Purpose. The immunological mechanisms of peri-implant crestal bone loss have, hitherto, not been elucidated. We hypothesized\r\nthat bacterial products from the microgap cause upregulation of cytokines in otherwise healthy peri-implant cells, which results in\r\nosteoclast formation and, ultimately, in bone resorption. Materials and Methods. We used RT-PCR and ELISA to assay mediators\r\nof osteoclastogenesis in rat and human macrophages (r-and hMO); bone marrow derived stromal cells (r-and hBMCs); and\r\nhuman gingival fibroblasts (hGF)ââ?¬â?with or without stimulation by LPS. TRAP positive multinucleate cells were assessed for\r\ntheir resorptive ability. Results. We show that IL-1a, IL-1Ã?Ÿ, and IL-6 were expressed by all examined cell types, and TNF-a was\r\nupregulated in hGF. Secretion of IL-1a and IL-1Ã?Ÿ proteins was stimulated in hMO by LPS, and IL-6 protein secretion was highly\r\nstimulated in hBMCs and hGF. Both LPS and RANKL stimulated macrophages to form osteoclast-like TRAP positive cells, which\r\nresorbed calcium phosphate substrates. Conclusion. Taken together, the results of our study support the hypothesis that bacterial\r\nendotoxins upregulate enhanced mediators of osteoclastogenesis in resident cells found in the healthy peri-implant compartment\r\nand that the local synergistic action of cytokines secreted by such cells results in the genesis of resorptively active osteoclasts
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