Randomized trial shows live microbes increase RANKL in osteoblast-like PDLFs, suggesting new pathways for periodontal disease treatment.
BACKGROUND/AIM: Human 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 METHODS: .). Gene expression was quantified by qRT-PCR, and the RANKL/osteoprotegerin (OPG) ratio was calculated. Cell viability was assessed using metabolic assays. RESULTS: . Co-stimulation synergistically increased the RANKL/OPG ratio and IL-17A expression, whereas heat-killed microbes had no effect. CONCLUSION: RANKL 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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