Toothache when eating hot food

When a doctor examines your teeth, he or she can also use a probe to detect sensitive spots on the teeth.

Dentine hypersensitivity is a painful symptom caused by external stimuli such as temperature (cold, hot), chemicals (acid, sweet) and mechanical action (friction or biting hard objects). It is characterized by rapid onset, sharp pain and short duration. Tooth hypersensitivity is not an independent disease, but a common symptom of various dental diseases, with the peak age of onset being around 40 years old. The onset is rapid and the pain is brief but unbearable.

Dental hypersensitivity can occur in any dental disease that destroys the integrity of the enamel and exposes the dentin, such as wear, wedge-shaped defects, tooth fractures, caries, and periodontal atrophy that exposes the tooth neck. However, not all teeth with exposed dentin will show symptoms. It is usually related to the duration of dentin exposure and the speed of reparative dentin formation. Although most clinical cases are caused by dentin exposure, which is an important reason, it cannot explain all clinical manifestations. For example, sensitive symptoms can go from non-existence to existence and from existence to non-existence with changes in health and climate, which cannot be explained by the speed of reparative dentin formation. Individual teeth with intact enamel can also become sensitive. Soviet scholars called this disease "increased sensitivity of enamel and dentin", which is more accurate in short as "tooth hypersensitivity".

The pathogenesis of dental hypersensitivity is still unclear, and there are currently three hypotheses.

1. The neural theory believes that there are pulp nerve endings in the dentin, so sensation can be transmitted from the surface of the dentin to the pulp. However, there is no consensus on morphological and functional observations. Many scholars believe that only a part of the unmyelinated nerves in the odontoblast layer of the dental pulp enters the pre-dentin and the inner layer of the dentin, and no nerve structure is found in the outer 2/3. Many experimental results also do not support the view that "the nerves' responses to various stimuli are direct." Potassium chloride, histamine, acetylcholine, etc. do not cause pain when acting on superficial dentin; local anesthetics acting on the dentin surface cannot reduce the sensitivity of dentin.

2. The dentin fiber conduction theory holds that the protoplasmic processes of odontoblasts contain acetylcholine, which can cause nerve conduction and produce pain when stimulated. Opponents believe that experimental interference with human odontoblasts did not reduce dentin sensitivity, indicating that odontoblasts do not have the characteristics of sensory organs and may only play a passive role in dentin hypersensitivity.

3. The fluid dynamics theory holds that the pain caused by air, hypertonic solutions or temperature stimulation is because these stimuli cause the fluid in the dentinal tubules to move, mechanically stirring the contents of the pulp, and then indirectly exciting the free nerve endings therein, transmitting impulses and producing pain. The energy accompanying the movement of the fluid can be converted into electrical signals by the receptors in the dental pulp. Approximately 25% of the volume of dentin is occupied by free fluid, which is similar in composition and properties to other body fluids and communicates with the pulp tissue fluid. Dentinal tubules are capillaries with a diameter of 0.8 to 2.5 μm; therefore, the effects of fluid dynamics depend on the permeability of dentinal tubules or the condition of the dentin surface. Stimuli that cause dentin fluid to move outward include air drying, hypertonic solutions and cold stimulation. Stimuli that cause dentin fluid to move inward include mechanical stimulation or heating. Dentin exposure is very sensitive in the early stage, and the sensitivity is naturally relieved later due to the deposition of minerals in the dentinal tubules or the formation of reparative dentin by the pulp.