Dentin has a relatively high water content due to its tubular structur
e. Once dentin is exposed, this intratubular water is free to move in
response to thermal, osmotic, evaporative, or tactile stimuli. Fluid s
hifts across dentin are thought to cause sufficient shear forces on od
ontoblasts, nerve endings, nearby fibroblasts, and blood vessels to ca
use significant mechanical irritation, disruption, or damage, dependin
g on the magnitude of the fluid shift. Even in the absence of fluid sh
ifts, the water-filled tubules provide diffusion channels for noxious
(i.e., bacterial products) substances which diffuse inward toward the
pulp, where they can activate the immune system, provide chemotactic s
timuli, cytokine production, and produce pain and pulpal inflammation.
Viewed from this perspective, dentin is a poor barrier to external ir
ritants. However, pulpal tissues react to these challenges by increasi
ng the activity of nerves, blood vessels, the immune system, and inter
stitial fluid turnover, to make the exposed dentin less permeable eith
er physiologically, via increased outward fluid flow, or microscopical
ly, by lining tubules with proteins, mineral deposits, or tertiary den
tin, thereby enhancing the barrier properties of dentin, and providing
additional protection to pulpal tissues. These reactions involve dent
in and pulp, both in the initiation of the processes and in their reso
lution. These responses of the dental pulp to irritation of dentin dem
onstrate the dynamic nature of the pulpo-dentin complex.