Evidence map›Paper›PMID 41652412›Full record

ArticleBMC medical genomics2026

Genome-wide profiling of salivary promoter-region DNA methylation in periodontitis: the Tromsø Study.

Natalia Petrenya, Birgitta Jönsson, Elin Hadler-Olsen, Lena Larsson, Arnar Flatberg, Vidar Beisvåg, Gro Eirin Holde, Svetlana N Zykova, Farah Asa'ad

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Article in BMC medical genomics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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2 · The registry

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

9 authors.

Natalia PetrenyaThe Public Dental Health Service Competence Centre of Northern Norway (TkNN), P.O. Box 2406, Tromsø, N-9271, Norway. natalia.petrenya@tromsfylke.no.
Birgitta JönssonThe Public Dental Health Service Competence Centre of Northern Norway (TkNN), P.O. Box 2406, Tromsø, N-9271, Norway.
Elin Hadler-OlsenThe Public Dental Health Service Competence Centre of Northern Norway (TkNN), P.O. Box 2406, Tromsø, N-9271, Norway.
Lena LarssonDepartment of Periodontology, Institute of Odontology, The Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden.
Arnar FlatbergGenomics Core Facility, Department of Clinical and Molecular Medicine, Norwegian University of Science and Technology (NTNU), Trondheim, Norway.
Vidar BeisvågGenomics Core Facility, Department of Clinical and Molecular Medicine, Norwegian University of Science and Technology (NTNU), Trondheim, Norway.
Gro Eirin HoldeThe Public Dental Health Service Competence Centre of Northern Norway (TkNN), P.O. Box 2406, Tromsø, N-9271, Norway.
Svetlana N ZykovaThe Public Dental Health Service Competence Centre of Northern Norway (TkNN), P.O. Box 2406, Tromsø, N-9271, Norway.
Farah Asa'adDepartment of Oral Biochemistry, Institute of Odontology, The Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden. farah.asaad@gu.se.

Funding

TUA-Research Funding TUAGBG-71180/966377
6 · The paper itself

Abstract

backgroundMethylation of DNA is an epigenetic reversible process that regulates gene expression. Aberrant promoter methylation is associated with chronic inflammation; however, the genome-wide DNA promoter methylation signature in periodontitis remains unexplored.

methodsThe present study is an epigenome-wide association study (EWAS) aimed at investigating salivary DNA methylation patterns within gene promoter regions in individuals with Stage III/IV periodontitis compared to healthy controls. Cases (all available individuals with Stage III/IV and probing pocket depths (PPD) > 5 mm, n = 50, 48% women) were participants in an oral health examination (40–54-year-old subsample, n = 1668) of the population-based seventh survey of the Tromsø Study, conducted from 2015 to 2016. Periodontally healthy controls with similar age and sex to the cases (n = 50, 58% women) were randomly selected from the same subsample. We used the Illumina DNA methylation BeadChip technology, targeting ~ 935 K unique methylation sites. The R package RnBeads was used to study the difference in methylation. Separate lists of all significantly (comb.p.adj.fdr < 0.05) hypomethylated (hypoMPs, n = 3411) and hypermethylated (hyperMPs, n = 3437) promoters in participants with periodontitis relative to controls were used as inputs for enrichment analysis (g:Profiler) and network visualization (Cystoscape).

resultsGene ontology terms enriched among the hypoMPs included DNA biosynthesis, cell cycle/checkpoint, nuclear chromosome, endoplasmic reticulum, regulation of inflammatory response and leucocyte activation, cell adhesion, TRIF-dependent Toll-like receptor signaling, tyrosine phosphorylation of STAT proteins, regulation of PI3K/Akt, collagen extracellular matrix, and mucopolysaccharide metabolic process. HyperMPs were enriched in mRNA catabolism, mitochondrial electron transport, intrinsic apoptotic signaling, B-lymphocyte differentiation, actin cytoskeleton, regulation of extracellular matrix organization, epithelial-mesenchymal transition, ubiquitination, wound healing, acylglycerol metabolism, and serine/threonine signaling. NF-κB, GMEB-1, and IRF-8 were enriched in hypoMPs; ZFP85, ELF-5, and HNF4-alpha in hyperMPs.

conclusionsWe identified a differential DNA promoter methylation signature in participants with Stage III/IV periodontitis in middle adulthood. Our study highlights biological pathways involved in inflammation, immune response, tissue destruction, and repair that may be epigenetically dysregulated.

Indexed as

DNA MethylationGenome-Wide Association StudyPeriodontitisPromoter Regions, GeneticSalivaAdultCase-Control StudiesEpigenesis, GeneticFemaleHumansMaleMiddle AgedDNA methylationEnrichment analysisEpigenomicsIllumina methylation BeadChip technologyNetwork visualizationPeriodontitis

Identifiers

PMID41652412
PMCPMC13231653

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LicenceCC BY-NC-ND
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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.