A variety of theories have been suggested to help explain the mechanism involved in the etiology of dentinal hypersensitivity.11 The transducer theory, the modulation theory, the “gate” control and vibration theory, and the hydrodynamic theory have all been presented and discussed throughout the years. The latter, “hydrodynamic theory”, developed in the 1960’s and based upon two decades of research, is now widely accepted as the cause of tooth sensitivity.12 The hydrodynamic theory asserts that when the fluid within the dentinal tubules, absent of a smear layer, is subjected to thermal, chemical, tactile or evaporative stimuli, the movement of the fluid stimulates the mechanical receptors which are sensitive to fluid pressure, resulting in the transmission of the stimuli to the pulpal nerves (Figure 2) ultimately causing the pain response.11

Figure 2.  Depiction of Brannstrom’s Hydrodynamic Theory.
Image: Brannstrom’s Hydrodynamic Theory

Berman11 describes thisreaction as:

“The coefficient of thermal expansion of the tubule fluid is about ten times that of the tubule wall. Therefore, heat applied to dentin will result in expansion of the dentinal fluid, and a cold stimulus will result in contraction of the fluid, both creating an excitation of the 'mechano-receptor'.”

Based on the hydrodynamic theory, dentinal hypersensitivity is a transient tooth pain. In order to exhibit a response to the stimuli, the tubules would have to be open at the dentin surface as well as the pulpal surface of the tooth. Anatomically, the tubules in the area closest to the pulp chamber are wider, and the number of tubules per unit area increases almost two-fold from the outer surface to the pulp.12

The most important variable affecting the fluid flow in dentin is the radius of the dentinal tubules. If the radius is reduced by one-half, the fluid flow within the tubules falls to one-sixteenth of its original rate. Consequently, the creation of a smear layer or the occlusion of the tubules will significantly reduce sensitivity.13,14