Complex Intratissue Microbiota Forms Biofilms in Periodontal Lesions

Baek, Keumjin; Ji, Sang-Hoon; Choi, Youngnim

doi:10.1177/0022034517732754

Cited by 32 publications

(47 citation statements)

References 41 publications

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“…The characteristics of the intratissue bacterial communities in OLP lesions were quite different from those in periodontitis lesions 11 . The bacterial communities within the gingival tissues had similar alpha diversities but decreased beta diversities compared with the plaque communities.…”

Section: Discussionmentioning

confidence: 75%

“…isolation of E. coli strains from OLP tissues. We previously reported that a key periodontal pathogen, Porphyromonas gingivalis, invades gingival tissues and is highly enriched in the intratissue bacterial communities at periodontal lesions 11,12 . Similarly, a species enriched within the tissues of OLP lesions may have a role in the pathogenesis of OLP.…”

Section: Resultsmentioning

confidence: 99%

“…The bacterial communities within the gingival tissues had similar alpha diversities but decreased beta diversities compared with the plaque communities. In addition, Fusobacterium nucleatum and P. gingivalis, the two species highly enriched within gingival tissues, accumulate in the subgingival plaque when the periodontal status converts from health to periodontitis 11,22 . Although periodontitis is a polymicrobial infection, P. gingivalis serves as a multipotent pathogen that drives the dysbiosis of the subgingival microbiome, damages the epithelial barriers with powerful proteinases, invades gingival tissues, and evades host immunity to cause persistent infection 13,[23][24][25][26] .…”

Section: Discussionmentioning

confidence: 99%

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Characterization of intratissue bacterial communities and isolation of Escherichia coli from oral lichen planus lesions

Baek

Lee

et al. 2020

Sci Rep

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Oral lichen planus (OLP) is a chronic T cell-mediated inflammatory disease of unknown etiology. We previously proposed that the intracellular bacteria detected in oLp lesions are important triggering factors for T cell infiltration. This study aimed to identify OLP-associated bacterial species through the characterization of intratissue bacterial communities of OLP lesions. Seven pairs of bacterial communities collected from the mucosal surface and biopsied tissues of oLp lesions were analyzed by high-throughput sequencing of the 16S rRNA gene. The intratissue bacterial communities were characterized by decreased alpha diversity but increased beta diversity compared with those on the mucosal surface. While the relative abundance of most taxa was decreased within the tissues, that of Escherichia coli was significantly increased. Four E. coli strains were isolated from additional OLP biopsies and verified as K12 strains by whole-genome sequencing. The distribution of E. coli in sections of control (n = 12) and OLP (n = 22) tissues was examined by in situ hybridization. E. coli was detected in most OLP tissues, suggesting its potential role in the pathogenesis of OLP. The oral E. coli strains isolated from oLp tissues will be useful to investigate their role as triggering factors for t cell infiltration. Oral lichen planus (OLP) is a T cell-mediated chronic mucocutaneous disease of unknown etiology and is currently incurable. OLP occurs in 0.5-4% of the global population and appears more prevalent in females than males at a ratio of 1.5:1 1-3. The main histological features of OLP include band-like lymphocytic infiltration at the superficial part of connective tissue, the presence of liquefaction degeneration in the basal cell layer and the absence of epithelial dysplasia 4. Although the etiology and pathogenesis of OLP are not completely understood, unknown antigens are thought to trigger T cell infiltration and inflammatory responses of infiltrated lymphocytes such as CD4 + and CD8 + T cells 5. What triggers the activation and recruitment of T cells is an important question to find new therapeutics for OLP. Recently, many researchers have attempted to understand the relationship between human diseases and the human microbiome through high-throughput sequencing technology. To date, four research groups have studied the oral microbiota associated with OLP by sequencing the 16S rRNA gene, and differences in the microbiota of saliva and buccal mucosa between healthy controls and OLP patients have been reported 2,6-9. We previously reported increased bacterial invasion into the lamina propria, the presence of bacteria within basal epithelial cells and T cells in OLP lesions, and the induction of T cell chemokines by oral bacteria 6. In addition, Mizuki et al. reported that Mycoplasma salivarium was detected by immunohistochemistry in the epithelium and lymphocyte infiltrate area in 58.5% of OLP tissues from Japanese patients 10. These results suggest that oral bacteria may have a role in the pathogenesis of OLP. Howeve...

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Section: Discussionmentioning

confidence: 75%

Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Characterization of intratissue bacterial communities and isolation of Escherichia coli from oral lichen planus lesions

Baek

Lee

et al. 2020

Sci Rep

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“…Porphyromonas gingivalis exploits various mechanisms to subvert the host innate immune response and therefore alone it may not induce sufficient inflammation to cause alveolar bone loss. Porphyromonas gingivalis ‐induced alveolar bone loss is dependent on the invasion of periodontal tissues by commensal bacteria . Incorporating the findings from the present study, QSIs could re‐establish bacterial communities within periodontal tissues that are favorable for periodontal health through a reduction of the total bacterial invasion of periodontal tissues.…”

Section: Discussionmentioning

confidence: 52%

Effects of quorum‐sensing inhibition on experimental periodontitis induced by mixed infection in mice

Amara

Song

et al. 2018

European J Oral Sciences

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This study aimed to verify, in in vivo settings, whether quorum-sensing inhibition molecules could attenuate alveolar bone loss induced by Porphyromonas gingivalis/Fusobacterium nucleatum co-infection and reduce the bacterial colonization of periodontal tissues. In BALB/c mice, periodontitis was induced through oral inoculation with P. gingivalis and F. nucleatum six times during a 42-d period. Quorum sensing inhibitors (a furanone compound and D-ribose) were administered simultaneously with bacterial infection. Linear and volumetric modifications of interproximal alveolar bone levels were compared between groups using micro-computed tomography. Total bacteria, and P. gingivalis and F. nucleatum DNA in periodontal tissues, were quantified using real-time PCR. Radiographic linear measurements demonstrated a significant reduction of alveolar bone loss, of approximately 40%, in mice treated with quorum sensing inhibitors when compared with the co-infection group. This was confirmed by a significant increase of residual bone volume in the test group. While total bacterial genes in the treatment group significantly decreased by 93% in periodontal tissue samples when quorum sensing inhibitors were administered, no significant differences of P. gingivalis DNA were found. Quorum sensing inhibitors reduced periodontal breakdown and bacterial infection in periodontal tissues after co-infection with P. gingivalis and F. nucleatum.

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“…Patients with acute rheumatic fever had higher levels of serum antibodies that react with ENO1 and bacterial enolase than did patients with streptococcal pharyngitis or healthy control subjects, suggesting the role of streptococcal enolase as a cross-reactive antigen in post-streptococcal autoimmune diseases [23]. The gingival tissues of periodontal lesions are infected with complex bacterial communities, including T. denticola and P. gingivalis , and patients with periodontitis frequently experience bacteremia after tooth brushing or even chewing [24,25]. Although TdEno has the highest homology with ENO1 among the enolases of human-associated bacteria, it is expected that not only TdEno but also the enolases of diverse periodontitis-associated bacteria contribute to the production of anti-ENO1 antibodies in periodontitis.…”

Section: Discussionmentioning

confidence: 99%

Treponema denticola enolase contributes to the production of antibodies against ENO1 but not to the progression of periodontitis

et al. 2018

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Autoantibodies against alpha-enolase (ENO1) are often detected in various infectious and autoimmune diseases. Anti-ENO1 antibody titers were reported to be associated with the severity of periodontitis in patients with rheumatoid arthritis. Because the enolase of the periodontal pathogen Treponema denticola (TdEno) has the highest homology with ENO1 among the enolases of human-associated bacteria, we hypothesized that anti-ENO1 autoantibodies produced during the immune response to TdEno may contribute to the progression of periodontitis and tested it in human and mouse systems. In human subjects with healthy periodontium or chronic periodontitis, a strong positive correlation between the levels of anti-TdEno and anti-ENO1 antibodies was observed. In addition, the purified anti-TdEno antibodies recognized ENO1 as well as TdEno in a dot blot, confirming the cross-reactivity between TdEno and ENO1. However, anti-ENO1 antibody titers were not associated with the severity of periodontitis. To further investigate the role of TdEno in the production of anti-ENO1 antibodies and the progression of periodontitis, mice received an oral gavage of P. gingivalis alone, subcutaneous immunization with TdEno alone, or both P. gingivalis oral gavage and TdEno immunization. Immunization with TdEno induced not only anti-TdEno but also anti-mouse Eno1 (mEno1) antibodies and increased the expression of TNFα in the gingival tissues. However, alveolar bone loss was not increased by TdEno immunization. In conclusion, autoreactive anti-ENO1/mEno1 antibodies that are produced as byproducts during the antibody response to TdEno play a minimal role in the progression of periodontitis in the absence of rheumatoid arthritis.

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Complex Intratissue Microbiota Forms Biofilms in Periodontal Lesions

Cited by 32 publications

References 41 publications

Characterization of intratissue bacterial communities and isolation of Escherichia coli from oral lichen planus lesions

Characterization of intratissue bacterial communities and isolation of Escherichia coli from oral lichen planus lesions

Effects of quorum‐sensing inhibition on experimental periodontitis induced by mixed infection in mice

Treponema denticola enolase contributes to the production of antibodies against ENO1 but not to the progression of periodontitis

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