2nd portion of the biopsy was snap frozen in liquid nitrogen. 15 sections, about 5 μm thick, were prepared in a cryostat and used for immune histochemical staining. The analysis of the sections included determination of the size of the lesions as well as assessments of various cells and cell markers. In all samples of both PIM and GM discrete infiltrates of inflammatory cells (ICT) were found in the connective tissue lateral to the junctional epithelium. The ICT of PIM occupied on the average 0.17±0.14 mm2 of the soft tissue, while the corresponding lesion in GM occupied an area that was 0.25 mn2±0.21 mm2 large. The density of CD19 positive cells was 7 times higher in GM than in PIM (3.7 versus 0.5) while the densities of CD3 positive cells were 7.5 (GM) and 4.7 (PM> respectively. The density of PMN elastase positive cells was about 3 times higher in GM than in PIM (3.7 versus 1.2). Care must be exercised when these differences are interpreted. It is possible that a prolonged exposure of the implant site to the oral environment may induce both qualitative and quantitative changes of the infiltrate in PIM.</abstract><subject lang="en"><genre>keywords</genre><topic>gingiva</topic><topic>periimplant mucosa</topic><topic>biopsy: immunohistochemistry</topic><topic>humans</topic><topic>histometry</topic><topic>implants: morphometry</topic><topic>titanium</topic></subject><relatedItem type="host"><titleInfo><title>Journal of Clinical Periodontology</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">0303-6979</identifier><identifier type="eISSN">1600-051X</identifier><identifier type="DOI">10.1111/(ISSN)1600-051X</identifier><identifier type="PublisherID">JCPE</identifier><part><date>1997</date><detail type="volume"><caption>vol.</caption><number>24</number></detail><detail type="issue"><caption>no.</caption><number>2</number></detail><extent unit="pages"><start>119</start><end>123</end><total>5</total></extent></part></relatedItem><identifier type="istex">E7ABEB667EEF0F98A99E194838522F21D9BA7EA9</identifier><identifier type="ark">ark:/67375/WNG-5VC73FPG-V</identifier><identifier type="DOI">10.1111/j.1600-051X.1997.tb00477.x</identifier><identifier type="ArticleID">JCPE119</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>Blackwell Publishing Ltd</recordOrigin></recordInfo></mods><json:item><extension>json</extension><original>false</original><mimetype>application/json</mimetype><uri>https://api.istex.fr/document/E7ABEB667EEF0F98A99E194838522F21D9BA7EA9/metadata/json</uri></json:item></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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