Seminar on dentin hypersensitivity..pptx

Dentine Hypersensitivity

1. Dentin Hypersensitivity Good Morning Presented By – Dr. Rohan Shrivastava PG 1 st year

2. 20XX Presentation title 2 CONTENTS Introduction Definition Prevalence & Distribution Etiology Anatomy of dentin-pulp complex Functional characteristics of pulp nociceptors Response of pulp nociceptors to injury/inflammation Mechanism of dentine sensitivity Theories of DH Clinical features Diagnosis & differential diagnosis Prevention of DH Management of DH Conclusion

3. INTRODUCTION 3

4. Dentinal hypersensitivity is one of the most commonly encountered clinical problems. It is clinically described as an exaggerated response to application of stimulus to exposed dentin, regardless of its location. 4

5. It can be a challenging condition for patients to describe and dental professionals to accurately diagnose. Patients may or may not report this painful and often chronic condition to their dentist or dental hygienist and when they do, they report experiencing short, sharp pain after a variety of stimuli. 5

6. A definitive diagnosis of dentinal hypersensitivity can be challenging and practitioners must rule out other problems such as caries, fractured or cracked teeth, defective restorations, occlusal trauma or gingival conditions that could be the underlying cause of the dental pain a patient experiences. 6

7. Johnson & coworkers in 1982, stated that, “dentin hypersensitivity is an enigma, being frequently encountered yet ill understood”. According to Pashley (1990), DH is an inaccurate term for the condition. 7

8. Dowell & Addy in 1983 stated, there being no evidence that the dentin is in any way different or the pulpal response exaggerated. Therefore, DENTIN SENSITIVITY may be more correct. 8

9. DEFINITION 9

10. Acc. To MARTIN ADDY (1983): “ Dentinal hypersensitivity is characterized by short sharp pain arising from exposed dentin in response to stimuli typically thermal, evaporative, tactile, osmotic or chemical and which cannot be ascribed to any other form of dental defect or pathology”. 10 Dowell P, Addy M (1983) Dentine Hypersensitivity – a review. Aetiology , symptoms and theories of pain production. J Clin Periodontal 10, 341-350

11. A modification was suggested (2003)- “Dentine hypersensitivity is defined as a distinctive short sharp pain arising from exposed dentine characteristically in response to an array of stimuli including thermal, tactile, evaporative, osmotic or chemical, which cannot be attributed to any other form of dental defect, disease or pathology”. 11 Canadian Advisory Board on Dentin Hypersensitivity (2003) Consensus based recommendations for the diagnosis and management of dentin hypersensitivity J Can Dent Assoc 69,221-226

12. 12 PREVALENCE

13. 13 The prevalence of dentin hypersensitivity varies from 4 – 74 % for Adults. For children and adolescents, the values ranges from 4.7 – 45.2 %. In patients with periodontitis its 60 – 98 %. Dentine Hypersensitivity Thiago Saads Carvalho ,  Samira Helena João-Souza , 05 July 2019   https://doi.org/10.1002/9781119372684.ch7.2

14. 14 DISTRIBUTION

15. 15 Gender – females > males Age – 20 to 50 years, peak b/w 30-40 years. Teeth – Canines > 1 st PMs > Incisors & 2 nd PMs > Molars Surface – buccal surface Site – cervical area

16. 16 FACTORS THAT MAY AFFECT DH

17. 17 AGE GENDER DIET PLAQUE SOCIO-ECONOMIC STATUS OCCUPATION SPECIFIC ORAL HYGIENE PRACTICES

18. 18 ETIOLOGY

19. 19 GINGIVAL RECESSION Periodontal disease Frenum involvement Toothbrush abrasion Poor oral hygiene Inadequate attached gingiva Periodontal surgery(pocket reduction) Iatrogenic loss during restorative procedures

20. 20 Aggressive scaling and root planning Acute or chronic trauma Occlusal trauma, tooth malposition Excessive oral hygiene

21. 21 ENAMEL LOSS Abrasion Attrition Erosion Abfraction Note- exposed cementum and/or dentine are readily abraded, dentine abrades 25 times faster than enamel and cementum abrades 35 times faster.

22. 22

23. 23 OTHER REASONS Bleaching Genetic ( gap joint of CEJ, thin periodontium) Poor plaque control Cervical decay Bruxism Crown preparation

24. 24 DH after bleaching procedures: Sensitive teeth after bleaching happens for two reasons. Bleaching molecules penetrates into the teeth Blood flow and pressure increased Irritation of tooth nerves Teeth becomes more sensitive to stimuli

25. 25 DH after bleaching procedures: Sensitive teeth after bleaching happens for two reasons. 2. Increased tooth porosity and removal of the protective protein Pores get open and exposed to external environment Irritation of tooth nerves Teeth becomes more sensitive to stimuli

26. 26 Avoiding DH with bleaching: As general rule, if you have teeth sensitive to whitening, stick to products with lower peroxide levels(5-6%) with 5 minutes application time. Stick to room temperature beverages. Soft tooth brush & Lukewarm water.

27. 27 How to Relieve sensitive teeth after whitening: Brush your teeth before whitening, not after whitening. Use a Desensitizing Gel to calm the nerves of the teeth prior to whitening.

28. 28 Rinse out your mouth thoroughly after bleaching with water, or better use a PH rebalancing mouth rinse. Use your finger to gently apply to your teeth one of the calcium-based desensitizing pastes.

29. 29 ANATOMY OF DENTIN- PULP COMPLEX

30. 30 Dentin – protected by hard tissue (enamel/cementum) Dentin – organic component (collagen fibers in a matrix of collagenous proteins) and an inorganic component (hydroxyapatite crystals). Within the dentin dentinal tubules run from the pulp to the outer dental surfaces.

31. 31 The number of tubules varies: PULP : DEJ (4 : 1) Diameter of tubules: PULP > DEJ Periodontoblastic space – dentinal fluids (22% of total volume of dentin).

32. 32 FUNCTIONAL CHARACTERISTICS OF PULPAL NOCICEPTORS

33. 33 Three types of nerve fibers ( A- δ fibers, A- β fibers, and C-fibers ) found within the dentin. Majority of axons (70-80%) entering the pulp are non-myelinated. A-fibers are responsible for dentin sensitivity.

34. 34 A- β fibers , respond to non-noxious mechanical & electrical stimulus (pre-pain sensation). A- δ fibers & A- β fibers lead to pain sensation(from pre-pain).

35. 35 After the peripheral pulp tissue is destroyed due to any stimulus This distortion acts as stimulus for C- fibers activation.

36. 36 A-fibers – fast conducting, sharp, short duration, localized pain. C-fibers – slow conducting, dull, diffused pain.

37. 37 RESPONSE OF PULP NOCICEPTORS TO INJURY/INFLAMMATION

38. 38 INJURY / INFLAMMATION Type & Intensity of applied stimulus Depends on

39. 39 Exposed sensitive dentinal tubules Pulp irritation occurs Nerve activation & neuropeptide release Inflammation & nerve sensitization Dentine Hypersensitivity

40. 40 MECHANISM OF DH

41. 41 In 1900, GYSI said dentin sensitivity is “ of secondary nature and is not physiologic”. Dental canaliculi contain “a watery organic substance” Pressure on the dentinal canaliculi is transmitted from one end of the tubule to the other end causes water flow as the same.

42. 42 Symons showed that:- interfering with the contents of the tubules at the outer end resulted in changes in capillary forces Outward flow of contents Pain occurs as a result

43. 43 DIRECTION OF MOVEMENT OF DENTINAL FLUID CENTRIFUGAL FLUID MOVEMENT Cooling Drying Evaporation Hypertonic solution Tactile

44. 44 DIRECTION OF MOVEMENT OF DENTINAL FLUID NATURE OF THE PAIN Rapid movement of fluid More painful/Sharp pain 75% of pain Transmitted by A- δ fibers

45. 45 DIRECTION OF MOVEMENT OF DENTINAL FLUID CENTRIPETAL FLUID MOVEMENT Heating Probing

46. 46 DIRECTION OF MOVEMENT OF DENTINAL FLUID NATURE OF THE PAIN Slow movement of fluid Less painful/Dull pain 25% of pain Transmitted by C - fibers

47. 47 “ The coefficient of thermal expansion of the tubule fluid is about 10 times that of the tubule wall ”. Therefore, heat applied to the dentin will result in expansion of the fluid and cold will result in contraction of the fluid. Both create an excitation of the “ mechanoreceptors” Berman LH. Dentinal sensation and hypersensitivity. A review of mechanisms and treatment alternatives. J Periodontal 1985;56;216-22

48. 48 Fluid flow is most affected by radius of dentinal tubule. If the radius is reduced by ½, the fluid flow within the tubule falls to 1/16 th of its original rate. Micheleih V, Pashley DH, Whitford GM, Dentin permeability. A comparision of functional versus anatomical tubular radii. J Dent Res 1978;57:1019-24

49. 49 THEORIES OF DH

50. 50 NEURAL THEORY Also called as direct innervation theory. This theory advocates that thermal, or mechanical stimuli, directly affect nerve endings within the dentinal tubules through direct communication with pulpal nerve fibers.

51. 51 Presentation title 20XX Dentinal Tubules showing exposed Odontoblastic Process Electron microscopic picture

52. 52 ODONTOBLASTIC TRANSDUCTION THEORY A ccording to this theory, odontoblastic processes are exposed on the dentine surface and can be excited by a variety of chemical and mechanical stimuli

53. 53 Neurotransmitters are released impulses are transmitted towards the nerve endings Causing sensitivity and pain

54. 54 HYDRODYNAMIC THEORY I t is also called as fluid movement theory. Postulated by Gysi in 1900 and developed by Brannstrom in 1963. Exposed dentinal tubules

55. 55 Fluid disturbances by temperature, physical or osmotic changes Stimulation of Baroreceptors Leads to neural discharge Excitation of nerve endings

56. 56 OTHER THEORIES M odulation theory :- Nerve impulses are modulated through the liberation of polypeptides from the odontoblasts, when injured.

57. 57 Gate control theory :- by Melzack & Wall in 1965. Transmission of impulses to the brain are modulated by spinal gating system.

58. 58 When activity of spinal cord transmission cells exceed a threshold, pain is perceived. A-beta fibers inhibit transmission and small A-delta and C fibers facilitate it.

59. 59 V ibration theory :- Vibratory motion leads to fluid disturbance and hence nerve stimulation occurs.

60. 60 CLINICAL FEATURES

61. 61 Mild to severe discomfort due to pain. Sensitivity sometimes felt at one tooth or several teeth and sometimes felt in all quadrants .

62. 62 Pain which is felt can be rapid in onset , sharp in character and of short duration . Presence of gingival recession or enamel/cementum loss.

63. 63 Cementum Loss Enamel Loss

64. 64 DIAGNOSIS

65. 65 Patient history and examination Pain evoked by any stimuli (source of pain) Consider detailed written dietary histories. Consider detailed written oral habits (e.g. Frequency, duration and timing of brushing, estimation of brushing force, frequency of brush change).

66. 66 Any symptoms during brushing. Sensitivity : - site character severity duration Treat any and all secondary conditions that include symptoms similar to Dentin Hypersensitivity

67. 67 The patient’s response to various triggering stimuli should be recorded. The stimuli are sorted into four categories:- Mechanical Chemical Electrical Thermal

68. 68 MECHANICAL (TACTILE) stimuli Sharp tipped probe Mechanical pressure stimulator (Yeaple’s probe) Jay sensitive sensor probe

69. 69 Presentation title 20XX Jay sensitive sensor probe Yeaple’s probe

70. 70 CHEMICAL stimuli Hypertonic solution Acidic solution (not used now) Cold air (1cm distance, 1sec) Cold water stimulation at, 3sec – 3mins.

71. 71 THERMOELECTRIC TECHNIQUES Fine tipped thermal probe initiation. ELECTRICAL STIMULATION Electric pulp testers.

72. 72 Presentation title 20XX Electric pulp tester Thermal probe

73. 73 OTHER METHODS Scaling procedures Single-tufted brush Dental pulp stethoscope Evaporative stimuli Electronic threshold measurement device Microprocessor temperature controlled air delivery system

74. 20XX Presentation title 74 TESTS VERBAL RATING SCALE (VRS) ( 0 ) = no discomfort ( 1 ) = mild discomfort ( 2 ) = significant discomfort ( 3 ) = significant discomfort lasting more than 10 seconds

75. 20XX Presentation title 75 TESTS VISUALANALOGUE SCALE (VAS) ( 0 ) = no pain to (10) = extreme pain

76. 20XX Presentation title 76

77. 20XX Presentation title 77 TESTS FACES PAIN SCALE REVISED (FPS-R) This is self reported measure of pain intensity developed for children (4-16 years) It was adapted from the Faces Pain Scale in order to make it possible to score on the widely accepted 0 – 10 metric.

78. 20XX Presentation title 78

79. 79 DIFFERENTIAL DIAGNOSIS

80. 80 Cracked tooth syndrome Fractured restoration Restoration in traumatic occlusion Chipped teeth, hypoplastic enamel Dental or root caries Postoperative sensitivity Marginal leakage of restoration Pulpitis

81. 81 Gingival inflammation Vital bleaching procedures Atypical odontalgia Palatogingival grooves

82. 82 PREVENTION OF DH

83. 83 Suggestions for patients: Avoid gingival recession due to poor plaque removal by practicing good oral hygiene techniques. Avoid using large amount of dentifrice or reapplying it during brushing. Avoid medium or hard bristle toothbrush .

84. 84 Avoid brushing teeth immediately after ingesting acidic foods . Avoid brushing teeth with excessive pressure or for extended period of time . Avoid excessive flossing or improper use of interproximal cleaning device. Avoid using toothpicks inappropriately.

85. 85 Suggestions for dental professionals: Avoid over instrumenting the root surfaces during scaling and root planning. Avoid over polishing exposed dentin during stain removal.

86. 86 Avoid violating the biological width during restoration placement, as they may cause recession. Avoid burning the gingival tissues during in-office bleaching.

87. 87 MANAGEMENT OF DH

88. Management of DH Nerve Desensitization Potassium nitrate (it is present in toothpaste in 5% concentration) Anti-inflammatory agents Corticosteroids Cover dentinal tubules Sclerosing dentinal tubules Dentine sealers Periodontal soft tissue grafting. Crown placement/restorative material Laser Homeopathy- Propolis 88 Presentation title 20XX

89. 89 Presentation title 20XX Ion salts Calcium hydroxide Ferrous oxide Potassium oxalate Sodium fluoride Stannous fluoride Strontium chloride Bio-active glass Potassium oxalate Protein precipitants Formaldehyde/glutaraldehyde Zinc chloride Silver nitrate Strontium chloride hexahydrate Sclerosing dentinal tubules Casein phosphopeptides burnishing Fluoride iontophoresis

90. 90 CALCIUM HYDROXIDE Apply calcium hydroxide paste for 3-5 mins through burnishing by wooden stick or rubber tip. It promotes peritubular dentin formation and thus blocking the tubule .

91. 91 High pH may provoke odontoblastic process protein coagulation , precipitation of protein , clogging the tubule and decreasing hydraulic conductance .

92. 92 FLUORIDES Fluorides such as sodium and stannous fluoride can reduce dentine hypersensitivity. It creates a barrier by precipitation of the calcium fluoride crystals in the dentinal tubules.

93. 93 It increases the resistance of dentin to acid dissolution thus, also helps in dentin remineralization. Aqueous solution provides immediate effect when applied for 3-5 mins in-office.

94. 94 IONTOPHORESIS Charged drug is delivered via an electrode. Leads to deep penetration of ions in the tubules leading to tubule occlusion. Since calcium fluoride is an unstable compound, iontophoresis increases the depth of penetration.

95. 95 Presentation title 20XX FLUORIDE IONTOPHORESIS DEVICE

96. 96 OXALATES Topical use of 3% potassium oxalate on exposed dentin after periodontal procedures results in a reduction of DH. Desensitizing action of potassium oxalate occurs by the deposition of calcium oxalate crystals on the dentin surface.

97. 97 If the dentin is previously etched with 37% phosphoric acid, it will increase the penetration depth of oxalate compound in the dentinal tubules and thus, pain relief can be expected for longer period of time.

98. 98 CPP-ACP CPP-ACP is stable and prevents dissolution of Ca. & P. Home use of CPP-ACP containing dentifrice has been found to help inhibit demineralization and to promote remineralization.

99. 99 Mechanism of CPP-ACPF Elevates level of calcium, phosphate and fluoride ions at the tooth surface. Depressing enamel demineralization and enhancing remineralization.

100. 100 PRO-ARGININ Consists of :- 8% arginine (amino acid) bicarbonate (as pH buffer) calcium carbonate (as calcium source) 1450 ppm fluoride (as sodium monofluorophosphate)

101. 101 Applied using low speed Handpiece with paste. Paste containing the compounds seals the dentinal tubules.

102. 102 NOVAMIN ( bioglass ) Consists of :- Calcium Phosphorous Sodium Silica Oxygen Comes as the brand name DenShield

103. 103 NOVAMIN particles Hydroxyl-carbonate apatite Occlusion of dentinal tubules Relieve Hypersensitivity

104. 104 LASERS In 1985, laser irradiation had been applied for the treatment of DH. They work by coagulation of proteins in the dentinal fluid and hence reduce permeability of dentin.

105. 105 PROPOLIS It is efficient in the treatment of DH. It also has an effect on tissue regeneration and wound healing. Propolis contains high content of Flavonoids.

106. 106 Flavonoids suppress the information of free radicals by binding heavy metal ions . Acts as an antioxidant, antimicrobial, anti-inflammatory and immunostimulatory .

107. 107 ADHESIVE MATERIALS They are also called as dentinal tubule sealers . They simply block the dentinal tubules. They cause coagulation of plasma proteins of the tubule fluid, resulting in the reduction of dentinal permeability.

108. Treatment Flow Chart 20XX Presentation title 108

109. 109 Presentation title 20XX

110. 110 RECENT TRENDS

111. 111 Recent approaches to advancing the treatment of dentinal hypersensitivity is to increase the potential to remineralize the tooth structure by increasing salivary calcium and phosphate levels as well as increasing the salivary pH and stimulating the formation of calcium phosphate or hydroxyapatite.

112. 112 CONCLUSION

113. 113 Presentation title 20XX DH is a common dental complaint. Identification of the various risk factors should be ascertained and a determination should be made of whether the pain is local or generalized. Self applied treatments such as desensitizing dentifrices are still largely used as home made desensitizing agent. The adhesive systems are one of the most effective clinical treatments and the lasers are expected to play an important role in treating DH.

114. 114 Presentation title 20XX Canadian Advisory Board on Dentin Hypersensitivity (2003) Consensus based recommendations for the diagnosis and management of dentin hypersensitivity J Can Dent Assoc 69,221-226 Berman LH. Dentinal sensation and hypersensitivity. A review of mechanisms and treatment alternatives. J Periodontal 1985;56;216-22 Micheleih V, Pashley DH, Whitford GM, Dentin permeability. A comparision of functional versus anatomical tubular radii. J Dent Res 1978;57:1019-24 Garberoglio R, Brännström M. Scanning electron microscopic investigation of human dentinal tubules.  Arch Oral Biol.  1976;21:355–362. Matthews B, Hughes SHS. The ultrasonic and receptor transduction mechanisms of dentine. In: Iggo A, Hamman W, editors.  Progress in brain research.  Amsterdam: Elsevier; 1988. pp. 69–76. Mumford JM.  Orofacial pain. Aetiology , diagnosis and treatment.  3. Philadelphia: Churchill Livingstone; 1982. pp. 152–179.  Nähri M, Jyväsjärvi E, Virtannen A. Role of intradental A- and C- type fibres in dental pain mechanisms.  Proc Finn Dent Soc.  1992;88(Suppl 1):507–516.  Matthews B, Andrew D, Wanachantararak S. Biology of the dental pulp with special reference to its vasculature and innervation. In: Embery G, Edgar WM, Orchardson R, Addy M, editors.  Tooth wear and sensitivity.  London: Taylor and Francis; 2000. pp. 39–51.  Nuttall NM (2001) A guide to the UK adult dental health survey 1998. British Dental Association; London, pp 1-7; 35; 47-55 REFERENCES