Evidence map›Paper›PMID 29289808›Full record

ArticleArchives of oral biology2018

MyD88-mediated innate sensing by oral epithelial cells controls periodontal inflammation.

Andrea E Delitto, Fernanda Rocha, Ann M Decker, Byron Amador, Heather L Sorenson, Shannon M Wallet

Abstract read
In one paragraph

Article in Archives of oral biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.2field-weighted citation impact, top 45% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

9 citing papers in PubMed, 11 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Article
  5. Article
  6. Probiotics During the Therapeutic Management of Periodontitis.Advances in experimental medicine and biology · 2022
    Review
  7. Article
  8. Immunological Pathways Triggered byMediators of inflammation · 2019
    Review
  9. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

Andrea E DelittoDepartment of Oral Biology, University of Florida, Gainesville, FL 32610, United States.
Fernanda RochaDepartment of Oral Biology, University of Florida, Gainesville, FL 32610, United States.
Ann M DeckerDepartment of Periodontology, University of Michigan, Ann Arbor, MI 48109, United States.
Byron AmadorDepartment of Oral Biology, University of Florida, Gainesville, FL 32610, United States.
Heather L SorensonDepartment of Oral Biology, University of Florida, Gainesville, FL 32610, United States.
Shannon M WalletDepartment of Oral Biology, University of Florida, Gainesville, FL 32610, United States. Electronic address: swallet@dental.ufl.edu.
University of Florida · USUniversity of Michigan–Ann Arbor · US

Funding

Comprehensive Training Program in Oral BiologyT90DE021990 · NIDCR · UNIVERSITY OF FLORIDA · PI Jose A Lemos · 2011 to 2026
$8.2M
Tissue-Targeted Enzyme for Localized Tryptophan Catabolism to Direct Subcutaneous and Oral Mucosal Inflammatory ResponsesR01DE027301 · NIDCR · UNIVERSITY OF FLORIDA · PI KESELOWSKY, BENJAMIN GEORGE · 2017 to 2020
$2.0M
Epithelial Cell Function in the Progression of Periodontal DiseaseR01DE023567 · NIDCR · UNIVERSITY OF FLORIDA · PI WALLET, SHANNON MARGARET · 2013 to 2016
$1.5M
Comprehensive Training Program in Oral BiologyR90DE022530 · NIDCR · UNIVERSITY OF FLORIDA · PI LEMOS, JOSE A · 2011 to 2025
$995k
NIDCR NIH HHS R01 DE023567NIDCR NIH HHS R01 DE027301NIDCR NIH HHS R90 DE022530NIDCR NIH HHS T90 DE021990
6 · The paper itself

Abstract

Periodontal diseases are a class of non-resolving inflammatory diseases, initiated by a pathogenic subgingival biofilm, in a susceptible host, which if left untreated can result in soft and hard tissue destruction. Oral epithelial cells are the first line of defense against microbial infection within the oral cavity, whereby they can sense the environment through innate immune receptors including toll-like receptors (TLRs). Therefore, oral epithelial cells directly and indirectly contribute to mucosal homeostasis and inflammation, and disruption of this homeostasis or over-activation of innate immunity can result in initiation and/or exacerbation of localized inflammation as observed in periodontal diseases. Dynamics of TLR signaling outcomes are attributable to several factors including the cell type on which it engaged. Indeed, our previously published data indicates that oral epithelial cells respond in a unique manner when compared to canonical immune cells stimulated in a similar fashion. Thus, the objective of this study was to evaluate the role of oral epithelial cell innate sensing on periodontal disease, using a murine poly-microbial model in an epithelial cell specific knockout of the key TLR-signaling molecule MyD88 (B6

Indexed as

Aggregatibacter actinomycetemcomitansAlveolar Bone LossAnimalsEpithelial CellsImmunity, InnateInflammationMiceMyeloid Differentiation Factor 88Periodontal DiseasesPorphyromonas gingivalisReal-Time Polymerase Chain ReactionSignal TransductionMyeloid Differentiation Factor 88Epithelial cellsHomeostasisInflammationMyD88Periodontal disease

Identifiers

PMID29289808
PMCPMC5816687
OpenAlexW2772688759

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.