Managing Dentin Hypersensitivity

Managing dentin hypersensitivity
Robin Orchardson and David G. Gillam

J Am Dent Assoc 2006;137;990-998
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CLINICAL PRACTICE
PRACTICAL SCIENCE
Managing dentin hypersensitivity

Robin Orchardson, BDS, PhD, FDS RCPSG; David G. Gillam, BDS, MSc, DDS
JADA, Vol. 137
IO
N
RT
Background. The objective of this review is to
ICLE
inform practitioners about dentin hypersensitivity
N
C
U
U
(DH) and its management. This clinical information
A ING ED 3
RT
is described in the context of the underlying biology.
ICLE
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.
JADA 2006;137:990-8.
Dr. Orchardson is a senior lecturer, University of Glasgow Dental School, 378 Sauchiehall St., Glasgow
G2 3JZ, Scotland, e-mail R.Orchardson@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.
http://jada.ada.org July 2006

Copyright 2006 American Dental Association. All rights reserved.
990
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 GlaxoSmithKline. Dr. Gillam has been an assistant
director for SmithKline-Beecham and Block
Drug Company (now GlaxoSmithKline).
ABSTRACT
CON
ome 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.
CLINICAL PRACTICE PRACTICAL SCIENCE
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.
Stimulus:
thermal, mechanical,
evaporative, chemical
Acts on
Exposed dentin; open
tubules
CHARACTERISTICS OF HYPERSENSITIVE
DENTIN
Increase rate of dentinal

fluid flow
Generation of action
potentials in intradental
nerves
dentin
pulp
Action potentials pass to brain

to cause pain
nerve
Figure 1. Outline of the hydrodynamic mechanism by which stimuli

activate intradental nerves to cause pain.
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
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 sen-
JADA, Vol. 137 http://jada.ada.org

July 2006
991
Clinical features. Definition. DH is characterized 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 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
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
pulp
3. Decrease intradental
nerve excitability
nerve
Figure 2. Stages in the hydrodynamic sequence outlined in

Figure 1 that can be targeted by desensitizing treatments.
sitive. 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
EVALUATING DESENSITIZING AGENTS
AND TREATMENTS FOR DENTIN
HYPERSENSITIVITY
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).
Research involves conducting laboratory
studies that screen potential treatments and
identify their mechanisms of action. To evaluate
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JADA, Vol. 137
CLINICAL MANAGEMENT OF DENTIN

HYPERSENSITIVITY
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 selfadministered by the patient at home or be applied
by a dental professional in the dental office. Athome 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

dentin
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-tohead against existing products to determine its
effective equivalency or superiority with its
comparators.
PREVENTION OF DENTIN
HYPERSENSITIVITY
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
Adhesive material or surgery

+ prevention
Pain persists
Topical agent + prevention

+ desensitizing toothpaste
Pain persists
Eliminate predisposing factors
+ desensitizing toothpaste or mouthwash
Diagnosis of dentin hypersensitivity
Figure 3. Pain ladder showing increasing pain and complexity of

desensitizing treatments. Adapted with permission of the World
Health Organization.32
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
patients diet that may contribute to DH. The
diary also could present an opportunity for practitioners to review their patients oral hygiene
practices.
AT-HOME TREATMENTS
Desensitizing toothpastes/dentifrices. Toothpastes 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 col-

July 2006
993
options can be graded by their complexity

(Figure 332).
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 patients 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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JADA, Vol. 137
mouth and, thus, reduce the efficacy of the cariesreducing 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.
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 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 oxalatebased 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

leagues.38 These authors undertook a metaanalysis 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 potassiumcontaining toothpastes have been published.
Some of these studies compared different toothpaste 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 toothpaste 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 monofluorophosphate, 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

July 2006
995
TABLE 1
Some studies indicated that
oxalates significantly reduced
Solutions and products tested in clinical trials.
sensitivity,56-58 while others
TYPE
CHEMICAL/CONCENTRATION
PRODUCT (STUDY)
reported that the effects of
oxalate did not differ signifiSodium fluoride, stannous Dentinbloc, Colgate Oral
Fluoride
fluoride, hydrogen
Pharmaceuticals, Canton,
cantly from those of a
fluoride
Mass. (Morris and
placebo.53,58
colleagues53)
Calcium phosphates. Cal* (Hodosh54)
1-15% solutions
Potassium Nitrate
cium phosphates may reduce
* (Frechoso and colleagues55)
5%, 10% in gel
dentin sensitivity effecProtect, Sunstar Butler,
3% potassium oxalate
Oxalate
tively.59 Calcium phosphates
Chicago (Camps and Pashley56)
Oxa-gel, Art-dent Ltda,
occlude dentinal tubules in
Araraquara, So Paulo, Brazil
vitro62,63 and decrease in vitro
(Pillon and colleagues57)
64
dentin permeability.
Sensodyne Sealant,
6.8% ferric oxalate
Adhesives and resins.
GlaxoSmithKline, Jersey City,
N.J. (Gillam and colleagues58)
Because many topical desensitizing agents do not adhere
* (Geiger and colleagues59)
1.5 molars per liter
Calcium Phosphate
calcium chloride + 1.0
to the dentin surface, their
mol/L potassium oxalate
effects are temporary.
*
Nonmarketed
product.
Stronger and more adhesive
materials offer improved and TABLE 2
longer-lasting desensitization
Adhesives and resins tested in clinical trials.
(Figure 3). In the 1970s,
TYPE
PRODUCT (STUDY)
Brnnstrm and colleagues65
suggested using resin
Fluoride Varnish
Duraphat, Colgate Oral Pharmaceuticals, Canton, Mass.
(Gaffar,66 Corona and colleagues67)
impregnation to desensitize
Fluoline, PD Dental, Altenwalde, Germany (Duran and
dentin. Current DH treatSengun68)
ments involve using adheOxalic Acid and
MS Coat, Sun Medical, Shiga, Japan (Prati and
sives, including varnishes,
Resin
colleagues69)
Pain-Free, Parkell, Farmingale, N.Y. (Morris and
bonding agents and restoracolleagues53)
tive materials. Practitioners
Sealants, Primers
Seal & Protect, Dentsply, Konstanz, Germany (Baysan and
should be aware that clinical
Lynch70)
trials of adhesive desensiDentin Protector, Ivoclar Vivadent, Ellwangen, Germany
(Schwarz and colleagues71)
tizing materials tend to be
Gluma Desensitizer, Heraeus Kulzer, Dormagen, Germany
pragmatic. Many of these
(Duran and Sengun,68 Dondi dallOrologio and colleagues,72
Singal and colleagues73)
trials are single-blind studies
Gluma Alternate, Heraeus Kulzer, Wehrheim, Germany
because true double-blind
(Dondi dallOrologio and colleagues74)
Health-Dent Desensitizer, Healthdent, Oswego, N.Y.
conditions are difficult to
(Duran and Sengun,68 Dondi dallOrologio and colleagues74)
achieve. Table 253,66-77 prePrime & Bond 2.1, Dentsply Caulk, Milford, Del. (Swift
and colleagues75)
sents a list of products tested
Scotchbond, 3M Dental Products, St. Paul, Minn. (Prati
since 1999 that claim to
and colleagues,69 Ferrari and colleagues76)
Single Bond, 3M Dental Products (Duran and Sengun68)
occlude tubules in hypersensitive dentin.
Etch and Primer
Scotchbond, 3M Dental Products (Ferrari and colleagues76)
Systemp.desensitizer, Ivoclar Vivadent, Schaan,
Other procedures. IontoLiechtenstein (Stewardson and colleagues77)
phoresis. This procedure uses
Etch and Primer
Scotchbond Multi-Purpose 3M Dental Products
electricity to enhance diffuand Adhesive
(Dondi dallOrologio and colleagues74)
sion of ions into the tissues.
Primer and
SE Bond, Kuraray, Okayama, Japan (Duran and Sengun68)
Dental iontophoresis is used
Adhesive
most often in conjunction
with fluoride pastes78 or solutions73 and reportedly reduces DH.73,78
the type of laser and the treatment parameters.79
Lasers. The effectiveness of lasers for treating
Studies have reported that the
DH varies from 5 to 100 percent, depending on
neodymium:yttrium-aluminum-garnet (YAG)
START
No
Patient complains of transient dentinal pain

in response to stimulation (Note 1)
No treatment required
Yes
Yes
Differential diagnosis: Is there an identifiable

cause for the dentinal pain? (Note 2)
Diagnose and treat as

appropriate
No
MANAGEMENT STRATEGY
Confirm diagnosis of DH
Treat with consideration for convenience
and cost-effectiveness (Note 3)
1. Preventive advice
2. At-home treatment (for example,
desensitizing toothpaste)
Review
(2-4 weeks)
(Note 4)
Pain relief
No further treatment;
reinforce preventive
advice; continue to
review
Continue with
preventive advice and
desensitizing toothpaste
In-office treatment:
1. Topical agents (for
example, fluorides, oxalates)
2. Adhesive materials
Review
(Note 4)
Pain relief
Pain persists
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
CONCLUSIONS
Professionals should appreciate

the role causative factors play in
DH confirmed
DH not confirmed
localizing and initiating hypersensitive lesions. It is important to
identify these factors so that preFigure 4. Flowchart for the clinical management of dentin hypersensitivity (DH).
(Adapted with permission of George Warman Publications [UK] Ltd., from Addy and
vention can be included in the
Urquhart.83) Note 1. Pain evoked by thermal, evaporative (jet of air), probe, osmotic or
treatment plan. Active managechemical stimuli.30 Note 2. Alternative causes of tooth pain include caries, chipped teeth,
ment of DH usually will involve a
cracked tooth syndrome, fractured or leaking restorations, gingivitis, palatogingival
grooves, postrestoration sensitivity or pulpitis.1 Note 3. Treatment may be delivered in a
combination of at-home and instratified manner, as indicated in Figure 3. With localized or severe DH, practitioners may
office therapies. In practice, the
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
regimen adopted will depend on
patients or practitioners preference and circumstances. Note 5. If mild sensitivity persists
the perceived severity of the conat 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
dition and the number of teeth
be appropriate.
involved. Active treatment may
begin with an at-home method,
laser,80 the erbium:YAG laser71 and galium-alusuch as a desensitizing dentifrice. This alone may
minium-arsenide low level laser67 all reduce DH,
alleviate the condition, but if not, an in-office
but the reductions were not significantly different
treatment may be used. When DH is localized to
from those of a placebo80 or positive controls.67 In
one or two teeth, however, the practitioner may
addition to these equivocal results, lasers repreelect to use an in-office method as the first choice
sent a more expensive and complex treatment
of treatment. In all cases, regular reviews are recommended1 so that appropriate action can be
modality.
Miscellaneous treatments. A large number of
taken.
anecdotal reports support alternative approaches
Practical Science is prepared in cooperation with the ADA Council on
for tooth desensitization. Although these reports
Scientific Affairs, the Division of Science and The Journal of the
are not truly evidence-based, they may apply to
American Dental Association. The mission of Practical Science is to
Review diagnosis
of DH
996
JADA, Vol. 137

No pain relief (Note 5)
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
spotlight scientific knowledge about the issues and challenges facing

todays practicing dentists.
The authors thank Helen Ristic, Department of Scientific Information, Division of Science, American Dental Association, for conducting
literature searches and obtaining references.

July 2006
997
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