Peri-Implant Crestal Bone Loss: A Putative Mechanism
Identifieur interne : 004215 ( Ncbi/Curation ); précédent : 004214; suivant : 004216Peri-Implant Crestal Bone Loss: A Putative Mechanism
Auteurs : Yuko Ujiie ; Reynaldo Todescan ; John E. DaviesSource :
- International Journal of Dentistry [ 1687-8728 ] ; 2012.
Abstract
Url:
DOI: 10.1155/2012/742439
PubMed: 23091492
PubMed Central: 3467942
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PMC:3467942Le document en format XML
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<author><name sortKey="Ujiie, Yuko" sort="Ujiie, Yuko" uniqKey="Ujiie Y" first="Yuko" last="Ujiie">Yuko Ujiie</name>
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<author><name sortKey="Todescan, Reynaldo" sort="Todescan, Reynaldo" uniqKey="Todescan R" first="Reynaldo" last="Todescan">Reynaldo Todescan</name>
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<author><name sortKey="Davies, John E" sort="Davies, John E" uniqKey="Davies J" first="John E." last="Davies">John E. Davies</name>
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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Peri-Implant Crestal Bone Loss: A Putative Mechanism</title>
<author><name sortKey="Ujiie, Yuko" sort="Ujiie, Yuko" uniqKey="Ujiie Y" first="Yuko" last="Ujiie">Yuko Ujiie</name>
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<author><name sortKey="Todescan, Reynaldo" sort="Todescan, Reynaldo" uniqKey="Todescan R" first="Reynaldo" last="Todescan">Reynaldo Todescan</name>
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<author><name sortKey="Davies, John E" sort="Davies, John E" uniqKey="Davies J" first="John E." last="Davies">John E. Davies</name>
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<series><title level="j">International Journal of Dentistry</title>
<idno type="ISSN">1687-8728</idno>
<idno type="eISSN">1687-8736</idno>
<imprint><date when="2012">2012</date>
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<front><div type="abstract" xml:lang="en"><p><italic>Purpose</italic>
. The immunological mechanisms of peri-implant crestal bone loss have, hitherto, not been elucidated. We hypothesized that bacterial products from the microgap cause upregulation of cytokines in otherwise healthy peri-implant cells, which results in osteoclast formation and, ultimately, in bone resorption. <italic>Materials and Methods</italic>
. We used RT-PCR and ELISA to assay mediators of osteoclastogenesis in rat and human macrophages (r-and hMO); bone marrow derived stromal cells (r-and hBMCs); and human gingival fibroblasts (hGF)—with or without stimulation by LPS. TRAP positive multinucleate cells were assessed for their resorptive ability. <italic>Results</italic>
. We show that IL-1<italic><italic>α</italic>
</italic>
, IL-1<italic><italic>β</italic>
</italic>
, and IL-6 were expressed by all examined cell types, and TNF-<italic><italic>α</italic>
</italic>
was upregulated in hGF. Secretion of IL-1<italic><italic>α</italic>
</italic>
and IL-1<italic><italic>β</italic>
</italic>
proteins was stimulated in hMO by LPS, and IL-6 protein secretion was highly stimulated in hBMCs and hGF. Both LPS and RANKL stimulated macrophages to form osteoclast-like TRAP positive cells, which resorbed calcium phosphate substrates. <italic>Conclusion</italic>
. Taken together, the results of our study support the hypothesis that bacterial endotoxins upregulate enhanced mediators of osteoclastogenesis in resident cells found in the healthy peri-implant compartment and that the local synergistic action of cytokines secreted by such cells results in the genesis of resorptively active osteoclasts.</p>
</div>
</front>
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