“Tooth sensitivity” is a more standard term, usually we are used to call it “dentin hypersensitivity”. The abbreviation is “DH”. Dental hypersensitivity is a specific painful condition caused by external stimuli (mechanical, chemical, temperature, osmotic pressure, etc.) to exposed dentin. Characteristics Rapid onset, sharp pain, and short duration. It is rapidly triggered by stimulation and disappears immediately after cessation of stimulation. The incidence rate is 8%~30%, with a high incidence in people around 40 years old. It is a common and frequent disease in the oral clinic. It is more widely involved. Such as: wedge-shaped defect, periodontal atrophy root exposure, dental trauma dentin exposure, severe wear, dental preparation, cavity preparation, scaling, scraping, tooth decoloration, jaw adjustment, etc. DH pathogenesis Three theories exist about the pathogenesis of DH: one is the neurological theory: it is believed that “the nerve endings of the dental pulp, which may extend to the enamel-dentin boundary, are directly stimulated to produce pain”. However, histological and morphological studies found that “the pulpal nerve only partially extends into the pre-dentin and inner dentin layers, while no nerve structures are seen in the outer 2/3 of it”. Let’s look at an experiment: as you know: “potassium chloride, bradykinin”, all of which have a strong stimulating effect on the nerve, should cause a strong pain response when applied to freshly exposed dentin. Experimental results: It did not cause a painful reaction. Moreover, when the test was continued deeper into the dentin, there was still no response, and it was only when the pulp was touched all the way down that it caused pain. If there were nerve fibers present in the superficial layer of the dentin, we should have been able to relieve and disappear the allergic symptoms by applying anesthetics (e.g., dicaine, etc.) to the allergic tooth surface. However, this effect did not occur. Therefore, the “nerve theory” is not well founded in experiments. In 1968, Frank, a histologist, reported that a pain response was observed in the dentin tubules. In 1968, histologist Frank reported that a complex of nerve and dentin-forming cell protrusions was observed in the dentin tubules, which could perform the function of “receptors”. However, after the introduction of electron microscopy, it was confirmed by scanning that it was the “collagen fibers” in the dentin and not the “complex” structure. To date, no nerve conduction material has been found. The dentin cells do not have the characteristics of “sensory apparatus”. The third is the “fluid dynamics theory”, which is based on the presence of dentin fluid in the dentin tubules. The flow of this fluid causes the expansion and compression of the dentin-making cells and their protrusions, which mechanically agitates the nerve endings of the dental pulp and produces pain. This theory can explain many of the phenomena that produce pain when dentin is stimulated. For example, when a piece of absorbent paper is placed on a freshly exposed dentin surface, a painful sensation is felt after a few minutes; when the paper is soaked, no pain is produced. This means that the pain sensation occurs due to the ability of the absorbent paper to make the fluid in the dentin tubules flow outward. The wet paper no longer absorbs water, so it cannot make the dentin fluid flow, so it does not produce pain. Hot and cold stimuli cause pain in allergic teeth because of the flow of dentin fluid caused by thermal expansion and contraction. So why are allergic teeth afraid of sweet and sour? It is because the concentration of gram molecular osmolarity of dentin fluid is low and it has to flow in the direction of higher gram molecular osmolarity. When there is sugar and acid on the surface of the tooth, especially when there is hypertonic fluid, it will cause the dentin fluid to flow outward, so allergic teeth are also afraid of acidity and sweetness. Many clinical phenomena can be explained by the “fluid dynamics theory”, so this theory can be accepted and respected by most people. The body has the ability to defend and resist various pathogenic factors of dental sensitivity. Clinically, when pulp is opened for an old tooth, it is found that the pulp apex is very small from the pulp floor and the root canal is particularly thin. The pulp chamber and root canal have been occupied by secondary dentin. This secondary dentin has a low permeability, which reduces the flow of dentin fluid; there are also various substances from saliva, which can be deposited in the tubules, making the diameter of the tubules smaller and inhibiting the flow of fluid in the tubules, thus reducing the stimulation of dentin fluid to the pulp nerve. We all have the experience that after scaling, the patient will feel the tooth soreness and fear of hot and cold. Usually we do not do special treatment, and the symptoms will disappear on their own after three or four days. For example, there are some elderly patients with wedge defects whose damage is even to the extent of pulp penetration, but they have no obvious history of dental allergy or pulpitis. Such patients are also very common. These, in clinical practice, can be confirmed. This is where the body’s defenses come into play. What should be considered in the treatment of dental sensitivity? RoBenthal, an endodontist, proposes six aspects of treatment of DH: 1. physical methods to close or block the outer end of the dentin tubules; 2. chemical methods to coagulate the protoplasm of the dentin tubules; 3. chemical substances reacting with tooth tissue to form precipitates and block the tubules; 4. inducing dentin formation and closing the proximal pulpal end of the dentin tubules; 5. anesthetic qualities penetrating into the pulp via the tubules and blocking the pulpal nerve Some substances penetrate into the pulp through the tubules to inhibit the excitation of the pulp nerve. To summarize these six rules, there are two points: one is to change the permeability of the dentin tubules; the other is to reduce the excitability of the pulpal nerve. Then, clinically, there are four mechanisms of using drugs for desensitization: (1) plugging effect: drugs that produce insoluble precipitates are applied to the tooth surface to produce precipitates to plug the dentin tubules. For example, 10% silver nitrate. (2) Corrosion: the use of corrosive drugs to coagulate and denature proteins in the dentin, reducing the permeability of the tubules. Such as phenolic drugs. (3) Covering effect: the use of dendritic materials to form a protective film on the dentin surface to isolate the irritation; (4) Biological effect: the dentin cells will be activated to form the restorative dentin drugs. (4) Biological action: the dentin cells are activated to form restorative dentin. For example, fluoride nodules. The majority of the current clinical desensitization methods are applied to these mechanisms. In 1935, the famous American endodontist Grossman proposed six criteria: 1, no irritation to the pulp; 2, relatively painless when used; 3, easy to handle; 4, rapid action; 5, stable effect; 6, no tooth staining. To date, there is no desensitizer that fully meets the above criteria. Therefore, the search for ideal desensitizing agents and desensitizing methods is the goal of everyone’s unremitting efforts.