ANY perception of pain emanating from a tooth can be caused by mechanical, chemical, thermal (temperature), or bacterial stimuli. Stimulation sources may include toothbrushing, digital (finger) probing, desiccation (a blast of air), acids, sweet or sour hot and cold products, and acid products from plaque bacteria. This is because dentine—the main bulk of a tooth—is mineralised tissue transected from the pulp chamber (at the centre of the tooth) to enamel or cementum (the surfaces) by microscopic tubules. Within the tubules are protoplasmic projections, with the cell body itself in the pulp chamber. Only pain is felt when these cells are stimulated.

So, it is quite common for dental practitioners to hear persons describe dental pain as an “edging” or “shocking” when they eat or drink anything sweet or sour, when the food is hot or cold, or even simply when brushing. If you experience this, then you are among numerous adults who suffer from dentine hypersensitivity.

There are currently four hypotheses of pain transmission through dentine, of which the hydrodynamic theory is the most widely accepted. According to this theory, the movement of fluids within the dentine and pulp stimulates the nerves, causing pain. All external stimuli translate into hydrodynamic changes that alter the pulp equilibrium and elicit pain. So, even contact with air can result in pain.

There are varied predisposing factors to dentinal hypersensitivity, but no single cause. The tooth becomes sensitive after enamel loss or root surface exposure. Enamel loss follows mechanical wear (biting surface wear), neck abrasion, or possibly tooth flexure after grinding, which fractures enamel rods. Chemical erosion (acidic foods or stomach regurgitation), gingival recession (retracting gums), and subsequent tooth root exposure allow more rapid and extensive exposure of dentinal tubules because the cementum layer overlying the root surface is thin and easily removed.
The many causes of gingival retraction include normal ageing, chronic periodontal disease, abnormal tooth position in the dental arch, periodontal surgery, incorrect brushing habits, and root preparation for crowns. All the precipitating factors allow the exposure of dentinal tubules, which create the condition for dentine hypersensitivity.

Treatment modalities fall into two main categories: chemical and physical. All available treatments work to differing degrees depending on the treatment and severity of the patient’s hypersensitivity. Pain is extremely subjective, so effective treatment often depends on the individual’s pain threshold. Some desensitising agents can be used at home; others require a visit to the dentist.

Chemical desensitising agents can be sub-classified by their action: anti-inflammatory, protein precipitating, and tubule blocking.
Corticosteroids—one of the many groups of chemical agents—have been used topically for their anti-inflammatory effects but are not particularly effective.
The second group of chemical agents, the protein precipitants, includes silver nitrate and zinc chloride. Silver nitrate was widely used in the past. Unfortunately, both substances cause teeth to stain permanently and are harmful to gums and pulp. Strontium chloride and formaldehyde (in Sensodyne

toothpaste) belong to the group of agents that precipitate proteins within the tubule. Other drugs used to treat the condition include calcium hydroxide, fluoride, and sodium citrate.
Patients may also be treated with composites (fillings), resin varnishes, sealants, soft tissue grafts, glass ionomer cements, and laser sealing of the tubules.