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j o u r n a l o f d e n t i s t ry 4 1 s 4 ( 2 0 1 3 ) s 3 s 1 7

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journal homepage: www.intl.elsevierhealth.com/journals/jden

Dentine sensitivity: Past, present and future


Maria Mantzourania, Deepak Sharmab,*
a
b

Oral Care Scientic and Professional Affairs, Johnson & Johnson Consumer Services EAME Ltd, Foundation Park, Maidenhead, UK
Oral Care Research & Development, Johnson & Johnson Consumer & Personal Products Worldwide, Skillman, NJ, USA

keywords

abstract

Dentine sensitivity
Tooth sensitivity
Dentine hypersensitivity
Tubule occlusion
Nerve stabilisation
Potassium oxalate
Mouthrinse

Objectives: This review denes dentine sensitivity (DS), its prevalence, its aetiology, the
mechanism(s) responsible for DS, its diagnosis and its treatment. The review then examines
the modes of action of various treatments for DS including potassium salts, strontium salts,
bioglasses, arginine/calcium carbonate and professional treatments such as adhesives and
oxalates. The methods used to evaluate the various treatment modalities are discussed,
including laboratory studies and randomised controlled clinical trials.
Data sources and study selection: A literature search was conducted using PubMed, Ovid Medline
and Cochrane reviews for information on DS and its treatments, as well as laboratory and
clinical studies used to evaluate the efcacy of various DS treatments. With regard to efcacy
of treatments for DS only reports of clinical studies that were randomised, controlled and
blinded were reviewed. The authors offer new insights into the shortcomings of the recent
systematic review of the use of oxalates for DS.
Conclusions: The authors introduce the concept of a novel desensitising mouthrinse
containing 1.4% potassium oxalate: Listerine Advanced Defence Sensitive mouthrinse.
Readers of this supplement issue of the Journal of Dentistry are invited to review the
signicance of managing the clinical problem of DS. They are also invited to assess data from
laboratory and randomised controlled clinical studies in order to understand the advantages
offered by regular use of 1.4% potassium oxalate-containing mouthrinse, Listerine Advanced
Defence Sensitive, in particular its resistance to daily erosive and/or abrasive challenges.
2013 Elsevier Ltd. All rights reserved.

1.

Introduction

Dentine sensitivity (DS) is a global clinical oral health problem


in the adult population. It is dened as pain arising from
exposed dentine in response to stimuli, typically thermal,
evaporative, tactile, osmotic or chemical, which cannot be
ascribed to any other form of dental defect or pathology1-4 and
satises all the criteria to be classied as a true pain syndrome.5
It is clinically described as a brief, sharp, bright type of pain
with a rapid onset, although it may also be followed by a
dull, aching pain. The pain may be localised or generalised,

affecting one or multiple tooth surfaces simultaneously.6 The


denition of DS therefore has two aspects: one describing the
clinical presentation and the second identifying the condition
by exclusion of other pathologies, highlighting the need for
correct differential diagnosis.7
Considerable research effort has been invested and
expended on understanding the processes leading to DS
and on developing effective treatments to alleviate and
prevent this painful condition. This article will describe the
current understanding of the prevalance and aetiology of
DS, and will provide an overview of various management
options.

* Corresponding author at: Medical Device Governance Group, Johnson & Johnson Consumer & Personal Products Worldwide,
Division of Johnson & Johnson Consumer Companies, Inc., SF 305, 199 Grand View Road, Skillman, NJ 08558, USA. Tel.: 908-904-3067;
fax: 908-874-2739.
E-mail address: DSharma6@its.jnj.com (D. Sharma)
0300-5712/$ see front matter 2013 Elsevier Ltd. All rights reserved.

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2.

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Data sources and study selection

A literature search was conducted using PubMed, Ovid


Medline and Cochrane reviews for information on DS and its
treatments, as well as laboratory and clinical studies used to
evaluate the efcacy of various DS treatments. With regard to
efcacy of treatments for DS, only reports of clinical studies
that were randomised, controlled and blinded were reviewed.

3.

Prevalence: How common is this clinical


problem?

It is generally accepted that screening for this clinical


condition is not routinely conducted except when prompted
by patients, and DS is therefore under-diagnosed and undertreated.8 Many patients suffer in silence and it is the dental
professionals role to identify the problem, make the patient
aware of it, address it and manage it. Based on a survey
conducted in 2007 by Martin Akel & Associates, Strassler and
colleagues reported that 78.7% of dentists and hygienists who
responded thought that the prevalence of DS was increasing.9
When questioned about the single most common cause of
DS, 47% thought it was gingival recession, 25% attributed it
to abrasion and just 3% thought it was erosion. Seventy-nine
per cent thought that erosion and toothwear were increasing
in prevalence, while 74.5% thought that the prevalence of
gingival recession was increasing. When asked if they thought
DS was a challenge to long-term oral health, 78.2% agreed.
Over half of the respondents (52.8%) thought that DS was
a challenge to general health, 59% thought it was of public
health importance and 88% thought that it affected their
patients quality of life.9
Studies have demonstrated huge variations in prevalence
of DS, ranging from 1% to 98%.10-13 This broad range does
not help in understanding this clinical problem and poses
many questions regarding the validity of the methods used.
However, if one looks more closely at these studies, it is
apparent that they fall into three distinct categories: (a) selfreported assessments, (b) professional/clinical examinations
and (c) professional examinations of periodontally involved
patient groups.
Self-reported assessments are based on self-administered
questionnaires that aim to collect information on demography; consumption of, for example, carbonated drinks;
management of DS; and other similar questions.14,15 Selfreport methods have the advantage of providing the patients
individual perspective, however there are a number of
limitations associated with this approach, including response
distortions;16-18 variations in the reliability and validity of
the instruments used in the surveys;19,20 and the design
and reliable analysis and interpretation of the data derived
using these methods.21,22 These limitations explain in part
the large variation (984%) in DS prevalence in self-reported
assessments.10-13,15,23-30
The second category of studies of DS prevalence clinical
examination studies has reported DS prevalence as ranging
from 1% to 34%.10,24,25,3136
Interestingly, the prevalence of DS is found to be much
higher in patients with periodontal conditions, ranging
from 60% to 98%.12,31,37 It can peak in the rst few days after
scaling and root planing or periodontal surgery, and is usually
substantially reduced by 8 weeks after the procedure, although

the duration can vary from months to more than 30 years.4


In many ways, this observation is to be expected as patients
with periodontal problems have more exposed dentine due
to gingival recession, and studies have conrmed that scaling
and root-planing procedures in periodontal therapy result in
an increase in the number of teeth that respond to painful
stimuli,38,39 as does periodontal surgery.4042 Studies have also
conrmed that meticulous plaque control reduced DS39 and
that post-operative DS gradually decreased approximately
6 weeks after periodontal surgery.42
Peak incidence for DS occurs between the third and fourth
decades of life, with subsequent reductions in incidence34 due
to the natural processes of ageing.43 In general, there appears
to be a higher prevalence of DS in women than men,10,25,44
which may reect better female oral hygiene awareness.2
Intra-orally, DS is mostly reported on the buccal cervical
surfaces of permanent teeth, with canines and rst premolars
being the most affected sites and molars the least affected.4547

4.

Subjective nature of pain

Another factor that may explain the wide range in selfreported prevalence assessments is the subjective nature of
pain. The experience of a sensory event is highly subjective
and can vary substantially between individuals.4850 In the
case of pain, positive expectations can reduce the subjective
experience of pain evoked by a consistently noxious stimulus,
whereas negative expectations may result in the amplication
of pain.5154
Another major disadvantage of self-reported assessments
of DS is incorrect diagnosis of the pain by the respondent
(patient). One cannot emphasise enough that all other dental
diseases with a similar pain should be excluded before
conrming the diagnosis of DS, and this can only be done
by a clinician. Self-reported assessments of the prevalence
of DS need to be interpreted with caution by clinicians and
researchers.
Clinical examination studies usually evaluate DS using
various quantitative probes. The Yeaple probe and the
scratchometer55 measure tactile sensitivity. Subjective
probes, such as the Schiff Cold Air Scale, measure perception
of pain from an air-blast stimulus. Subjective sensitivity
measurements are often recorded using a visual analogue
scale. However, even those studies may be compromised by
the patients subjective perception of pain, which appears to
be altered by sensory factors, prompting a heightened pain
response.56

5.

Aetiology and risk factors

Several theories have been proposed in order to explain


the biological mechanism of DS, with the hydrodynamic
theory57,58 being the most widely accepted. This states that
dentinal uid ow induced by any perturbation of dentinal
uid within the dentinal tubules activates pulpal nociceptors,
resulting in pain.57,59-61 More specically, most pain-inducing
stimuli (cold, evaporative and osmotic) increase outward
uid ow within the dentinal tubules, causing uid shear
forces over mechanoreceptor nerves in the central end of
tubules. This, in turn, activates the intradentinal AG nerves
at the pulpdentinal interface, thereby generating pain. So,

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the true physiological stimulus is inward or outward uid


shifts. Studies performed in vivo revealed that the response
of the pulpal nerves was proportional to the rate of uid ow
(Fig. 1).62,63 In addition, it was found that cold stimuli cause
uid ow away from the pulp and produce a greater and more
rapid pulp-nerve response compared with heat, which causes
an inward ow.62 This would explain why the cold stimulus
seems the strongest pain-inducing stimulus to people with DS.26

5.1

Osmotic stimulation

As osmotic stimuli also induce pain, it is important to


understand the osmolality of a solution, so as to establish
whether a solution is hypertonic or isotonic. This is particularly
relevant in the case of DS.
The osmolality of a solution is a measure of its water
concentration relative to pure water, which has an osmolality
of zero. As water-soluble solutes are added to water, the mole
fraction of water decreases. A solution of 0.9% NaCl has an
osmolality of 0.290 osmoles/kg of solution (290 mOsm/kg).
The osmolality of plasma is approximately the same as that
of 0.9% NaCl, ie, they have the same water concentration and
they are isosmotic.64
Toothpastes have osmolalities much higher than 290 mOsm/
kg. Pashley found most toothpaste osmolalities to be between
3993 and 4028 mOsm/kg,65 although Colgate Baking Soda
toothpaste had an osmolality of 9999 mOsm/kg.65 Thus,
although most commercial toothpastes have osmolalities that
are 13.8 times that of plasma, Colgate Baking Soda toothpaste
has an osmolality that is 34 times that of plasma. These
measurements demonstrated that these toothpastes are very
hypertonic; they contain 1/14th to 1/34th of the water found in
plasma or dentinal uid. Thus, if undiluted toothpastes are
put on dentine, they will draw water out of the tubules, which
may lead to DS. During toothbrushing, toothpastes are diluted
by saliva, making them less concentrated and hence less
hypertonic. Most bleaching gels are also hypertonic, with an
osmolality ranging from 4900 to 5500 mOsm/kg.66
Fortunately, osmotic stimuli are short lived. As water from
body uids diffuses into the hypertonic solutions, it dilutes the
solutes, causing the osmotic gradient to collapse.67 Detailed
information on how osmotically active solutes interact with
dentine can be found elsewhere.6871 Based on the information
above, it is important to emphasise the need for making
dental-care products as isotonic as possible.

5.2

Structural differences between sensitive and


non-sensitive dentine

Consistent with the ndings of the hydrodynamic theory


are the differences in the structure of sensitive versus nonsensitive dentine. Sensitive dentine appears to have more
dentinal tubules per unit area than non-sensitive dentine
(eight times as many tubules at the root surface compared
with non-sensitive teeth) and the channels are wider, with
the average diameter of tubules in sensitive teeth being two
times greater than that of tubules in non-sensitive teeth
(0.83 Pm versus 0.4 Pm, respectively).46 It has also been shown
that smear layers in sensitive dentine are thinner and undercalcied compared with those on non-sensitive dentine.72 The
greater number of open and wider tubules leads to increased
uid permeability through dentine and therefore increased
stimulus transmission and, eventually, the pain response.

Fig. 1 Schematic representation of uid movement after


hydrodynamic stimuli are applied to the exposed dentine
surface, stimulating the peripheral and central mechanisms
of dentinal pain. Reproduced from Vieira and Santiago63 with
permission from General Dentistry, 2013. Academy of
General Dentistry. All rights reserved. On the Web at
www.agd.org. License # 37067.

5.3

Prerequisites for dentine sensitivity

In order to produce DS and generate pain, two criteria must be


fullled (Fig. 2): dentine must be exposed (lesion localisation)
and its tubules must be open/permeable from the pulp to
the surface (lesion initiation).73 Dentine exposure may be the
result of hard tissue loss (enamel) (Fig. 3)74 or soft tissue loss
(periodontal tissue or gingival recession) (Fig. 4).74,75 Enamel
loss can occur because of attrition,76 abrasion or erosion,77,78
with increased dentine wear and tubule exposure being the
result of the synergistic effect of erosion and abrasion.79
Attrition describes wear at sites of direct contact between
teeth,80 with bruxism having been identied as a cause of
pathological toothwear.81 Abrasion describes toothwear
caused by objects other than teeth, such as toothbrushes/
toothpaste. Abrasive toothpastes have been identied as
possibly being responsible for lesion development,82 and while
it is possible that toothpaste may erode dentine, abrasiveness
may also produce a smear layer, thereby reducing sensitivity.83
It is also interesting to note that toothpastes containing
detergents may remove the smear layer and open the
tubules.81,83 It is not surprising that canines and premolars
are the teeth most affected with toothbrushing owing to their
position within the dental arch; the buccal cervical areas are
the sites most affected.84,85 Some of these lesions, however, are
located subgingivally where toothbrush trauma cannot occur
and clinicians have used the term abfraction to describe
them instead.86 The process whereby abfraction or cervical
stress lesions are formed is thought to involve eccentric
occlusal loading, leading to cusp exure. This in turn leads
to compressive and tensile stresses at the cervical fulcrum,
resulting in weakening of the cervical tooth structure.87-89
Erosion is currently thought to be the major factor involved
in tooth wear and is dened as the dissolution of teeth by acids

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Fig. 2 Prerequisites for dentine sensitivity. OH, oral hygiene.

Fig. 3 Enamel loss exposing dentine in molars. Reproduced


from Chu et al74 with permission from General Dentistry,
2013. Academy of General Dentistry. All rights reserved.
On the Web at www.agd.org. License # 37067.

Fig. 4 Gingival recession exposing tooth roots. Reproduced


from Chu et al74 with permission from General Dentistry,
2013. Academy of General Dentistry. All rights reserved.
On the Web at www.agd.org. License # 37067.

that are not of bacterial origin (Fig. 5).74,90 Acids can be extrinsic
or intrinsic. Extrinsic acid exposure is associated with dietary
acids, such as citrus fruit/drinks, carbonated drinks, etc.15,90
Intrinsic acids mainly comprise gastric acid, which moves
to the oral cavity as a result of gastro-oesophageal reux,29
vomiting syndromes, such as bulimia,91 or from vomiting
caused by drugs that act as irritants to the gastric mucosa. For
erosive toothwear to occur, a two-stage process is required:
rst the acids demineralise the tooth surface and soften it;
second, during this period the softened enamel is subject
to friction or abrasion, which can permanently remove it,
resulting in the erosive lesion.90 In normal conditions, these
softened surfaces remineralise through the action of saliva
and uoride, but the process can take up to 2 hours. It is

important to note that in vivo, the titratable acidity of the acid


challenge is one of the most important parameters. Buffering
capacity is commonly quantied by the titratable acidity: the
greater the buffering capacity of an acid solution, the more
saliva is required to neutralise the acid. With this in mind, low
pH does not mean high erosive potential. Industrial erosion
can also occur and results from occupational exposure to
acids or acidic vapours such as might be experienced by
workers in battery factories92,93 or wine tasters.94

5.4

Bleaching sensitivity

Another chemical factor that can trigger tooth sensitivity


similar to DS is the effect of bleaching agents, which cause

j o u r n a l o f d e n t i s t ry 4 1 s 4 ( 2 0 1 3 ) s 3 s 1 7

Fig. 5 Dental erosion due to frequent intake of acidic


beverages. Reproduced from Chu et al74 with permission
from General Dentistry, 2013. Academy of General
Dentistry. All rights reserved. On the Web at www.agd.org.
License # 37067.

bleaching sensitivity. It has been found that approximately 50%


of patients who undergo peroxide-based whitening treatments
experience bleaching sensitivity. However, this is a shortterm effect and is directly proportional to the concentration
of peroxide and duration of treatments, with most patients
recovering after approximately 3 days.95-98 The mechanism
of nociceptor activation in bleaching sensitivity is currently
unknown. As many aspects of DS and bleaching sensitivity
symptoms differ, it has been hypothesised that the mechanism
of pain generation also differs in these two conditions. It is
thought that the mechanism of bleaching sensitivity-induced
pain is the direct activation of intradental nerve activity by
hydrogen peroxide.99 In this paper we will focus on DS only.

6.

accumulation on root surfaces can lead to demineralisation


of the root surface, which in turn leads to the opening of
the dentinal tubules, and therefore to pain.103 It has been
demonstrated that patients with poor plaque control on their
root surfaces report more problems with DS.103105 On the other
hand, clinical studies have reported more gingival recession
with aggressive and/or improper oral hygiene practices.85 The
most brushed teeth (canines and premolars) and therefore
the ones with the lowest plaque scores exhibited the most
gingival recession and the most DS despite having no plaque
present.85
Plaque control plays a key role in reducing the patency of
dentinal tubules and may therefore actually promote the
natural repair of DS.106 It is this removal of plaque, by either
mechanical (toothbrushing) or chemical means, that has
been found to reduce the diameter of dentinal tubules and
therefore helps to alleviate DS.102 Dental professionals must
therefore promote this message of maintaining good oral
hygiene to patients with DS.

8.

Diagnosis

As mentioned previously, DS is essentially diagnosed by


exclusion.1 It is therefore imperative before we discuss any
treatment modalities for DS and their mechanisms of action,
that we emphasise the need for the correct differential
diagnosis as there are conditions that mimic DS.7 A variety
of conditions present with similar symptoms and need to
be appropriately identied and treated before a diagnosis
of DS is considered.8,42 These conditions include gingival
inammation; dental caries; chipped or cracked teeth;
fractured cusps; fractured restorations or restorations with
decient margins and marginal leakage; post-operative
sensitivity; periodontal disease; pulpitis or other endodontic
problems; and sensitivity due to bleaching.8,42 A thorough
history and clinical and radiographic examinations are
therefore essential even though the condition can be difcult
to diagnose given the many variations in its presentation.

Gingival recession

Soft tissue loss or gingival recession, which is the other major


factor in exposing dentine, has been described as an enigma.100
It allows for rapid and extensive exposure of dentinal tubules as
the cementum that overlies the root surface is thin and easily
removed100-102 but its aetiology appears to be multifactorial. One
of its causes is the anatomy of the buccal plate of the alveolar
bone. As the buccal alveolar bone provides much of the local
blood supply for buccal gingivae, the loss of buccal bone in
periodontal disease can result in loss of buccal gingivae.84
Hence, tooth anatomy, orthodontic movements, etc., can
predispose sites to gingival recession. Another indirect cause of
gingival recession is poor oral hygiene, leading to periodontal
disease. However, gingival recession resulting from periodontal
disease and bone loss rarely occurs on buccal/cervical sites.
This observation brings us to the following paradox when it
comes to DS: recession and plaque control.

9.

The paradox of plaque control

It has been reported that patients who maintain good


levels of plaque control are less likely to report DS.102 Plaque

Treatment

Knowledge of the background information described so


far is essential in order to better understand and evaluate
the treatment options available for DS. A large number
of treatment options exist for managing DS, but they all
fall under two basic categories: (a) nerve stabilisation/
desensitisation107-110 or (b) occlusion of the exposed dentinal
tubules. Over-the-counter products have several benets
including ease of use, convenience of self-application and
easier access but in some cases can require several weeks
before taking effect. Generally, stronger and more powerful
treatments are available from a dental ofce and can provide
instant relief. However the effects of the in-ofce treatment
may not last until the next visit.

9.1

7.

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Nerve stabilisation

Potassium salts are known to be nerve-numbing agents110 and


were used to lessen pain before the discovery of anaesthetics.
In 1974, Hodosh reported that potassium nitrate (KNO3) was
effective in reducing DS.107 Reductions in DS were observed

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with application of 115% solutions of KNO3, and pastes


containing 10% KNO3. Several other potassium salts are also
effective, such as potassium chloride, potassium citrate and
potassium bicarbonate.111 Potassium salts have the advantage
of being compatible with uoride, which is frequently added
to dentifrices to prevent caries.112
The mechanism of action of KNO3 is not completely
understood. Previously, it was thought that the nitrate ion was
the active ingredient because of silver nitrates desensitising
ability. Further investigations clearly identied potassium as
the essential component, and it is currently hypothesised
that potassium, and to a lesser extent divalent strontium,111,113
act directly on the nerves located in the pulp (Fig. 6).111,113
Potassium ions must pass through the dentinal tubules to
reach the pulpal nerves, resulting in a lag time of 48 weeks
before pain relief is experienced by the patient. A potassium
concentration of 8 mM is required to inactivate intradental
nerves at the pulpal ends of the tubules.109111,113117 Once at
the nerve site, potassium alters the cells electrical potential,
resulting in depolarisation.115117 Subsequently, the cell is less
responsive to stimuli. The nerve cannot repolarise, so its
excitability is reduced.110,111,113,115 This proposed mechanism of
action is mainly based on in vivo animal studies117 in which
the intradental nerve activity of cats teeth was reduced by
potassium but not sodium salts. Recently, it was demonstrated
that potassium ions could indeed produce a temporary
block of impulse conduction in sensory nerve endings in
the dentine or pulp in vivo when applied to the exposed
dentine of human volunteers.114 This in vivo study in humans
conrmed the previous ndings in animals. Other studies
have also shown relief of symptoms when using toothpaste
containing 5% potassium nitrate,118,119 and a 2.4% potassium
nitrate mouthrinse formulation.120 Despite these encouraging
ndings, it is worth noting that a recent systematic Cochrane
review failed to nd strong evidence supporting the efcacy of
potassium nitrate toothpaste for DS.121
Strontium and other divalent cations may operate by
a different mechanism from potassium, such that the
membrane of the nerve cell is stabilised but the potential of
the cell is unchanged.113

9.2

Tubule occlusion

According to the hydrodynamic mechanism of pain


stimulation previously described, tubules must be patent in
order for surface stimuli to result in intratubule uid shifts.57,71
Blocking or occluding these exposed tubules is a simple but
effective way of decreasing sensitivity (Fig. 6). There are
several mechanisms by which exposed dentinal tubules can
be occluded to decrease DS. Mechanical formation of a natural
smear layer by burnishing dentine induces tubule occlusion.
Introduction of topically applied compounds that form
insoluble materials that precipitate in the tubules and on the
surface, or that facilitate the formation of natural biological
minerals, are also effective. Such compounds include abrasive
particles, strontium or stannous salts, calcium phosphate,
soluble oxalates and bioactive glasses.122
Most of the above desensitising agents act by physically
blocking open dentine tubules. However, their efcacy is
largely dependent on an individuals pain threshold.123,124
These desensitising agents are applied topically, either by a
dental professional or at home by the patient. Non-invasive
treatment options include topical agents and toothpastes

Fig. 6 Treatment of dentine sensitivity. Dentine sensitivity


can be treated by stabilising intradental nerves with
potassium or by partially occluding tubules with crystals or
precipitates. The length and thickness of the arrows indicate
the magnitude of uid shifts in response to hydrodynamic
stimuli.

containing desensitising agents, as will be described below.


These are considered to be the simplest, most cost-effective
and efcacious rst line of treatment for most patients.125
Treatments designed for home use have been traditionally
dominated by desensitising toothpastes with proven
benets.109,125,126 Over the years, more toothpastes have
emerged that offer a combination of desensitising agents,
uoride, anti-calculus agents and/or whitening ingredients,
comprising a more complete preventative oral care approach.
The most widely used of these agents are described in more
detail below.

9.2.1

Strontium

Strontium has been investigated as a treatment for DS since


1956, when Pawlowska reported the benecial properties
of a 25% strontium/water solution and a 75% glycerin
paste.127 Strontium chloride, the original active ingredient in
Sensodyne, was rst introduced commercially over 50 years
ago. Strontium has several possible mechanisms of action for
alleviating DS, although little evidence exists to support any of
them.113 One possible mechanism is precipitation of particles
on the surface of the dentine that prevent uid movement.128
Strontium can replace calcium in hydroxyapatite due to the
similar chemistry of these elements,113 thereby strengthening
demineralised dentine. Strontium has been shown to in-

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corporate into bone, enamel and dentine.128 It can also have a


stabilising effect on the nerve cell membrane.113
Clinical investigations have resulted in mixed opinions
about the effectiveness of strontium. Zappa129 reviewed early
clinical studies of strontium and reported that these studies
suggested that 10% strontium chloride was effective in
relieving sensitivity, but that the role of strontium was unclear
because of the presence of other ingredients in the treatment.
Cummins130 has also surveyed recent clinical studies and
found that there are insufcient data for making any absolute
conclusions about the efcacy of strontium treatment due to
the diversity of testing methods used in the studies.
While a number of studies support the superior efcacy
of 10% strontium chloride toothpaste compared with an
inactive control,127,128,130,131 several more-recent studies claim
there is no benet from strontium treatment.130,132 Arrais et
al.133 compared the occluding abilities of three dentifrices for
the treatment of DS: Sensodyne, Emoform and Sorriso. In
addition to their active ingredients (10% strontium chloride,
potassium nitrate and sodium mono-uorophosphate,
respectively) each contained abrasive materials such as
calcium carbonate and silica. It is possible that these abrasives
play an important role in reducing sensitivity by occluding
dentinal tubules. The three dentifrices occluded tubules to
a statistically signicantly greater extent compared with no
brushing and brushing without a dentifrice, but were not
signicantly different from each other.
Strontium chloride, although still available commercially in
some areas, has for the most part been replaced by strontium
acetate due to its improved clinical efcacy134,135 and its
compatibility with uoride and potassium nitrate.

9.2.2

Bioglasses

A number of treatments exist that occlude dentinal tubules


via generation of natural mineral formation by introducing
compounds that form insoluble precipitates. Recently,
products have been developed that contain bioactive
and biocompatible glasses that occlude dentine tubules.
Bioglasses consist of specic proportions of SiO2, Na2O and
P2O5 and have been shown to promote crystal growth of new
calcium phosphate on the tooth surface.122,136 Bioactive glass is
unstable in aqueous environments and therefore it can only
be formulated as anhydrous paste.
Wang et al.136 used hydraulic conductance in dentine discs
to analyse the occluding properties of a bioglass-containing
dentifrice (NovaMin) and two commercial desensitising
dentifrices (Sensodyne Freshmint and Colgate Sensitive).
The dentifrices were compared with EDTA treatment and
brushing with distilled water. Treated discs were then
subjected to either 6% citric acid or 24-h immersion in
articial saliva. NovaMin was found to be the most effective
at occluding tubules, with relative permeability reduced
by 81.5%. Both NovaMin and Sensodyne occluded tubules
statistically signicantly more than did brushing with distilled
water but were not signicantly different from each other. In
contrast, Colgate Sensitive was not signicantly different from
brushing with distilled water. Dentine permeability increased
with all dentifrices following both the citric acid and articial
saliva post-treatments. Further, in vitro studies have found
bioactive glass biocompatible,137 and a recent clinical study
demonstrated its effectiveness in reducing DS when applied
as prophylaxis paste.138

9.2.3

S9

Arginine

Biomolecules have also been used in desensitising treatments


because of their ability to form precipitates on the surface
of dentine. Colgate Sensitive Pro-Relief dentifrice contains
calcium carbonate and 8% arginine. This product attempts to
mimic the natural process of DS reduction that occurs because
of the presence of calcium, phosphate and glycoproteins in
saliva. Arginine, an amino acid naturally present in saliva,
works in conjunction with calcium carbonate and phosphate
to create a plug in dentinal tubules that prevents uid ow.130
The hypothesised mechanism of action suggests that the
positively charged arginine is attracted to negatively charged
dentine. The alkaline pH promotes deposition of calcium,
phosphate, arginine and carbonate on the dentine surface
and inside the dentine tubules.139 Electron spectroscopy for
chemical analysis (ESCA) of dentine samples treated with
8% arginine revealed increased levels of calcium, oxygen and
phosphorus, consistent with remineralisation.139
Results from a 12-week clinical trial, which used tactile
and air-blast stimuli to determine sensitivity, showed that
the 8% arginine-containing prophylaxis paste (for in-ofce
treatment) was statistically signicantly more effective in
reducing DS than a control paste (Nupro pumice prophylaxis
paste), after 4 weeks. No statistically signicant difference was
observed between the 8% arginine-containing paste and the
control at 12 weeks.140 A combination of 0.8% arginine, PVM/
MA copolymer, pyrophosphates and 0.05% sodium uoride
in a mouthrinse formulation was shown to decrease dentine
uid ow as measured by hydraulic conductance.141 Occlusion
of the dentine surface using the same arginine mouthrinse
formulation was demonstrated with additional in vitro
techniques.142 A randomised, controlled, clinical study showed
that this 0.8% arginine formulation attained a statistically
signicant improvement in the mean tactile scores compared
with those achieved with potassium nitrate, as well as an
enhancement in air-blast sensitivity mean scores after 2, 4
and 6 weeks of product use.143 Another randomised clinical
study showed that the 0.8% arginine mouthrinse formulation
provided a signicant reduction in DS after 8 weeks of product
use compared with a negative control mouthrinse.144

9.2.4

Professional treatments

Resins and dental restoratives can be applied professionally


and create a polymerised surface-sealing layer that covers
exposed tubules. These materials are applied to exposed
dentine of cervical lesions and are effective immediately.
The key components in these resins are hydroxyethyl
methacrylate (HEMA), benzalkonium chloride, glutaraldehyde
and uoride (reviewed by Pashley145). Glutaraldehyde can
induce coagulation and precipitation of plasma proteins in
dentinal uid, such as serum albumin, forming cross links
in dentine tubules. Further reaction of glutaraldehyde with
albumin leads to polymerisation of HEMA, which physically
blocks the dentinal tubules.146,147 Products containing high
concentrations of uoride (300022,500 ppm) are effective in
reducing DS.148-150 High-concentration uoride varnish (applied
in the ofce setting) is effective in providing instant relief
from DS, and Ling et al.151,152 have shown that topical uoride
treatments reduce DS. A varnish containing potassium
uoride, polyethylenglycol and other methacrylates
(VivaSens) as well as a desensitiser that continuously

S10

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releases amine uoride (Seal&Protect) were both effective in


relieving cervical DS during the time course of a clinical study,
as evaluated both by air stimulation and a questionnaire
related to oral health/quality of life status.153 Kanouse and
Ash154 reported that sodium monouorophosphate, which is
commonly added to dentifrices, can reduce sensitivity.
Fluoride on the dentine surface induces precipitation
of calcium uoride crystals, which may occlude dentinal
tubules. The desensitising effect of products containing
high concentrations of CaF2 has not been well documented
but a double-blind study that evaluated the effectiveness
of a commercially available uoride lacquer (Biuorid 12
containing 6% CaF2 and 6% NaF) in reducing DS, found a distinct
reduction in sensitivity after 1, 2 and 3 weeks in the Biuorid
12 group.155 Interestingly, 24% of patients did not experience a
benecial effect with Biuorid 12, suggesting that there must
be patient-specic factors, such as oral hygiene technique,
that modify the interaction between the dentine surface and
the active desensitising ingredients in that product. In vitro
studies of uid movement across dentine discs showed that
treatment with acidulated phosphate uoride gel failed to
achieve tubule occlusion.148
Invasive treatments are also available but must be performed
by a dental professional. Invasive procedures include gingival
grafting,156 application of restorative materials,157 laser
application,158 or even root canal treatments in rare cases.
The following section focuses on the oxalate products
available for the treatment of DS. These provide a non-invasive
treatment option that is professionally applied.

9.2.5

Oxalate

Soluble oxalate salts have been known to occlude tubules


by reacting with naturally occurring calcium ions in the oral
uids to precipitate as insoluble calcium oxalate crystals.146
This precipitate blocks uid ow in the dentinal tubules,148
leading to decreased hypersensitivity. Using in vitro hydraulic
conductance models, several researchers have demonstrated
a decrease in uid ow across dentine samples with
exposed tubules treated with oxalates.159,160 Furthermore,
precipitates of oxalates are relatively resistant to dissolution
in acidic environments, increasing their durability.160 Oxalatecontaining treatments for DS have become well established
since their introduction in the 1970s.160-163
The reduction of hydraulic conductance (ie, dentine
permeability) in fty etched dentine discs treated with
potassium oxalate-containing dentifrices was examined
by Santiago et al.161 Five treatments were assessed: OxaGel, experimental agent DD-1, experimental agent DD-2,
placebo gel and deionised water. The experimental agents
DD-1 and DD-2 contained carboxymethylcellulose and
carboxypolymethylene thickeners; the occluding agents
were 6% monohydrate potassium oxalate and potassium
oxalate, respectively. Following a 3-min treatment, hydraulic
conductance was measured immediately, after 5, 15 and 30 min,
and after an acid etch. No statistically signicant difference
was observed between the oxalate-containing treatments,
nor was there a signicant difference between the placebo
treatments. There was, however, a statistically signicant
difference between the oxalate-containing treatments and the
placebos. A decrease in dentine permeability was observed for
the placebos; however, acid etching restored lost permeability.
This decrease in permeability with placebo was associated

with inorganic and organic particles remaining after the


initial acid etch, which can occlude tubules once uid begins
to ow. The oxalate treatments, however, were resistant to the
acid-etching challenges.
Using scanning electron microscopy (SEM) to analyse
dentine discs for tubule occlusion, Gillam et al.162 examined a
number of professional and over-the-counter DS treatments
using the dentine-disc model. Dentine discs, sectioned from
the crowns of extracted teeth, were treated with various DS
treatments including oxalate-containing dentine sealants (for
professional use), solutions, non-abrasive gels, desensitising
toothpastes and a benchmark uoride dentifrice. Active
ingredients included, but were not limited to, potassium
oxalate, ferric oxalate, stannous uoride, KNO3 and strontium
acetate. It was concluded that the ferric oxalate-containing
product, Sensodyne Sealant, occluded almost all of the
tubules and was superior to the potassium oxalate-containing
product Butler Protect. Furthermore, silica- and calciumbased abrasive components may contribute a therapeutic
effect as particles of these materials were also observed in the
tubules. However, the authors did not fracture the discs to see
if there was subsurface tubule occlusion; such studies often
reveal extensive subsurface occlusion.163
A number of clinical trials have been conducted to
determine the validity of in-ofce oxalate treatments. Muzzin
and Johnson164 compared 30% dipotassium oxalate with 3%
monohydrogen-monopotassium oxalate for the treatment
of DS in vivo using a randomised split-mouth trial. Results
showed a signicant decrease from baseline in DS immediately
and after 4 weeks for 3% monohydrogen-monopotassium
oxalate treatment. In addition, highly statistically signicant
decreases in DS were observed 1 and 2 weeks post treatment
with 30% dipotassium oxalate followed by 3% monohydrogenmonopotassium oxalate. It was concluded that a decrease
in DS can be achieved by treatment with monohydrogenmonopotassium oxalate alone or with 30% dipotassium
oxalate followed by 3% monohydrogen-monopotassium
oxalate.
Protect a common oxalate desensitising treatment (2.7%
potassium oxalate, pH 2.5) was evaluated for efcacy in
treating DS in vivo by Camps and Pashley.165 Sensitivity was
determined by scratching and air-blast stimuli. Reduced
sensitivity to air-blast stimuli after oxalate treatment was
experienced for 62% of active-treated teeth compared with
30% for placebo. The mean scratching force ( standard
deviation) required to elicit pain increased from 44 17 cN
to 53 17 cN for placebo and to 95 24 cN after oxalate
treatment. Only 8% of teeth remained sensitive to scratching
after oxalate treatment compared with 37% for placebo.
Gillam et al.166 evaluated the effect of ferric oxalate on DS
both in vitro and in vivo. Participants in the trial were treated
with Sensodyne Sealant for 1 min and their level of DS was
assessed using tactile and evaporative stimuli and a Biomet
thermal probe after 5 min and after 4 weeks. No statistical
difference was observed between the ferric oxalate treatment
and placebo. Based on the response to tactile and evaporative
stimuli, there was a reduction in DS from baseline that
returned to baseline at 4 weeks. However, using the Biomet
thermal probe an immediate reduction in DS was observed
with the active treatment alone, and this was maintained for
4 weeks.166 The authors concluded that ferric oxalate works
rapidly to reduce DS but that long-term efcacy investigations
were still needed.

j o u r n a l o f d e n t i s t ry 4 1 s 4 ( 2 0 1 3 ) s 3 s 1 7

Pamir et al.167 compared the efcacy of three occluding


agents Seal & Protect (resin), VivaSens (HEMA based)
and BisBlock (oxalic acid) with that of placebo (distilled
water). All three marketed treatments signicantly alleviated
sensitivity compared with baseline and with the placebo after
4 weeks of treatment, but were not signicantly different from
each other. There was however, a signicant placebo effect.
Erdemir et al.149 examined three DS treatments PainFree (HEMA based and 2% oxalic acid), BisBlock, and Seal &
Protect 10 min, and 1, 2, 3 and 4 weeks after treatment. There
was no placebo arm in this study, so it is not clear if the results
were inuenced by a placebo effect. All three treatments
reduced pain from DS for up to 4 weeks, but a signicant
sensitivity reduction was found with Seal & Protect and PainFree compared with Bis-Block after 2 and 4 weeks.
In a recent systematic review of the efcacy of oxalates in
treating DS, Cunha-Cruz et al. reviewed 174 reports of clinical
trials on DS treatment.168 Nineteen trials tested the efcacy
of oxalates in reducing DS, four of which did not meet the
inclusion criteria for the review and were excluded and
three more studies were similar reports of already included
individual studies. The remaining 12 reports were subjected
to detailed analysis. All were randomised controlled trials. For
the purposes of a meta-analysis a number of these trials were
excluded. The oldest study was conducted in 1987 and two
more were performed in 1989 and 1991, before the criteria
for such clinical trials were well established. In a study by
Morris et al.,169 the authors used Pain-Free desensitiser,
which is a mixture of 1% oxalic acid and a copolymer of 90%
methylmethacrylate and 10% styrene sulphonic acid. As this
treatment creates a layer of polymer on the dentine surface,
its mode of action is distinct from the other oxalates reported
in this meta-analysis. We believe that this study should have
been excluded from the systematic review. In a study by
Gillam et al.,166 the authors evaluated 6.8% ferric oxalate in
a dilute nitric acid solution. When that solution reacts with
dentine, it forms a complex mixture of insoluble salts of ferric
phosphate, calcium phosphate and calcium oxalate. There
is concern regarding that study because calcium oxalate
crystals may have been in the minority and any ferric and
calcium phosphate that formed in dentinal tubules would
have dissolved before the 4-week assessment. In the study
by Cuenin et al.,170 only one hydrodynamic stimulus was
assessed: air-blast (evaporative) stimulus on a 14 pain scale
that lacked resolution. Furthermore, the control solution was
3% sodium chloride acidied with hydrochloric acid to pH 2.4
to match the pH of 3% monohydrogen-monopotassium
oxalate. The control thus became an active treatment (D
Pashley, personal communication) and may have etched
dentine, releasing calcium and phosphate ions that might
precipitate in the tubules as relatively insoluble calcium
acid phosphates. This was conrmed when the treated teeth
were extracted and the treated surfaces were examined
by SEM. These details were unknown to the authors at the
time of the study but can be used today to reinterpret their
results. No strong acids should be used in the formulation of
desensitising products because they form complex mixtures
of calcium phosphates in tubules that do not persist for more
than a few days. While biological apatite has a solubility
product constant of 10-27, the solubility product constant of
strong acid (ie, hydrochloric acid) reaction products, such as
dicalcium phosphate dehydrate, is only 10-7. Such precipitates
would rapidly solubilise in saliva.171

S11

Trials included in the systematic review168 that used


30% dipotassium oxalate followed by 3% monopotassiummonohydrogen oxalate were awed in that the 30% dipotassium oxalate (pH 7.0) is very hypertonic (3260 mOsm/
kg) and would tend to draw dentinal uid out of the tubules
as the oxalate was trying to diffuse into the tubules.
When the investigators applied half-neutralised 3% oxalic
acid, which gave a mild acid etch, the released calcium
probably reacted with neutral oxalate ions to form calcium
oxalate crystals on the surface, not in the tubules. Those
studies164,172,173 were performed early in the development of
oxalates and that technique is no longer used clinically. The
study authors would have been unaware of these potential
problems in 1989 and the authors of the systematic review
were not aware of these complications.
Thus, if one limits the clinical trials to those that only used
3% monohydrogen-monopotassium oxalate,164,165,167,174177 and
excludes the study by Cuenin et al.170 (because the control
was acidied with hydrochloric acid), the aggregate results
of those clinical trials suggest that this oxalate treatment is
effective.168 Indeed, the authors of the review acknowledge
that 3% monohydrogen-monopotassium oxalate may
have some benecial effect; this treatment appears to be a
rational rst line of oxalate treatment.168
All of these clinical trials involved a single treatment and
did not refer to a mouthrinse as a delivery vehicle. We are
not aware of any topical treatments for the surface of a tooth
with aqueous solutions of any substance that have a lasting,
substantive presence on tooth structure following one
treatment. Calcium oxalate has a relatively high solubility
product constant of about 2 10-9. Salts with high solubility
product constants do tend to dissolve in saliva over time,
although the degree of saturation is also important.

9.3

Evaluation of treatment modalities

So far we have reviewed the available technologies for DS


in relation to home-management products, as well as the
professionally applied oxalate treatments. These treatment
modalities have traditionally been evaluated by in vitro, in
situ and clinical studies, which remain the gold standard
when assessing the efcacy of an available technology in the
treatment of a clinical condition such as DS. In vitro studies
focus on surface characteristics, such as the occlusion of
tubules, and are an essential component in evaluating the
efcacy of such technologies. Examples of methodologies
used for in vitro studies are: SEM,162 hydraulic conductance,178
energy-dispersive X-ray analysis179 etc. In vitro methodologies
have many limitations, and there is a constant need to
apply new methods to in vitro studies. One such method is
Fourier transform infrared spectroscopy, which has been
shown to be an effective and non-destructive approach for
surface analysis, and which also ensures high comparability
of spectra before and after treatment.180,181 The limitations
and advantages of the current in vitro methodologies are
extensively discussed later in this supplement.
Any technology that addresses the problem of DS must
be able to withstand the acidic challenges of the oral
environment. That is why the application of acids during in
vitro studies is often used to test how stable these occlusion
technologies are, in an attempt to mimic the conditions in
the oral environment.

S12

j o u r n a l o f d e n t i s t ry 4 1 s 4 ( 2 0 1 3 ) s 3 s 1 7

Fig. 7 Pain ladder guide to treatment for dentine sensitivity.

In situ studies are also a quick and efcient way to evaluate


technologies as they allow dentine surface characteristics to
be examined while present in the oral environment. Crossover and split-mouth designs can produce rapid results and
give a good indication of the efcacy of a technology.
Despite the utility of other investigations, the gold standard
for evaluation of treatments remains clinical studies. Ideally,
a double-blind, parallel-group (control and study group)
study is indicated, patient assignment to the groups should
be randomised and stratication of the study components
should be based on common characteristics. A wash-out
period should be introduced before starting the study, during
which subjects are to avoid use of any desensitising agents.
The study group selection criterion should be the diagnosis
of DS, based on observation of the bucco-cervical surfaces of
permanent teeth. In head to head trials an active comparator
arm should be included to allow evaluation of the relative
efcacy and tolerability of the test treatments. All trials should
include appropriate negative and positive controls.
A systematic evaluation of the existing studies is also
required and is a good means by which to demonstrate
clinical efcacy and to develop protocols and clinical
guidance. Systematic reviews are largely dependent on the
availability of clinical trials. With regard to DS, there have
been three such systematic reviews: 1) a Cochrane review
evaluating potassium-containing toothpastes for dentine
hypersensitivity,121 which did not show any clear evidence to
support potassium containing toothpastes; 2) a systematic
review on the effectiveness of laser treatment in dentinal
hypersensitivity,182 which demonstrated only weak evidence
that laser therapy can reduce DS; and 3) a systematic review
on the efcacy of oxalates to treat dentine hypersensitivity,168
which concluded that the existing evidence is not supportive
of the use of oxalates in those delivery vehicles, with the
exception of 3% monohydrogen-monopotassium oxalate.
Based on all this information and the current evaluation
of the treatment modalities in DS, it is evident that along

with robust in vitro and in situ studies more randomised


controlled clinical studies are needed, using more universally
standardised protocols. Such clinical trials can then be
incorporated in future meta-analyses and appropriate
conclusions can be drawn.
The studies described in the following articles in this
supplement are intended to contribute towards the development of a more robust body of evidence relating to the
treatment of DS. In vitro and clinical studies will be described
in detail, introducing a novel technology for the management
of DS.

10.

Introducing a new technology

Mouthrinses are becoming accepted as better delivery vehicles


compared with pastes and gels due to a variety of factors such
as patient ease of use and compliance with mouthwashes;
the osmolality of toothpastes in combination with the need
to use a brush, which leads to increased pain sensation; and
of course difculties with access when referring for in-ofce
treatments. In addition, desensitising technologies based
on occlusion have the potential for increased intratubular
occlusion when in liquid form. Therefore, an alternative to
in-ofce application of oxalate toothpaste and gels is oxalate
application via a mouthrinse available as an over-the-counter
product.
The present supplement introduces a novel technology:
a mouthrinse containing 1.4% potassium oxalate for the
management of DS. This technology forms calcium oxalate
crystals within the dentinal tubules that physically block
hydrodynamic stimulus transmission, thus providing relief
from dentinal sensitivity. It has been tested and compared
with the existing technologies for home management of DS
and found to be the most effective home-use treatment for
DS compared with the leading recommended toothpastes
and mouthrinses. This unique patented technology, in

j o u r n a l o f d e n t i s t ry 4 1 s 4 ( 2 0 1 3 ) s 3 s 1 7

combination with the vehicle of a mouthrinse, provides the


clinician with both a preventative and a treatment option
(Fig. 7) that abides by the principles of the ideal treatment,6 ie
a product that:
must withstand the inuences of oral environment and
external pressures placed on the oral cavity (eg, acid
resistance),
must provide effective in situ results,
is supported by evidence from well-conducted studies,
including clinical trials,
is well tolerated.
Various aspects of this new technology will be described in
detail in the ensuing articles in this supplement.

3.
4.

5.
6.
7.

8.

9.

11.

Conclusions

DS affects numerous dental patients. It can affect not only


their quality of life but it can also prevent them from receiving
necessary dental care. These patients are at risk from further
degradation of tooth structure if the personal habits that lead
to this condition are not addressed. Clinical data suggest
that potassium nitrate-containing desensitising toothpastes
must be used for at least 24 weeks before any statistically
signicant reduction in DS can be detected in clinical trials.132
Patients tend to become frustrated by the lack of prompt
response to desensitising toothpastes. Rapid and long-lasting
relief from sensitivity can, however, be achieved with products
that occlude dentinal tubules, and it has been suggested that
increased mineral density on the dentine surface can assist
with resistance to wear. The novel technology described in the
following articles in this supplement effectively addresses this
widespread clinical problem: it assists patients in their daily
management of DS and provides dental professionals with
an effective, evidence-based, rst-line treatment solution for
their patients that they can recommend with condence.

Conict of interest
Preparation of this article was sponsored by Johnson &
Johnson Consumer & Personal Products Worldwide. Maria
Mantzourani is an employee of Johnson & Johnson Consumer
Services EAME Ltd. Deepak Sharma is an employee of Johnson
& Johnson Consumer & Personal Products Worldwide, Division
of Johnson & Johnson Consumer Companies, Inc.

Acknowledgements
The authors thank Dr Pashley for critical review of the
manuscript. Editorial assistance was provided by Dr Julie
Ponting of Anthemis Consulting Ltd, funded by Johnson &
Johnson Consumer Services EAME Ltd.

10.

11.

12.

13.

14.

15.

16.

17.

18.

19.
20.
21.

22.

23.

24.

25.

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