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2006;137;990-998J Am Dent Assoc

Robin Orchardson and David G. GillamManaging dentin hypersensitivity

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JADA, Vol. 137 http://jada.ada.org July 2006 991

CLINICAL PRACTICE PRACTICAL SCIENCE

We obtained and read the full-text copies of therelevant publications. We also searched the bibli-

ographies of these articles to identify materialthat we may have missed in our MEDLINE

search. We placed this material in context with

the existing body of knowledge about DH.

CHARACTERISTICS OF HYPERSENSITIVEDENTIN

Clinical features.Definition. DH is character-ized by short sharp pain arising from exposed

dentin in response to stimulitypically thermal,evaporative, tactile, osmotic or chemicalthat

cannot be ascribed to any other dental defect ordisease.1 DH usually is diagnosed after other pos-

sible conditions have been eliminated. Alternativecauses of pain include chipped or fractured teeth,

cracked cusps, carious lesions, leaky restorationsand 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 dueto differences in the populations studied and the

methods of investigation (for example, question-naires or clinical examinations). The prevalence

of DH is between 60 and 98 percent in patientswith periodontitis.7A majority of patients, how-

ever, do not seek treatment to desensitize theirteeth because they do not perceive DH to be a

severe oral health problem.8

In response to ques-tionnaires, dentists have reported that DH affects

between 109 and 25 percent10 of their patients.Schuurs and colleagues9 also reported that den-

tists believe DH presents a severe problem foronly 1 percent of their diagnosed patients.

Distribution. While DH mostly occurs inpatients who are between 30 and 40 years old,2 it

may affect patients of any age. It affects womenmore often than men, though the sex difference

rarely is statistically significant. The conditionmay affect any tooth, but it most often affects

canines and premolars

3,4

; the affected teeth tendto vary among studies and populations, and dif-

ferent distribution patterns have beendescribed.11

Etiology.Mechanisms of sensitivity. Dentin isnaturally sensitive owing to its close structuraland functional relationship with the dental pulp.12

This inherent sensitivity usually is not a problembecause other tissues cover the dentin. Micro-

scopic examination reveals that patent dentinaltubules are more numerous and wider in hyper-

sensitive dentin than in nonsensitive dentin.13,14

These observations are consistent with the

hypothesis that dentinal pain is mediated by ahydrodynamic mechanism.15 In the hydrodynamic

sequence, a pain-provoking stimulus applied todentin increases the flow of dentinal tubular

fluid. In turn, this mechanically activates thenerves 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 thepulp more effectively activate intradental nerves

than do stimuli such as heating or probing thatcause fluid to flow toward the pulp.12,16 The obser-

vation that about 75 percent of patients with DHcomplain of pain on receiving cold stimuli sup-

ports this hypothesis.

3

Lesion localization. More than 90 percent of

hypersensitive surfaces are at the cervical marginon 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 ofdentin, either by loss of enamel or by gingival

recession. Gingival recession is the more impor-tant of these two factors.18 Normal toothbrushing

will not remove enamel, but it has been cited inthe etiology of gingival recession.18

Lesion initiation. Not all exposed dentin is sen-

Stimulus:

thermal, mechanical,evaporative, chemical

Acts on

Exposed dentin; opentubules

Increase rate of dentinalfluid flow

Generation of actionpotentials in intradental

nerves

Action potentials pass to brainto cause pain

dentin

pulp

nerve

Figure 1. Outline of the hydrodynamic mechanism by which stimuliactivate intradental nerves to cause pain.

Copyright 2006 American Dental Association. All rights reserved.

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992 JADA, Vol. 137 http://jada.ada.org July 2006

sitive. The localized DH lesion has to be initiated.

This occurs when the smear layer or tubularplugs are removed, which opens the outer ends of

the dentinal tubules.17

Abrasion and erosion maybe implicated here, but acid erosion seems to be

the predominant factor.18 Plaque is not a signifi-cant 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 hypersensi-tivity may occur after periodontal procedures

such as deep scaling, root planing or gingivalsurgery.20 Hypersensitivity also may occur after

tooth whitening and restorative procedures.21

EVALUATING DESENSITIZING AGENTS

AND TREATMENTS FOR DENTINHYPERSENSITIVITY

Principles.An understanding of the hydro-dynamic mechanism of dentin sensitivity pro-

vides a basis for developing desensitizing thera-pies. Desensitizing agents may target various

points in the hydrodynamic sequence, whichcan be interrupted by various actions (Figure 2).

Research involves conducting laboratorystudies that screen potential treatments and

identify their mechanisms of action. To evaluate

claims made by desensitizing products manufac-turers, practitioners should be aware of the limi-

tations and strengths of these research methods.Dentin disk model. Small dentin disks pre-

pared from extracted teeth can be used to mea-

sure the permeability of dentin. Permeability isderived from the hydraulic conductance or ease of

fluid flow through the dentin.22 Some desensi-tizing agents such as oxalates reduce dentin per-

meability, while others such as potassium nitratedo not. Treated dentin disks can be examined

using a scanning electron microscope to visualizesurface deposits and tubule occlusion.23 By incor-

porating the dentin disk specimens in intraoralappliances, experiments can be conducted in situ

under natural conditions in the mouth.24 It also ispossible to replicate the outward flow of dentinal

fluid,25 which can oppose pulpward diffusion ofdesensitizing agents.

Recording conduction in isolated nervefibers. 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 rapidscreening of potential desensitizing agents, they

generally do not mimic natural conditions or indi-cate how the agent will behave when exposed to

saliva and masticatory forces.Clinical trials. The ultimate test of any treat-

ment is how well it works in the clinic. A random-ized, blinded and controlled trial is the gold

standard for determining efficacy.30 In such a clin-ical trial, the product is compared with the same

formulation minus the active ingredient, whichcan 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 itscomparators.

CLINICAL MANAGEMENT OF DENTINHYPERSENSITIVITY

Classifying treatments for DH can be challenging

because its modes of action often are unknown. Itcan be simpler to classify treatments according to

their mode of delivery. Treatments can be self-

administered by the patient at home or be appliedby a dental professional in the dental office. At-

home methods tend to be simple and inexpensiveand can treat simultaneously generalized DH

affecting many teeth.31 In-office treatments aremore complex and generally target DH localized

to one or a few teeth. These various treatment

dentin

pulp

nerve

Stimulus:

thermal, mechanical,evaporative, chemical

1. Avoid the pain-producing stimulus

2. Occlude the dentinal tubules

a. Formation of smear layer, plug tubule openings

b. Increase formation of

intratubular dentin

c. Induce formation

of tertiary dentin

3. Decrease intradental nerve excitability

Figure 2. Stages in the hydrodynamic sequence outlined inFigure 1 that can be targeted by desensitizing treatments.



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options can be graded by their complexity(Figure 332).

History, examination and diagnosis.Adiagnosis of DH should be determined only when

the practitioner has considered differential diag-

noses after conducting a methodical history andexamination of the patient. As we mentioned pre-

viously, DH is defined as a transient tooth painarising in response to stimulation.1 The other

causes of transient tooth pain must be excludedfor a diagnosis of DH to be made. Quantifying the

initial degree of sensitivity provides a baselinefrom which to chart subsequent changes in the

condition. Pain scores can be quantified using adescriptive 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 aprobe or jet of air. The patients own evaluation of

the severity of his or her sensitivity also shouldbe recorded, as it is important to establish the

severity of the condition as it affects daily life.30

PREVENTION OF DENTINHYPERSENSITIVITY

Evidence suggests that many professionals do notconsider the preventive aspects of DH.1,11 One

study demonstrated the value of prevention byfinding that the efficacy of laser desensitizing

treatment increased when etiologic factors wereremoved.33 The development of a sound treatment

plan for any oral health condition should considercausative factors. Similarly, any treatment plan

for DH should include identifying and elimi-nating predisposing etiologic factors such as

endogenous or exogenous acids and toothbrushtrauma.

The role erosive agents play in the develop-ment of DH is well-established.2,18 Exogenous

dietary sources like fruits, fruit juices and winecontain acids that can remove smear layers and

open dentinal tubules. Endogenous acids arisingfrom gastric acid reflux or regurgitation also can

produce DH, which characteristically affectspalatal surfaces.

Toothbrushing with an abrasive toothpaste can

abrade the dentin surface18 and may open updentinal tubules if combined with erosive agents.

Patients should avoid toothbrushing for at leasttwo to three hours after consuming acidic foods or

drinks to reduce the deleterious coeffects of acidsand 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 theyrecord their food and drink consumption over a

period of consecutive days spanning a week andweekend. The diary may reveal changes in the

patients diet that may contribute to DH. Thediary also could present an opportunity for practi-

tioners to review their patients oral hygienepractices.

AT-HOME TREATMENTS

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 dentinaltubules (those that contained strontium salts and

fluorides) or destroy vital elements within thetubules (those that contained formaldehyde).

Now, most desensitizing toothpastes contain apotassium salt such as potassium nitrate, potas-

sium chloride or potassium citrate, though onestudy34 reported that a remineralizing toothpaste

containing sodium fluoride and calcium phos-phates 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 ofintradental nerves by altering their membrane

potential.26,37 The efficacy of potassium nitrate toreduce DH, however, is not supported strongly by

the literature, according to Poulsen and col-

Adhesive material or surgery+ prevention

Eliminate predisposing factors+ desensitizing toothpaste or mouthwash

Pain persists

Pain persists

Topical agent + prevention+ desensitizing toothpaste

Diagnosis of dentin hypersensitivity

1

2

3

Figure 3. Pain ladder showing increasing pain and complexity ofdesensitizing treatments. Adapted with permission of the WorldHealth Organization.32




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leagues.38 These authors undertook a meta-analysis of clinical trials on potassium nitrate

toothpastes published up to 1998. Eight studiessatisfied 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 signifi-cantly decreased DH when compared with base-

line or negative controls. A product containing 5percent potassium nitrate and 0.454 percent stan-

nous fluoride in a silica base produced signifi-cantly greater reduction in DH than did a tooth-

paste containing 5 percent potassium nitrate and0.243 percent sodium fluoride in a silica base39,40

or than did an alternative formulation containing5 percent potassium nitrate and 0.76 percent

sodium monofluorophosphate in a dicalcium phos-phate base.41,42

An in vitro study of hydraulic conductance indentin disks25 confirmed the findings of these clin-

ical trials.39-42 The product containing 5 percentpotassium nitrate and 0.454 percent stannous flu-

oride in a silica base, which caused significantlygreater reduction in DH, also demonstrated the

lowest hydraulic conductance (permeability) andgreatest inward potassium ion flux in dentin

disks.Two studies support the desensitizing effective-

ness 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 desen-sitizing and abrasive agents. Further studies are

needed to determine that these various ingredi-ents do not interfere with each other. Two studies

found that the antiplaque ingredients triclosan orzinc citrate did not compromise the desensitizing

efficacy of potassium nitrate or citrate.44,46

Toothpaste application. Practitioners shouldeducate patients on how to use dentifrices and

monitor their toothbrushing techniques. Denti-frices should be applied by toothbrushing. There

is no evidence to suggest that finger application ofthe paste increases effectiveness.1 Many patients

habitually rinse their mouths with water aftertoothbrushing. 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. Studieshave found that mouthwashes containing potas-

sium nitrate and sodium fluoride,48,49 potassium

citrate or sodium fluoride50 or a mixture of fluo-rides51 can reduce DH. In only one of these

studies,48 however, was the effect of the activemouthwash significantly greater than that of the

control product. Another study52 concluded that achewing gum containing potassium chloride sig-

nificantly reduced DH, but the study did notinclude a control group.

DH severity should be reassessed two to fourweeks after commencement of treatment to deter-

mine the effectiveness of the first level of desensi-tizing treatment (Figure 3). If at-home care fails

to reduce DH compared with baseline levels, thenext level of treatment, an in-office method

(Figure 3), should be started.

IN-OFFICE TREATMENTS

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 desensitizingtreatment.

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 usedfor desensitization (Table 153-59).

Fluoride. Fluorides such as sodium fluorideand stannous fluoride can reduce dentin sensi-

tivity.53 Fluorides decrease the permeability ofdentin in vitro,22 possibly by precipitation of insol-

uble 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 solution

54

or an adhesivegel.55 Potassium nitrate does not reduce dentin

permeability in vitro,22 but potassium ions doreduce nerve excitability in animal models.26,37

Oxalate. In 1981, Greenhill and Pashley22

reported that 30 percent potassium oxalatecaused a 98 percent reduction in dentin perme-

ability in vitro. Since then, numerous oxalate-based desensitizing products have become avail-

able. Oxalate products reduce dentin permeabilityand occlude tubules more consistently in labora-

tory studies60,61 than they do in clinical trials.36



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Some studies indicated thatoxalates significantly reduced

sensitivity,56-58 while othersreported that the effects of

oxalate did not differ signifi-

cantly from those of aplacebo.53,58

Calcium phosphates. Cal-cium phosphates may reduce

dentin sensitivity effec-tively.59 Calcium phosphates

occlude dentinal tubules invitro62,63 and decrease in vitro

dentin permeability.64

Adhesives and resins.Because many topical desen-sitizing agents do not adhere

to the dentin surface, theireffects are temporary.

Stronger and more adhesivematerials offer improved and

longer-lasting desensitization(Figure 3). In the 1970s,

Brnnstrm and colleagues65

suggested using resin

impregnation to desensitizedentin. Current DH treat-

ments involve using adhe-sives, including varnishes,

bonding agents and restora-tive materials. Practitioners

should be aware that clinicaltrials of adhesive desensi-

tizing materials tend to bepragmatic. Many of these

trials are single-blind studiesbecause true double-blind

conditions are difficult toachieve. Table 253,66-77 pre-

sents a list of products testedsince 1999 that claim to

occlude tubules in hypersen-sitive dentin.Other procedures.Ionto-

phoresis. This procedure uses

electricity to enhance diffu-

sion of ions into the tissues.Dental iontophoresis is used

most often in conjunctionwith fluoride pastes78 or solu-

tions73 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)

TABLE 1

Solutions and products tested in clinical trials.

TYPE CHEMICAL/CONCENTRATION PRODUCT (STUDY)

* Nonmarketed product.

Fluoride

Potassium Nitrate

Oxalate

Calcium Phosphate

Sodium fluoride, stannous

fluoride, hydrogenfluoride

1-15% solutions5%, 10% in gel

3% potassium oxalate

6.8% ferric oxalate

1.5 molars per liter

calcium chloride + 1.0mol/L potassium oxalate

Dentinbloc, Colgate Oral

Pharmaceuticals, Canton,Mass. (Morris andcolleagues53)

* (Hodosh54)* (Frechoso and colleagues55)

Protect, Sunstar Butler,Chicago (Camps and Pashley56)Oxa-gel, Art-dent Ltda,

Araraquara, So Paulo, Brazil(Pillon and colleagues57)

Sensodyne Sealant,GlaxoSmithKline, Jersey City,N.J. (Gillam and colleagues58)

* (Geiger and colleagues59)

TABLE 2

TYPE PRODUCT (STUDY)

Fluoride Varnish

Oxalic Acid andResin

Sealants, Primers

Etch and Primer

Etch and Primerand Adhesive

Primer andAdhesive

Duraphat, Colgate Oral Pharmaceuticals, Canton, Mass.(Gaffar,66 Corona and colleagues67)Fluoline, PD Dental, Altenwalde, Germany (Duran andSengun68)

MS Coat, Sun Medical, Shiga, Japan (Prati andcolleagues69)

Pain-Free, Parkell, Farmingale, N.Y. (Morris andcolleagues53)

Seal & Protect, Dentsply, Konstanz, Germany (Baysan andLynch70)Dentin Protector, Ivoclar Vivadent, Ellwangen, Germany(Schwarz and colleagues71)Gluma Desensitizer, Heraeus Kulzer, Dormagen, Germany(Duran and Sengun,68 Dondi dallOrologio and colleagues,72

Singal and colleagues73)Gluma Alternate, Heraeus Kulzer, Wehrheim, Germany(Dondi dallOrologio and colleagues74)Health-Dent Desensitizer, Healthdent, Oswego, N.Y.(Duran and Sengun,68 Dondi dallOrologio and colleagues74)Prime & Bond 2.1, Dentsply Caulk, Milford, Del. (Swiftand colleagues75)Scotchbond, 3M Dental Products, St. Paul, Minn. (Pratiand colleagues,69 Ferrari and colleagues76)Single Bond, 3M Dental Products (Duran and Sengun68)

Scotchbond, 3M Dental Products (Ferrari and colleagues76)Systemp.desensitizer, Ivoclar Vivadent, Schaan,Liechtenstein (Stewardson and colleagues77)

Scotchbond Multi-Purpose 3M Dental Products(Dondi dallOrologio and colleagues74)

SE Bond, Kuraray, Okayama, Japan (Duran and Sengun68)

Adhesives and resins tested in clinical trials.




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laser,80 the erbium:YAG laser71 and galium-alu-

minium-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 repre-sent a more expensive and complex treatment

modality.Miscellaneous treatments.A large number of

anecdotal reports support alternative approachesfor tooth desensitization. Although these reports

are not truly evidence-based, they may apply to

some clinical situations. Forexample, periodontal surgery

involving coronally positionedflaps reportedly eliminates DH in

extensively exposed root dentin.81

If the DH is associated with anabfraction lesion, occlusal adjust-

ment may be effective.82

MANAGEMENT STRATEGY

Some dental professionals lack

confidence in treating DH. Thissituation may arise because they

do not fully understand thebiology, etiology, diagnosis and

management of this condition. Amanagement strategy is outlined

in a flowchart (Figure 41,30,83). DHis a transient pain evoked by stim-

ulation of dentin with thermal,mechanical, evaporative, osmotic

or chemical stimuli.30 The condi-tion should be diagnosed only

after excluding other possiblecauses of pain.1,30

CONCLUSIONS

Professionals should appreciatethe role causative factors play in

localizing and initiating hypersen-sitive lesions. It is important to

identify these factors so that pre-vention can be included in the

treatment plan. Active manage-ment of DH usually will involve a

combination of at-home and in-office therapies. In practice, the

regimen adopted will depend onthe perceived severity of the con-

dition and the number of teethinvolved. 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-officetreatment 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 choiceof treatment. In all cases, regular reviews are rec-

ommended1 so that appropriate action can betaken.

Practical Science is prepared in cooperation with the ADA Council onScientific Affairs, the Division of Science and The Journal of theAmerican Dental Association. The mission of Practical Science is to

Patient complains of transient dentinal painin response to stimulation (Note 1)

Differential diagnosis:Is there an identifiable

cause for the dentinal pain? (Note 2)

Confirm diagnosis of DHTreat with consideration for convenienceand cost-effectiveness (Note 3)1. Preventive advice2. At-home treatment (for example,desensitizing toothpaste)

Review

(2-4 weeks)(Note 4)

Review(Note 4)

Continue withpreventive advice anddesensitizing toothpaste

No further treatment;reinforce preventiveadvice; continue toreview

In-office treatment:1. Topical agents (forexample, fluorides, oxalates)2. Adhesive materials

Review diagnosisof DH

No

No

Yes

Yes

No pain relief (Note 5) Pain relief

Pain relief

Pain persists

DH confirmed DH not confirmed

No treatment required

Diagnose and treat as

appropriate

START

Figure 4. Flowchart for the clinical management of dentin hypersensitivity (DH).(Adapted with permission of George Warman Publications [UK] Ltd., from Addy andUrquhart.83) Note 1. Pain evoked by thermal, evaporative (jet of air), probe, osmotic orchemical stimuli.30 Note 2. Alternative causes of tooth pain include caries, chipped teeth,cracked tooth syndrome, fractured or leaking restorations, gingivitis, palatogingivalgrooves, postrestoration sensitivity or pulpitis.1 Note 3. Treatment may be delivered in astratified manner, as indicated in Figure 3. With localized or severe DH, practitioners mayprefer to treat the patient directly, using an in-office procedure. Note 4. Some form offollow-up is recommended.1 However, the follow-up interval may vary, depending onpatients or practitioners preference and circumstances. Note 5. If mild sensitivity persistsat the initial follow-up appointment, the practitioner may continue with preventive andat-home therapies. If the sensitivity is more severe, some form of in-office treatment maybe appropriate.



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spotlight scientific knowledge about the issues and challenges facingtodays practicing dentists.

The authors thank Helen Ristic, Department of Scientific Informa-tion, Division of Science, American Dental Association, for conductingliterature searches and obtaining references.

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