A possible mechanism of maxillofacial abscess formation: involvement of Porphyromonas endodontalis lipopolysaccharide via the expression of inflammatory cytokines

Abstract

In a previous study, we developed a specific monoclonal antibody against Porphyromonas endodontalis lipopolysaccharide, and demonstrated that this lipopolysaccharide was detected in bacterially infected root canal fluid. We suggest here that P. endodontalis lipopolysaccharide in the infectious materials plays a stimulatory role in maxillofacial abscess formation via the expression of inflammatory cytokines. Our epidemiological study showed that this lipopolysaccharide was detected in significant levels the infectious material of patients with periapical periodontitis and odontogenic abscesses. Interestingly, infectious material-induced expression of tumor necrosis factor-alpha, interleukin-1beta, or neutrophil chemoattractant KC genes in mouse macrophages, was significantly neutralized by monoclonal antibody against the lipopolysaccharide. In addition, we also detected a significant amount of tumor necrosis factor-alpha in the infectious material. These results suggest that P. endodontalis lipopolysaccharide plays an important role in the pathogenic mechanism of maxillofacial abscess formation via the expression of inflammatory cytokines.

Efficacy of Endodontic Treatment for Endotoxin Reduction in Primarily Infected Root Canals and Evaluation of Cytotoxic Effects

“…Endotoxins are the main virulence factor of these bacteria (7) and exert various biological effects that result in the amplification of inflammatory and immune responses (8). Studies suggest that endotoxins are involved in the pathogenesis of pulpal and periapical inflammation (6,(9)(10)(11)(12)(13)(14)(15). A positive correlation between endotoxin concentration in the root canal and the presence of endodontic signs and symptoms has been shown (16).…”

Porphyromonas endodontalis Lipopolysaccharides Induce RANKL by Mouse Osteoblast in a Way Different from That of Escherichia coli Lipopolysaccharide

“…When it comes to P. endodontalis, it is less potent than Streptococcus mutans in stimulating mononuclear cells but more effective in directly inducing IL-6 and IL-1expression by osteoblastic cells (4). This might be significant because these characteristics may enable P. endodontalis to escape the immune response mounted by leukocytes but possess the ability to cause bone resorption at the sites of endodontic infection.…”

“…Studies have revealed that the content of endotoxin or LPS in infected root canals is higher in teeth with symptomatic apical periodontitis, teeth with periradicular bone destruction, or teeth with persistent exudation than in those without them (11). P. endodontalis LPS has been detected in samples from infected root canals or in the pus samples of acute abscesses of about 90% of the patients tested; it can play an integral role as a potent stimulator of inflammatory cytokines that are involved in the formation of acute abscesses (4).…”

“…This species is almost exclusively found in infections of the dental pulp and has been implicated in the etiology of infected root canals and apical periodontitis (2,3). As a major constituent of outer membrane and a main virulence factor of gramnegative bacteria, lipopolysaccharide (LPS) has been proved to play a critical role in initiating and developing periapical periodontitis and the odontogenic abscess by mediating inflammation and inducing cells to secrete proinflammatory cytokines (4).…”

Bacterial pathogenesis and mediators in apical periodontitis

“…Studies have revealed that the content of endotoxin or LPS in infected root canals is higher in teeth with symptomatic apical periodontitis, teeth with periradicular bone destruction, or teeth with persistent exudation than in those without them (32)(33)(34)(35)(36). Murakami et al (37) detected Porphyromonas endodontalis LPS in samples from infected root canals or in the pus samples of acute abscesses of about 90% of the patients tested. They suggested that P. endodontalis LPS can play an integral role as a potent stimulator of inflammatory cytokines that are involved in the formation of acute abscesses (37).…”