Porphyromonas gingivalis Exacerbates Ligature-Induced, RANKL-Dependent Alveolar Bone Resorption via Differential Regulation of Toll-Like Receptor 2 (TLR2) and TLR4
Ligature
Periodontal pathogen
DOI:
10.1128/iai.02084-14
Publication Date:
2014-07-22T03:31:36Z
AUTHORS (7)
ABSTRACT
Toll-like receptors (TLRs) play a key role in the innate immune responses to periodontal pathogens disease. The present study was performed determine roles of TLR2 and TLR4 signaling alveolar bone resorption, using Porphyromonas gingivalis-associated ligature-induced periodontitis model mice. Wild-type (WT), Tlr2(-/-), Tlr4(-/-) mice (8 10 weeks old) C57/BL6 background were used. Silk ligatures applied maxillary second molars presence or absence live P. gingivalis infection. Ligatures removed from on day 14, kept for another 2 before sacrifice final analysis (day 28). On there no differences resorption gingival RANKL expression between treated with ligation plus infection alone. Gingival interleukin-1β (IL-1β) tumor necrosis factor alpha (TNF-α) increased, whereas IL-10 decreased WT Tlr2(-/-) but not 28, showed significantly increased loss compared those alone, such an increase diminished TNF-α upregulation downregulation observed only mice, In all induced by antagonized local anti-RANKL antibody administration. This suggests that exacerbates ligature-induced, RANKL-dependent via differential regulation signaling.
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