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Dentin hypersensitivity educational teaching resource

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  • After viewing this lecture, attendees should be able to:
    describe the oral anatomy as it relates to dentin hypersensitivity.
    discuss the etiology and physiologic mechanism of dentin hypersensitivity.
    describe the prevalence and epidemiology of dentin hypersensitivity.
    describe the diagnosis and management of dentin hypersensitivity.
  • Dentin hypersensitivity is best defined as a “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 defect or pathology”1
  • The 4 main dental tissues are:
    Enamel
    Dentin
    Cementum
    Dental Pulp
    Enamel is the most highly calcified and hardest tissue in the body; it is acid-soluble.
    Enamel is insensitive, as it has no nerves.
    Enamel grows only when a tooth is formed (typically complete by 12 years of age) and it darkens throughout life as enamel is lost.
    Enamel cannot be renewed but fluoride and saliva can help to preserve it.
  • The anatomic tooth crown is the portion of the tooth covered by enamel.
    The anatomic root is the lower two-thirds of a tooth. The roots are normally subgingival, buried in bone, and serve to anchor the tooth in position.
    The pulp cavity houses the dental pulp, an organ of myelinated and unmyelinated nerves, arteries, veins, lymph channels, connective tissue cells, and various other cells involved in formative or developmental, nutritive, sensory, protective, and defensive or reparative processes.
  • Presence of tubules renders dentin permeable to fluid movement
    Number of tubules per unit area varies depending on the location because of the decreasing area of the dentin surfaces in the pulpal direction.15
    Dentinal tubules are conical, being wider at the pulpal end than the periphery. They follow a sinuous course from the amelodentinal junction and from the cementodentinal junction. These tubules are interconnected by an intricate and profuse system of canaliculi that branch off from the main tubules at different angles.15
    Additional Info:
    The tubules run parallel to each other in an S-shaped course.
    The tubules are filled with a fluid. External stimuli will cause movement of the dentinal fluid, a hydrodynamic movement, which can result in short, sharp pain episodes. These details are important in the understanding of dentin hypersensitivity.
  • The hydrodynamic theory proposes that when dentin becomes exposed and “trigger” stimuli occur, the fluid in the tubules moves rapidly. It is believed that this movement of fluid stimulates the free nerve endings of the A-beta (A-β) and A-delta (A-δ) located around the odontoblast body and the inner dentin layer which results in short, sharp pain.2
  • The hydrodynamic theory proposes that when dentin becomes exposed and “trigger” stimuli occur, the fluid in the tubules moves rapidly. It is believed that this movement of fluid stimulates the free nerve endings of the A-beta (A-β) and A-delta (A-δ) located around the odontoblast body and the inner dentin layer which results in short, sharp pain.2
  • There are two essential elements of the hydrodynamic mechanism:2
    When dentinal tubules are exposed after enamel or cementum is lost, fluid within the dentinal tubules may flow inward or outward depending on pressure differences in the surrounding tissue. These intratubular fluid shifts activate the mechanoreceptors in the intratubular nerves or in the superficial pulp, (pulpal sensory nerves) and are perceived as pain by the patient.
  • The 2 processes required for hypersensitivity are:
    dentin must be exposed
    dentin tubules must be open to:
    dentin surface
    patent to the pulp
  • Triggers ( Stimulus causes fluid movement inward or outward)
    Thermal stimuli — pain in response to cold, sometimes to heat
    Cold = Inward movement
    Hot = Outward movement
    Tactile stimuli — pain in response to touch (eg, toothbrushing, flossing, dental explorer)
    Tactile (touch) – inward movement
    Evaporative stimuli — sensitivity in response to blowing air on the tooth surface
    Evaporative (air) – outward movement
    Osmotic stimuli — pain in response to sugar/acid
    Osmotic (sweet or sour) – outward movement
  • Trigger stimuli, such as hot and cold, tactile, evaporative, and osmotic, cause movement of intratubular fluid. It is this movement that activates mechanoreceptors in the intratubular nerves or in the superficial pulp. Therefore, it is important to point out that the true physiologic stimulus is the inward or outward fluid shifts, not the actual trigger.
    Example:
    The sensation of cold and hot actually cause fluid to move in opposite directions. The mechanoreceptors in A-beta (A-β) and A-delta (A-δ) fibers detect movement, they do not respond to temperature. Therefore, it is not the temperature of the stimuli that stimulates the receptor, but rather the movement of the fluid.
    A cold stimulus causes the tissue fluid volume to shrink slightly, and heat causes it to expand.15
  • The most important factor in the etiology of dentin hypersensitivity is exposed dentin5,6 as a result of gingival recession associated with exposure of root surfaces and/or as a result of loss of enamel associated with tooth wear or trauma; followed by opening of the dentinal tubules (ie, loss of cementum or removal of any smear layer).15
    Dentin can be exposed as a result of:
    Gingival recession (exposure of root surfaces)
    Loss of enamel from tooth wear or trauma
    Loss of cementum
    The removal or absence of a smear layer
  • Periodontal disease and trauma (ie, toothbrushing) are the two major causes of gingival recession.
    Gingival recession is irreversible. However, in some cases it may be repaired with periodontal surgery.
  • Abrasion is the wear of teeth caused by objects other than another tooth (eg, toothbrush). Abrasion occurs particularly on the cervical area of the tooth where gingival recession has occurred. Exposed dentin will abrade faster than enamel because it is softer.
    Attrition is the wearing of the enamel surface over time at sites of direct contact between teeth.
    Abfraction is the loss of tooth surface at the cervical areas of teeth caused by tensile and compressive forces (occlusal load) from chewing or tooth grinding. It results in cervical stress lesions which are usually deep “V” or notch-shaped cavities.
    Erosion is the dissolution of the surface layer of enamel or dentin by acids. It occurs when acidic solutions come into contact with the teeth and cause a loss of mineral that is beyond the repair of saliva. There are two sources: Extrinsic acids are ingested (food, beverages, medicines) and Intrinsic acids originate in the stomach where they are produced (eg, gastric reflux or bulimia).
    Multifactorial – tooth wear is typically advanced by interaction of the above causes. Erosion and abrasion almost always interact and can contribute to enamel loss at the cervical area.
  • Not all dentin is sensitive or responsive to triggers that would normally elicit symptoms of dentin hypersensitivity.
    In non-sensitive dentin, the smear layer covers the opening of tubules and may, in some cases, completely block the opening, reducing the diameter of the exposed tubule.
    In hypersensitive dentin, the removal of the smear layer exposes the dentin tubule, increasing the diameter of the exposed area.
    Tooth wear also increases the diameter of the exposed tubules as it moves toward the pulp. Dentin tubules are funnel-shaped, with the wider end at the pulp. As the dentin is worn inward toward the pulp, the tubule diameter increases in size.
  • Dentin becomes exposed through enamel or cenmentum loss and/or gingival recession
    Opening of tubules by removal of the smear layer initiates the lesion
    Disturbed flow stimulates A-β and some A-δ nerve fibers - It is believed that this movement of fluid in the dentinal tubules stimulates the free nerve endings of the A-β (A-beta) and A-δ (A-delta) located around the odontoblast body and the inner dentin layer which results in short, sharp pain
  • Aggressive toothbrushing
    Periodontal diseases
    Periodontal therapy
    Tooth whitening/bleaching
    Although there are many causes of noncarious cervical lesions of dentin, improper brushing, especially in the presence of an acidic diet, is a major cause.15
  • Aggressive toothbrushing
    Periodontal diseases
    Periodontal therapy
    Tooth whitening/bleaching
    Although there are many causes of noncarious cervical lesions of dentin, improper brushing, especially in the presence of an acidic diet, is a major cause.15
  •  
    Erosion — acts alone, or in combination with abrasion to cause enamel loss
     
    Extrinsic acids — ingested
    Food, beverages, medicine
    Intrinsic acids — internal
    Originate in the stomach
     
    Extrinsic/intrinsic acids cause surface softening of enamel, which takes hours to re-harden and results in greater susceptibility to physical insult
  • Prevalence of dentin hypersensitivity varies from 4% to 57%, with a figure of 15% fairly consistently reported. Symptoms can present at any age, but the majority of individuals range from ages 20 to 40 with a peak prevalence at the end of the third decade.3
    Women are more frequently affected, and at a younger mean age.
    Reports in the dental literature list factors contributing to an increased prevalence of dentin hypersensitivity, and many clinicians report an apparent earlier age of onset, even in the teens and early twenties.
    Whereas dentin hypersensitivity traditionally has been regarded as a condition of older patients with receding gingivae, it is thought that lifestyle changes in the current diet, such as frequent and increasing ingestion of highly acidic foods and beverages (fresh fruits, salads, fruit juices and carbonated beverages) contribute to increased rates of erosive tooth wear and, therefore, earlier onset.
  • Dentin hypersensitivity is most commonly found in:
    Canines and premolars
    Buccal cervical regions
    The individual sites around the mouth with the highest prevalence of dentin hypersensitivity are associated with gingival recession and are located on the facial surfaces of canines > premolars > incisors > molars.15
  • Published studies vary substantially due to different research methods and differences in populations surveyed (age, etc.).
    However, this quote from Dr. Connie Drisko, dean of the Medical College of Georgia, a periodontist and former dental hygienist who delivered an address at the World Dental Congress in Vienna in 2002, sums it up best:
    “It is obvious given the studies reported from around the world, that dentinal sensitivity is pandemic and that the prevalence and location of affected teeth are indeed similar among different study populations. It is also interesting to observe that only a small percentage of subjects have taken advantage of using the most common means of treating their dentin hypersensitivity, namely use of a dentrifrice formulated to treat hypersensitivity. It is noteworthy that as the adult population lives longer and maintains greater numbers of teeth, with more tooth wear, so that it is likely that many more adults will likely suffer dentinal hypersensitivity in the future. This underscores the need for prevention and early treatment of dentinal hypersensitivity.”11
  • There are a number of factors that may contribute to an increased prevalence of dentin hypersensitivity:
    Dietary Changes – is likely the most common factor in younger patients. Higher intake of acidic food/drinks with low pH.
    Bleaching – While the popularity of tooth bleaching is expanding exponentially, a common side effect of external tooth bleaching is tooth sensitivity. All forms of vital tooth bleaching are associated with some level of sensitivity.12,13,15 It is estimated that 55% to 75% of bleaching/tooth whitening patients suffer from some level of sensitivity.14
  • Differential diagnosis:
    Exclude other conditions with identical symptoms which require different management:
    Dental caries
    Chipped teeth
    Fractured restorations
    Marginal leakage
    Restorative materials
    Cracked tooth syndrome
    Palato-gingival groove
    Differential diagnosis is essential in order to exclude other conditions with similar symptoms where dentin is exposed and sensitive.15
  • The complete history should account for:
    Sign and symptoms
    Intensity
    Frequency and duration
    Dietary changes
    Other related events
    The clinical examination includes:
    Visual assessment
    Physical assessment: Dental explorer (probe): tactile stimulus
    Periodontal probe: Depth of periodontal pocket
    Percussion testing
    Response to cold air
    A final diagnosis also includes radiographic analysis.
  • Other related events to consider when diagnosing dentin hypersensitivity include:
    Dental caries
    Periodontal diseases & treatment
    Fractured tooth
    Fractured restoration
    Restorative margin leakage
    Pulpitis
    Occlusal trauma
    Oral hygiene habits
    Tooth whitening/bleaching
  • Tooth sensitivity is one of the most common forms of dental pain
    Usually occurs on the side opposite the dominant hand
    The buccal cervical sites on the canine and pre-molars are the most common sites for tooth sensitivity
  • Root sensitivity is typically a result of gingival recession that may be compounded by tooth wear
    Sensitivity in the crown may be caused by some form or combination of factors attributed to tooth wear
  • All forms of vital tooth bleaching are associated with some level of sensitivity
    Bleaching sensitivity is caused by the easy passage of hydrogen peroxide and urea through the intact enamel, through the dentin in the interstitial spaces into the pulp within 5 to 15 minutes
  • This image is taken from Van Haywood’s contribution to the “Consensus-Based Recommendations for the Diagnosis and Management of Dentin Hypersensitivity,” which were compiled by Dr. Haywood and his colleagues at the Medical College of Georgia, under the auspices of Dean Dr. Connie Drisko. The concept of the stool delineates the three treatment options for the avoidance or treatment of bleaching sensitivity:
    • Bleaching material with KNO3 (avoidance)
    • Dentifrice with KNO3
    • Professional KNO3 product (treatment)
  • Pain can occur in response to:
    Cold beverages
    Eating cold food
    Breathing cold air
    Toothbrushing
    Improper dental floss use
    Eating sour/acid food
    Eating sweet/sugary liquids and foods
    Bleaching/whitening procedures
  • Thermal—pain in response to cold or hot
    Evaporative—blowing air on the tooth surface
    Tactile—pain in response to touch
    Osmotic—pain in response to sugar/acid
    Dental treatment—this type of sensitivity is transient and will resolve with removal of treatment or over time
  • Use fluoride-rich dentifrices with low abrasivity
    Modify behavior with oral hygiene instructions:
    decrease the frequency and severity of the acid challenge by changing eating and drinking habits
    – frequency on intake
    – not holding liquid or swishing it in the mouth.
    Patient education – patients should not brush immediately after eating or drinking high-acidity foods or beverages
    Decrease abrasive forces – low abrasivity toothpaste, correct brushing techniques (decrease overzealous brushing).
    Apply topical fluoride
    Enhance the defense mechanisms of the body – increase salivary flow.
    Provide nutritional counseling
  • Gingival Recession:
    Correct toothbrushing technique
    Plaque control
    Avoidance of harmful habits
    Periodontal disease management
    Replacement of restorations with defective margins
    Smoking cessation
  • Management of Dentin Hypersensitivity: Treatment
    Obturate tubules or alter fluid flow in dentinal tubules
    Modify or block pulpal nerve response with potassium nitrate dentifrice
  • Nerve Inactivators
    Potassium salt (nitrate-KNO3)
    Tubule Obtundants
    Strontium chloride
    Calcium hydroxide
    Fluorides
    Sodium citrate
    Potassium oxalate
    Iontophoresis with NaF
    Protein Precipitators
    Strontium chloride
    Silver nitrate
    Formaldehyde
  • Composite resins
    Bonding agents
    Sealants
    Glass-ionomer cements
    Varnishes
    Soft tissue grafts
    Lasers
  • For persistent pain from dentin hypersensitivity (depending on severity and extent of pain) the recommended approach to management is a continuum from least invasive/expensive to most invasive/expensive according to the Canadian Advisory Board on Dentin Hypersensitivity.
  • In-office by dental professional
    Chemicals (oxalates)
    Physical agents
    Restorations
    Endodontic (root canal)
    Tooth extraction
  • [header]
    REFERENCES
     
    [body]
     
    1. Ajcharanukul O, Kraivaphan P, Wanachantarak S, Vongsavan N, Matthers B. Effects of potassium ions on dentin sensitivity in man. Arch Oral Biol. 2007;52(7);632-639.
    2. Matthews B, Vongsavan N. Interaction between neural and hydrodynamic mechanisms in dentine and pulp. Arch Oral Biol. 1994:39(Suppl):87S-95S.
    3. Strassler HE, Drisko CL, Alexander DC. Dentin hypersensitivity: its inter-relationship to gingival recession and acid erosion. Inside Dentistry. 2008;29(5 Special Issue):3-8.
    4. Dentin hypersensitivity: current state of the art and science. In: Pashley DH, Tay FR, Haywood VB, et al. Dentin Hypersensitivity: Consensus-Based Recommendations for the Diagnosis and Management of Dentin Hypersensitivity. Inside Dentistry. 2008;4(9 Special Issue):8-18.
    5. Watson PJ. Gingival recession. J Dent. 1984;12(1):29-35.
    6. Smith RG. Gingival recession. Reappraisal of an enigmatic condition and a new index for monitoring. J Clin Periodontol. 1997;24(3):201-205.
    7. Dentin hypersensitivity and gingival recession. In: Pashley DH, Tay FR, Haywood VB, et al. Dentin Hypersensitivity: Consensus-Based Recommendations for the Diagnosis and Management of Dentin Hypersensitivity. Inside Dentistry. 2008;4(9 Special Issue):19-24.
    8. Imfeld T. Dental erosion. Definition, classification and links. Eur J Oral Sci. 1996;104(2 (Pt 2)):151-155.
    9. ten Cate JM, Imfeld T. Dental erosion. Summary. Eur J Oral Sci. 1996;104(2 (Pt 2)):241-244.
    10. Addy, Martin, Dentin Hypersensitivity: new perspective on an old problem. Int Dent J. 2002;52:367-375.
    11. Drisko, CH. Dentin hypersensitivity – dental hygiene and periosntal considerations. Intl Dental Journal. 2002;52;385-393.
    12. Auschill TM, Hellwig E, Schmidate S, et al. Efficacy, side-effects and patient’s acceptance of different bleaching techniques (OTC, in-office, at home). Oper Dent 2005;30 (2): 155-163
    13. Broening WD, Blalock JS, Fraizer KB, et al. Duration and timing of sensitivity related to bleaching. J Esthet Restor Dent. 2007; 19(5): 256-264
    14. Haywood VB, Leonard R, Nelson CF, et al. Effectiveness, side effects and long-term status of nightguard vital bleaching. J Am Dent Assoc. 1994;125(9):1219-1226.
    15. Dentin hypersensitivity: consensus-based recommendations for the diagnosis and management of dentin hypersensitivity. In: Pashley DH, Tay FR, Haywood VB, et al. Dentin Hypersensitivity: Consensus-Based Recommendations for the Diagnosis and Management of Dentin Hypersensitivity. Inside Dentistry. 2008;4(9 Special Issue):1-7.
    16. Considerations for managing bleaching sensitivity. In: Pashley DH, Tay FR, Haywood VB, et al. Dentin Hypersensitivity: Consensus-Based Recommendations for the Diagnosis and Management of Dentin Hypersensitivity. Inside Dentistry. 2008;4(9 Special Issue):25-31.
    17. Lussi A, Hellwig E. Risk assessment and preventative measures. In: Lussi A, ed. Dental Erosion: From Diagnosis to Therapy. Basel, Switzerland: Karger; 2006:190-199. Whitford GM. Monographs in Oral Science; vol 20.
    18. Dentin Hypersensitivity: Etiology, Diagnosis and Successful Management. Advancements in Oral Health Educational Module.
    19. 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.
  • Transcript

    • 1. DENTIN HYPERSENSITIVITY Physiology, Etiology, Epidemiology, Diagnosis, and Treatment
    • 2. Dentin Hypersensitivity After viewing this lecture, attendees should be able to: • describe the oral anatomy as it relates to dentin hypersensitivity. • discuss the etiology and physiologic mechanism of dentin hypersensitivity. • describe the prevalence and epidemiology of dentin hypersensitivity. • describe the diagnosis and management of dentin hypersensitivity.
    • 3. Dentin Hypersensitivity Dentin hypersensitivity is best defined as a “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 defect or pathology.”1
    • 4. • Enamel • Dentin • Cementum • Dental Pulp The 4 main dental tissues: Enamel Dentin Cementum Dental Pulp Oral Anatomy: Dental Tissues
    • 5. • Anatomic Crown • Anatomic Root • Pulp Chamber The 3 parts of a tooth: Anatomic Crown Anatomic Root Pulp Chamber Oral Anatomy: Dental Tissues
    • 6. Oral Anatomy: Dental Tissues Enamel Dentin Cementum Dental Pulp
    • 7. Oral Anatomy: Dentinal Tubules • Presence of tubules renders dentin permeable to fluid movement • Number of tubules per unit area varies • Dentinal tubules are conical Dentin Pulp Tubule Fluid Nerve Fibers Odontoblast Cell
    • 8. Dentin Hypersensitivity: Physiology Thedentalpulpisrichlyinnervated. Accordingtoconductionvelocities,thenerveunitscanbeclassifiedintoAgroup—havingtheconductionvelocitymorethan2m/sandCgroup—withconduction velocitylessthan2m/s Thesharp,betterlocalizedpainismediatedbyAdelta fibers,whereasCfiberactivationseemstobeconnected withthedullradiatingpainsensation.
    • 9. Dentin Hypersensitivity: Physiology The most widely accepted mechanism of action for dentin hypersensitivity is the Hydrodynamic Theory, which was first proposed by Gysi in 1900 and validated by Brannstrom in 1996.2 Mechanism of Dentin Hypersensitivity
    • 10. Dentin Hypersensitivity: Physiology There are two essential elements of the hydrodynamic mechanism:2 • Fluid flow through dentinal tubules • Pulpal sensory nerves Mechanism of Dentin Hypersensitivity
    • 11. Dentin Hypersensitivity: Physiology Two processes required:3 • dentin must be exposed • dentin tubules must be open to: – dentin surface – patent to the pulp Hydrodynamic Theory Enamel Exposed Dentin Receding Gingiva Tubules Odontoblast
    • 12. Dentin Hypersensitivity: Physiology Trigger stimuli include:3 • Thermal – Hot – Cold • Tactile • Evaporative • Osmotic Hydrodynamic Theory
    • 13. Dentin Hypersensitivity: Physiology The true physiologic stimulus is the inward or outward fluid shifts, not the actual trigger.4 Hydrodynamic Theory Fluid-filled Tubules Dentin Nerve Fibers Odontoblast Cell
    • 14. Dentin Hypersensitivity: Physiology • Mathews et al (1994 – stimuli such as cold causes fluid flow away from the pulp, produces more rapid and greater pulp nerve responses than those such as heat, which causes an inward flow. • This certainly would explain the rapid and severe response to cold stimuli compared to the slow dull response to heat Insert Text Here 14
    • 15. Dentin Hypersensitivity: Physiology • The dehydration of dentin by air blasts or absorbent paper causes outward fluid movement and stimulates the mechanoreceptor of the odontoblast, causing pain. • Prolonged air blast causes formation of protein plug into the dentinal tubules, reducing the fluid movement and thus decreasing pain Insert Text Here 15
    • 16. Dentin Hypersensitivity: Physiology Hydrodynamic theory showing pain because of fluid movement 16
    • 17. Dentin Hypersensitivity: Etiology The most important factor in the etiology of dentin hypersensitivity is exposed dentin.5,6 Hydrodynamic Theory • The result of gingival recession (exposure of root surfaces) • The result of loss of enamel from tooth wear or trauma • Loss of cementum • Removal or absence of a smear layer Receding Gingiva Tooth Wear
    • 18. Dentin Hypersensitivity: Etiology Gingival Recession is caused by:7 • Physiologic factors – Hormonal fluctuations – Poor nutrition – Aging • Periodontal diseases – Gingivitis – Periodontitis • Periodontal therapy – Scaling and root planning – Surgery • Restoration margins • Chronic trauma – Oral hygiene (toothbrushing) – Habits (tobacco smoking & chewing) • Predisposing anatomic factors – Thin gingiva – Prominent roots – Dehiscences – Fenestrations – Frenum pulls – Roots moved outside alveolar housing by orthodontics
    • 19. • Physical Loss – Abrasion—mechanical – Attrition—tooth/tooth – Abfraction—lesions • Chemical dissolution – Erosion -Extrinsic acids -Intrinsic acids • Multifactorial etiology – Erosion, abrasion, attrition, abfraction Tooth Wear can occur as a result of:3,8 Dentin Hypersensitivity: Etiology
    • 20. Dentin Hypersensitivity: Etiology • Not all exposed dentin is sensitive3 Dentinal Tubules • Surface appearance • Open/patent tubules • Greater number of tubules • Tubules larger in diameter • Absence of smear layer • Tubules open from tooth wear Characteristics of Sensitive Dentin: Dentin Tooth Wear Receding Gingiva
    • 21. Dentin Hypersensitivity: Etiology • Dentin becomes exposed through enamel or cementum loss and/or gingival recession • Opening of tubules by removal of the smear layer initiates the lesion • Disturbed flow stimulates A-beta (A-β) and some A-delta (A-δ) nerve fibers Understanding Dentin Hypersensitivity Pain4
    • 22. Dentin Hypersensitivity: Etiology • Aggressive toothbrushing • Periodontal diseases • Periodontal therapy • Tooth whitening/bleaching Understanding Dentin Hypersensitivity Pain
    • 23. Dentin Hypersensitivity: Etiology Understanding Dentin Hypersensitivity Pain
    • 24. Dentin Hypersensitivity: Etiology • Erosion—acts alone, or in combination with abrasion to cause enamel loss • Extrinsic/intrinsic acids cause surface softening of enamel which takes hours to re-harden and results in greater susceptibility to physical insult Understanding Dentin Hypersensitivity Pain9 3. Strassler HE, Drisko CL, Alexander DC.
    • 25. • Incidence: 15% (4% to 57%) • Age range: 15 – 70+ years • Peak incidence: 20 – 40 years • Gender: Female > Males Global Prevalence3 Dentin Hypersensitivity: Epidemiology Pain or discomfort caused by cold, hot, sweet, sour, foods/drinks or tooth brushing.
    • 26. Dentin Hypersensitivity: Epidemiology • Teeth: Canines (cuspids) and premolars (bicuspids) • Sites: Buccal cervical regions Most Commonly Found3 Canine Premolar Canine In: Pashley DH, Tay FR, Haywood VB, et al. Dentin Hypersensitivity: Consensus-Based Recommendations for the Diagnosis and Management of Dentin Hypersensitivity.
    • 27. Frequency of Dentate Adults who Responded Positively to Having or Ever Having Sensitive Teeth Dentin Hypersensitivity: Epidemiology In a multi-national survey conducted with 11,000 adults in 2002, 48% of participants said at some point they had consulted a dentist due to sensitive teeth.10,11 27
    • 28. Insert Text Here 28
    • 29. Dentin Hypersensitivity: Epidemiology • Dietary changes – Acidic food/drinks • Periodontal procedures • Cosmetic treatments – Bleaching/whitening12-14 – Restorative • Aging – Retain natural teeth There are a number of factors that may contribute to an increased prevalence of dentin hypersensitivity:3
    • 30. Dentin Hypersensitivity: Management • Differential diagnosis • Exclude or treat other causes of dentin pain • Identify etiological factors • Prevent, remove or modify etiological factors • Management/treatment Management begins with patient education and modification of risk factors15
    • 31. Dentin Hypersensitivity: Management/Diagnosis Complete History • Sign and symptoms • Intensity • Frequency and duration • Dietary changes • Other related events Clinical Examination • Visual assessment • Physical assessment – Dental explorer (probe): tactile stimulus • Periodontal probe – Depth of periodontal pocket • Percussion testing • Response to cold air Dentin Hypersensitivity is a diagnosis of exclusion Radiographic examination • Rule out periapical lesions
    • 32. Differential Diagnosis • Cracked tooth syndrome • Fractured restoration • Chipped teeth • Dental caries • Periodontal disease • Post-restorative sensitivity • Marginal leakage • Pulpitis • Palatogingival groove • Bleaching sensitivity Needs to rule out:15 Non-Odontogenic Origin • Musculoskeletal • Neuropathic • Neurovascular • Inflammatory (sinusitis) • Systemic (cardiac, herpes, zoster, sickle cell anemia, neoplasm) • Psychogenic • Referred pain Dentin Hypersensitivity: Management/Diagnosis
    • 33. • Tooth sensitivity is one of the most common forms of dental pain • Usually occurs on the side opposite the dominant hand • The buccal cervical sites on the canine and pre-molars are the most common sites for tooth sensitivity Incidences3 Dentin Hypersensitivity: Management/Diagnosis
    • 34. Dentin Hypersensitivity: Management/Diagnosis • Root sensitivity is typically a result of gingival recession that may be compounded by tooth wear • Sensitivity in the crown may be caused by some form or combination of factors attributed to tooth wear Tooth Wear3 Receding Gingiva Dentin Wear Enamel Wear
    • 35. • All forms of vital tooth bleaching are associated with some level of sensitivity • Bleaching sensitivity is caused by the easy passage of hydrogen peroxide and urea through the intact enamel, through the dentin in the interstitial spaces into the pulp within 5 to 15 minutes16 Tooth Whitening/Bleaching16 Dentin Hypersensitivity: Management/Diagnosis
    • 36. Dentin Hypersensitivity: Management/Diagnosis Tooth hypersensitivity differs from dentinal or pulpal pain. In case of dentin hypersensitivity, patient’s ability to locate the source of pain is very good, whereas in case of pulpal pain, it is very poor The character of thepain does not outlast the stimulus; the pain is intensified by thermal changes, sweet and sour The pain can be duplicated by hot or cold application or by scratching the dentin Insert Text Here 36
    • 37. Prevention and Treatment of Bleaching Hypersensitivity 16. Pashley DH, Tay FR, Haywood VB, et al. Dentin Hypersensitivity: Management/Diagnosis
    • 38. Dentin Hypersensitivity: Management/Diagnosis • Cold beverages • Eating cold food • Breathing cold air • Toothbrushing • Improper dental floss use • Eating sour/acid food • Eating sweet/sugary liquids and foods • Bleaching/whitening procedures Occurrence of pain:3
    • 39. • Thermal—pain in response to cold or hot • Evaporative—blowing air on the tooth surface • Tactile—pain in response to touch • Osmotic—pain in response to sugar/acid • Dental treatment—this type of sensitivity is transient and will resolve with removal of treatment or over time Dentin Hypersensitivity: Management/Diagnosis Sensitivity may occur in response to various stimuli:3
    • 40. Dentin Hypersensitivity: Management/Etiological Factors Tooth Wear/Erosion: • Use fluoride-rich dentifrice • Behavior modification • Decrease abrasive forces • Application of topical fluoride • Enhance the defense mechanisms of the body • Provide nutritional counseling Management of Pre-disposing Factors17
    • 41. Dentin Hypersensitivity: Management/Etiological Factors Gingival Recession: • Correct toothbrushing technique • Plaque control • Avoidance of harmful habits • Periodontal disease management • Replacement of restorations with defective margins • Smoking cessation Management of Pre-disposing Factors17
    • 42. Dentin Hypersensitivity: Treatment • Obturate tubules or alter fluid flow in dentinal tubules • Modify or block pulpal nerve response Management of Dentin Hypersensitivity3,4 KNO3
    • 43. CHEMICAL AGENTS18 Nerve Inactivators • Potassium salt (nitrate- KNO3) Tubule Obtundants • Strontium chloride • Calcium hydroxide • Fluorides • Sodium citrate • Potassium oxalate • Iontophoresis with NaF Management of Dentin Hypersensitivity Protein Precipitators • Strontium chloride • Silver nitrate • Formaldehyde Dentin Hypersensitivity: Treatment
    • 44. Potassium salt (nitrate-KNO3) Insert Text Here 44
    • 45. Potassium salt (nitrate-KNO3) • Potassium ion is a desensitization agent because it diffuses through dentin tubules and increases the extracellular potassium concentration at the nerve ending, eliminating the potassium ion concentration gradient across the nerve cell membrane. Without this concentration gradient, the nerve cell will not depolarize and will not respond to stimuli; thus the sensation of pain will not be transmitted. Potassium ion can be delivered in a variety of salt forms (e.g., potassium nitrate, potassium citrate). The most common potassium salt used in sensitivity dentifrices is potassium nitrate (KNO3) Insert Text Here 45
    • 46. Insert Text Here 46
    • 47. Tubule Blocking or Occluding Agents 47
    • 48. Insert Text Here 48
    • 49. Tubule Blocking or Occluding Agents • Calcium sodium phosphosilicate (Novamin®, Sensodyne® Repair & Protect). • In saliva, Novamin® releases calcium and phosphate ions and raises the pH. Under these conditions, calcium phosphate salts precipitate from solution to not only block dentin tubules but also to form an insoluble calcium phosphate layer on the surface of enamel Insert Text Here 49
    • 50. Tubule Blocking or Occluding Agents Insert Text Here 50
    • 51. PHYSICAL AGENTS18 Dentin Hypersensitivity: Treatment Management of Dentin Hypersensitivity • Composite resins • Bonding agents • Sealants • Glass-ionomer cements • Varnishes • Soft tissue grafts • Lasers
    • 52. Insert Text Here 52
    • 53. Insert Text Here 53
    • 54. Dentin Hypersensitivity: Treatment At-home treatments—patient applied • Anti-sensitivity dentifrice • Fluoride-based gels • Rinses Options for Treatment19
    • 55. Dentin Hypersensitivity: Treatment In-office by dental professional • Chemicals (oxalates) • Physical agents • Restorations • Endodontic (root canal) • Tooth extraction Options for Treatment19 (listed as least invasive to most)
    • 56. Dentin Hypersensitivity: “the common cold of dentistry.”3 Dentin Hypersensitivity
    • 57. Dentin Hypersensitivity—References 1. Ajcharanukul O, Kraivaphan P, Wanachantarak S, et al. Effects of potassium ions on dentin sensitivity in man. Arch Oral Biol. 2007;52(7);632-639. 2. Matthews B, Vongsavan N. Interaction between neural and hydrodynamic mechanisms in dentine and pulp. Arch Oral Biol. 1994:39(Suppl):87S-95S. 3. Strassler HE, Drisko CL, Alexander DC. Dentin hypersensitivity: its inter-relationship to gingival recession and acid erosion. Inside Dentistry. 2008;29(5 Special Issue):3-8. 4. Dentin hypersensitivity: current state of the art and science. In: Pashley DH, Tay FR, Haywood VB, et al. Dentin Hypersensitivity: Consensus-Based Recommendations for the Diagnosis and Management of Dentin Hypersensitivity. Inside Dentistry. 2008;4(9 Special Issue):8-18. 5. Watson PJ. Gingival recession. J Dent. 1984;12(1):29-35. 6. Smith RG. Gingival recession. Reappraisal of an enigmatic condition and a new index for monitoring. J Clin Periodontol. 1997;24(3):201-205. 7. Dentin hypersensitivity and gingival recession. In: Pashley DH, Tay FR, Haywood VB, et al. Dentin Hypersensitivity: Consensus-Based Recommendations for the Diagnosis and Management of Dentin Hypersensitivity. Inside Dentistry. 2008;4(9 Special Issue):19-24. 8. Imfeld T. Dental erosion. Definition, classification and links. Eur J Oral Sci. 1996;104(2 (Pt 2)):151-155. 9. ten Cate JM, Imfeld T. Dental erosion. Summary. Eur J Oral Sci. 1996;104(2 (Pt 2)):241-244. 10. Addy, Martin, Dentin hypersensitivity: new perspective on an old problem. Int Dent J. 2002;52:367-375. 11. Drisko, CH. Dentin hypersensitivity – dental hygiene and periodontal considerations. Int Dent J. 2002;52;385-393. 12. Auschill TM, Hellwig E, Schmidate S, et al. Efficacy, side-effects and patient’s acceptance of different bleaching techniques (OTC, in-office, at home). Oper Dent. 2005;30(2):155-163. 13. Broening WD, Blalock JS, Fraizer KB, et al. Duration and timing of sensitivity related to bleaching. J Esthet Restor Dent. 2007; 19(5): 256-264
    • 58. Dentin Hypersensitivity—References 14. Haywood VB, Leonard R, Nelson CF, et al. Effectiveness, side effects and long-term status of nightguard vital bleaching. J Am Dent Assoc. 1994;125(9):1219-1226. 15. Dentin hypersensitivity: consensus-based recommendations for the diagnosis and management of dentin hypersensitivity. In: Pashley DH, Tay FR, Haywood VB, et al. Dentin Hypersensitivity: Consensus-Based Recommendations for the Diagnosis and Management of Dentin Hypersensitivity. Inside Dentistry. 2008;4(9 Special Issue):1-7. 16. Considerations for managing bleaching sensitivity. In: Pashley DH, Tay FR, Haywood VB, et al. Dentin Hypersensitivity: Consensus-Based Recommendations for the Diagnosis and Management of Dentin Hypersensitivity. Inside Dentistry. 2008;4(9 Special Issue):25-31. 17. Lussi A, Hellwig E. Risk assessment and preventative measures. In: Lussi A, ed. Dental Erosion: From Diagnosis to Therapy. Basel, Switzerland: Karger; 2006:190-199. Whitford GM. Monographs in Oral Science; vol 20. 18. Dentin Hypersensitivity: Etiology, Diagnosis and Successful Management. Advancements in Oral Health Educational Module. 19. 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.

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