Conclusion
RANKL was involved in peri-implantitis, and regulated by TLR2, LOX-1 and Erk1/2 signaling against P. gingivalis infection. As the novel inflammation pathway triggers, TLR2 and LOX-1 which mediate RANKL production seems to be potential drug targets of peri-implantitis.
Methods
Therefore, we collected peri-implant crevicular fluid (PICF) and gingival tissues from healthy implants and peri-implantitis patients. The expression of RANKL in samples was tested by ELISA, Western blot and immunofluorescence staining. The production of RANKL in THP-1 macrophages stimulated with P. gingivalis was detected by qRT-PCR and Western blot. Then macrophages were pre-treated with neutralizing antibodies of Toll-like receptor 2 (TLR2) or lectin-type oxidized LDL receptor 1 (LOX-1) and inhibitors of TLR2, LOX-1 or Erk1/2 before P. gingivalis stimulation to evaluate the roles of TLR2, LOX-1 and Erk1/2 in RANKL production by qRT-PCR and Western blot.
Purpose
To explore whether receptor activator of nuclear factor kappa-B ligand (RANKL) is involved in the nosogenesis of peri-implantitis and to reveal the regulatory mechanism in Porphyromonas gingivalis induced RANKL production.
Results
The protein level of RANKL was higher in PICF of peri-implantitis patients than healthy implants. We observed increased RANKL expression in P. gingivalis infected macrophages compared to controls. RANKL induced by P. gingivalis stimulation was mediated by TLR2 and Erk1/2 signaling pathway in THP-1 macrophages. LOX-1 is involved in TLR2 induced RANKL expression.