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Peri‐implant versus periodontal wound healing

Identifieur interne : 000419 ( Istex/Corpus ); précédent : 000418; suivant : 000420

Peri‐implant versus periodontal wound healing

Auteurs : Pinar Emecen-Huja ; Tim D. Eubank ; Vladimir Shapiro ; Vedat Yildiz ; Dimitris N. Tatakis ; Binnaz Leblebicioglu

Source :

RBID : ISTEX:71C463B777A43E6E232DE5EDEB159D209CAD6F95

English descriptors

Abstract

Peri‐implant gingival healing following one‐stage implant placement was investigated and compared to periodontal healing.

Url:
DOI: 10.1111/jcpe.12127

Links to Exploration step

ISTEX:71C463B777A43E6E232DE5EDEB159D209CAD6F95

Le document en format XML

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Aim
<p>Peri‐implant gingival healing following one‐stage implant placement was investigated and compared to periodontal healing.</p>
Methods
<p>Healing at surgical sites [implant (I) and adjacent teeth (T+)] was compared to non‐operated tooth (T−) in non‐smokers receiving one‐stage implant. Periodontal Indices (
<hi rend="fc">PI</hi>
,
<hi rend="fc"> GI</hi>
) were recorded at surgery and up to 12 weeks post‐operatively. Peri‐implant (
<hi rend="fc">PICF</hi>
) and gingival crevicular fluids (
<hi rend="fc">GCF</hi>
) were analysed for cytokines, collagenases and inhibitors. Data were analysed by linear mixed model regression analysis and repeated measures
<hi rend="smallCaps">anova</hi>
.</p>
Results
<p>Forty patients (22 females; 21–74 years old) completed the study. Surgical site
<hi rend="fc">GI</hi>
, increased at week 1, decreased significantly during early healing (weeks 1–3;
<hi rend="italic">p</hi>
 = 0.0003) and continually decreased during late healing (weeks 6–12) for I (
<hi rend="italic">p</hi>
 < 0.01).
<hi rend="fc">PICF</hi>
volume decreased threefold by week 12 (
<hi rend="italic">p</hi>
 = 0.0003).
<hi rend="fc">IL</hi>
‐6,
<hi rend="fc">IL</hi>
‐8,
<hi rend="fc">MIP</hi>
‐1β and
<hi rend="fc">TIMP</hi>
‐1 levels significantly increased at surgical sites at week one, significantly decreasing thereafter (
<hi rend="italic">p</hi>
 < 0.016). Week one
<hi rend="fc">IL</hi>
‐6,
<hi rend="fc">IL</hi>
‐8 and
<hi rend="fc">MIP</hi>
‐1β levels were ~threefold higher and
<hi rend="fc">TIMP</hi>
‐1 levels 63% higher, at I compared to T+ (
<hi rend="italic">p</hi>
 = 0.001).</p>
Conclusion
<p>Peri‐implant gingival healing, as determined by crevicular fluid molecular composition, differs from periodontal healing. The observed differences suggest that peri‐implant tissues, compared to periodontal tissues, represent a higher pro‐inflammatory state.</p>
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<p>Peri‐implant gingival healing following one‐stage implant placement was investigated and compared to periodontal healing.</p>
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<p>Healing at surgical sites [implant (I) and adjacent teeth (T+)] was compared to non‐operated tooth (T−) in non‐smokers receiving one‐stage implant. Periodontal Indices (
<fc>PI</fc>
,
<fc> GI</fc>
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<fc>PICF</fc>
) and gingival crevicular fluids (
<fc>GCF</fc>
) were analysed for cytokines, collagenases and inhibitors. Data were analysed by linear mixed model regression analysis and repeated measures
<sc>anova</sc>
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<p>Forty patients (22 females; 21–74 years old) completed the study. Surgical site
<fc>GI</fc>
, increased at week 1, decreased significantly during early healing (weeks 1–3;
<i>p</i>
 = 0.0003) and continually decreased during late healing (weeks 6–12) for I (
<i>p</i>
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<fc>PICF</fc>
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<i>p</i>
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<fc>IL</fc>
‐6,
<fc>IL</fc>
‐8,
<fc>MIP</fc>
‐1β and
<fc>TIMP</fc>
‐1 levels significantly increased at surgical sites at week one, significantly decreasing thereafter (
<i>p</i>
 < 0.016). Week one
<fc>IL</fc>
‐6,
<fc>IL</fc>
‐8 and
<fc>MIP</fc>
‐1β levels were ~threefold higher and
<fc>TIMP</fc>
‐1 levels 63% higher, at I compared to T+ (
<i>p</i>
 = 0.001).</p>
</section>
<section xml:id="jcpe12127-sec-0004">
<title type="main">Conclusion</title>
<p>Peri‐implant gingival healing, as determined by crevicular fluid molecular composition, differs from periodontal healing. The observed differences suggest that peri‐implant tissues, compared to periodontal tissues, represent a higher pro‐inflammatory state.</p>
</section>
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<p>
<b>Conflict of interest and sources of funding statement</b>
</p>
<p>The authors report no conflict of interest. This study was supported by NIDCR grant R21 DE018718 and by the OSU Division of Periodontology.</p>
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<title>Peri‐implant versus periodontal wound healing</title>
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<title>Peri‐implant versus periodontal wound healing</title>
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<name type="personal">
<namePart type="given">Pinar</namePart>
<namePart type="family">Emecen‐Huja</namePart>
<affiliation>Division of Periodontology, College of Dentistry, The Ohio State University, OH, Columbus, USA</affiliation>
<affiliation>Current Address: Division of Periodontology, College of Dentistry, University of Kentucky, Lexington, Kentucky, USA</affiliation>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal">
<namePart type="given">Tim D.</namePart>
<namePart type="family">Eubank</namePart>
<affiliation>Department of Internal Medicine, College of Medicine, The Ohio State University, OH, Columbus, USA</affiliation>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal">
<namePart type="given">Vladimir</namePart>
<namePart type="family">Shapiro</namePart>
<affiliation>Division of Periodontology, College of Dentistry, The Ohio State University, OH, Columbus, USA</affiliation>
<affiliation>Current Address: Private Practice, OH, Cincinnati, USA</affiliation>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal">
<namePart type="given">Vedat</namePart>
<namePart type="family">Yildiz</namePart>
<affiliation>Center for Biostatistics, The Ohio State University, OH, Columbus, USA</affiliation>
<role>
<roleTerm type="text">author</roleTerm>
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</name>
<name type="personal">
<namePart type="given">Dimitris N.</namePart>
<namePart type="family">Tatakis</namePart>
<affiliation>Division of Periodontology, College of Dentistry, The Ohio State University, OH, Columbus, USA</affiliation>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal">
<namePart type="given">Binnaz</namePart>
<namePart type="family">Leblebicioglu</namePart>
<affiliation>Division of Periodontology, College of Dentistry, The Ohio State University, OH, Columbus, USA</affiliation>
<affiliation>Address:E‐mail:</affiliation>
<affiliation>E-mail: leblebicioglu.1@osu.edu</affiliation>
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<publisher>Blackwell Publishing Ltd</publisher>
<dateIssued encoding="w3cdtf">2013-08</dateIssued>
<dateCreated encoding="w3cdtf">2013-05-25</dateCreated>
<dateValid encoding="w3cdtf">2013-05-12</dateValid>
<edition>Emecen‐Huja P , Eubank TD , Shapiro V , Yildiz V , Tatakis DN , Leblebicioglu B. Peri‐implant versus periodontal wound healing. J Clin Periodontol 2013; doi: 10.1111/jcpe.12127.</edition>
<copyrightDate encoding="w3cdtf">2013</copyrightDate>
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<abstract>Peri‐implant gingival healing following one‐stage implant placement was investigated and compared to periodontal healing.</abstract>
<abstract>Healing at surgical sites [implant (I) and adjacent teeth (T+)] was compared to non‐operated tooth (T−) in non‐smokers receiving one‐stage implant. Periodontal Indices (PI, GI) were recorded at surgery and up to 12 weeks post‐operatively. Peri‐implant (PICF) and gingival crevicular fluids (GCF) were analysed for cytokines, collagenases and inhibitors. Data were analysed by linear mixed model regression analysis and repeated measures anova.</abstract>
<abstract>Forty patients (22 females; 21–74 years old) completed the study. Surgical site GI, increased at week 1, decreased significantly during early healing (weeks 1–3; p = 0.0003) and continually decreased during late healing (weeks 6–12) for I (p < 0.01). PICF volume decreased threefold by week 12 (p = 0.0003). IL‐6, IL‐8, MIP‐1β and TIMP‐1 levels significantly increased at surgical sites at week one, significantly decreasing thereafter (p < 0.016). Week one IL‐6, IL‐8 and MIP‐1β levels were ~threefold higher and TIMP‐1 levels 63% higher, at I compared to T+ (p = 0.001).</abstract>
<abstract>Peri‐implant gingival healing, as determined by crevicular fluid molecular composition, differs from periodontal healing. The observed differences suggest that peri‐implant tissues, compared to periodontal tissues, represent a higher pro‐inflammatory state.</abstract>
<note type="funding">NIDCR - No. R21 DE018718; </note>
<note type="funding">The Ohio State University</note>
<subject>
<genre>keywords</genre>
<topic>crevicular fluid</topic>
<topic>cytokines</topic>
<topic>dental implant</topic>
<topic>gingiva</topic>
<topic>periodontal surgery</topic>
<topic>wound healing</topic>
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<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>2013</date>
<detail type="volume">
<caption>vol.</caption>
<number>40</number>
</detail>
<detail type="issue">
<caption>no.</caption>
<number>8</number>
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