IADR Abstract Archives
Azithromycin Regulates Human Osteoclast Formation and Activity in an in vitro Inflammatory Environment
Objectives: Periodontal disease is a pathologic condition whereby inflammation is modulated by complex interactions between bacteria and host cells leading to destruction of the soft and hard tissues of the periodontium. Azithromycin is a macrolide antibiotic with both bacteriostatic and immunomodulatory properties. Clinically it can be considered a novel adjunct in cases of periodontitis non-responsive to conventional periodontal treatment.
The aim of the study was to determine the effect of azithromycin on osteoclast formation and resorptive activity in an in vitro inflammatory environment.
Methods: Peripheral blood mononuclear cells were isolated from whole blood of healthy volunteers. The cells were stimulated with Porphyromonas gingivalis (P. gingivalis) LPS for 24 hours, then differentiated into osteoclasts with macrophage colony stimulating factor (M-CSF) and receptor activator of nuclear factor kappa B (RANK) ligand. The effects of azithromycin at concentrations of 20 and 40 μg/mL were tested. Immunohistochemistry was used to determine tartrate-resistant acid phosphatase (TRAP) expression, indicative of osteoclast formation. Dentine resorption assays were used to detect osteoclast activity and production of key inflammatory cytokines were measured using enzyme-linked immunosorbent assay’s.
Results: The results demonstrated that P. gingivalis LPS induced an "inflammation-like" milieu with significant increases in monocyte chemoattractant protein-1 (MCP-1), interleukin-1 beta (IL-1β) and interleukin-6 (IL-6) concentrations in cell supernatant compared to unstimulated control cells (p<0.05). Preliminary analyses suggest that azithromycin may modulate osteoclast formation and activity as evidenced by decreased TRAP staining and resorptive activity.
Conclusions: This study expands our current understanding of azithromycin’s effect on in vitro osteoclastogenesis. This may provide a basis for future targeted and clinically appropriate use of antibiotics in the management of non-responsive periodontitis.
Supported by the Australian Dental Research Foundation and Colin Cormie Scholarship (ADRF).
The aim of the study was to determine the effect of azithromycin on osteoclast formation and resorptive activity in an in vitro inflammatory environment.
Methods: Peripheral blood mononuclear cells were isolated from whole blood of healthy volunteers. The cells were stimulated with Porphyromonas gingivalis (P. gingivalis) LPS for 24 hours, then differentiated into osteoclasts with macrophage colony stimulating factor (M-CSF) and receptor activator of nuclear factor kappa B (RANK) ligand. The effects of azithromycin at concentrations of 20 and 40 μg/mL were tested. Immunohistochemistry was used to determine tartrate-resistant acid phosphatase (TRAP) expression, indicative of osteoclast formation. Dentine resorption assays were used to detect osteoclast activity and production of key inflammatory cytokines were measured using enzyme-linked immunosorbent assay’s.
Results: The results demonstrated that P. gingivalis LPS induced an "inflammation-like" milieu with significant increases in monocyte chemoattractant protein-1 (MCP-1), interleukin-1 beta (IL-1β) and interleukin-6 (IL-6) concentrations in cell supernatant compared to unstimulated control cells (p<0.05). Preliminary analyses suggest that azithromycin may modulate osteoclast formation and activity as evidenced by decreased TRAP staining and resorptive activity.
Conclusions: This study expands our current understanding of azithromycin’s effect on in vitro osteoclastogenesis. This may provide a basis for future targeted and clinically appropriate use of antibiotics in the management of non-responsive periodontitis.
Supported by the Australian Dental Research Foundation and Colin Cormie Scholarship (ADRF).