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Chapters

0:00 Introduction
0:25 Use a toothpaste for sensitive teeth
0:40 Limit foods and drinks that trigger your pain
0:53 Peppermint tea bags
1:09 Hydrogen peroxide mouth rinse
1:22 Rinse with salt water
1:36 Clove oil
1:52 Cold compress around jaw



Dentin hypersensitivity (DH,[4] DHS)[5] is dental pain which is sharp in character and of short duration, arising from exposed dentin surfaces in response to stimuli, typically thermal, evaporative, tactile, osmotic, chemical or electrical; and which cannot be ascribed to any other dental disease.[5][3][6][7]

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,[3] the latter term is the most accurate. The real cause of dentine hypersensitivity is controversial. There have been several theories put forward to try and explain the cause of dentine hypersensitivity. These include the odontoblastic transduction theory, the neural theory and the hydrodynamic theory.[9]

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.[10]

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.[11]

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.

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.[9] The main cause of DH is gingival recession (receding gums) with exposure of root surfaces, loss of the cementum layer and smear layer. Receding gums can be a sign of long-term trauma from excessive or forceful toothbrushing or abrasive toothpaste (dental abrasion), or a sign of chronic periodontitis (gum disease).[10] A less common cause is acid erosion, which is the loss of hard dental tissues due to acids e.g. related to gastroesophageal reflux disease, bulimia or excessive consumption of acidic foods and drinks. Repeated exposures to a low pH cause the mineral content of the teeth on the outer layer of enamel to dissolve therefore leaving the dentine exposed and leading to hypersensitivity. Other causes include dental bleaching, smoking tobacco (which can lead to recession and therefore sensitivity) cracked teeth and abfraction or grinding of teeth. Evidence of abfraction may be shown by wedge shaped defects that are developed at the cervical region of the teeth known as abfraction lesions. There is no direct relationship between abfraction lesions and diet, periodontal disease or abrasion.[12]

Most experts on this topic state that the pain of DH is in reality a normal, physiologic response of the nerves in a healthy, non-inflamed dental pulp in the situation where the insulating layers of gingiva and cementum have been lost;[5][3] i.e., dentin hypersensitivity is not a true form of allodynia or hyperalgesia. To contradict this view, not all exposed dentin surfaces cause DH.[3] Others suggest that due to the presence of patent dentinal tubules in areas of hypersensitive dentin, there may be increased irritation to the pulp, causing a degree of reversible inflammation.[12]


The diagnosis of DH may be challenging.[5] It is a diagnosis of exclusion, reached once all other possible explanations for the pain have been ruled out.[5] A thorough patient history and clinical examination are required.[5] The examination includes a pain provocation test by blasting air fr

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