The role of 5-lipoxygenase in Aggregatibacter actinomycetemcomitans-induced alveolar bone loss

Abstract

Aim

Leukotrienes (LTs) are pro-inflammatory lipid mediators formed by the enzyme 5-lipoxygenase (5-LO). The involvement of 5-LO metabolites in periodontal disease (PD) is not well defined. This study aimed to assess the role of 5-LO in experimental PD induced by Aggregatibacter actinomycetemcomitans (Aa).

Material and Methods

In vivo experiments were carried out using SV129 wild type (WT) and 5-LO deficient (5lo^-/-) mice inoculated with Aa. Osteoclasts were stimulated in vitro with AaLPS in the presence or not of selective inhibitors of the 5-LO pathway, or LTB4 or platelet-activating factor (PAF), since PAF has already been shown to increase osteoclast activity.

Results

In 5lo^-/- mice there was no loss of alveolar bone and less TRAP-positive osteoclasts in periodontal tissues, after Aa inoculation, despite local production of TNF-α and IL-6. The differentiation and activity of osteoclasts stimulated with AaLPS were diminished in the presence of BLT1 antagonist or 5-LO inhibitor, but not in the presence of cystenil leukotriene receptor antagonist. The osteoclast differentiation induced by PAF was impaired by the BLT1 antagonism.

Conclusion

In conclusion, LTB4 but not CysLTs is important for Aa-induced alveolar bone loss. Overall, LTB4 affects osteoclast differentiation and activity and is a key intermediate of PAF-induced osteoclastogenesis.

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