Dentin hypersensitivity

Sharp, short lived tooth pain
A degree of dentin sensitivity is normal, but pain is not usually experienced in everyday activities like drinking a cooled drink. Therefore, although the terms dentin sensitivity and sensitive dentin are used interchangeably to refer to dental hypersensitivity,
Mechanical–tactile – dental probe during dental examination,

The most commonly accepted model is called the hydrodynamic or fluid movement theory proposed by Brannstrom in 1964. According to this theory, when the exposed dentine surface is subjected to thermal, chemical, tactile or evaporative stimuli, the flow of the fluid within the tubules will be increased. Fluid movement inside the dentinal tubules may be away from or towards the pulp. Dentine contains many thousands of microscopic tubular structures that radiate outwards from the pulp; these dentinal tubules are typically 0.5 2 micrometres in diameter. Changes in the flow of the plasma like biological fluid present in the dentinal tubules can trigger mechanoreceptors present on nerves located at the pulpal aspect, thereby eliciting a pain response. This hydrodynamic flow can be increased by cold, (air pressure), drying, sugar, sour (dehydrating chemicals), or forces acting on to the tooth. Hot or cold food or drinks, and physical pressure are typical triggers in those individuals with teeth sensitivity. Movement of dentinal fluid away from the pulp can be caused by triggers such as cold and drying and movement towards the pulp can be caused by heat. Research has shown that triggers causing dentinal fluid to move away from the pulp elicit more of a painful response. The odontoblastic transduction theory was suggested by Rapp et al. and puts forward the idea that odontoblasts act as receptor cells, and conduct impulses via synaptic junctions to the end of the nerves and therefore cause the feeling of pain. However, there is not much evidence to support this theory. The neural theory proposes that thermal or mechanical stimuli can directly influence nerve endings within the dentinal tubules via direct communication with the nerve endings of the pulp. There are two common ways in which dentine can be exposed; gingival recession and tooth wear. If a negative result for the pain provocation test occurs, no treatment for dentinal hypersensitivity is indicated and another diagnosis should be sought, such as other causes of orofacial pain.

There is no universally accepted, gold standard treatment which reliably relieves the pain of dental hypersensitivity in the long term, and consequently many treatments have been suggested which have varying degrees of efficacy when scientifically studied. Generally, they can be divided into in office (i. e. intended to be applied by a dentist or dental therapist), or treatments which can be carried out at home, available over the counter or by prescription. OTC products are more suited for generalized, mild to moderate dentin hypersensitivity associated with several teeth, and in office treatments for localized, severe DH associated with one or two teeth. Non invasive, simple treatments which can be carried out at home should be attempted before in office procedures are carried out. The purported mechanism of action of these treatments is either occlusion of dentin tubules (e. g. resins, varnishes, toothpastes) or desensitization of nerve fibres/blocking the neural transmission (e. g. potassium chloride, potassium citrate, potassium nitrate).

At home treatments include desensitizing toothpastes or dentifrices, potassium salts, mouthwashes and chewing gums. A variety of toothpastes are marketed for dentin hypersensitivity, including compounds such as strontium chloride, strontium acetate, arginine, calcium carbonate, hydroxyapatite and calcium sodium phosphosilicate. Desensitizing chewing gums and mouthwashes are also marketed. Potassium containing toothpastes are common; however, the mechanism by which they may reduce hypersensitivity is unclear. Animal research has demonstrated that potassium ions placed in deep dentin cavities cause nerve depolarization and prevent re polarization. It is not known if this effect would occur with the twice daily, transient and small increase in potassium ions in saliva that brushing with potassium containing toothpaste creates. In individuals with dentin hypersensitivity associated with exposed root surfaces, brushing twice daily with toothpaste containing 5% potassium nitrate for six to eight weeks reduces reported sensitivity to tactile, thermal and air blast stimuli. However, meta analysis reported that these individuals' subjective report of sensitivity did not significantly change after six to eight weeks of using the potassium nitrate toothpaste. Desensitizing toothpastes containing potassium nitrate have been used since the 1980s while toothpastes with potassium chloride or potassium citrate have been available since at least 2000. It is believed that potassium ions diffuse along the dentinal tubules to inactivate intradental nerves. However, as of 2000, this has not been confirmed in intact human teeth and the desensitizing mechanism of potassium containing toothpastes remains uncertain. Since 2000, several trials have shown that potassium containing toothpastes can be effective in reducing dentin hypersensitivity, although rinsing the mouth after brushing may reduce their efficacy. Studies have found that mouthwashes containing potassium salts and fluorides can reduce dentine hypersensitivity. A randomized clinical trial published in 2018 found promising results in controlling and reducing hypersensitivity when potassium oxalate mouthrinse was used in conjugation with toothbrushing. As of 2006, no controlled study of the effects of chewing gum containing potassium chloride has been made, although it has been reported as significantly reducing dentine hypersensitivity. Nano hydroxyapatite (nano HAp) is considered one of the most biocompatible and bioactive materials and has gained wide acceptance in dentistry in recent years. An increasing number of reports have shown that nano hydroxyapatite shares characteristics with the natural building blocks of enamel having the potential, due to its particle size, to occlude exposed dentinal tubules helping to reduce hypersensitivity and enhancing teeth remineralization. For this reason, the number of toothpastes and mouthwashes that already incorporate nano hydroxyapatite as a desensitizing agent is increasing. Dentine hypersensitivity is commonly experienced by patients. Studies reveal prevalence rates can range from 3 98%. Prevalence is found to be higher in patient questionnaire studies, 74%,  over diagnostic studies, 15 30%. Diagnostic studies are where patients are diagnosed on classical symptoms (rapid, sharp, short duration). This discrepancy in range can be explained by DH being underreported due to the difficulties patients face when describing symptoms. The scale of symptoms for DH are so variant, some patients are unable to eat ice cream or drink cold water, whereas for others, discomfort is episodic in nature. Episodic symptoms of DH is the likely reason why some patients fail to report the discomfort. Hence having a negative effect on the number of diagnoses. If a patient does not complain of the symptoms then no additional screening checks are in place for dentin hypersensitivity and often the diagnosis is missed. It must be remembered that DH is seen as a diagnosis of exclusion. Although DH affects all age groups, varying from 20–50 years, it most commonly peaks between 30–40 years. Females are more affected by DH. It can be said that this is due to females having diets high in erosive acids and diligent oral hygiene methods. Another contributing factor to this theory, is that females attend the dentist on a more regular basis, discuss health problems more readily than males which can lead to some bias in the DH being more prevalent in females. Hence the findings from some studies that DH does not significantly affect females over males. A large number of DH cases are linked to periodontal disease and follow as a result of periodontal treatment. Surgical and non surgical periodontal treatment is said to have the same effect on DH. As part of the periodontitis disease process, recession and root exposure are prevalent. The aim of periodontal treatment is to reduce the inflammation that presents. Treatment strategies also lead to the removal of cementum, smear layer and exposure of dentinal tubules, furthermore causing DH for patients. Within the elderly generation periodontal disease is more prevalent however, DH is not a common diagnosis in the elderly. DH decreases during 40–50 years, a plausible explanation or this is the result of sclerosing of canals and formation of tertiary dentine. DH can present on several teeth in the whole of the mouth, on teeth in one part of the mouth or on a single tooth. Premolars and canines tend to present with hypersensitivity more readily followed by molars5, this is true for upper and lower arches. Maxillary teeth are more commonly affected. Sites of teeth affected are cervical aspect buccal sites on teeth.

Dentin hypersensitivity may affect individuals' quality of life. Over time, the dentin pulp complex may adapt to the decreased insulation by laying down tertiary dentin, thereby increasing the thickness between the pulp and the exposed dentin surface and lessening the symptoms of hypersensitivity. Similar process such as formation of a smear layer (e. g. from toothbrushing) and dentin sclerosis. These physiologic repair mechanisms, which occur at a naturally slow pace, are likely to occur with or without any form of treatment.