Cells that stop dividing help teeth emerge in mice
Mouse experiments found that suppressing senescence in tissue surrounding developing teeth delayed eruption, supporting its role in normal development.
Limit: The study examined tooth development, not effects on aging
Edited by Boris Djordjevic · AgingResearch.News
Experiments in mice showed that senescence, a state in which cells stop dividing, helped teeth erupt. Senescent cells progressively accumulated in the dental follicle, the tissue surrounding a developing tooth, during normal eruption. This accumulation was suppressed in mice with a disrupted copy of Runx2, a gene involved in tooth development. These mice had delayed tooth eruption.
Giving normal mice nicotinamide mononucleotide to inhibit dental follicle senescence also delayed eruption. Human dental follicle samples from people with cleidocranial dysplasia, a genetic disorder that can delay permanent teeth, had fewer cells positive for senescence markers than samples from healthy controls. Further experiments in dental follicle cells linked RUNX2 disruption to changes in chemical tags on DNA-packaging proteins and reduced senescence.
Why it matters
Senescence is relevant to aging biology, but it also participates in development. Understanding its role in tissue remodeling may help distinguish its useful functions from its roles in disease.
Caveats
The causal evidence came from mice; the human findings were comparisons between patients and healthy controls, not an intervention. The study examined tooth development, not aging.
- RUNX2
- Cellular senescence
- Epigenetic regulation of gene expression
- Delayed tooth eruption
- Cleidocranial dysplasia
- Mice
The paper
Cell Death Discovery, Oct 26, 2026, CC BY
