Peri-Implant Crestal Bone Loss: A Putative Mechanism
Identifieur interne : 003102 ( Main/Merge ); précédent : 003101; suivant : 003103Peri-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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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">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></author><author><name sortKey="Todescan, Reynaldo" sort="Todescan, Reynaldo" uniqKey="Todescan R" first="Reynaldo" last="Todescan">Reynaldo Todescan</name></author><author><name sortKey="Davies, John E" sort="Davies, John E" uniqKey="Davies J" first="John E." last="Davies">John E. Davies</name></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">23091492</idno><idno type="pmc">3467942</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3467942</idno><idno type="RBID">PMC:3467942</idno><idno type="doi">10.1155/2012/742439</idno><date when="2012">2012</date><idno type="wicri:Area/Pmc/Corpus">002D52</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">002D52</idno><idno type="wicri:Area/Pmc/Curation">002D52</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Curation">002D52</idno><idno type="wicri:Area/Pmc/Checkpoint">001D37</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Checkpoint">001D37</idno><idno type="wicri:Area/Ncbi/Merge">004215</idno><idno type="wicri:Area/Ncbi/Curation">004215</idno><idno type="wicri:Area/Ncbi/Checkpoint">004215</idno><idno type="wicri:doubleKey">1687-8728:2012:Ujiie Y:peri:implant:crestal</idno><idno type="wicri:Area/Main/Merge">003102</idno></publicationStmt><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></author><author><name sortKey="Todescan, Reynaldo" sort="Todescan, Reynaldo" uniqKey="Todescan R" first="Reynaldo" last="Todescan">Reynaldo Todescan</name></author><author><name sortKey="Davies, John E" sort="Davies, John E" uniqKey="Davies J" first="John E." last="Davies">John E. Davies</name></author></analytic><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></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><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><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Adell, R" uniqKey="Adell R">R Adell</name></author><author><name sortKey="Lekholm, U" uniqKey="Lekholm U">U Lekholm</name></author><author><name sortKey="Rockler, B" uniqKey="Rockler B">B Rockler</name></author><author><name sortKey="Br Nemark, Pi" uniqKey="Br Nemark P">PI Brånemark</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Cox, Jf" uniqKey="Cox J">JF Cox</name></author><author><name sortKey="Zarb, Ga" uniqKey="Zarb G">GA Zarb</name></author></analytic></biblStruct><biblStruct><analytic><author><name 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Perala</name></author><author><name sortKey="Chapman, Rj" uniqKey="Chapman R">RJ Chapman</name></author><author><name sortKey="Gelfand, Ja" uniqKey="Gelfand J">JA Gelfand</name></author><author><name sortKey="Callahan, Mv" uniqKey="Callahan M">MV Callahan</name></author><author><name sortKey="Adams, Df" uniqKey="Adams D">DF Adams</name></author><author><name sortKey="Lie, T" uniqKey="Lie T">T Lie</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Kao, Rt" uniqKey="Kao R">RT Kao</name></author><author><name sortKey="Curtis, Da" uniqKey="Curtis D">DA Curtis</name></author><author><name sortKey="Richards, Dw" uniqKey="Richards D">DW Richards</name></author><author><name sortKey="Preble, J" uniqKey="Preble J">J Preble</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Remick, Dg" uniqKey="Remick D">DG Remick</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Lazzara, Rj" uniqKey="Lazzara R">RJ Lazzara</name></author><author><name sortKey="Porter, Ss" uniqKey="Porter S">SS Porter</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Baumgarten, H" uniqKey="Baumgarten H">H Baumgarten</name></author><author><name sortKey="Cocchetto, R" uniqKey="Cocchetto R">R Cocchetto</name></author><author><name sortKey="Testori, T" uniqKey="Testori T">T Testori</name></author><author><name sortKey="Meltzer, A" uniqKey="Meltzer A">A Meltzer</name></author><author><name sortKey="Porter, S" uniqKey="Porter S">S Porter</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Jimi, E" uniqKey="Jimi E">E Jimi</name></author><author><name sortKey="Nakamura, I" uniqKey="Nakamura I">I Nakamura</name></author><author><name sortKey="Duong, Lt" uniqKey="Duong L">LT Duong</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Kobayashi, K" uniqKey="Kobayashi K">K Kobayashi</name></author><author><name sortKey="Takahashi, N" uniqKey="Takahashi N">N Takahashi</name></author><author><name sortKey="Jimi, E" uniqKey="Jimi E">E Jimi</name></author></analytic></biblStruct></listBibl></div1></back></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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