Pathogenesis of Important Virulence Factors of Porphyromonas gingivalis via Toll-Like Receptors

Abstract

Periodontitis is a common intraoral infection and is inextricably linked to systemic diseases. Recently, the regulation between host immunologic response and periodontal pathogens has become a hotspot to explain the mechanism of periodontitis and related systemic diseases. Since Porphyromonas gingivalis ( P. gingivalis ) was proved as critical periodontal pathogen above all, researches focusing on the mechanism of its virulence factors have received extensive attention. Studies have shown that in the development of periodontitis, in addition to the direct release of virulent factors by periodontal pathogens to destroy periodontal tissues, over-low or over-high intrinsic immune and inflammatory response mediated by Toll-like receptors (TLRs) can lead to more lasting destruction of periodontal tissues. It is very necessary to sort out how various cytopathic factors of P. gingivalis mediate inflammation and immune responses between the host through TLRs so as to help precisely prevent, diagnose, and treat periodontitis in clinic. This review summarizes the role of three most widely studied pathogenic factors produced by P. gingivalis (lipopolysaccharide, gingipains, pili) and their interactions with TLRs at the cellular and molecular level in the progress of periodontitis.

Persistent Exposure to Fusobacterium nucleatum Triggers Chemokine/Cytokine Release and Inhibits the Proliferation and Osteogenic Differentiation Capabilities of Human Gingiva-Derived Mesenchymal Stem Cells

“…Polymicrobial infection with Porphyromonas gingivalis and F. nucleatum has been shown to can aggravate periodontal alveolar bone loss and induce an increased inflammatory response in a mouse periodontitis model (Polak et al, 2009). The stimulatory mechanism of inflammatory bone resorption in periodontitis induced by P. gingivalis has been comprehensive reported (Hanazawa, 1998;Jia et al, 2019), whereas the defined effect of F. nucleatum on oral tissue destruction has rarely been explored. Our current study confirms that F. nucleatum significantly alters the biological properties of GMSCs by promoting cell migration and chemokine/cytokine release and decreasing the proliferation and osteogenic differentiation ability.…”

Periodontal disease and systemic health

“…P. gingivalis, Tanerella forsythensi and Troponema denticola, are directly associated with chronic periodontitis. A. actinomycetemcomitans has been observed in thee early stages of periodontal disease and in aggressive periodontitis (8,9). these bacterial species have the ability to activate local defense mechanisms, destroy the epithelium and other structures of the gingiva, while inactivating ther repairs systems.…”

“…activated neutrophils present at the site of inflammation are immobilized and produce reactive oxygen species (SrO) that are capable of destroying the pathogens. rOS overproduction can damage the surrounding host tissue (8)(9)(10).…”

“…are three important biological stages in the progression of periodontal disease: inflammation, connective tissue degradation and the last one bone turnover. Inflammation in periodontal disease is response to bacterial plaque acumulation, permanent presence of bacterial multispecies, leads to chronic inflammation and abundance of oral inflammatory biomarkers (6,8,9). Many studies have detected various inflammation biomarkers to be increased both saliva or gingival crevicular fluid (gCf) in patients with periodontitis.…”

Quercetin inhibits virulence properties of Porphyromas gingivalis in periodontal disease

“…P. gingivalis possesses various potential virulence factors including gingipain proteases, haemagglutinin, fimbriae, capsule, lipopolysacharides and major outer-membrane proteins to evade the host immune defense system and destroy host connective tissues 7 , 8 . One major virulence factor is gingipain proteases consist of lysine-specific protease (Lys-gingipain (Kgp)) and arginine-specific protease (Arg-gingipain (Rgp)).…”