A review of T helper 17 cell-related cytokines in serum and saliva in periodontitis

Medara, Nidhi; Lenzo, Jason C.; Walsh, Katrina A; Reynolds, Eric C.; Darby, Ivan; O'Brien-Simpson, Neil M

doi:10.1016/j.cyto.2020.155340

Cited by 16 publications

(10 citation statements)

References 397 publications

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“…However, the levels of IL-33 in GCF in the present study were higher in patients from G3 (OSA) and G4 (P-OSA) with positive correlations with periodontal parameters in PD in G3 (OSA) and PD and BOP (%) in G4 (P-OSA). In periodontitis, the expression of IL-33 in gingival epithelial and connective tissue cells acts as an alarmin of tissue damage for the immune system, inducing RANKL expression and triggering the recruitment of RANKL-expressing B and T cells [ 33 , 34 ]. Sozer et al (2018) reported serum IL-33 concentrations significantly higher in patients with OSA, and hypothesized that OSA influences the levels of IL-33 and is involved in the systemic inflammation produced in OSA [ 35 ].…”

Section: Discussionmentioning

confidence: 99%

“…Interestingly, TNF-α plays both anti-inflammatory and pro-inflammatory roles in inflammation: initiating a strong inflammatory response and regulating the intensity and duration of inflammatory processes, respectively. This cytokine plays a variety of roles in the development of periodontitis, including attracting cells to sites of tissue damage and inflammation, and promoting the breakdown of extracellular matrix and bone resorption by increasing the production of IL-1β, IL-6, collagenases, MMPs, and RANKL in gingival epithelial cells [ 33 ]. TNF-α levels in saliva and serum were not significantly different between patients with periodontitis and healthy patients; in fact, TNF-α levels were lower in periodontitis patients.…”

Section: Discussionmentioning

confidence: 99%

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Biomarkers for the severity of periodontal disease in patients with obstructive sleep apnea:IL-1 β, IL-6, IL-17A, and IL-33

Corral¹,

Daza²,

Jimenez³

et al. 2023

Heliyon

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Biomarkers for the severity of periodontal disease in patients with obstructive sleep apnea:IL-1 β, IL-6, IL-17A, and IL-33

Corral¹,

Daza²,

Jimenez³

et al. 2023

Heliyon

View full text Add to dashboard Cite

“…It is encoded by the TNFA gene located on chromosome 6p21 [ 107 ] and was first purified and characterized by Aggarwal et al in 1985 [ 108 ]. It is generally produced by macrophages [ 109 ], T cells and NK cells [ 110 ]; however, it can also be secreted by fibroblasts present in the periodontal ligament, gingival keratinocytes and osteoblasts [ 111 ]. It is first synthesized as a type II transmembrane protein on the cell surface of 27 kDa and consists of 233 amino acids, which undergo proteolytic cleavage between alanine 76 and valine 77 residues by a matrix metalloproteinase named the TNF-α, converting enzyme (TACE), releasing the soluble TNF-α homotrimer of 17 kDa, and consisting of 157 amino acids [ 112 ].…”

Section: Oral Biomarkersmentioning

confidence: 99%

Potential Impact of Prosthetic Biomaterials on the Periodontium: A Comprehensive Review

et al. 2023

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The success of a prosthetic treatment is closely related to the periodontal health of the individual. The aim of this article was to review and present the importance of prosthetic restorative materials on the condition of the periodontium, the changes that occur in the composition of the subgingival microbiota and the levels of inflammatory markers in gingival crevicular fluid. Articles on the influence of different prosthetic restorative materials on subgingival microbiota and proinflammatory cytokines were searched for using the keywords “prosthetic biomaterials”, “fixed prosthesis”, “periodontal health”, “subgingival microbiota”, “periodontal biomarkers” and “gingival crevicular fluid” in PubMed/Medline, Science Direct, Scopus and Google Scholar. The type of material used for prosthesis fabrication together with poor marginal and internal fit can result in changes in the composition of the subgingival microbiota, as well as increased accumulation and retention of dentobacterial plaque, thus favoring the development of periodontal disease and prosthetic treatment failure. Biological markers have helped to understand the inflammatory response of different prosthetic materials on periodontal tissues with the main purpose of improving their clinical application in patients who need them. Metal-free ceramic prostheses induce a lower inflammatory response regardless of the fabrication method; however, the use of CAD/CAM systems is recommended for their fabrication. In addition, it is presumed that metal-ceramic prostheses cause changes in the composition of the subgingival microbiota producing a more dysbiotic biofilm with a higher prevalence of periodontopathogenic bacteria, which may further favor periodontal deterioration.

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“…Homeostatic oral Th17 cells are commensal-independent and IL-6-dependent, whereas the development and maintenance of Th17 cell-associated periodontal diseases is largely dependent upon the local microbiomes and require a pro-inflammatory microenvironment ( 97 ). Many pro-inflammatory cytokines, including IL‐1β, IL‐6, IL‐21, IL‐22, IL‐23, and IL‐17, take part in the pathogenesis of periodontal diseases ( 98 ) ( Figure 2 ). These cytokines are either stimulated or balanced by the Th17 cell-associated immune responses.…”

Section: The Function Of Cd4 + T Cells In Periodon...mentioning

confidence: 99%

mTOR Signaling in the Regulation of CD4+ T Cell Subsets in Periodontal Diseases

Jiang

Huang

et al. 2022

Front. Immunol.

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Periodontal disease results from the inflammatory infiltration by the microbial community which is marked through tooth mobility and alveolar bone resorption. The inflammation in periodontal disease is mediated by CD4+ T cells through cytokine secretion and osteoclastogenetic activity. Historically, the inflammatory model in periodontal disease is described through disruption of the balance between two subsets of T helper cells which are T-helper type 1 (Th1) and T-helper type 2 (Th2). However, more and more studies have found that apart from subsets of helper T cells, regulatory T-cells and Th17 cells are also involved in the pathogenesis of periodontal diseases. Growing evidence proves that helper T cells differentiation, activation, and subset determination are under the strong impact of mTOR signaling. mTOR signaling could promote Th1 and Th17 cell differentiation and inhibit Treg commitment through different mTOR complexes, therefore we anticipate a regulation effect of mTOR signaling on periodontal diseases by regulating CD4+ T cell subsets. This review aims to integrate the topical researches about the role of different types of Th cells in the pathogenesis of periodontal diseases, as well as the regulation of mTOR signaling in the specification and selection of Th cell commitment.

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A review of T helper 17 cell-related cytokines in serum and saliva in periodontitis

Cited by 16 publications

References 397 publications

Biomarkers for the severity of periodontal disease in patients with obstructive sleep apnea:IL-1 β, IL-6, IL-17A, and IL-33

Biomarkers for the severity of periodontal disease in patients with obstructive sleep apnea:IL-1 β, IL-6, IL-17A, and IL-33

Potential Impact of Prosthetic Biomaterials on the Periodontium: A Comprehensive Review

mTOR Signaling in the Regulation of CD4+ T Cell Subsets in Periodontal Diseases

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