A6 Tooth Sensitivity

Topic

Tooth sensitivity, also known as dentin hypersensitivity, is a sharp, short-lived pain that occurs when a thermal, evaporative, osmotic, or tactile stimulus acts upon exposed dentin. Unlike dental pain from other sources, this sharp pain subsides as soon as the triggering stimulus is removed, a characteristic that clinically distinguishes it from other types of tooth pain.

Dentin becomes exposed when gingival recession, abrasion, or erosion removes the enamel or root cementum that normally covers it, thereby revealing the dentinal tubules that run through it. The more this network of dentinal tubules is exposed, the greater the dentin permeability becomes—that is, the ease with which any external stimulus can reach the interior of the dentin.

When an external stimulus acts upon this exposed dentin—with its increased permeability—it triggers rapid movement of the fluid filling the dentinal tubules. This displacement of dentinal fluid is the central stage of the mechanism: the stimulus does not act directly on a nerve but instead first moves the fluid within the dentinal tubules, and it is this fluid movement that ultimately generates the sensation of pain.

The speed of this dentinal fluid movement depends on the pressure gradient generated by the stimulus along the dentinal tubule and, above all, on the radius of each tubule: dentinal fluid flow increases when the pressure gradient rises, but it increases much more sharply when the tubule radius increases, because this dependency is proportional to the fourth power of the radius rather than a simple linear relationship. Consequently, dentinal tubules that are only slightly wider produce disproportionately more intense movements of the dentinal fluid. Among the various stimuli capable of moving dentinal fluid, cold is particularly effective: cooling the dentinal fluid causes it to contract, generating a rapid centrifugal flow—that is, a movement of the fluid outward from the dentinal tubule toward the exposed dentin surface. This rapid centrifugal flow is far more effective at triggering a pain response than a slow or low-velocity flow.

This movement of dentinal fluid—whether the rapid centrifugal flow caused by cold or the flow generated by other stimuli—activates the mechanoreceptors of A-delta nerve fibers located at the pulp-dentin junction, the boundary between the dentin and the dental pulp. When these A-delta fiber mechanoreceptors are activated, they generate the signal that the nervous system interprets as the sharp, short-lived pain characteristic of tooth sensitivity.

Treatments for tooth sensitivity target two different points in this mechanism: some, such as varnishes or precipitated hydroxyapatite, occlude the dentinal tubules, thereby directly reducing the dentinal fluid movement that triggers sharp pain; others, such as potassium nitrate, do not prevent fluid movement but instead block nerve conduction in A-delta fibers, so that even if mechanoreceptors are activated, the signal is not interpreted as sharp pain. In both cases, the goal is to interrupt, at some point, the chain of events leading from exposed dentin to the sharp pain that defines tooth sensitivity.

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