Virulence Factors of the Periodontal Pathogens: Tools to Evade the Host Immune Response and Promote Carcinogenesis

Periodontitis is the most common chronic, inflammatory oral disease that affects more than half of the population in the United States. The disease leads to destruction of the tooth-supporting tissue called periodontium, which ultimately results in tooth loss if uncured. The interaction between the periodontal microbiota and the host immune cells result in the induction of a non-protective host immune response that triggers host tissue destruction. Certain pathogens have been implicated periodontal disease formation that is triggered by a plethora of virulence factors. There is a collective evidence on the impact of periodontal disease progression on systemic health. Of particular interest, the role of the virulence factors of the periodontal pathogens in facilitating the evasion of the host immune cells and promotion of carcinogenesis has been the focus of many researchers. The aim of this review is to examine the influence of the periodontal pathogens Aggregatibacter actinomycetemcomitans (A. actinomycetemcomitans), Porphyromonas gingivalis (P. gingivalis), and Fusobacterium nucleatum (F. nucleatum) in the modulation of the intracellular signaling pathways of the host cells in order to evade the host immune response and interfere with normal host cell death and the role of their virulence factors in this regard.

Automated summary

Periodontitis, a common chronic oral disease in the US, causes destruction of tooth-supporting tissue and can lead to tooth loss. The interaction between periodontal bacteria and immune cells triggers a harmful immune response and tissue destruction. Certain pathogens, such as A. actinomycetemcomitans, P. gingivalis, and F. nucleatum, have been linked to periodontal disease formation and their virulence factors play a role in evading immune response and promoting carcinogenesis. This review examines how these pathogens modulate host cell signaling pathways and interfere with normal cell death.