ArticleJournal of dental research2020
Histone Methylation: Achilles Heel and Powerful Mediator of Periodontal Homeostasis.
Article in Journal of dental research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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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.
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.
Who cites it
17 citing papers in PubMed, 37 citations in OpenAlex.
- KDM6B/Pdk1 glycolytic pathway-driven ZEB2 lactylation promotes cellular cementum formation.International journal of oral science · 2026Article
- The role of genome-wide DNA methylation and polymorphisms in periodontitis etiology: A narrative review.Biomolecules & biomedicine · 2025Review
- Role and mechanisms of histone methylation in osteogenic/odontogenic differentiation of dental mesenchymal stem cells.International journal of oral science · 2025Review
- miR-708-3p targetedly regulates LSD1 to promote osteoblast differentiation of hPDLSCs in periodontitis.Odontology · 2025Article
- Interplay between epigenetics, senescence and cellular redox metabolism in cancer and its therapeutic implications.Redox biology · 2024Review
- Epigenetic alterations and advancement of lymphoma treatment.Annals of hematology · 2024Review
- Mesenchymal stem cells under epigenetic control - the role of epigenetic machinery in fate decision and functional properties.Cell death & disease · 2023Review
- Changes inGenes · 2023Article
- Review
- Epigenetics in susceptibility, progression, and diagnosis of periodontitis.The Japanese dental science review · 2022Review
- Study on Optimizing Novel Antimicrobial Peptides with Bifunctional Activity to Prevent and Treat Peri-Implant Disease.Antibiotics (Basel, Switzerland) · 2022Article
- Inhibition of NOS1 promotes the interferon response of melanoma cells.Journal of translational medicine · 2022Article
- Association between Maternal Periodontitis and Development of Systematic Diseases in Offspring.International journal of molecular sciences · 2022Review
- Epigenetic Regulation of Methylation in Determining the Fate of Dental Mesenchymal Stem Cells.Stem cells international · 2022Review
- Metabolic Remodeling Impacts the Epigenetic Landscape of Dental Mesenchymal Stem Cells.Stem cells international · 2022Review
- A Review of Antimicrobial Activity of Dental Mesenchymal Stromal Cells: Is There Any Potential?Frontiers in oral health · 2021Review
- Epigenetic regulation of inflammation in periodontitis: cellular mechanisms and therapeutic potential.Clinical epigenetics · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
The packaging of DNA around nucleosomes exerts dynamic control over eukaryotic gene expression either by granting access to the transcriptional machinery in an open chromatin state or by silencing transcription via chromatin compaction. Histone methylation modification affects chromatin through the addition of methyl groups to lysine or arginine residues of histones H3 and H4 by means of histone methyl transferases or histone demethylases. Changes in histone methylation state modulate periodontal gene expression and have profound effects on periodontal development, health, and therapy. At the onset of periodontal development, progenitor cell populations such as dental follicle cells are characterized by an open H3K4me3 chromatin mark on RUNX2, MSX2, and DLX5 gene promoters. During further development, periodontal progenitor differentiation undergoes a global switch from the H3K4me3 active methyl mark to the H3K27me3 repressive mark. When compared with dental pulp cells, periodontal neural crest lineage differentiation is characterized by repressive H3K9me3 and H3K27me3 marks on typical dentinogenesis-related genes. Inflammatory conditions as they occur during periodontal disease result in unique histone methylation signatures in affected cell populations, including repressive H3K9me3 and H3K27me3 histone marks on extracellular matrix gene promoters and active H3K4me3 marks on interleukin, defensin, and chemokine gene promoters, facilitating a rapid inflammatory response to microbial pathogens. The inflammation-induced repression of chromatin on extracellular matrix gene promoters presents a therapeutic opportunity for the application of histone methylation inhibitors capable of inhibiting suppressive trimethylation marks. Furthermore, inhibition of chromatin coregulators through interference with key inflammatory mediators such as NF-kB by means of methyltransferase inhibitors provides another avenue to halt the exacerbation of the inflammatory response in periodontal tissues. In conclusion, histone methylation dynamics play an intricate role in the fine-tuning of chromatin states during periodontal development and harbor yet-to-be-realized potential for the treatment of periodontal disease.
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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.