Abstract: Periodontal diseases are featured by chronic infection, inflammation and degeneration of the periodontal tissue that is induced by anaerobic gram-negative bacteria (e.g., Porphyromonas gingivalis). We have recently reported that butyrate, a metabolite produced by periodontopathic bacteria, induced death of the gingival epithelial cells mainly via autophagy. Another study showed that the release of high-mobility group box-1 (HMGB1), a molecule that acts as a group of proinflammatory cytokine when released extracellularly, was detected in the culture medium of gingival epithelial cells after butyrate-induced cell death. These results suggest a possible connection between autophagy and periodontal diseases.
P. gingivalis, a causative bacterium of periodontal diseases and butyrate producer, can persist and proliferate in host epithelial cells. The bacterium is internalized in phagosomes of the host cells and then transferred to autophagosomes, where it persists and proliferates. Inhibition of autophagy by 3-methyladenine or wortmannin caused lysosomal fusion with phagosomes containing P. gingivalis, and the lysosomal enzymes digest the bacterium. This suggests that P. gingivalis can utilize a part of the host autophagy mechanism for their own protection from being damaged by host anti-bacterial system.
In this chapter, we provide an overview of the relationship between autophagy and the processes of periodontal disease and propose a hypothesis for the mechanism of periodontal disease via autophagy.