Evidence map›Paper›PMID 24338806›Full record

ReviewEuropean journal of immunology2014

Breaking bad: manipulation of the host response by Porphyromonas gingivalis.

George Hajishengallis, Richard J Lamont

Registry-linked trialAbstract readReview
In one paragraph

Review in European journal of immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05657015 (Lepidium Sativum Extract Versus Simvastatin as an Adjunctive Local Delivery Agents to Non-Surgical Periodontal Therapy), which is not on this map. Cited by 220 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
220citing papers in PubMed, 3 pooled it
–field-weighted citation impact
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.

NCT05657015 phase4completednot on this mapstarted 2021, after this paper: background citation

Lepidium Sativum Extract Versus Simvastatin as an Adjunctive Local Delivery Agents to Non-Surgical Periodontal Therapy: A Randomized Controlled Clinical Trial With Biochemical Analysis

TypeinterventionalSponsorAin Shams UniversityRan2021 to 2022Enrolled30ConditionsPeriodontitisArmsLepidium Sativum, Simvastatin
3 · Its place in the literature

Who cites it

220 citing papers in PubMed, 3 syntheses or guidelines pooled it.

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160 more citing papers are in PubMed but not listed here.

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

2 authors.

George HajishengallisDepartment of Microbiology, School of Dental Medicine, University of Pennsylvania, Philadelphia, PA, USA.
Richard J Lamont

Funding

MOLECULAR ASPECTS OF ORAL PLAQUE FORMATIONR01DE012505 · NIDCR · UNIVERSITY OF WASHINGTON · PI Richard J Lamont, JAN S POTEMPA · 1998 to 2026
$9.5M
P GINGIVALIS INTERACTIONS WITH GINGIVAL EPITHELIAL CELLSR01DE011111 · NIDCR · UNIVERSITY OF WASHINGTON · PI HARIBABU BODDULURI, Richard J Lamont · 1995 to 2026
$5.4M
P. gingivalis as a keystone pathogenR01DE015254 · NIDCR · UNIVERSITY OF PENNSYLVANIA · PI HAJISHENGALLIS, GEORGIOS · 2004 to 2018
$4.6M
Streptococcus-Candida Communication in Oral BiofilmsR01DE016690 · NIDCR · UNIVERSITY OF BRISTOL · PI JENKINSON, HOWARD F, LAMONT, RICHARD J · 2006 to 2016
$3.8M
Oral Immunity and Adjuvant ReceptorsR01DE017138 · NIDCR · UNIVERSITY OF PENNSYLVANIA · PI HAJISHENGALLIS, GEORGIOS · 2006 to 2014
$3.8M
P.gingivalis Interactions with Gingival Epithelial CellsR37DE011111 · NIDCR · UNIVERSITY OF LOUISVILLE · PI LAMONT, RICHARD J · 2009 to 2018
$3.6M
Role of JAKs in innate responses to P. gingivalisR01DE017921 · NIDCR · UNIVERSITY OF LOUISVILLE · PI LAMONT, RICHARD J · 2010 to 2019
$3.3M
Novel mechanisms and 'complement-ary' therapy in periodontitisR01DE021685 · NIDCR · UNIVERSITY OF PENNSYLVANIA · PI HAJISHENGALLIS, GEORGIOS · 2012 to 2016
$2.0M
Aging and novel therapeutic interventions in periodontal diseaseRC4DE021580 · NIDCR · UNIVERSITY OF PENNSYLVANIA · PI HAJISHENGALLIS, GEORGIOS · 2010 to 2010
$1.6M
Pathogenic mechanisms of F. alocisR21DE022867 · NIDCR · UNIVERSITY OF LOUISVILLE · PI LAMONT, RICHARD J · 2012 to 2013
$404k
NIDCR NIH HHS DE011111NIDCR NIH HHS DE012505NIDCR NIH HHS DE015254NIDCR NIH HHS DE016690NIDCR NIH HHS DE017138NIDCR NIH HHS DE017921NIDCR NIH HHS DE021580NIDCR NIH HHS DE021685NIDCR NIH HHS DE022867NIDCR NIH HHS R01 DE011111NIDCR NIH HHS R01 DE012505NIDCR NIH HHS R01 DE015254NIDCR NIH HHS R01 DE016690NIDCR NIH HHS R01 DE017138NIDCR NIH HHS R01 DE017921NIDCR NIH HHS R01 DE021685NIDCR NIH HHS R21 DE022867NIDCR NIH HHS R37 DE011111NIDCR NIH HHS RC4 DE021580
6 · The paper itself

Abstract

Recent metagenomic and mechanistic studies are consistent with a new model of periodontal pathogenesis. This model proposes that periodontal disease is initiated by a synergistic and dysbiotic microbial community rather than by a select few bacteria traditionally known as "periopathogens." Low-abundance bacteria with community-wide effects that are critical for the development of dysbiosis are now known as keystone pathogens, the best-documented example of which is Porphyromonas gingivalis. Here, we review established mechanisms by which P. gingivalis interferes with host immunity and enables the emergence of dysbiotic communities. We integrate the role of P. gingivalis with that of other bacteria acting upstream and downstream in pathogenesis. Accessory pathogens act upstream to facilitate P. gingivalis colonization and co-ordinate metabolic activities, whereas commensals-turned pathobionts act downstream and contribute to destructive inflammation. The recent concepts of keystone pathogens, along with polymicrobial synergy and dysbiosis, have profound implications for the development of therapeutic options for periodontal disease.

Indexed as

AnimalsCoinfectionDysbiosisHost-Pathogen InteractionsHumansInflammationPeriodontal DiseasesPorphyromonas gingivalisDysbiosisImmune subversionInflammationPeriodontitisP. gingivalis

Identifiers

PMID24338806
PMCPMC3925422

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Registered trials

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.