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Updated: Apr 30, 2026
Porphyromonas gingivalis as a Model Organism for Assessing Interaction of Anaerobic Bacteria with Host Cells
Published on: December 17, 2015
Live Porphyromonas gingivalis and Candida albicans Synergistically Induce RANKL in Osteoblast-like PDLFs But Not in
Masayo Abe1, Kohei Kamijyo2, Shintaro Oda1
1Division of Microbiology and Immunology, Department of Oral Biology and Tissue Engineering, Meikai University School of Dentistry, Sakado, Japan.
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:
PDLFs were cultured in standard or osteogenic medium and stimulated with TLR2/TLR4 ligands, a Dectin-1 ligand, or infected with live or heat-killed Porphyromonas gingivalis (P.g.) and Candida albicans (C.a.). Gene expression was quantified by qRT-PCR, and the RANKL/osteoprotegerin (OPG) ratio was calculated. Cell viability was assessed using metabolic assays.
Results:
Undifferentiated PDLFs failed to upregulate RANKL in response to TLR2/TLR4 ligands, a Dectin-1 ligand, or stimulation with live or heat-killed P.g. or C.a., even though TLR2 stimulation increased IL-17A expression. In contrast, osteoblast-like PDLFs exhibited increased cell viability and robust RANKL induction following stimulation with live C.a., and these responses were further enhanced by co-stimulation with live P.g. and C.a. 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.
