Journal
JOURNAL OF ORAL PATHOLOGY & MEDICINE
Volume 33, Issue 3, Pages 162-169Publisher
WILEY
DOI: 10.1111/j.0904-2512.2004.00045.x
Keywords
bone resorption; lipopolysaccharide (LPS); macrophage; periapical lesion; polymyxin B
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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-1alpha (IL-1alpha) and tumor necrosis factor-alpha (TNF-alpha) 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-1alpha and anti-TNF-alpha 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-1alpha and TNF-alpha from macrophages. These pro-inflammatory cytokines up-regulate the production of MMP-1 by macrophages to promote periapical bone resorption.
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