Dentine hypersensitivity is prevalent amongst a large portion of individuals 30 to 40 years of age. It causes oral discomfort generated by pain, leads to nutritional deficiency due to dietary restrictions in some individuals. The nociceptive stimulus commonly reported in the majority of cases is that of cold, followed by the mechanical stimulus of toothbrushing and the chemical stimulus of diet with a high concentration of sugar (1).

Pain of dentinal origin is sharp, located, and of short duration. The hydrodynamic theory proposed by Brännströn e Aström (2), in 1964, is still currently accepted to explain the relationship between pain of dentinal origin and the displacement of odontoblasts in the dentinal tubules.

Thermal, physical and chemical stimuli would cause the displacement of the pulp-dentinal fluid, thus stimulating the pulpar nervous terminations.

Under normal conditions, dentine is covered by enamel or cement and does not suffer direct stimulation. Only with the exposure of the peripheral terminations of dentinal tubules is a situation of strong dentinal sensitivity manifested, termed hypersensitivity. Occlusion of the exposed dentinal tubules can reduce the intensity of dentinal sensitivity. This can be accomplished through passive mechanisms, such as precipitation of salivary calcium phosphate inside the dentinal tubules, adsorption of plasma proteins and saliva constituents, as well by active mechanisms such as deposit of intracanalicular crystalline material and secretion of protein material from the interior of the tubules, diminishing dentinal permeability and sensitivity (3). Type A fibers are responsible for dentinal sensitivity and are probably activated by the hydrodynamic mechanism. Therefore, their activation is directly associated to the presence of opened or occluded tubules. However, hypersensitivity sometimes remains in spite of the effective blocking of the tubules, suggesting that other mechanisms contribute to nerve activation instead of or in addition to the hydrodynamic mechanism. Dentine hypersensitivity may occur as a result of sensitization induced by nerve inflammation in the dentinepulpar boundary of teeth with opened dentinal tubules. This partially explains the large sensitivity variation of exposed dentine and, furthermore, nerve activation may result in the release of neuropeptides from the activated nervous terminations and, consequently, induce neurogenic inflammation. The symptoms of dentine hypersensitivity would, up to a certain point, be self-sustainable (4).

The most common factors responsible for dentine hypersensitivity are abrasion, caused by toothbrushing with inadequate intensity; abfraction, caused by tooth flexion associated with ill-directed occlusal forces, parafunctional habits or occlusal disequilibrium; erosion, as an effect of acids in the oral cavity; anatomic predisposition due to structural deficiency in the enamel-cement junction; cavity preparations in teeth with pulp vitality that expose the dentine; as well as improperly controlled dentinal acid conditioning (5,6). Any treatment, which reduces the dentinal permeability, must diminish dentinal sensitivity. The occlusion of dentinal tubules leads to reduction of dentinal permeability and, proportionally, also decreases the degree of dentinal sensitivity (7). According to the hydrodynamic theory, the effectiveness of dentine desensitization agents is directly related to their capacity to promote the sealing of the dentinal canaliculi (8). With the advent of laser technology and its growing utilization in dentistry, an additional therapeutic option is available for the treatment of dentinal pain. The laser, by interacting with the tissue, causes different tissue reactions, according to its active medium, wavelength and power density and to the optical properties of the target tissue (9).

The laser photobiomodulating action in the dental pulp was reported by Villa et al. (10), with histological studies of dental pulp of mice after irradiation with laser, in teeth previously eroded with high rotation in order to expose the dentine.

The profiling of the odontoblasts was observed, showing evidence of a large quantity of tertiary dentine production, causing the physiological obliteration of the dentinal tubules. The non-irradiated control teeth showed intense inflammatory process that, in some cases, evolved to necrosis.