Pathogenesis
The hydrodynamic theory (Brännström, 1966): dentinal tubules are fluid-filled. When an external stimulus (cold, air, sweet, pressure) is applied to exposed dentin, it causes rapid fluid movement WITHIN the tubules — either inward or outward depending on the stimulus.
This fluid movement mechanically stimulates A-delta nerve fibers at the inner end of the tubules (pulp-dentinal border), triggering a rapid, sharp pain — typically lasting <10-30 seconds and resolving when the stimulus is removed.
Cold stimuli cause fluid movement toward the pulp (thermal contraction of fluid); heat causes outward fluid movement; evaporation (air blast, dental drying) causes outward fluid movement due to surface drying.
C-fibers may also be involved in some cases, causing a slower, duller ache — but A-delta fiber stimulation is the primary mechanism for the characteristic sharp, immediate pain of DH.
Tubule occlusion — natural resolution: over time, the pulp attempts to protect itself by depositing reactionary dentin (tertiary dentin), narrowing and eventually sealing the tubules from the pulp side. This explains why many cases of DH gradually improve without treatment.