JADA Continuing Education
Managing dentin hypersensitivity
Robin Orchardson, BDS, PhD, FDS RCPSG and
David G. Gillam, BDS, MSc, DDS
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ABSTRACT
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Background. The objective of this review is to inform practitioners about dentin hypersensitivity (DH) and its management. This clinical information is described in the context of the underlying biology.
Types of Studies Reviewed. The authors used MEDLINE to find relevant English-language literature published in the period 1999 to 2005. They used combinations of the search terms "dentin*," "tooth," "teeth," "hypersensit*," "desensiti*" and "desensitiz*." They read abstracts and then full articles to identify studies describing etiology, prevalence, clinical features, controlled clinical trials of treatments and relevant laboratory research on mechanisms of action.
Results. The prevalence of DH varies widely, depending on the mode of investigation. Potassium-containing toothpastes are the most widely used at-home treatments. Most in-office treatments employ some form of "barrier," either a topical solution or gel or an adhesive restorative material. The reported efficacy of these treatments varies, with some having no better efficacy than the control treatments. Possible reasons for this variability are discussed. A flowchart summarizes the various treatment strategies.
Clinical Implications. DH is diagnosed after elimination of other possible causes of the pain. Desensitizing treatment should be delivered systematically, beginning with prevention and at-home treatments. The latter may be supplemented with in-office modalities.
Key Words: At-home treatments; clinical features; desensitizing treatments; dentin hypersensitivity; etiology; in-office treatments; prevention; toothpastes
Some dental professionals are confused about the diagnosis, etiology and mechanisms of dentin hypersensitivity (DH).1 Practitioners also report that they lack the confidence to manage the condition effectively. In this article, we review the current literature on DH to provide practitioners with information that they can use in the diagnosis and clinical management of DH in their practice.
We used MEDLINE to source relevant English-language literature published in the period 1999 to 2005. We used various combinations of the search terms "dentin*," "tooth," "teeth," "hypersensit*," "desensiti*" and "desensitiz*." We read all the abstracts identified in the search to identify studies describing etiology, prevalence, clinical features and controlled clinical trials of treatments. We also identified laboratory studies of the mechanisms of action of these therapies. We obtained and read the full-text copies of the relevant publications. We also searched the bibliographies of these articles to identify material that we may have missed in our MEDLINE search. We placed this material in context with the existing body of knowledge about DH.
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CHARACTERISTICS OF HYPERSENSITIVE DENTIN
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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.1 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.2 The clinical features of DH are well-documented.2–4
Prevalence.
The prevalence of DH varies from 45 to 57 percent.6 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.7 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.8 In response to questionnaires, dentists have reported that DH affects between 109 and 25 percent10 of their patients. Schuurs and colleagues9 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,2 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 premolars3,4; the affected teeth tend to vary among studies and populations, and different distribution patterns have been described.11
Etiology.
Mechanisms of sensitivity.
Dentin is naturally sensitive owing to its close structural and functional relationship with the dental pulp.12 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.13,14 These observations are consistent with the hypothesis that dentinal pain is mediated by a hydrodynamic mechanism.15 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.12,16 The observation that about 75 percent of patients with DH complain of pain on receiving cold stimuli supports this hypothesis.3
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Figure 1. Outline of the hydrodynamic mechanism by which stimuli activate intradental nerves to cause pain.
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Lesion localization.
More than 90 percent of hypersensitive surfaces are at the cervical margin on the buccal or labial aspects of the teeth.3 It has been proposed that DH develops in two phases.17 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.18 Normal toothbrushing will not remove enamel, but it has been cited in the etiology of gingival recession.18
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.17 Abrasion and erosion may be implicated here, but acid erosion seems to be the predominant factor.18 Plaque is not a significant factor in DH; patients with DH tend to have good plaque control.14,19
DH is more frequently encountered in patients with periodontitis,7,11 and transient hypersensitivity may occur after periodontal procedures such as deep scaling, root planing or gingival surgery.20 Hypersensitivity also may occur after tooth whitening and restorative procedures.21
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EVALUATING DESENSITIZING AGENTS AND TREATMENTS FOR DENTIN HYPERSENSITIVITY
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Principles.
An understanding of the hydrodynamic mechanism of dentin sensitivity provides a basis for developing desensitizing therapies. Desensitizing agents may target various points in the hydrodynamic sequence, which can be interrupted by various actions (Figure 2).
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Figure 2. Stages in the hydrodynamic sequence outlined in Figure 1 that can be targeted by desensitizing treatments.
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Research involves conducting laboratory studies that screen potential treatments and identify their mechanisms of action. To evaluate claims made by desensitizing products’ manufacturers, practitioners should be aware of the limitations and strengths of these research methods.
Dentin disk model.
Small dentin disks prepared from extracted teeth can be used to measure the permeability of dentin. Permeability is derived from the hydraulic conductance or ease of fluid flow through the dentin.22 Some desensitizing agents such as oxalates reduce dentin permeability, while others such as potassium nitrate do not. Treated dentin disks can be examined using a scanning electron microscope to visualize surface deposits and tubule occlusion.23 By incorporating the dentin disk specimens in intraoral appliances, experiments can be conducted in situ under natural conditions in the mouth.24 It also is possible to replicate the outward flow of dentinal fluid,25 which can oppose pulpward diffusion of desensitizing agents.
Recording conduction in isolated nerve fibers.
This model identifies agents (for example, potassium salts)26,27 or procedures (for example, use of lasers)28,29 that may block nerve conduction. Although these in vitro methods allow for rapid screening of potential desensitizing agents, they generally do not mimic natural conditions or indicate how the agent will behave when exposed to saliva and masticatory forces.
Clinical trials.
The ultimate test of any treatment is how well it works in the clinic. A randomized, blinded and controlled trial is the gold standard for determining efficacy.30 In such a clinical trial, the product is compared with the same formulation minus the active ingredient, which can be called "minus active," "negative control" or "placebo." A product also can be tested "head-to-head" against existing products to determine its effective equivalency or superiority with its comparators.
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CLINICAL MANAGEMENT OF DENTIN HYPERSENSITIVITY
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Classifying treatments for DH can be challenging because its modes of action often are unknown. It can be simpler to classify treatments according to their mode of delivery. Treatments can be self-administered by the patient at home or be applied by a dental professional in the dental office. At-home methods tend to be simple and inexpensive and can treat simultaneously generalized DH affecting many teeth.31 In-office treatments are more complex and generally target DH localized to one or a few teeth. These various treatment options can be graded by their complexity (Figure 332).
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Figure 3. Pain ladder showing increasing pain and complexity of desensitizing treatments. Adapted with permission of the World Health Organization.32
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History, examination and diagnosis.
A diagnosis of DH should be determined only when the practitioner has considered differential diagnoses after conducting a methodical history and examination of the patient. As we mentioned previously, DH is defined as a transient tooth pain arising in response to stimulation.1 The other causes of transient tooth pain must be excluded for a diagnosis of DH to be made. Quantifying the initial degree of sensitivity provides a baseline from which to chart subsequent changes in the condition. Pain scores can be quantified using a descriptive category scale (for example, pain is mild, moderate, severe) or a visual analog scale (for example, 0–100). To elicit a pain response for recording purposes, the practitioner can use a probe or jet of air. The patient’s own evaluation of the severity of his or her sensitivity also should be recorded, as it is important to establish the severity of the condition as it affects daily life.30
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PREVENTION OF DENTIN HYPERSENSITIVITY
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Evidence suggests that many professionals do not consider the preventive aspects of DH.1,11 One study demonstrated the value of prevention by finding that the efficacy of laser desensitizing treatment increased when etiologic factors were removed.33 The development of a sound treatment plan for any oral health condition should consider causative factors. Similarly, any treatment plan for DH should include identifying and eliminating predisposing etiologic factors such as endogenous or exogenous acids and toothbrush trauma.
The role erosive agents play in the development of DH is well-established.2,18 Exogenous dietary sources like fruits, fruit juices and wine contain acids that can remove smear layers and open dentinal tubules. Endogenous acids arising from gastric acid reflux or regurgitation also can produce DH, which characteristically affects palatal surfaces.
Toothbrushing with an abrasive toothpaste can abrade the dentin surface18 and may open up dentinal tubules if combined with erosive agents. Patients should avoid toothbrushing for at least two to three hours after consuming acidic foods or drinks to reduce the deleterious coeffects of acids and abrasion.1,18
Most patients are unable to remember details of their food and drink consumption. They should be asked to keep a daily diet diary in which they record their food and drink consumption over a period of consecutive days spanning a week and weekend. The diary may reveal changes in the patient’s diet that may contribute to DH. The diary also could present an opportunity for practitioners to review their patients’ oral hygiene practices.
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AT-HOME TREATMENTS
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Desensitizing toothpastes/dentifrices.
Tooth-pastes are the most widely used dentifrices for delivering over-the-counter desensitizing agents. The first desensitizing toothpastes to appear on the market claimed either to occlude dentinal tubules (those that contained strontium salts and fluorides) or destroy vital elements within the tubules (those that contained formaldehyde). Now, most desensitizing toothpastes contain a potassium salt such as potassium nitrate, potassium chloride or potassium citrate, though one study34 reported that a remineralizing toothpaste containing sodium fluoride and calcium phosphates reduced DH.
Potassium salts.
Toothpastes containing potassium nitrate have been used since 1980.35 Since then, pastes containing potassium chloride or potassium citrate have been made available.36 Potassium ions are thought to diffuse along dentinal tubules and decrease the excitability of intradental nerves by altering their membrane potential.26,37 The efficacy of potassium nitrate to reduce DH, however, is not supported strongly by the literature, according to Poulsen and colleagues.38 These authors undertook a meta-analysis of clinical trials on potassium nitrate toothpastes published up to 1998. Eight studies satisfied their inclusion criteria, but only four studies provided sufficient information to be included in their final meta-analysis.
Since 2000, several trial results of potassium-containing toothpastes have been published. Some of these studies compared different tooth-paste formulations. For instance, six studies39–44 found that pastes containing 5 percent potassium nitrate or 3.75 percent potassium chloride significantly decreased DH when compared with baseline or negative controls. A product containing 5 percent potassium nitrate and 0.454 percent stannous fluoride in a silica base produced significantly greater reduction in DH than did a tooth-paste containing 5 percent potassium nitrate and 0.243 percent sodium fluoride in a silica base39,40 or than did an alternative formulation containing 5 percent potassium nitrate and 0.76 percent sodium monofluorophosphate in a dicalcium phosphate base.41,42
An in vitro study of hydraulic conductance in dentin disks25 confirmed the findings of these clinical trials.39–42 The product containing 5 percent potassium nitrate and 0.454 percent stannous fluoride in a silica base, which caused significantly greater reduction in DH, also demonstrated the lowest hydraulic conductance (permeability) and greatest inward potassium ion flux in dentin disks.
Two studies support the desensitizing effectiveness of pastes containing potassium citrate.45,46 Many toothpastes contain other ingredients such as fluorides (for example, sodium monofluoro-phosphate, sodium fluoride, stannous fluoride) and antiplaque agents in conjunction with desensitizing and abrasive agents. Further studies are needed to determine that these various ingredients do not interfere with each other. Two studies found that the antiplaque ingredients triclosan or zinc citrate did not compromise the desensitizing efficacy of potassium nitrate or citrate.44,46
Toothpaste application.
Practitioners should educate patients on how to use dentifrices and monitor their toothbrushing techniques. Dentifrices should be applied by toothbrushing. There is no evidence to suggest that finger application of the paste increases effectiveness.1 Many patients habitually rinse their mouths with water after toothbrushing. Rinsing with water may cause the active agent to be diluted and cleared from the mouth and, thus, reduce the efficacy of the caries-reducing effect of fluoride toothpastes.47
Mouthwashes and chewing gums.
Studies have found that mouthwashes containing potassium nitrate and sodium fluoride,48,49 potassium citrate or sodium fluoride50 or a mixture of fluorides51 can reduce DH. In only one of these studies,48 however, was the effect of the active mouthwash significantly greater than that of the control product. Another study52 concluded that a chewing gum containing potassium chloride significantly reduced DH, but the study did not include a control group.
DH severity should be reassessed two to four weeks after commencement of treatment to determine the effectiveness of the first level of desensitizing treatment (Figure 3). If at-home care fails to reduce DH compared with baseline levels, the next level of treatment, an in-office method (Figure 3), should be started.
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IN-OFFICE TREATMENTS
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Desensitizing agents intended for at-home use by patients generally are simple to administer. Dental professionals can deliver a wider range of more complex and more potent desensitizing treatment.
Topically applied desensitizing agents.
Before the discovery of local anesthetics, dentists would use toxic chemicals such as silver nitrate, zinc chloride, potash and arsenic compounds to obtund dentin. Now, less toxic materials are used for desensitization (Table 153–59).
Fluoride.
Fluorides such as sodium fluoride and stannous fluoride can reduce dentin sensitivity.53 Fluorides decrease the permeability of dentin in vitro,22 possibly by precipitation of insoluble calcium fluoride within the tubules.
Potassium nitrate.
Potassium nitrate, which usually is applied via a desensitizing toothpaste, also can reduce dentin sensitivity when applied topically in an aqueous solution54 or an adhesive gel.55 Potassium nitrate does not reduce dentin permeability in vitro,22 but potassium ions do reduce nerve excitability in animal models.26,37
Oxalate.
In 1981, Greenhill and Pashley22 reported that 30 percent potassium oxalate caused a 98 percent reduction in dentin permeability in vitro. Since then, numerous oxalate-based desensitizing products have become available. Oxalate products reduce dentin permeability and occlude tubules more consistently in laboratory studies60,61 than they do in clinical trials.36 Some studies indicated that oxalates significantly reduced sensitivity,56–58 while others reported that the effects of oxalate did not differ significantly from those of a placebo.53,58
Calcium phosphates.
Calcium phosphates may reduce dentin sensitivity effectively.59 Calcium phosphates occlude dentinal tubules in vitro62,63 and decrease in vitro dentin permeability.64
Adhesives and resins.
Because many topical desensitizing agents do not adhere to the dentin surface, their effects are temporary. Stronger and more adhesive materials offer improved and longer-lasting desensitization (Figure 3). In the 1970s, Brännström and colleagues65 suggested using resin impregnation to desensitize dentin. Current DH treatments involve using adhesives, including varnishes, bonding agents and restorative materials. Practitioners should be aware that clinical trials of adhesive desensitizing materials tend to be pragmatic. Many of these trials are single-blind studies because true double-blind conditions are difficult to achieve. Table 253,66–77 presents a list of products tested since 1999 that claim to occlude tubules in hypersensitive dentin.
Other procedures.
Ionto-phoresis.
This procedure uses electricity to enhance diffusion of ions into the tissues. Dental iontophoresis is used most often in conjunction with fluoride pastes78 or solutions73 and reportedly reduces DH.73,78
Lasers.
The effectiveness of lasers for treating DH varies from 5 to 100 percent, depending on the type of laser and the treatment parameters.79 Studies have reported that the neodymium:yttrium-aluminum-garnet (YAG) laser,80 the erbium:YAG laser71 and galium-aluminium-arsenide low level laser67 all reduce DH, but the reductions were not significantly different from those of a placebo80 or positive controls.67 In addition to these equivocal results, lasers represent a more expensive and complex treatment modality.
Miscellaneous treatments.
A large number of anecdotal reports support alternative approaches for tooth desensitization. Although these reports are not truly evidence-based, they may apply to some clinical situations. For example, periodontal surgery involving coronally positioned flaps reportedly eliminates DH in extensively exposed root dentin.81 If the DH is associated with an abfraction lesion, occlusal adjustment may be effective.82
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MANAGEMENT STRATEGY
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Some dental professionals lack confidence in treating DH. This situation may arise because they do not fully understand the biology, etiology, diagnosis and management of this condition. A management strategy is outlined in a flowchart (Figure 41,30,83). DH is a transient pain evoked by stimulation of dentin with thermal, mechanical, evaporative, osmotic or chemical stimuli.30 The condition should be diagnosed only after excluding other possible causes of pain.1,30
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Figure 4. Flowchart for the clinical management of dentin hypersensitivity (DH). (Adapted with permission of George Warman Publications [UK] Ltd., from Addy and Urquhart.83) Note 1. Pain evoked by thermal, evaporative (jet of air), probe, osmotic or chemical stimuli.30 Note 2. Alternative causes of tooth pain include caries, chipped teeth, cracked tooth syndrome, fractured or leaking restorations, gingivitis, palatogingival grooves, postrestoration sensitivity or pulpitis.1 Note 3. Treatment may be delivered in a stratified manner, as indicated in Figure 3. With localized or severe DH, practitioners may prefer to treat the patient directly, using an in-office procedure. Note 4. Some form of follow-up is recommended.1 However, the follow-up interval may vary, depending on patient’s or practitioner’s preference and circumstances. Note 5. If mild sensitivity persists at the initial follow-up appointment, the practitioner may continue with preventive and at-home therapies. If the sensitivity is more severe, some form of in-office treatment may be appropriate.
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CONCLUSIONS
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Professionals should appreciate the role causative factors play in localizing and initiating hypersensitive lesions. It is important to identify these factors so that prevention can be included in the treatment plan. Active management of DH usually will involve a combination of at-home and in-office therapies. In practice, the regimen adopted will depend on the perceived severity of the condition and the number of teeth involved. Active treatment may begin with an at-home method, such as a desensitizing dentifrice. This alone may alleviate the condition, but if not, an in-office treatment may be used. When DH is localized to one or two teeth, however, the practitioner may elect to use an in-office method as the first choice of treatment. In all cases, regular reviews are recommended1 so that appropriate action can be taken.
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FOOTNOTES
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DISCLOSURE: Dr. Orchardson has received funding from GlaxoSmithKline (Jersey City, N.J.), Procter & Gamble (Cincinnati), Reckitt Toiletry Products (Derby, England) and Unilever Dental Research (Port Sunlight, England) and has been a consultant to Glaxo-SmithKline. Dr. Gillam has been an assistant director for SmithKline-Beecham and Block Drug Company (now GlaxoSmithKline).
Dr. Orchardson is a senior lecturer, University of Glasgow Dental School, 378 Sauchiehall St., Glasgow G2 3JZ, Scotland, e-mail "R.Orchardson{at}dental.gla.ac.uk". Address reprint requests to Dr. Orchardson. Dr. Gillam is a senior clinician, 4-Front Research, Capenhurst, Cheshire, England, and an honorary senior lecturer, Department of Restorative Dentistry, Eastman Dental Institute for Oral Health Care Sciences, University College London.
Practical Science is prepared in cooperation with the ADA Council on Scientific Affairs, the Division of Science and The Journal of the American Dental Association. The mission of Practical Science is to spotlight scientific knowledge about the issues and challenges facing today’s practicing dentists.
The authors thank Helen Ristic, Department of Scientific Information, Division of Science, American Dental Association, for conducting literature searches and obtaining references.
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