Figure 2.

Proposed model of A. actinomycetemcomitans and F. alocis interactions with the host within the gingival pocket. In the early stages of periodontitis, A. actinomycetemcomitans makes use of lactic acid produced by Streptococcus sp. as a nutrient to increase its numbers. A. actinomycetemcomitans releases OMVs that are packed with outer membrane proteins (Omp) OmpA1, Omp 100, and the virulence factors CdtB, and LtxA. Omp100 mediates initial adhesion of the bacterium, and OmpA1 binds to its putative ligand on gingival epithelial cells and induces F-actin rearrangements resulting in A. actinomycetemcomitans cells being internalized. Production of H₂O₂ by Streptococcus sp. causes A. actinomycetemcomitans to migrate deeper in the gingival pocket, where the bacterial cells are exposed to the host immune response. The release of CtdB in this environment inhibits phagocytosis and LtxA release by A. actinomycetemcomitans will promote neutrophil degranulation or cell death when present at high concentrations. The release of OMVs by A. actinomycetemcomitans or EVs by F. alocis might contribute to the pathogenicity of these organisms by evasion of the host immune response and promoting bone resorption.