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DENTINAL
HYPERSENSITIVITY
PRESENTER:
DR. MRINALINI
CONTENT
INTRODUCTION
DEFINITION
ETIOLOGY
MECHANISM OF DENTIN
SENSITIVITY
THEORIES ASSOCIATED WITH
HYPERSENSITIVITY
PREDISPOSING FACTORS
METHODS OF MEASURING
HYPERSENSITIVITY
(DIAGNOSIS)
MANAGEMENT OF
HYPERSENSITIVITY
CONCLUSION
REFERENCES
INTRODUCTION
1987, Johnson and Coworkers: Dentine Hypersensitivity is an
enigma being frequently encountered yet ill understood
Generally used to describe a common painful condition of teeth
Dowell and Addy,1981: Short sharp pain arising from exposed dentine in response to stimuli,
typically thermal, evaporative, tactile, osmotic, chemical and which cannot be ascribed to any
other dental defect or pathology
DENTINAL
HYPERSENSITIVITY
Sharp
transient
pain
Stimulated
pain
Dentin
exposure
Exclusion
of other
dental
defects
Prevalance: 15-80%
in general population
72-98% in
periodontal patients
Age incidence: 20-50
yrs( because of
appearance and
progression of
gingival recession)
Gender: Female
Distribution: Buccal
and cervical(Enamel
is thinnest and site of
gingival recession
Teeth: Canine and 1st
Premolar followed by
Incisor and 2nd
Premolar, least often
molars
ETIOLOGY
Lesion localisation:
Dentine has to
become exposed
Causes: Enamel
loss
Gingival recession
Lesion initiation
Attrition, Abrasion, Erosion,
Abfraction
Others: Improper
instrumentation, Enamel and
Cementum do not meet at CEJ
Requires opening of dentinal tubules
Tooth paste with abrasives, erosive
agents etc causes removal of dentin
smear layer after few minutes of
exposure and cause bulk loss of
dentin
PLUG/ SMEAR LAYER:
Elements of protein and
sediments derived from
salivary calcium
phosphate and seals the
tubule inconsistently and
transiently
Mechanical + Chemical
factor: remove smear layer
Sensitive dentin: 8 times more
dentinal tubules, also tubules
are thicker than non sensitive
ones (Orchardson(2006),
Cummins D (2010),
Miglani(2010)
DEJ: Profuse branching of
tubules at DEJ, thus most
sensitive
Rate of fluid flow is directly
proportional to tubule radius to
the power 4
Rate of fluid flow is directly
proportional to tubule radius to
the power 4
Mainly A delta fibers (present
at periphery)
Stimuli that move fluid away
from pulp dentin complex
produce more pain(cold, drying,
evaporation, hypertonic solution)
SENSITIVE TO HYPERSENSITIVE
•Dentinal tubules first exposed , become more sensitive to tactile, evaporative and osmotic
stimuli.
•Over time, because of poor plaque control becomes hypersensitive.
•Mechanism: Localised pulpal inflammation, Sprouting of pulpal nerves, Expression of
inflammatory sodium channels.
•Often such hypersensitivity disappears due to protective mechanism.
•Problem: when endogenous protective mechanism fail to correct hypersensitivity.
•Normal: outward movement of fluid because of pulpal pressure, prevents ingress of endotoxins
Pulpal inflammation
Release of chemical mediators( Histamine, Bradykinin)
Make pulpal nerves more sensitive than normal and cause surrounding fibroblast to divide more
rapidly
Fibroblasts release more nerve growth factor
Nerve terminals sprout
Increase in nerve density will cause hypersensitivity
•Inflammatory mediators: Upregulate new sodium channels that are easily activated
• Neural theory or
Direct nerve
innervation
theory
Theories
• Odontoblastic
transduction
theory
Associated
• Fluid
Hydrodynamic
theory
Dentin
Sensitivity
THEORIES
OBJECTIVE
ASSESSMENT
Mechanical or Tactile
stimuli: Dental
explorer(No.23): 5-
10gm force
SUBJECTIVE
EVALUATION
VERBAL RATING
SCALE: 0-4(No, mild,
moderate and marked
discomfort)
Visual Analogue Scale
Questionnaire
Hand held scratch
device: Dr. Kleinberg
CLINICAL ASSESSMENT
Torsion gauge
Sharp explorer like
probe
Indicator: Records the
force of displacement in
centinewtons
Probed at CEJ
A tooth that fails to
respond at 80 centi
newtons is non sensitive
THERMAL
SENSITIVITY
EPT
Dental Pulp Stethoscope: Stark
Osmotic stimulation( least
preffered): NaCl, glucose,
sucrose, CaCl2
Cold water test: Varies temp
of 15ml water
Thermoelectric device:
Provides a continuous
application of heat/ cold
Directing a burst of cold air
from a dental syringe onto the
test tooth( 1sec, 65-70F, 45psi,
1cm distance & perpendicular)
Air thermal device: Dr. K. C.
Yeh: Air was heated to
100F(close to mouth temp.)
,temperature was reduced until
subject felt pain or discmfort
DIFFERENTIAL
DIAGNOSIS
Cracked tooth
syndrome
Dental caries
Teeth in acute
hyperfunction
Chipped teeth
Fractured
restoration
Post restorative
sensitivity
Overenthusiastic brushers
Chewing smokeless tobacco
or snuff tobacco
Periodontally treated patients
Gingival recession
Bulimics
High acid food intake
Xerostomia
Poor oral hygiene practices
RISK OF
SENSITIVITY
Brushing: Avoid
abrasive paste, soft
bristle brush, no
brush after 1 hr of
acid food or drink
Premature occlusal
contact: Splint,
occlusal
adjustment
Gingival
recession:
Periodontist for
graft or flap
surgery
Exogenous acid :
Carbonated drinks,
citrus fruits,
Alcohol, Yoghurt -
Diet counselling
Endogenous acid:
GERD- Doctor
consultation
Poor oral hygiene:
Oral hygiene
practices
PREVENTION OF DENTINAL
HYPERSENSITIVITY
MANAGEMENT
Classification(Scherman and Jacobeen,1992)
CHEMICALAGENTS
Corticosteroids
Silver nitrate
Strontium chloride
Formaldehyde
Potassium nitrate or oxalate
Fluorides
Sodium citrate
Iontophoresis with 2% NaF
PHYSICALAGENTS
Composites
Resins
Varnishes
Sealants
Soft tissue grafts
GIC
Lasers
At home: Paste,
Mouthwash (F
& K nitrate)
Chewing gums
(KCl)
In office
Mode of
administr
ation Disturb neural
response to
pain stimulus
Block the fluid
flow and
occlude tubule
Mechanis
m of
action
“MECHANISM,
•Most likely: Reduction in the diameter of dentinal tubules so as to limit the displacement
of fluid in them.
•Can be attained by:
•Formation of smear layer produced by burnishing the exposed surface.
•Topical application of agents that forms insoluble ppt within tubules.
•Impregnation of tubules with plastic resins.
•Sealing of tubules with plastic resins.
•Act via ppt of crystalline salts on the dentine surface, which blocks tubules.
•Desensitizing agents for a continuous period of atleast 2 weeks.
STRONTIUM CHLORIDE
(10%)
•In-vitro studies: Slightly reduces dentinal
fluid flow, the occurrence thought to be
produced by abrasive filler occluding the
tubule orifice
•Skurnick: Decreased sensitivity in 93% cases
•Anderson and Matthews: ineffective
POTASSIUM NITRATE
• Greenhill and Pashley: ineffective in in-vitro
study even at 30% conc.
•Others: 5% effective
•Hodash,1974: effective at 1-15%
concentration
•Tarber: 5% for 1 week was effective in 92%,
histologic examination: did not induce any
pulpal damage
SODIUM MONOFLUOROPHOSPHATE
Arowojolu(2001): Better than strontium
chloride
Effective results after 6 weeks
VARNISH: 5% NaF by Clark et al(1985)
HEMA containing primers like GLUMA(5% Gluteraldehyde and 35% HEMA)
CORTICOSTEROID: Antiinflammatory effect decreases sensitivity, causes complete
obliteration of dentin, eg. Prednisolone+ Parachlorophenol+ m-cresyl acetate+ gum camphor
BURNISHING OF DENTIN
Tooth pick or orange wood stick creates partial smear layer
Reduces fluid movement by 50-80%
Pashley: Compared Burnishing NaF, Kaolin, Glycerin, alone and in various combination,
Results indicated that important variable was not any constituents of the paste rather
burnishing process itself
SILVER NITRATE
•Powerful protein precipitate
•Greenhill and Pashley: Silver nitrate either
alone or in combination with formalin ppt
silver chloride and elemental silver
•May cause pulpal inflammation
•Most studies: Ineffective and deleterious
CALCIUM HYDROXIDE
Block dentinal tubules, promotes peritubular
dentin formation
Mjor(1967); Increased radiodensity
Grene: Better than potassium nitrate at all time
intervals throughout cold stimulation
HYDROXYAPATITE:
Shetty et al: HPT as in-office agent showed
potential as an effective desensitizing agent
providing quick relief
FLUORIDE:
MOA- Reparative dentin formation and CaF
ppt(insoluble)
Clement and Hoyt and Bibby (33.3% NaF):
Very effective but may produce pulpal
inflammation when applied to dentin
FLUORIDE IONTOPHORESIS
A low voltage electric current is used to impregnate the tooth with fluoride ions
2-6 times more fluoride can be impregnated
Carlo (non-controlled study): significant relief from sensitivity in 90% cases
OXALATES
Inexpensive, easy to apply, well tolerated
Potassium oxalate and Ferric oxalate solutions:
Calcium ion in dentinal fluid form calcium
oxalate
Short effect, long term use can lead to
digestive problem
LASERS
Example: Nd:YAG, Er:YAG
Expensive and complex technique
Kumar et al: Nd:YAG with 5% NaF better than
when used alone
Yilmaz(2011):Er:Cr:YSGG immediate result
and was effective even after 3 months
Occlude by coagulating protein of fluid inside
tubule
VARNISH
Short duration result
DENTIN BONDING AGENT
Easy, Aesthetic
Brannstorm: Immediate and lasting blocakde
in 20 patients studied for a period of 2-20
months.
Narhi et al( Animal study) : No neural activity
after resin impregnation
COMPOSITE AND GIC
Long lasting, Indicated only if loss of tooth
structure is present
GC TOOTH MOUSSE:
Minimum 6 weeks of topical application
NANO STRUCTURE BIOACTIVE GLASS:
Mitchell et al(2011)- Produced an immediate reduction in fluid conductance
maintaining it for a minimum of 7 days
Main constituent is silicate that ppt Ca and PO4, SEM: tubule occlusion
ARGININE:
Cummins D(2009), 8% arginine+ CaCO3+ 1450ppm F: Established alkaline
environment leading to precipitation of salivary calcium and phosphate on the
surface as well as in the tubule
PORTLAND CEMENT:
Porto IC(2009)- Occlusion of tubule through remineralisation
Clinical and Dietary
history+ Examination:
Diagnosis
At home
products(3-4
weeks):
CaPO4, F,
Oral hygiene
practice
In office:
APF gel,
Laser,
Varnish etc
LAST RESORT: CONSIDER RCT
REFERENCES:
1. Davari AR, Ataei E, Assarzadeh H. Dentin hypersensitivity: etiology, diagnosis and treatment;
a literature review. Journal of Dentistry. 2013 Sep;14(3):136.
2. Taha S. Clinician's guide to the diagnosis and management of tooth sensitivity. New York:
Springer; 2014.
3. Brännström M, Åström A. A study on the mechanism of pain elicited from the dentin. Journal
of dental research. 1964 Jul;43(4):619-25.
4. Orchardson R, Gillam DG. Managing dentin hypersensitivity. J Am Dent Assoc.
2006;137:990–998.
5. Porto IC, Andrade AK, Montes MA. Diagnosis and treatment of dentinal hypersensitivity. J
Oral Sci. 2009;51:323–332.
6. Miglani S, Aggarwal V, Ahuja B. Dentin hypersensitivity: Recent trends in management. J
Conserv Dent. 2010;13:218–224.
7. Kopycka-Kedzierawski DT, Meyerowitz C, Litaker MS, Chonowski S, Heft MW, Gordan VV,
Yardic RL, Madden TE, Reyes SC, Gilbert GH, National Dental PBRN Collaborative Group.
8. Management of Dentin Hypersensitivity by National Dental Practice-Based Research
Network practitioners: results from a questionnaire administered prior to initiation of a
clinical study on this topic. BMC oral health. 2017 Dec 1;17(1):41.
9. Cummins D. Recent advances in dentin hypersensitivity: clinically proven treatments for
instant and lasting sensitivity relief. Am J Dent. 2010;23 Spec No A:3A–13A
10. Cummins D. Dentin hypersensitivity: from diagnosis to a breakthrough therapy for
everyday sensitivity relief. J Clin Dent. 2009;20:1–9.
11. Poulsen S, Errboe M, Lescay Mevil Y, Glenny AM. Potassium containing toothpastes for
dentine hypersensitivity. Cochrane Database Syst Rev. 2006
12. Lee Y, Chung WG. Management of dentin hypersensit-ivity. J Korean Academy
Endodontics. 2011;12

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Dentinal hypersensitivity

  • 2. CONTENT INTRODUCTION DEFINITION ETIOLOGY MECHANISM OF DENTIN SENSITIVITY THEORIES ASSOCIATED WITH HYPERSENSITIVITY PREDISPOSING FACTORS METHODS OF MEASURING HYPERSENSITIVITY (DIAGNOSIS) MANAGEMENT OF HYPERSENSITIVITY CONCLUSION REFERENCES
  • 3. INTRODUCTION 1987, Johnson and Coworkers: Dentine Hypersensitivity is an enigma being frequently encountered yet ill understood Generally used to describe a common painful condition of teeth Dowell and Addy,1981: Short sharp pain arising from exposed dentine in response to stimuli, typically thermal, evaporative, tactile, osmotic, chemical and which cannot be ascribed to any other dental defect or pathology
  • 5. Prevalance: 15-80% in general population 72-98% in periodontal patients Age incidence: 20-50 yrs( because of appearance and progression of gingival recession) Gender: Female Distribution: Buccal and cervical(Enamel is thinnest and site of gingival recession Teeth: Canine and 1st Premolar followed by Incisor and 2nd Premolar, least often molars
  • 6. ETIOLOGY Lesion localisation: Dentine has to become exposed Causes: Enamel loss Gingival recession Lesion initiation Attrition, Abrasion, Erosion, Abfraction Others: Improper instrumentation, Enamel and Cementum do not meet at CEJ Requires opening of dentinal tubules Tooth paste with abrasives, erosive agents etc causes removal of dentin smear layer after few minutes of exposure and cause bulk loss of dentin
  • 7. PLUG/ SMEAR LAYER: Elements of protein and sediments derived from salivary calcium phosphate and seals the tubule inconsistently and transiently Mechanical + Chemical factor: remove smear layer
  • 8. Sensitive dentin: 8 times more dentinal tubules, also tubules are thicker than non sensitive ones (Orchardson(2006), Cummins D (2010), Miglani(2010) DEJ: Profuse branching of tubules at DEJ, thus most sensitive Rate of fluid flow is directly proportional to tubule radius to the power 4 Rate of fluid flow is directly proportional to tubule radius to the power 4 Mainly A delta fibers (present at periphery) Stimuli that move fluid away from pulp dentin complex produce more pain(cold, drying, evaporation, hypertonic solution)
  • 9. SENSITIVE TO HYPERSENSITIVE •Dentinal tubules first exposed , become more sensitive to tactile, evaporative and osmotic stimuli. •Over time, because of poor plaque control becomes hypersensitive. •Mechanism: Localised pulpal inflammation, Sprouting of pulpal nerves, Expression of inflammatory sodium channels. •Often such hypersensitivity disappears due to protective mechanism. •Problem: when endogenous protective mechanism fail to correct hypersensitivity.
  • 10. •Normal: outward movement of fluid because of pulpal pressure, prevents ingress of endotoxins Pulpal inflammation Release of chemical mediators( Histamine, Bradykinin) Make pulpal nerves more sensitive than normal and cause surrounding fibroblast to divide more rapidly Fibroblasts release more nerve growth factor Nerve terminals sprout Increase in nerve density will cause hypersensitivity •Inflammatory mediators: Upregulate new sodium channels that are easily activated
  • 11. • Neural theory or Direct nerve innervation theory Theories • Odontoblastic transduction theory Associated • Fluid Hydrodynamic theory Dentin Sensitivity
  • 13. OBJECTIVE ASSESSMENT Mechanical or Tactile stimuli: Dental explorer(No.23): 5- 10gm force SUBJECTIVE EVALUATION VERBAL RATING SCALE: 0-4(No, mild, moderate and marked discomfort) Visual Analogue Scale Questionnaire Hand held scratch device: Dr. Kleinberg CLINICAL ASSESSMENT
  • 14. Torsion gauge Sharp explorer like probe Indicator: Records the force of displacement in centinewtons Probed at CEJ A tooth that fails to respond at 80 centi newtons is non sensitive
  • 15. THERMAL SENSITIVITY EPT Dental Pulp Stethoscope: Stark Osmotic stimulation( least preffered): NaCl, glucose, sucrose, CaCl2 Cold water test: Varies temp of 15ml water Thermoelectric device: Provides a continuous application of heat/ cold Directing a burst of cold air from a dental syringe onto the test tooth( 1sec, 65-70F, 45psi, 1cm distance & perpendicular) Air thermal device: Dr. K. C. Yeh: Air was heated to 100F(close to mouth temp.) ,temperature was reduced until subject felt pain or discmfort
  • 16. DIFFERENTIAL DIAGNOSIS Cracked tooth syndrome Dental caries Teeth in acute hyperfunction Chipped teeth Fractured restoration Post restorative sensitivity
  • 17. Overenthusiastic brushers Chewing smokeless tobacco or snuff tobacco Periodontally treated patients Gingival recession Bulimics High acid food intake Xerostomia Poor oral hygiene practices RISK OF SENSITIVITY
  • 18. Brushing: Avoid abrasive paste, soft bristle brush, no brush after 1 hr of acid food or drink Premature occlusal contact: Splint, occlusal adjustment Gingival recession: Periodontist for graft or flap surgery Exogenous acid : Carbonated drinks, citrus fruits, Alcohol, Yoghurt - Diet counselling Endogenous acid: GERD- Doctor consultation Poor oral hygiene: Oral hygiene practices PREVENTION OF DENTINAL HYPERSENSITIVITY
  • 19. MANAGEMENT Classification(Scherman and Jacobeen,1992) CHEMICALAGENTS Corticosteroids Silver nitrate Strontium chloride Formaldehyde Potassium nitrate or oxalate Fluorides Sodium citrate Iontophoresis with 2% NaF PHYSICALAGENTS Composites Resins Varnishes Sealants Soft tissue grafts GIC Lasers
  • 20. At home: Paste, Mouthwash (F & K nitrate) Chewing gums (KCl) In office Mode of administr ation Disturb neural response to pain stimulus Block the fluid flow and occlude tubule Mechanis m of action
  • 21. “MECHANISM, •Most likely: Reduction in the diameter of dentinal tubules so as to limit the displacement of fluid in them. •Can be attained by: •Formation of smear layer produced by burnishing the exposed surface. •Topical application of agents that forms insoluble ppt within tubules. •Impregnation of tubules with plastic resins. •Sealing of tubules with plastic resins. •Act via ppt of crystalline salts on the dentine surface, which blocks tubules. •Desensitizing agents for a continuous period of atleast 2 weeks.
  • 22. STRONTIUM CHLORIDE (10%) •In-vitro studies: Slightly reduces dentinal fluid flow, the occurrence thought to be produced by abrasive filler occluding the tubule orifice •Skurnick: Decreased sensitivity in 93% cases •Anderson and Matthews: ineffective POTASSIUM NITRATE • Greenhill and Pashley: ineffective in in-vitro study even at 30% conc. •Others: 5% effective •Hodash,1974: effective at 1-15% concentration •Tarber: 5% for 1 week was effective in 92%, histologic examination: did not induce any pulpal damage SODIUM MONOFLUOROPHOSPHATE Arowojolu(2001): Better than strontium chloride Effective results after 6 weeks
  • 23. VARNISH: 5% NaF by Clark et al(1985) HEMA containing primers like GLUMA(5% Gluteraldehyde and 35% HEMA) CORTICOSTEROID: Antiinflammatory effect decreases sensitivity, causes complete obliteration of dentin, eg. Prednisolone+ Parachlorophenol+ m-cresyl acetate+ gum camphor BURNISHING OF DENTIN Tooth pick or orange wood stick creates partial smear layer Reduces fluid movement by 50-80% Pashley: Compared Burnishing NaF, Kaolin, Glycerin, alone and in various combination, Results indicated that important variable was not any constituents of the paste rather burnishing process itself
  • 24. SILVER NITRATE •Powerful protein precipitate •Greenhill and Pashley: Silver nitrate either alone or in combination with formalin ppt silver chloride and elemental silver •May cause pulpal inflammation •Most studies: Ineffective and deleterious CALCIUM HYDROXIDE Block dentinal tubules, promotes peritubular dentin formation Mjor(1967); Increased radiodensity Grene: Better than potassium nitrate at all time intervals throughout cold stimulation HYDROXYAPATITE: Shetty et al: HPT as in-office agent showed potential as an effective desensitizing agent providing quick relief FLUORIDE: MOA- Reparative dentin formation and CaF ppt(insoluble) Clement and Hoyt and Bibby (33.3% NaF): Very effective but may produce pulpal inflammation when applied to dentin
  • 25. FLUORIDE IONTOPHORESIS A low voltage electric current is used to impregnate the tooth with fluoride ions 2-6 times more fluoride can be impregnated Carlo (non-controlled study): significant relief from sensitivity in 90% cases
  • 26. OXALATES Inexpensive, easy to apply, well tolerated Potassium oxalate and Ferric oxalate solutions: Calcium ion in dentinal fluid form calcium oxalate Short effect, long term use can lead to digestive problem LASERS Example: Nd:YAG, Er:YAG Expensive and complex technique Kumar et al: Nd:YAG with 5% NaF better than when used alone Yilmaz(2011):Er:Cr:YSGG immediate result and was effective even after 3 months Occlude by coagulating protein of fluid inside tubule VARNISH Short duration result DENTIN BONDING AGENT Easy, Aesthetic Brannstorm: Immediate and lasting blocakde in 20 patients studied for a period of 2-20 months. Narhi et al( Animal study) : No neural activity after resin impregnation COMPOSITE AND GIC Long lasting, Indicated only if loss of tooth structure is present
  • 27. GC TOOTH MOUSSE: Minimum 6 weeks of topical application NANO STRUCTURE BIOACTIVE GLASS: Mitchell et al(2011)- Produced an immediate reduction in fluid conductance maintaining it for a minimum of 7 days Main constituent is silicate that ppt Ca and PO4, SEM: tubule occlusion ARGININE: Cummins D(2009), 8% arginine+ CaCO3+ 1450ppm F: Established alkaline environment leading to precipitation of salivary calcium and phosphate on the surface as well as in the tubule PORTLAND CEMENT: Porto IC(2009)- Occlusion of tubule through remineralisation
  • 28.
  • 29.
  • 30. Clinical and Dietary history+ Examination: Diagnosis At home products(3-4 weeks): CaPO4, F, Oral hygiene practice In office: APF gel, Laser, Varnish etc LAST RESORT: CONSIDER RCT
  • 31. REFERENCES: 1. Davari AR, Ataei E, Assarzadeh H. Dentin hypersensitivity: etiology, diagnosis and treatment; a literature review. Journal of Dentistry. 2013 Sep;14(3):136. 2. Taha S. Clinician's guide to the diagnosis and management of tooth sensitivity. New York: Springer; 2014. 3. BrännstrĂśm M, ÅstrĂśm A. A study on the mechanism of pain elicited from the dentin. Journal of dental research. 1964 Jul;43(4):619-25. 4. Orchardson R, Gillam DG. Managing dentin hypersensitivity. J Am Dent Assoc. 2006;137:990–998. 5. Porto IC, Andrade AK, Montes MA. Diagnosis and treatment of dentinal hypersensitivity. J Oral Sci. 2009;51:323–332. 6. Miglani S, Aggarwal V, Ahuja B. Dentin hypersensitivity: Recent trends in management. J Conserv Dent. 2010;13:218–224. 7. Kopycka-Kedzierawski DT, Meyerowitz C, Litaker MS, Chonowski S, Heft MW, Gordan VV, Yardic RL, Madden TE, Reyes SC, Gilbert GH, National Dental PBRN Collaborative Group.
  • 32. 8. Management of Dentin Hypersensitivity by National Dental Practice-Based Research Network practitioners: results from a questionnaire administered prior to initiation of a clinical study on this topic. BMC oral health. 2017 Dec 1;17(1):41. 9. Cummins D. Recent advances in dentin hypersensitivity: clinically proven treatments for instant and lasting sensitivity relief. Am J Dent. 2010;23 Spec No A:3A–13A 10. Cummins D. Dentin hypersensitivity: from diagnosis to a breakthrough therapy for everyday sensitivity relief. J Clin Dent. 2009;20:1–9. 11. Poulsen S, Errboe M, Lescay Mevil Y, Glenny AM. Potassium containing toothpastes for dentine hypersensitivity. Cochrane Database Syst Rev. 2006 12. Lee Y, Chung WG. Management of dentin hypersensit-ivity. J Korean Academy Endodontics. 2011;12

Editor's Notes

  1. Known as common cold of dentistry, toothbrush disease
  2. 2 process to occur for hypersensitivity: lesionlocalisation and lesion initiation
  3. Poiseuille’s equation: inversely proportional to length
  4. Smith and Ash scratch device(1964): ss wire which moves along highest arc of curvature on facial surface of sensitive tooth. Scratching force could be increased by a screw Yeaple probe(1980): pen like handpiece with a probe tip and electronic control unit that allowed force of 0.05-1 N., Used for studies Scratchometer
  5. Successive increase of 5 centinewtons till pain is felt
  6. Cold water test: 7 degree celcius, syringe with diff temp water(0 to 20) beginning with warmest. Application time not more than 3 sec. if no response next lower temp. In between give a time gap for 3 minutes Heat test: GP or hot water, vaseline coated toth, hot water bath under rubber dam Thermoelectric device: thermally and electrically conductive probe tip Osmotc stimulation: non controllable thus not used Consisted of digital readout sensitive voltameter connected to a digital printer teeth. Stimulus intensity measured in volts. Pulp test lip is placed on gingival third of enamel and stimulated. Electric gel of 5.4-5.6 pH is used. Once patient feels warm tingling sensation, it is switched off and voltage is read. 15 volts and above: Range of non sensitivity
  7. Corticosteroids: Induce remineralisation leading to tubular occlusion
  8. Tooth paste/powder, Mouthwash, Chewing gum Toothpaste: Earlier strontium salts and fluoride with formaldehyde (formaldehyde destroyed vital elements of tubules) Nowadays, Potassium salts( KCl, KNO3, Kcitrate)- Move along the tubule and block axonic action of intradental nerve fibers and reduce excitability of tooth Should be used with soft bristle brush and minimum amount of water