ArticleIn vivo (Athens, Greece)
Live
Article in In vivo (Athens, Greece). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND/
aimHuman periodontal ligament fibroblasts (PDLFs) can acquire osteoblast-like characteristics within periodontal lesions and contribute to osteoclastogenesis through the expression of receptor activator of nuclear factor (NF) κB ligand (RANKL). However, the microbial and cellular conditions required for RANKL induction remain unclear. This study compared the microbial responsiveness of undifferentiated and osteoblast-like PDLFs to clarify the mechanisms regulating RANKL expression. MATERIALS AND
methodsPDLFs were cultured in standard or osteogenic medium and stimulated with TLR2/TLR4 ligands, a Dectin-1 ligand, or infected with live or heat-killed
resultsUndifferentiated PDLFs failed to upregulate RANKL in response to TLR2/TLR4 ligands, a Dectin-1 ligand, or stimulation with live or heat-killed
conclusionRANKL induction in PDLFs requires osteoblast-like differentiation and multifactorial stimulation provided by live microbes, including synergistic interactions between bacteria and fungi. These findings offer new insights into the mechanisms driving periodontal bone destruction.
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