Activation of RANKL‐induced osteoclasts and memory T lymphocytes by Porphyromonas gingivalis is serotype dependant

Abstract

P. gingivalis serotypes K1 and K2, but not others, are associated with an increased production of the osteoclastogenesis-related factor RANKL. This important information suggests that these serotypes could elicit a greater bone resorption in vivo and have a role in the periodontitis pathogenesis.

Resident memory T cells: Possible players in periodontal disease recurrence

“…It has been shown that Trm cells produce IFN‐γ and that high expression of IFN‐γ is responsible for inflammatory bone loss . A higher frequency of CD4 memory T cells reactive to serotypes K1 and K2 of Porphyromonas gingivalis was detected in periodontitis tissue compared with healthy gingiva, suggesting a role of memory cells in the recurrence of periodontitis …”

Capsular‐defective Porphyromonas gingivalis mutant strains induce less alveolar bone resorption than W50 wild‐type strain due to a decreased Th1/Th17 immune response and less osteoclast activity

“…Bacterial encapsulation has long been recognized as a way to protect microorganisms from clearance by host immune defenses, by reducing the ability of immune cells to gain access to the bacteria, which leads to withstand bacterial phagocytosis. Encapsulation, however, also has a direct effect on eliciting host adaptive immune response through activation of effector Th1 and Th17 lymphocytes . In this context, this study sought to clarify whether capsular deficiency in P. gingivalis moderates the Th1‐ and Th17‐pattern of immune response during periodontitis and whether this immune attenuation is associated with less alveolar bone resorption.…”

“…It has been reported that capsule of the P. gingivalis W50 strain, belonging to the K1 serotype, is composed of mannuronic acid, glucuronic acid, galacturonic acid, galactose, and N‐acetylglucosamine, composition that differs from that of the other capsular serotypes . Thus, genetic variations in the capsular polysaccharide loci, which could be reflected in the differences in capsular sugar composition and structure, might be associated to differential immunostimulatory capacity between the different capsular serotypes and between the capsulated and non‐encapsulated strains of P. gingivalis , as it has been described in dendritic cells and T lymphocytes and also reported in the present investigation.…”

“…The capsule of all serotypes has been analyzed for the induction of immune response in macrophages, dendritic cells, and T lymphocytes, and it has been demonstrated that the capsule of the K1 serotype induces a higher Th1‐ and Th17‐pattern of immune response compared with the other serotypes . In addition, the encapsulated serotype K1 of P. gingivalis triggers a strong RANKL‐induced osteoclast differentiation and activity in vitro, and this increment was significantly higher than that induced by the other capsulated serotypes …”

“…[11][12][13] In addition, the encapsulated serotype K1 of P. gingivalis triggers a strong RANKL-induced osteoclast differentiation and activity in vitro, and this increment was significantly higher than that induced by the other capsulated serotypes. 14 Identification and characterization of the capsular polysaccharide (K-antigen) locus of P. gingivalis allowed the generation of strain W50 (serotype K1)-based isogenic capsular-deficient mutants. 15 The analysis of such mutants has shown that encapsulation deregulates the production of proinflammatory cytokines by fibroblasts and macrophages, 16,17 thus further demonstrating that encapsulation is a hallmark of virulence heterogeneity of P. gingivalis.…”