Maintaining homeostatic control of periodontal epithelial tissue

Chang, Ana M.; Kantrong, Nutthapong; Darveau, Richard P.

doi:10.1111/prd.12369

Cited by 17 publications

(13 citation statements)

References 101 publications

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“…For example, a study using the CRISPR/Cas9 system to engineer and test previously identified human haplotypes within the interleukin-8 gene (IL-8; also known as CXCL8) have provided new evidence of the active involvement of host genetics to increase neutrophil migration in vitro and hence its potential to influence an individual's susceptibility to disease [ 7 ]. Furthermore, there is growing awareness behind the host protective role of the microbial dental plaque biofilm as a key player for the maintenance of healthy homeostasis [ 8 , 9 ]. Studies by To et al and Myers et al have shown the unique immunosuppressive potential of healthy subgingival and supra-gingival plaque, respectively [ 10 , 11 ].…”

Section: Introductionmentioning

confidence: 99%

Clinically Healthy Human Gingival Tissues Show Significant Inter-individual Variability in GCF Chemokine Expression and Subgingival Plaque Microbial Composition

Bamashmous¹,

Kotsakis²,

Jain³

et al. 2021

Front. Oral. Health

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Aim: Clinically healthy gingival tissue is maintained through controlled regulation of host defense mechanisms against plaque biofilm overgrowth. One key component is the transit of neutrophils from the vasculature into gingival tissue where the expression of different neutrophil chemokines are tightly regulated. This cross-sectional study examines the inter-individual variability in chemokine profiles within gingival crevicular fluid (GCF) in relation to the subgingival bacterial community in a state of gingival health.Methods: Gingival crevicular fluid and subgingival plaque samples were collected from mesiobuccal surfaces of all six Ramfjord teeth of 20 systemically healthy individuals (14.55 ± 1.67 years). A multiplex immunoassay was carried out to quantify the expression of 40 different chemokines in the healthy gingival tissue. Neutrophils were assessed indirectly by myeloperoxidase (MPO) in GCF using traditional ELISA. Characterization of healthy subgingival plaque was conducted with the Illumina Miseq targeting the 16S rRNA gene.Results: In health, there are distinct variations within individual gingival crevicular fluid chemokine expression profiles, as well as in the concentration of neutrophils, that divided the participants into high or low chemokine expressing groups. Specifically, key differences were identified within MIF (2683.54 ± 985.82 pg per 30-s sample), IL-8/CXCL8 (170.98 ± 176.96 pg per 30-s sample), Gro-α/CXCL1 (160.42 ± 94.21 pg per 30-s sample), ENA-78/CXCL5 (137.76 ± 76.02 pg per 30-s sample), IL-1β (51.39 ± 37.23 pg per 30-s sample), TNF-α (1.76 ± 1.79 pg per 30-s sample), and IFN-γ (0.92 ± 0.54 pg per 30-s sample). Of these identified chemokines, the highest correlation was associated between IL-8/CXCL8 and neutrophils (r = 0.54, p = 0.014). Furthermore, species characterization of healthy subgingival plaque revealed significant inter-individual variability that identified two unique groups unrelated to the previously identified chemokine groups.Conclusion: The lack of concordance between the microbial composition and chemokine profile during health may be a reflection of the unique microbial composition of each individual coupled with variations within their host response, emphasizing the vast complexity of the defense mechanisms in place to maintain gingival health.

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Section: Introductionmentioning

confidence: 99%

Clinically Healthy Human Gingival Tissues Show Significant Inter-individual Variability in GCF Chemokine Expression and Subgingival Plaque Microbial Composition

Bamashmous¹,

Kotsakis²,

Jain³

et al. 2021

Front. Oral. Health

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“…There is a mutually beneficial relationship between the microbial community and the host ( Ye et al., 2013 ; Chang et al., 2021 ). For example, resident oral bacteria are able to prevent colonization by exogenous organisms, which have the potential to be pathogenic ( Shu et al., 2020 ).…”

Section: Oral Mucositismentioning

confidence: 99%

Roles of Toll-Like Receptors in Radiotherapy- and Chemotherapy-Induced Oral Mucositis: A Concise Review

Hao

Wang

et al. 2022

Front. Cell. Infect. Microbiol.

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Radiotherapy and/or chemotherapy-induced oral mucositis (RIOM/CIOM) is a common complication in cancer patients, leading to negative clinical manifestations, reduced quality of life, and impacting compliance with anticancer treatment. The composition and metabolic function of the oral microbiome, as well as the innate immune response of the oral mucosa are severely altered during chemotherapy or radiotherapy, promoting the expression of inflammatory mediators by direct and indirect mechanisms. Commensal oral bacteria-mediated innate immune signaling via Toll-like receptors (TLRs) ambiguously shapes radiotherapy- and/or chemotherapy-induced oral damage. To date, there has been no comprehensive overview of the role of TLRs in RIOM/CIOM. This review aims to provide a narrative of the involvement of TLRs, including TLR2, TLR4, TLR5, and TLR9, in RIOM/CIOM, mainly by mediating the interaction between the host and microorganisms. As such, we suggest that these TLR signaling pathways are a novel mechanism of RIOM/CIOM with considerable potential for use in therapeutic interventions. More studies are needed in the future to investigate the role of different TLRs in RIOM/CIOM to provide a reference for the precise control of RIOM/CIOM.

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“…Oral epithelial cells are sentinel cells provided with a multitude of PRRs and upon PAMP stimulation produce interleukins (ILs), in particular IL-8 ( 149 ). IL-8 is mostly recognised via the neutrophil chemokine receptor CXCR2, which play a crucial role for the neutrophil recruitment into periodontal crevice ( 150 ).…”

Section: Dysregulated Immunitymentioning

confidence: 99%

Neutrophils Orchestrate the Periodontal Pocket

et al. 2021

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The subgingival biofilm attached to tooth surfaces triggers and maintains periodontitis. Previously, late-onset periodontitis has been considered a consequence of dysbiosis and a resultant polymicrobial disruption of host homeostasis. However, a multitude of studies did not show “healthy” oral microbiota pattern, but a high diversity depending on culture, diets, regional differences, age, social state etc. These findings relativise the aetiological role of the dysbiosis in periodontitis. Furthermore, many late-onset periodontitis traits cannot be explained by dysbiosis; e.g. age-relatedness, attenuation by anti-ageing therapy, neutrophil hyper-responsiveness, and microbiota shifting by dysregulated immunity, yet point to the crucial role of dysregulated immunity and neutrophils in particular. Furthermore, patients with neutropenia and neutrophil defects inevitably develop early-onset periodontitis. Intra-gingivally injecting lipopolysaccharide (LPS) alone causes an exaggerated neutrophil response sufficient to precipitate experimental periodontitis. Vice versa to the surplus of LPS, the increased neutrophil responsiveness characteristic for late-onset periodontitis can effectuate gingiva damage likewise. The exaggerated neutrophil extracellular trap (NET) response in late-onset periodontitis is blameable for damage of gingival barrier, its penetration by bacteria and pathogen-associated molecular patterns (PAMPs) as well as stimulation of Th17 cells, resulting in further neutrophil activation. This identifies the dysregulated immunity as the main contributor to periodontal disease.

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Maintaining homeostatic control of periodontal epithelial tissue

Cited by 17 publications

References 101 publications

Clinically Healthy Human Gingival Tissues Show Significant Inter-individual Variability in GCF Chemokine Expression and Subgingival Plaque Microbial Composition

Clinically Healthy Human Gingival Tissues Show Significant Inter-individual Variability in GCF Chemokine Expression and Subgingival Plaque Microbial Composition

Roles of Toll-Like Receptors in Radiotherapy- and Chemotherapy-Induced Oral Mucositis: A Concise Review

Neutrophils Orchestrate the Periodontal Pocket

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