Brännström's Hydrodynamic Theory of Dentin Sensitivity: Fluid Movement & Nerve Activation

Dentin is not a solid mineral mass; it is a porous, living tissue permeated by millions of microscopic channels called dentinal tubules. In the cervical root region exposed by gum recession, tubule density averages between 20,000 and 30,000 tubules per square millimeter.

Each tubule has an average diameter of 0.8 to 2.0 micrometers and spans the full distance from the outer cementum boundary to the inner dental pulp. Inside each tubule resides dentinal fluid (an extracellular fluid communicating with the pulpal interstitial space) and the cytoplasmic process of an odontoblast cell.

Brännström’s hydrodynamic theory provides the scientifically accepted mechanism for dentin hypersensitivity following gingival recession and cementum loss. The theory posits that external thermal, tactile, or osmotic stimuli cause rapid micro-displacement of fluid within open dentinal tubules.

Brännström's genius was recognizing that dentinal fluid obeys basic fluid mechanics (Poiseuille's law). When a cold liquid or burst of cold air touches an open tubule, the fluid contracts rapidly. Following capillary laws, this volumetric contraction pulls fluid outward toward the tooth surface at velocities of 2 to 3 millimeters per second.

This rapid fluid displacement creates mechanical shear stress at the base of the tubule. Wrapped around the odontoblastic cell bodies are unmyelinated endings of A-delta sensory nerve fibers (and some A-beta fibers). The hydrodynamic shear physically deforms these mechanosensitive nerve membranes, opening stretch-activated ion channels that fire an electrical action potential to the brain.

This inward or outward fluid movement deforms nerve terminals wrapped around odontoblast cell bodies within the subodontoblastic plexus of Raschkow. The resulting mechanical deformation activates mechanoreceptive A-beta and A-delta sensory nerve fibers, triggering sharp, rapid pulpal pain sensations.

Understanding hydrodynamic theory directly guides modern sensitivity treatments. Because fluid flow is proportional to the fourth power of the tubule radius, even partial occlusion of the tubule opening dramatically abolishes fluid movement and stops pain.

This explains why treatments that deposit calcium fluoride crystals, glutaraldehyde protein plugs, or resin adhesives provide immediate relief—they seal the hydraulic pipeline. In contrast, potassium nitrate toothpastes do not stop fluid flow; they diffuse potassium ions down the pipeline to raise the electrical firing threshold of the A-delta nerves.

Cold stimuli trigger outward fluid contraction, which elicits the fastest fluid velocity and consequently the most excruciating pain response in patients. Effective desensitizing agents work fundamentally by either occluding the open tubule lumens or chemically depolarizing nerve membrane potentials.

Dentin hypersensitivity is explained scientifically by the hydrodynamic theory formulated by Martin Brännström in the 1960s. Dentin is traversed by 20,000 to 45,000 microscopic tubules per square millimeter, each filled with dentinal fluid (an ultrafiltrate of plasma).

When physical, thermal, or osmotic stimuli are applied to an exposed root surface, they induce rapid shifts in dentinal fluid volume. Cold stimuli cause fluid contraction, generating an outward flow velocity of 2 to 3 millimeters per second; heat causes expansion, producing an inward flow.

This rapid fluid movement generates mechanical shear stresses against the odontoblast process and nearby nerve endings within the inner tubule and pulpal interface, triggering mechanosensitive ion channels.

The pain response in dentin hypersensitivity is mediated primarily by myelinated A-delta and unmyelinated A-beta sensory nerve fibers originating in the subodontoblastic plexus of Raschkow located in the dental pulp.

Terminal neurofilaments extend 100 to 200 micrometers into the pulpal end of dentinal tubules, intimately associated with the odontoblast cell membrane. When hydrodynamic fluid displacement deforms the odontoblast and its nerve terminal, mechanosensitive piezo channels and transient receptor potential (TRP) channels open, initiating rapid sodium influx.

This depolarizes the nerve membrane, transmitting a sharp, stabbing, short-duration pain signal along the trigeminal pathway to the primary somatosensory cortex.