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The role of lipopolysaccharide in infectious bone resorption of periapical lesion
Author(s) -
Hong ChiYuan,
Lin SzeKwan,
Kok SangHeng,
Cheng ShihJung,
Lee MingShu,
Wang TongMei,
Chen ChuanShuo,
Lin LiDeh,
Wang JuoSong
Publication year - 2004
Publication title -
journal of oral pathology and medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.887
H-Index - 83
eISSN - 1600-0714
pISSN - 0904-2512
DOI - 10.1111/j.0904-2512.2004.00045.x
Subject(s) - fusobacterium nucleatum , lipopolysaccharide , bone resorption , lesion , tumor necrosis factor alpha , resorption , macrophage , porphyromonas gingivalis , medicine , polymyxin b , periodontitis , pathology , immunology , chemistry , microbiology and biotechnology , in vitro , biology , biochemistry , antibiotics
Background: The role of lipopolysaccharide (LPS) in periapical lesion‐induced bone resorption was investigated. Polymyxin B (PMB), a specific inhibitor of LPS, was evaluated to treat the apical lesion. Methods: Lipopolysaccharide isolated from two common endodontic pathogens, Fusobacterium nucleatum and Porphyromonas endodontalis , stimulated mouse macrophage (J774) to release interleukin‐1α (IL‐1α) and tumor necrosis factor‐α (TNF‐α) in a time‐dependent manner. Results: Combination of LPS further enhanced the stimulation. PMB inhibited these effects significantly. LPS also stimulated matrix metalloproteinase‐1 (MMP‐1) gene expression in J774, whereas anti‐IL‐1α and anti‐TNF‐α antibodies, as well as PMB, diminished this effect. A disease model of periapical lesion was established in Wistar rat. Administration of PMB reduced the extent of lesion‐associated bone resorption by 76% to approximately 80%, and simultaneously reduced the numbers of MMP‐1‐producing macrophages. Conclusions: It is suggested that LPS released from the infected root canal triggers the synthesis of IL‐1α and TNF‐α from macrophages. These pro‐inflammatory cytokines up‐regulate the production of MMP‐1 by macrophages to promote periapical bone resorption.