Pathway 13-7-2 DETECTION First Step - Pulp Testing and SENSITIVITY OF DENTIN

Pulp Testing

• The electrical pulp tester stimulates sensory A fibers at the dentin-pulp border zone.
• The electrical pulp tester uses a current strong enough to overcome the enamel and dentin resistance.
• Pulp C fibers are not stimulated by a conventional pulp tester.
• The incisal edge of anterior teeth is the optimal placement site for the electrode, based on lowest response threshold.
• Cold tests, like CO2 snow or refrigerants, activate A fibers through hydrodynamic forces in dentinal tubules.
• Heat tests, using heated gutta-percha or hot water, also activate A fibers through hydrodynamic forces in dentinal tubules.
• C fibers are generally not activated by cold or heat tests unless injury to the pulp occurs.
• Cold tests are not known to injure the pulp.
• Heat tests have a greater potential to injure the pulp if not used properly.

Dentin Sensitivity Mechanisms

• Fluid movement in dentinal tubules is the primary mechanism for dentin sensitivity.
• Stimuli like heat, cold, air blasts, and probing, displace fluid in tubules, triggering the hydrodynamic mechanism.
• The hydrodynamic theory suggests that mechanical stimulation of dentinal tubules leads to mechanotransduction.
• Mechanotransducers on pulpal afferent nerves support this theory.
• Fluid movement within tubules is converted to electrical signals by receptors in axon terminals innervating the tubules.
• Single-fiber recordings show a positive correlation between pressure changes and nerve impulses, indicating that outward fluid movements (negative pressure) generate a stronger response.

Thermal Pain Perception

• Applying heat or cold to the outer surface of premolar teeth causes pain before any significant temperature changes reach the tooth's pulp.
• This pain response is short-lived, lasting only one to two seconds.
• Despite dentin's low thermal diffusivity, the tooth responds quickly to thermal stimulation, often within less than a second.
• Evidence suggests that thermal stimulation triggers a rapid movement of fluid within the dentinal tubules.
• This fluid movement activates sensory nerve terminals in the pulp.
• Heat causes fluid expansion within the tubules faster than dentin, driving fluid towards the pulp.
• Cold causes fluid contraction faster than dentin, resulting in outward fluid flow.
• It's theorized that the rapid fluid movement across the axon terminal membrane activates a mechanosensitive receptor.
• This process resembles how fluid movement activates hair cells in the cochlea of the ear.
• Axon terminals contain membrane channels through which charged ions pass.
• The initial receptor current, if strong enough, can trigger voltage-gated sodium channels to depolarize the cell.
• This depolarization leads to a series of impulses transmitted to the brain.
• Some ion channels are activated by voltage, chemicals, or mechanical pressure.
• In pulpal nerve fibers activated by hydrodynamic forces, pressure is transduced, activating mechanosensitive ion channels.

Dentinal Tubule Structure and Capillary Forces

• Dentinal tubules are narrow capillary tubes.
• Smaller diameter leads to increased fluid force due to capillary action.
• Dehydration of the dentin surface via air blast or absorbent paper causes rapid outward movement of fluid in the tubules.
• Desiccation can cause dentinal fluid to flow outward at a rate of 2 to 3 mm/s.
• Hyperosmotic solutions like sucrose or calcium chloride can cause pain when applied to exposed dentin due to dehydration.

### Hydrodynamic Mechanism

• A-fibers are activated by hydrodynamic stimuli like heat, cold, and air blasts applied to exposed dentin.
• C-fibers may be activated if heat is applied long enough to increase the temperature of the dentin-pulp border by several degrees Celsius, particularly if the heat produces injury.

C-Fiber Activation

• Slow tooth heating produces no response until the temperature reaches 111°F (43.8°C), at which time C fibers are activated, presumably due to heat-induced injury to the pulp.
• C fibers are called polymodal nociceptors due to their ability to detect and respond to numerous stimuli.

TRPV1 Receptor

• Capsaicin, the active ingredient in hot peppers, activates C fibers and a subset of A-delta fibers.
• Capsaicin activates the TRPV1 receptor, which is expressed primarily on a major subclass of nociceptors.
• The TRPV1 receptor responds to heat (110°F/43°C), certain inflammatory mediators, and acid (pH < 6).
• TRPV1 is considered a molecular integrator of various noxious stimuli.

TRPV1 Antagonists and Dental Implications

• Capsazepine, a TRPV1 antagonist, can inhibit acid-, heat-, and capsaicin-activated trigeminal neurons.
• TRPV1 antagonists are being developed for the treatment of pulpal pain.
• Eugenol, found in zinc oxide eugenol temporary restorations, activates and desensitizes TRPV1, which may contribute to its analgesic effect.

### Dentin Sensitivity

• Open dentin tubules allow easier transmission of pain stimuli
• Acid etching removes the smear layer, opening tubules and making dentin more sensitive to air blasts and probing
• Probing can create pressure, compress dentin, and cause fluid displacement, stimulating sensory receptors in the pulp
• Multiple nerve endings can be stimulated simultaneously when probing dentin due to the density of tubules
• Low-threshold mechanoreceptors, called "algoneurons" by authors, may explain pain sensations from weak mechanical stimuli like air puffs and water sprays
• This "algoneuron" theory complements, but doesn't contradict, the hydrodynamic theory

Odontoblast Displacement

• Strong hydraulic forces within dentinal tubules can displace odontoblasts.
• Desiccation of exposed dentin, such as with an air syringe or cavity-drying agents, causes rapid fluid movement within the tubules.
• This fluid movement forces odontoblast nuclei and cell bodies upward in the tubules.
• Displaced odontoblasts undergo autolysis and disappear from the tubules.
• Stem cells from the pulp's cell-rich zone may eventually replace displaced odontoblasts.

Hydrodynamic Theory and Dentin Hypersensitivity

• The hydrodynamic theory explains the mechanism of dentin hypersensitivity.
• Exposed dentin can be sensitive or hypersensitive.
• Evidence suggests that exposure to inflammation leads to the expression of new sodium channels in nerve tissue.
• Increased density or sensitivity of sodium channels may contribute to dentin hypersensitivity.
• Dentin hypersensitivity is associated with the exposure of dentin normally covered by cementum or enamel.
• Gingival recession can expose cementum, which can be worn away by brushing, flossing, or toothpicks.
• Exposed dentin responds to stimuli like mechanical pressure and dehydrating agents.
• Dentin hypersensitivity may subside after a few weeks due to occlusion of tubules by mineral deposits, reducing hydrodynamic forces.
• Reparative dentin deposition over exposed tubules may also decrease sensitivity due to lower innervation.
• Some dentin hypersensitivity doesn't desensitize spontaneously, potentially due to inflammatory changes in the pulp or mechanical changes in dentinal tubule patency.

Treating Hypersensitive Teeth

• Goal: Reduce the diameter of dentinal tubules to limit fluid movement
• Modalities:
  • Smear Layer Formation: Burnishing exposed root surface creates a layer, blocking tubules
  • Oxalate Compounds: Insoluble precipitates form within tubules
  • HEMA (with/without glutaraldehyde): Occludes tubules with precipitated plasma proteins
  • Dentin Bonding Agents: Seals off the tubules