CDEWorld > Courses > Dentin Hypersensitivity: Differential Diagnosis, Tests, and Etiology

Dentin Hypersensitivity: Differential Diagnosis, Tests, and Etiology

Richard D. Trushkowsky, DDS; and Franklin Garcia-Godoy, DDS, MS, PhD, PhD

February 2014 Issue - Expires February 28th, 2017

Compendium of Continuing Education in Dentistry

Abstract

Dentin hypersensitivity (DHS) is a painful condition that affects up to 57% of the adult population. It occurs as a result of exposure of dentin to the oral environment. Ensuring the correct diagnosis of this condition is based on history and examination. An oral screening for DHS should encompass such elements as patient history, clinical examination that includes radiographs, a variety of tests, identification of risk factors, and a differential diagnosis. An understanding of dentinal fluid and odontoblasts is also beneficial for diagnosis.

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Dentin hypersensitivity (DHS) is characterized by short painful responses to stimuli—typically thermal, evaporative, tactile, osmotic, or chemical—which cannot be ascribed to any other form of dental defect or pathology1 (Figure 1). In 2003 the Canadian Advisory Board on Dentine Hypersensitivity suggested that the term disease should be substituted for pathology. In 1900, Gysi said dentin sensitivity is “of secondary nature and is not physiologic.” He also claimed that dentin sensitivity is “sufficiently provided for by the pulp and periosteum so that supply of nerves in dentin would be superfluous.” He further stated that the dentinal canaliculi contain “a watery organic substance.” The pressure on the dentinal canaliculi is transmitted from one end of the tubule, which is open and full of water, to the other end, which is loosely woven to the odontoblasts. The canaliculi are “interwoven with nerves and they felt pressure as a sensation of pain.”2 Munch also showed that any stimulation on dentin was perceived as pain.2 Symons learned that interfering with the contents of the tubules at the outer end resulted in changes in capillary forces and caused an outward flow, and that pain was a result of this outward flow.2 The application of heat, however, caused the fluid to flow toward the pulp and did not produce pain as readily.2

Although many theories have been suggested over the last century, the hydrodynamic hypothesis that was initially proposed in the 1960s remains the one that is usually accepted. This theory was established by Brännström and Astrom and relates to the design of dentin and the movement of fluid in the dentinal tubules as a result of various stimuli.3 DHS is a painful condition affecting 8% to 57% of the adult population and is a result of exposure of dentin to the oral environment.4 Since several other oral disorders, such as untreated dental caries, a cracked tooth, or marginal leakage around a restoration, may result in dental pain and pulpal pain, a proper diagnosis is needed.

Diagnosis and Clinical Management

About a decade ago Addy5 suggested the following approach to diagnosis and clinical management of DHS; the correct diagnosis is based on patient history and examination.

• Consider a differential diagnosis, as suggested by DHS, which alone may explain the symptoms or identify the presence of other conditions contributing to the pain of DHS.

• Treat any and all secondary conditions that induce symptoms similar to DHS (differential diagnosis).

• Identify etiological and predisposing factors, particularly with respect to erosion and abrasion. Consider detailed, written, dietary histories and oral hygiene habits (eg, frequency, duration, and timing of brushing; estimation of brushing force; frequency of brush change). Some of the aspects of tooth brushing behavior are best apprised by observing the patient in the dental practice.

• Remove or modify identified etiologic or predisposing factors. Offer dietary advice to minimize erosion and oral hygiene instruction to minimize abrasion and to distinguish abrasion from erosion.

• Recommend or provide treatment appropriate to the individual needs of the sufferer. The number of teeth involved and the severity of the pain are important variables and should influence treatment options.

In order to circumvent an incorrect diagnosis, under-diagnosis, and under- or over-treatment of patients reporting pain, an oral screening should be undertaken.

Patient History

The patient should be asked whether any tooth or teeth hurt when eating or drinking hot, iced, cold, sweet, or acidic food or beverages. The patient should then be asked if any symptoms occur during brushing or following restorative procedures. If the patient answers positively to any of these questions, a more detailed history needs to be obtained. The dentist should inquire as to the site, character, severity, and duration of pain. The source of the pain needs to be identified. The source of any extrinsic or intrinsic acid needs to be determined (eg, acids in juices, fruits, carbonated drinks, and wines).6

A Clinical Examination, Including Radiographs, Directly Related to DHS

A clinical examination directly related to dentin hypersensitivity should be performed, with exclusion of all differential diagnoses, including the following: cracked tooth syndrome; fractured restoration; restoration in traumatic occlusion; chipped teeth; dental or root caries; postoperative sensitivity; pulpal response to restorative treatment or material; marginal leakage of restoration; pulpitis (pulpal status); gingival inflammation; vital bleaching procedures; and atypical odontaglia.

The patient’s response to various triggering stimuli should be recorded. The stimuli are sorted into four categories: mechanical, chemical, electrical, and thermal.7

Mechanical (tactile) stimuli involve running a sharp tipped probe on the exposed dentinal surface. A mechanical pressure stimulator, such as the Yeaple probe, can be used in a research setting. The probe should be placed at a right angle to the surface of the tooth, and the pressure (in grams) is progressively increased until the pain onset is reached. The Yeaple probe uses an electromagnetic device to control the amount of force applied. Force corresponding to 70 g with no pain is considered non-sensitive. The force is increased in 5-g intervals, with care taken not to apply too much scratching pressure, as this could prompt more problems. Kakar A8 described the Jay Sensitivity Sensor Probe, an instrument to evaluate tactile sensitivity in clinical settings, as follows: “Notable features of this instrument for improved clinical operations include a microprocessor-controlled evaluation of force limits in pre-set increments, audible beeps for each programmed force limit, a digital readout of the force eliciting patient responses, factory calibration to preclude additional daily calibration and foot control for operator’s ease.”9

Chemical (osmotic) stimuli are created by using hypertonic solutions of glucose or sucrose. Acid solutions were used previously, but their low pH resulted in tubular demineralization and symptoms. These solutions create their effect by means of osmotic pressure that causes intratubular fluid movement. This solution is applied with a cotton-tipped applicator. However, since a graded response cannot be obtained, this test has limited validity. Cold air currents/air from the dental chair can be applied at a distance of 1 cm and should be at right angles to the tooth. Ideally, the pressure should be 45 psi and at a temperature of 19°C to 24°C. Unfortunately, use of the air for more than 1 second creates temperature variations. The test is useful mainly for screening and should be used after the tactile test to eliminate any residual effect. Cold-water stimulation at 7°C is perfect for identification of DHS. Ideally, a group of syringes with water at a variety of temperatures ranging between 0°C to 20°C are required. Initially, the warmest is used, followed by decreasing temperatures. Exposure of the tooth to the water should not exceed 3 seconds, and if no reaction is induced, a 3-minute wait is required prior to the next lower temperature. The temperature should be decreased in increments of 5°C and stopped when 0°C is reached and there is no response.

Thermoelectric techniques involve constant heat or cold application, which allows quantification of the applied provocation. A fine-tipped thermal probe is used on the tooth surface. The test should be initiated at 25°C and then decreased by 5°C until pain is experienced. The probe must make adequate contact with the tooth so that the temperature gradient is transmitted. However, normally the cold air or liquid would be the stimulus to cause fluid movement in the tubules, rather than a probe that also introduces a pressure element that may modify the results. Electrical stimulation can also be used, but the results may be modified due to current loss through the periodontium and possible stimulation of periodontal nerves.7

Tests

Despite the variety of tests available, unfortunately they are all subjective. Pain perception will depend on the individual disposition, psychological factors, amount of fear or anxiety present, ethnic differences, and social impacts. Ideally, a more objective technique would be used in order to adequately quantify the patient’s response. Though there are several scales that can be used, they are limited in scope.

Verbal Rating Scale (VRS)—The VRS uses a numerical program with a pain cognizance rating from 0 to 3: (0 = no discomfort, 1 = mild discomfort, 2 = significant discomfort, 3 = significant discomfort lasting more than 10 seconds). However, the scale provides limited responses, and narrative of the pain sensation is not feasible.

Visual Analog Scale (VAS)—With the VAS, the patient marks the pain intensity on a 10-cm straight line (0 = no pain, 10 = extreme pain). Global evaluation of dentin sensitivity determines the “intensity of stimulus needed to produce pain (stimulus-based techniques)” and the “subjective evaluation of pain induced by a stimulus (response-based techniques).” The first technique is based on pain threshold, while the latter is based on intensity.10

Numerical Rating Scale (NRS)—These scales consist of a range of numbers from which patients select the number most representative of their pain, usually from 0 to 10 or 0 to 100, with 0 representing no pain and the highest number representing the “worst pain I have experienced.”

Faces Pain Scale-Revised (FPS-R)—This is a self-reported measure of pain intensity developed for children. It was adapted from the Faces Pain Scale in order to make it possible to score on the widely accepted 0 to 10 metric. It shows a close linear relationship to visual analog pain scales across the age range of 4 to 16 years.11,12

Visual Analogue Thermometer (VAT)—The VAT consists of a rigid plasticized cardboard strip of white color with a horizontal black opening 10 cm long by 2 cm wide. The opening is covered with a red opaque band that slides from left to right by means of a strip located on the back of the thermometer. The left signifies no pain and the right, unbearable pain. As the strip is moved across the opening, the increasing intensity of pain is shown by the red band.13

Ferreira-Valente et al explored the validity of four pain-intensity rating scales.14 It was found that the NRS can provide data for parametric analysis and is relatively simple to administer and score. The VRS does not have equal breaks between levels, which limits the evaluation of the degree of differences over time. Women also seem to report higher pain intensity ratings across temperatures, which will modify results.

Identification of Risk Factors

Dentin sensitivity may occur as a result of enamel loss. Enamel loss can occur due to attrition, abrasion, or erosion. In actuality, a combination of these factors in various proportions is what usually leads to enamel loss. Erosion is thought to be a main factor in tooth wear and is defined as the dissolution of teeth by acids, which are not bacterial in origin. Erosion can be caused by extrinsic or intrinsic acids. Erosion by extrinsic sources can be further subdivided into dietary or environmental causes. Intrinsic erosion is triggered by exposure of teeth to gastric juices. Dietary erosion can occur as a result of drinks containing acids, such as fruit juices, soda, and wine, as well as such foods as citrus fruits and yogurt. Raw food seems to bring increased risks of dental erosion. Citric acid, which is found in many drinks, may possibly demineralize tooth structure by chelating calcium.

Industrial erosion can be a by-product of work such as that done by employees in battery manufacturing facilities and wine tasters. Swimmers who are exposed to pools with pH at 2.7 may suffer erosion to their teeth. Improperly used nighttime bleaching agents can also erode both dentin and enamel. Some mouth rinses have a low pH and can dissolve the smear layer, thereby opening the tubules. Brushing immediately after exposure may potentiate the effect. Intrinsic erosion may be exhibited by patients with gastric reflux resulting from a hiatus hernia, chronic alcoholism, and a variety of eating disorders.

Abfraction is believed to be a result of eccentric loading, causing cusp flexure and resulting in compressive and tensile forces in the cervical area. These weakened areas may potentiate the effects of abrasion and erosion. Gingival recession will expose more of the root surface and, consequently, the dentinal tubules as cementum is removed. Tooth brushing with increased frequency and with a hard toothbrush will often cause recession on the buccal surface of teeth. Usually, these areas are free of plaque, but some authors feel plaque and bacterial contamination may cause dentin sensitivity.15 This has been an area of controversy, as many patients referred for periodontal treatment display dentin hypersensitivity.16

Differential Diagnosis

There are many conditions that may provoke the same symptoms as DHS, and these must be eliminated prior to making a diagnosis of DHS. Cracked tooth syndrome (CTS) refers to an incomplete fracture of a vital posterior tooth that involves the dentin and occasionally extends to the pulp.17,18 A more recent definition of the nature of this condition is “a fracture plane of unknown depth and direction passing through tooth structure that, if not already involving, may progress to communicate with the pulp and/or periodontal ligament.”19 The history elicited from the patient can give certain characteristic clues. Pain on biting that ceases after the pressure has been withdrawn is a classic sign.18

There are two classic patterns of crack formation.17 In the first pattern, the crack is centrally situated and, following the dentinal tubules, may extend to the pulp; in the second pattern, the crack is more peripherally directed and may result in cuspal fracture. Pressure applied to the crown of a cracked tooth leads to separation of the tooth components along the line of the crack. Such separation in dentin causes movement of fluid in the dentinal tubules, stimulating odontoblasts in the pulp as well as the stretching and rupturing odontoblastic processes while lying in the tubules.20 Vitality testing usually gives a positive response, and the tooth is not normally tender to percussion in an axial direction. However, symptoms can be provoked when pressure is applied to an individual cusp.21 The pain of pulpitis often occurs without provocation, and, particularly after thermal tests, may persist after the stimulus has been removed. This would differentiate pulpitis from dentin hypersensitivity pain, which subsides after removal of the stimulus. Additional tests for pulpitis could include painful response to percussion, chewing, and tooth mobility.22

Dentinal Fluid and Odontoblasts

The space between the odontoblastic process and the tubule wall (the periodontoblastic space) is thought to be occupied with dentinal fluid, but the proof of this has yet to be established.23 It is believed the odontoblastic cell layer creates a barrier that restrains the passage of fluids, ions, and other molecules along the extracellular pathways. It is also believed that circumstances not involving external stimuli that encompass tissue-damaging (eg, caries, caries preparation, abrasion) dentinal fluid are solely under odontoblastic control. Since most studies discussing dentinal fluid flow and consistency are based on cavity preparations that may disrupt the tight junctions between odontoblasts, fluid from the pulp, blood vessels, or both may diffuse into the dentin. If this occurs, the fluid exists only as a reaction to trauma.24,25

Although there is disagreement regarding the origin of dental fluid, it is usually acknowledged that dentin sensitivity to extrinsic irritants is facilitated by alterations in hydraulic conductance.26 Human teeth are more sensitive to outward than inward flow.26 Dentin exposed to external stimuli results in a fluid shift across the dentin to create a neurovascular response (pain sensation).27 The cell bodies of the sensory neurons of the pulp are located in the trigeminal ganglion. The majority of the nerve bundles reach the coronal dentin, where they fan out to form the nerve plexus of Raschkow. There, they anastomose and terminate as free nerve endings that synapse onto and into the odontoblastic cell layer (approximately 100 μm to 200 μm deep in the dentinal tubules) and the odontoblastic cell processes.28 A recent report demonstrated that human dental pulp fibroblasts express thermosensitive transient receptor potential (TRP) channels. TRP channels are a group of nonselective calcium-permeable cationic channels that act as polymodal sensors of environmental stimuli (eg, thermal and chemical). TRPM8 and TRPA1 are cold-sensing TRP channels.29 El Karim et al believed that human odontoblasts can express functional TRP channels that may possibly be involved in mediating thermal sensation in teeth.30 More recently TRPC1, 5, 6, TRPM2, and TRPM3 have been shown to be implicated in pain transduction.31

Treatments

Treatments for dentin hypersensitivity are abundant and varied, and a detailed review is outside of the scope of this text. Treatments can usually be classified into home or professional treatment. The therapeutic aims of both home and professional treatments are to interfere with pulp neural response or to block fluid movement by occluding the tubules.32,33

Conclusion

DHS is a common dental complaint, and prior to treatment, a differential diagnosis is critical. The diagnosis is usually one of exclusion. Identification of the various risk factors should be ascertained, and a determination should be made of whether the pain is local or generalized. Eliminating or minimizing these risk factors should be accomplished prior to treatment. Unfortunately, most currently available tests are subjective; ideally, a more objective technique is required in order to adequately quantify the patient’s response. Although many theories have been suggested over the past century, the hydrodynamic hypothesis that was initially proposed in the 1960s by Brännström remains the one that is usually accepted, but it is not totally clear. This is due to the complex nature of the odontoblasts, nerve endings, and fluid content of the tubules. It has been suggested that the odontoblasts, which form the outermost layer of the dental pulp, act as sensory receptor cells. Some studies have indicated that human odontoblasts express functional TRP channels, which may play a vital role in facilitating thermal sensation in teeth.34 Further research is needed to ascertain the validity of these studies and to develop tests for DHS that are not as subjective as current modalities.

REFERENCES

1. Dowell P, Addy M. Dentine hypersensitivity—a review. Aetiology, symptoms and theories of pain production. J Clin Periodontol. 1983;10(4):341-350.

2. Stark MM, Pelzner R. Measurement of dentinal hypersensitivity. Compend Contin Educ Dent. 1982;(suppl 3):S105-S107.

3. Magloire H, Maurin JC, Couble ML, et al. Topical review. Dental pain and odontoblasts: facts and hypotheses. J Orofac Pain. 2010;24(4):335-349.

4. Markowitz K, Pashley DH. Personal reflections on a sensitive subject. J Dent Res. 2007;86(4):292-295.

5. Addy M. Dentine hypersensitivity: new perspectives on an old problem. Int Dent J. 2002;52:367-375.

6. Gernhardt CR. How valid and applicable are current diagnostic criteria and assessment methods for dentin hypersensitivity? An overview. Clin Oral Investig. 2013;17(suppl 1):S31-S40.

7. Martínez-Ricarte J, Faus-Matoses V, Faus-Llácer VJ, et al. Dentinal sensitivity: concept and methodology for its objective evaluation. Med Oral Patol Oral Cic Bucal. 2008;13(3):E201-E206.

8. Kakar A, inventor; Kakar A, assignee. Apparatus and method for measuring dentin hypersensitivity. The Patent Office Journal (India), Application No. 1680/DEL/2009 A, page 2970. February 18, 2011.

9. Sowinski J, Kakar A, Kakar K. Clinical evaluation of the Jay Sensitivity Probe: a new microprocessor-controlled instrument to evaluate dentine hypersensitivity. Am J Dent. 2013;26(spec no B):5B-12B.

10. Porto IC, Andrade AK, Montes MA. Diagnosis and treatment of dentinal hypersensitivity. J Oral Sci. 2009;51(3):323-332.

11. Spagrud LJ, Piira T, von Baeyer CL. Children’s self-report of pain intensity: the faces pain scale—revised. Am J Nurs. 2003;103(12):62-64.

12. Tomlinson D, von Baeyer CL, Stinson JN, Sung L. A systematic review of faces scales for the self-report of pain intensity in children. Pediatrics. 2010;126(5):e1168-e1198.

13. Choinière M, Amsel R. A visual analogue thermometer for measuring pain intensity. J Pain Symptom Manage. 1996;11(5):299-311.

14. Ferreira-Valente MA, Pais-Ribeiro JL, Jensen MP. Validity of four pain intensity rating scales. Pain. 2011;152(10):2399-2404.

15. Lawson K, Gross KB, Overman PR, Anderson D. Effectiveness of chlorhexidine and sodium fluoride in reducing dentin hypersensitivity. J Dent Hyg. 1991;65(7):340-344.

16. Addy M, Mostafa P, Newcombe RG. Dentine hypersensitivity: the distribution of recession, sensitivity and plaque. J Dent. 1987:15(6):242-248.

17. Cameron CE. Cracked-tooth syndrome. J Am Dent Assoc. 1964;68:405-411.

18. Ehrmann EH, Tyas MT. Cracked tooth syndrome: diagnosis, treatment and correlation between symptoms and post-extraction findings. Aust Dent J. 1990;35(2):105-112.

19. Ellis SG. Incomplete tooth fracture—proposal for a new definition. Br Dent J. 2001;190(8):424-428.

20. Rosen H. Cracked tooth syndrome. J Prosthet Dent. 1982;47(1):36-43.

21. Trushkowsky R. Restoration of a cracked tooth with a bonded amalgam. Quintessence Int. 1991;22(5):397-400.

22. Mejàre IA, Axelsson S, Davidson T, et al. Diagnosis of the condition of the dental pulp: a systematic review. Int Endod J. 2012;45(7):597-613.

23. Torneck CD. Dentin–pulp complex. In: Ten Cate AR, ed. Oral Histology: Development Structure, and Function. 5th ed. St. Louis, MO: Mosby Elsevier; 1998:150-196.

24. Turner DF, Marfurt CF, Sattelberg C. Demonstration of physiological barrier between pulpal odontoblasts and its perturbation following routine restorative procedures: a horseradish peroxidase tracing study in the rat. J Dent Res. 1989;68(8):1262-1268.

25. Turner DF. Immediate physiological response of odontoblasts. Proc Finn Dent Soc. 1992;88(suppl 1):55-63.

26. Charoenlarp P, Wanachantararak S, Vongsavan N, Matthews B. Pain and the rate of dentinal fluid flow produced by hydrostatic pressure stimulation of exposed dentine in man. Arch Oral Biol. 2007;52(7):625-631.

27. Pashley DH. Dentine permeability and its role in the pathobiology of dentine sensitivity. Arch Oral Biol. 1994;39(suppl):73S-80S.

28. Abd-Elmeguid A, Yu DC. Dental pulp neurophysiology: part 1. Clinical and diagnostic implications. J Can Dent Assoc. 2009;75(1):55-59.

29. El Karim IA, Linden GJ, Curtis TM, et al. Human dental pulp fibroblasts express the “cold-sensing” transient receptor potential channels TRPA1 and TRPM8. J Endod. 2011;37(4);473-478.

30. El Karim IA, Linden GJ, Curtis TM, et al. Human odontoblasts express functional thermo-sensitive TRP channels: implications for dentin sensitivity. Pain. 2011;152(10):2211-2223.

31. Premkumar LS, Abooj M. TRP channels and analgesia. Life Sci. 2013;92(8-9):415-424.

32. Trushkowsky RD, Oquendo A. Treatment of dentin hypersensitivity. Dent Clin North Am. 2011;55(3):599-608.

33. Kanapka JA. Over-the-counter dentifrices in the treatment of tooth hypersensitivity. Review of clinical studies. Dent Clin North Am. 1990;34(3):545-560.

34. Allard B, Magliore H, Couble ML, et al. Voltage-gated sodium channels confer excitability to human odontoblasts: possible role in tooth pain transmission. J Biol Chem. 2006;281(39):29002-29010.

ABOUT THE AUTHORS

Richard D. Trushkowsky, DDS
Associate Director, Advanced Program for International Denstists in Esthetic Dentistry, New York University College of Dentistry, New York, New York

Franklin Garcia-Godoy, DDS, MS, PhD, PhD
Chair, Department of Bioscience Research, Senior Executive, Associate Dean for Research, College of Dentistry, University of Tennessee Health Science Center, Memphis, Tennessee

Queries to the author regarding this course may be submitted to authorqueries@aegiscomm.com.

Related Content:

Innovations for Combating Dentin Hypersensitivity Current State of the Art: dentalaegis.com/go/cced539

Fig 1. Flow chart for treatment of dentin hypersensitivity. (Adapted from Canadian Advisory Board on Dentin Hypersensitivity. Consensus-based recommendations for the diagnosis and management of dentin hypersensitivity. J Can Dent Assoc. 2003; 69(4):221-226. Used with permission from Canadian Dental Association.)

Figure 1

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SOURCE: Compendium of Continuing Education in Dentistry | February 2014

Learning Objectives:

  • explain how dentin hypersensitivity is characterized
  • discuss the diagnosis and clinical management of dentin hypersensitivity
  • describe the various elements involved in diagnosing dentin hypersensitivity