To be hypersensitive, dentin must be exposed and the exposed tubules must be open and patent to both the oral cavity and the pulp [10, 15]. Exposure of dentin through the loss of gingival and periodontal tissue may be caused by either too meticulous or by neglected oral hygiene (Fig. 15.3). The exact mechanism by which too meticulous oral hygiene causes loss of tissue is not very well understood and often implies brushing force and brush bristle characteristics. Several studies have shown the injury potential of sharp nonrounded filament tips on gingival abrasion [16, 17]. Surprisingly there is no information on the role of toothpastes in this process. Such a role could be both physical, through abrasion, and chemical, through cytotoxicity of ingredients such as detergents to the soft tissues [18]. In any case, modifying factors like inserting frenula, thin gingival biotypes, a lack of keratinized gingiva, or absence of the buccal bone may be implicated and should be considered. The mechanism by which neglected oral hygiene causes recessions runs through acute and chronic periodontal diseases and nonsurgical and surgical treatments.

Exposure of dentin by the loss of enamel is often ascribed to abrasion. However, most abrasives are softer than enamel and it must be concluded that toothpaste abrasion alone would play a clinically insignificant role in exposure of dentin [18]. In contrast, acids from intrinsic or extrinsic sources are more harmful for enamel by dissolution and by softening. The softened enamel is subsequently abraded away by mechanical forces. Shear forces of the oral soft tissues may be sufficient to abrade the softened enamel [19], but toothbrushing surely will as will grinding and clenching [20]. So when there is exposure of dentin as a result of loss of enamel, the patient’s history should reveal the role of intrinsic or extrinsic acids (Table 15.1).

Since nonsensitive dentin reveals few if any open dentinal tubules at the surface [13], it is assumed that the tubules are covered by a “smear layer,” consisting of protein components and calcium phosphate deposits derived from saliva [23] (Fig. 15.4). To initiate dentin hypersensitivity this layer has to be removed, and in vitro and in situ studies implicate erosive wear, as the smear layer is sensitive to acids [24, 25]. When acids have softened the smear layer and dentin, the materials are more susceptible to physical forces, such as toothbrushing. Clinical data suggest that physical forces alone are not a key factor in removing the smear layer and opening exposed dentin tubules [10]. Also toothpaste will remove the smear layer [25, 26] probably by a combined abrasive and detergent action. Moore and Addy [27] have suggested that certain “mild” surfactants and “gentle” abrasives might have advantages over their more traditional counterparts in toothpastes marketed for the relief of dentin hypersensitivity [27]. However, this hypothesis does not appear to have been clinically validated in well-designed clinical studies [15]. One study showed no difference in desensitizing effect after elicitation using the evaporative method when using four desensitizing toothpastes different in abrasivity with RDA 60, 108, 150, or 210, respectively [28].

Subsequent to tubule exposure, toothpaste may reduce patency by secondary abrasive smearing or deposition of toothpaste constituents onto the dentin surface and into tubules. This makes the role of toothpaste without active ingredients to reduce dentin hypersensitivity inconclusive, even of fluoride containing pastes. Additionally it suggests that when using desensitizing toothpastes application with a fingertip or cotton swab after brushing may be beneficial.

Dentin hypersensitivity may disturb the patient during eating, drinking, toothbrushing, and sometimes even breathing. The resulting restrictions on everyday activities can have an important effect on the patient’s quality of life [35]. Oral health-related quality of life (OHRQoL) is a relatively new concept in dentistry. It is an aspect of dental health addressing the patient’s perception of whether his/her current oral health status has an impact upon his/her actual quality of life [35]. Therefore, OHRQoL may provide a new perspective when looking at a patient, by measuring treatment efficacy in terms of patient satisfaction. There is only little research into the relevance of the various quality of life questionnaires in the treatment of dentin hypersensitivity, yet it may be very valuable to the patient to evaluate the treatment according to these values. Boiko et al. [36] developed, based on in-depth and focus group interviews, a dentin hypersensitivity experience questionnaire (Table 15.2) to capture subjective impacts on patients. The questions can be phrased like “Having the sensations in my teeth takes a lot of the pleasure out of eating and drinking” after which the patients can indicate to what extent he agrees or disagrees.

For home use, both toothpaste and mouthrinses are available. There are a few studies on chewing gum but the results are not very reliable [43, 44]. The working mechanisms fall under two basic categories, being nerve desensitization and occlusion of exposed dental tubules (Table 15.4).