bubble_chart Overview

Tooth hypersensitivity, also known as hypersensitive dentine or dentine hypersensitivity, is a painful symptom caused by external stimuli such as temperature (cold, heat), chemical substances (acid, sweet), and mechanical actions (friction or biting hard objects). It is characterized by rapid onset, sharp pain, and short duration. Tooth hypersensitivity is not an independent disease but rather a common symptom of various dental conditions, with the peak incidence occurring around the age of 40.

bubble_chart Etiology

Any dental condition that compromises the integrity of the enamel and exposes the dentin—such as abrasion, wedge-shaped defects, tooth fractures, dental caries, or gingival recession leading to exposed tooth necks—can result in dentin hypersensitivity. However, not all teeth with exposed dentin exhibit symptoms, which are typically related to the duration of dentin exposure and the speed of reparative dentin formation. While most clinical cases are caused by dentin exposure, which is a significant factor, this alone cannot explain all clinical manifestations. For instance, sensitivity symptoms may appear or disappear with changes in health or climate, a phenomenon that cannot be accounted for solely by the rate of reparative dentin formation. In rare cases, even teeth with intact enamel can experience sensitivity. Soviet scholars referred to this condition as "increased sensitivity of enamel and dentin," more accurately termed "dentin hypersensitivity."

bubble_chart Pathogenesis

The mechanism of dentin hypersensitivity is not yet fully understood, and there are currently three hypotheses.

1. Neural Theory: It suggests that there are dental pulp nerve endings in the dentin, allowing sensations to be transmitted from the dentin surface to the pulp. However, observations from both morphological and functional perspectives have not yielded consistent conclusions. Many scholars believe that the unmyelinated nerves in the odontoblast layer of the pulp only partially extend into the predentin and inner dentin, with no nerve structures observed in the outer two-thirds. Numerous experimental results also do not support the view that "nerves respond directly to various stimuli." Potassium chloride, histamine, acetylcholine, and other substances applied to superficial dentin do not produce pain, and local anesthetics applied to the dentin surface do not reduce dentin sensitivity.

2. Dentinal Fiber Conduction Theory: This theory posits that the protoplasmic processes of odontoblasts contain acetylcholinesterase, which can trigger nerve conduction and pain upon stimulation. Opponents argue that experimental interference with human odontoblasts did not reduce dentin sensitivity, indicating that odontoblasts do not possess the characteristics of sensory receptors and may only play a passive role in dentin hypersensitivity.

3. Hydrodynamic Theory: This theory proposes that pain caused by air, hypertonic solutions, or temperature stimuli results from the movement of fluid within the dentinal tubules, mechanically agitating the pulp contents and indirectly exciting the free nerve endings, thereby generating pain signals. The energy accompanying fluid movement can be converted into electrical signals by the pulp's receptors. Approximately 25% of dentin volume is occupied by free fluid, whose composition and properties are similar to other bodily fluids and communicate with the pulp tissue fluid. Dentinal tubules are capillaries with diameters of 0.8–2.5 μm, so the hydrodynamic effect depends on the permeability of the dentinal tubules or the condition of the dentin surface. Stimuli that cause outward movement of dentinal fluid include air drying, hypertonic solutions, and cold stimuli. Inward movement of dentinal fluid is induced by mechanical stimuli or heating. Exposed dentin in the initial stage is highly sensitive, but the natural alleviation of sensitivity over time is due to mineral deposition within the dentinal tubules or the formation of reparative dentin by the pulp.

bubble_chart Clinical Manifestations

The main manifestation is sharp pain, where stimuli such as brushing teeth, eating hard foods, sour, sweet, cold, or hot items can trigger soreness, with mechanical stimuli being the most sensitive. The most reliable diagnostic method involves sliding a sharp probe over the tooth surface to locate one or several sensitive areas. Foreign reports mention a mechanical stimulator that adjusts the pressure of a stainless steel needle via a screw to test tooth sensitivity, while others use electrically controlled thermometers for testing. However, to date, the degree of tooth sensitivity can only be expressed based on the patient's subjective perception.

bubble_chart Treatment Measures

The hydrodynamic theory is widely accepted in the mechanism of dentin hypersensitivity. According to this theory, effective treatment for hypersensitivity must involve sealing the dentinal tubules to reduce or prevent fluid movement within the dentin. Due to the spontaneous desensitization process of this condition, evaluating the efficacy of any drug treatment is extremely challenging.

Common treatment methods include:

1. Fluorides: Various forms of fluoride can be used to treat dentin hypersensitivity. Fluoride ions reduce the diameter of dentinal tubules, thereby decreasing hydraulic conductance. In vitro experiments have shown that acidulated sodium fluoride solution or 2% neutral sodium fluoride solution can reduce hydraulic conductance by 24.5% and 17.9%, respectively, while iontophoresis with sodium fluoride solution can reduce it by up to 33%.

(1) 0.76% sodium monofluorophosphate gel (pH=6) maintains an effective fluoride concentration and is currently the most effective among fluoride treatments.

(2) Apply 75% sodium fluoride glycerin repeatedly to the sensitive area for 1–2 minutes; alternatively, use a wooden applicator dipped in the solution to rub the affected area for 1–2 minutes.

(3) Iontophoresis with 2% sodium fluoride solution:

1) Use a DC therapy device: the positive electrode is held by the patient, while the negative electrode, moistened with sodium fluoride solution, contacts the sensitive area. The current intensity is 0.5–1 mA, adjusted to the patient’s comfort level, with an application time of 10 minutes.

2) Drug ion introduction via electrolytic toothbrush: A dry cell (1.5V) is installed at the end of the toothbrush handle, with the handle serving as the anode (held by the hand) and the brush head as the cathode for drug introduction. Brush with this device 2–3 times daily for 3–5 minutes each time. Regularly check if the current pathway is normal and if the battery is nearly depleted.

2. Strontium chloride: A neutral salt with high water solubility and low toxicity. It is convenient and safe to use in toothpaste. 10% strontium chloride toothpaste is widely used abroad, and domestic products are also available. For topical application, 75% strontium chloride glycerin or 25% strontium chloride solution is used. Among the extensively studied drugs, strontium exhibits strong adsorption to all calcified tissues, including dentin. Its effect on dentin hypersensitivity is attributed to the blockage of open dentinal tubules through the formation of strontium-calcium apatite.

3. Silver ammonia nitrate: Isolate and dry the sensitive area, apply silver ammonia nitrate solution, then reduce it with clove oil until it turns black. The resulting protein silver and reduced silver precipitate in the dentinal tubules, blocking conduction. Care must be taken to protect oral soft tissues to avoid burns.

4. Silver iodide: Apply 3% iodine tincture for 0.5 minutes, then apply 10–30% silver nitrate solution to the sensitive area, resulting in a gray-white precipitate. Repeat the process 1–2 times after 0.5 minutes for effectiveness. This method relies on silver nitrate coagulating proteins in the dental hard tissue to form a protective layer, while the reaction between iodine tincture and silver nitrate produces nascent silver iodide, which deposits in the dentinal tubules to block conduction.

5. Electrocoagulation: Isolate the area, apply a small cotton ball soaked in 10% formalin to the sensitive spot, and electrocoagulate with a spherical electrode for 1 second. Replace the formalin-soaked cotton ball and repeat every 5 seconds. Each electrocoagulation should not exceed 1 second, with intervals of at least 5 seconds. Perform 10–15 repetitions per visit.

Formaldehyde in formalin has excellent diffusion properties, especially at high temperatures, where it effectively fixes organic matter.

6. Laser: YAG laser at 15W power. Irradiate the sensitive area for 0.5 seconds per session, with 10–20 sessions constituting one treatment course, which is the safe threshold for treating dentin hypersensitivity. The mechanism likely involves the laser’s thermal effect on the dentinal tubules, instantly sealing exposed tubules through coagulation, thereby achieving desensitization.

7. Other drugs: 4% magnesium sulfate solution, 5% potassium nitrate solution, and 30% potassium oxalate solution can all be used for the treatment of dentin hypersensitivity.

8. Restorative Treatment For those who do not respond to repeated drug desensitization, filling or artificial crown restoration may be considered. In cases of severe wear close to the dental pulp, pulp devitalization therapy may be necessary when required.