Evidence map›Paper›PMID 33902163›Full record

ArticleJournal of periodontology2021

Dysbiosis revisited: Understanding the role of the oral microbiome in the pathogenesis of gingivitis and periodontitis: A critical assessment.

Frank A Scannapieco, Anna Dongari-Bagtzoglou

Open access · greenAbstract read
In one paragraph

Article in Journal of periodontology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
79citing papers in PubMed, 3 pooled it
10.9field-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

79 citing papers in PubMed, 3 syntheses or guidelines pooled it, 107 citations in OpenAlex.

  1. Pooled it
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  13. Observational
  14. Association of theInternational journal of molecular sciences · 2026
    Article
  15. [The Oral Microbiome: Maintenance of Homeostasis, Disease Associations, and Mechanisms of Pathogenesis].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2026
    Review
  16. Article
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  20. Iron Oxide-Based Magnetic Nanoparticles in Oral Infection Control.International journal of nanomedicine · 2026
    Review

19 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 at 2 institutions in 1 country.

Frank A ScannapiecoDepartment of Oral Biology, School of Dental Medicine, University at Buffalo, The State University of New York, Buffalo, NY.ORCID 0000-0002-8804-6593
Anna Dongari-BagtzoglouDepartment of Oral Health and Diagnostic Sciences, Division of Periodontology, UConn Health, Farmington, CT.
UConn Health · USUniversity at Buffalo, State University of New York · US

Funding

Oral Epithelial Cells, Candida and PMN ActivationR01DE013986 · NIDCR · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI Anna I Dongari-Bagtzoglou · 2000 to 2026
$9.2M
NIDCR NIH HHS R01 DE013986
6 · The paper itself

Abstract

This commentary provides background, historical context, and a critical assessment of the concept that microbial dysbiosis drives the pathogenesis of periodontal diseases. It is long known that periodontal pathogenesis is dependent on tooth-borne microbial biofilms (dental plaque) that trigger host inflammation resulting in periodontal destruction and tooth loss in some patients. Ecological principles governing plaque biofilm development, along with localized host responses, are both rooted in evolution. Interpretation of available evidence suggests that, in most patients, alveolar bone loss results from interactions of a highly diverse commensal microbiota with the host, and not from "overgrowth" of a few "pathobionts" that results in a "dysbiosis." Most previously described dysbiotic chronic diseases, for example, inflammatory bowel diseases and dermatitis, are characterized by decreased microbial diversity (likely due to frank overgrowth of one or a few microbial taxa). Most common forms of periodontitis do not appear to conform to this general principle, and the associated microbiome in fact almost always shows increased bacterial diversity compared with periodontal health. This diversity is driven by interactions of genetic and environmental factors working in concert within specific windows of time. Periodontal pathogenesis is likely the result of "personalized pathology," insofar as each patient likely has a variable constellation of microbes and host risk factors influencing specific tissue sites where disease activity occurs, and during a limited window of time (a tissue-destructive "burst"). The concept of cooperative virulence of higher abundance commensals in periodontal pathogenesis, which does not conform to the model of dysbiosis observed for other diseases, is discussed.

Indexed as

GingivitisMicrobiotaPeriodontal DiseasesPeriodontitisDysbiosisHumanscalculusgenomicshost-parasite interactionsmicrobiologypathogenesis of periodontal diseases

Identifiers

PMID33902163
PMCPMC8380683
OpenAlexW3158460262

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.