Evidence map›Paper›PMID 24976068›Full record

ReviewMolecular oral microbiology2014

The inflammophilic character of the periodontitis-associated microbiota.

G Hajishengallis

Open access · bronzeAbstract readReview
In one paragraph

Review in Molecular oral microbiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 258 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
258citing papers in PubMed, 5 pooled it
23.3field-weighted citation impact, top 1% 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

258 citing papers in PubMed, 5 syntheses or guidelines pooled it, 391 citations in OpenAlex.

  1. Pooled it
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  13. Fermentation-Derived 6-Shogaol fromInternational journal of molecular sciences · 2026
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198 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

1 author at 1 institution in 1 country.

G HajishengallisDepartment of Microbiology, University of Pennsylvania School of Dental Medicine, Philadelphia, PA, USA.
University of Pennsylvania · US

Funding

P. gingivalis as a keystone pathogenR01DE015254 · NIDCR · UNIVERSITY OF PENNSYLVANIA · PI HAJISHENGALLIS, GEORGIOS · 2004 to 2018
$4.6M
Oral Immunity and Adjuvant ReceptorsR01DE017138 · NIDCR · UNIVERSITY OF PENNSYLVANIA · PI HAJISHENGALLIS, GEORGIOS · 2006 to 2014
$3.8M
Novel mechanisms and 'complement-ary' therapy in periodontitisR01DE021685 · NIDCR · UNIVERSITY OF PENNSYLVANIA · PI HAJISHENGALLIS, GEORGIOS · 2012 to 2016
$2.0M
NIDCR NIH HHS DE015254NIDCR NIH HHS DE017138NIDCR NIH HHS DE021685NIDCR NIH HHS R01 DE015254NIDCR NIH HHS R01 DE017138NIDCR NIH HHS R01 DE021685
6 · The paper itself

Abstract

In periodontitis, dysbiotic microbial communities exhibit synergistic interactions for enhanced protection from host defenses, nutrient acquisition, and persistence in an inflammatory environment. This review discusses evidence that periodontitis-associated communities are 'inflammo-philic' (=loving or attracted to inflammation) in that they have evolved to not only endure inflammation but also to take advantage of it. In this regard, inflammation can drive the selection and enrichment of these pathogenic communities by providing a source of nutrients in the form of tissue breakdown products (e.g. degraded collagen peptides and heme-containing compounds). In contrast, those species that cannot benefit from the altered ecological conditions of the inflammatory environment, or for which host inflammation is detrimental, are likely to be outcompeted. Consistent with the concept that inflammation fosters the growth of dysbiotic microbial communities, the bacterial biomass of human periodontitis-associated biofilms was shown to increase with increasing periodontal inflammation. Conversely, anti-inflammatory treatments in animal models of periodontitis were shown to diminish the periodontal bacterial load, in addition to protecting from bone loss. The selective flourishing of inflammophilic bacteria can perpetuate inflammatory tissue destruction by setting off a 'vicious cycle' for disease progression, in which dysbiosis and inflammation reinforce each other. Therefore, the control of inflammation appears to be central to the treatment of periodontitis, as it is likely to control both dysbiosis and disease progression.

Indexed as

DysbiosisInflammationMicrobiotaAlveolar Bone LossAnimalsAnti-Inflammatory AgentsBacterial LoadBiofilmsDisease Models, AnimalDisease ProgressionHost-Pathogen InteractionsHumansPeriodontitisPorphyromonas gingivalisAnti-Inflammatory AgentsdysbiosisinflammationperiodontitisP. gingivalisToll-like receptors

Identifiers

PMID24976068
PMCPMC4232466
OpenAlexW2169722961

What OpenQuestion holds

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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.