Figure 7
From: Expression of the Hutchinson-Gilford Progeria Mutation Leads to Aberrant Dentin Formation
Schematic working model proposing the major hypothesis. During initial dentinogenesis in WT, odontoblasts form a primary dentin until the tooth becomes functional. When contacts between antagonistic cusps are established, then the formation of secondary dentin starts immediately, and continues throughout life. However, in HGPS mice, progerin-induced cellular senescence of odontoblasts occurred by progerin results in impaired physiological secondary dentin formation, which is an intermediate outcome. Physiologically, this thinner dentin may be recognized as an injury, such as dentin trauma. Subsequently, odontoblast-like cells differentiated from dental pulp cells might rapidly produce tertiary dentin until the pulp is completely obliterated in the HGPS mice. Paracrine factors released from odontoblasts undergoing senescence accelerate tertiary dentin formation by stimulating odontogenic differentiation of pulp cells.
