Mechanobiological and Molecular Alterations in the Aging Dentin-Pulp Complex

The dental pulp-dentin complex is a dynamic tissue system whose structure and biological functions evolve over time under physiological, molecular, and environmental influences. This study aimed to characterize age-related alterations in apoptotic, inflammatory, and autophagy-associated signaling pathways, alongside nanoscale mechanical changes, and to evaluate their potential impact on pulp tissue homeostasis and cellular adaptive capacity.

Human teeth (n = 90) were divided into three age groups: young (≤17 years), mature (18-50 years), and old (>51 years). Immunohistochemistry was performed to assess the expression of CD34, BID, Caspase-8, NFκB, STAT3, JAK1, COX-2, LAMP2, and MAP LC3II. Nanoindentation and atomic force microscopy (AFM) were used to measure dentin hardness and modulus of elasticity.

BID expression increased with age, whereas Caspase-8 showed a relative decrease (p < 0.05). Anterior teeth exhibited higher marker positivity than molars for BID (p = 0.029), Caspase-8 (p = 0.004), STAT3 (p = 0.001), and JAK1 (p = 0.026). Mechanical analysis revealed the lowest modulus of elasticity in young root dentin and the highest in old coronal dentin, reflecting progressive age-dependent structural changes.

Aging of the dentin-pulp complex involves coordinated modulation of apoptotic, autophagic, and inflammatory pathways, closely linked to altered mechanical properties. This interplay likely influences pulp vitality and adaptive cellular responses, highlighting potential targets for age-adapted dental therapeutic strategies.