Evidence map›Paper›PMID 35754944›Full record

ReviewThe Japanese dental science review2022

Epigenetics in susceptibility, progression, and diagnosis of periodontitis.

Shigeki Suzuki, Satoru Yamada

Open access · goldAbstract readReview
In one paragraph

Review in The Japanese dental science review, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
6.7field-weighted citation impact, top 2% 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

30 citing papers in PubMed, 46 citations in OpenAlex.

  1. Article
  2. Review
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  7. Review
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  10. Review
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  12. Frontiers in pharmacology · 2025
    Article
  13. Review
  14. Article
  15. Article
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  19. Article
  20. Dental Stem Cells and Lipopolysaccharides: A Concise Review.International journal of molecular sciences · 2024
    Review
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 1 institution in 1 country.

Shigeki SuzukiDepartment of Periodontology and Endodontology, Tohoku University Graduate School of Dentistry, Sendai 980-8575, Japan.
Satoru YamadaDepartment of Periodontology and Endodontology, Tohoku University Graduate School of Dentistry, Sendai 980-8575, Japan.
Tohoku University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Periodontitis is characterized by irreversible destruction of periodontal tissue. At present, the accepted etiology of periodontitis is based on a three-factor theory including pathogenic bacteria, host factors, and acquired factors. Periodontitis development usually takes a decade or longer and is therefore called chronic periodontitis (CP). To search for genetic factors associated with CP, several genome-wide association study (GWAS) analyses were conducted; however, polymorphisms associated with CP have not been identified. Epigenetics, on the other hand, involves acquired transcriptional regulatory mechanisms due to reversibly altered chromatin accessibility. Epigenetic status is a condition specific to each tissue and cell, mostly determined by the responses of host cells to stimulations by local factors, like bacterial inflammation, and systemic factors such as nutrition status, metabolic diseases, and health conditions. Significantly, epigenetic status has been linked with the onset and progression of several acquired diseases. Thus, epigenetic factors in periodontal tissues are attractive targets for periodontitis diagnosis and treatments. In this review, we introduce accumulating evidence to reveal the epigenetic background effects related to periodontitis caused by genetic factors, systemic diseases, and local environmental factors, such as smoking, and clarify the underlying mechanisms by which epigenetic alteration influences the susceptibility of periodontitis.

Indexed as

5mC, 5-methylcytocineAP, aggressive periodontitisATAC-seq, assay for transposase-accessible chromatin sequencingceRNA, competing endogenous RNACP, chronic periodontitisDNA methylationECM, extracellular matrixEpigeneticsEpigenomeGWAS, genome-wide association studyH3K27ac, acetylation of histone H3 lysine 27H3K27me3, trimethylation of histone H3 lysine 27H3K4me3, trimethylation of histone H3 lysine 4H3K9ac, histone H3 lysine 9HATs, histone acetyltransferasesHDACs, histone deacetylasesHistone modificationslncRNAs, long ncRNAsLPS, lipopolysaccharidem6A, N6-methyladenosinencRNAs, non-coding RNAsPDL, periodontal ligamentPeriodontal ligamentPeriodontitissEV, small extracellular vesicles

Identifiers

PMID35754944
PMCPMC9218144
OpenAlexW4283075359

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.