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Improving oral implant osseointegration in a murine model via Wnt signal amplification

Identifieur interne : 002619 ( Pmc/Corpus ); précédent : 002618; suivant : 002620

Improving oral implant osseointegration in a murine model via Wnt signal amplification

Auteurs : Sylvain Mouraret ; Daniel J. Hunter ; Claire Bardet ; Antoine Popelut ; John B. Brunski ; Catherine Chaussain ; Philippe Bouchard ; Jill A. Helms

Source :

RBID : PMC:4993043

Abstract

Aim

To determine the key biological events occurring during implant failure and then we use this knowledge to develop new biology-based strategies that improve osseointegration.

Materials and Methods

Wild-type and Axin2LacZ/LacZ adult male mice underwent oral implant placement, with and without primary stability. Peri-implant tissues were evaluated using histology, alkaline phosphatase (ALP) activity, tartrate resistant acid phosphatase (TRAP) activity and TUNEL staining. In addition, mineralization sites, collagenous matrix organization and the expression of bone markers in the peri-implant tissues were assessed.

Results

Maxillary implants lacking primary stability show histological evidence of persistent fibrous encapsulation and mobility, which recapitulates the clinical problems of implant failure. Despite histological and molecular evidence of fibrous encapsulation, osteoblasts in the gap interface exhibit robust ALP activity. This mineralization activity is counteracted by osteoclast activity that resorbs any new bony matrix and consequently, the fibrous encapsulation remains. Using a genetic mouse model, we show that implants lacking primary stability undergo osseointegration, provided that Wnt signalling is amplified.

Conclusions

In a mouse model of oral implant failure caused by a lack of primary stability, we find evidence of active mineralization. This mineralization, however, is outpaced by robust bone resorption, which culminates in persistent fibrous encapsulation of the implant. Fibrous encapsulation can be prevented and osseointegration assured if Wnt signalling is elevated at the time of implant placement.


Url:
DOI: 10.1111/jcpe.12187
PubMed: 24164629
PubMed Central: 4993043

Links to Exploration step

PMC:4993043

Le document en format XML

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<title>Aim</title>
<p id="P1">To determine the key biological events occurring during implant failure and then we use this knowledge to develop new biology-based strategies that improve osseointegration.</p>
</sec>
<sec id="S2">
<title>Materials and Methods</title>
<p id="P2">Wild-type and
<italic>Axin2
<sup>LacZ/LacZ</sup>
</italic>
adult male mice underwent oral implant placement, with and without primary stability. Peri-implant tissues were evaluated using histology, alkaline phosphatase (ALP) activity, tartrate resistant acid phosphatase (TRAP) activity and TUNEL staining. In addition, mineralization sites, collagenous matrix organization and the expression of bone markers in the peri-implant tissues were assessed.</p>
</sec>
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<title>Results</title>
<p id="P3">Maxillary implants lacking primary stability show histological evidence of persistent fibrous encapsulation and mobility, which recapitulates the clinical problems of implant failure. Despite histological and molecular evidence of fibrous encapsulation, osteoblasts in the gap interface exhibit robust ALP activity. This mineralization activity is counteracted by osteoclast activity that resorbs any new bony matrix and consequently, the fibrous encapsulation remains. Using a genetic mouse model, we show that implants lacking primary stability undergo osseointegration, provided that Wnt signalling is amplified.</p>
</sec>
<sec id="S4">
<title>Conclusions</title>
<p id="P4">In a mouse model of oral implant failure caused by a lack of primary stability, we find evidence of active mineralization. This mineralization, however, is outpaced by robust bone resorption, which culminates in persistent fibrous encapsulation of the implant. Fibrous encapsulation can be prevented and osseointegration assured if Wnt signalling is elevated at the time of implant placement.</p>
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<journal-title>Journal of clinical periodontology</journal-title>
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<surname>Mouraret</surname>
<given-names>Sylvain</given-names>
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<xref ref-type="aff" rid="A2">2</xref>
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<contrib contrib-type="author">
<name>
<surname>Hunter</surname>
<given-names>Daniel J.</given-names>
</name>
<xref ref-type="aff" rid="A1">1</xref>
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<name>
<surname>Bardet</surname>
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<name>
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<name>
<surname>Bouchard</surname>
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<name>
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<given-names>Jill A.</given-names>
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Division of Plastic and Reconstructive Surgery, Department of Surgery, Stanford School of Medicine, Stanford, CA, USA</aff>
<aff id="A2">
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Department of Periodontology, Service of Odontology, Rothschild Hospital, AP-HP, Paris 7 – Denis, Diderot University, U.F.R. of Odontology, Paris, France</aff>
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Dental School University Paris Descartes PRES Sorbonne Paris Cité, Montrouge, France</aff>
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<corresp id="FN1">Address: Jill A. Helms, 257 Campus Drive, PSRL Building, Stanford, CA 94305, USA,
<email>jhelms@stanford.edu</email>
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<pub-date pub-type="nihms-submitted">
<day>16</day>
<month>8</month>
<year>2016</year>
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<pub-date pub-type="epub">
<day>08</day>
<month>12</month>
<year>2013</year>
</pub-date>
<pub-date pub-type="ppub">
<month>2</month>
<year>2014</year>
</pub-date>
<pub-date pub-type="pmc-release">
<day>22</day>
<month>8</month>
<year>2016</year>
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<volume>41</volume>
<issue>2</issue>
<fpage>172</fpage>
<lpage>180</lpage>
<pmc-comment>elocation-id from pubmed: 10.1111/jcpe.12187</pmc-comment>
<abstract>
<sec id="S1">
<title>Aim</title>
<p id="P1">To determine the key biological events occurring during implant failure and then we use this knowledge to develop new biology-based strategies that improve osseointegration.</p>
</sec>
<sec id="S2">
<title>Materials and Methods</title>
<p id="P2">Wild-type and
<italic>Axin2
<sup>LacZ/LacZ</sup>
</italic>
adult male mice underwent oral implant placement, with and without primary stability. Peri-implant tissues were evaluated using histology, alkaline phosphatase (ALP) activity, tartrate resistant acid phosphatase (TRAP) activity and TUNEL staining. In addition, mineralization sites, collagenous matrix organization and the expression of bone markers in the peri-implant tissues were assessed.</p>
</sec>
<sec id="S3">
<title>Results</title>
<p id="P3">Maxillary implants lacking primary stability show histological evidence of persistent fibrous encapsulation and mobility, which recapitulates the clinical problems of implant failure. Despite histological and molecular evidence of fibrous encapsulation, osteoblasts in the gap interface exhibit robust ALP activity. This mineralization activity is counteracted by osteoclast activity that resorbs any new bony matrix and consequently, the fibrous encapsulation remains. Using a genetic mouse model, we show that implants lacking primary stability undergo osseointegration, provided that Wnt signalling is amplified.</p>
</sec>
<sec id="S4">
<title>Conclusions</title>
<p id="P4">In a mouse model of oral implant failure caused by a lack of primary stability, we find evidence of active mineralization. This mineralization, however, is outpaced by robust bone resorption, which culminates in persistent fibrous encapsulation of the implant. Fibrous encapsulation can be prevented and osseointegration assured if Wnt signalling is elevated at the time of implant placement.</p>
</sec>
</abstract>
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<kwd>dental</kwd>
<kwd>fibrointegration</kwd>
<kwd>fibrous encapsulation</kwd>
<kwd>histology</kwd>
<kwd>
<italic>in vivo</italic>
</kwd>
<kwd>maxilla</kwd>
<kwd>mice</kwd>
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<kwd>oral cavity</kwd>
<kwd>Wnt</kwd>
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