original article

DENTIN HYPERSENSITIVITY
Harlan J. Shiau, DDS, DMSc

ABSTRACT
Context: In dental practice, dentin hypersensitivity is a commonly presenting condition, 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 beverage, 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 variants (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, randomized control trials. Efforts also were made to identify rigorous meta-analysis in the
literature on the subject of dentin hypersensitivity treatment.

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

Conclusion: Although multiple treatment approaches appear to provide clinical

success in managing dentin hypersensitivity, the entire body of clinical research literature 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 measures and therapies focusing on disrupting pathophysiology form the core of effective dentin hypersensitivity management.

Introduction

Corresponding Author: Harlan J. Shiau, DDS,

DMSc, Assistant Professor, Department
of Periodontics, University of Maryland
Dental School, Baltimore, MD 21201;
Email:hshiau@umaryland.edu
J Evid Base Dent Pract 2012:S1:
[220-228]
1532-3382/$36.00
2012 Elsevier Inc. All rights reserved.

entin hypersensitivity (DH) is characterized by short or transient sharp pain

arising from exposed dentin in response to an array of stimulisuch as thermal, mechanical, osmotic, or chemical elements.1,2 Generally, as a predisposing factor 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

Keywords: Dentin hypersensitivity

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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 stimulus range from toothbrush bristle to metallic materials, such
as an eating utensil or dental instrument.4 Developing evidence-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

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

Epidemiology of DH
Despite 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 hypersensitivity range from 3% to 73% of the adult population of
Western Europe and the United States.7,9,10 Again, the heterogeneity 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 populations 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 incidence of DH is unclear. On one hand, the severity of the
condition increasing with age has been attributed to the increased prevalence of periodontal disease, periodontal treatment, gingival recession, and erosive toothwear on exposing
dentine to external stimuli.4,13 All of the aforementioned scenarios 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 DH
Theories 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 mineralization process; odontoblasts are crucially involved in dentin
formation and repair.14 The macrostructure of dentin consists
of tubule units, surrounded by hypermineralized tissue: peritubular dentin (Fig.1, A and B). The dentin tubule contains
serum-like fluid and an odontoblast cell process. Ultrastructural studies have confirmed the close physical proximity of
sensory nerves to the odontoblast (process and cell body).15

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.)

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

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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 mediate 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 odontoblastic transduction theory.

Figure 2. (A) A simplified diagram of the dentinopulpal 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.)

The hydrodynamic theory, often attributed to Brnnstrm,16

is the most widely accepted contemporary explanation for
DH. Hyperesthesia results from fluids within the dentinal tubules becoming disturbed by temperature, or physical or osmotic 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 dentin 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 analogous 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 greater 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 Hypermineralization of peritubular dentine, that is, the dentin adjacent
to odontoblastic process, as well as the precipitation of minerals from saliva or fluid within the tubules, results in reactive sclerosis.20 Scanning electron microscopic evaluation of
hypersensitive dentin confirms the presence of widely open
dentin tubules.17

predisposes DH.21 For example, toothbrush abrasion, along

with abrasive components contained in dentifrice, may contribute to the loss of enamel structure. Simultaneous exposure 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 recession, 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.

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 peripheral 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,

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Clinical Diagnosis
An 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 management of DH. A careful differential diagnosis must be developed 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 history 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 diagnosing 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 structured data collection will best allow the clinician to track
a patients DH symptoms during the course of treatment.

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 nitrate
Potassium 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 dentifrices (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 4weeks.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

Management of DH

Strontiumsalts

The management of DH should first consider preventive

strategies directed at predisposing etiological factors
again, related to the localization of the lesion via abrasion/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 frequency of consumption and interval between consumption
should be monitored in considering pellicle reformation
and rehardening of the acid-softened surface.22 Contributing factors to gingival recession, such as overzealous brushing, factitial habits, and tongue jewelry should also be considered. Excessive frequency of brushing has been noted in
many subjects plagued by DH.20

Strontium 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 (strontium) replacement of calcium in the hydroxyapatite scaffold to strengthen demineralized dentin.30 Strontium salts
have been incorporated into toothpastes and have been
reported in several clinical studies.31-34 Generally, these studies 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% strontium 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 suggested that the silica abrasive component of the dentifrice
may be responsible in part for desensitizing properties.36

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 representative 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) designed to physically block, to the use of periodontal soft
tissue grafting, and, finally, more recently, the use of lasers.

223

Fluorides
Fluoride 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 indicates effectiveness of 2 separate 5% sodium fluoride varnish products in sensitizing efficacy, as measured by VAS response to air and cold tests, over a 24-week period.38 Topical

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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 cellulose, 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

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

Oxalates

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

Phosphate, Fluorides

Oxalates are used to manage DH by leveraging their ability to form precipitates within dentin tubules, consequently 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 systematic review found only 3% monohydrogen-monopotassium
oxalate as effective in decreasing DH, but recommended
more stringent studies.44

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

Glutaraldehyde

2.4. Mucogingival plastic surgery

A combination product composed of an aqueous solution

of 5% glutaraldehyde and 35% hydroxyethyl methacrylate
(Gluma Desensitizer; Heraeus, Germany) has been described to be an effective desensitizing agent for up to 7 to
9months. Glutaraldehyde blocks dentinal tubules counteracting the hydrodynamic mechanism, responsible for DH.
Reductions in DH ranging from 5% to 27% are reported, although the issue of placebo effect is raised.45 The proposed
mechanism of glutaraldehyde involves the reaction with serum albumin in dentinal fluid, leading to precipitate formation, 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

applications.51 The action of bioactive glass in management

of DH is occlusion of open dentinal tubules. This biomaterial precipitates hydroxycarbonate apatite layer, thereby
blocking patent tubules. Under the brand name Novamin
(Dentsply; USA), this component is available in officeprescribed 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 tubules.53 Subsequent studies investigated the potential of use
of bioactive glasscontaining pastes in postoperative management of dentinal hypersensitivity associated with periodontal surgery.54 Bioactive glass induction of natural mineral formation in situ is a similar strategy used by recently
developed arginine-containing compounds.

Resins and Adhesives

The basis for the use of resins and adhesives is to seal the
dentin tubules and thus prevent the transmission of hydrodynamic stimuli to the pulpal nerve complex.The deposition
of a thin film coating using professionally applied polymerbased 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

Arginine
Arginine 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 formation of a protective salivary glycoprotein with calcium
and phosphatea process favored under alkaline pH conditions. These observations underpinned the commercial
research and development of a formulation containing arginine, an amino acid positively charged at physiological pH;
bicarbonate, functioning as a pH buffer; and calcium carbonate, functioning as a source of calcium. The mechanism

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

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microscopy, scanning electron microscopy, and atomic force

microscopyconfirming occlusion of patent tubules.55,56
Studies evaluating fluid movement via hydraulic conductance experiments have shown inhibition of the hydrodynamic mechanism of DH.55 Studies evaluating efficacy of
8% argininecalcium carbonatefluoridecontaining toothpaste 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 hypersensitivity when topically applied.59 As with other treatments of
DH, the susceptibility to acid challenge negatively impacts
maintenance of relief from discomfort.35

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, inoffice, or combination treatments depends on the
patients severity of discomfort and magnitude of
quality-of-life disruption.
Patient presents with signs and symptoms consistent
with a working diagnosis of dentin hypersensitivity (DH)
Alternative diagnosis assessed and excluded

Periodontal surgery

DH Management plan formed:

Mucogingival surgery aimed at root coverage attempts to

minimize areas of exposed dentin. The vast majority of periodontal clinical research on root coverage procedures measures outcome success with respect to physical change
(e.g. percent root coverage achieved), rather than patientbased 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; further rigorous, well-executed clinical trials are needed.61

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?)

Lasers
Low-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 remains to be fully elucidated. Some experiments suggest that
low-output lasers of the diode type may operate by mediating an analgesic effect controlled by decreasing nerve
transmission.63

OTHER:
Address para-function related to attrition?

Selection of At-Home vs. In-Office

based on severity of pain and impact on
quality-of-life

II. DIRECTED THERAPY

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

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

Combination
Office applied desensitizing agents
Resins/adhesives
Periodontal surgery/Endodontic Tx

Overall, there is considerable potential for development of

laser application in managing DH; certainly, further investigation is required addressing issues of recurrence of DH and
safety.

In-Office

of arginine-calcium carbonate formulations in addressing DH have been established via confocal laser scanning

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Practical Considerations in DH
Management

9.

First, the clinician should develop a preventive strategy toward 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 removal (erosion or zealous toothbrush use). Another example would be the counseling of a patient to reduce or eliminate 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 component 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 approaches at managing DH. Products, including at-home strategies
containing fluorides, strontium chlorides, and more contemporary materials, such as bioactive glass and arginine, have
been broadly studied and are shown to be safe and beneficial 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 research cannot currently proclaim one technique to be vastly
superior to another in DH management.

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