Dentine Hypersensitivity - An Enigma?

Sumangali Anand1, Anu Priya S2, Anand Raju3, Arun Priya S4

Email for correspondence:mamatadental@yahoo.co.in

INTRODUCTION

According to Addy et al. dentine hypersensitivityis defined as ‘pain derived from exposed dentine inresponse to chemical, thermal, tactile or osmoticstimuli which cannot be explained as arising from anyother dental defect or pathology.’ A recentmodification to this definition has been madeto replace the term ‘pathology’ with the word‘disease’.1, 2

The condition, etiology, and treatment of dentinhypersensitivity, have been reported in the literaturefor over 100 years. As early as 1884, Calvo stated thatthere is a great need of a medicament that, whilelessening the sensibility of dentine, will not impairthe vitality of the pulp.3

Article InfoReceived: July 12, 2011Review Completed: August, 15, 2011Accepted: September, 17, 2011Available Online: January, 2012© NAD, 2011 - All rights reserved

REVIEW

ABSTRACT:

Tooth sensitivity is a very common clinical presentation whichcan cause considerable concern for patients. This condition isfrequently encountered by dentists, endodontists, periodontists,hygienists and dental therapists. This condition generally involvesthe facial surfaces of teeth near the cervical aspect and is verycommon in premolars and canines.

The most widely accepted theory of how the pain occurs isBrannstrom's hydrodynamic theory, fluid movement within thedentinal tubules. The dental professional, using a variety ofdiagnostic techniques, will discern the condition from otherconditions that may cause sensitive teeth. The management ofthis condition requires a good understanding of the complexityof the problem, as well as the variety of treatments available.

This review considers the mechanism, aetiology, diagnosis andmanagement of dentinal hypersensitivity.

Key words: Dentinal hypersensitivity, hydrodynamic theory,desensitizing agents, cervical sensitivity.

Professor1

Department of Conservative Dentistry,Mamata Dental College, Khammam, A.P.

Senior lecturer2

AECS Maaruti College of Dental Sciences andResearch Centre, Bangalore.

Dental Surgeon3

Bangalore

Senior Lecturer4

Dept. of Oral Surgery,K.V.G. Dental College and Hospital, Sullia.

INDIAN JOURNAL OF DENTAL ADVANCEMENTS

Jour nal homepage: www. nacd. in

doi: 10.5866/3.4.659

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MECHANISM FOR DENTINAL SENSATION

Although the morphological characteristics ofthe dentinal tubule have been described throughnumerous studies, the precise mechanism of paintransmission from the exposed dentin surface to theterminal nerve ending is only theorized. The theoriesthat have been proposed include the transducer,neural, modulation, gate control, and hydrodynamictheory. 2

THEORIES FOR DENTINAL HYPERSENSITIVITY

Odontoblastic transduction theory

According to this theory, odontoblasticprocesses are exposed on the dentine surface andcan be excited by a variety of chemical andmechanical stimuli. As a result of such stimulationneurotransmitters are released and impulses aretransmitted towards the nerve endings.

Indian J Dent Adv 2011; 3(4): 659-667

Fig: Schematic representation of odontoblast transductiontheory. The odotoblastic process extends to the full length

of the dentinal tubule.

To date no neurotransmitters have been foundto be produced or released by odontoblasticprocesses.

Neural theory

As an extension of the odontoblastic theory, thisconcept advocates that thermal, or mechanicalstimuli, directly affect nerve endings within thedentinal tubules through direct communication withpulpal nerve fibres.

This theory has been supported by theobservation of the presence of unmyelinated nervefibres in the outer layer of root dentine and thepresence of putative neurogenic polypeptides, thistheory is still considered theoretical with little solidevidence to support it.

Fig: Schematic representation of Neural theory. Nerve endings within

the dentinal tubules are directly triggered by the stimulus

Hydrodynamic theory

The most widely accepted theory for dentinalhypersensitivity is the hydrodynamic theoryproposed by Brannstrom et al. This theorypostulates that fluids within the dentinal tubules aredisturbed either by thermal, physical or osmoticchanges and these fluid changes or movementsstimulate a baroreceptor which leads to neuraldischarge. The basis of this theory is that the fluidfilled dentinal tubules are open to the oral cavity atthe dentine surface as well as towards the pulp. Theexcitement of nerve fibres by different kinds ofstimuli can be explained by the hydrodynamic theory.

Example:

1. Dehydration associated with desiccationfollowing air movement over the exposed dentinesurface results in outward movement of dentinal fluidtowards the dehydrated surface, which triggers nervefibres and results in a painful sensation.

2. Thermal changes can result in expansion orcontraction of the dentinal tubules resulting inchanges in dentinal fluid flow and associatedexcitation of nerve fibres causing pain.

3. High osmotic stimuli such as sugar, acid andsalt can also result in fluid flow within the dentinaltubules and induce nerve stimulation and painfulsensations.

4. Physical stimulation such as mechanicalabrasion of the exposed dentine surface may besufficient to induce unwanted fluid flow within thedentinal tubules with resulting pain from thestimulated nerve fibres.1, 4, 5, 6

Fig: Diagrammatic representation of hydrodynamic theory showing

fluid moving away from the pulp in response to a cold stimulus

Dentine Hypersensitivity - An Enigma? Sumangali, et, al.

Indian J Dent Adv 2011; 3(4): 659-667

Two phases in dentine hypersentivitydevelopment

There are two phases to the development of dentinehypersensitivity.

1. ‘Lesion localisation’ by exposure of dentine

2. ‘Lesion initiation’ by opening of dentinaltubules.

Given the buccal cervical site of predilection ofthe condition, lesion localisation will mainly resultfrom abrasion and erosive influences to enamel andthe gingivae. Clinical evidence indicates that gingivalrecession accounts for a much greater dentine areaexposure than cervical enamel loss. Lesion initiationrequires removal of cementum or smear layers. Thesecould be achieved by abrasive or erosive agents. Theevidences suggests that erosion is themore dominant factor but can be potentiated byabrasion.5, 7, 8

Etiology of Cervical Tooth Sensitivity

Scientific hypothesis of dentin hypersensitivitymentioned above assists us in understanding thecondition and treatment of cervical tooth sensitivity,the clinical cause is exposed and open dentinaltubules.

In the ideal anatomical position, only the enamelof most teeth is exposed to the oral environment, anddentin that is protected by enamel or cementum isnot sensitive. Cervical tooth sensitivity occurs whenthis protective layer is removed and the underlyingdentinal tubules are exposed. This exposure can bethe result of numerous etiologic factors that includeabrasion, erosion, attrition, abfraction, and gingivalrecession. These etiologic factors can be attributedto a multitude of conditions (eg, aging, improperoral hygiene habits, dietary habits, low pH mouthrinses). 1, 3, 8

Diagnosis

The reasons for tubules to be exposed should beassessed during a visual examination of the teeth aswell as a detailed dietary history should be elicited.Useful diagnostic tools are the air/water syringe(thermal), dental explorer (touch), percussion testing,bite stress tests, and other thermal tests such as anice cube and assessment of occlusion.

A comprehensive dental examination will ultimatelyrule out other underlying conditions for whichsensitivity is a symptom such as cracked tooth,fractured restoration, chipped teeth, dental caries,gingival inflammation, post-restorative sensitivity,marginal leakage, and pulpitis. Excessive dietary acidssuch as citrus juices and fruits, carbonated drinks,wines, and ciders have been identified as potentialrisk factors for dental hypersensitivity.

The dietary history provided by the patient willassist in identifying the risk factors the patient mayhave for tooth sensitivity.

In addition other risk factors will be ferreted outduring an examination such as toothbrush abrasion,chemical erosion, thin enamel, gingival recession,exposed dentin, and eating disorders. The patient willbe able to assist in diagnosis by identifying the paininciting stimuli, i.e., thermal, tactile, etc., as well asdescribing the pain. The response to stimuli variesfrom patient to patient. Factors such as individualpain tolerance, emotional state, and environment cancontribute to the variety of responses between andamong patients.

The most common cited reason for exposeddentinal tubules is gingival recession (predisposingfactor). Chronic exposure to bacterial plaque,toothbrush abrasion, gingival laceration from oralhabits such as toothpick use, excessive flossing, crownpreparation, inadequate attached gingiva, andgingival loss secondary to disease or surgery aresome but not all causes of gingival recession. Gingivalrecession is the reduction of the height of themarginal gingival to a location apical to the CEJ.Recessed areas may become sensitive due to the lossof cementum, ultimately exposing dentin. Probingdepths, recessed areas, and sensitivity reported bythe patient must be accurately recorded andmonitored to provide a reference for the patient’sdisease activity over time.6, 7, 8, 9, 10

Differential diagnosis

Factors to consider in the differential diagnosis ofdentine hypersensitivity

1. Abscessed or non-vital tooth withperiapical radiolucency or draining fistula; necroticwith sensitivity to occlusion; partially necrotic in one

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canal, with vital tissue elsewhere (in which case toothtests vital to stimuli). Pain typically occursspontaneously or upon occlusion or tapping.

2. Cracked tooth showing vertical fracture orsingle cusp partial fracture. Pain typically occurs onrelease of biting or tapping of a single cusp.

Fig: Schematic representation of a cracked tooth

3. Dental caries. Greatest degree of sensitivityexperienced when dental decay passes the dentine-enamel junction. As caries penetrates further into thetooth, sensitivity lessens until pulp becomes involved.

Fig : Pit and fissure caries

4. Gingival recession. Often occurs post-periodontal surgery, when a large portion of the rootis exposed, or due to ageing, mechanical trauma orocclusal trauma.

Fig: Gingival recession seen with respsect to the mandibular central

and lateral incisors.

5. Toothbrush abrasion. Caused by use of ahard toothbrush or a soft toothbrush with abrasivetoothpaste or by aggressive brushing, and generallylocated on the side opposite the dominant hand.Abrasion may either instigate gingival recession orstem from greater accessibility to softer root surfacesfrom recession.

Fig: Abrasion of the tooth roots associated with tooth brushing

6. Abfraction lesions. Generally associatedwith occlusal trauma where the anatomic crown ofthe tooth has flexure. Although non-carious, theselesions can become very sensitive and even progressinto the pulp. They may be multifactorial whereabrasion and erosive forces combine to producetooth surface loss.

Fig: Schematic representation of abfraction

Fig: Abfraction lesions seen on mandibular premolars and first molar

Dentine Hypersensitivity - An Enigma? Sumangali, et, al.

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7. Erosive lesions. Associated with acid reflux,hiatus hernia, purging, bulimia (intrinsic causes), anddiet (extrinsic causes). Intrinsic acid lesions typicallyoccur on the palatal surfaces, while extrinsic acidlesions tend to occur on the buccal surfaces.Consuming large quantities of carbonated cola drinksand fruit drinks, which have a very low pH, causestooth surface loss, as does toothbrushing followingan acidic assault, which removes the acid-softenedenamel or dentine.

Fig: Erosion: buccal surfaces of right maxillary cuspid and firstpremolar tooth showing loss of enamel. Both central and right lateral

incisor teeth show white areas at their labial surfaces indicatingincipient decalcificatio

Fig: Erosion related to acid in soft drinks

8. Diet sensitivity. Generally associated with alow pH material, such as fresh tomatoes, orange juice,cola drinks. Areas with exposed dentine are etched,causing sudden sensitivity. Diet choices mayaggravate sensitivity from erosion.

9. Genetic sensitivity. Patients will bereporting with history of sensitive teeth and it is notknown whether sensitivity correlates to the 10 percent of teeth that do not have cementum coveringall the dentine at the DEJ, or is a factor of lower overallpatient pain threshold values.

10. Restorative sensitivity. Triggered followingplacement of a restoration for several possiblereasons: certain amalgams having a history of 24-48hours sensitivity due to shrinkage, rather than theusual expansion, during setting; contamination ofcomposites during placement or improper etchingof the tooth on composites, which results in micro-leakage; improper tooth-drying technique; incorrectpreparation of glass ionomer or zinc phosphatecements; general pulpal insult from cavitypreparation technique; thermal or occlusal causes;galvanic reaction to dissimilar metals that creates asudden shock or ‘tin foil’ taste in the mouth.

11. Medication sensitivity is cause due tomedications that dry the mouth (e.g. antihistamines,high blood pressure medication), therebycompromising the protective effects of saliva andaggravating diet-related trauma or proliferatingplaque. Even a reduction in salivary flow due toageing or medications can lower the pH of the salivabelow the level at which caries occurs (6.0-6.8 forDentine caries; < 5.5 for enamel caries) and increaseerosive lesions to exposed dentine.

12. Bleaching sensitivity. Commonlyassociated with carbamide peroxide vital toothbleaching and thought to be due to the by-productsof 10 per cent carbamide peroxide (3 per centhydrogen peroxide and 7 per cent urea) readilypassing through the enamel and dentine into thepulp in a matter of minutes. Sensitivity takes the formof a reversible pulpitis caused from the dentine fluidflow and pulpal contact of the material, whichchanges osmolarity, without apparent harm to thepulp. Sensitivity is caused by all other forms ofbleaching (in-office, with or without light activation,and new, over-the-counter) and depends on peroxideconcentration.6, 7, 8, 9, 10, 11, 12, 13, 14, 15

Fig: Schematic representation of few lesions included in thedifferential diagnosis of dentinal hypersensitivity.

Dentine Hypersensitivity - An Enigma? Sumangali, et, al.

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Treatments

Treating dentinal hypersensitivity is challengingtask for the dental professional because of thedifficulty related to measuring the pain responsesince the response varies from patient to patient. Inaddition if the dentin exposure is due to personalhabits, it may be difficult for patients to change theirbehavior.1, 5, 7, 8, 10 If the diagnosis confirms dentinalhypersensitivity in the absence of underlyingdiseases or structural problems, then the followingsteps can be initiated:

(1) Identify the etiologic factor. Remove, reduceor modify the risk factors by educating the patientabout dietary acids and other oral care habits (oralhygiene habits- frequency, brushing, timing ofbrushing, technique of brushing, force exerted whilebrushing and the abrasives used in the tooth paste)

(2) Recommend different tooth brushingmethods, if appropriate

(3) Initiate treatment by recommending adesensitizing agent for home use

(4) Applying topical desensitizing agentsprofessionally.

Treatment can be invasive in nature or noninvasive

Non-invasive treatment includes:

a) Topical agents

b) Dentifrices that contain a desensitizing activeingredient. (potassium nitrate, stannous fluoride,strontium chloride hexahydrate, and aluminum,potassium or ferric oxalates and fluorides

c) Anti-inflammatory agents: Corticosteroids

Invasive procedures include:

a) Dentine sealers

� Glass ionomer cements

� Composites

� Resins

� Varnishes

� Sealants

� Methyl methacrylate

b) Pulpectomy

c) Gingival surgery/Periodontal soft tissuegrafting

d) Crown placement/restorative material

e) Lasers

Other active agents that have been proven to beeffective as a desensitizing agents are Proteinprecipitants, Formaldehyde, Glutaraldehyde, Silvernitrate, Strontium chloride hexahydrate, Caseinphosphopeptides, Burnishing, Fluorideiontophoresis.1, 5, 7, 8, 10

Topical desensitizing agents:

These topical desensitizing interfere with thetransmission of pain stimulus at the level of the A-delta fibers around the odontoblasts or exert ablocking effect on the open dentine tubules. Someprotein precipitants may act in the both the ways.15

Potassium nitrate

Hodosh study was the first to report thatpotassium nitrate was a “superior desensitizer”.

The mechanism of action of potassium nitrate isunknown, although an oxidizing effect or blockingof tubules by crystallization has been proposed, butnot proven. A more likely explanation is that thepotassium ions are the active component and thatpotassium nitrate reduces dentinal sensory nerveactivity due to the depolarizing activity of the K+ ionand it aso prevents the repolarization of the nerve.Potassium nitrate does not induce any pulpalchanges.1, 5, 6, 9, 10, 11, 15

Fig: Schematic representation of the action of potassium nitrate on

dentinal tubules

Dentine Hypersensitivity - An Enigma? Sumangali, et, al.

Indian J Dent Adv 2011; 3(4): 659-667

Calcium hydroxide

Several studies have reported on theeffectiveness of calcium hydroxide in managingdentinal hypersensitivity. Its mode of action has beenproposed to be via occlusion of dentinal tubulesthrough the binding of loose protein radicals bycalcium ions and increasing mineralization of theexposed dentine. Although immediately effective,the action of calcium hydroxide diminishesrapidly requiring multiple applications to maintainits effect.1, 5, 6, 9, 10, 11

Casein phosphopeptides

A relatively new product on the marketcomposed of casein phosphopeptides has been usedfor the management of dentinal hyperersensitivity.

Sodium monofluorophosphate

Toothpastes containing sodiummonofluorophosphate have been shown to beeffective in managing dentinal hypersensitivity. Themechanism of action of sodiummonofluorophosphate is unclear. It does not appearto act by occluding dentinal tubules since scanningelectronmicroscopic studies have failed todemonstrate any visual changes to the dentinesurface treated with sodium monofluorophosphate.1, 5, 6, 9, 10, 11

Sodium fluoride

Many clinical studies have shown that treatmentof exposed root surfaces with fluoride toothpasteand concentrated fluoride solutions is very efficientin managing dentinal hypersensitivity. Theimprovement appears to be due to an increase in theresistance of dentine to acid decalcification as wellas to precipitations in the exposed dentinal tubules.Tal et al. suggested that the probable desensitizingeffects of fluoride are related to precipitated fluoridecompounds mechanically blocking exposed dentinaltubules or fluoride within the tubules blockingtransmission of stimuli.1, 5, 6, 9, 10, 11

Stannous fluoride

Stannous fluoride in either an aqueous solutionor in glycerine gelled with carboxymethyl celluloseis effective in controlling dentinal hypersensitivity.

The mode of action appears to be through theinduction of a high mineral content which creates acalcific barrier blocking the tubular openings on thedentine surface. Alternatively, stannous fluoride mayprecipitate on the dentine surface leading toocclusion of the exposed dentinal tubules andreducing the fluid flow to the pulp.1, 5, 6, 9, 10, 11 14, 15

Figure: Open tubules following treatment with non-sensitivityfluoride toothpaste.

Figure: Closed tubules following treatment with SnF2 dentifrice.

Oxalate salts

Oxalate salts generally used are potassiumoxalate and ferric oxalate. These salts are applied byrubbing or burnishing. They act via occlusion ofdentinal tubules and reducing the tubule fluid flowin either direction.15

Arginine-calcium carbonate

Treatment with the arginine-calcium carbonatedesensitizing paste is simple. The paste is gentle togingival tissues, does not elicit pain when applied.The dental professional applies a small amount of

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paste to sensitive tooth surfaces by burnishing it inwith a slowly rotating soft prophy cup. Paste can alsobe applied to accessible spots by massagingthoroughly with a cotton-tipped applicator and tofurcations and other hard-to-reach areas with amicrobrush. The dental professional should carefullyburnish the arginine-calcium carbonatedesensitizing paste into all sensitive areas, focusingon the CEJ and exposed cementum and dentin.1, 5, 6, 9,

10, 11

Fluoride iontophoresis

Iontophoresis is the process of influencing ionicmotion by an electric current and has been used as adesensitizing procedure in conjunction with sodiumfluoride. Studies report that there is an immediatereduction in sensitivity after treatment withiontophoresis, but the symptoms gradually returnover the ensuing six months.1, 5, 6, 9, 10, 11

Formaldehyde or glutaraldehyde

Formaldehyde and glutaraldehyde, act throughtheir ability to precipitate salivary proteins in dentinaltubules. This effect has been questioned since variousformulations have been found to have little or noeffect on dentinal hypersensitivity. Given that theseagents are very strong tissue fixatives, they should beused with extreme caution to ensure they do not comein contact with the vital gingival tissues. 1, 5, 6, 9, 10, 11

Anti-inflammatory agents

Corticosteroids

Anti-inflammatory agents such ascorticosteroids have been proposed for use tomanage dentine hypersensitivity.

However, trials have not found them to beparticularly useful. While it is presumed that theseagents may induce mineralization leading to tubuleocclusion, this view has yet to be validated and thevalidity of using such agents has been questioned. 1,

5, 6, 9, 10, 11

Dentine sealers

Resins and adhesives

Sealing of dentinal tubules with resins andadhesives has been advocated for many years as a

means of managing dentinal hypersensitivity. Thistechnique is generally reserved for cases of specificand localized dentinal hypersensitivity rather thangeneralized dentinal pain.1, 5, 6, 9, 10, 11

Fig: Schematic representation of composite resin restoration

Periodontal surgery

There are numerous soft tissue graftingprocedures which can be carried out to coverexposed root surfaces including lateral sliding grafts,free gingival grafts, connective tissue grafts, coronallyrepositioned flaps and in some cases guided tissueregeneration for treatment for the treatment oflocalized gingival recession using bioresorbablemembrane or skin allograft. Soft tissue grafting forlocalized recession defects requires careful planningand an understanding of the anatomical defect tobe treated. In general, soft tissue grafting for themanagement of sensitivity is not regarded as a verypredictable treatment strategy.1, 5, 6, 9, 10, 11

Fig: Schematic representation of gingival flaps surgery forgingival recession.

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Indian J Dent Adv 2011; 3(4): 659-667

Lasers

Both the Nd:YAG and CO2 lasers have been

studied for their use in managing dentinalhypersensitivity.11, 14, 23

Both applications rely on their ability to occludethe dentinal tubules. The Nd:YAG laser has been usedin conjunction with sodium fluoride varnish withencouraging results showing up to 90 per cent of thedentinal tubules being occluded through use of thiscombined therapy.

CO2 laser irradiation and stannous fluoride gelhas also been shown to be effective for inducingtubule occlusion for up to six months after treatment.While still largely experimental, this techniquerequires further scientific investigation before itbecomes a clinically acceptable means of treatment.1, 5, 6, 9, 10, 11, 12, 13

Future therapies

Gene therapy may further be included in thetreatment of dentinal hypersensitivity. It includes thetreatment of sensory nerves to dental restorativeprocedures as well as to surgical and non surgicaldebridement that elicit dentine hypersensitivity. Onesuch method is blocking the increased productionof nerve growth factor by pulpal fibroblasts near thelesion thought to contribute to tooth hypersensitivityafter restorative procedures.14

Conclusion

The ultimate goal in the treatment of dentinehypersensitivity is the immediate and permanentrelief of pain. For many patients, conventionaldesensitising agents often produce unsatisfactoryresults, since the action is usually directed toward theocclusion of the opened dentinal tubules withoutconsidering the causative factors that created theproblem. Once a definitive diagnosis of dentinehypersensitivity has been made, after considering adifferential diagnosis, a careful assessment of theaetiologic factors must be considered, which in turnif identified and correctly managed may enhance theoutcome of the currently used desensitizing agentsand ensure more successful management.

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13. Aldo Brugnera Junior, Ana Eliza Garrini, Antonio Pinheiro,Dilma Helena, Souza Campos, Elisângela Donamaria: LaserTherapy In The Treatment Of Dental Hypersensitivity~AHistologic Study And Clinical Application: Laser Therapy12:16-21.

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Dentine Hypersensitivity - An Enigma? Sumangali, et, al.

Indian J Dent Adv 2011; 3(4): 659-667