Evidence map›Paper›PMID 19493882›Full record

ReviewJournal of dental research2009

Epigenetics: connecting environment and genotype to phenotype and disease.

S P Barros, S Offenbacher

Registry-linked trialAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Journal of dental research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT01663298 (FGF2 Promoter Hypermethylation and Implant Wound Healing Among Smokers and Diabetics), which is not on this map. Cited by 93 papers.

0numbers the graph read from it
0cells of the map it votes in
93citing papers in PubMed
7.3field-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.

NCT01663298 completednot on this mapstarted 2010, after this paper: background citation

FGF2 Promoter Hypermethylation and Implant Wound Healing Among Smokers and Diabetics

TypeobservationalSponsorUniversity of North Carolina, Chapel HillRan2010 to 2016Enrolled44ConditionsSmoking, DiabetesArmsDental implant surgery
3 · Its place in the literature

Who cites it

93 citing papers in PubMed, 257 citations in OpenAlex.

  1. Article
  2. Brain-Behavior Relationships: Neural Mechanisms of Impulsivity and Compulsivity in Neuropsychiatric Disorders.Cognitive and behavioral neurology : official journal of the Society for Behavioral and Cognitive Neurology · 2025
    Review
  3. Review
  4. Article
  5. Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. DNA methylation in necrotizing enterocolitis.Expert reviews in molecular medicine · 2024
    Review
  12. Article
  13. Review
  14. Article
  15. Review
  16. Review
  17. Article
  18. AQP5-1364A/C Polymorphism AffectsInternational journal of molecular sciences · 2022
    Article
  19. Review
  20. Article

33 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 1 institution in 1 country.

S P BarrosCenter for Oral and Systemic Diseases, Department of Periodontology, School of Dentistry, University of North Carolina at Chapel Hill, Room 222, CB 7455, Chapel Hill, NC 27599, USA. barross@dentistry.unc.edu
S Offenbacher
University of North Carolina at Chapel Hill · US

Funding

Zonisamide in Patients with Neuropathic Pain Associated with Diabetic NeuropathyM01RR000046 · NCRR · UNIV OF NORTH CAROLINA CHAPEL HILL · PI JOY, MELANIE S · 1985 to 2008
$38.5M
NCRR NIH HHS M01 RR000046NCRR NIH HHS RR-00046NIDCR NIH HHS DE-01243
6 · The paper itself

Abstract

Genetic information is encoded not only by the linear sequence of DNA, but also by epigenetic modifications of chromatin structure that include DNA methylation and covalent modifications of the proteins that bind DNA. These "epigenetic marks" alter the structure of chromatin to influence gene expression. Methylation occurs naturally on cytosine bases at CpG sequences and is involved in controlling the correct expression of genes. DNA methylation is usually associated with triggering histone deacetylation, chromatin condensation, and gene silencing. Differentially methylated cytosines give rise to distinct patterns specific for each tissue type and disease state. Such methylation-variable positions (MVPs) are not uniformly distributed throughout our genome, but are concentrated among genes that regulate transcription, growth, metabolism, differentiation, and oncogenesis. Alterations in MVP methylation status create epigenetic patterns that appear to regulate gene expression profiles during cell differentiation, growth, and development, as well as in cancer. Environmental stressors including toxins, as well as microbial and viral exposures, can change epigenetic patterns and thereby effect changes in gene activation and cell phenotype. Since DNA methylation is often retained following cell division, altered MVP patterns in tissues can accumulate over time and can lead to persistent alterations in steady-state cellular metabolism, responses to stimuli, or the retention of an abnormal phenotype, reflecting a molecular consequence of gene-environment interaction. Hence, DNA epigenetics constitutes the main and previously missing link among genetics, disease, and the environment. The challenge in oral biology will be to understand the mechanisms that modify MVPs in oral tissues and to identify those epigenetic patterns that modify disease pathogenesis or responses to therapy.

Indexed as

EnvironmentChromatinDNA-Binding ProteinsDNA MethylationEpigenesis, GeneticGene ExpressionGene SilencingGenotypeHumansMouth DiseasesPhenotypeTranscriptional ActivationChromatinDNA-Binding Proteins

Identifiers

PMID19493882
PMCPMC3317936
OpenAlexW2086120628

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.