Journal of Evidence Based Dental Practice
Original ArticleDentin Hypersensitivity
Introduction
Dentin hypersensitivity (DH) is characterized by short or transient sharp pain arising from exposed dentin in response to an array of stimuli—such as thermal, mechanical, osmotic, or chemical elements.1, 2 Generally, as a predisposing factor to DH, the dentin needs to become exposed, as a result of loss of enamel and/or gingival recession.
The diagnosis of DH typically excludes other forms of dental disease or pathology. The hyperesthesia attributed to DH ranges from a minor annoyance to becoming moderately disruptive of essential daily activities, even effecting specific diet choices and personal plaque control ability. Notably in patients who have completed active periodontal therapy, the failure to address DH will have an adverse effect on intraprocedure discomfort and overall patient compliance to maintenance therapy.3
In practical terms, the most common trigger of DH is cold stimuli.4, 5, 6 For instance, exposure to cold winter air when breathing through the mouth may trigger hyperesthesia, as well as contact with air from the air/water syringe of a dental chair. DH pain may also occur in response to chemical stimuli such as acidic foods or sweets.7 Sources of mechanical stimulus range from toothbrush bristle to metallic materials, such as an eating utensil or dental instrument.4 Developing evidence-based management of DH presents a challenge in the face of heterogeneous stimuli. For example, one observation in appraisals of DH distribution is that not all patients who report “sensitive teeth” are diagnosed as DH, given specific clinical diagnostic/testing criteria.8
Section snippets
Epidemiology of DH
Despite common empirical presentation in the office, a wide range of DH prevalence is reported in the literature. For example, estimates as to the prevalence of dentine hypersensitivity range from 3% to 73% of the adult population of Western Europe and the United States.7, 9, 10 Again, the heterogeneity of prevalence may likely be related to assessment methods, ranging from questionnaires to clinical detection, and possibly related to study location, ranging from private practice to
Mechanism of DH
Theories for the mechanism of DH are intimately related to the anatomy and histology of the dentin-pulpal complex. Recall that odontoblast cells synthesize the dentin's collagen matrix (majority Type I) and are instrumental in the mineralization process; odontoblasts are crucially involved in dentin formation and repair.14 The macrostructure of dentin consists of tubule units, surrounded by hypermineralized tissue: peritubular dentin (Fig. 1, A and B). The dentin tubule contains serum-like
Clinical Diagnosis
An imperative component of any clinical treatment is to ascertain a proper diagnosis and to address predisposing factors of the condition; this is most appropriate in management of DH. A careful differential diagnosis must be developed considering other clinical conditions that may mimic DH: postoperative restorations, cracked tooth syndrome, sensitivity from bleaching, fractured restorations, and dental caries and related pulpitis are some worthy entities to rule out. Also relevant may be a
Management of DH
The management of DH should first consider preventive strategies directed at predisposing etiological factors—again, related to the “localization” of the lesion via abrasion/erosion and/or gingival recession.23 Therefore, some practical measures might be taken related to modification or counseling of dietary intake and oral hygiene technique. Consumption of acidic foods/liquids should be regulated. Fruit, fruit juices, and soft drinks contain concentrations as much as 3% citric and malic acids.
Practical Considerations in DH Management
First, the clinician should develop a preventive strategy toward DH, focusing on predisposing factors (see Fig. 4). These measures, for example, might be aimed at reducing the risk of exposing dentin by identifying the cause of enamel removal (erosion or zealous toothbrush use). Another example would be the counseling of a patient to reduce or eliminate intake of acidic foods deemed contributory to erosion of enamel. Only with predisposing factors addressed should the clinician begin to
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