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• W2004692124 abstract "Purpose . 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. Materials and Methods . 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. Results . We show that IL-1 α , IL-1 β , and IL-6 were expressed by all examined cell types, and TNF- α was upregulated in hGF. Secretion of IL-1 α and IL-1 β 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. Conclusion . 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." @default.
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• W2004692124 date "2012-01-01" @default.
• W2004692124 modified "2023-09-23" @default.
• W2004692124 title "Peri-Implant Crestal Bone Loss: A Putative Mechanism" @default.
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• W2004692124 doi "https://doi.org/10.1155/2012/742439" @default.
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