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  • This common complaint is defined as dentinal hypersensitivity, but it is also known as root sensitivity, or just sensitivity.
  • It is clinically described as an exaggerated response to application of a stimulus to exposed dentine, regardless of its location. Some authors have substituted the word “dentine” and added the site, such as cervical or root, resulting in various other terminologies (e.g., cervical sensitivity/hypersensitivity) to describe the same clinical condition.
  • A slightly higher incidence of dentin hypersensitivity has been observed in females, which may reflect oral hygiene and dietary practices.
  • The crowded odontoblast gives it that sigmoid shape.
  • These nerves are from the sensory afferent nerve of the trigeminal nerve and the sympathetic branches of the superior cervical ganglion.
  • the impact of tensile and compressive forces during tooth flexure (abfraction), Physical wear as a result of tensile or shear stress in the cemento-enamel region provoking microfractures in enamel and dentine (fatigue wear)
  • The transducer theory, the modulation theory, the “gate” control and vibration theory, and the hydrodynamic theory
  • Why is that LA and protein precipitant(silver nitrate) are unable to abolish the pain
    Bradykinin and histamine don’t seem to evoke pain when applied, why?
  • LA and protein precipitants do not abolish the sensitivity
  • The exogenous dietary acids include carbonated drinks, citrus fruits, wines, yogurt, and professional hazards (workers in battery manufacturing, wine tasters).
  • but it can occur in patients significantly younger or older. various external stimuli that are typically thermal, evaporative, tactile, electrical, osmotic, or chemical,
  • The relationship between DHS and ageing is unclear. While it is true that with increasing age recession is increased it is also a fact that dentin permeability and neural sensitivity decreases with age. This is probably as a result of the sclerosed dentin tubules, secondary dentin formation and prolong use of fluoride dentifrices
  • Treatment for sensitivity caused by mouthguard vital tooth bleaching consists of removal of the mouthguard for 2 to 3 days, reduction of wearing time, and re-adjustment of the guard.
  • These tactile and evaporative stimuli(with air jet) should reliably provoke the dentin hypersensitivity-associated pain.
  • Patient should be advised to take something alkaline (milk) or drink using the straw.
  • Also, the patients should be instructed to avoid brushing for at least 2 hours after acidic drinks to prevent agonist effect of acidic erosion on tooth brush abrasion.
  • Ammonium hexafluorosilicate has been used as a desensitizing agent. It can present a continuous effect of dentinal tubule occlusion via precipitation of a mixture of calcium fluoride and fluoridated apatite. If the precipitate is predominantly composed of fluoridated apatite, it can form stable crystals deposited deep inside the dentinal tubules.
  • It has been shown that the effect of oxalates on DH diminishes over a period of time. This can be attributed to the removal of the calcium oxalate crystals by brushing or dietary acids. The condition can be improved by acid etching of the dentinal surface, thus increasing the penetration of calcium oxalate crystals deep into the dentinal tubules.
  • . Saliva provides calcium and phosphate, which over time will occlude and block open dentinal tubules from external stimuli associated with dentinal hypersensitivity. Reduced salivary flow, hyposalivation and xerostomia are risk factors for caries and tooth demineralization and may exacerbate dentinal hypersensitivity.
  • The use of a Er: YAG laser has been shown to be effective for desensitizing hypersensitive dentin for up to 6 months. The desensitizing effect was attributed to the deposition of insoluble salts into the exposed dentinal tubules.
  • Nanotechnology refers broadly to a field of applied science and technology whose unifying theme is the control of matter on the molecular level in scales smaller than 1>m, normally 1-100nm, and the fabrication of devices within that size range.

    1. 1. Dr Aghimien osaronse University of Benin School of Dentistry. Nigeria DENTIN HYPERSENSITIVITY AND CURRENT TRENDS IN MANAGEMENT
    2. 2. outline Introduction Definition of dentin hypersensitivity DHS Epidemiology Relevant anatomy: dentin-pulp complex Odontoblast and its processes Dentinal tubules Sclerosed dentin Neurovascular bundle Etiopathogenesis lesion localisation lesion initiation
    3. 3. Theories of DHS neural nerve transduction hydrodynamic Management of DHS o diagnosis; history examination differential diagnosis investigation/tools definitive diagnosis o prevention/removal of predisposing factors
    4. 4. o Treatment classification of treatment options traditional method current trends in treatment • Arginine-base product Pro-Arginine™ • Laser • Bio-glass • Casein phosphopeptide • nanodentistry CONCLUSSION REFERENCES
    5. 5. introduction Dentin hypersensitivity is said to be one of most painful and chronic dental condition. Previously described as an enigma because it was poorly understood. It has a higher prevalence among periodontally compromised patients, 60%–98% (Von Troil et al, 2002).
    6. 6. Definition As defined by an international workshop on DH: “Dentine hypersensitivity is characterized by short, sharp pain arising from exposed dentine in response to stimuli, typically thermal, evaporative, tactile, osmotic or chemical and which cannot be ascribed to any other dental defect or pathology”( Holland et al, 1997).
    7. 7. • Dentine Hypersensitivity is a transient tooth pain, characterized by a short, sharp pain arising from exposed dentine in response to a stimulus that cannot be attributed to any other form of dental defect or pathology(Andy M, 2002).
    8. 8. Epidemiology It occurs in patients 30 to 40 years old, but it can occur in patients significantly younger or older.  female are more commonly affected than males. Canines and premolars are more affected
    9. 9. OOOCH….
    10. 10. Dentin-pulp complex The close relation (embryologically, histologically and functionally) between them warrant their discussion as a unit. Relevant anatomic consideration as it relates to this discussion would be considered. These include; Odontoblast and its processes Dentinal tubules Sclerosed dentin Neurovascular bundle
    11. 11. Odontoblast and its processes They are formed from the ectomesenchymal differentiation of cells of the dental papilla and are responsible for the formation of dentin. Their processes extend into the dentin. They are more in the coronal dentin than the root dentin The processes tend to traverse the entire length of the tubule
    12. 12. Dentinal tubules They are channels via which the odontoblastic processes traverse. They extend the entire length of the dentin permitting diffusion of nutrients through out the dentin They run a sigmoid shape in the coronal dentin but straight in the root dentin, this is determine by the course of the odontoblast. Dentinal tubules branch majorly in the root dentin than in coronal dentin.
    13. 13. Dentinal fluid The odontoblastic processes are surrounded by dentinal fluid inside the tubules. The dentinal fluid forms around 22% of total volume of dentin. It is an ultrafiltrate of blood from the pulp via dentinal tubules and forms a communication medium between the pulp (via the odontoblastic layer) and outer regions of the dentin.
    14. 14. Sclerosed dentin Results from continuous deposition of peritubular dentin. Mineral deposition within the tubules without dentin formation mineralisation of the odontoblastic processes and intra-tubular collagen fibrils. These ultimately reduce permeability of the dentin thereby prolonging the pulp vitality
    15. 15. Neurovascular supply A plexus( of Raschkow) of nerve exist in the coronal part of the crown. No plexus exist in the root area as they are supply by ascending branched.  the nerve further extend for a short distance into the dentinal tubules hence, called intra-tubular nerves.
    16. 16. Within the dentinal tubules there are two types of nerve fibers, myelinated (A-fibers) and unmyelinated (C-fibers). The A-fibers are responsible for the sensation of dentinal hypersensitivity, perceived as pain in response to all stimuli.  it is said that the density of the intra-tubular nerve varies as high as one for every two tubules
    17. 17. Etiopathogenesis Regardless of the cause it is important to state that apart from been expose, the dentinal tubule should be patent for sensitivity to occur. Two phases are involved in the pathogenesis of dentin hypersensitivity; Lesion localisation Lesion initiation
    18. 18. Lesion localisation This involves the exposure of the dentin a as result of various mechanical or chemical processes; 1. Attrition due to bruxism 2. Erosion 3. Abfraction 4. Abrasion 5. Pocket reduction surgery 6. Tooth preparation for crown 7. Excessive flossing 8. Secondary to periodontal diseases
    19. 19. This involves the actual mechanism that results in the sensitivity felt by the patient. It is on this ground that different theories have been postulated as to how the response is brought about. 1. Direct innervation/neural theory 2. Odontoblastic receptor theory 3. Hydrodynamic/fluid movement theory/Brannstrom 1964
    20. 20. Neural theory It explains that the nerve is the primary receptor that excites the action potential. But; Newly erupted teeth are sensitive even when the plexus of nerves and intra-tubular nerve are not yet establish Is the outer layer of the dentin directly innervated?
    21. 21. Odontoblastic receptor theory Odontoblast was postulated as the receptor. It was assume that the odontoblast is of same neural crest origin as the nerve hence, it should retain the ability to transduce and propagate impulses. But; No organise junction exist between the axon and the odontoblastic process Membrane potential of the odontoblastic process is too low to permit transduction
    22. 22. Consistent with the odontoblastic theory are; Odontoblastic process traverse the entire length of the tubule There is the possibility of gap junction between the odontoblast.
    23. 23. Hydrodynamic theory Fluid movement within the tubule distort the pulpal environment and is sense by the free nerve ending of the Raschkow plexus. The wider tubules increase the fluid movement and thus the pain response. The profuse branching of the tubules at the dentin-enamel junction explains the increase sensitivity felt. The response of pulpal nerves, mainly A delta intra-dentinal afferent fibers, depends upon the pressure applied, i.e. intensity of stimuli.
    24. 24. It has been noted that stimuli which tend to move the fluid away from the pulp–dentine complex produce more pain. These stimuli include cooling, drying, evaporation and application of hypertonic chemical substances.
    26. 26. IMPORTANT STEPS TO FOLLOW 1. Correct diagnosis of dentin hypersensitivity including a patient’s history screening and a brief clinical examination 2. Identification of etiologic and predisposing factors 3. Differential diagnosis, to exclude all other dental conditions 4. If present, treatment of all conditions with symptoms similar to dentin hypersensitivity 5. Removal or minimization of etiologic and predisposing factors
    27. 27. Occur in females than males; this is in keeping with their dietary practices Middle age group of 30-40 years are commonly affected Pain is described as sharp, short lasting irrespective of the stimuli and usually of chronic duration History of excessive tooth brushing, flossing and oral habit should be checked.
    28. 28. Past dental treatment like vital tooth bleaching, periodontal procedures 54%– 55% (Howard E. S, 2009). Medical condition that results in tooth wear lesion bulemics and gastrointestinal reflux disease Social practices involving intake of acidic foods and drinks(quantity and frequency)
    29. 29. EXAMINATION Evidence of tooth wear lesion (attrition, abrasion, erosion) Gingival recession
    30. 30. Exposed root surfaces
    31. 31. Recession and attrition
    32. 32. investigations • It is important to note that DHS is a diagnosis of exclusion hence, effort should be made to rule out other conditions that would mimic this presentation. The following diagnostic tools could help; 1. Air jet 2. Cold water jet 3. Electrical devices 4. Dental explorer 5. Periodontal probe 6. Radiographs 7. Caries diagnostic devices 8. Percussion testing 9. Assessment of occlusion 10. Bite stress tests
    33. 33. Differentials Bite stress test, transillumination could help diagnosis a fracture Percussion test could exclude pulpitis and periodontal involvement Radiographs or other caries detecting devices exclude caries(root) Occlusion assessment could rule out traumatic occlusion from high restoration
    34. 34. Differential diagnosis Cracked tooth syndrome Fractured restorations Restorations left in traumatic occlusion Chipped teeth Dental caries, root caries Postoperative sensitivity Pulpal response to restorative treatment or certain materials Marginal leakage of restorations Pulpitis, pulpal status Vital bleaching procedures
    35. 35. Definitive diagnosis A simple clinical method of diagnosing DHS includes a jet of air or using an exploratory probe on the exposed dentin, in a mesio-distal direction,
    36. 36. Prevention/eliminate predisposing factors 1) Ensure proper toothbrush consistency, ensure proper brushing technique, highly abrasive tooth powder or pastes should be avoided. 2) Avoid over-brushing with excessive pressure or for an extended period of time or excessive flossing 3) Avoid brushing immediately after taking acidic drinks 4) Avoid over-polishing exposed dentin during stain removal.
    37. 37. Prevention cont’d 5) Avoid over-instrumenting the root surfaces during scaling and root planing, particularly in the cervical area of the tooth. 6) Avoid violating the biologic width during restoration placement, as this may cause recession. 7) Patient with gastrointestinal reflux disease should be properly managed by the physician and fabrication of occlusal splint to cover the affected areas, to prevent their contact with the acids.
    38. 38. Treatment of DHS • Classification of treatment options • Ideal properties of a desensitizing agent • Traditional methods of treatment • Current trends in treatment
    39. 39. Two main group of products are available; To occlude or plug the tubules Nerve desensitisers
    40. 40. CLASSIFICATION OF DESENSITIZING AGENTS 1. Base on mode of administration: at-home in-office 2. Base on mode of action Nerve desensitization Protein precipitation Plugging dentinal tubules Dentine adhesive sealers Lasers Homeopathic medication 3.’’ Others’’ gingival graft
    41. 41. 1. Mode of administration At home desensitizing agents In-office treatment 2. On the basis of mechanism of action A. Nerve desensitization Potassium nitrate B. Protein precipitation Gluteraldehyde Silver nitrate Zinc chloride Strontium chloride hexahydrate
    42. 42. C. Plugging dentinal tubules STROTIUM ACETATE…..SENSODYNE RAPID ACTION Sodium fluoride Stannous fluoride Potassium oxalate Calcium phosphate Calcium carbonate Bio active glasses (SiO –P O –CaO–Na O) D. Dentine adhesive sealers Fluoride varnishes Oxalic acid and resin Glass ionomer cements Composites Dentin bonding agents
    43. 43. E. Periodontal soft tissue grafting. F. Anti-inflammatory corticosteroids G. Crown placement and restorative materials H. Lasers  Neodymium:yttrium aluminum garnet (Nd- YAG) laser  GaAlAs (galium-aluminium-arsenide laser)  Erbium-YAG laser  He:Ne laser I. Homeopathic medication Propolis
    44. 44. Ideal properties of a desensitizing agent (Grossman et al, 1965) 1. Rapidly acting with long-term effects, 2. non-irritant to pulp, 3. painless 4. easy to apply, and 5. Should not stain the tooth.
    45. 45. Traditional treatment methods A. Adhesive composite resin, GIC and dentin bonding agents;  Indicated when the exposed sensitive root surface has surface loss due to abrasion, erosion and/or abfraction leaving a notching of the root.  The adhesive resins can seal the dentinal tubules effectively by forming a hybrid layer.  Newer bonding agents modify the smear layer and incorporate it into the hybrid layer.
    46. 46.  Hydroxyethyl methacrylate (HEMA), forms deep resinous tags and occludes the dentinal tubules. 5% of Gluteraldehyde could be added to 35% of HEMA causing coagulation of the proteins inside the dentinal tubules
    47. 47. B. Fluoride varnish:(e.g. sodium fluoride, stannous fluoride) Fluorides decrease the dentinal permeability by precipitation of calcium fluoride crystals inside the dentinal tubules. 5% sodium fluoride varnish painted over exposed root surfaces is effective treatment of DHS.
    48. 48. C. oxalate.  precipitates and occlude the open dentinal tubules.  Oxalate reacts with the calcium ions of dentine and forms calcium oxalate crystals inside the dentinal tubules as well as on the dentinal surface.  Topical application of 3% potassium oxalate can reduce DHS post periodontal surgery.  Avoid using with tray for a long time as it can cause gastric irritation.
    49. 49. D. desensitizing dentifrices.  desensitizing ingredient in toothpastes is potassium nitrate.  It acts by penetrating the A-fibres of the nerves reducing its excitabilty.  for a potassium nitrate toothpaste it must contain 5% potassium nitrate. It takes up to two weeks to show any effectiveness
    50. 50. Others. Gingival graft; This is indicated when recession is progressive, aesthetic is a major concern and when the treatment is not responding to convention treatment, including coronally reposition flaps, lateral sliding graft, free gingival and connective tissue graft Anti-inflammatory Topical application 0.5% solution of prednisolone on exposed root surface will induce remineralisation leading to tubular occlusion.
    51. 51. Fluoride Iontophoresis can also be used, a technique that utilizes a low galvanic current to accelerate ionic exchanges and precipitation of insoluble calcium with fluoride gels to occlude the open tubules.
    52. 52. Current trends in treatment of DHS a. Arginine-base product Pro- Arginine™ b. Laser c. Bio-glass d. Casein phosphopeptide e. nanodentistry
    53. 53. Arginine-base product Utilizes arginine, an amino acid; bicarbonate, a pH buffer; and calcium carbonate, a source of calcium. Mechanism of action is based upon the role that saliva plays in naturally reducing dentinal hypersensitivity Arginine at a neutral pH is positively charged and bind to the negatively charged tubules thereby attracting a calcium-rich layer from the saliva to infiltrate and block the dentinal tubules. The dentin plug contained high amounts of phosphate, calcium and carbonate and also significantly reduced the flow of dentinal fluid in the tubules.
    54. 54. A slow speed hand piece is use to apply the paste on the exposed tubule.  It provides instant relief from discomfort that lasted 4 weeks after a single application with 71.7% reduction in sensitivity measured by air- blast and an 84.2% reduction by the “scratch” test immediately following application (Kleinberg I.S, 2002). Significant relieve is experienced when applied before dental procedure.
    55. 55. Occlusion of dentinal tubules by the Pro-Argin™ technology
    56. 56. Laser MECHANISM OF ACTION a. Occlusion of dentinal tubules e.g. Nd-YAG b. Alteration of nerve transmission. GaAlAs c. Coagulation of proteins within the dentinal tubules and blockage of fluid movement. d. deposition of insoluble salts into the exposed dentinal tubules: Er: YAG laser LASER can be carried out alone or in association with surface treatment.
    57. 57. Casein phosphopeptide–amorphous calcium phosphate CCP-ACP The phosphoseryl sequences within the casein phosphopeptide get attached to the ACP which maintain a supersaturated solution of bioavailable calcium and phosphates. The stabilised CCP-ACP is able to remineralised subsurface enamel lesion which is also important in treatment of dentine sensitivity.
    58. 58. ACP can be used to control bleaching sensitivity when incorporated into bleaching gels. Direct application on teeth by brushing could relieve sensitivity.
    59. 59. Bioglass (NovaMin) e.g. calcium sodium phosphosilicate bioactive glass e.g. NovaMinR Has silica as the main component, acting as a nucleation site for the precipitation of calcium and phosphate. Upon its application an apatite layer is formed which occlude the tubule. Relieve should be expected after 6 weeks of home used.
    60. 60. THE PLACE OF NANODENTISTRY Nanodentistry will make possible the maintenance of comprehensive oral health by employing nanomaterials, biotechnology, including tissue engineering, and ultimately dental nanorobotics(robots at the nanoscale.). These nanorobots will be able to bring about a variety of functions as they exert precise control over matter.
    61. 61. In the area dentine sensitivity nanorobots could selectively and precisely occlude selected tubules in minutes, offering patients a quick and permanent cure (Mallanagouda et al., 2008; Jhaver, 2005; Freitas, 2005). isn’t this wonderful?
    62. 62. Dentin hypersensitivity is always a diagnosis of exclusion, it is confirmed only after all possible other conditions have been diagnostically eliminated
    63. 63. The importance of implementing preventative strategies in identifying and eliminating predisposing factors in particularly erosive factors (e.g. dietary acids) cannot be ignored if you as the practitioner is going to treat this troublesome, stubborn and recalcitrant clinical condition successfully.
    64. 64. Conclusion Depending on the severity of dentinal hypersensitivity, clinical management may include both in-office and self-applied at- home therapies, including recent and novel technologies that have been introduced. The least invasive, most cost-effective treatment is the use of an effective desensitizing toothpaste.
    65. 65. 1. Christian R. Gernhardt. How valid and applicable are current diagnostic criteria and assessment methods for dentin hypersensitivity? An overview. Clin Oral Invest (2013) 17. 2. Mikkilineni M, Rao AS, Tummala M, Elkanti S. Nanodentistry: New buzz in dentistry. Eur J Gen Dent 2013;2:109-13 3. Maryam Moezizadeh Future of dentistry, nanodentistry, ozone therapy and tissue engineering . Journal of Developmental Biology and Tissue Engineering Vol. 5(1), pp. 1-6, April 2013 4. Patrick R. Schmidlin and Phlipp Sahrmann. Current management of dentin hypersensitivity. Clin Oral Investig. 2013 March; 17(Suppl 1): 55–59 5. Rita Chandki et al. ‘NANODENTISTRY’: Exploring the beauty of miniature. J Clin Exp Dent. 2012;4(2):e119-24.
    66. 66. 5, Nutalapati R. et al: Nanodentistry – The New Horizon. The Internet Journal of Nanotechnology. 2011 Volume 3 Number 2. 6. Preeti SK et al : A Paradigm Shift-from Fiction to Reality. Journal of undian prosthodontic society , 2011 March; 11(1): 1–6. 7. Sanjay Miglani, Vivek Aggarwal, and Bhoomika Ahuja Dentin hypersensitivity: Recent trends in management. Journal of Conservative Dentistry 2010 Oct-Dec; 13(4): 218–224 8. Howard E. S, Francis G. S. Dentinal Hypersensitivity: Etiology, Diagnosis and Management. The Academy of Dental Therapeutics and stomatology. 2009
    67. 67. 9. Peter Jacobsen et al. Restorative Dentistry An Integrated Approach 2nd Edition. 5: 35-43. 2008 10. José M. R et al. Dentinal sensitivity: Concept and methodology for its objective evaluation. Med Oral Patol Oral Cir Bucal. 2008 Mar1;13(3):E201-6 11. Bartold PM. Dentin hypersensitivity; A review. Australian dental journal 2006; 51:(3):212-218 12. Gillam D.G., R. Orchardson. Advances in the treatment of root dentine sensitivity: mechanisms and treatment principles Endodontic Topics 2006, 13, 13–33 13 Walters PA. Dentinal Hypersensitivity: A Review. Journal of Contemporary Dental Practices 2005 May;(6)2:107-117.
    68. 68. 14. Antonio Nanci et al. Oral histology; development, structure and function, 6th Edition. 8:192-240. 1998