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

Abstract

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.

Periodontopathogens Porphyromonas gingivalis and Fusobacterium nucleatum and Their Roles in the Progression of Respiratory Diseases

“…Although there are randomized controlled trials demonstrating that periodontal treatment improves lung function and reduces the frequency of pulmonary disease exacerbations [ 159 , 160 , 161 , 162 , 163 , 164 ], there is no clear evidence that the treatment against P. gingivalis and F. nucleatum reduces the risk or incidence of respiratory diseases. Gingipains and FadA are, respectively, the main virulence factors of P. gingivalis and F. nucleatum that induce the production of pro-inflammatory cytokines in the lower respiratory tract and lung and act synergistically with other respiratory pathogenic bacteria [ 165 , 166 ]. Thus, targeted therapy against key virulence factors produced by P. gingivalis and F. nucleatum , such as gingipains and FadA, may ameliorate respiratory diseases.…”

Porphyromonas gingivalis, a bridge between oral health and immune evasion in gastric cancer

“…The fact that distant organs can be affected emphasizes that P. gingivalis has systemic tumorigenic and tumor enhancer effects ( 39 – 41 ). The damage mechanisms of P. gingivalis may include biological processes such as modifying and evading the innate immune response, promoting inflammation, and suppressing apoptosis ( 42 , 43 ) ( Figure 1 ).…”

From Cells to Environment: Exploring the Interplay between Factors Shaping Bone Health and Disease

“…Osteoimmunity acts as the connecting link between the microbiota and the bone [ 82 ]. In instances of dysbiosis, harmful bacteria within the dental biofilm generate virulence factors that trigger inflammation in the periodontal tissues [ 85 ]. These factors encompass LPS, which activate the host’s immune reaction, inducing the release of pro-inflammatory cytokines such as IL-1, IL-6, and TNF-α.…”

“…These factors encompass LPS, which activate the host’s immune reaction, inducing the release of pro-inflammatory cytokines such as IL-1, IL-6, and TNF-α. These cytokines not only heighten inflammation within the periodontal region but also influence osteoclast function, promoting the breakdown of bone tissue [ 85 ]. The persistent and prolonged state of inflammation resulting from dysbiosis disturbs the equilibrium between formation and breakdown, ultimately resulting in a gradual loss of alveolar bone over an extended period.…”