Evidence map›Paper›PMID 25077073›Full record

ReviewFrontiers in cellular and infection microbiology2014

Historical and contemporary hypotheses on the development of oral diseases: are we there yet?

Bob T Rosier, Marko De Jager, Egija Zaura, Bastiaan P Krom

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in cellular and infection microbiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 102 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
102citing papers in PubMed, 4 pooled it
11.1field-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

102 citing papers in PubMed, 4 syntheses or guidelines pooled it, 196 citations in OpenAlex.

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  4. Meta-analysis of caries microbiome studies can improve upon disease prediction outcomes.APMIS : acta pathologica, microbiologica, et immunologica Scandinavica · 2022
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  9. Multicohort external validation ofFrontiers in cellular and infection microbiology · 2026
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42 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

4 authors at 1 institution in 2 countries.

Bob T RosierDepartment of Preventive Dentistry, Academic Centre for Dentistry Amsterdam (ACTA), University of Amsterdam and Free University Amsterdam Amsterdam, Netherlands.
Marko De JagerPhilips Research Eindhoven, Netherlands.
Egija ZauraDepartment of Preventive Dentistry, Academic Centre for Dentistry Amsterdam (ACTA), University of Amsterdam and Free University Amsterdam Amsterdam, Netherlands.
Bastiaan P KromDepartment of Preventive Dentistry, Academic Centre for Dentistry Amsterdam (ACTA), University of Amsterdam and Free University Amsterdam Amsterdam, Netherlands.
Philips (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dental plaque is an oral biofilm that much like the rest of our microbiome has a role in health and disease. Specifically, it is the cause of very common oral diseases such as caries, gingivitis, and periodontitis. The ideas about oral disease development have evolved over time. In the nineteenth century, scientists could not identify bacteria related to disease due to the lack of technology. This led to the "Non-Specific Plaque Hypothesis" or the idea that the accumulation of dental plaque was responsible for oral disease without discriminating between the levels of virulence of bacteria. In the twentieth century this idea evolved with the techniques to analyze the changes from health to disease. The first common hypothesis was the "Specific Plaque Hypothesis" (1976) proposing that only a few species of the total microflora are actively involved in disease. Secondly, the "Non-Specific Plaque Hypothesis" was updated (1986) and the idea that the overall activity of the total microflora could lead to disease, was enriched by taking into account difference in virulence among bacteria. Then, a hypothesis was considered that combines key concepts of the earlier two hypotheses: the "Ecological Plaque Hypothesis" (1994), which proposes that disease is the result of an imbalance in the microflora by ecological stress resulting in an enrichment of certain disease-related micro-organisms. Finally, the recent "Keystone-Pathogen Hypothesis" (2012) proposes that certain low-abundance microbial pathogens can cause inflammatory disease by interfering with the host immune system and remodeling the microbiota. In this comprehensive review, we describe how these different hypotheses, and the ideas around them, arose and test their current applicability to the understanding of the development of oral disease. Finally, we conclude that an all-encompassing ecological hypothesis explaining the shifts from health to disease is still lacking.

Indexed as

Dental CariesDental PlaqueHumansMouth DiseasesPeriodontal Diseasesdental plaqueecological plaque hypothesiskeystone pathogen hypothesisnon-specific plaque hypothesisspecific plaque hypothesis

Identifiers

PMID25077073
PMCPMC4100321
OpenAlexW2058313496

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.