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Managing dentin hypersensitivity

Robin Orchardson and David G. Gillam
JADA 2006;137(7):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
ome dental professionals
S 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 rel-
evant 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, clin-
ical features and controlled clinical
trials of treatments. We also identi-
fied laboratory studies of the mech-
anisms of action of these therapies.
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).
990 JADA, Vol. 137 http://jada.ada.org July 2006
Copyright ©2006 American Dental Association. All rights reserved.
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ABSTRACT ✷
A
J
A D
A
1
✷
N
RT
CON
Background. The objective of this review is to
IO
ICLE
inform practitioners about dentin hypersensitivity
T
T
A
N
I
C
(DH) and its management. This clinical information U
A ING ED 3
U
is described in the context of the underlying biology. RT
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 treat-
ments 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 “bar-
rier,” 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 vari-
ability 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 Sci-
ences, University College London.
 Downloaded from jada.ada.org on May 27, 2014
We obtained and read the full-text copies of the
relevant publications. We also searched the bibli-
ographies 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.
CHARACTERISTICS OF HYPERSENSITIVE
DENTIN
Clinical features. Definition. DH is character-
ized 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 pos-
sible 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, question-
naires or clinical examinations). The prevalence
of DH is between 60 and 98 percent in patients
with periodontitis.7 A majority of patients, how-
ever, 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 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 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 dif-
ferent 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. Micro-
scopic examination reveals that patent dentinal
tubules are more numerous and wider in hyper-
sensitive dentin than in nonsensitive dentin.13,14
Copyright ©2006 American Dental Association. All rights reserved.
CLINICAL PRACTICE PRACTICAL SCIENCE
Stimulus:
thermal, mechanical,
evaporative, chemical
Acts on
Exposed dentin; open
tubules
Increase rate of dentinal
fluid flow
dentin
Generation of action
potentials in intradental
nerves 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 obser-
vation that about 75 percent of patients with DH
complain of pain on receiving cold stimuli sup-
ports 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 impor-
tant 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-
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CLINICAL PRACTICE PRACTICAL SCIENCE

claims made by desensitizing products’ manufac-

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
dentin
c. Induce formation
pulp of tertiary dentin
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 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 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 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, 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
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 is
derived 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 nitrate
do not. Treated dentin disks can be examined
using a scanning electron microscope to visualize
surface deposits and tubule occlusion.23 By incor-
porating 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 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, 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.
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 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

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

Copyright ©2006 American Dental Association. All rights reserved.
 Downloaded from jada.ada.org on May 27, 2014
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 diag-
noses after conducting a methodical history and
examination of the patient. As we mentioned pre-
viously, 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
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 elimi-
nating predisposing etiologic factors such as
endogenous or exogenous acids and toothbrush
trauma.
The role erosive agents play in the develop-
ment 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
Copyright ©2006 American Dental Association. All rights reserved.
CLINICAL PRACTICE PRACTICAL SCIENCE
Adhesive material or surgery 3
+ prevention
Pain persists
2
Topical agent + prevention
+ desensitizing toothpaste
Pain persists
1
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
patient’s diet that may contribute to DH. The
diary also could present an opportunity for practi-
tioners to review their patients’ oral hygiene
practices.
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 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, potas-
sium chloride or potassium citrate, though one
study34 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 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-
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 Downloaded from jada.ada.org on May 27, 2014
CLINICAL PRACTICE PRACTICAL SCIENCE
leagues.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 signifi-
cantly decreased DH when compared with base-
line or negative controls. A product containing 5
percent 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 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 phos-
phate base.41,42
An in vitro study of hydraulic conductance in
dentin disks25 confirmed the findings of these clin-
ical trials.39-42 The product containing 5 percent
potassium nitrate and 0.454 percent stannous flu-
oride 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 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 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. Denti-
frices 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
994 JADA, Vol. 137 http://jada.ada.org July 2006
Copyright ©2006 American Dental Association. All rights reserved.
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 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 active
mouthwash significantly greater than that of the
control product. Another study52 concluded that a
chewing gum containing potassium chloride sig-
nificantly 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 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, 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 sensi-
tivity.53 Fluorides decrease the permeability of
dentin 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 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 perme-
ability in vitro. Since then, numerous oxalate-
based desensitizing products have become avail-
able. Oxalate products reduce dentin permeability
and occlude tubules more consistently in labora-
tory 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 signifi-
cantly from those of a
placebo.53,58
Calcium phosphates. Cal-
cium phosphates may reduce
dentin sensitivity effec-
tively.59 Calcium phosphates
occlude dentinal tubules in
vitro62,63 and decrease in vitro
64
dentin permeability.
Adhesives and resins.
Because many topical desen-
sitizing agents do not adhere
to the dentin surface, their
effects are temporary.
Stronger and more adhesive
materials offer improved and TABLE 2
longer-lasting desensitization
(Figure 3). In the 1970s,
Brännström and colleagues65
suggested using resin
impregnation to desensitize
dentin. Current DH treat-
ments involve using adhe-
sives, including varnishes,
bonding agents and restora-
tive materials. Practitioners
should be aware that clinical
trials of adhesive desensi-
tizing 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 pre-
sents a list of products tested
since 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 conjunction
with 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
Copyright ©2006 American Dental Association. All rights reserved.
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CLINICAL PRACTICE PRACTICAL SCIENCE
TABLE 1
Solutions and products tested in clinical trials.
TYPE CHEMICAL/CONCENTRATION PRODUCT (STUDY)
Fluoride Sodium fluoride, stannous Dentinbloc, Colgate Oral
fluoride, hydrogen Pharmaceuticals, Canton,
fluoride Mass. (Morris and
colleagues53)
Potassium Nitrate 1-15% solutions —* (Hodosh54)
5%, 10% in gel —* (Frechoso and colleagues55)
Oxalate 3% potassium oxalate Protect, Sunstar Butler,
Chicago (Camps and Pashley56)
Oxa-gel, Art-dent Ltda,
Araraquara, São Paulo, Brazil
(Pillon and colleagues57)
6.8% ferric oxalate Sensodyne Sealant,
GlaxoSmithKline, Jersey City,
N.J. (Gillam and colleagues58)
Calcium Phosphate 1.5 molars per liter —* (Geiger and colleagues59)
calcium chloride + 1.0
mol/L potassium oxalate
* Nonmarketed product.
Adhesives and resins tested in clinical trials.
TYPE PRODUCT (STUDY)
Fluoride Varnish Duraphat, Colgate Oral Pharmaceuticals, Canton, Mass.
(Gaffar,66 Corona and colleagues67)
Fluoline, PD Dental, Altenwalde, Germany (Duran and
Sengun68)
Oxalic Acid and MS Coat, Sun Medical, Shiga, Japan (Prati and
Resin colleagues69)
Pain-Free, Parkell, Farmingale, N.Y. (Morris and
colleagues53)
Sealants, Primers Seal & Protect, Dentsply, Konstanz, Germany (Baysan and
Lynch70)
Dentin Protector, Ivoclar Vivadent, Ellwangen, Germany
(Schwarz and colleagues71)
Gluma Desensitizer, Heraeus Kulzer, Dormagen, Germany
(Duran and Sengun,68 Dondi dall’Orologio and colleagues,72
Singal and colleagues73)
Gluma Alternate, Heraeus Kulzer, Wehrheim, Germany
(Dondi dall’Orologio and colleagues74)
Health-Dent Desensitizer, Healthdent, Oswego, N.Y.
(Duran and Sengun,68 Dondi dall’Orologio and colleagues74)
Prime & Bond 2.1, Dentsply Caulk, Milford, Del. (Swift
and colleagues75)
Scotchbond, 3M Dental Products, St. Paul, Minn. (Prati
and colleagues,69 Ferrari and colleagues76)
Single Bond, 3M Dental Products (Duran and Sengun68)
Etch and Primer Scotchbond, 3M Dental Products (Ferrari and colleagues76)
Systemp.desensitizer, Ivoclar Vivadent, Schaan,
Liechtenstein (Stewardson and colleagues77)
Etch and Primer Scotchbond Multi-Purpose 3M Dental Products
and Adhesive (Dondi dall’Orologio and colleagues74)
Primer and SE Bond, Kuraray, Okayama, Japan (Duran and Sengun68)
Adhesive
the type of laser and the treatment parameters.79
Studies have reported that the
neodymium:yttrium-aluminum-garnet (YAG)
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CLINICAL PRACTICE PRACTICAL SCIENCE

No
some clinical situations. For
START Patient complains of transient dentinal pain
in response to stimulation (Note 1)
No treatment required example, periodontal surgery
involving coronally positioned
Yes
flaps reportedly eliminates DH in
Yes
Differential diagnosis: Is there an identifiable Diagnose and treat as extensively exposed root dentin.81
cause for the dentinal pain? (Note 2) appropriate
If the DH is associated with an
No abfraction lesion, occlusal adjust-
ment may be effective.82

Confirm diagnosis of DH MANAGEMENT STRATEGY

Treat with consideration for convenience
and cost-effectiveness (Note 3) Some dental professionals lack
1. Preventive advice
2. At-home treatment (for example, confidence in treating DH. This
desensitizing toothpaste)
situation may arise because they
do not fully understand the
biology, etiology, diagnosis and
management of this condition. A
No pain relief (Note 5)
Review Pain relief
management strategy is outlined
(2-4 weeks)
(Note 4)
in a flowchart (Figure 41,30,83). DH
is a transient pain evoked by stim-
No further treatment; ulation of dentin with thermal,
Continue with reinforce preventive
preventive advice and advice; continue to mechanical, evaporative, osmotic
review
desensitizing toothpaste or chemical stimuli.30 The condi-
tion should be diagnosed only
In-office treatment: Pain relief
after excluding other possible
1. Topical agents (for
example, fluorides, oxalates)
Review
(Note 4)
causes of pain.1,30
2. Adhesive materials
CONCLUSIONS
Pain persists
Professionals should appreciate
Review diagnosis the role causative factors play in
of DH
DH confirmed DH not confirmed localizing and initiating hypersen-
sitive lesions. It is important to
Figure 4. Flowchart for the clinical management of dentin hypersensitivity (DH). identify these factors so that pre-
(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
chemical stimuli.30 Note 2. Alternative causes of tooth pain include caries, chipped teeth,
treatment plan. Active manage-
cracked tooth syndrome, fractured or leaking restorations, gingivitis, palatogingival ment of DH usually will involve a
grooves, postrestoration sensitivity or pulpitis.1 Note 3. Treatment may be delivered in a combination of at-home and in-
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 office therapies. In practice, the
follow-up is recommended.1 However, the follow-up interval may vary, depending on regimen adopted will depend 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 the perceived severity of the con-
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-alu- such 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 repre- elect 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 rec-
modality. ommended1 so that appropriate action can be
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

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

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spotlight scientific knowledge about the issues and challenges facing
today’s practicing dentists.
The authors thank Helen Ristic, Department of Scientific Informa-
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