Advances in the pathogenesis of periodontitis: summary of developments, clinical implications and future directions

Page, Roy C.; Offenbacher, Steven; Schroeder, Hubert E.; Seymour, G. J.; Kornman, Kenneth S.

doi:10.1111/j.1600-0757.1997.tb00199.x

Cited by 846 publications

(759 citation statements)

References 68 publications

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“…However, there are considerable quantitative differences in this regulatory capacity by the two 13 13 biofilms. The subgingival biofilm is more potent than the supragingival biofilm in this respect, causing a 4-fold greater RANKL/OPG ratio enhancement at 6 h, and a remarkable 112-fold after 24 h. The higher capacity of the subgingival biofilm to enhance the RANKL/OPG ratio and potentially bone resorption, is well in line with the strong association of subgingival biofilms with periodontitis [1,2,6], in which bone destruction is a major histopathological trait [26,27].…”

Section: Discussionmentioning

confidence: 88%

The RANKL–OPG system is differentially regulated by supragingival and subgingival biofilm supernatants

et al. 2011

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Periodontitis is an inflammatory condition that destroys the tooth supporting tissues, including the alveolar bone. It is triggered by polymicrobial biofilms attaching on tooth surfaces, which can be supragingival or subgingival. Bone resorption is triggered by receptor activator of NF-B ligand (RANKL) and blocked by its soluble decoy receptor osteoprotegerin (OPG), which are cytokines of the tumor necrosis factor ligand and receptor families, respectively. The present study aimed to comparatively investigate the effects of the Zürich in vitro supragingival and subgingival biofilm models, on RANKL and OPG gene expression in primary human gingival fibroblasts (GF) cultures. The cells were challenged with biofilm culture supernatants for up-to 24h. RANKL and OPG gene expression in the cells was analyzed by quantitative real-time polymerase chain reaction (qPCR) and their relative RANKL/OPG ratio was calculated. Both biofilm supernatants induced RANKL expression, but the subgingival caused a more pronounced up-regulation compared to the supragingival (10-fold at 6h and 100-fold at 24h). Changes in OPG expression in response to either biofilm were more limited. Accordingly, the subgingival biofilm caused a greater enhancement of the relative RANKL/OPG ratio (4-fold at 6h and 110-fold 24h). In conclusion, subgingival biofilms exhibit a stronger potency for inducing molecular mechanisms of bone resorption than supragingival biofilms, in line with their higher virulence nature for the development of periodontitis. AbstractPeriodontitis is an inflammatory condition that destroys the tooth supporting tissues, including the alveolar bone. It is triggered by polymicrobial biofilms attaching on tooth surfaces, which can be supragingival or subgingival. Bone resorption is triggered by RANKL and blocked by its soluble decoy receptor OPG, which are cytokines of the tumor necrosis factor ligand and receptor families, respectively. The present study aimed to comparatively investigate the effects of the Zürich in vitro supragingival and subgingival biofilm models, on RANKL and OPG gene expression in primary human GF cultures. The cells were challenged with the biofilms for up-to 24 hours. RANKL and OPG gene expression in the cells was analysed by qPCR and their relative RANKL/OPG ratio was calculated. Both biofilms induced RANKL expression, but the subgingival caused a more pronounced up-regulation compared to the supragingival (10-fold at 6 h and 100-fold at 24 h). Changes in OPG expression in response to either biofilm were more limited. Accordingly, the subgingival biofilm caused a greater enhancement of the relative RANKL/OPG ratio (4-fold at 6 h and 110-fold 24 h). In conclusion, subgingival biofilms exhibit a stronger potency for inducing molecular mechanisms of bone resorption than supragingival biofilms, in line with their higher virulence nature for the development of periodontitis.

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Section: Discussionmentioning

confidence: 88%

The RANKL–OPG system is differentially regulated by supragingival and subgingival biofilm supernatants

et al. 2011

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“…Immunohistochemistry studies reveal dense cellular infiltration, including numerous T and B cells in periodontitis lesions. In addition, high levels of inflammatory mediators such as IL-1␤, TNF-␣, PGE 2 , IFN-␥, and IL-8 can be detected in inflamed gingival tissues and gingival crevicular fluid (1,2).…”

Section: Il-8 and Ido Expression By Human Gingivalmentioning

confidence: 99%

IL-8 and IDO Expression by Human Gingival Fibroblasts via TLRs

Mahanonda

Sa‐Ard‐Iam

Montreekachon

et al. 2007

The Journal of Immunology

132

104

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Human gingival fibroblasts (HGFs), a predominant cell type in tooth-supporting structure, are presently recognized for their active role in the innate immune response. They produce a variety of inflammatory cytokines in response to microbial components such as LPS from the key periodontal pathogen, Porphyromonas gingivalis. In this study, we demonstrated that HGFs expressed mRNA of TLRs 1, 2, 3, 4, 5, 6, and 9, but not TLRs 7, 8, and 10. Stimulation of HGFs with highly purified TLR2 ligand (P. gingivalis LPS), TLR3 ligand (poly(I:C)), TLR4 ligand (Escherichia coli LPS), and TLR5 ligand (Salmonella typhimurium flagellin) led to expression of IL-8 and IDO. A potent TLR 9 ligand, CpG oligodeoxynucleotide 2006 had no effect, although HGFs showed a detectable TLR9 mRNA expression. No significant enhancement on IL-8 or IDO expression was observed when HGFs were stimulated with various combinations of TLR ligands. Surprisingly, the TLR9 ligand CpG oligodeoxynucleotide 2006 was able to specifically inhibit poly(I:C)-induced IL-8 and IDO expression. TNF-α enhanced TLR ligand-induced IL-8 production in HGFs, whereas IFN-γ enhanced TLR ligand-induced IDO expression. HGF production of IDO in response to P. gingivalis LPS, IFN-γ, or the two in combination inhibited T cell proliferation in MLRs. The observed T cell inhibition could be reversed by addition of either 1-methyl-dl-tryptophan or l-tryptophan. Our results suggest an important role of HGFs not only in orchestrating the innate immune response, but also in dampening potentially harmful hyperactive inflammation in periodontal tissue.

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“…Among those, periodontal diseases are complex polymicrobial inflammatory diseases associated with dysbiosis of the dental biofilm that induces a long-lasting chronic inflammation of the periodontal supporting tissues, leading to alveolar bone destruction, and eventual tooth loss [6]. Over the years, strong evidence has accumulated to indicate that the pathogenic microbiota and the chronic inflammation established in periodontitis contribute to the onset and/or progression of several systemic inflammatory diseases such as cardiovascular diseases [7,8], diabetes [9], obesity [10], metabolic syndrome [11], respiratory disease [12], cancer [13], chronic kidney disease (CKD) [14] and rheumatoid arthritis (RA) [15].…”

Section: Introductionmentioning

confidence: 99%

Defining the gut microbiota in individuals with periodontal diseases: an exploratory study

Lourenςo

Spencer

Alm

et al. 2018

Journal of Oral Microbiology

122

109

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Background: This exploratory study aimed to characterize the gut microbiome of individuals with different periodontal conditions, and correlate it with periodontal inflammation and tissue destruction.Methods: Stool samples were obtained from individuals presenting periodontal health (PH = 7), gingivitis (G = 14) and chronic periodontitis (CP = 23). The intestinal microbiome composition was determined by Illumina MiSeq sequencing.Results: A lower alpha-diversity in the gut microbiome of individuals with CP was observed, although no significant difference among groups was found (p > 0.01). Firmicutes, Proteobacteria, Verrucomicrobia and Euryarchaeota were increased, whereas Bacteroidetes were decreased in abundance in patients with periodontitis compared to PH. Prevotella (genus), Comamonadaceae (family) and Lactobacillales (order) were detected in higher numbers in G, while Bacteroidales (order) was predominant in PH (p < 0.01). Significant correlations (rho = 0.337–0.468, p < 0.01) were found between OTUs representative of periodontal pathogens and attachment loss. Mogibacteriaceae, Ruminococcaceae and Prevotella were able to discriminate individuals with periodontal diseases from PH (overall accuracy = 84%). Oral taxa were detected in high numbers in all stool samples.Conclusions: Individuals with periodontal diseases present a less diverse gut microbiome consistent with other systemic inflammatory diseases. High numbers of oral taxa related to periodontal destruction and inflammation were detected in the gut microbiome of individuals regardless of periodontal status.

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Advances in the pathogenesis of periodontitis: summary of developments, clinical implications and future directions

Cited by 846 publications

References 68 publications

The RANKL–OPG system is differentially regulated by supragingival and subgingival biofilm supernatants

The RANKL–OPG system is differentially regulated by supragingival and subgingival biofilm supernatants

IL-8 and IDO Expression by Human Gingival Fibroblasts via TLRs

Defining the gut microbiota in individuals with periodontal diseases: an exploratory study

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