CHARACTERISTICS OF HYPERSENSITIVE DENTIN
Clinical features. Definition. DH is characterized by short sharp pain arising from exposed dentin in response to stimuli—typically thermal, evaporative, tactile, osmotic or chemical—that cannot be ascribed to any other dental defect or disease. DH usually is diagnosed after other possible conditions have been eliminated. Alternative causes of pain include chipped or fractured teeth, cracked cusps, carious lesions, leaky restorations and palatogingival grooves. The clinical features of DH are well-documented.
Prevalence. The prevalence of DH varies from 45 to 57 percent. These variations are likely due to differences in the populations studied and the methods of investigation (for example, questionnaires or clinical examinations). The prevalence of DH is between 60 and 98 percent in patients with periodontitis. A majority of patients, however, do not seek treatment to desensitize their teeth because they do not perceive DH to be a severe oral health problem. In response to questionnaires, dentists have reported that DH affects between 109 and 25 percent of their patients. Schuurs and colleagues also reported that dentists believe DH presents a severe problem for only 1 percent of their diagnosed patients.
Distribution. While DH mostly occurs in patients who are between 30 and 40 years old, it may affect patients of any age. It affects women more often than men, though the sex difference rarely is statistically significant. The condition may affect any tooth, but it most often affects canines and premolars; the affected teeth tend to vary among studies and populations, and different distribution patterns have been described.
Etiology. Mechanisms of sensitivity. Dentin is naturally sensitive owing to its close structural and functional relationship with the dental pulp. This inherent sensitivity usually is not a problem because other tissues cover the dentin. Microscopic examination reveals that patent dentinal tubules are more numerous and wider in hypersensitive dentin than in nonsensitive dentin. These observations are consistent with the hypothesis that dentinal pain is mediated by a hydrodynamic mechanism. In the hydrodynamic sequence, a pain-provoking stimulus applied to dentin increases the flow of dentinal tubular fluid. In turn, this mechanically activates the nerves situated at the inner ends of the tubules or in the outer layers of the pulp (Figure 1). Cooling, drying, evaporation and hypertonic chemical stimuli that stimulate fluid to flow away from the pulp more effectively activate intradental nerves than do stimuli such as heating or probing that cause fluid to flow toward the pulp. The observation that about 75 percent of patients with DH complain of pain on receiving cold stimuli supports this hypothesis.
Lesion localization. More than 90 percent of hypersensitive surfaces are at the cervical margin on the buccal or labial aspects of the teeth. It has been proposed that DH develops in two phases. First, lesion localization occurs by exposure of dentin, either by loss of enamel or by gingival recession. Gingival recession is the more important of these two factors. Normal toothbrushing will not remove enamel, but it has been cited in the etiology of gingival recession.
Lesion initiation. Not all exposed dentin is sensitive. The localized DH lesion has to be initiated. This occurs when the smear layer or tubular plugs are removed, which opens the outer ends of the dentinal tubules. Abrasion and erosion may be implicated here, but acid erosion seems to be the predominant factor. Plaque is not a significant factor in DH; patients with DH tend to have good plaque control.
DH is more frequently encountered in patients with periodontitis, and transient hypersensitivity may occur after periodontal procedures such as deep scaling, root planing or gingival surgery. Hypersensitivity also may occur after tooth whitening and restorative procedures.
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