A Murine Model of Lipopolysaccharide-Induced Peri-Implant Mucositis and Peri-Implantitis
Identifieur interne : 002690 ( Pmc/Curation ); précédent : 002689; suivant : 002691A Murine Model of Lipopolysaccharide-Induced Peri-Implant Mucositis and Peri-Implantitis
Auteurs : Flavia Q. Pirih [États-Unis] ; Sarah Hiyari [États-Unis] ; Ho-Yin Leung [États-Unis] ; Ana D. V. Barroso [Brésil] ; Adrian C. A. Jorge [Brésil] ; Jeniffer Perussolo [Brésil] ; Elisa Atti [États-Unis] ; Yi-Ling Lin [États-Unis] ; Sotirios Tetradis [États-Unis] ; Paulo M. Camargo [États-Unis]Source :
- The Journal of oral implantology [ 0160-6972 ] ; 2014.
Abstract
Dental implants are a vastly used treatment option for tooth replacement. Dental implants are however susceptible to inflammatory diseases such as peri-implant mucositis and peri-implantitis, which are highly prevalent and may lead to implant loss. Unfortunately, the understanding of the pathogenesis of peri-implant mucositis and peri-implantitis is fragmented and incomplete. Therefore, the availability of a reproducible animal model to study these inflammatory diseases would facilitate the dissection of their pathogenic mechanisms. The objective of this study is to propose a murine model of experimental peri-implant mucositis and peri-implantitis.
Screw-shaped titanium implants were placed in the upper healed edentulous alveolar ridges of C57BL/6J mice eight weeks after tooth extraction. Following four weeks of osseointegration,
LPS-injections resulted in a significant increase in soft tissue edema around the head of the implants as compared to the control groups. Micro-CT analysis revealed significantly greater bone loss in the LPS-treated implants. Histological analysis of the specimens demonstrated that the LPS-group had increased soft tissue vascularity, which harbored a dense mixed inflammatory cell infiltrate, and the bone exhibited noticeable osteoclast activity.
The induction of peri-implant mucositis and peri-implantitis in mice via localized delivery of bacterial LPS has been demonstrated. We anticipate that this model will contribute to the development of more effective preventive and therapeutic approaches for these two conditions.
Url:
DOI: 10.1563/aaid-joi-D-14-00068
PubMed: 24967609
PubMed Central: 4391986
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<series><title level="j">The Journal of oral implantology</title>
<idno type="ISSN">0160-6972</idno>
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<front><div type="abstract" xml:lang="en"><sec id="S1"><title>Introduction</title>
<p id="P1">Dental implants are a vastly used treatment option for tooth replacement. Dental implants are however susceptible to inflammatory diseases such as peri-implant mucositis and peri-implantitis, which are highly prevalent and may lead to implant loss. Unfortunately, the understanding of the pathogenesis of peri-implant mucositis and peri-implantitis is fragmented and incomplete. Therefore, the availability of a reproducible animal model to study these inflammatory diseases would facilitate the dissection of their pathogenic mechanisms. The objective of this study is to propose a murine model of experimental peri-implant mucositis and peri-implantitis.</p>
</sec>
<sec id="S2"><title>Materials and Methods</title>
<p id="P2">Screw-shaped titanium implants were placed in the upper healed edentulous alveolar ridges of C57BL/6J mice eight weeks after tooth extraction. Following four weeks of osseointegration, <italic>Porphyromonas gingivalis</italic>
-lipolysaccharide (LPS) injections were delivered to the peri-implant soft tissues for six weeks. No-injections and vehicle injections were utilized as controls. Peri-implant mucositis and peri-implantitis were assessed clinically, radiographically (micro-CT) and histologically following LPS-treatment.</p>
</sec>
<sec id="S3"><title>Results</title>
<p id="P3">LPS-injections resulted in a significant increase in soft tissue edema around the head of the implants as compared to the control groups. Micro-CT analysis revealed significantly greater bone loss in the LPS-treated implants. Histological analysis of the specimens demonstrated that the LPS-group had increased soft tissue vascularity, which harbored a dense mixed inflammatory cell infiltrate, and the bone exhibited noticeable osteoclast activity.</p>
</sec>
<sec id="S4"><title>Conclusion</title>
<p id="P4">The induction of peri-implant mucositis and peri-implantitis in mice via localized delivery of bacterial LPS has been demonstrated. We anticipate that this model will contribute to the development of more effective preventive and therapeutic approaches for these two conditions.</p>
</sec>
</div>
</front>
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<pmc article-type="research-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<pmc-dir>properties manuscript</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-journal-id">7801086</journal-id>
<journal-id journal-id-type="pubmed-jr-id">5309</journal-id>
<journal-id journal-id-type="nlm-ta">J Oral Implantol</journal-id>
<journal-id journal-id-type="iso-abbrev">J Oral Implantol</journal-id>
<journal-title-group><journal-title>The Journal of oral implantology</journal-title>
</journal-title-group>
<issn pub-type="ppub">0160-6972</issn>
<issn pub-type="epub">1548-1336</issn>
</journal-meta>
<article-meta><article-id pub-id-type="pmid">24967609</article-id>
<article-id pub-id-type="pmc">4391986</article-id>
<article-id pub-id-type="doi">10.1563/aaid-joi-D-14-00068</article-id>
<article-id pub-id-type="manuscript">NIHMS674268</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Article</subject>
</subj-group>
</article-categories>
<title-group><article-title>A Murine Model of Lipopolysaccharide-Induced Peri-Implant Mucositis and Peri-Implantitis</article-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>Pirih</surname>
<given-names>Flavia Q.</given-names>
</name>
<xref ref-type="aff" rid="A1">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Hiyari</surname>
<given-names>Sarah</given-names>
</name>
<xref ref-type="aff" rid="A1">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Leung</surname>
<given-names>Ho-Yin</given-names>
</name>
<xref ref-type="aff" rid="A1">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Barroso</surname>
<given-names>Ana D. V.</given-names>
</name>
<xref ref-type="aff" rid="A2">2</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Jorge</surname>
<given-names>Adrian C. A.</given-names>
</name>
<xref ref-type="aff" rid="A3">3</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Perussolo</surname>
<given-names>Jeniffer</given-names>
</name>
<xref ref-type="aff" rid="A3">3</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Atti</surname>
<given-names>Elisa</given-names>
</name>
<xref ref-type="aff" rid="A4">4</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Lin</surname>
<given-names>Yi-Ling</given-names>
</name>
<xref ref-type="aff" rid="A5">5</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Tetradis</surname>
<given-names>Sotirios</given-names>
</name>
<xref ref-type="aff" rid="A4">4</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Camargo</surname>
<given-names>Paulo M.</given-names>
</name>
<xref ref-type="aff" rid="A1">1</xref>
</contrib>
</contrib-group>
<aff id="A1"><label>1</label>
University of California, Los Angeles, School of Dentistry, Section of Periodontics, United States</aff>
<aff id="A2"><label>2</label>
Universidade Federal do Espirito Santo, School of Dentistry, Brazil</aff>
<aff id="A3"><label>3</label>
Universidade Estadual de Ponta Grossa, School of Dentistry, Brazil</aff>
<aff id="A4"><label>4</label>
University of California, Los Angeles, School of Dentistry, Section of Oral Radiology, United States</aff>
<aff id="A5"><label>5</label>
University of California, Los Angeles, School of Dentistry, Section of Oral Pathology, United States</aff>
<author-notes><corresp id="CR1">Corresponding author: Dr. Paulo M. Camargo <email>pcamargo@dentistry.ucla.edu</email>
Phone: 310-825-0928 Fax: 310-206-3282 UCLA School of Dentistry Section of Periodontics 10833 Le Conte Ave CHS 53042-D Los Angeles, CA 90095</corresp>
</author-notes>
<pub-date pub-type="nihms-submitted"><day>25</day>
<month>3</month>
<year>2015</year>
</pub-date>
<pub-date pub-type="epub"><day>26</day>
<month>6</month>
<year>2014</year>
</pub-date>
<pub-date pub-type="ppub"><month>10</month>
<year>2015</year>
</pub-date>
<pub-date pub-type="pmc-release"><day>15</day>
<month>10</month>
<year>2015</year>
</pub-date>
<volume>41</volume>
<issue>5</issue>
<fpage>e158</fpage>
<lpage>e164</lpage>
<pmc-comment>elocation-id from pubmed: 10.1563/aaid-joi-D-14-00068</pmc-comment>
<abstract><sec id="S1"><title>Introduction</title>
<p id="P1">Dental implants are a vastly used treatment option for tooth replacement. Dental implants are however susceptible to inflammatory diseases such as peri-implant mucositis and peri-implantitis, which are highly prevalent and may lead to implant loss. Unfortunately, the understanding of the pathogenesis of peri-implant mucositis and peri-implantitis is fragmented and incomplete. Therefore, the availability of a reproducible animal model to study these inflammatory diseases would facilitate the dissection of their pathogenic mechanisms. The objective of this study is to propose a murine model of experimental peri-implant mucositis and peri-implantitis.</p>
</sec>
<sec id="S2"><title>Materials and Methods</title>
<p id="P2">Screw-shaped titanium implants were placed in the upper healed edentulous alveolar ridges of C57BL/6J mice eight weeks after tooth extraction. Following four weeks of osseointegration, <italic>Porphyromonas gingivalis</italic>
-lipolysaccharide (LPS) injections were delivered to the peri-implant soft tissues for six weeks. No-injections and vehicle injections were utilized as controls. Peri-implant mucositis and peri-implantitis were assessed clinically, radiographically (micro-CT) and histologically following LPS-treatment.</p>
</sec>
<sec id="S3"><title>Results</title>
<p id="P3">LPS-injections resulted in a significant increase in soft tissue edema around the head of the implants as compared to the control groups. Micro-CT analysis revealed significantly greater bone loss in the LPS-treated implants. Histological analysis of the specimens demonstrated that the LPS-group had increased soft tissue vascularity, which harbored a dense mixed inflammatory cell infiltrate, and the bone exhibited noticeable osteoclast activity.</p>
</sec>
<sec id="S4"><title>Conclusion</title>
<p id="P4">The induction of peri-implant mucositis and peri-implantitis in mice via localized delivery of bacterial LPS has been demonstrated. We anticipate that this model will contribute to the development of more effective preventive and therapeutic approaches for these two conditions.</p>
</sec>
</abstract>
<kwd-group><kwd>Peri-implant mucositis</kwd>
<kwd>Peri-implantitis</kwd>
<kwd>Implants</kwd>
<kwd>Mouse</kwd>
<kwd>Dental Implants</kwd>
<kwd>Lipopolysaccharide</kwd>
</kwd-group>
</article-meta>
</front>
</pmc>
</record>
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