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Peer-reviewedCC BY 4.0Biomolecules

Synergistic Epigenetic and Post-Transcriptional Regulation of Alveolar Bone Resorption

  • Sennan Yang1,2,3
  • Xinyu Zhang1,2,3
  • Bowei Shi3
  • Wei Xu3
  • Shiyu Lin1,2,4
  • Jin Yang1,2,3
  • Xinyong Li1,2
  • Lemei Zhu1,2
  • Dan Luo1,2
4 affiliations
  1. 1Hunan Key Laboratory of the Research and Development of Novel Pharmaceutical Preparations, School of Public Health, Changsha Medical University, Changsha 410219, China
  2. 2Hunan Provincial University Key Laboratory of the Fundamental and Clinical Research on Neurodegenerative Diseases, Changsha Medical University, Changsha 410219, China
  3. 3School of Dental Medicine, Changsha Medical University, Changsha 410219, China
  4. 4School of Traditional Chinese Medicine, Changsha Medical University, Changsha 410219, China
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Abstract

Alveolar bone resorption, which accompanies periodontitis, post-extraction mechanical unloading, and aging-related inflammation, is governed by interacting epigenetic and post-transcriptional mechanisms. Evidence from DNA methylation, histone modification, non-coding RNA (ncRNA), RNA-binding protein, and N6-methyladenosine (m6A) studies indicates that these layers jointly regulate the balance between bone formation and resorption, although their causal hierarchy and tissue specificity remain incompletely defined. This review integrates that evidence into a graded framework that separates mechanisms demonstrated functionally in alveolar bone or periodontal models from those supported only by correlational data or extrapolated from long-bone, calvarial, and osteoporosis models, and assigns each mechanism to the cell types in which it has been demonstrated. Because the effects of individual regulators (for example, DNMTs, HDACs, and m6A writers) depend on cell type, differentiation stage, dose, and timing, conflicting reports are examined explicitly. We further dissect the bidirectional crosstalk between epigenetic modifiers and ncRNAs, distinguishing experimentally verified links from hypothetical ones, and critically assess emerging therapeutic strategies—small-molecule epigenetic inhibitors, oligonucleotide therapeutics, and biomaterial-assisted delivery—together with their safety and delivery barriers. By formalizing an evidence-graded conceptual framework, this review provides a basis for mechanism-based strategies against alveolar bone resorption.

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Cite

BibTeXRIS
BibTeX
@article{yang2026synergistic,
  title = {{Synergistic Epigenetic and Post-Transcriptional Regulation of Alveolar Bone Resorption}},
  author = {Sennan Yang and Xinyu Zhang and Bowei Shi and Wei Xu and Shiyu Lin and Jin Yang and Xinyong Li and Lemei Zhu and Dan Luo},
  journal = {Biomolecules},
  year = {2026},
  month = oct,
  doi = {10.3390/biom16111581},
  url = {https://www.mdpi.com/2218-273X/16/11/1581},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Synergistic Epigenetic and Post-Transcriptional Regulation of Alveolar Bone Resorption
AU  - Sennan Yang
AU  - Xinyu Zhang
AU  - Bowei Shi
AU  - Wei Xu
AU  - Shiyu Lin
AU  - Jin Yang
AU  - Xinyong Li
AU  - Lemei Zhu
AU  - Dan Luo
PY  - 2026
DA  - 2026/10/30
JO  - Biomolecules
DO  - 10.3390/biom16111581
UR  - https://www.mdpi.com/2218-273X/16/11/1581
AB  - Alveolar bone resorption, which accompanies periodontitis, post-extraction mechanical unloading, and aging-related inflammation, is governed by interacting epigenetic and post-transcriptional mechanisms. Evidence from DNA methylation, histone modification, non-coding RNA (ncRNA), RNA-binding protein, and N6-methyladenosine (m6A) studies indicates that these layers jointly regulate the balance between bone formation and resorption, although their causal hierarchy and tissue specificity remain incompletely defined. This review integrates that evidence into a graded framework that separates mechanisms demonstrated functionally in alveolar bone or periodontal models from those supported only by correlational data or extrapolated from long-bone, calvarial, and osteoporosis models, and assigns each mechanism to the cell types in which it has been demonstrated. Because the effects of individual regulators (for example, DNMTs, HDACs, and m6A writers) depend on cell type, differentiation stage, dose, and timing, conflicting reports are examined explicitly. We further dissect the bidirectional crosstalk between epigenetic modifiers and ncRNAs, distinguishing experimentally verified links from hypothetical ones, and critically assess emerging therapeutic strategies—small-molecule epigenetic inhibitors, oligonucleotide therapeutics, and biomaterial-assisted delivery—together with their safety and delivery barriers. By formalizing an evidence-graded conceptual framework, this review provides a basis for mechanism-based strategies against alveolar bone resorption.
SN  - 2218-273X
ER  -