Abstract: In autophagy, damaged proteins, organelles, and nutrients are transported to lysosomes for degradation, elimination, and recycling. This process is a highly conserved mechanism among eukaryotic cells. Inflammation is a vital protective host response to tissue damage and pathogenic infection. However, excessive inflammation can cause tissue damage and diseases. Autophagy inhibits the assembly of inflammasomes by degrading endogenous stimuli, including DNA and reactive oxygen species. This process also controls interleukin(IL)-1β secretion by targeting pro-IL-1β for degradation. Periodontal pathogens destroy periodontal tissues through the interaction of Toll-like receptor(TLR) with various components, such as lipopolysaccharide, peptidoglycan, and bacterial DNA. As a consequence, inflammatory cells are recruited and inflammatory cytokines are released. In local periodontal tissues, TLR or nucleotide-binding oligomerization domain-like receptor activates innate immune responses, induces autophagy-related pathways, and recognizes pathogen- and damage-associated molecular patterns. Autophagy can also influence inflammatory responses by negatively regulating TLR signals. This review focuses on recent progress in the mutual regulation of autophagy and inflammation. This review also describes the potential relations between autophagy and periodontitis to elucidate disease pathogenesis and to develop new therapies.

Key words: autophagy, inflammation, Toll-like receptor, periodontitis