Dentine Hypersensitivity

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original article

Keywords: Dentin hypersensitivity

Corresponding Author: Harlan J. Shiau, DDS, DMSc, Assistant Professor, Department of Periodontics, University of Maryland Dental School, Baltimore, MD 21201; Email: [email protected]

J Evid Base Dent Pract 2012:S1: [220-228]

1532-3382/$36.00

2012 Elsevier Inc. All rights reserved.

Department of Periodontics, University of Maryland Dental School, Baltimore, MD 21201.

DENTIN HYPERSENSITIVITY

Harlan J. Shiau, DDS, DMSc

ABSTRACTContext: In dental practice, dentin hypersensitivity is a commonly presenting con-dition, which consists of sharp pain arising from exposed dentin in response to a varied assortment of stimuli; for example, dietary factors, such as an ice-cold bever-age, to even environmental considerations, such as the exposure to atmospheric air on a cold winters day. The heterogeneity of this presentation, ranging from minor inconvenience to the patient, to a near incapacitating quality-of-life disturbance, as well as the wide range of treatment strategies, as is discussed in this article, certainly pose a challenge to the clinician.

Evidence Acquisition: A search was performed on the MEDLINE database (2002 to present) by way of OVID. Search terms, such as dentin hypersensitivity and vari-ants (eg, dentinal hypersensitivity, cervical dentin hypersensitivity) were used. Select references of review-type articles from the original search were sought.

Evidence Synthesis: Efforts were made to identify multiple comparative clinical treatment studies that were of highest quality study designspecifically, random-ized control trials. Efforts also were made to identify rigorous meta-analysis in the literature on the subject of dentin hypersensitivity treatment.

Conclusion: Although multiple treatment approaches appear to provide clinical success in managing dentin hypersensitivity, the entire body of clinical research lit-erature is far from being unequivocal in pronouncing one superior strategy. Equally as important is the clinicians consideration of the predisposing factors that initially localized the lesion on the tooth surface. Together, personalized preventive mea-sures and therapies focusing on disrupting pathophysiology form the core of effec-tive dentin hypersensitivity management.

InTRoDuCTIon

Dentin hypersensitivity (DH) is characterized by short or transient sharp pain arising from exposed dentin in response to an array of stimulisuch as ther-mal, mechanical, osmotic, or chemical elements.1,2 Generally, as a predisposing fac-tor 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

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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 stimu-lus range from toothbrush bristle to metallic materials, such as an eating utensil or dental instrument.4 Developing evi-dence-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

EpIDEMIology of DHDespite 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 hyper-sensitivity range from 3% to 73% of the adult population of Western Europe and the United States.7,9,10 Again, the het-erogeneity 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 institutional settings. Reviews of available studies conclude that the incidence of hypersensitivity in most popu-lations ranges from 10% to 30% of the general population.8,11 Some studies indicate there is a higher female incidence in DH compared with males.12,13 The literature reports that DH most commonly affects premolars and incisor teeth. Some studies indicate that the molar teeth are least likely to be affected by DH.13 The role of age in the distribution or in-cidence of DH is unclear. On one hand, the severity of the condition increasing with age has been attributed to the in-creased prevalence of periodontal disease, periodontal treat-ment, gingival recession, and erosive toothwear on exposing dentine to external stimuli.4,13 All of the aforementioned sce-narios would presumably act to increase the susceptibility to classic DH stimulus. At the same time, some reports indicate the occurrence of DH to be at peak presentation at the between the third and fourth decades, followed by a gradual decline thereafter.4

MECHAnISM of DHTheories for the mechanism of DH are intimately related to the anatomy and histology of the dentin-pulpal complex. Recall that odontoblast cells synthesize the dentins collagen matrix (majority Type I) and are instrumental in the mineral-ization process; odontoblasts are crucially involved in dentin formation and repair.14 The macrostructure of dentin consists of tubule units, surrounded by hypermineralized tissue: peri-tubular dentin (fig. 1, A and B). The dentin tubule contains serum-like fluid and an odontoblast cell process. Ultrastruc-tural studies have confirmed the close physical proximity of sensory nerves to the odontoblast (process and cell body).15

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.4-6 for instance, exposure to cold winter air when

Figure 1. (a) Histologic cross-section of tooth showing enamel, labeled a, and dentin, labeled B. (Source: Photo taken by user:dozenist. http://commons.wikimedia.org/wiki/File:Crosssectiontooth11-24-05.jpg#filehistory

A

B

Creative Commons license/gnu.) (B) With smear layer removed the ultrastructure of open dentin tubules are visualized clearly. (Courtesy of Drs gary Hack and Ru-Ching Hsia.)

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predisposes DH.21 for example, toothbrush abrasion, along with abrasive components contained in dentifrice, may con-tribute to the loss of enamel structure. Simultaneous expo-sure of these regions to abrasion and dietary acid challenge has been shown to enhance softening of remaining tooth structure.22 Here, susceptibility to further structural damage occurred with even just a few brush strokes. Gingival reces-sion, which may occur with aging, chronic periodontitis, or destructive habits, also contributes as a predisposing factor of DH. In general, patients with periodontitis have a relatively greater prevalence of DH, presumably because of the greater risk and extent of root exposure as a result of periodontal destruction.

Historically, a few theories on the mechanism of pain from DH had been advanced. The dentinal receptor mechanism theory describes a role of direct stimulation of the sensory nerve endings in dentin. Nonetheless, there are experimental and microscopic findings that conclude it improbable that neural cells exist in the outer dentin. In the odontoblastic transduction theory, the odontoblast cell functions to medi-ate membrane potential changes through a synaptic junction with pulpal innervation. In this scenario, the odontoblastic processes are exposed at the dentin surface and are thus susceptible to excitation by chemical and mechanical stimuli. There is not widespread scientific backing for the odonto-blastic transduction theory.

The hydrodynamic theory, often attributed to Brnnstrm,16 is the most widely accepted contemporary explanation for DH. Hyperesthesia results from fluids within the dentinal tu-bules becoming disturbed by temperature, or physical or os-motic changes. These fluid changes or movements stimulate a baroreceptor, which leads to a neural signal. The hydro-dynamic theory forms a plausible explanation for the classic stimuli of DH. for instance, air movement desiccates the den-tin surface, yielding an outward flow of dentinal fluid toward the dehydrated surface. The consequent movement triggers nerve fibers and generates a painful sensation. In an analo-gous method, thermal stimulus would result in contraction of the dentin tubules, resulting in changes in dentinal fluid flow, again, generating excitation of nerves. Osmotic stimuli, such as acids, salt, and sugar, also result in dentinal fluid movement (fig. 2, A and B).

Diameter, patency status, and number of open tubules are likely factors that distinguish the DH-affected tooth versus the nonsensitive tooth. Teeth affected by DH have a great-er number of patent tubules, almost 8 times per unit area, compared with nonsensitive teeth.17 Tubule diameter is also greater in teeth affected by DH versus nonsensitive teeth.18 It is suggested that this patency (or lack of patency) is related to acid demineralization and inability to remineralize. Exposed dentin tubules close as a result of reactive sclerosis and the deposition of secondary and tertiary dentine.19 Hypermin-eralization of peritubular dentine, that is, the dentin adjacent to odontoblastic process, as well as the precipitation of min-erals from saliva or fluid within the tubules, results in reac-tive sclerosis.20 Scanning electron microscopic evaluation of hypersensitive dentin confirms the presence of widely open dentin tubules.17

A predisposing condition for DH is the access to dentin that arises from gingival recession and loss of cementum or loss of enamel. Under normal conditions, dentin is covered by enamel or cementum; only with the exposure of the pe-ripheral termination of the dentinal tubules is DH possible. Loss of enamel, as a result of abrasion or erosion, followed by the action of dietary acids maintaining tubule patency,

Figure 2. (A) A simplified diagram of the dentino-pulpal complex. a, Dentin tubule; B, odontoblast cell and extending process, note proximally associated nerves (yellow); C, nerve/nerve plexus in pulp region. (Source: Illustrated by H.J. Shiau.) (B) Upon challenge by a stimulus (thermal, mechanical, evaporative, chemical), the exposed dentin and open tubules permit a change in rate of fluid flow in the dentin tubule. An action potential is generated involving the trigeminal sensory nerves (yellow). (Source: Illustrated by H.J. Shiau.)

A

B

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fig. 3 summarizes the strategies used in directed therapy of DH. The remaining part of the article focuses on select strategies from this table.

potassium nitratePotassium nitrate is the most common therapeutic agent taking the strategy of nerve desensitization. Potassium nitrate is an effective treatment modality that is currently used in most over-the-counter desensitization toothpastes and a variety of at-home and in-office gels. The mechanism of potassium nitrate is likely related to its ability to increase the extracellular potassium ion concentration, consequently depolarizing the nerve and preventing it from re-polarizing. In general, patients report favorable outcomes in the use of potassium nitrate in managing their DH symptoms.26 In one of the earliest studies, potassium nitratecontaining denti-frices (5% potassium nitrate) have been demonstrated to be safe on the pulp, and, with daily use, to be effective in desensitizing affected teeth for up to 4 weeks.27 However, a recent cochrane review of potassium nitratecontaining toothpastes, factoring in a meta-analysis of 6 studies, was unable to offer strong support for the use of potassium salts in the management of DH.28

Strontium saltsStrontium salts precipitate insoluble metal compounds on the tooth surface, thus occluding or partially occluding open tubules.29 Alternative explanations described in the literature include nerve depolarization effects or (stron-tium) replacement of calcium in the hydroxyapatite scaf-fold to strengthen demineralized dentin.30 Strontium salts have been incorporated into toothpastes and have been reported in several clinical studies.31-34 Generally, these stud-ies reported an improvement in the patients perception of DH-related symptoms. An example of a commonly available dentrifice using strontium salts is Sensodyne Rapid Relief (GlaxoSmithKline, United Kingdom), which has 8% stron-tium acetate in silica base (and sodium fluoride). Dietary acidic challenge does not significantly alter the occlusion of tubules provided by strontium acetate.35 A more recent investigation affirmed the tubule-occluding properties in situ of a strontium acetatecontaining toothpaste, but sug-gested that the silica abrasive component of the dentifrice may be responsible in part for desensitizing properties.36

fluoridesFluoride products, such as sodium fluoride and stannous fluoride, have demonstrated positive effects in occluding dentin tubules and offering clinical sensitivity relief. Topically applied fluoride creates a barrier by precipitating CaF2 on the dentin surface.37 One randomized control study indi-cates effectiveness of 2 separate 5% sodium fluoride var-nish products in sensitizing efficacy, as measured by VAS re-sponse to air and cold tests, over a 24-week period.38 Topical

ClInICAl DIAgnoSISAn 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 manage-ment of DH. A careful differential diagnosis must be devel-oped 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 thorough dietary history and information on oral hygiene practices. Again, a proper his-tory of the nature of pain, clinical evaluation, radiographic examination, and use of diagnostic tests, such as percussion, palpation, and pulp vitality testing will aid in confirming DH by excluding other conditions. A clinical technique of diag-nosing DH may involve the use of air from a triple-syringe or use of an exploratory probe on the exposed dentin. The severity or degree of pain can be quantified according to either a categorical scale (ie, slight, moderate, or severe pain) or using a visual analogue scale (VAS).21 Such struc-tured data collection will best allow the clinician to track a patients DH symptoms during the course of treatment.

MAnAgEMEnT of DHThe management of DH should first consider preventive strategies directed at predisposing etiological factorsagain, related to the localization of the lesion via abra-sion/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. Soda, recently receiving attention because of unhealthy sugar content, also contains phosphoric acid in concentration of 0% to 1%.24,25 The fre-quency of consumption and interval between consumption should be monitored in considering pellicle reformation and rehardening of the acid-softened surface.22 contribut-ing factors to gingival recession, such as overzealous brush-ing, factitial habits, and tongue jewelry should also be con-sidered. Excessive frequency of brushing has been noted in many subjects plagued by DH.20

Directed therapy aims to interfere, whether transiently or permanently, with the mechanism of DH. conceptually, there are 2 major strategies in managing DH: (1) impede or diminish neural transmission, and (2) physically occlude or plug the patent tubule. This second strategy is repre-sentative of a broad number of treatment modalities that range from the use of ions/salts/ proteins to plug tubules, to application of restorative materials (dentin sealers) de-signed to physically block, to the use of periodontal soft tissue grafting, and, finally, more recently, the use of lasers.

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applications.51 The action of bioactive glass in management of DH is occlusion of open dentinal tubules. This bioma-terial precipitates hydroxycarbonate apatite layer, thereby blocking patent tubules. Under the brand name Novamin (Dentsply; USA), this component is available in office-prescribed dentifrices and in-office prophylaxis pastes. The aforementioned toothpaste formulation has demonstrated short-term 6-week clinical effectiveness in reducing DH pain compared with both strontium-based toothpaste and placebo.52 In vitro studies confirm via scanning electron microcopy and assessment by hydraulic conductance that bioactive glass containing dentifrice occludes dentinal tu-bules.53 Subsequent studies investigated the potential of use of bioactive glasscontaining pastes in postoperative man-agement of dentinal hypersensitivity associated with peri-odontal surgery.54 Bioactive glass induction of natural min-eral formation in situ is a similar strategy used by recently developed arginine-containing compounds.

ArginineArginine and calcium carbonate formulations have been developed to manage DH symptoms based on naturally occurring biological process of tubule occlusion by salivary glycoproteins. Saliva transports calcium and phosphate in proximity to dentin tubules to induce occlusion and for-mation of a protective salivary glycoprotein with calcium and phosphatea process favored under alkaline pH con-ditions. These observations underpinned the commercial research and development of a formulation containing ar-ginine, an amino acid positively charged at physiological pH; bicarbonate, functioning as a pH buffer ; and calcium car-bonate, functioning as a source of calcium. The mechanism

fluoride gel (1.23% sodium fluoride) has been suggested for use in decreasing postoperative sensitivity associated with tooth-bleaching procedures.39,40 Stannous fluoride, often in an aqueous solution carrier or with carboxymethyl cellu-lose, is effective in addressing DH.41 Again, the mechanism is likely the specific precipitation of stannous fluoride on the dentine surface, or general generation of high mineral content to block tubules.42

oxalatesOxalates are used to manage DH by leveraging their abil-ity to form precipitates within dentin tubules, consequent-ly blocking dentinal fluid flow.43 The oxalates, such as 3% monohydrogen-monopotassium oxalate, have the added benefit of relative insolubility in acid, rendering them very resistant to dissolution on treatment.44 A recent system-atic review found only 3% monohydrogen-monopotassium oxalate as effective in decreasing DH, but recommended more stringent studies.44

glutaraldehydeA combination product composed of an aqueous solution of 5% glutaraldehyde and 35% hydroxyethyl methacrylate (Gluma Desensitizer ; Heraeus, Germany) has been de-scribed to be an effective desensitizing agent for up to 7 to 9 months. Glutaraldehyde blocks dentinal tubules counter-acting the hydrodynamic mechanism, responsible for DH. Reductions in DH ranging from 5% to 27% are reported, al-though the issue of placebo effect is raised.45 The proposed mechanism of glutaraldehyde involves the reaction with se-rum albumin in dentinal fluid, leading to precipitate forma-tion, and subsequent narrowing or blocking of the tubule.46 Studies using scanning electron microscopy and confocal laser scanning microscopy have verified that intratubular blocking via protein coagulation occurs to some degree.47

Resins and AdhesivesThe basis for the use of resins and adhesives is to seal the dentin tubules and thus prevent the transmission of hydro-dynamic stimuli to the pulpal nerve complex. The deposition of a thin film coating using professionally applied polymer-based materials, such as resins and dentin-bonding agents, generates an artificial smear layer to seal open tubules.48 Dentin-bonding system products, not originally intended for managing DH specifically, have demonstrated efficacy in decreasing sensitivity, although in varying magnitudes.49 clinically, this treatment selection usually occurs after the exhaustion of at-home strategies.50

Bioactive glassAs a biomaterial, bioactive glass has been used in dentistry over the past 4 decades. This class of glass-ceramic com-pounds was developed as a bone repair and regenera-tion material in orthopedic, maxillofacial, and periodontal

Figure 3. Main strategies used in directed therapy of dentin hypersensitivity.

Strategies of Directed Therapies of Dentin Hypersensitivity

1. IMpEDE nEuRAl TRAnSMISSIon Example: Potassium nitrate

2. pHySICAlly CoVER/plug TuBulES

2.1. Plugging Tubules

2.1.1. Ions/Salts: Example: Strontium salts, Oxalates,Calcium Phosphate, Fluorides

2.1.2. Protein precipitates: Example: Formaldehyde, Glutaraldehyde

2.2. Dentin Sealers

2.2.1. Glass ionomers

2.2.2. composites

2.2.3. Dentin adhesives

2.2.4. Other

2.3. Lasers

2.4. Mucogingival plastic surgery

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microscopy, scanning electron microscopy, and atomic force microscopyconfirming occlusion of patent tubules.55,56 Studies evaluating fluid movement via hydraulic conduc-tance experiments have shown inhibition of the hydrody-namic mechanism of DH.55 Studies evaluating efficacy of 8% argininecalcium carbonatefluoridecontaining tooth-paste in reduction of DH symptoms show superiority over 2% potassium ioncontaining toothpastes in an 8-week study.57,58 Arginine formulation containing dentifrice has an advantage of providing immediate relief of dentin hypersen-sitivity when topically applied.59 As with other treatments of DH, the susceptibility to acid challenge negatively impacts maintenance of relief from discomfort.35

periodontal surgeryMucogingival surgery aimed at root coverage attempts to minimize areas of exposed dentin. The vast majority of peri-odontal clinical research on root coverage procedures mea-sures outcome success with respect to physical change (e.g. percent root coverage achieved), rather than patient-based outcomes.60 A recent systematic review identified and analyzed 9 studiesall of which noted a decrease in cervical dentin hypersensitivity observed following root coverage surgery. However, the authors caution that the predictability of the procedure(s) may be in question; fur-ther rigorous, well-executed clinical trials are needed.61

lasersLow-output devices, such as the He-Ne laser or diode-type laser, have been investigated as a prospective treatment for DH. Original publications of He-Ne lasers applied to treat dentin hypersensitivity used low-output power at 6 mW in both continuous wave and pulsed modes. Effectiveness varied considerably from 5% to 100%.62 The mechanism involved in laser treatment of dentine hypersensitivity re-mains to be fully elucidated. Some experiments suggest that low-output lasers of the diode type may operate by me-diating an analgesic effect controlled by decreasing nerve transmission.63

Higher output lasers, such as the Nd:YAG and cO2 laser have also been evaluated in the treatment of DH. The mechanism of Nd:YAG laser effects on DH is thought to be the laser-induced blocking or contraction of dentinal tubules and/or analgesia.64,65 The cO2 laser addresses DH by similarly occluding or narrowing the dentinal tubules.66 This study also reported the safety of using the laser in not creating thermal damage to the pulpa similar finding for many other studies applying lasers to DH treatment.67

Overall, there is considerable potential for development of laser application in managing DH; certainly, further investiga-tion is required addressing issues of recurrence of DH and safety. of arginine-calcium carbonate formulations in address-

ing DH have been established via confocal laser scanning

Figure 4. The management of dentin hypersensitivity includes (I) preventive measures, addressing predisposing/contributing factors and (II) direct therapy, which targets the mechanism of dentin hypersensitivity. Selection of at-home, in-office, or combination treatments depends on the patients severity of discomfort and magnitude of quality-of-life disruption.

I. PREVENTIVE

ORAL HYGIENE:(Proper brushing technique; Proper type of toothbrush; Timing of toothbrushing related to acidic intake)DIET INVENTORY & HISTORY: (Acidic foods/drinks; Identify eating disorders)MEDICAL CONSULTATION:(e.g. Erosion related to regurgitation and vomiting related to a medical condition?)OTHER:Address para-function related to attrition?

II. DIRECTED THERAPY

At-Home

In-Office

Combination

Home applied desensitizing agents: (1)Over the counter available(2)Office directed, home-applied

Office applied desensitizing agentsResins/adhesives Periodontal surgery/Endodontic Tx

Patient presents with signs and symptoms consistent with a working diagnosis of dentin hypersensitivity (DH)

Alternative diagnosis assessed and excluded

DH Management plan formed:

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9. chabanski MB, Gillam DG, Bulman DG, Newman HN. Prevalence of cer-vical dentine sensitivity in a population of patients referred to a special-ist Periodontology Department. J clin Periodontol 1996;23(11):989-92.

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11. Ye W, feng XP, Li R. The prevalence of dentine hypersensitivity in chi-nese adults. J Oral Rehabil 2010;39(3):182-7.

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14. Holland GR. Morphological features of dentine and pulp related to den-tine sensitivity. Arch Oral Biol 1994;39(Suppl):3S-11S.

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29. Miller S, Truong T, et al. Recent advances in stannous fluoride technol-ogy: antibacterial efficacy and mechanism of action towards hypersen-sitivity. Int Dent J 1994;44(1 Suppl 1):83-98.

pRACTICAl ConSIDERATIonS In DH MAnAgEMEnTfirst, the clinician should develop a preventive strategy to-ward 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 re-moval (erosion or zealous toothbrush use). Another exam-ple would be the counseling of a patient to reduce or elimi-nate intake of acidic foods deemed contributory to erosion of enamel. Only with predisposing factors addressed should the clinician begin to formulate directed therapy toward the hypersensitivity, aimed at interfering with the mechanism of DH. At-home strategies in the form of dentifrices and rinses, using the active ingredients and materials described previously, are generally safe, cost-effective, and reversible. More-invasive in-office treatments form the next compo-nent of directed therapy; a suggested working algorithm is presented based on the currently available and reviewed DH treatments discussed in this article (fig. 4)

The literature presents many clinically successful approach-es at managing DH. Products, including at-home strategies containing fluorides, strontium chlorides, and more contem-porary materials, such as bioactive glass and arginine, have been broadly studied and are shown to be safe and benefi-cial to patients with DH. The reviews of individual strategies correctly point out that, in many instances, there does not exist a large body of systematic and rigorous controlled studies to demonstrate efficacy clinically. As such, clinical re-search cannot currently proclaim one technique to be vastly superior to another in DH management.

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JOURNAL Of EVIDENcE-BASED DENTAL PRAcTIcE SPEcIAL ISSUEPERIODONTAL AND IMPLANT TREATMENT

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Dentin HypersensitivityIntroductionEpidemiology of DHMechanism of DHClinical DiagnosisManagement of DHPotassium nitrateStrontium saltsFluoridesOxalatesGlutaraldehydeResins and AdhesivesBioactive glassArgininePeriodontal surgeryLasers

Practical Considerations in DH ManagementREFERENCES