dentine sensitivity past, present and future

7/26/2019 Dentine Sensitivity Past, Present and Future

1/15

j o u rn al o f d e n t is try 41s 4 (20 13 ) s 3s 17

1. Introduction

Dentine sensitivity (DS) is a global clinical oral health problemin the adult population. It is defined as pain arising fromexposed dentine in response to stimuli, typically thermal,

evaporative, tactile, osmotic or chemical, which cannot beascribed to any other form of dental defect or pathology1-4andsatisfies all the criteria to be classified as a true pain syndrome.5

It is clinically described as a brief, sharp, bright type of painwith a rapid onset, although it may also be followed by adull, aching pain. The pain may be localised or generalised,

affecting one or multiple tooth surfaces simultaneously.6Thedefinition 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 forcorrect differential diagnosis.7

Considerable research effort has been invested andexpended on understanding the processes leading to DSand on developing effective treatments to alleviate andprevent this painful condition. This article will describe the

current understanding of the prevalance and aetiology ofDS, and will provide an overview of various managementoptions.

k e y w o r d s

Dentine sensitivity

Tooth sensitivity

Dentine hypersensitivity

Tubule occlusion

Nerve stabilisation

Potassium oxalate

Mouthrinse

a b s t r a c t

Objectives: This review defines 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 efficacy of various DS treatments. With regard to efficacy

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

significance 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.

Dentine sensitivity: Past, present and future

Maria Mantzourania, Deepak Sharmab,*

aOral Care Scientific and Professional Affairs, Johnson & Johnson Consumer Services EAME Ltd, Foundation Park, Maidenhead, UKbOral Care Research & Development, Johnson & Johnson Consumer & Personal Products Worldwide, Skillman, NJ, USA

* 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: [email protected](D. Sharma)

0300-5712/$ see front matter 2013 Elsevier Ltd. All rights reserved.

Available online at www.sciencedirect.com

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


2/15

S4 j o u rn a l o f d en t i st ry 4 1s4 ( 2013 ) s3 s17

2. Data sources and study selection

A literature search was conducted using PubMed, OvidMedline and Cochrane reviews for information on DS and its

treatments, as well as laboratory and clinical studies used toevaluate the efficacy of various DS treatments. With regard toefficacy of treatments for DS, only reports of clinical studies

that were randomised, controlled and blinded were reviewed.

3. Prevalence: How common is this clinicalproblem?

It is generally accepted that screening for this clinical

condition is not routinely conducted except when promptedby patients, and DS is therefore under-diagnosed and under-treated.8Many patients suffer in silence and it is the dental

professionals role to identify the problem, make the patientaware of it, address it and manage it. Based on a surveyconducted in 2007 by Martin Akel & Associates, Strassler andcolleagues 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 ofDS, 47% thought it was gingival recession, 25% attributed it

to abrasion and just 3% thought it was erosion. Seventy-nineper cent thought that erosion and toothwear were increasingin prevalence, while 74.5% thought that the prevalence of

gingival recession was increasing. When asked if they thoughtDS was a challenge to long-term oral health, 78.2% agreed.Over half of the respondents (52.8%) thought that DS wasa challenge to general health, 59% thought it was of public

health importance and 88% thought that it affected theirpatients 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 posesmany questions regarding the validity of the methods used.

However, if one looks more closely at these studies, it isapparent that they fall into three distinct categories: (a) self-reported assessments, (b) professional/clinical examinationsand (c) professional examinations of periodontally involved

patient groups.Self-reported assessments are based on self-administered

questionnaires that aim to collect information on demo-

graphy; consumption of, for example, carbonated drinks;management of DS; and other similar questions.14,15 Self-report methods have the advantage of providing the patients

individual perspective, however there are a number of

limitations associated with this approach, including responsedistortions;16-18 variations in the reliability and validity of

the instruments used in the surveys;19,20 and the designand reliable analysis and interpretation of the data derivedusing these methods.21,22 These limitations explain in partthe large variation (984%) in DS prevalence in self-reported

assessments.10-13,15,23-30

The second category of studies of DS prevalence clinicalexamination studies has reported DS prevalence as ranging

from 1% to 34%.10,24,25,3136

Interestingly, the prevalence of DS is found to be muchhigher in patients with periodontal conditions, rangingfrom 60% to 98%.12,31,37It can peak in the first few days afterscaling 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.4In many ways, this observation is to be expected as patientswith periodontal problems have more exposed dentine dueto gingival recession, and studies have confirmed that scaling

and root-planing procedures in periodontal therapy result inan increase in the number of teeth that respond to painfulstimuli,38,39as does periodontal surgery.4042Studies have also

confirmed that meticulous plaque control reduced DS39 and

that post-operative DS gradually decreased approximately6 weeks after periodontal surgery.42

Peak incidence for DS occurs between the third and fourthdecades of life, with subsequent reductions in incidence34dueto the natural processes of ageing.43In general, there appearsto be a higher prevalence of DS in women than men,10,25,44

which may reflect better female oral hygiene awareness.2Intra-orally, DS is mostly reported on the buccal cervicalsurfaces of permanent teeth, with canines and first 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 self-reported prevalence assessments is the subjective nature of

pain. The experience of a sensory event is highly subjectiveand can vary substantially between individuals.4850 In thecase of pain, positive expectations can reduce the subjective

experience of pain evoked by a consistently noxious stimulus,whereas negative expectations may result in the amplificationof pain.5154

Another major disadvantage of self-reported assessmentsof DS is incorrect diagnosis of the pain by the respondent(patient). One cannot emphasise enough that all other dentaldiseases with a similar pain should be excluded before

confirming the diagnosis of DS, and this can only be done

by a clinician. Self-reported assessments of the prevalenceof 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 thescratchometer55 measure tactile sensitivity. Subjectiveprobes, such as the Schiff Cold Air Scale, measure perceptionof pain from an air-blast stimulus. Subjective sensitivitymeasurements are often recorded using a visual analogue

scale. However, even those studies may be compromised bythe patients subjective perception of pain, which appears tobe altered by sensory factors, prompting a heightened pain

response.56

5. Aetiology and risk factors

Several theories have been proposed in order to explainthe biological mechanism of DS, with the hydrodynamic

theory57,58 being the most widely accepted. This states thatdentinal fluid flow induced by any perturbation of dentinalfluid within the dentinal tubules activates pulpal nociceptors,

resulting in pain.57,59-61More specifically, most pain-inducingstimuli (cold, evaporative and osmotic) increase outwardfluid flow within the dentinal tubules, causing fluid shearforces over mechanoreceptor nerves in the central end of

tubules. This, in turn, activates the intradentinal Anerves

at the pulpdentinal interface, thereby generating pain. So,


3/15

j o u rn al o f d e n t is try 41s 4 (20 13 ) s 3s 17 S5

the true physiological stimulus is inward or outward fluidshifts. Studies performed in vivo revealed that the responseof the pulpal nerves was proportional to the rate of fluid flow(Fig. 1).62,63 In addition, it was found that cold stimuli cause

fluid flow away from the pulp and produce a greater and morerapid pulp-nerve response compared with heat, which causesan inward flow.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 tounderstand the osmolality of a solution, so as to establishwhether 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 molefraction of water decreases. A solution of 0.9% NaCl has anosmolality 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 andthey are isosmotic.64

Toothpastes have osmolalities much higher than 290 mOsm/

kg. Pashley found most toothpaste osmolalities to be between3993 and 4028 mOsm/kg,65 although Colgate Baking Sodatoothpaste had an osmolality of 9999 mOsm/kg.65 Thus,

although most commercial toothpastes have osmolalities thatare 13.8 times that of plasma, Colgate Baking Soda toothpastehas an osmolality that is 34 times that of plasma. Thesemeasurements demonstrated that these toothpastes are very

hypertonic; they contain 1/14thto 1/34thof the water found inplasma or dentinal fluid. Thus, if undiluted toothpastes areput 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 lesshypertonic. 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 frombody fluids diffuses into the hypertonic solutions, it dilutes thesolutes, causing the osmotic gradient to collapse.67Detailedinformation on how osmotically active solutes interact withdentine can be found elsewhere.6871Based on the informationabove, 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 findings of the hydrodynamic theory

are the differences in the structure of sensitive versus non-sensitive dentine. Sensitive dentine appears to have moredentinal 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, withthe average diameter of tubules in sensitive teeth being twotimes greater than that of tubules in non-sensitive teeth

(0.83 m versus0.4 m, respectively).46It has also been shownthat smear layers in sensitive dentine are thinner and under-calcified compared with those on non-sensitive dentine.72The

greater number of open and wider tubules leads to increasedfluid permeability through dentine and therefore increased

stimulus transmission and, eventually, the pain response.

5.3 Prerequisites for dentine sensitivity

In order to produce DS and generate pain, two criteria must befulfilled (Fig. 2): dentine must be exposed (lesion localisation)and its tubules must be open/permeable from the pulp to

the surface (lesion initiation).73Dentine exposure may be the

result of hard tissue loss (enamel) (Fig. 3)74or soft tissue loss(periodontal tissue or gingival recession) (Fig. 4).74,75 Enamel

loss can occur because of attrition,76abrasion or erosion,77,78with increased dentine wear and tubule exposure being theresult of the synergistic effect of erosion and abrasion.79

Attrition describes wear at sites of direct contact betweenteeth,80 with bruxism having been identified as a cause ofpathological toothwear.81 Abrasion describes toothwearcaused by objects other than teeth, such as toothbrushes/

toothpaste. Abrasive toothpastes have been identified aspossibly being responsible for lesion development,82and whileit 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 containingdetergents may remove the smear layer and open thetubules.81,83 It is not surprising that canines and premolarsare the teeth most affected with toothbrushing owing to theirposition within the dental arch; the buccal cervical areas arethe sites most affected.84,85Some of these lesions, however, are

located subgingivally where toothbrush trauma cannot occurand clinicians have used the term abfraction to describethem instead.86 The process whereby abfraction or cervical

stress lesions are formed is thought to involve eccentricocclusal loading, leading to cusp flexure. This in turn leadsto 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 defined as the dissolution of teeth by acids

Fig. 1 Schematic representation of fluid movement afterhydrodynamic stimuli are applied to the exposed dentinesurface, stimulating the peripheral and central mechanismsof dentinal pain. Reproduced from Vieira and Santiago63withpermission from General Dentistry, 2013. Academy ofGeneral Dentistry. All rights reserved. On the Web atwww.agd.org. License # 37067.


4/15


that are not of bacterial origin (Fig. 5).74,90Acids can be extrinsic

or intrinsic. Extrinsic acid exposure is associated with dietaryacids, such as citrus fruit/drinks, carbonated drinks, etc.15,90Intrinsic acids mainly comprise gastric acid, which movesto the oral cavity as a result of gastro-oesophageal reflux,29

vomiting syndromes, such as bulimia,91 or from vomitingcaused by drugs that act as irritants to the gastric mucosa. Forerosive toothwear to occur, a two-stage process is required:

first the acids demineralise the tooth surface and soften it;second, during this period the softened enamel is subjectto friction or abrasion, which can permanently remove it,resulting in the erosive lesion.90 In normal conditions, thesesoftened surfaces remineralise through the action of saliva

and fluoride, 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. Bufferingcapacity is commonly quantified by the titratable acidity: thegreater the buffering capacity of an acid solution, the moresaliva is required to neutralise the acid. With this in mind, low

pH does not mean high erosive potential. Industrial erosioncan also occur and results from occupational exposure toacids or acidic vapours such as might be experienced by

workers in battery factories92,93or 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

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

Fig. 3 Enamel loss exposing dentine in molars. Reproducedfrom Chu et al74with 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. Reproducedfrom Chu et al74with permission from General Dentistry,2013. Academy of General Dentistry. All rights reserved.On the Web at www.agd.org. License # 37067.


5/15


bleaching sensitivity. It has been found that approximately 50%of patients who undergo peroxide-based whitening treatmentsexperience bleaching sensitivity. However, this is a short-

term effect and is directly proportional to the concentrationof peroxide and duration of treatments, with most patientsrecovering after approximately 3 days.95-98 The mechanism

of nociceptor activation in bleaching sensitivity is currentlyunknown. As many aspects of DS and bleaching sensitivitysymptoms differ, it has been hypothesised that the mechanismof 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 byhydrogen peroxide.99In this paper we will focus on DS only.

6. Gingival recession

Soft tissue loss or gingival recession, which is the other majorfactor in exposing dentine, has been described as an enigma.100It allows for rapid and extensive exposure of dentinal tubules as

the cementum that overlies the root surface is thin and easilyremoved100-102but its aetiology appears to be multifactorial. Oneof 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 inperiodontal disease can result in loss of buccal gingivae. 84

Hence, tooth anatomy, orthodontic movements, etc., canpredispose sites to gingival recession. Another indirect cause ofgingival recession is poor oral hygiene, leading to periodontaldisease. 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 itcomes to DS: recession and plaque control.

7. The paradox of plaque control

It has been reported that patients who maintain good

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

accumulation on root surfaces can lead to demineralisationof the root surface, which in turn leads to the opening ofthe dentinal tubules, and therefore to pain.103 It has beendemonstrated that patients with poor plaque control on their

root surfaces report more problems with DS.103105On the otherhand, clinical studies have reported more gingival recessionwith aggressive and/or improper oral hygiene practices.85The

most brushed teeth (canines and premolars) and therefore

the ones with the lowest plaque scores exhibited the mostgingival recession and the most DS despite having no plaquepresent.85

Plaque control plays a key role in reducing the patency ofdentinal tubules and may therefore actually promote thenatural repair of DS.106It is this removal of plaque, by either

mechanical (toothbrushing) or chemical means, that hasbeen found to reduce the diameter of dentinal tubules andtherefore helps to alleviate DS.102Dental professionals must

therefore promote this message of maintaining good oralhygiene to patients with DS.

8. Diagnosis

As mentioned previously, DS is essentially diagnosed by

exclusion.1 It is therefore imperative before we discuss anytreatment 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.7A varietyof conditions present with similar symptoms and need tobe appropriately identified and treated before a diagnosisof DS is considered.8,42 These conditions include gingivalinflammation; dental caries; chipped or cracked teeth;fractured cusps; fractured restorations or restorations withdeficient margins and marginal leakage; post-operative

sensitivity; periodontal disease; pulpitis or other endodontic

problems; and sensitivity due to bleaching.8,42 A thoroughhistory and clinical and radiographic examinations are

therefore essential even though the condition can be difficultto diagnose given the many variations in its presentation.

9. Treatment

Knowledge of the background information described so

far is essential in order to better understand and evaluatethe treatment options available for DS. A large numberof 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 dentinaltubules. Over-the-counter products have several benefitsincluding ease of use, convenience of self-application and

easier access but in some cases can require several weeksbefore taking effect. Generally, stronger and more powerfultreatments are available from a dental office and can provide

instant relief. However the effects of the in-office treatmentmay not last until the next visit.

9.1 Nerve stabilisation

Potassium salts are known to be nerve-numbing agents110and

were used to lessen pain before the discovery of anaesthetics.In 1974, Hodosh reported that potassium nitrate (KNO

3) was

effective in reducing DS.107Reductions in DS were observed

Fig. 5 Dental erosion due to frequent intake of acidicbeverages. Reproduced from Chu et al74with permissionfrom General Dentistry, 2013. Academy of GeneralDentistry. All rights reserved. On the Web at www.agd.org.

License # 37067.


6/15


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 andpotassium bicarbonate.111Potassium salts have the advantage

of being compatible with fluoride, which is frequently addedto 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 desensitisingability. Further investigations clearly identified potassium asthe essential component, and it is currently hypothesised

that potassium, and to a lesser extent divalent strontium,111,113act directly on the nerves located in the pulp (Fig. 6).111,113Potassium ions must pass through the dentinal tubules to

reach the pulpal nerves, resulting in a lag time of 48 weeksbefore pain relief is experienced by the patient. A potassiumconcentration of 8 mM is required to inactivate intradental

nerves at the pulpal ends of the tubules. 109111,113117 Once atthe nerve site, potassium alters the cells electrical potential,resulting in depolarisation.115117Subsequently, the cell is less

responsive to stimuli. The nerve cannot repolarise, so its

excitability is reduced.110,111,113,115

This proposed mechanism ofaction is mainly based on in vivoanimal studies117 in whichthe intradental nerve activity of cats teeth was reduced by

potassium but not sodium salts. Recently, it was demonstratedthat potassium ions could indeed produce a temporaryblock of impulse conduction in sensory nerve endings in

the dentine or pulp in vivo when applied to the exposeddentine of human volunteers.114This in vivostudy in humansconfirmed the previous findings in animals. Other studieshave also shown relief of symptoms when using toothpaste

containing 5% potassium nitrate,118,119and a 2.4% potassiumnitrate mouthrinse formulation.120Despite these encouragingfindings, it is worth noting that a recent systematic Cochrane

review failed to find strong evidence supporting the efficacy of

potassium nitrate toothpaste for DS.121

Strontium and other divalent cations may operate by

a different mechanism from potassium, such that themembrane of the nerve cell is stabilised but the potential ofthe cell is unchanged.113

9.2 Tubule occlusion

According to the hydrodynamic mechanism of pain

stimulation previously described, tubules must be patent inorder for surface stimuli to result in intratubule fluid shifts.57,71Blocking 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 canbe occluded to decrease DS. Mechanical formation of a naturalsmear layer by burnishing dentine induces tubule occlusion.

Introduction of topically applied compounds that forminsoluble materials that precipitate in the tubules and on thesurface, or that facilitate the formation of natural biological

minerals, are also effective. Such compounds include abrasiveparticles, strontium or stannous salts, calcium phosphate,soluble oxalates and bioactive glasses.122

Most of the above desensitising agents act by physicallyblocking open dentine tubules. However, their efficacy islargely dependent on an individuals pain threshold.123,124

These desensitising agents are applied topically, either by adental professional or at home by the patient. Non-invasive

treatment options include topical agents and toothpastes

containing desensitising agents, as will be described below.These are considered to be the simplest, most cost-effectiveand efficacious first line of treatment for most patients.125

Treatments designed for home use have been traditionallydominated by desensitising toothpastes with provenbenefits.109,125,126 Over the years, more toothpastes haveemerged that offer a combination of desensitising agents,

fluoride, 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 since1956, when Pawlowska reported the beneficial propertiesof a 25% strontium/water solution and a 75% glycerin

paste.127Strontium chloride, the original active ingredient inSensodyne, was first introduced commercially over 50 yearsago. Strontium has several possible mechanisms of action for

alleviating DS, although little evidence exists to support any ofthem.113One possible mechanism is precipitation of particleson the surface of the dentine that prevent fluid movement.128

Strontium can replace calcium in hydroxyapatite due to thesimilar chemistry of these elements,113thereby strengthening

demineralised dentine. Strontium has been shown to in-

Fig. 6 Treatment of dentine sensitivity. Dentine sensitivitycan be treated by stabilising intradental nerves withpotassium or by partially occluding tubules with crystals orprecipitates. The length and thickness of the arrows indicatethe magnitude of fluid shifts in response to hydrodynamicstimuli.


7/15


corporate into bone, enamel and dentine.128It can also have astabilising effect on the nerve cell membrane.113

Clinical investigations have resulted in mixed opinionsabout the effectiveness of strontium. Zappa129reviewed early

clinical studies of strontium and reported that these studiessuggested that 10% strontium chloride was effective inrelieving 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 andfound that there are insufficient data for making any absoluteconclusions about the efficacy of strontium treatment due to

the diversity of testing methods used in the studies.While a number of studies support the superior efficacy

of 10% strontium chloride toothpaste compared with an

inactive control,127,128,130,131 several more-recent studies claimthere is no benefit from strontium treatment.130,132Arrais etal.133compared the occluding abilities of three dentifrices for

the treatment of DS: Sensodyne, Emoform and Sorriso. Inaddition to their active ingredients (10% strontium chloride,potassium nitrate and sodium mono-fluorophosphate,respectively) each contained abrasive materials such as

calcium carbonate and silica. It is possible that these abrasivesplay an important role in reducing sensitivity by occludingdentinal tubules. The three dentifrices occluded tubules to

a statistically significantly greater extent compared with nobrushing and brushing without a dentifrice, but were notsignificantly different from each other.

Strontium chloride, although still available commercially insome areas, has for the most part been replaced by strontiumacetate due to its improved clinical efficacy134,135 and its

compatibility with fluoride and potassium nitrate.

9.2.2 Bioglasses

A number of treatments exist that occlude dentinal tubules

via generation of natural mineral formation by introducingcompounds that form insoluble precipitates. Recently,

products have been developed that contain bioactiveand biocompatible glasses that occlude dentine tubules.Bioglasses consist of specific proportions of SiO

2, Na

2O and

P2O

5and have been shown to promote crystal growth of new

calcium phosphate on the tooth surface.122,136Bioactive glass isunstable in aqueous environments and therefore it can onlybe formulated as anhydrous paste.

Wang et al.136used hydraulic conductance in dentine discsto analyse the occluding properties of a bioglass-containingdentifrice (NovaMin) and two commercial desensitising

dentifrices (Sensodyne Freshmint and Colgate Sensitive).

The dentifrices were compared with EDTA treatment andbrushing with distilled water. Treated discs were thensubjected to either 6% citric acid or 24-h immersion in

artificial saliva. NovaMin was found to be the most effectiveat occluding tubules, with relative permeability reducedby 81.5%. Both NovaMin and Sensodyne occluded tubules

statistically significantly more than did brushing with distilledwater but were not significantly different from each other. Incontrast, Colgate Sensitive was not significantly different from

brushing with distilled water. Dentine permeability increasedwith all dentifrices following both the citric acid and artificialsaliva post-treatments. Further, in vitro studies have foundbioactive glass biocompatible,137 and a recent clinical studydemonstrated its effectiveness in reducing DS when applied

as prophylaxis paste.138

9.2.3 Arginine

Biomolecules have also been used in desensitising treatmentsbecause of their ability to form precipitates on the surface

of dentine. Colgate Sensitive Pro-Relief dentifrice containscalcium carbonate and 8% arginine. This product attempts tomimic 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 phosphateto create a plug in dentinal tubules that prevents fluid flow.130The hypothesised mechanism of action suggests that thepositively charged arginine is attracted to negatively chargeddentine. The alkaline pH promotes deposition of calcium,

phosphate, arginine and carbonate on the dentine surfaceand inside the dentine tubules.139 Electron spectroscopy forchemical analysis (ESCA) of dentine samples treated with

8% arginine revealed increased levels of calcium, oxygen andphosphorus, 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-officetreatment) was statistically significantly more effective inreducing DS than a control paste (Nupropumice prophylaxis

paste), after 4 weeks. No statistically significant difference wasobserved between the 8% arginine-containing paste and thecontrol at 12 weeks.140A combination of 0.8% arginine, PVM/

MA copolymer, pyrophosphates and 0.05% sodium fluoridein a mouthrinse formulation was shown to decrease dentinefluid flow as measured by hydraulic conductance.141Occlusion

of the dentine surface using the same arginine mouthrinseformulation was demonstrated with additional in vitrotechniques.142A randomised, controlled, clinical study showedthat this 0.8% arginine formulation attained a statistically

significant improvement in the mean tactile scores compared

with those achieved with potassium nitrate, as well as anenhancement in air-blast sensitivity mean scores after 2, 4

and 6 weeks of product use.143Another randomised clinicalstudy showed that the 0.8% arginine mouthrinse formulationprovided a significant reduction in DS after 8 weeks of productuse compared with a negative control mouthrinse.144

9.2.4 Professional treatments

Resins and dental restoratives can be applied professionallyand create a polymerised surface-sealing layer that coversexposed tubules. These materials are applied to exposed

dentine of cervical lesions and are effective immediately.

The key components in these resins are hydroxyethylmethacrylate (HEMA), benzalkonium chloride, glutaraldehydeand fluoride (reviewed by Pashley145). Glutaraldehyde caninduce coagulation and precipitation of plasma proteins indentinal fluid, such as serum albumin, forming cross linksin dentine tubules. Further reaction of glutaraldehyde with

albumin leads to polymerisation of HEMA, which physicallyblocks the dentinal tubules.146,147 Products containing highconcentrations of fluoride (300022,500 ppm) are effective in

reducing DS.148-150High-concentration fluoride varnish (appliedin the office setting) is effective in providing instant relieffrom DS, and Ling et al.151,152have shown that topical fluoride

treatments reduce DS. A varnish containing potassiumfluoride, polyethylenglycol and other methacrylates

(VivaSens) as well as a desensitiser that continuously


8/15


releases amine fluoride (Seal&Protect) were both effective inrelieving cervical DS during the time course of a clinical study,as evaluated both by air stimulation and a questionnairerelated to oral health/quality of life status.153 Kanouse and

Ash154reported that sodium monofluorophosphate, which iscommonly added to dentifrices, can reduce sensitivity.

Fluoride on the dentine surface induces precipitation

of calcium fluoride crystals, which may occlude dentinal

tubules. The desensitising effect of products containinghigh concentrations of CaF

2has not been well documented

but a double-blind study that evaluated the effectivenessof a commercially available fluoride lacquer (Bifluorid 12containing 6% CaF

2and 6% NaF) in reducing DS, found a distinct

reduction in sensitivity after 1, 2 and 3 weeks in the Bifluorid

12 group.155Interestingly, 24% of patients did not experience abeneficial effect with Bifluorid 12, suggesting that there mustbe patient-specific factors, such as oral hygiene technique,

that modify the interaction between the dentine surface andthe active desensitising ingredients in that product. In vitrostudies of fluid movement across dentine discs showed thattreatment with acidulated phosphate fluoride gel failed to

achieve tubule occlusion.148

Invasive treatments are also available but must be performedby a dental professional. Invasive procedures include gingival

grafting,156 application of restorative materials,157 laserapplication,158or 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-invasivetreatment option that is professionally applied.

9.2.5 Oxalate

Soluble oxalate salts have been known to occlude tubulesby reacting with naturally occurring calcium ions in the oral

fluids to precipitate as insoluble calcium oxalate crystals.146

This precipitate blocks fluid flow in the dentinal tubules,148leading to decreased hypersensitivity. Using in vitro hydraulic

conductance models, several researchers have demonstrateda decrease in fluid flow across dentine samples withexposed tubules treated with oxalates.159,160 Furthermore,

precipitates of oxalates are relatively resistant to dissolutionin acidic environments, increasing their durability.160Oxalate-containing treatments for DS have become well establishedsince their introduction in the 1970s.160-163

The reduction of hydraulic conductance (ie, dentinepermeability) in fifty etched dentine discs treated withpotassium oxalate-containing dentifrices was examined

by Santiago et al.161 Five treatments were assessed: Oxa-

Gel

, experimental agent DD-1, experimental agent DD-2,placebo gel and deionised water. The experimental agentsDD-1 and DD-2 contained carboxymethylcellulose and

carboxypolymethylene thickeners; the occluding agentswere 6% monohydrate potassium oxalate and potassiumoxalate, respectively. Following a 3-min treatment, hydraulic

conductance was measured immediately, after 5, 15 and 30 min,and after an acid etch. No statistically significant differencewas observed between the oxalate-containing treatments,

nor was there a significant difference between the placebotreatments. There was, however, a statistically significantdifference between the oxalate-containing treatments and theplacebos. 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 fluid beginsto flow. The oxalate treatments, however, were resistant to theacid-etching challenges.

Using scanning electron microscopy (SEM) to analysedentine discs for tubule occlusion, Gillam et al.162examined anumber 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 DStreatments including oxalate-containing dentine sealants (forprofessional use), solutions, non-abrasive gels, desensitising

toothpastes and a benchmark fluoride dentifrice. Activeingredients included, but were not limited to, potassiumoxalate, ferric oxalate, stannous fluoride, KNO

3and strontium

acetate. It was concluded that the ferric oxalate-containingproduct, Sensodyne Sealant, occluded almost all of thetubules and was superior to the potassium oxalate-containing

product Butler Protect. Furthermore, silica- and calcium-based abrasive components may contribute a therapeuticeffect as particles of these materials were also observed in thetubules. However, the authors did not fracture the discs to see

if there was subsurface tubule occlusion; such studies oftenreveal extensive subsurface occlusion.163

A number of clinical trials have been conducted to

determine the validity of in-office oxalate treatments. Muzzinand Johnson164 compared 30% dipotassium oxalate with 3%monohydrogen-monopotassium oxalate for the treatment

of DS in vivo using a randomised split-mouth trial. Resultsshowed a significant decrease from baseline in DS immediatelyand after 4 weeks for 3% monohydrogen-monopotassiumoxalate treatment. In addition, highly statistically significant

decreases in DS were observed 1 and 2 weeks post treatmentwith 30% dipotassium oxalate followed by 3% monohydrogen-monopotassium oxalate. It was concluded that a decrease

in DS can be achieved by treatment with monohydrogen-

monopotassium oxalate alone or with 30% dipotassiumoxalate followed by 3% monohydrogen-monopotassiumoxalate.

Protect a common oxalate desensitising treatment (2.7%potassium oxalate, pH 2.5) was evaluated for efficacy intreating DS in vivo by Camps and Pashley.165Sensitivity wasdetermined by scratching and air-blast stimuli. Reducedsensitivity to air-blast stimuli after oxalate treatment wasexperienced for 62% of active-treated teeth compared with

30% for placebo. The mean scratching force ( standarddeviation) required to elicit pain increased from 44 17 cNto 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.166evaluated the effect of ferric oxalate on DS

both in vitroand in vivo. Participants in the trial were treatedwith Sensodyne Sealant for 1 min and their level of DS wasassessed using tactile and evaporative stimuli and a Biometthermal probe after 5 min and after 4 weeks. No statistical

difference was observed between the ferric oxalate treatmentand placebo. Based on the response to tactile and evaporativestimuli, there was a reduction in DS from baseline that

returned to baseline at 4 weeks. However, using the Biometthermal probe an immediate reduction in DS was observedwith the active treatment alone, and this was maintained for4 weeks.166The authors concluded that ferric oxalate worksrapidly to reduce DS but that long-term efficacy investigations

were still needed.


9/15


Pamir et al.167 compared the efficacy of three occludingagents Seal & Protect (resin), VivaSens (HEMA based)and BisBlock (oxalic acid) with that of placebo (distilledwater). All three marketed treatments significantly alleviated

sensitivity compared with baseline and with the placebo after4 weeks of treatment, but were not significantly different fromeach other. There was however, a significant placebo effect.

Erdemir et al.149 examined three DS treatments Pain-

Free(HEMA based and 2% oxalic acid), BisBlock, and Seal &Protect 10 min, and 1, 2, 3 and 4 weeks after treatment. Therewas no placebo arm in this study, so it is not clear if the results

were influenced by a placebo effect. All three treatmentsreduced pain from DS for up to 4 weeks, but a significantsensitivity reduction was found with Seal & Protect and Pain-

Free compared with Bis-Block after 2 and 4 weeks.In a recent systematic review of the efficacy of oxalates in

treating DS, Cunha-Cruz et al. reviewed 174 reports of clinical

trials on DS treatment.168Nineteen trials tested the efficacyof oxalates in reducing DS, four of which did not meet theinclusion criteria for the review and were excluded andthree more studies were similar reports of already included

individual studies. The remaining 12 reports were subjectedto detailed analysis. All were randomised controlled trials. Forthe purposes of a meta-analysis a number of these trials were

excluded. The oldest study was conducted in 1987 and twomore were performed in 1989 and 1991, before the criteriafor 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 thistreatment creates a layer of polymer on the dentine surface,

its mode of action is distinct from the other oxalates reportedin this meta-analysis. We believe that this study should havebeen 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 withdentine, it forms a complex mixture of insoluble salts of ferric

phosphate, calcium phosphate and calcium oxalate. Thereis concern regarding that study because calcium oxalatecrystals may have been in the minority and any ferric andcalcium phosphate that formed in dentinal tubules would

have dissolved before the 4-week assessment. In the studyby Cuenin et al.,170 only one hydrodynamic stimulus wasassessed: air-blast (evaporative) stimulus on a 14 pain scale

that lacked resolution. Furthermore, the control solution was3% sodium chloride acidified with hydrochloric acid to pH 2.4to match the pH of 3% monohydrogen-monopotassium

oxalate. The control thus became an active treatment (D

Pashley, personal communication) and may have etcheddentine, releasing calcium and phosphate ions that mightprecipitate in the tubules as relatively insoluble calcium

acid phosphates. This was confirmed when the treated teethwere extracted and the treated surfaces were examinedby SEM. These details were unknown to the authors at the

time of the study but can be used today to reinterpret theirresults. No strong acids should be used in the formulation ofdesensitising products because they form complex mixturesof calcium phosphates in tubules that do not persist for more

than a few days. While biological apatite has a solubilityproduct constant of 10-27, the solubility product constant of

strong acid (ie, hydrochloric acid) reaction products, such asdicalcium phosphate dehydrate, is only 10-7. Such precipitates

would rapidly solubilise in saliva.171

Trials included in the systematic review168 that used30% dipotassium oxalate followed by 3% monopotassium-monohydrogen oxalate were flawed in that the 30% di-potassium oxalate (pH 7.0) is very hypertonic (3260 mOsm/

kg) and would tend to draw dentinal fluid out of the tubulesas 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 calciumoxalate crystals on the surface, not in the tubules. Thosestudies164,172,173 were performed early in the development ofoxalates and that technique is no longer used clinically. Thestudy authors would have been unaware of these potentialproblems 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,164,165,167,174177and

excludes the study by Cuenin et al.170 (because the controlwas acidified with hydrochloric acid), the aggregate resultsof those clinical trials suggest that this oxalate treatment iseffective.168 Indeed, the authors of the review acknowledge

that 3% monohydrogen-monopotassium oxalate mayhave some beneficial effect; this treatment appears to be arational first line of oxalate treatment.168

All of these clinical trials involved a single treatment anddid not refer to a mouthrinse as a delivery vehicle. We arenot 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 onetreatment. Calcium oxalate has a relatively high solubilityproduct constant of about 2 10-9. Salts with high solubilityproduct 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 DSin relation to home-management products, as well as theprofessionally applied oxalate treatments. These treatmentmodalities have traditionally been evaluated by in vitro, insitu and clinical studies, which remain the gold standardwhen assessing the efficacy of an available technology in thetreatment of a clinical condition such as DS. In vitrostudies

focus on surface characteristics, such as the occlusion oftubules, and are an essential component in evaluating theefficacy of such technologies. Examples of methodologies

used for in vitrostudies are: SEM,162hydraulic conductance,178

energy-dispersive X-ray analysis179

etc. In vitromethodologieshave many limitations, and there is a constant need toapply new methods to in vitrostudies. One such method is

Fourier transform infrared spectroscopy, which has beenshown to be an effective and non-destructive approach forsurface analysis, and which also ensures high comparability

of spectra before and after treatment.180,181The limitationsand advantages of the current in vitro methodologies areextensively discussed later in this supplement.

Any technology that addresses the problem of DS mustbe able to withstand the acidic challenges of the oralenvironment. That is why the application of acids during invitrostudies is often used to test how stable these occlusion

technologies are, in an attempt to mimic the conditions in

the oral environment.


10/15


In situstudies are also a quick and efficient way to evaluate

technologies as they allow dentine surface characteristics tobe examined while present in the oral environment. Cross-over and split-mouth designs can produce rapid results andgive a good indication of the efficacy of a technology.

Despite the utility of other investigations, the gold standardfor 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 stratification of the study componentsshould be based on common characteristics. A wash-out

period should be introduced before starting the study, duringwhich subjects are to avoid use of any desensitising agents.The study group selection criterion should be the diagnosisof DS, based on observation of the bucco-cervical surfaces of

permanent teeth. In head to head trials an active comparatorarm should be included to allow evaluation of the relativeefficacy 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 demonstrateclinical efficacy and to develop protocols and clinical

guidance. Systematic reviews are largely dependent on theavailability of clinical trials. With regard to DS, there havebeen three such systematic reviews: 1) a Cochrane review

evaluating potassium-containing toothpastes for dentinehypersensitivity,121which did not show any clear evidence tosupport potassium containing toothpastes; 2) a systematic

review on the effectiveness of laser treatment in dentinalhypersensitivity,182which demonstrated only weak evidencethat laser therapy can reduce DS; and 3) a systematic review

on the efficacy of oxalates to treat dentine hypersensitivity,168which concluded that the existing evidence is not supportiveof the use of oxalates in those delivery vehicles, with theexception 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 universallystandardised protocols. Such clinical trials can then beincorporated in future meta-analyses and appropriateconclusions can be drawn.

The studies described in the following articles in thissupplement are intended to contribute towards the develop-ment of a more robust body of evidence relating to the

treatment of DS. In vitroand clinical studies will be described

in detail, introducing a novel technology for the managementof DS.

10. Introducing a new technology

Mouthrinses are becoming accepted as better delivery vehiclescompared with pastes and gels due to a variety of factors suchas patient ease of use and compliance with mouthwashes;

the osmolality of toothpastes in combination with the needto use a brush, which leads to increased pain sensation; andof course difficulties with access when referring for in-office

treatments. In addition, desensitising technologies based

on occlusion have the potential for increased intratubularocclusion when in liquid form. Therefore, an alternative toin-office application of oxalate toothpaste and gels is oxalate

application via a mouthrinse available as an over-the-counterproduct.

The present supplement introduces a novel technology:

a mouthrinse containing 1.4% potassium oxalate for themanagement of DS. This technology forms calcium oxalatecrystals within the dentinal tubules that physically blockhydrodynamic stimulus transmission, thus providing relief

from dentinal sensitivity. It has been tested and comparedwith the existing technologies for home management of DSand found to be the most effective home-use treatment for

DS compared with the leading recommended toothpastes

and mouthrinses. This unique patented technology, in

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


11/15


combination with the vehicle of a mouthrinse, provides theclinician with both a preventative and a treatment option(Fig. 7) that abides by the principles of the ideal treatment,6iea product that:

must withstand the influences of oral environment andexternal pressures placed on the oral cavity (eg, acidresistance),

must provide effective in situresults,

is supported by evidence from well-conducted studies,including clinical trials,

is well tolerated.

Various aspects of this new technology will be described indetail in the ensuing articles in this supplement.

11. Conclusions

DS affects numerous dental patients. It can affect not onlytheir quality of life but it can also prevent them from receivingnecessary dental care. These patients are at risk from furtherdegradation of tooth structure if the personal habits that lead

to this condition are not addressed. Clinical data suggestthat potassium nitrate-containing desensitising toothpastesmust be used for at least 24 weeks before any statistically

significant reduction in DS can be detected in clinical trials.132Patients tend to become frustrated by the lack of promptresponse to desensitising toothpastes. Rapid and long-lasting

relief from sensitivity can, however, be achieved with productsthat occlude dentinal tubules, and it has been suggested thatincreased mineral density on the dentine surface can assistwith resistance to wear. The novel technology described in the

following articles in this supplement effectively addresses thiswidespread clinical problem: it assists patients in their dailymanagement of DS and provides dental professionals with

an effective, evidence-based, first-line treatment solution for

their patients that they can recommend with confidence.

Conflict of interest

Preparation of this article was sponsored by Johnson &Johnson Consumer & Personal Products Worldwide. MariaMantzourani is an employee of Johnson & Johnson ConsumerServices EAME Ltd. Deepak Sharma is an employee of Johnson

& Johnson Consumer & Personal Products Worldwide, Divisionof Johnson & Johnson Consumer Companies, Inc.

Acknowledgements

The authors thank Dr Pashley for critical review of themanuscript. Editorial assistance was provided by Dr JuliePonting of Anthemis Consulting Ltd, funded by Johnson &

Johnson Consumer Services EAME Ltd.

r e f e r e n c e s

1. Holland GR, Narhi MN, Addy M, Gangarosa L, Orchardson R.Guidelines for the design and conduct of clinical trials ondentine hypersensitivity.Journal of Clinical Periodontology1997; 24: 808-13.

2. Addy M. Etiology and clinical implications of dentine

hypersensitivity. Dental Clinics of North America1990; 34: 503-14.

3. West NX. Dentine hypersensitivity. Monographs in Oral Science2006; 20: 173-89.

4. Markowitz K, Pashley DH. Discovering new treatments forsensitive teeth: the long path from biology to therapy.Journalof Oral Rehabilitation2008; 35: 300-15.

5. Curro FA. Tooth hypersensitivity in the spectrum of pain.Dental Clinics of North America1990; 34: 429-37.

6. Orchardson R, Gillam DG. Managing dentin hypersensitivity.Journal of the American Dental Association 2006; 137: 990-8.

7. Dowell P, Addy M, Dummer P. Dentine hypersensitivity:aetiology, differential diagnosis and management. BritishDental Journal1985; 158: 92-6.

8. Canadian Advisory Board on Dentin Hypersensitivity.Consensus-based recommendations for the diagnosisand management of dentin hypersensitivity.Journal of theCanadian Dental Association2003; 69: 221-6.

9. Strassler HE, Drisko CL, Alexander DC. Dentinehypersensitivity: its inter-relationship to gingival recessionand acid erosion. Newtown, PA: Aegis Publications, 2008.

10. Flynn J, Galloway R, Orchardson R. The incidence ofhypersensitive teeth in the West of Scotland.Journal ofDentistry1985; 13: 230-6.

11. Murray LE, Roberts AJ. The prevalence of self-reportedhypersensitive teeth.Archives of Oral Biology1994; 39(Suppl):S129.

12. Chabanski MB, Gillam DG, Bulman JS, Newman HN.

Prevalence of cervical dentine sensitivity in a population ofpatients referred to a specialist periodontology department.Journal of Clinical Periodontology1996; 23: 989-92.

13. Liu HC, Lan WH, Hsieh CC. Prevalence and distribution ofcervical dentin hypersensitivity in a population in Taipei,Taiwan.Journal of Endodontics1998; 24: 45-7.

14. Gillam DG, Bulman JS, Jackson RJ, Newman HN. Comparisonof 2 desensitizing dentifrices with a commercially availablefluoride dentifrice in alleviating cervical dentine sensitivity.

Journal of Periodontology1996; 67: 737-42.15. Oderinu OH, Savage KO, Uti OG, Adegbulugbe IC. Prevalence

of self-reported hypersensitive teeth among a group ofNigerian undergraduate students. The Nigerian PostgraduateMedical Journal2011; 18: 205-9.

16. Edwards AL. The relationship between the judgeddesirability of a trait and the probability that it will beendorsed.Journal of Applied Psychology 1953; 37: 90-3.

17. Newcomb MD. Nuclear attitudes and reactions: associationswith depression, drug use, and quality of life.Journal ofPersonality and Social Psychology1986; 50: 906-20.

18. Paulhaus DL. Measurement and control of response bias. In:Robinson JP, Shaver PR, Wrightsman LS, editors. Measuresof personality and social psychological attitudes. Volume 1:Measures of social psychological attitudes. San Diego, CA:Academic Press; 1991. p.17-59.

19. Nunnally JC. Psychometric theory, 2nd ed. New York, NY:McGraw-Hill; 1978.

20. Nunnally JC, Bernstein IH. Psychometric theory, 3rd ed. NewYork, NY: McGraw-Hill; 1994.

21. Spector PE. Using self-report questionnaires in OB research:A comment on the use of a controversial method.Journal ofOrganizational Behavior 1994; 15: 385-92

22. Spector PE. Method variance in organisational research:

Truth or urban legend. Organisational Research Methods 2006;9: 221-31.23. Jensen AL. Hypersensitivity controlled by iontophoresis:

Double blind clinical investigation.Journal of the AmericanDental Association1964: 68: 216-25

24. Graf H, Galasse R. Morbidity, prevalence and intraoraldistribution of hypersensitive teeth.Journal of Dental Research1977: 56(Special Issue A): 162 (Abstract 479).

25. Fischer C, Fischer RG, Wennberg A. Prevalence anddistribution of cervical dentine hypersensitivity in apopulation in Rio de Janeiro, Brazil.Journal of Dentistry1992;20: 272-6.

26. Irwin CR, McCusker P. Prevalence of dentine hypersensitivityin a general dental population.Journal of the Irish Dental

Association1997; 43: 7-927. Gillam DG, Seo HS, Bulman JS, Newman HN. Perceptions of

dentine hypersensitivity in a general practice population.

Journal of Oral Rehabilitation1999; 26: 710-4.


12/15


28. Clayton DR, McCarthy D, Gillam DG. A study of theprevalence and distribution of dentine sensitivity in apopulation of 1758-year-old serving personnel on an RAFbase in the Midlands.Journal of Oral Rehabilitation2002; 29:14-23.

29. Bamise CT, Kolawole KA, Oloyede EO, Esan TA. Toothsensitivity experience among residential universitystudents. International Journal of Dental Hygiene2010; 8: 95-100.

30. Bartlett D, Harding M, Sherriff M, Shirodaria S, Whelton H.A new index to measure tooth wear methodology andpractical advice. Community Dental Health2011; 28: 182-7.

31. Taani DQ, Awartani F. Prevalence and distribution of dentinhypersensitivity and plaque in a dental hospital population.Quintessence International2001; 32: 372-6.

32. Rees JS, Addy M. A cross-sectional study of dentinehypersensitivity.Journal of Clinical Periodontology2002; 29:997-1003.

33. Bamise CT, Olusile AO, Oginni AO, Dosumu OO. Theprevalence of dentine hypersensitivity among adult patientsattending a Nigerian teaching hospital. Oral Health &Preventive Dentistry2007; 5: 49-53.

34. Que K, Ruan J, Fan X, Liang X, Hu D. A multi-centre andcross-sectional study of dentine hypersensitivity in China.

Journal of Clinical Periodontology2010; 37: 631-7.35. Amarasena N, Spencer J, Ou Y, Brennan D. Dentine

hypersensitivity in a private practice patient population inAustralia.Journal of Oral Rehabilitation2011; 38: 52-60.36. Ye W, Feng XP, Li R. The prevalence of dentine

hypersensitivity in Chinese adults.Journal of OralRehabilitation2012; 39: 182-7.

37. Rees JS, Jin LJ, Lam S, Kudanowska I, Vowles R. Theprevalence of dentine hypersensitivity in a hospital clinicpopulation in Hong Kong.Journal of Dentistry2003; 31: 453-61.

38. Fischer C, Wennberg A, Fischer RG, Attstrom R. Clinicalevaluation of pulp and dentine sensitivity aftersupragingival and subgingival scaling. Endodontics and DentalTraumatology 1991; 7: 259-65.

39. Tammaro S, Wennstrom JL, Bergenholtz G. Root-dentinsensitivity following non-surgical periodontal treatment.

Journal of Clinical Periodontology2000; 27: 690-7.40. Nishida M, Katamsi D, Uchida A, Asano K, Ujimoto H, Kaya

H, et al. Hypersensitivity of the exposed root surface aftersurgical periodontal treatment.Journal of the Osaka UniversityDental School1976; 16: 73-85.

41. Wallace JA, Bissada NF. Pulpal and root sensitivity ratedto periodontal therapy. Oral Surgery, Oral Medicine, and OralPathology1990; 69: 743-7.

42. Al-Sabbagh M, Beneduce C, Andreana S, Ciancio SG.Incidence and time course of dentinal hypersensitivity afterperiodontal surgery. General Dentistry2010; 58: e14-9.

43. Bartold PM. Dentinal hypersensitivity: a review.AustralianDental Journal2006; 51: 212-8.

44. Orchardson R, Collins WJ. Clinical features of hypersensitiveteeth. British Dental Journal1987; 162: 253-6.

45. Kawasaki A, Ishikawa K, Suge T, Shimizu H, Suzuki K,Matsuo T, et al. Effects of plaque control on the patencyand occlusion of dentine tubules in situ.Journal of OralRehabilitation2001; 28: 439-49.

46. Absi EG, Addy M, Adams D. Dentine hypersensitivity. A studyof the patency of dentinal tubules in sensitive and non-sensitive cervical dentine.Journal of Clinical Periodontology1987; 14: 280-4.

47. Dababneh RH, Khouri AT, Addy M. Dentine hypersensitivity an enigma? A review of terminology, mechanisms, aetiologyand management. British Dental Journal1999; 187: 606-11.

48. McGrath PA. The measurement of human pain. Endodonticsand Dental Traumatology1986; 2: 124-9.

49. McGrath PA. Psychological aspects of pain perception.Archives of Oral Biology1994; 39(Suppl): 55S-62S.

50. Coghill RC, McHaffie JG, Yen YF. Neural correlates ofinterindividual differences in the subjective experienceof pain. Proceedings of the National Academy of Sciences of theUnited States of America2003; 100: 8538-42.

51. Benedetti F, Arduino C, Amanzio M. Somatotopic activationof opioid systems by target-directed expectations ofanalgesia. The Journal of Neuroscience1999; 19: 3639-48.

52. Price DD. Psychological and neural mechanisms of theaffective dimension of pain. Science2000; 288: 1769-72.

53. Dannecker EA, Price DD, Robinson ME. An examinationof the relationships among recalled, expected, and actualintensity and unpleasantness of delayed onset muscle pain.The Journal of Pain2003; 4: 74-81.

54. Robinson ME, Gagnon CM, Dannecker EA, Brown JL, JumpRL, Price DD. Sex differences in common pain events:expectations and anchors. The Journal of Pain2003; 4: 40-5.

55. Camps J, Pashley D. In vivo sensitivity of human root dentinto air blast and scratching.Journal of Periodontology2003; 74:1589-94.

56. Addy M, West NX, Barlow A, Smith S. Dentinehypersensitivity: is there both stimulus and placeboresponses in clinical trials? International Journal of DentalHygiene2007; 5: 53-9.

57. Brnnstrm M, Astrom A. Hydrodynamics of dentine; itspossible relationship to dentinal pain. International Dental

Journal1972; 22: 219-27.58. Brnnstrm M, Johnson G, Nordenvall KJ. Transmission

and control of dentinal pain: resin impregnation for thedesensitization of dentin.Journal of the American Dental

Association1979; 99: 612-8.59. Brnnstrm M, Linden LA, Astrom A. The hydrodynamics

of the dental tubule and of pulp fluid. A discussion of itssignificance in relation to dentinal sensitivity. Caries Research

1967; 1: 310-7.60. Brnnstrm M, Johnson G. The sensory mechanism inhuman dentin as revealed by evaporation and mechanicalremoval of dentin.Journal of Dental Research1978; 57: 49-53.

61. Brnnstrm M, Astrom A. A study on the mechanism of painelicited from the dentin.Journal of Dental Research1964; 43:619-25.

62. Matthews B, Vongsavan N. Interactions between neural andhydrodynamic mechanisms in dentine and pulp.Archives ofOral Biology1994; 39(Suppl): 87S-95S.

63. Vieira AH, Santiago SL. Management of dentinalhypersensitivity. General Dentistry2009; 57: 120-6.

64. Guyton AC, Hall JE. Medical physiology 10th ed. New York,NY: WB Saunders Company; 2000 p.270-2.

65. Pashley DH. Dentine permeability and its role in thepathobiology of dentine hypersensitivity.Archives of OralBiology1994; 39(Suppl): 73S-80S.

66. Hanks CT, Fat JC, Wataha JC, Corcoran JF. Cytotoxicity anddentin permeability of carbamide peroxide and hydrogenperoxide vital bleaching materials, in vitro.Journal of DentalResearch1993; 72: 931-8.

67. Pashley DH. Sensitivity of dentin to chemical stimuli.Endodontic and Dental Traumatology1986; 2: 130-7.

68. Pashley DH, Livingston MJ, Whitford GM. The effect ofmolecular size on reflection coefficients in human dentine.

Archives of Oral Biology1979; 24: 455-60.69. Pashley DH, Whitford GM. Permeability of human dentine in

vitro interpreted from reflection coefficients.Archives of OralBiology1980; 25: 141-4.

70. Pashley DH, Parsons GS. Pain produced by topical anestheticointment. Endodontic and Dental Traumatology1987; 3: 80-2.

71. Pashley DH. Dentin permeability: Theory and practice. In:Spangberg L, editor. Experimental endodontics. Boca Raton,

FL: CRC Press, Inc.; 1990. p.19-49.72. Rimondini L, Baroni C, Carrassi A. Ultrastructure ofhypersensitive and non-sensitive dentine. A study on replicamodels.Journal of Clinical Periodontology1995; 22: 899-902.

73. Addy M. Clinical aspects of dentine hypersensitivity.Proceedings of the Finnish Dental Society1992; 88(Suppl 1): 23-30.

74. Chu CH, Lam A, Lo EC. Dentin hypersensitivity and itsmanagement. General Dentistry2011; 59: 115-22.

75. Addy M, Hughes J, Pickles MJ, Joiner A, Huntington E.Development of a method in situ to study toothpasteabrasion of dentine. Comparison of 2 products.Journal ofClinical Periodontology2002; 29: 896-900.

76. Lussi A, Schaffner M. Progression of and risk factors fordental erosion and wedge-shaped defects over a 6-yearperiod. Caries Research2000; 34: 182-7.

77. Beyer M, Reichert J, Heurich E, Jandt KD, Sigusch BW. Pectin,alginate and gum arabic polymers reduce citric acid erosion


13/15


effects on human enamel. Dental Materials2010; 26: 831-9.78. Heurich E, Beyer M, Jandt KD, Reichert J, Herold V,

Schnabelrauch M, et al. Quantification of dental erosion a comparison of stylus profilometry and confocal laserscanning microscopy (CLSM). Dental Materials2010; 26: 326-36.

79. Addy M, Pearce N. Aetiological, predisposing andenvironmental factors in dentine hypersensitivity.Archives ofOral Biology1994; 39(Suppl): 33S-8S.

80. Smith P, Wax Y, Adler F. Population variation in tooth, jaw,and root size: a radiographic study of two populations ina high-attrition environment.American Journal of Physical

Anthropology1989; 79: 197-206.81. Smith BG, Knight JK. An index for measuring the wear of

teeth. British Dental Journal1984; 156: 435-8.82. West NX, Hooper SM, OSullivan D, Hughes N, North M,

Macdonald EL, et al. In siturandomised trial investigatingabrasive effects of two desensitising toothpastes on dentinewith acidic challenge prior to brushing.Journal of Dentistry2012; 40: 77-85.

83. Adams D, Addy M, Absi EG. Abrasive and chemical effectsof dentifrices. In: Embry G, Rolla G, editors. Clinical andbiological aspects of dentifrices. Oxford: Oxford UniversityPress; 1992. p.345-55.

84. Addy M. Dentin hypersensitivity: definition, prevalence,distribution, aetiology. In: Addy M, Embry G, Edgar WM,

Orchardson R, editors. Tooth wear and sensitivity: Clinicaladvances in restorative dentistry. London: Martin Dunitz;2000. p.239-48.

85. Addy M, Mostafa P, Newcombe RG. Dentine hypersensitivity:the distribution of recession, sensitivity and plaque.Journalof Dentistry1987;15:242-8.

86. Grippo JO, Simring M, Schreiner S. Attrition, abrasion,corrosion and abfraction revisited: a new perspectiveon tooth surface lesions.Journal of the American Dental

Association2004; 135: 1109-18.87. Grippo JO. Abfractions: a new classification of hard tissue

lesions of teeth.Journal of Esthetic Dentistry1991; 3: 14-9.88. Braem M, Lambrechts P, Vanherle G. Stress-induced cervical

lesions. The Journal of Prosthetic Dentistry1992; 67: 718-22.89. Pindborg JJ. Pathology of the dental hard tissues.

Copenhagen: Munksgaard; 1970. p. 312-21.90. Zero DT, Lucci A. Etiology of enamel erosion: intrinsic

and extrinsic factors. In: Addy M, Embry G, Edgar WM,Orchardson R, editors. Tooth wear and sensitivity: Clinicaladvances in restorative dentistry. London: Martin Dunitz;2000. p.121-39.

91. Spigset O. Oral symptoms in bulimia nervosa. A survey of 34cases.Acta Odontologica Scandinavica1991; 49: 335-9.

92. Petersen PE, Gormsen C. Oral conditions among Germanbattery factory workers. Community Dentistry and OralEpidemiology1991; 19: 104-6.

93. Amin WM, Al-Omoush SA, Hattab FN. Oral health status ofworkers exposed to acid fumes in phosphate and batteryindustries in Jordan. International Dental Journal2001; 51: 169-74.

94. Gray A, Ferguson MM, Wall JG. Wine tasting and dentalerosion. Case report.Australian Dental Journal1998; 43: 32-4.

95. Browning WD, Blalock JS, Frazier KB, Downey MC, Myers

ML. Duration and timing of sensitivity related to bleaching.Journal of Esthetic and Restorative Dentistry2007; 19: 256-64.96. Amengual J, Forner L. Dentine hypersensitivity in dental

bleaching: case report. Minerva Stomatologica2009; 58: 181-5.97. Tsubura S. Clinical evaluation of three months nightguard

vital bleaching on tetracycline-stained teeth using Polanight10% carbamide gel: 2-year follow-up study. Odontology2010;98: 134-8.

98. Kugel G, Gerlach RW, Aboushala A, Ferreira S, Magnuson B.Long-term use of 6.5% hydrogen peroxide bleaching stripson tetracycline stain: a clinical study. Compendium ofContinuing Education in Dentistry2011; 32: 50-6.

99. Markowitz K. Pretty painful: why does tooth bleaching hurt?Medical hypotheses2010; 74: 835-40.

100. Smith RG. Gingival recession. Reappraisal of an enigmaticcondition and a new index for monitoring.Journal of ClinicalPeriodontology1997; 24: 201-5.

101. Bevenius J, Lindskog S, Hultenby K. The micromorphology in

vivo of the buccocervical region of premolar teeth in youngadults. A replica study by scanning electron microscopy.ActaOdontologica Scandinavica1994; 52: 323-34.

102. Manochehr-Pour M, Bhat M, Bissada N. Clinical evaluationof two potassium nitrate toothpastes for the treatment ofdental hypersensitivity. Periodontal Case Reports1984; 6: 25-30.

103. Hiatt WH, Johansen E. Root preparation. I. Obturation ofdentinal tubules in treatment of root hypersensitivity.Journalof Periodontology1972; 43: 373-80.

104. Trowbridge HO, Silver DR. A review of current approaches toin-office management of tooth hypersensitivity. Dental Clinicsof North America1990; 34: 561-81.

105. Cox CF. Etiology and treatment of root hypersensitivity.American Journal of Dentistry1994; 7: 266-70.

106. Suge T, Kawasaki A, Ishikawa K, Matsuo T, Ebisu S. Effects ofplaque control on the patency of dentinal tubules: an in vivostudy in beagle dogs.Journal of Periodontology2006; 77: 454-9.

107. Hodosh M. A superior desensitizer potassium nitrate.Journal of the American Dental Association1974; 88: 831-2.

108. Tarbet WJ, Silverman G, Stolman JM, Fratarcangelo PA.Clinical evaluation of a new treatment for dentinalhypersensitivity.Journal of Periodontology1980; 51: 535-40.

109.Nagata T, Ishida H, Shinohara H, Nishikawa S, Kasahara S,Wakano Y, et al. Clinical evaluation of a potassium nitratedentifrice for the treatment of dentinal hypersensitivity.

Journal of Clinical Periodontology1994; 21: 217-21.110. Peacock JM, Orchardson R. Effects of potassium ions onaction potential conduction in A- and C-fibers of rat spinalnerves.Journal of Dental Research1995; 74: 634-41.

111. Markowitz K, Kim S. Hypersensitive teeth. Experimentalstudies of dentinal desensitizing agents. Dental Clinics ofNorth America1990; 34: 491-501.

112. Silverman G. The sensitivity-reducing effect of brushingwith a potassium nitrate-sodium monofluorophosphatedentifrice. Compendium of Continuing Education in Dentistry1985; 6: 131-3, 6.

113. Markowitz K, Kim S. The role of selected cations in thedesensitization of intradental nerves. Proceedings of theFinnish Dental Society1992; 88(Suppl 1): 39-54.

114. Ajcharanukul O, Kraivaphan P, Wanachantararak S,Vongsavan N, Matthews B. Effects of potassium ions ondentine sensitivity in man.Archives of Oral Biology2007; 52:632-9.

115. Peacock JM, Orchardson R. Action potential conduction blockof nerves in vitro by potassium citrate, potassium tartrateand potassium oxalate.Journal of Clinical Periodontology1999;26: 33-7.

116. Orchardson R, Gillam DG. The efficacy of potassium salts asagents for treating dentin hypersensitivity.Journal of OrofacialPain2000; 14: 9-19.

117. Markowitz K, Bilotto G, Kim S. Decreasing intradental nerveactivity in the cat with potassium and divalent cations.

Archives of Oral Biology1991; 36: 1-7.118. Nagata T, Ishida H, Shinohara H, Nishikawa S, Kasahara S,

Wakano Y, et al. Clinical evaluation of a potassium nitratedentifrice for the treatment of dentinal hypersensitivity.

Journal of Clinical Periodontology1994; 21: 217-21.119. Schiff T, Bonta Y, Proskin HM, DeVizio W, Petrone M, Volpe

AR. Desensitizing efficacy of a new dentifrice containing5.0% potassium nitrate and 0.454% stannous fluoride.American Journal of Dentistry2000; 13: 111-5.

120. Morris A, Gallob J, Amini P, Santos S, Qaqish J, Peng P, et al.Efficacy of a potassium nitrate mouthrinse for relievingdentinal hypersensitivity. Abstract 1575, presented at the87th General Session & Exhibition of the InternationalAssociation for Dental Research, Miami, USA; 14 April 2009.Available from: http://iadr.confex.com/iadr/2009miami/webprogram/Paper119832.html

121. Poulsen S, Errboe M, Lescay Mevil Y, Glenny AM. Potassiumcontaining toothpastes for dentine hypersensitivity. CochraneDatabase of Systematic Reviews2006; (3): CD001476.

122. Wang Z, Jiang T, Sauro S, Wang Y, Thompson I, Watson TF, etal. Dentine mineralization induced by two bioactive glassesdeveloped for air abrasion purposes.Journal of Dentistry2011;39: 746-56.

123. Addy M, Dowell P. Dentine hypersensitivity a review.


14/15


Clinical and in vitro evaluation of treatment agents.Journalof Clinical Periodontology1983; 10: 351-63.

124. Scherman A, Jacobsen PL. Managing dentin hypersensitivity:what treatment to recommend to patients.Journal of the

American Dental Association1992; 123: 57-61.125. Jacobsen PL, Bruce G. Clinical dentin hypersensitivity:

understanding the causes and prescribing a treatment.The Journal of Contemporary Dental Practice2001; 2: 1-12.

126. Kanapka JA. Over-the-counter dentifrices in the treatmentof tooth hypersensitivity. Review of clinical studies. DentalClinics of North America1990; 34: 545-60.

127. Pawlowska K. Strontium chloride: Its importance indentistry and prophylaxis. Czasopismo Stomatologiczne1956;9: 353-61.

128. Minkoff S, Axelrod S. Efficacy of strontium chloride in dentalhypersensitivity.Journal of Periodontology1987; 58: 470-4.

129. Zappa U. Self-applied treatments in the managementof dentine hypersensitivity.Archives of Oral Biology1994;39(Suppl): 107S-12S.

130. Cummins D. Recent advances in dentin hypersensitivity:Clinically proven treatments for instant and lastingsensitivity relief.American Journal of Dentistry2010; 23(Specialissue A): 3A-13A.

131. Shapiro WB, Kaslick RS, Chasens AI, Weinstein D. Controlledclinical comparison between a strontium chloride and asodium monofluorophosphate toothpaste in diminishing

root hypersensitivity.Journal of Periodontology1970; 41: 523-5.132. Jackson RJ. Potential treatment modalities for dentinehypersensitivity: home use products. In: Addy M, Embery G,Edgar WM, Orchardson R, editors. Tooth wear and sensitivity:Clinical advances in restorative dentistry. London: MartinDunitz; 2000. p.327-38.

133. Arrais UAG, Micheloni CD, Giannini M, Chan DC. Occludingeffect of dentifrices on dentinal tubules.Journal of Dentistry2003; 31: 577-84.

134. Pearce NX, Addy M, Newcombe RG. Dentine hypersensitivity:A clinical trial to compare 2 strontium desensitizingtoothpastes with a conventional fluoride toothpaste.Journalof Periodontology1994; 65: 113-9.

135. Olley RC, Pilecki P, Hughes N, Jeffery P, Austin RS, Moazzez R,Bartlett D. An in situstudy investigating dentine tubuleocclusion of dentifrices following acid challenge.Journal ofDentistry2012; 40: 585-93.

136. Wang Z, Sa Y, Sauro S, Chen H, Xing W, Ma X, Jiang T, Wang Y.Effect of desensitizing toothpastes on dentinal tubuleocclusion: A dentine permeability measurement and SEM invitro study.Journal of Dentistry2010; 38: 400-10.

137. Bakry AS, Tamura Y, Otsuki M, Kasugai S, Ohya K, Tagami J.Cytotoxicity of 45S5 bioglass paste used for dentinehypersensitivity treatment.Journal of Dentistry2011; 39: 599-603.

138.Neuhaus KW, Milleman JL, Milleman KR, Mongiello KA,Simonton TC, Clark CE, et al. Effectiveness of a calciumsodium phosphosilicate containing prophylaxis pastein reducing dentine hypersensitivity immediately and 4weeks after a single application: a double-blind randomizedcontrolled trial.Journal of Clinical Periodontology2013; 40: 349-57.

139. Petrou I, Heu R, Stranick M, Lavender S, Zaidel L, Cummins D,

et al. A breakthrough therapy for dentine hypersensitivity:How dental products containing 8% arginine and calciumcarbonate work to deliver effective relief of sensitive teeth.

Journal of Clinical Dentistry2009; 20(Special issue): 23-31.140. Schiff T, Delgado E, Zhang Y-P, Cummins D, DeVizio W,

Mateo LR. Clinical evaluation of the efficacy of an in-officedesensitizing paste containing 8% arginine and calciumcarbonate in providing instant and lasting relief of dentinhypersensitivity.American Journal of Dentistry2009; 22(SI A):8A-15A.

141. Mello SV, Arvanitidou E, Vandeven M. The development ofa new desensitising mouthwash containing arginine, PVM/MA copolymer, pyrophosphates, and sodium fluorideAhydraulic conductance study.Journal of Dentistry2013;41(Suppl1): 20-5.

142. Mello SV, Arvanitidou E, Stranick MA, Santana R, KutesY, Huey B. Mode of action studies of a new desensitizingmouthwash containing 0.8% arginine, PVM/MA copolymer,

pyrophosphates, and 0.05% sodium fluoride.Journal ofDentistry 2013; 41(Suppl 1): S12-9.

143. Elias Boneta AR, Galn Sals RM, Mateo LR, Stewart B, MelloS, Arvanitidou LS, et al. Efficacy of a mouthwash containing0.8% arginine,PVM/MA copolymer, pyrophosphates, and0.05% sodium fluoride compared to a commercial mouthwashcontaining 2.4% potassium nitrate and 0.022% sodiumfluoride and a control mouthwash containing 0.05% sodiumfluoride on dentine hypersensitivity: A six-week randomizedclinical study.Journal of Dentistry 2013; 41(Suppl 1): S34-41.

144. Hu D, Stewart B, Mello S, Arvanitidou L, Panagakos F, De VizioW, et al. Efficacy of a mouthwash containing 0.8% arginine,PVM/MA copolymer, pyrophosphates, and 0.05% sodiumfluoride compared to a negative control mouthwash ondentin hypersensitivity reduction. A randomized clinicaltrial.Journal of Dentistry2013; 41(Suppl 1): S26-33.

145. Pashley DH. Potential treatment modalities for dentinehypersensitivity: in-office products. In: Addy M, Embry G,Edgar WM, Orchardson R, editors. Tooth wear and sensitivity:Clinical advances in restorative dentistry. London: MartinDunitz; 2000. p. 351-66.

146. Pashley DH. Dentin permeability, dentin sensitivity andtreatment through tubule occlusion.Journal of Endodontics1986; 12: 465-74.

147. Qin CY, Xu J, Zhang Y. Spectroscopic investigation ofthe function of aqueous 2-hydroxyethylmethacrylate/

glutaraldehyde solution as a dentin desensitizer. EuropeanJournal of Oral Sciences2006; 114: 354-9.148. Greenhill JD, Pashley DH. The effects of desensitizing agents

on the hydraulic conductance of human dentin in vitro.Journal of Dental Research1981; 60: 686-98.

149.Erdemir U, Yildiz E, Kilic I, Yucel T, Ozel S. The efficacyof three desensitizing agents used to treat dentinhypersensitivity. Journal of the American Dental Association2010; 141: 285-96.

150. Prabhakar AR, Manojkumar AJ, Basappa N. In vitroremineralization of enamel subsurface lesions andassessment of dentine tubule occlusion from NaF dentifriceswith and without calcium.Journal of the Indian Society ofPedodontics and Preventive Dentistry2013; 31: 29-35.

151. Ling TY, Gillam DG, Barber PM, Mordan NJ, Critchell J. Aninvestigation of potential desensitizing agents in the dentinedisc model: a scanning electron microscopy study.Journal ofOral Rehabilitation1997; 24: 191-203.

152. Ling TY, Gillam DG. The effectiveness of desensitizing agentsfor the treatment of cervical dentine sensitivity (CDS) areview. The Journal of the Western Society of Periodontology/Periodontal Abstracts1996; 44: 5-12.

153. Jalali Y, Lindh L. A randomized prospective clinicalevaluation of two desensitizing agents on cervical dentinesensitivity. A pilot study. Swedish Dental Journal 2010; 34: 79-86.

154. Kanouse MC, Ash MM Jr. The effectiveness of a sodiummonofluorophosphate dentifrice on dental hypersensitivity.

Journal of Periodontology1969; 40: 38-40.155. Kielbassa AM, Attin T, Hellwig E, Schade-Brittinger C. In vivo

study on the effectiveness of a lacquer containing CaF2/NaF

in treating dentine hypersensitivity. Clinical Oral Investigations1997; 1: 95-9.

156. Park JB. Treatment of multiple gingival recessions usingsubepithelial connective tissue grafting with a single-incision technique.Journal of Oral Science2009; 51: 31721.

157. Powell LV, Gordon GE, Johnson GH. Sensitivity restored ofClass V abrasion/erosion lesions.Journal of the AmericanDental Association 1990; 121: 694-6.

158. Yilmaz HG, Kurtulmus-Yilmaz S, Cengiz E, Bayindir H,Aykac Y. Clinical evaluation of Er,Cr:YSGG and GaAlAs lasertherapy for treating dentine hypersensitivity: A randomizedcontrolled clinical trial.Journal of Dentistry2011; 39: 249-54.

159. Pashley DH, Livingston MJ, Reeder OW, Horner J. Effects ofthe degree of tubule occlusion on the permeability of humandentine in vitro.Archives of Oral Biology1978; 23: 1127-33.

160. Pashley DH, Galloway SE. The effects of oxalate treatmenton the smear layer of ground surfaces of human dentine.

Archives of Oral Biology1985; 30: 731-7.161. Santiago SL, Pereira JC, Martineli AC. Effect of commercially

available and experimental potassium oxalate-based dentin


15/15


desensitizing agents in dentin permeability: influence oftime and

dentine sensitivity past, present and future

Documents