Effects of Toll‐like receptor 4 on Porphyromonas gingivalis‐induced bone loss in mice

Abstract

Toll-like receptor 4 (TLR-4)/myeloid differentiation protein-2 complex ligation by lipopolysaccharide induces production of pro-inflammatory cytokines and co-stimulatory molecules on antigen presenting cells. The aim of this study was to determine the role of the TLR-4 in bone loss-resistant C57BL mice and in bone loss-susceptible BALB/c mice after infection with Porphyromonas gingivalis. The BALB/c and C57BL/10 mice, either normal or TLR-4 deficient, were infected or sham-infected orally four times, at 4 day intervals, with 10(9) colony forming units of P. gingivalis. At 47 days, defleshed jaws were stained and photographed in a standardized position. We measured the surface area of the root trunk to assess the alveolar bone loss. Porphyromonas gingivalis-infected wild-type BALB/c mice lost 13.8% more bone than P. gingivalis-infected wild-type C57BL/10 mice. In contrast, P. gingivalis-infected TLR-4-deficient C57BL/10 mice lost 12.7% more bone than P. gingivalis-infected TLR-4-deficient BALB/c mice. Porphyromonas gingivalis-infected wild-type C57BL/6 and TLR-2 knockout C57BL/6 mice had similar bone levels to sham-infected control mice. Toll-like receptor 4 is protective for C57BL/10 but detrimental to BALB/c mice, since its absence allowed C57BL/10 but not BALB/c mice to lose alveolar bone. Toll-like receptor 2 does not contribute to this protection in genetically similar C57BL/6 mice.