Periodontitis lesions are the main source of salivary cytomegalovirus
Identifieur interne : 004218 ( Istex/Corpus ); précédent : 004217; suivant : 004219Periodontitis lesions are the main source of salivary cytomegalovirus
Auteurs : S. Ahin ; I. Saygun ; A. Kubar ; J. SlotsSource :
- Oral Microbiology and Immunology [ 0902-0055 ] ; 2009-08.
English descriptors
- KwdEn :
- Ages years, Clin, Clin microbiol, Clin virol, Copy counts, Cytomegalovirus, Ebvpositive subjects, Edentulous, Edentulous patients, Edentulous subjects, Gingival, Gingival index, Gingivitis, Gingivitis patients, Hcmv, Hcmvpositive, Hcmvpositive subjects, Healthy individuals, Herpesvirus, Herpesviruses, Human cytomegalovirus, Human herpesvirus, Human periodontitis, Immunol, Kubar, Lesion, Main source, Microbiol, Natural teeth, Oral herpesviruses, Oral microbiol immunol, Periodontal, Periodontal disease, Periodontal diseases, Periodontal examination, Periodontal pocket depth, Periodontal therapy, Periodontal treatment, Periodontitis, Periodontitis lesions, Periodontitis patients, Periodontol, Renal allograft, Saliva, Salivary, Salivary cytomegalovirus, Salivary hcmv, Salivary herpesviruses, Salivary load, Saygun, Southern california, Undetectable levels, Valacyclovir, Virol, Virological sampling, Whole saliva.
- Teeft :
- Ages years, Clin, Clin microbiol, Clin virol, Copy counts, Cytomegalovirus, Ebvpositive subjects, Edentulous, Edentulous patients, Edentulous subjects, Gingival, Gingival index, Gingivitis, Gingivitis patients, Hcmv, Hcmvpositive, Hcmvpositive subjects, Healthy individuals, Herpesvirus, Herpesviruses, Human cytomegalovirus, Human herpesvirus, Human periodontitis, Immunol, Kubar, Lesion, Main source, Microbiol, Natural teeth, Oral herpesviruses, Oral microbiol immunol, Periodontal, Periodontal disease, Periodontal diseases, Periodontal examination, Periodontal pocket depth, Periodontal therapy, Periodontal treatment, Periodontitis, Periodontitis lesions, Periodontitis patients, Periodontol, Renal allograft, Saliva, Salivary, Salivary cytomegalovirus, Salivary hcmv, Salivary herpesviruses, Salivary load, Saygun, Southern california, Undetectable levels, Valacyclovir, Virol, Virological sampling, Whole saliva.
Abstract
Background: Herpesviruses play causal or cooperative roles in childhood infections, tumorigenesis, ulcerogenesis, and periodontitis. Saliva is a common vehicle of herpesvirus horizontal transmission, but the source of salivary herpesviruses remains obscure. To evaluate the significance of periodontal disease in shedding of oral herpesviruses, this study determined the genome‐copy counts of human cytomegalovirus (HCMV) and Epstein–Barr virus (EBV) in whole saliva of subjects with periodontitis, gingivitis, or no natural teeth.
Url:
DOI: 10.1111/j.1399-302X.2009.00528.x
Links to Exploration step
ISTEX:8535373C14E8EDE86F281FC3E0B6ABE9F8CBA9E7Le document en format XML
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Saliva is a common vehicle of herpesvirus horizontal transmission, but the source of salivary herpesviruses remains obscure. To evaluate the significance of periodontal disease in shedding of oral herpesviruses, this study determined the genome‐copy counts of human cytomegalovirus (HCMV) and Epstein–Barr virus (EBV) in whole saliva of subjects with periodontitis, gingivitis, or no natural teeth.</div></front></TEI><istex><corpusName>wiley</corpusName><keywords><teeft><json:string>periodontitis</json:string><json:string>hcmv</json:string><json:string>periodontal</json:string><json:string>herpesviruses</json:string><json:string>salivary</json:string><json:string>gingivitis</json:string><json:string>cytomegalovirus</json:string><json:string>herpesvirus</json:string><json:string>virol</json:string><json:string>microbiol</json:string><json:string>periodontitis patients</json:string><json:string>valacyclovir</json:string><json:string>gingival</json:string><json:string>periodontitis lesions</json:string><json:string>salivary hcmv</json:string><json:string>clin</json:string><json:string>immunol</json:string><json:string>oral microbiol immunol</json:string><json:string>kubar</json:string><json:string>hcmvpositive</json:string><json:string>periodontol</json:string><json:string>copy counts</json:string><json:string>human herpesvirus</json:string><json:string>periodontal disease</json:string><json:string>saygun</json:string><json:string>salivary cytomegalovirus</json:string><json:string>edentulous subjects</json:string><json:string>human cytomegalovirus</json:string><json:string>hcmvpositive subjects</json:string><json:string>ebvpositive subjects</json:string><json:string>periodontal therapy</json:string><json:string>whole saliva</json:string><json:string>healthy individuals</json:string><json:string>saliva</json:string><json:string>edentulous</json:string><json:string>lesion</json:string><json:string>ages years</json:string><json:string>periodontal pocket depth</json:string><json:string>gingivitis patients</json:string><json:string>periodontal examination</json:string><json:string>gingival index</json:string><json:string>virological sampling</json:string><json:string>edentulous patients</json:string><json:string>periodontal treatment</json:string><json:string>periodontal diseases</json:string><json:string>salivary herpesviruses</json:string><json:string>undetectable levels</json:string><json:string>southern california</json:string><json:string>main source</json:string><json:string>natural teeth</json:string><json:string>human periodontitis</json:string><json:string>clin virol</json:string><json:string>oral herpesviruses</json:string><json:string>renal allograft</json:string><json:string>clin microbiol</json:string><json:string>salivary load</json:string></teeft></keywords><author><json:item><name>S. Şahin</name><affiliations><json:string>Department of Periodontology</json:string></affiliations></json:item><json:item><name>I. Saygun</name><affiliations><json:string>Department of Periodontology</json:string></affiliations></json:item><json:item><name>A. Kubar</name><affiliations><json:string>Department of Virology, Gülhane Military Medical Academy, Ankara, Turkey</json:string></affiliations></json:item><json:item><name>J. Slots</name><affiliations><json:string>School of Dentistry, University of Southern California, Los Angeles, CA, USA</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>cytomegalovirus</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Epstein–Barr virus</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>periodontal disease</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>saliva</value></json:item></subject><articleId><json:string>OMI528</json:string></articleId><arkIstex>ark:/67375/WNG-3N70VPQN-D</arkIstex><language><json:string>eng</json:string></language><originalGenre><json:string>article</json:string></originalGenre><abstract>Background: Herpesviruses play causal or cooperative roles in childhood infections, tumorigenesis, ulcerogenesis, and periodontitis. Saliva is a common vehicle of herpesvirus horizontal transmission, but the source of salivary herpesviruses remains obscure. To evaluate the significance of periodontal disease in shedding of oral herpesviruses, this study determined the genome‐copy counts of human cytomegalovirus (HCMV) and Epstein–Barr virus (EBV) in whole saliva of subjects with periodontitis, gingivitis, or no natural teeth.</abstract><qualityIndicators><score>5.066</score><pdfWordCount>2238</pdfWordCount><pdfCharCount>14874</pdfCharCount><pdfVersion>1.3</pdfVersion><pdfPageCount>3</pdfPageCount><pdfPageSize>595.276 x 782.362 pts</pdfPageSize><refBibsNative>true</refBibsNative><abstractWordCount>69</abstractWordCount><abstractCharCount>532</abstractCharCount><keywordCount>4</keywordCount></qualityIndicators><title>Periodontitis lesions are the main source of salivary cytomegalovirus</title><pmid><json:string>19572898</json:string></pmid><genre><json:string>article</json:string></genre><host><title>Oral Microbiology and Immunology</title><language><json:string>unknown</json:string></language><doi><json:string>10.1111/(ISSN)1399-302X</json:string></doi><issn><json:string>0902-0055</json:string></issn><eissn><json:string>1399-302X</json:string></eissn><publisherId><json:string>OMI</json:string></publisherId><volume>24</volume><issue>4</issue><pages><first>340</first><last>342</last><total>3</total></pages><genre><json:string>journal</json:string></genre></host><namedEntities><unitex><date><json:string>2009</json:string></date><geogName></geogName><orgName><json:string>University of Southern California, Los Angeles</json:string><json:string>University of Southern California</json:string><json:string>SPSS Inc, Chicago</json:string></orgName><orgName_funder></orgName_funder><orgName_provider></orgName_provider><persName><json:string>S. Sahin</json:string><json:string>John Wiley</json:string><json:string>To</json:string><json:string>A. Kubar</json:string><json:string>I. Saygun</json:string><json:string>J. Slots</json:string><json:string>S. Background</json:string></persName><placeName><json:string>Ankara</json:string><json:string>Brazil</json:string><json:string>Turkey</json:string><json:string>Los Angeles</json:string><json:string>CA</json:string></placeName><ref_url></ref_url><ref_bibl><json:string>Sahin et al.</json:string><json:string>Sunde et al.</json:string></ref_bibl><bibl></bibl></unitex></namedEntities><ark><json:string>ark:/67375/WNG-3N70VPQN-D</json:string></ark><categories><wos></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 - Medicine</json:string><json:string>3 - Microbiology (medical)</json:string><json:string>1 - Health Sciences</json:string><json:string>2 - Dentistry</json:string><json:string>3 - General Dentistry</json:string><json:string>1 - Life Sciences</json:string><json:string>2 - Immunology and Microbiology</json:string><json:string>3 - Immunology</json:string><json:string>1 - Life Sciences</json:string><json:string>2 - Immunology and Microbiology</json:string><json:string>3 - Microbiology</json:string></scopus></categories><publicationDate>2009</publicationDate><copyrightDate>2009</copyrightDate><doi><json:string>10.1111/j.1399-302X.2009.00528.x</json:string></doi><id>8535373C14E8EDE86F281FC3E0B6ABE9F8CBA9E7</id><score>1</score><fulltext><json:item><extension>pdf</extension><original>true</original><mimetype>application/pdf</mimetype><uri>https://api.istex.fr/document/8535373C14E8EDE86F281FC3E0B6ABE9F8CBA9E7/fulltext/pdf</uri></json:item><json:item><extension>zip</extension><original>false</original><mimetype>application/zip</mimetype><uri>https://api.istex.fr/document/8535373C14E8EDE86F281FC3E0B6ABE9F8CBA9E7/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/8535373C14E8EDE86F281FC3E0B6ABE9F8CBA9E7/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main">Periodontitis lesions are the main source of salivary cytomegalovirus</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><availability><licence>© 2009 John Wiley & Sons A/S</licence></availability><date type="published" when="2009-08"></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">Periodontitis lesions are the main source of salivary cytomegalovirus</title><title level="a" type="short">Source of salivary cytomegalovirus</title><author xml:id="author-0000"><persName><forename type="first">S.</forename><surname>Şahin</surname></persName><affiliation>Department of Periodontology</affiliation></author><author xml:id="author-0001"><persName><forename type="first">I.</forename><surname>Saygun</surname></persName><affiliation>Department of Periodontology</affiliation></author><author xml:id="author-0002"><persName><forename type="first">A.</forename><surname>Kubar</surname></persName><affiliation>Department of Virology, Gülhane Military Medical Academy, Ankara, Turkey<address><country key="TR"></country></address></affiliation></author><author xml:id="author-0003"><persName><forename type="first">J.</forename><surname>Slots</surname></persName><affiliation>School of Dentistry, University of Southern California, Los Angeles, CA, USA<address><country key="US"></country></address></affiliation></author><idno type="istex">8535373C14E8EDE86F281FC3E0B6ABE9F8CBA9E7</idno><idno type="ark">ark:/67375/WNG-3N70VPQN-D</idno><idno type="DOI">10.1111/j.1399-302X.2009.00528.x</idno><idno type="unit">OMI528</idno><idno type="toTypesetVersion">file:OMI.OMI528.pdf</idno></analytic><monogr><title level="j" type="main">Oral Microbiology and Immunology</title><title level="j" type="alt">ORAL MICROBIOLOGY IMMUNOLOGY</title><idno type="pISSN">0902-0055</idno><idno type="eISSN">1399-302X</idno><idno type="book-DOI">10.1111/(ISSN)1399-302X</idno><idno type="book-part-DOI">10.1111/omi.2009.24.issue-4</idno><idno type="product">OMI</idno><idno type="publisherDivision">ST</idno><imprint><biblScope unit="vol">24</biblScope><biblScope unit="issue">4</biblScope><biblScope unit="page" from="340">340</biblScope><biblScope unit="page" to="342">342</biblScope><biblScope unit="page-count">3</biblScope><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="2009-08"></date></imprint></monogr></biblStruct></sourceDesc></fileDesc><profileDesc><abstract xml:lang="en" style="main"><p><hi rend="bold">Background: </hi> Herpesviruses play causal or cooperative roles in childhood infections, tumorigenesis, ulcerogenesis, and periodontitis. Saliva is a common vehicle of herpesvirus horizontal transmission, but the source of salivary herpesviruses remains obscure. To evaluate the significance of periodontal disease in shedding of oral herpesviruses, this study determined the genome‐copy counts of human cytomegalovirus (HCMV) and Epstein–Barr virus (EBV) in whole saliva of subjects with periodontitis, gingivitis, or no natural teeth.</p><p><hi rend="bold">Methods: </hi> Whole saliva was collected from 14 periodontitis patients, 15 gingivitis patients and 13 complete denture wearers. The study subjects were systemically healthy and had not received periodontal treatment in the past 3 months. Real‐time TaqMan polymerase chain reaction was used to determine the salivary load of HCMV and EBV.</p><p><hi rend="bold">Results: </hi> Salivary HCMV was detected in seven (50%) periodontitis patients, but not in any gingivitis or edentulous subjects (<hi rend="italic">P </hi>< 0.001). Salivary EBV was detected in 11 (79%) periodontitis patients, in five (33%) gingivitis patients, and in seven (54%) edentulous subjects (<hi rend="italic">P </hi>= 0.076). Salivary samples showed copy counts of HCMV in the range of 3.3 × 10<hi rend="superscript">3</hi>–4.2 × 10<hi rend="superscript">4</hi>/ml and of EBV in the range of 3.6 × 10<hi rend="superscript">2</hi>–1.6 × 10<hi rend="superscript">9</hi>/ml.</p><p><hi rend="bold">Conclusions: </hi> HCMV and EBV are commonly present in the saliva of periodontitis patients. Periodontitis lesions of systemically healthy subjects seem to constitute the main origin of salivary HCMV, but do not comprise the sole source of salivary EBV.</p></abstract><textClass><keywords xml:lang="en"><term xml:id="k1">cytomegalovirus</term><term xml:id="k2">Epstein–Barr virus</term><term xml:id="k3">periodontal disease</term><term xml:id="k4">saliva</term></keywords><keywords rend="tocHeading1"><term>Original articles</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/8535373C14E8EDE86F281FC3E0B6ABE9F8CBA9E7/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)1399-302X</doi><issn type="print">0902-0055</issn><issn type="electronic">1399-302X</issn><idGroup><id type="product" value="OMI"></id><id type="publisherDivision" value="ST"></id></idGroup><titleGroup><title type="main" sort="ORAL MICROBIOLOGY IMMUNOLOGY">Oral Microbiology and Immunology</title></titleGroup></publicationMeta><publicationMeta level="part" position="08004"><doi origin="wiley">10.1111/omi.2009.24.issue-4</doi><numberingGroup><numbering type="journalVolume" number="24">24</numbering><numbering type="journalIssue" number="4">4</numbering></numberingGroup><coverDate startDate="2009-08">August 2009</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="13" status="forIssue"><doi origin="wiley">10.1111/j.1399-302X.2009.00528.x</doi><idGroup><id type="unit" value="OMI528"></id></idGroup><countGroup><count type="pageTotal" number="3"></count></countGroup><titleGroup><title type="tocHeading1">Original articles</title></titleGroup><copyright>© 2009 John Wiley & Sons A/S</copyright><eventGroup><event type="firstOnline" date="2009-06-15"></event><event type="publishedOnlineFinalForm" date="2009-06-15"></event><event type="xmlConverted" agent="Converter:BPG_TO_WML3G version:2.3.2 mode:FullText source:FullText result:FullText" date="2010-03-10"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-02-06"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-11-03"></event></eventGroup><numberingGroup><numbering type="pageFirst" number="340">340</numbering><numbering type="pageLast" number="342">342</numbering></numberingGroup><correspondenceTo>Jørgen Slots, School of Dentistry, University of Southern California, MC‐0641, Los Angeles, CA 90089‐0641, USA
E‐mail: <email>jslots@usc.edu</email></correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:OMI.OMI528.pdf"></link></linkGroup></publicationMeta><contentMeta><unparsedEditorialHistory>Accepted for publication March 19, 2009</unparsedEditorialHistory><countGroup><count type="figureTotal" number="0"></count><count type="tableTotal" number="1"></count></countGroup><titleGroup><title type="main">Periodontitis lesions are the main source of salivary cytomegalovirus</title><title type="shortAuthors"><i>Şahin et al</i>.</title><title type="short"><i>Source of salivary cytomegalovirus</i></title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#a1"><personName><givenNames>S.</givenNames><familyName>Şahin</familyName></personName></creator><creator creatorRole="author" xml:id="cr2" affiliationRef="#a1"><personName><givenNames>I.</givenNames><familyName>Saygun</familyName></personName></creator><creator creatorRole="author" xml:id="cr3" affiliationRef="#a2"><personName><givenNames>A.</givenNames><familyName>Kubar</familyName></personName></creator><creator creatorRole="author" xml:id="cr4" affiliationRef="#a3"><personName><givenNames>J.</givenNames><familyName>Slots</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="a1"><unparsedAffiliation>Department of Periodontology</unparsedAffiliation></affiliation><affiliation xml:id="a2" countryCode="TR"><unparsedAffiliation>Department of Virology, Gülhane Military Medical Academy, Ankara, Turkey</unparsedAffiliation></affiliation><affiliation xml:id="a3" countryCode="US"><unparsedAffiliation>School of Dentistry, University of Southern California, Los Angeles, CA, USA</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en"><keyword xml:id="k1">cytomegalovirus</keyword><keyword xml:id="k2">Epstein–Barr virus</keyword><keyword xml:id="k3">periodontal disease</keyword><keyword xml:id="k4">saliva</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><!--
Şahin S, Saygun I, Kubar A, Slots J. Periodontitis lesions are the main source of salivary cytomegalovirus.
Oral Microbiol Immunol 2009: 24: 340–342. © 2009 John Wiley & Sons A/S.
--><p><b>Background: </b> Herpesviruses play causal or cooperative roles in childhood infections, tumorigenesis, ulcerogenesis, and periodontitis. Saliva is a common vehicle of herpesvirus horizontal transmission, but the source of salivary herpesviruses remains obscure. To evaluate the significance of periodontal disease in shedding of oral herpesviruses, this study determined the genome‐copy counts of human cytomegalovirus (HCMV) and Epstein–Barr virus (EBV) in whole saliva of subjects with periodontitis, gingivitis, or no natural teeth.</p><p><b>Methods: </b> Whole saliva was collected from 14 periodontitis patients, 15 gingivitis patients and 13 complete denture wearers. The study subjects were systemically healthy and had not received periodontal treatment in the past 3 months. Real‐time TaqMan polymerase chain reaction was used to determine the salivary load of HCMV and EBV.</p><p><b>Results: </b> Salivary HCMV was detected in seven (50%) periodontitis patients, but not in any gingivitis or edentulous subjects (<i>P </i>< 0.001). Salivary EBV was detected in 11 (79%) periodontitis patients, in five (33%) gingivitis patients, and in seven (54%) edentulous subjects (<i>P </i>= 0.076). Salivary samples showed copy counts of HCMV in the range of 3.3 × 10<sup>3</sup>–4.2 × 10<sup>4</sup>/ml and of EBV in the range of 3.6 × 10<sup>2</sup>–1.6 × 10<sup>9</sup>/ml.</p><p><b>Conclusions: </b> HCMV and EBV are commonly present in the saliva of periodontitis patients. Periodontitis lesions of systemically healthy subjects seem to constitute the main origin of salivary HCMV, but do not comprise the sole source of salivary EBV.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Periodontitis lesions are the main source of salivary cytomegalovirus</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Source of salivary cytomegalovirus</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Periodontitis lesions are the main source of salivary cytomegalovirus</title></titleInfo><name type="personal"><namePart type="given">S.</namePart><namePart type="family">Şahin</namePart><affiliation>Department of Periodontology</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">I.</namePart><namePart type="family">Saygun</namePart><affiliation>Department of Periodontology</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">A.</namePart><namePart type="family">Kubar</namePart><affiliation>Department of Virology, Gülhane Military Medical Academy, Ankara, Turkey</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">J.</namePart><namePart type="family">Slots</namePart><affiliation>School of Dentistry, University of Southern California, Los Angeles, CA, USA</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">2009-08</dateIssued><edition>Accepted for publication March 19, 2009</edition><copyrightDate encoding="w3cdtf">2009</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><extent unit="figures">0</extent><extent unit="tables">1</extent></physicalDescription><abstract>Background: Herpesviruses play causal or cooperative roles in childhood infections, tumorigenesis, ulcerogenesis, and periodontitis. Saliva is a common vehicle of herpesvirus horizontal transmission, but the source of salivary herpesviruses remains obscure. To evaluate the significance of periodontal disease in shedding of oral herpesviruses, this study determined the genome‐copy counts of human cytomegalovirus (HCMV) and Epstein–Barr virus (EBV) in whole saliva of subjects with periodontitis, gingivitis, or no natural teeth.</abstract><abstract>Methods: Whole saliva was collected from 14 periodontitis patients, 15 gingivitis patients and 13 complete denture wearers. The study subjects were systemically healthy and had not received periodontal treatment in the past 3 months. Real‐time TaqMan polymerase chain reaction was used to determine the salivary load of HCMV and EBV.</abstract><abstract>Results: Salivary HCMV was detected in seven (50%) periodontitis patients, but not in any gingivitis or edentulous subjects (P < 0.001). Salivary EBV was detected in 11 (79%) periodontitis patients, in five (33%) gingivitis patients, and in seven (54%) edentulous subjects (P = 0.076). Salivary samples showed copy counts of HCMV in the range of 3.3 × 103–4.2 × 104/ml and of EBV in the range of 3.6 × 102–1.6 × 109/ml.</abstract><abstract>Conclusions: HCMV and EBV are commonly present in the saliva of periodontitis patients. Periodontitis lesions of systemically healthy subjects seem to constitute the main origin of salivary HCMV, but do not comprise the sole source of salivary EBV.</abstract><subject lang="en"><genre>keywords</genre><topic>cytomegalovirus</topic><topic>Epstein–Barr virus</topic><topic>periodontal disease</topic><topic>saliva</topic></subject><relatedItem type="host"><titleInfo><title>Oral Microbiology and Immunology</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">0902-0055</identifier><identifier type="eISSN">1399-302X</identifier><identifier type="DOI">10.1111/(ISSN)1399-302X</identifier><identifier type="PublisherID">OMI</identifier><part><date>2009</date><detail type="volume"><caption>vol.</caption><number>24</number></detail><detail type="issue"><caption>no.</caption><number>4</number></detail><extent unit="pages"><start>340</start><end>342</end><total>3</total></extent></part></relatedItem><identifier type="istex">8535373C14E8EDE86F281FC3E0B6ABE9F8CBA9E7</identifier><identifier type="ark">ark:/67375/WNG-3N70VPQN-D</identifier><identifier type="DOI">10.1111/j.1399-302X.2009.00528.x</identifier><identifier type="ArticleID">OMI528</identifier><accessCondition type="use and reproduction" contentType="copyright">© 2009 John Wiley & Sons A/S</accessCondition><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/8535373C14E8EDE86F281FC3E0B6ABE9F8CBA9E7/metadata/json</uri></json:item></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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