Dentinal hyper sensitivity / /certified fixed orthodontic courses by Indian dental academy


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Dentinal hyper sensitivity / /certified fixed orthodontic courses by Indian dental academy

  1. 1. INDIAN DENTAL ACADEMYLeader in Continuing Dental Education
  2. 2. Introduction“ An enigma, because it was frequently encountered yet poorly understood” Johnson. R.H 1982“Not the enigma it once was, there still much to be discovered” Martin Addy 2002
  4. 4. HISTORICAL PERSPECTIVE• Tomes 1856, “The dentine tubes are constantly filled by fluid, and the pulp at their inner extremities feels pressure made upon the fluid at the exposed ends of the tubes”• Whit (1870) “ the pain arising from the contact with sensitive dentine cannot be conveyed by direct contact with the ultimate fibres of the dentine nerve, but through some intermediary agent.”• Beers (1893) “ There is no doubt, but sensitiveness is due to the presence of the tube contents, whether nerve fibres enter or not. Dentine is nothing but [a] passive matrix, in which lie the sources of sensation.”
  5. 5. • Gysi, 1900 introduced hydrodynamic concept.• Hopewell-Smith (1923) “Dentine is not live, nor is it dead like enamel, it serves as an intermediate tissue between the external enamel and the internal living pulp, it does not generate sensations but transmits through its tubes impulses of various kinds to the pulp.”• Fish (1927) “there is a lymphatic fluid in the dentinal tubule and that tubules terminate with a lymphatic plexus, providing a continuous lymphatic flow through the various tubules and the pulp.”
  6. 6. • Orban (1940) “displacement of odontoblasts…. and pulp cells into the tubule”• Ivory & Kramer (1952) showed aspiration of odontoblasts• Anderson (1958) “receptors responsible for pain sensations were in the pulp, rather than the dentine.”• Brännström’s (1966) hydrodynamic explanation of dentine sensitivity
  7. 7. PULPO-DENTIN COMPLEX“an oversimplication”"odontoblast-dentin complex" and the pulp as two distinct tissues. (Goldberg and Lasfargues, 1995).• “function as an integrated unit which is generally termed the pulpo-dentin complex.”D.H. Pashley• Crit Rev Oral Bio Med7(2): 104-133 (1996)
  8. 8. Odontoblast-dentin complex • DENTINE MORPHOLOGY • DYNAMICS OF DENTIN
  9. 9. The extent of the odontoblast process• “there are no supporting cells or blood vessels, the ability of the odontoblast cell body to support a long cytoplasmic process is in question.” (Holland, 1976; Byers and Sugaya, 1995).• An odontoblast process at the DEJ or CDJ would be 3 mm or 3000 µm from the nearest capillary, which is a very long diffusion distance.
  10. 10. Changes in dentin structure with depth “area occupied by tubule lumina at the DEJ to be approximately 1% of the total surface area at the DEJ and 22% at the pulp”- Pashley (1984)• “It is clear that the water content or wetness of dentin is not uniform, but varies 20-fold from superficial to deep dentin.”
  11. 11. Dentin permeabilityDivided into two broad categories:1. Transdentinal movement2. Intradentinal movement• Dentin can be regarded as both a barrier or a permeable structure, depending upon its thickness, age, and other variables.• The permeability of dentin is not uniform but varies widely.• Highest at the pulp.• Lowest at the DEJ
  12. 12.
  13. 13. Balance between the permeation of noxioussubstances across dentin and their clearance by the pulpal circulation
  14. 14. • The outward fluid flow through tubules - first line of defense against the inward diffusion of noxious substances.• Dentinal fluid contains plasma proteins which can bind or agglutinate - protective role• A second defensive reaction causes the permeability of dentin to fall .
  15. 15. Control of dentin permeabilityPeripheral Reductions in Dentin Permeability• Relatively large molecules (e.g.,albumin, globulins, fibrinogen) exits pulpal blood vessels, gain access to extracellular spaces, and reach the dentinal tubules (Bergenholtz et al, 1993, 1996).Internal Reductions in Dentin Permeability• "reactionary dentinogenesis“• "reparative dentinogenesis".
  16. 16. Dynamics of Dentin
  17. 17. REACTIONS TO CAVITY PREPARATIONS: FLUID SHIFTS• Inward fluid shifts (because of frictional heat generation on the end of a poorly irrigated cutting bur).• Outward fluid shifts due to evaporative water loss (if only air cooling is used), and slight inward fluid shifts due to osmotic movement of cooling water into dentin (Horiuchi and Matthews, 1973).These fluid shifts occur in both directions at various stages of cavity preparation.
  18. 18. DISRUPTION OF ODONTOBLAST LAYER• Deep cavity preparation causes aspiration of odontoblasts (Byers et al, 1988),• More shallow preparation causes disruption of junctional complexes between odontoblasts (Ohsima, 1990),which decreases their barrier properties.• Loss of gap junctions interferes secretion of collagen matrix in a synchronous. coordinated manner, due to the loss of cell signaling between adjacent cells.
  19. 19. • The proteins that make up gap junctions are called connexins• How long it takes odontoblasts to reestablish the continuity of gap junctions and to revert to tissue rather than cellular function is unknown
  20. 20. PULPAL REACTIONS TO DENTIN EXPOSURE: NERVE RESPONSES• Sensory nerve fibers innervating dentin by release neuropeptides such as CGRP (Gazelius et al, 1987; Byers et al, 1988, 1992a; Heyeraas et al, 1994; Byers, 1996),• The depletion of the neuropeptides is in response to rapid fluid shifts produced by evaporative, thermal, and physical forces.• Reparative dentin is not well-innervated and seems to form much faster than innervated tubular dentin (Byers, 1984).
  21. 21. INNERVATION OF DENTIN• Developmental• Receptive Fields• Modification of Nerve Activity• Dentin Sensitivity• Nerve Reactions to Exposure of Dentin
  22. 22. Developmental• Nerves grow into the pulp early in bell stage of tooth development. Nerves enter the apex Only a few nerves are given off in the root (< 10%, Byers and Matthews, 1981), Forms Nerve plexus of Rashkow Terminate in predentin or dentin,
  23. 23. Receptive Fields• Individual A-8 fibers have discrete receptive areas on dentin which can be located by probing.• localized to a small spot on the dentin• surface, some single nerve fibers have two or three separate receptive areas separated from each other by many millimeters.
  24. 24. Modification of Nerve Activity• “Neurotrophic proteins such as NGF may produce analgesic activity in chronically inflamed teeth, making them asymptomatic. If this is confirmed, it may provide an explanation for the lack of correlation between the signs of pulpal inflammation and patient pain” (Hargreaves et al, 1996).
  25. 25. Nerve Reactions to Exposure of Dentin• The NGF travels up the axon to the trigeminal ganglion,where it stimulates the neuron to increase the synthesis of more CGRP (Lindsay et al, 1989, 1990) and, by mechanisms not yet completely understood, to cause branching and sprouting of nerve terminals beneath the exposed dentin.• increases the number of CGRP-positive nerve terminals in the region of exposed dentin within 48 hrs, but the response disappears within 7-10 days if there is no further irritation.
  26. 26. Dentin Sensitivity• Transducer theory• Modulation theory• “gate” control and vibration theory• The hydrodynamic theory
  27. 27. Transducer theory• Odontoblasts function as receptors• Coupled to nerves ,either electrically through gap junctions or through chemical synapses.• Receptors located beneath the odontoblasts
  28. 28. “Gate” control / Vibration theory• Melzack and Wall (1965) Pain mechanisms: a new theory. Science 1965; 150: 971–979• This theory states that pain is a function of the balance between the information traveling into the spinal cord through large nerve fibers and information traveling into the spinal cord through small nerve fibers
  29. 29. Large nerve fibers carry non-nociceptive information and small nerve fibers carry nociceptive information
  30. 30. • According to the gate control theory , A-β nerve fibers, which transmit information from vibration receptors.• Stimulate inhibitory interneurons in the spinal cord, which in turn act to reduce the amount of pain signal transmitted from A-δ and C fibers across the midline of the spinal cord and from there to the brain.. Melzack R. From the gate to the neuromatrix. Pain. 1999 Aug; Suppl 6:S121-6.
  31. 31. Pain Modulation theory• Levels Theory of Pain Control• Spinal Levels of Pain Control Level 1 Gate Control Theory Level 2 Central Biasing (hyperstimulation analgesia) Level 3 Endogenous Opiate (Pituitary level)
  32. 32. The hydrodynamic theory• Gysi, 1900 introduced hydrodynamic concept. “An attempt to explain the senstiveness of dentine” – Br J Dent Sci: 43:865 – 8• 1960s, Brannstrom demonstrated that pain producing stimuli induced fluid shifts across dentin in vitro.• Provided experimental data to support to develop a plausible theory.• Brannstrom M, Linden LA, Astrom A (1967). The hydrodynamics of the dental tubule and of pulp fluid. Caries Res L310-312.
  33. 33. Hydrodynamics (Blaise Pascal 1600)• Fluid movement• osmotic pressure• Volumetric changes• Hydrostatic pressures• Viscosity• Velocity
  34. 34. Fluid movement• The rate of this fluid flow depends upon the hydraulic conductance of dentin and the pulpal tissue pressure (Pashley,1990)• hydraulic conductance of dentin suddenly increases, permitting both a slow outward spontaneous fluid flow (Pashley,1992)
  35. 35. osmotic pressure• colloid osmotic pressure of plasma proteins could cause negative tissue pressures under special conditions of low to zero pulpal blood flow. Thus, under special conditions (intense sympathetic stimulation or adrenergic drug-induced vasoconstriction), dentinal fluid (and its contents) can be "aspirated" into the pulp. – Brown et al. (1969)
  36. 36. Volumetric changes“Thermal stimuli cause more rapid volumetric changes in dentinal fluid than in dentin itself, resulting in an outward (cold) or inward (hot) movement of fluid. The reason(s) why cold stimuli are more effective than hot stimuli is unclear. It may be due to the fact that the resistance to fluid movement across dentin is different when fluid moves inward vs. outward.” Horiuchi and Matthews (1973).
  37. 37. Hydrostatic pressures• Positive hydrostatic pressures always produced higher hydraulic conductances (and higher fluid shifts) than negative pressures• Positive hydrostatic pressures - inward fluid movement - displace the odontoblasts slightly away from the orifice .• Negative pressures would tend to seat them more firmly in the tubules .• Altered hydrodynamic resistances
  38. 38. Positive Negativehydrostatic hydrostatic
  39. 39. Viscosity• As dentinal fluid is cooled, its viscosity increases significantly .• Since dentinal fluid flow through tubules is inversely related to viscosity , decreases in temperature would decrease fluid flow but increase shear stresses on dentinal/pulpal nerves.• Heating dentin would do the reverse.
  40. 40. VelocityFluid flow is occurring between the tubule wall and odontoblasts and/or nerve terminals. velocities of fluid movement - sufficient shear forces to deform nerve terminals . Neural elements responsible for pain may not necessarily involve stretch sensitive ion channels but rather simple shear forces on free nerve endings.
  41. 41. DEFINITION• Dowell 1985• Orchardson and collins 1987• Dentine 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 (Holland 1997)
  42. 42. Two processes must to cause dentinal hypersensitivity……• Lesion localization: Dentin must be exposed to etiological agents• Lesion Initiation: Sensitivity must be induced by tubular exposure
  43. 43. Lesion localization• Loss of periodontal tissue Gingival recession• Loss of Enamel Attrition Abrasion Erosion Abfraction
  44. 44. Lesion Initiation• Cementum - extremely labile – offers little protection against sensitivity. (Bevenius 1994)• Non-sensitive dentin shows few tubules at the surface (Absi 1987)• Two category initiating agents: 1. Abrasive 2.Erosive
  45. 45. PREVALENCE AND DISTRIBUTION• Prevalence studies to date yield limited associations with etiological factors.• Distribution data suggests association between tooth cleaning ,gingival recession and hypersensitivity.• Bacterial plaque – negatively associated• Plaque induced sensitivity is different from dentin hypersensitivity
  46. 46. GINGIVAL RECESSION• The exposure of root surface by an apical shift in the position of the gingiva.
  47. 47. RECESSION Mechanical Destructive Factors Periodontal Disease(Tooth brushing) (Serino, JCP, 1994) Only buccal All tooth surfaces are surfaces are involved involved
  48. 48. • High muscle attachment and frenal pull (Trott, 1966)• Tooth malposition (Gorman, JP, 1967)• Irregular tooth alignment in the dental arch,(Stoner J,JP, 1980)• Areas with absence or a narrow zone (width) of attached gingiva (Tenenbaum H. JCP, 1982)
  49. 49. • Reduced thickness of the alveolar bone in the buccolingual side (Wennström, JCP, 1987)• Root prominence (Gartrell JR, 1976)• Alveolar bone dehiscence ( Lost, JCP, 1984)• Iatrogenic factors related to restorative and periodontal treatment procedures (Lindhe, 1987)
  50. 50. • Margins of gingival restorations (Donaldson D., JP, 1973)• Orthodontic tooth movement (Steiner, G, JP, 1981)• Viruses (Prato GP, JP, 2002)
  51. 51. Buccal recession maxillary molars and bicuspids  mandibular bicuspids  mandibular molars  Maxillary and mandibular incisors• (Harald Löe, JP, 1992; The Natural History of periodontal Disease in Man)
  52. 52. • Interproximal recession• Lingual recession It is characterized by the loss of periodontal connective tissue fibers, along with tooth cementum and alveolar bone.(Santarelli GA, 2001) cervical root caries.(Anson D., 1999)
  53. 53. Erosion• Defined as the chemical dissolution of teeth by acids.• Common site – Palatal surface of upper anteriors (O’Brien1993)• Caused by1. Regurgitated gastric juice – pH 1 to 22. Dietary acids – pH around 3 (Smith 1994)
  54. 54. Gastric acid• Gastro-esophageal reflux disease – enters mouth passively• Anorexia and Bulmia nervosa – enters forcibly• Chronic alcoholism – either passive regurgitation or chronic vomiting
  55. 55. ABRASION• The pathological wearing away of dental hard tissue through abnomal mechanical processes involving foreign objects or substances repeatedly introduced in the mouth and contacting the teeth. (Imfeld 1996)• Soft tissue damage - tooth brush• Hard tissue loss - tooth paste(Sangnes 1976,Davis and Winter 1980)
  56. 56. Variables influencing Abrasion• Brushing technique vertical vs Horizontal• Bristle Stiffness Hard filaments retain more paste• Brushing Force Manual –upto 500g ,Power – upto 200g• Time Spent• Frequency Excess of twice/day – encourages abrasion
  57. 57. Tooth Paste Abrasivity• Diatomaceous earth• Calcium carbonate• Dicalcium phosphate• Hydrated/anhydrous insoluble sodium metaphosphate• Silica• Aluminium oxide• Calcium pyrophosphate• Alumina• Pumice
  58. 58. ATTRITION• The physiological wearing away f dental hard tissues as a result of tooth –to –tooth contact without the intervention of foreign bodies (Imfeld 1996)• 29xm/year – molars• 15xm/year – Premolars (Lambrechs 1989)• High bite force and bruxism• “prerequisite for balanced occlussion”• “considered physiological” (Begg 1954)
  59. 59. Associations with abfractive lesions• An abfraction lesion is a wedge shaped (rarely saucer-shaped) defect at the cervical region of a tooth.• Tensile stress-induced microtrauma from hyperfunction or parafunction• High correlation between dentinal hypersensitivity and abfraction lesions.
  60. 60. DENTINAL PAIN……?• The International Association for the Study of Pain defines pain as “unpleasant sensory and emotional experience arising from actual or potential tissue damage ” – Carr DB (Ed). Vol1, Issue1, May 1993 Dentin hypersensitivity satisfies all the criteria to be classified as a true pain syndrome, and therefore needs to be treated accordingly. - Dababneh RH, Br Dent J 1999;187:606-11.
  61. 61. • Pain is complex, subjective, and assessed only indirectly, based on the patient’s overt communication, both verbal and behavioural.• Dentin hypersensitivity is a painful condition subject to these complexities.• “Unreported” pain does not mean “unimportant” pain
  62. 62. DIAGNOSIS• Diagnosis of exclusion• Symptoms mimicking dentin hypersensitivity must be ruled out• Appropriate to rely on patients’ perception of pain
  63. 63. Assessment of Hypersensitivity• Subjective evaluation Response based assessment• Objective evaluation Stimulus based assessment
  64. 64. Subjective evaluation• Verbal rating scales - Keele1948• Visual analogue scales – Ekowski 1972• Verbal descriptor checklist – Gracely 1978• McGill word descriptors – Melzack 1987• Hospital anxiety and Depression scale – Zigmond & Snaith 1983
  65. 65. Objective Assessment• Mechanical stimulation Pressure sensitive probes• Chemical (osmotic) stimulation Hypertonic solutions – sucrose or CaCl2• Electrical stimulation Electric pulp testers
  66. 66. • Dehydrating (evaporative) stimuli 20.C (room temp) air blasts• Thermal stimulation Cold water, air ethyl chloride contact cold probes• Hydrostatic pressure Fluid filtration
  67. 67. EXAMINE PATIENT TO EXCLUDE• Cracked tooth syndrome• Fractured restorations• Chipped teeth• Dental caries• Gingival inflammation• Post-restorative sensitivity• Marginal leakage• Pulpitis• Palatogingival grooves
  68. 68. Strategies for MANAGEMENT• Prevention• Tubule occlusion1. Endogeneos desensitization2. Exogenous desensitization• Altering tubule content• Modifying nerve excitablity
  69. 69. Tubule occlusion• Endogeneos desensitization Promote formation of smear layer or impermeable surface deposits Intratubular dentin Tertiary dentin
  70. 70. Tubule occlusionExogenous desensitization• Block tubule orifice with barrier• Tooth paste constituents• Topical agents• Restorative materials
  71. 71. Altering tubule content• Viscosity of tubular fluid could be raised by increasing its macromolecular protein content.• So that stimulus generates less fluid flow
  72. 72. Modifying nerve excitability• Potassium ions – reduces intradental nerve excitability• When applied to outer dentin surface might diffuse along the tubules and block intradental nerve function by raising the K+ ions concentration• A positive pressure could be applied to overcome the pulpal pressure, or the pulpal pressure could be reduced
  73. 73. TREATMENT MODALITIES• Home use products: Tooth pastes containing strontium /potassium salts Tooth paste containing sodium and amine fluoride Mouth rinses containing Aluminium lactate
  74. 74. In – office products• Agents that do not polymerize Varnishes/precipitants Primers containing HEMA• Agents that undergo setting or polymerization GIC, Resin reinforced GIC/COMPOMERS Resin primers, Bonding agents• MOUTH GUARDS• IONTOPHORESIS• LASERS• PERIODONTAL SURGERY/GRAFTING• CROWN PLACEMENT
  75. 75. Varnishes/precipitants• Shellacs• 5% sodium fluoride varnish• 1%NaF,0.4%SnF2,0.14%HF solutions• 3% mono-potassium-monohydrogen oxalate• 6% acidic ferric oxalate• Cacium phosphate preparations• Calcium hydroxide
  76. 76. Primers containing HEMA• 5% glutaraldehyde ,35% HEMA in water• 35% HEMA in water
  77. 77. MOUTH GUARDS• Mouthguard type appliance to deliver potassium nitrate (Reinhart 1990)Severe Bruxism cases - a vacuum formed muthguard with small amount of 5% KNO3 dentrifice (Jerome 1995)
  78. 78. IONTOPHORESIS• Pivati 1747• Galvani and Volta 1821- electricity can move different metal ions• LeDuc 1900 – Ionotheraphy & formulated laws• Iontophoresis is a method of electrically transporting ionic particles into hard or soft tissue (Sausen, 1955; Harris,1967; and Zadok et al., 1976).• Defined as the introduction by means of direct electrical current, of ions of soluble salts in to the tissues of the body for therapeutic purposes – Singh and Maibach 1994
  79. 79. • Fluoride, which is such an ionic particle, is negatively-charged.• when an electrical potential is applied, fluoride ion would be repelled from the negative electrode (cathode) and attracted to the positive (anode).• (Manning, 1961; Jensen, 1964; Murthy et al., 1973; and Gangarosa and Park, 1978) iontophoresis of fluoride was more effective in reducing dentin hypersensitivity than was topical application alone.
  80. 80. LASER• Increases excitability threshold of the free nervous terminations, causing an analgesic effect.• Stimulates pulp mesenchymal cells to differ in Odontoblasts, with the purpose to produce reparative dentin• Both red and infrared wavelength lasers have been effective.
  81. 81. Surgical methods for root coverage• Pedicle gingival grafts a. Laterally positioned grafts b. Double Papilla Flaps c. Transpositional flaps d. Coronally positioned flaps• Free autogenous gingival grafts• Connective tissue grafts or subepithelial connective tissue grafts• GTR• Semilunar Coronally Positioned flaps
  82. 82. • Future………NANOROBOTICS…?
  83. 83. conclusionWhile it may not be feasible to prevent dentineexposure ,it should be possible to preventexposed dentin from becoming undulysensitive.This requires identification and elimination ofthe various factors predisposing to persistenttubule patency.
  84. 84. References• Tooth wear and sensitivity – Martin Addy• Clinical Periodontology - Glickman• Oral Histology – Orbans• Oral Histology – TenCate• ImplantPeridontology - lindhe
  85. 85. • DYNAMICS OF THE PULPCHDENTIN COMPLEX, D.H. Pashley, Crit Rev Oral Biol Med 7(2):104-133 (1996)• Physiology of dentine hypersensitivity: clinical treatment, Charles Cox DMD,• Fluoride Levels in Dentin after lontophoresis of 2% NaF, J. M. WILSON, J Dent Res 63(6):897-900, June, 1984• ASSESSING THE EFFICACY OF THREE DENTIFRICES IN THE TREATMENT OF DENTINAL HYPERSENSITIVITY, G. SILVERMAN, JADA, Vol. 127, February 1996• Cervical Dentin Hypersensitivity: Etiology & Current Treatment, THOMAS A. COLEMAN,• Consensus-Based Recommendations for the Diagnosis and Management of Dentin Hypersensitivity, J Can Dent Assoc 2003; 69(4):221–6• DIAGNOSIS OF PERIODONTOCLASIA, F. V. SIMONTON,• THE DENTIN DISC SURFACE: A PLAUSIBLE MODEL FOR DENTIN PHYSIOLOGY AND DENTIN SENSITIVITY EVALUATION, D.G. GlLLAM, Adv Dent Res 11(4):487-501,1997• Displacement of the contents of dentinal tubules and sensory transduction in intradental nerves of the cat, D. Andrew and B. Matthews, J. Physiol. 2000;529;791-802• Nanodentistry, ROBERT A. FREITAS, JADA, Vol. 131, November 2000• Dentine hypersensitivity: new perspectives on an old problem, Martin Addy, International Dental Journal (2002) 52, 367–375• Transmission Electron Microscopic Characterization of Hypersensitive Human Radicular Dentin, M. YOSHIYAMA, J Dent Res 69(6):1293-1297, June, 1990• Scanning Electron Microscopic Characterization of Sensitive vs. Insensitive Human Radicular Dentin, M. YOSHIYAMA, J Dent Res 68(11):1498-1502, November, 1989