Biochemical and molecular characteristics of Porphyromonas gingivalis a key causative pathogen in periodontitis

Abstract

Periodontitis is an infection-driven inflammatory disease, which is characterized by gingival inflammation and bone loss. Periodontitis is associated with various systemic diseases, including cardiovascular, respiratory, musculoskeletal, and reproductive system-related abnormalities. The recent theory attributes the pathogenesis of periodontitis to oral microbial dysbiosis, in which Porphyromonas gingivalis acts as a critical agent by disrupting host immune homeostasis. Lipopolysaccharide, proteases, fimbriae, and some other virulence factors are among the strategies exploited by P. gingivalis to promote the bacterial colonization and facilitate the outgrowth of the surrounding microbial community. Virulence factors promote the coaggregation of P. gingivalis with other bacteria and the formation of dental biofilm. These virulence factors also modulate a variety of host immune components and subvert the immune response to evade bacterial clearance or induce an inflammatory environment. The antibody-based concept of P. gingivalis as a causative agent in human periodontitis is based on the humoral immune response; P. gingivalis is probably a causative agent in periodontal disease, and this humoral immune response is probably protective. P. gingivalis fimbriae promote monocytes and macrophage activation. Stimulation of memory T-cells derived from periodontitis patient with P. gingivalis has been shown to induce higher interleukin (IL)-4 production than in healthy controls. The induction of IL-4-producing memory T-cells in peripheral blood tended to coincide with that of autologous periodontitis lesion sites. The article focuses to discuss the virulence factors of periodontal pathogens, especially P. gingivalis, and their roles in regulating immune responses during periodontitis progression.