May 29th, 2026
Teeth do age, becoming more brittle and prone to fracture as the cell populations of the dental pulp become less capable of conducting the necessary maintenance processes. This has only relatively recently become a topic of interest in the dental community, and so relatively little is understood in detail of the mechanisms of tooth aging. Researchers here identify loss of NFATC1 in dental pulp cells as a driver of age-related dysfunction in the maintenance of tooth structural properties, and show that this mechanism is in large part a downstream consequence of the presence of senescent cells in that tissue. Clearance of senescent cells via senolytic therapies reduces the impact of aging on teeth.
Although tooth aging is causally linked to age-associated dental degeneration and regenerative disability, its pathogenesis remains largely unelucidated, despite extensive documentation of its phenotypic alterations. Over time, alongside senescence of the mineralized parenchyma, dental pulp undergoes irreversible changes impairing its renewal capacity. This leads to brittle teeth prone to fracture and susceptible to damage as pulpal degeneration progresses and dentinogenesis fails. These age-related issues remain unresolved due to the unknown drivers. Recognition of this problem in dentistry is relatively recent, dating back only two decades.
