Ecological considerations in the treatment of <i>Actinobacillus actinomycetemcomitans</i> and <i>Porphyromonas gingivalis</i> periodontal infections

Socransky, S. S.; Haffajee, A. D.; Ximénez‐Fyvie, Laurie Ann; Feres, Magda; Mager, Donna L.

doi:10.1111/j.1600-0757.1999.tb00165.x

Cited by 108 publications

(96 citation statements)

References 111 publications

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“…Presumably, they each play different, and potentially unique, roles in the ecosystem that develops within this niche in the oral cavity. Numerous investigations have noted a succession of bacterial species, which develop in an orderly fashion in the supragingival and subgingival areas of the gums and teeth (26,42). If the biofilm remains undisturbed, the bacterial mass accumulates and the bacteria multiply and metabolize in this ecology.…”

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confidence: 99%

“…The spirochetes are generally isolated during inflammation and disease, in contrast to healthy sites where few or no treponemes are isolated (41). Treponema pectinovorum and Treponema denticola are both gram-negative anaerobic spirochetes that are associated with adult and juvenile periodontitis (21,26,40,42). Generally, these species are isolated from the subgingival plaque along with a substantial variety of other genera and species that comprise the complex biofilm and create a milieu of nutrient and waste product interdependencies.…”

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confidence: 99%

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Cytokine Responses toTreponema pectinovorumandTreponema denticolain Human Gingival Fibroblasts

Nixon¹,

Steffen

Ebersole

2000

Infect Immun

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Human gingival fibroblasts were challenged with Treponema pectinovorum and Treponema denticola to test three specific hypotheses: (i) these treponemes induce different cytokine profiles from the fibroblasts, (ii) differences in cytokine profiles are observed after challenge with live versus killed treponemes, and (iii) differences in cytokine profiles are noted from different gingival fibroblast cell lines when challenged with these treponemes. Three normal gingival fibroblast cell cultures were challenged with T. pectinovorum and T. denticola strains, and the supernatants were analyzed for cytokine production (i.e., interleukin-1␣ [IL-1␣], IL-1␤, IL-6, IL-8, IL-10, gamma interferon, macrophage chemotactic protein 1 [MCP-1], platelet-derived growth factor, tumor necrosis factor alpha, and granulocyte-macrophage colony-stimulating factor). Unstimulated fibroblast cell lines produced IL-6, IL-8, and MCP-1. T. pectinovorum routinely elicited the greatest production of these cytokines from the fibroblast cell lines, increasing 10-to 50-fold over basal production. While T. denticola also induced IL-6 and IL-8 production, these levels were generally lower than those elicited by challenge with T. pectinovorum. MCP-1 levels were significantly lower after T. denticola challenge, and the kinetics suggested that this microorganism actually inhibited basal production by the fibroblasts. No basal or stimulated production of the other cytokines was observed. Significant differences were noted in the responsiveness of the various cell lines with respect to the two species of treponemes and the individual cytokines produced. Finally, dead T. pectinovorum generally induced a twofold-greater level of IL-6 and IL-8 than the live bacteria. These results supported the idea that different species of oral treponemes can elicit proinflammatory cytokine production by gingival cells and that this stimulation did not require live microorganisms. Importantly, a unique difference was noted in the ability of T. pectinovorum to induce a robust MCP-1 production, while T. denticola appeared to inhibit this activity of the fibroblasts. While the general cytokine profiles of the fibroblast cell cultures were similar, significant differences were noted in the quantity of individual cytokines produced, which could relate to individual patient variation in local inflammatory responses in the periodontium.

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confidence: 99%

Cytokine Responses toTreponema pectinovorumandTreponema denticolain Human Gingival Fibroblasts

Nixon¹,

Steffen

Ebersole

2000

Infect Immun

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“…Porphyromonasgingivalisis a Gram-negative anaerobic bacterium implicated as a major periodontal pathogen [18,19]. Recent studies demonstrated that P. gingivalisorchestrates inflammation through manipulation of host immunity and periodontal microbiota and that periodontal disease is initiated by polymicrobial synergy and dysbiosis [3,20].…”

Section: How Tlrs Activate Cytokine Production?mentioning

confidence: 99%

The Role of TLRs in the Pathogenesis of Periodontal Diseases

Gümüş¹

2016

J. Dent. Sci. Ther

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Periodontitis is a complex and multi-factorial inflammatory disease. Dysbiotic microbial communities of keystone pathogens induce host response, which are also responsible for tissuedestructive inflammation and inflammatory bone loss. Microbiata in the microbial dental biofilm stimulate innate immunity via the Toll-like receptor (TLR) family of pattern-recognition receptors. TLRs recognize the antigens and activate pro-inflammatory cytokines in the periodontal tissues. The transition from gingivitis to periodontitis requires both a dysbioticmicrobiota and a susceptible host. Understanding the role of TLRs signaling in the periodontal health and disease may be helpful for providing new insight to the pathogenesis of periodontitis and developing new therapeutic approaches.

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“…With regard to the disease process, the primary ecological niche of P. gingivalis is in the subgingival area, where toxic products, such as proteases, can readily access the periodontal tissues. However, initial colonization of the oral cavity by P. gingivalis involves attachment to sites remote from the subgingival area, including the supragingival tooth surface (28,39,43,47,57,58). Indeed, introduction of P. gingivalis into the mouths of human volunteers results in localization almost exclusively on supragingival surfaces (39).…”

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Porphyromonas gingivalis Genes Involved in Community Development with Streptococcus gordonii

et al. 2006

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Porphyromonas gingivalis, one of the causative agents of adult periodontitis, develops biofilm microcolonies on substrata of Streptococcus gordonii but not on Streptococcus mutans. P. gingivalis genome microarrays were used to identify genes differentially regulated during accretion of P. gingivalis in heterotypic biofilms with S. gordonii. Thirty-three genes showed up-or downregulation by array analysis, and differential expression was confirmed by quantitative reverse transcription-PCR. The functions of the regulated genes were predominantly related to metabolism and energy production. In addition, many of the genes have no current known function. The roles of two upregulated genes, ftsH (PG0047) encoding an ATP-dependent zinc metallopeptidase and ptpA (PG1641) encoding a putative tyrosine phosphatase, were investigated further by mutational analysis. Strains with mutations in these genes developed more abundant biofilms with S. gordonii than the parental strain developed. ftsH and ptpA may thus participate in a regulatory network that constrains P. gingivalis accumulation in heterotypic biofilms. This study provided a global analysis of P. gingivalis transcriptional responses in an oral microbial community and also provided insight into the regulation of heterotypic biofilm development.Periodontal diseases are a group of infections characterized by destruction of the supporting structures of the teeth. Porphyromonas gingivalis is a gram-negative anaerobe that is an important pathogen in severe manifestations of these diseases (15,41). With regard to the disease process, the primary ecological niche of P. gingivalis is in the subgingival area, where toxic products, such as proteases, can readily access the periodontal tissues. However, initial colonization of the oral cavity by P. gingivalis involves attachment to sites remote from the subgingival area, including the supragingival tooth surface (28,39,43,47,57,58). Indeed, introduction of P. gingivalis into the mouths of human volunteers results in localization almost exclusively on supragingival surfaces (39). The bacterial inhabitants of the supragingival tooth surface comprise a complex multispecies biofilm (42), and numerous in vitro studies have demonstrated the ability of P. gingivalis to attach to common constituents of the supragingival biofilm, including Actinomyces species and oral streptococci (12, 35). The molecular basis of P. gingivalis adhesion to Streptococcus gordonii has been investigated in some detail and has been shown to be multivalent (3,4,23,24,45). The P. gingivalis long fimbriae (FimA) bind to glyceraldehyde-3-phosphate dehydrogenase present on the streptococcal surface (27). In addition, the P. gingivalis short fimbriae (Mfa) engage the streptococcal SspA/B (antigen I/II) adhesins (33) through an approximately 80-amino-acid binding epitope of SspA/B termed BAR (11). Coadhesion mediated through these effectors is required for P. gingivalis to accumulate in a heterotypic biofilm with S. gordonii (23).In contrast to the synergistic rela...

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Ecological considerations in the treatment of Actinobacillus actinomycetemcomitans and Porphyromonas gingivalis periodontal infections

Cited by 108 publications

References 111 publications

Cytokine Responses toTreponema pectinovorumandTreponema denticolain Human Gingival Fibroblasts

Cytokine Responses toTreponema pectinovorumandTreponema denticolain Human Gingival Fibroblasts

The Role of TLRs in the Pathogenesis of Periodontal Diseases

Porphyromonas gingivalis Genes Involved in Community Development with Streptococcus gordonii

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