Expression of Toll-like receptor 2 and 4 in inflamed pulp in severe combined immunodeficiency mice.

INTRODUCTION: Toll-like receptors (TLRs) are important receptors mediating innate immune responses because they detect factors released from bacterial cell wall components during inflammatory reactions. However, the role of TLRs in dental pulp, which is bounded by hard tissues, is poorly understood. The purpose of this study was to investigate the relationship between the innate immune system and the defense of pulp tissue by using immunodeficient mice that lack an adaptive immune response METHODS: Mice with severe combined immunodeficiency (SCID) were used as a model because they lack an adaptive immune response. The expression of TLR-2 and TLR-4 in experimentally inflamed pulps in SCID mice was measured by quantitative real-time polymerase chain reaction and immunohistochemistry. Total RNA was isolated from pulp tissues at 0 to 24 hours after bacterial dentinal infection. Anti-TLR-2, anti-TLR-4 cells, anti-CD64, and antinestin cells were detected with labeled streptavidin-biotin methods. RESULTS: TLR-2 messenger RNA was detected at 3 hours after bacterial infection and then gradually increased from 9 to 24 hours. Numerous TLR-2- and CD64-positive cells detected on macrophages and dendritic-like cells, and TLR-4- and CD64-positive macrophages were detected in the early stage of pulpitis. CONCLUSION: These results suggest that the expression of TLR-2 and TLR-4 may be triggered by bacterial infection in irreversible pulpitis without a need for an adaptive immune response. Those signals may relate to pulpal responses to bacterial infection.

Expression of toll-like receptor 2 and 4 in dental pulp.

Toll-like receptors (TLRs) are important factors in innate immune responses because they mediate signals from bacterial cell wall components during inflammatory reactions. However, the role of TLR in dental pulp, which is bounded by hard tissues, is little understood. The present study investigated the expression of TLR-2 and TLR-4 in experimentally inflamed pulp by quantitative real-time polymerase chain reaction and immunohistochemistry. Total RNA isolated from pulp tissue from 0 to 72 hours after bacterial dentinal infection. The TLR-2 messenger RNA (mRNA) level was 30-fold higher than the TLR-4 mRNA level at 9 hours. The TLR-2 mRNA level in pulp began to increase by 3 hours after bacterial infection, reaching a maximum level after 9 hours and gradually decreasing from 9 to 72 hours. Numerous TLR-2- and CD64-positive cells detected on macrophage and dendritic-like cells, TLR-4-positive cells detected a little in the pulp at 9 hours. These results suggest that TLR-2 may be mainly regulated during the early stage of pulp inflammation triggered by bacterial infection.

Inhibitory effects of incadronate on the progression of rat experimental periodontitis by porphyromonas gingivalis infection.

BACKGROUND: Incadronate (YM175, disodium cycloheptylaminomethylenediphosphonate monohydrate), a bisphosphonate, has been suggested to prevent the bone resorption associated with periodontitis by inhibiting osteoclast activity. The purpose of this study was to investigate the effect of incadronate in preventing periodontal destruction in rats with Porphyromonas gingivalis-induced periodontitis. METHODS: Periodontitis was induced in 35 Wister rats by inoculating P. gingivalis into the oral cavity and feeding the rats a soft diet for 4 weeks. Incadronate or placebo was administered to the oral cavity of the rats 2 days per week for 2, 4, or 8 weeks. RESULTS: P. gingivalis infection resulted in destruction of the periodontal ligament, reduced bone density, and caused inflammatory cell migration. Radiographic, morphometric, and histological results showed that incadronate had the ability to increase the bone mineral density (quantum level score; cortex 518.9 [placebo 612.8]; sponge 579.8 [placebo 672.0]) and to prevent periodontal ligament destruction (width 0.16 mm [placebo 0.20 mm]; area 0.36 mm2 [placebo 0.54 mm2]) after 8 weeks' administration. Furthermore, the polymorphonuclear leukocyte (PMN) infiltration in gingival tissue was significantly decreased. CONCLUSION: These results showed that incadronate inhibits bone resorption and PMN migration in P. gingivalis-induced periodontitis.