CourseNumber:136 CervicalDentin … · CervicalDentin Hypersensitivity:Etiology,...

Continuing Education

Cervical DentinHypersensitivity: Etiology,

Diagnosis, and ManagementAuthored by Douglas A. Terry, DDS

Course Number: 136

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LEARNING OBJECTIVESAfter reading this article, the individual will learn:• The accepted mechanism of dentinal sensation.• The etiology, differential diagnosis, and management

of cervical dentin hypersensitivity (CDH).

ABOUT THE AUTHORSDr. Terry is a clinical assistant professorin the Department of RestorativeDentistry and Biomaterials at theUniversity of Texas Health ScienceCenter Dental Branch at Houston. He isan accredited member of the American

Academy of Cosmetic Dentistry, an active member of theEuropean Academy of Esthetic Dentistry, and an honorarymember of the Indian Academy of Restorative Dentistry. Heis a member of the International Association for DentalResearch. Dr. Terry has received a number of professionalawards and has received Fellowships in the American andInternational College of Dentists, AGD, and theInternational Academy of Dental Facial Aesthetics. He is amember and the US vice president of International OralDesign. Dr. Terry is the founder and CEO of Design Tech-nique International and the Institute of Esthetic andRestorative Dentistry. He maintains a private practice inHouston, Tex. Dr. Terry has served as a past researchassociate for REALITY Research Lab and a clinicalassociate for REALITY Publishing. He is an editorialmember of numerous peer-reviewed scientific journals andhas published more than 230 articles on various topics inaesthetic and restorative dentistry and has authored thetextbooks Natural Aesthetics With Composite Resin andAesthetic and Restorative Dentistry: Material Selectionand Technique. He has lectured internationally on varioussubjects in restorative and aesthetic dentistry. For moreinformation see Aesthetic & Restorative Dentistry:Material Selection & Technique at the Web siteseverestpublishingmedia.net, quintpub.com, and

amazon.com. He can be reached at (281) 481-3483 or atthe e-mail [email protected].

Disclosure: Dr. Terry reports no disclosures.

INTRODUCTIONCervical dentin hypersensitivity (CDH) is a common clinicalcondition that has been reported to annoy and affect 15% to20% of the adult population, and most clinical practitioners.1

Approximately 40 million adults in North America may havesome degree of dentin hypersensitivity at some time in theirlife, whereas in other areas of the world the prevalence mayapproach 50% of the population.2,3 Further, this incidenceshould continue to rise with the increase in life expectancyand patients retaining their natural dentitions longer. Thus,this clinical manifestation presents a significant clinicalchallenge in dentistry now and in the future.

CDH is a condition characterized by transient sharptooth pain arising from exposure of dentin and opening ofdentinal tubules as well as to inflammatory processes in theunderlying pulp tissue.1,4,5 The condition is associated witha variety of exogenous stimuli that elicit pain, includingthermal (cold), tactile (touch), evaporative, chemical (acidexposure), or osmotic changes (sweets or drying thesurface).4,6,7 A considerable variation exists in the degreeand extent of dentin hypersensitivity that can vary fromindividual to individual due to differences in patency ofexposed dentinal tubules, state of the pulp, and thedifferences in pain tolerance, emotional state, andenvironmental factors for each individual. The conditionmay affect any tooth, but it most often affects canines andpremolars.8-10

This scientific review describes the acceptedmechanism of dentinal sensation and discusses theetiology, differential diagnosis, and management of CDH.

MECHANISMS FOR CERVICAL DENTINHYPERSENSITIVITYAlthough the morphological characteristics of the dentinaltubule have been described through autoradiographic,histochemical, and electron microscopic studies, theprecise mechanism of pain transmission from the exposeddentin surface to the terminal nerve ending is only


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Recommendations for Fluoride VarnishUse in CariesManagement

Cervical Dentin Hypersensitivity:Etiology, Diagnosis, andManagementEffective Date: 04/1/2011 Expiration Date: 04/1/2013

theorized. Many theories have been proposed to explain themechanism of CDH,11,12 including the modulation,transducer, gate control, and hydrodynamic theories. One ofthese, the odontoblastic transducer mechanism theoryproposed by Rapp, et al13 suggested that odontoblasts act asreceptor cells, mediating changes in the membrane potentialof the odontoblasts via synaptic junctions with nerves.13,14

This theory is inconclusive and not well accepted.A hydrodynamic hypothesis for dentin sensitivity that was

proposed 100 years ago provided the catalyst for theconfirmatory evidence produced in the 1960s by Brännströmand Aström.15 This “Hydrodynamic theory” has become themost widely accepted theory for explaining the mechanism ofdentinal sensation.16 This theory postulates that the dentintubules, which are open and wide, contain a fluid. Variousstimuli (ie, thermal, tactile, chemical, or osmotic changes)displace the fluid in the dentinal tubules inwardly or outwardly.This liquid movement stimulates the odontoblast process, andthe subsequent mechanical disturbance stimulates abaroreceptor (a nerve receptor sensitive to pressure) thatleads to neural discharge (depolarization); this neural pulpalactivation is perceived as pain.15,17

Pain seems to be produced by a rapid outwarddisplacement of the fluid in the dentinal tubules at thepulpo-dentinal border that is initiated by strong capillaryforces, and if sufficiently rapid, it may activate nerveslocated some distance from the tubules corresponding tothe exposed dentin.15,18 Furthermore, studies of surfacemorphologies of hypersensitive and nonsensitive dentinreport that dentin which is exposed and sensitive exhibitsmore numerous, patent, and wider dentinal tubules than innonsensitive areas.12,19

Another scanning electron microscope study showedthat in hypersensitive dentin, the smear layer was thinner,different in structure, and was more likely to beundercalcified than nonsensitive dentin.12,20 These findingsappear consistent with the hydrodynamic theory. Accordingto Poiseuille’s law, the volume rate of flow within a tube isdirectly proportional to the fourth power of the tube’sinternal radius.21 Therefore, an increase in the tubulediameter results in an increase of fluid flow by a power of 4,thus pain is amplified when the tubules are open to the oralcavity.2 Therefore, a greater number of open and wider

tubules at the dentin surface enhances fluid permeabilitythrough dentin and thus increases the potential for stimulustransmission and subsequent pain response.12 Thesefindings support the theory of increased hydrodynamicpermeability of hypersensitive dentin15 and have providedstrategies for the treatment of hypersensitive dentin. Accor-dingly, dentin hypersensitivity can be treated by minimizingmovement of intratubular fluid (Figure 1).

ETIOLOGY AND PREDISPOSING INFLUENCESThere are numerous and varied etiological factors andpredisposing influences involved with CDH. More than 90%of hypersensitive surfaces occur at the cervical region onthe buccal and labial aspects of the involved teeth. In theideal anatomical position, most teeth have only the enamelexposed to the oral environment, and dentin that isprotected by enamel or cementum is not sensitive. Cervicaltooth sensitivity occurs when this enamel or cementumlayer is removed and the underlying dentinal tubules areopen and exposed to the oral environment.8

There are 2 phases in the development of CDH.10,12

First, “lesion localization” occurs by exposure of the dentinaltubules from either gingival recession and loss ofcementum or through loss of enamel from wear. Since all


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Cervical Dentin Hypersensitivity: Etiology, Diagnosis, and Management

Figure 1. Dentinal tubules are normally filled with odontoblasticprocesses and dentinal fluid, a transudate of plasma. Since manytubules contain mechanoreceptor nerve endings near the pulp,intrafluid movement can result in pain transmission. (Courtesy ofJorge Perdigâo, DMD, MS, PhD)

exposed dentin is not sensitive, this localized lesionrequires the second phase. The second phase, “lesioninitiation,” occurs when the smear layer or tubular plugs areremoved, which opens the outer ends of the dentinaltubules.10,12

This dentin exposure can be the result of numerousetiologic factors which include abrasion, corrosion, attrition,abfraction, and gingival recession.22 These etiologic co-factors can be attributed to a multitude of conditions andphenomena which include aging,23 improper oral habits,lack of or excessive tooth brushing,24 incorrect toothbrushing,25 improper use of bleaching agents,12,26 acidicdietary habits,13,27 low pH mouth rinses,12,13,28 bulimianervosa,12,13,29-32 pyrophosphates, poor oral hygiene,13

airborne acids,32,33 clenching,32,34-37 bruxism,13,35

overeruption,23 a developmental anomaly, occlusal dishar-mony,13 periodontal disease,23 and periodontal therapy.38

The following discussion of several of these phenomenamay provide the dental professional with insight andinformation for determining etiology through differentialdiagnosis and methods for prevention, management, andtreatment:

� With the increasing life span and the increasedretention of teeth by the older patient, dental professionalsmust be aware of the physiological changes associated withthe aging process. As age advances, the number of teethwith root exposure increases.13 One recent survey revealedthat 88% of people age 65 years and older have one or moresites with recession.39 The presence and extent of gingivalrecession also increases with age. Despite these dramaticimprovements in tooth retention for the older patient, therestill remains a substantial portion of the aged population withmissing natural teeth. With the absence of opposing teeth,dental extrusion can occur, resulting in root exposure andthe increased potential for dentin hypersensitivity.23

� Improper or inadequate oral hygiene maintenance canresult in accumulation of plaque, causing gingival inflammationthat can result in gingival recession.This root exposure can berelated to CDH and intensified by acids excreted by bacteria,which can result in further opening of the dentinal tubules.Malpositioned teeth and toothbrush trauma have beenreported to be the most frequent etiologic factors associatedwith gingival recession.39-41 The incidence of gingival

recession increases with age and is greater in males thanfemales of the same age.39-41

� Dentin hypersensitivity can be a consequence ofperiodontal disease and surgical and nonsurgicalperiodontal therapy.38,42-51 After periodontal treatment,there can be a reduction of the gingival protective barrier asa result of excision of tissue which exposes the root surface.In addition, removal of cementum during root planing mayexpose the dentin to external stimuli.13,42,47,52 Reports byTammaro, et al43 indicate a significant change in dentinhypersensitivity after scaling and root planing, while vonTroil, et al50 found that dentin hypersensitivity occurred inapproximately 50% of patients following scaling and rootplaning. Tamminen, et al48 reported that dentinhypersensitivity occurred after periodontal surgeries usingthe modified Widman flap procedure. This postoperativedentin hypersensitivity may be due to increased surfaceexposure of root dentin to external stimuli and gingivalrecession following periodontal surgery.53,54 In addition,age, sex, and type of therapy are factors that can influencepostoperative pain and postoperative dentin hyper-sensitivity during periodontal therapy.45

� Normal function generates considerable stresseswithin teeth and supporting tissues.55 Since teeth are notrigid structures, they undergo deformation (strain) when afunctional load is applied,2,56 and this strain is proportional tothe amount of stress. The functional load is influenced bythe number of teeth, the type of occlusion, and the occlusalbehavior of the patient (ie, premature contacts, para-functional habits).2 During occlusal loading, the toothundergoes a lateral or an axial bending called toothflexure.55,57-64 The tooth flexure theory posits that occlusalforces are transmitted through the cusp and can becomeconcentrated in the cervical region of the tooth.57,65 Thistheory has been demonstrated and supported byengineering studies60-64,66 reporting that these horizontalloading forces cause a microscopic flexing of the anatomicalcrown of the tooth. Subsequently, this physiologic bendinggenerates a maximal strain in the cervical region of the toothwith resulting tensile stress concentrations in the cervicalregion on the side of the tooth from which the force isdirected. At the same time, the opposite region of the tooth isunder compressive stresses. When the direction of the force


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changes (ie, bruxism), the tooth flexes in the opposite directionand the stresses correspondingly reverse at the cervicalregion.66,67 These cyclic tensile and compressive stresseswhich occur in the mouth during chewing or parafunctionalhabits can reach a fatigue limit and can result in tooth structureloss and dentin hypersensitivity.13,68-72

�Corrosion is tooth surface loss caused by chemical orelectrochemical action; there are 2 sources of origin:endogenous and exogenous. Endogenous sources ofcorrosion involve unique patterns of enamel loss that areassociated with endogenous acids from gastroesophagealreflux disease, bulimia,29-31 anorexia nervosa, hiatal

hernia,73 and pregnancy morning sickness. Anotherendogenous source is gingival crevicular fluid which can beacidic and corrosive when in contact with the cervicalregion of the tooth.32,74 Exogenous sources of corrosioninvolve a chemically-induced loss of tooth substance fromextrinsic origin and are associated with diet (ie, carbonatedsoft drinks, candies that contain phosphoric or citric acid,citrus fruits or juices, and baby bottle syndrome), airborneacids such as industrial chemicals, and chlorinatedswimming pool water.73,75-86 Corrosion produces a moresoftened enamel zone, and the dentin becomes exposed tothe oral environment. An acid environment can further open


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Table. Summary of Treatment Strategies for Dentin Hypersensitivity

DESENSITIZE THE NERVE—MAKING IT LESS RESPONSIVE TO STIMULATIONA. Potassium nitrate

COVER THE DENTINAL TUBULES—PREVENTING FLUID FLOWA. Plug the dentinal tubules

1. Ions/saltsAluminumAmmoniumhexafluorosilicate

Calcium hydroxideCalcium carbonateCalcium phosphateCalcium silicateDibasic sodium citrateFluorsilcatePotassium oxalateSilicateSodiummonofluorophosphate

Sodium fluorideSodium fluoride/stannousfluoride combination

Stannous fluorideStrontium acetate withfluoride

Strontium chlorideIn combination with anadhesive

2. Precipitates—proteins/amino acids

FormaldehydeGlutaraldehydeSilver nitrateStrontium chloridehexahydrate

Zinc chlorideCPP-ACPF

3. PhytocomplexesRhubarb rhaponicumSpinacia oleracia

4. ResinsDentin sealersMethyl methacrylateDentinal adhesivesResinous dentinaldesensitizers

VarnishesSealants

B. Composite/glass ionomer restorationC. Crown placementD. Periodontal soft-tissue graftingE. Laser therapy

the dentinal tubules, resulting in dentin hypersensitivity.� Postdental bleaching sensitivity and gingival irritation

are the 2 main adverse effects of vital tooth bleaching.Gingival irritation can be caused from prolonged contact ofthe peroxide gel with the gingival tissues.27,87 Toothsensitivity can be attributed to the penetration of thebleaching agent through enamel and dentin and into thepulp chamber during the whitening procedure. Thehypersensitivity that occurs in association with bleachinghas been attributed to patient factors, the concentration ofthe bleaching agent, length of exposure to the bleachingagent, pH of the bleaching solution, and factors related totray fabrication.88

ESTABLISHING A DIAGNOSISThe most important part of any clinical treatment is toestablish a good diagnosis and to find and eliminate thepredisposing factors of the condition. After considering allfactors related to cervical tooth sensitivity from corrosion,attrition, abrasion, abfraction, gingival recession, or acombination of these processes, a differential diagnosisshould be developed. Dentinal hypersensitivity must bedifferentiated from other clinical conditions that may causeteeth to be sensitive, and an appropriate diagnosis must bemade before any treatment is initiated. The characteristicresponse to a specific stimulus is that the pain should besharp, localized, brief, and usually diminishes after removalof the stimulus, but may remain as a dull ache.89

Clinical conditions that should be considered includepostrestorative sensitivity, postoperative sensitivity frombleaching, fractured teeth or restorations, dental caries, andirreversible pulpitis. This differential diagnosis providesinformation for determining etiology and can requireadditional information such as age, diet, oral hygiene routine,occupation, medical and dental factors, abnormal oral habits,and occlusal disharmonies.22,32,90 The information acquiredduring the differential diagnosis will provide a systematicapproach for the management of hypersensitive surfacesthrough preventive and restorative therapy.

Management of CDH begins with prevention andelimination of the predisposing factors associated withcontinued dentinal tubule exposure. Preoperative treatmentconsiderations and procedures may include preventive

measures such as fluoride therapy, iontophoresis, brushingwith desensitizing dentrifices, professional application ofpotassium oxalate or other tubule occluding agents,application of dentin adhesives, occlusal adjustments,91

dietary instruction, toothbrushing and oral hygieneinstruction, discontinuation of poor oral habits, and occlusalguard fabrication.

TREATMENT STRATEGIESThree fundamental treatment strategies should beconsidered for the management of CDH (Table). The firsttreatment strategy is to desensitize the nerve tissue bymodifying neural response within the dentin tubule.Potassium nitrate is an effective therapeutic agent that iscurrently used in all over-the-counter (OTC) desensitizationdentifrices with ADA and US Food and Drug Administrationapproval. Tarbet, et al92 demonstrated in well-conductedclinical trials that a toothpaste containing 5% potassiumnitrate was effective, with daily use, to desensitize for up to 4weeks, and that potassium nitrate does not induce changesin the pulp. Potassium nitrate is believed to increase theextracellular potassium ion concentration and thus maydepolarize the nerve and prevent it from repolarizing. Thischange disrupts the ionic tubular membrane transmissionand prevents sending pain signals to the brain until ionicconcentrations restabilize.

Potassium nitrate desensitizing gels (ie, in-office or homeapplication) can be used for preoperative and postoperativebleaching sensitivity. Haywood, et al93 concluded that 10 to30 minutes of wearing time of the gel in the tray before orafter whitening may reduce sensitivity in more than 90% ofpatients and make the bleaching procedure tolerable.87,93 Inaddition, additives such as 3% potassium nitrate and 0.11fluoride ion weight/volume have been reported to reduce butnot eliminate sensitivity when added to a 10% carbamideperoxide bleaching gel87,94 (Figures 2a and 2b).

A second treatment strategy is to occlude the distalterminal ends of the exposed dentinal tubules. The tubulescan be sealed through natural desensitization fromsecondary dentin formation or mineralization or byutilization of compounds that can precipitate to form anaccumulation of denatured protein or a calcified plugginglayer. These OTC and professionally applied desensitizing


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dentifrice treatments for cervical sensitivitycontain various chemicals that includedenaturing salts (ie, strontium chloride,formaldehyde) and precipitating agents (ie,sodium fluoride, stannous fluoride,monofluorophosphate, casein phosphopep-tide-amorphous calcium fluoride phos-phate,and oxalates) (Figure 3). This treatment iscost-effective, noninvasive, and can beapplied at home or in the dental office.

Other effective clinical techniques includeiontophoresis and adhesive resin application.Iontophoresis utilizes a charged electricalcurrent to accelerate and precipitate insolublecalcium with fluoride gels.95,96 Adhesive resinimpregnation is another clinical technique that has increasedin popularity in recent years and is currently considered oneof the most definitive and rapidly acting methods ofdesensitization. This procedure reduces sensitivity with theapplication of a dentin adhesive to form a hybrid layer, and thisresin barrier prevents continued diffusion of toxins andbacterial invasion toward the pulp while producing minimaladverse pulpal inflammation (Figure 4). A combination ofiontophoresis followed by resin impregnation is one of themost effective clinical techniques for eliminating cervical toothsensitivity.97 In addition, one clinical technique that utilizes anapplication of calcium hydroxide paste has been effective inrelieving cervical sensitivity by increasing peritubular dentinmineralization.98

A third treatment strategy when there is gingivalrecession and/or a cervical lesion is to cover the exposedsurface of the dentinal tubules by utilizing a periodontalsurgical procedure and/or dental restoration. Theperiodontal procedures include free autogenous mucosalgrafts, subepithelial connective tissue grafts, coronallyadvanced flap technique, guided periodontal tissueregeneration, and acellular dermal matrix grafts. Res-torative methods can involve the use of conventional glassionomers, resin-modified glass ionomers, compomers,flowable composites, hybrid composites, microfillcomposites, laboratory-processed composite and porcelainveneers, laboratory-processed composite Class V inlays,all-ceramic Class V inlays and crowns, and PFM crowns and bridges.99,100


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Figure 3. A customtray application of atopical paste contain-ing bio-availablecalcium, phosphate,and fluoride (GC MIPaste Plus [GCAmerica]) is appliedto the sensitive

regions of the teeth and allowed to dwell for 3 minutes before thepatient is allowed to expectorate.

Figures 2a and 2b. (a) A thick ribbon of gel containing potassium nitrate (Relief[Discus Dental]; UltraEz [Ultradent Products]) is applied to the cervical lesion withan applicator tip using a rubbing motion and allowed to dwell for 3 minutes beforethe patient is allowed to expectorate. (b) Hypersensitivity is frequently associatedwith tooth whitening and can be managed by applying a thick ribbon of gelcontaining potassium nitrate (Relief; UltraEz) to the sensitive areas of the teethusing an extra-soft brush.

a b

Figure 4. After totaletch technique isperformed, adesensitizingadhesive (GlumaComfort Bond +Desensitizer [HeraeusKulzer]) is applied tothe cervical lesionusing 3 coats, allowedto dwell for 15seconds, and light-cured for 20 seconds.

Since gingival recession is a primary cause of dentinexposure and a major predisposing factor for dentinhypersensitivity, a combined treatment modality should beconsidered for more advanced cervical lesions with rootcaries. This treatment strategy combines the use of a glassionomer to seal the exposed surfaces of the dentinal tubulesand to define the root emergence contour whilerepositioning the gingival contour using a connective tissuegraft procedure99,101,102 (Figures 5a to 5c). Postoperativesensitivity can be prevalent following periodontal proceduresand usually decreases considerably after one to 4 weeks.50

Addressing the occlusal status of a patient should also beexamined as has been shown in the retrospective studydone by Coleman, et al.91 Judicious occlusal analysis andequilibration can frequently eliminate CDH. It is suggestedthat a thorough oral hygiene protocol be integrated with theaforementioned strategies.

CONCLUSIONManagement of any clinical situation begins with prevention,knowledge of the various etiological factors and predisposinginfluences, and an understanding of the various therapeuticmethods available for treatment. Professionals shouldrecognize the role causative factors play in initiating dentinhypersensitivity and inform and communicate those variousclinical considerations and solutions effectively with theirpatients. This article has attempted to provide the dentalprofessional a general overview for understanding thebiology, etiology, and different mechanisms and clinicalmanifestations of CDH. By utilizing this knowledge withclinical experience and sound judgment, the dentalrestorative team can identify and determine etiology throughdifferential diagnosis and thus provide methods forprevention, management, and treatment of dentinhypersensitivity.


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Figures 5a to 5c.A maxillary first molarwith a Miller Class IIIgingival recessionassociated with anoncarious cervicallesion is successfullytreated by integratinga subepithelialconnective tissuegraft and aconventional glassionomer restoration(GC Fuji IX GP Extra[GC America]).

a

c

b

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54. Rees JS, Addy M. A cross-sectional study of buccalcervical sensitivity in UK general dental practice and asummary review of prevalence studies. Int J Dent Hyg.2004;2:64-69.

55. Yettram AL, Wright KW, Pickard HM. Finite element stressanalysis of the crowns of normal and restored teeth. J DentRes. 1976;55:1004-1011.

56. Ross GK, et al. Measurement of deformation of teeth invivo. J Dent Res. 1992;71A:569. Abstract 432.

57. Heymann HO, Sturdevant JR, Bayne S, et al. Examining

tooth flexure effects on cervical restorations: a two-yearclinical study. J Am Dent Assoc. 1991;122:41-47.

58. Grippo JO. Tooth flexure. J Am Dent Assoc. 1991;122:13.59. Gordon JE. The Science of Structure and Materials. New

York, NY: Scientific American Library; 1988.60. Selna LG, Shillingburg HT Jr, Kerr PA. Finite element

analysis of dental structures—axisymmetric and planestress idealizations. J Biomed Mater Res. 1975;9:237-252.

61. Rubin C, Krishnamurthy N, Capilouto E, et al. Stressanalysis of the human tooth using a three-dimensionalfinite element model. J Dent Res. 1983;62:82-86.

62. Goel VK, Khera SC, Ralston JL, et al. Stresses at thedentinoenamel junction of human teeth—a finite elementinvestigation. J Prosthet Dent. 1991;66:451-459.

63. Rees JS. The role of cuspal flexure in the development ofabfraction lesions: a finite element study. Eur J Oral Sci.1998;106:1028-1032.

64. Rees JS, Jacobsen PH. The effect of cuspal flexure on abuccal Class V restoration: a finite element study. J Dent.1998;26:361-367.

65. Tyas MJ. The Class V lesion—aetiology and restoration.Aust Dent J. 1995;40:167-170.

66. Terry DA, Leinfelder KF. Managing stress with compositeresin, part 2: the class V restoration. Dent Today.2007;26:104-113.

67. Grippo JO, Simring M. Dental ‘erosion’ revisited. J Am DentAssoc. 1995;126:619-620, 623-624, 627-630.

68. Thresher RW, Saito GE. The stress analysis of humanteeth. J Biomech. 1973;6:443-449.

69. Hood JA. Experimental studies on tooth deformation: stressdistribution in class V restorations. N Z Dent J.1972;68:116-131.

70. Powers JM, Craig RG, Ludema KC. Frictional behavior andsurface failure of human enamel. J Dent Res.1973;52:1327-1331.

71. Mayhew RB, Jessee SA, Martin RE. Association ofocclusal, periodontal, and dietary factors with the presenceof non-carious cervical dental lesions. Am J Dent.1998;11:29-32.

72. Ikeda T, Nakano M, Bando E, et al. The effect of lightpremature occlusal contact on tooth pain threshold inhumans. J Oral Rehabil. 1998;25:589-595.

73. Howden GF. Erosion as the presenting symptom in hiatushernia. A case report. Br Dent J. 1971;131:455-456.

74. Bodecker CF. Local acidity: a cause of dental erosion-abrasion; progress report of the Erosion-AbrasionCommittee of the New York Academy of Dentistry. AnnDent. 1945;4:50-55.

75. Grippo JO. Abfractions: a new classification of hard tissuelesions of teeth. J Esthet Dent. 1991;3:14-19.

76. Imfeld T. Dental erosion. Definition, classification and links.Eur J Oral Sci. 1996;104(2 pt 2):151-155.

77. Filler SJ, Lazarchik DA. Tooth erosion: An unusual case.Gen Dent. 1994;42:568.


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78. Allan DN. Dental erosion from vomiting: A case report. BrDent J. 1969;126:311-312.

79. Milosevic A, Slade PD. The orodental status of anorexicsand bulimics. Br Dent J. 1989;167:66-70.

80. White DK, Hayes RC, Benjamin RN. Loss of tooth structureassociated with chronic regurgitation and vomiting. J AmDent Assoc. 1978;97:833-835.

81. Kleier DJ, Aragon SB, Averbach RE. Dental managementof the chronic vomiting patient. J Am Dent Assoc.1984;108:618-621.

82. Rosenthal P, Rosenthal R. Tooth enamel erosion fromvomiting treated with an acrylic sealant. Clin Pediatr (Phila).1983;22:818.

83. Simmons MS, Thompson DC. Dental erosion secondary toethanol-induced emesis. Oral Surg Oral Med Oral Pathol.1987;64:731-733.

84. Eccles JD, Jenkins WG. Dental erosion and diet. J Dent.1974;2:153-159.

85. Burket LW, Lynch MA, Brightman VJ, et al. Burket’s OralMedicine: Diagnosis and Treatment. 8th ed. Philadelphia,PA: Lippincott; 1984:568.

86. Holloway PF, Mellanby M, Stewart RJC. Fruit drinks andtooth erosion. Br Dent J. 1958;104:305-309.

87. Hewlett ER. Etiology and management of whitening-induced tooth hypersensitivity. J Calif Dent Assoc.2007;35:499-506.

88. Jacobsen PL, Bruce G. Clinical dentin hypersensitivity:understanding the causes and prescribing a treatment. JContemp Dent Pract. 2001;2:1-12.

89. Addy M. Etiology and clinical implications of dentinehypersensitivity. Dent Clin North Am. 1990;34:503-514.

90. Grippo JO. Noncarious cervical lesions: the decision toignore or restore. J Esthet Dent. 1992;4 suppl:55-64.

91. Coleman TA, Grippo JO, Kinderknecht KE. Cervical dentinhypersensitivity. Part III: resolution following occlusalequilibration. Quintessence Int. 2003;34:427-434.

92. Tarbet WJ, Silverman G, Stolman JM, et al. Clinicalevaluation of a new treatment for dentinal hypersensitivity.J Periodontol. 1980;51:535-540.

93. Haywood VB, Caughman WF, Frazier KB, et al. Traydelivery of potassium nitrate-fluoride to reduce bleachingsensitivity. Quintessence Int. 2001;32:105-109.

94. Tam L. Effect of potassium nitrate and fluoride oncarbamide peroxide bleaching. Quintessence Int.2001;32:766-770.

95. Singal P, Gupta R, Pandit N. 2% sodium fluoride-iontophoresis compared to a commercially availabledesensitizing agent. J Periodontol. 2005;76:351-357.

96. Orbak R, Canakçi V, Tezel A. Clinical evaluation of an electron-ionizing toothbrush with a toothpaste containing stannousfluoride in treatment of dentine hypersensitivity followingperiodontal surgery.Dent Mater J. 2001;20:164-171.

97. Christensen GJ. Desensitization of cervical tooth structure.J Am Dent Assoc. 1998;129:765-766.

98. Berman LH. Dentinal sensation and hypersensitivity. Areview of mechanisms and treatment alternatives. JPeriodontol. 1985;56:216-222.

99. Terry DA, McGuire MK, McLaren E, et al. Perioestheticapproach to the diagnosis and treatment of carious andnoncarious cervical lesions: Part I. J Esthet Restor Dent.2003;15:217-232.

100.Terry DA, Leinfelder KF, Geller W. Aesthetic & RestorativeDentistry: Material Selection and Technique. Houston, TX:Everest Publishing Media; 2009.

101. Santamaria MP, Suaid FF, Nociti FH Jr, et al. Periodontalsurgery and glass ionomer restoration in the treatment ofgingival recession associated with a non-carious cervicallesion: report of three cases. J Periodontol. 2007;78:1146-1153.

102. Santamaria MP, Suaid FF, Casati MZ, et al. Coronallypositioned flap plus resin-modified glass ionomer restorationfor the treatment of gingival recession associated with non-carious cervical lesions: a randomized controlled clinical trial.J Periodontol. 2008;79:621-628.


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POST EXAMINATION INFORMATION

To receive continuing education credit for participation inthis educational activity you must complete the programpost examination and receive a score of 70% or better.

Traditional Completion Option:You may fax or mail your answers with payment to DentistryToday (see Traditional Completion Information on followingpage). All information requested must be provided in orderto process the program for credit. Be sure to complete your“Payment,” “Personal Certification Information,” “Answers,”and “Evaluation” forms. Your exam will be graded within 72hours of receipt. Upon successful completion of the post-exam (70% or higher), a letter of completion will be mailedto the address provided.

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POST EXAMINATION QUESTIONS

1. CDH most often affects:

a. Maxillary molar teeth.

b. Mandibular molar teeth.

c. Incisor teeth.

d. Canine and premolar teeth.

2. The most widely accepted theory for explaining themechanism of dentinal sensation is the:

a. Hydrodynamic theory.

b. Odontoblastic transducer mechanism theory.

c. Gate control theory.

d. Modulation theory.

3. The volume rate of flow within a tube is determinedby:

a. Brännström’s law.

b. Rapp’s law.

c. Poiseuille’s law.

d. Aston’s law.

4. Approximately ____% of hypersensitive surfacesoccur at the cervical region on the buccal and labialaspects of teeth.

a. 30.

b. 50.

c. 75.

d. 90.

5. Dentin exposure can result from:

a. Abrasion.

b. Corrosion.

c. Abfraction.

d. All of the above.

6. One recent survey revealed that ____% of people age65 years or older have one or more sites withgingival recession.

a. 65.

b. 77.

c. 88.

d. 93.

7. The incidence of gingival recession increases withage. The incidence of gingival recession is greater infemales than males of the same age.

a. The first statement is true, the second is false.

b. The first statement is false, the second true.

c. Both statements are true.

d. Both statements are false.


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8. Tooth surface loss caused by chemical orelectrochemical action is called:

a. Abrasion.

b. Wear.

c. Corrosion.

d. Abfraction.

9. Hypersensitivity associated with tooth bleaching hasbeen attributed to:

a. The pH of the bleaching agent.

b. Concentration of bleaching agent.

c. Length of exposure to the bleaching agent.

d. All of the above.

10. Pain from CDH usually diminishes after removal ofthe stimulus. The pain may remain as a dull ache.





11. The following is currently used in all over-the-counter (OTC) desensitization dentifrices:

a. Stannous fluoride.

b. Potassium nitrate.

c. Sodium fluoride.

d. Monofluorophosphate.

12. The following precipitating agent is used in OTC andprofessionally applied desensitizing dentifrices:

a. Strontium chloride.

b. Formaldehyde.

c. Sodium fluoride.

d. Both a and b.

13. Haywood, et al concluded that wearing a traycontaining potassium nitrate desensitizing gel for____ minutes may reduce dentin sensitivity in 90% orhigher of patients:

a. 5 to 10.

b. 10 to 30.

c. 30 to 60.

d. 60 to 90.

14. A toothpaste containing 5% potassium nitrate useddaily can desensitize for up to 4 weeks. However,such use may induce changes in the pulp.





15. A combination of iontophoresis followed by resinimpregnation:

a. Is contraindicated due to risk of pulpal changes.

b. Is rarely helpful in reducing dentin hypersensitivity.

c. Is one of the most definitive and rapidly actingmethods of desensitization.

d. Has not been studied for clinical effectiveness inreducing dentin hypersensitivity.

16. One clinical technique that relieves cervicalsensitivity by increasing peritubular dentinmineralization is:

a. Iontophoresis.

b. Calcium hydroxide paste.

c. Adhesive resin impregnation.

d. Glass ionomer.


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