Periodontitis is a chronic inflammatory condition that destroys the tooth‐supporting tissues and eventually leads to tooth loss. As one of the most prevalent oral conditions, periodontitis endangers the oral health of 70% of people throughout the world. Periodontitis is also related to various systemic diseases, such as diabetes mellitus, atherosclerosis, and rheumatoid arthritis, which not only has a great impact on population health status and the quality of life but also increases the social burden. Porphyromonas gingivalis (P. gingivalis) is a gram‐negative oral anaerobic bacterium that plays a key role in the pathogenesis of periodontitis. Porphyromonas gingivalis can express various of virulence factors to overturn innate and adaptive immunities, which makes P. gingivalis survive and propagate in the host, destroy periodontal tissues, and have connection to systemic diseases. Porphyromonas gingivalis can invade into and survive in host tissues by destructing the gingival epithelial barrier, internalizing into the epithelial cells, and enhancing autophagy in epithelial cells. Deregulation of complement system, degradation of antibacterial peptides, and destruction of phagocyte functions facilitate the evasion of P. gingivalis. Porphyromonas gingivalis can also suppress adaptive immunity, which allows P. gingivalis to exist in the host tissues and cause the inflammatory response persistently. Here, we review studies devoted to understanding the strategies utilized by P. gingivalis to escape host immunity. Methods for impairing P. gingivalis immune evasion are also mentioned.

Background Sialidase has an important role in the pathogenesis of periodontitis and Porphyromonas gingivalis is a sialidase‐producing organism implicated in periodontitis development. The aim of this study was to evaluate the anti‐virulence and anti‐inflammatory properties of the sialidase inhibitor, 2‐deoxy‐2,3‐didehydro‐N‐acetylneuraminic acid (DANA), in vitro and in vivo. Methods The effects of DANA on P. gingivalis sialidase and cell viability were determined, and the effects of DANA on P. gingivalis virulence were evaluated by assessment of growth curves, cell morphology, biofilm formation, fimbriae gene expression, and gingipains and lipopolysaccharide (LPS) activity. Anti‐inflammatory effects of DANA on LPS‐induced macrophages were assessed by measurement of tumor necrosis factor‐alpha (TNF‐α), interleukin (IL‐1β), inducible nitric oxide synthase (iNOS) secretions. The effect of DANA on P. gingivalis–induced periodontitis in rats was analyzed by radiography, stereoscopic microscopy, histopathology, and immunohistochemistry. Results Sialidase inhibition rate of 1mM DANA was 72.01%. Compared with untreated controls, treatment with DANA inhibited P. gingivalis growth and biofilm formation, and significantly decreased expression of the fimA, fimR, and fimS genes, as well as gingipains activity. DANA did not influence macrophage viability, but significantly inhibited TNF‐α, IL‐1β, and iNOS production in LPS‐stimulated macrophages. In the periodontitis rat model, DANA prevented alveolar bone absorption and inhibited TNF‐α and IL‐1β production. Conclusion DANA can reduce the growth, the biofilm formation and the virulence of P. gingivalis and exhibits anti‐inflammatory effects, as well as effects against rat periodontitis, suggesting that DANA should be considered for development as a new adjunctive treatment for periodontitis.

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