3. INTRODUCTION
ďą1987, Johnson and Coworkers: Dentine Hypersensitivity is an
enigma being frequently encountered yet ill understood
ďąGenerally 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
â˘Dentinal tubules first exposed , become more sensitive to tactile, evaporative and osmotic
stimuli.
â˘Over time, because of poor plaque control becomes hypersensitive.
â˘Mechanism: Localised pulpal inflammation, Sprouting of pulpal nerves, Expression of
inflammatory sodium channels.
â˘Often such hypersensitivity disappears due to protective mechanism.
â˘Problem: when endogenous protective mechanism fail to correct hypersensitivity.
10. â˘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
â˘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. ďąTorsion gauge
ďąSharp explorer like
probe
ďąIndicator: Records the
force of displacement in
centinewtons
ďąProbed at CEJ
ďąA 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
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. âMECHANISM,
â˘Most likely: Reduction in the diameter of dentinal tubules so as to limit the displacement
of fluid in them.
â˘Can be attained by:
â˘Formation of smear layer produced by burnishing the exposed surface.
â˘Topical application of agents that forms insoluble ppt within tubules.
â˘Impregnation of tubules with plastic resins.
â˘Sealing of tubules with plastic resins.
â˘Act via ppt of crystalline salts on the dentine surface, which blocks tubules.
â˘Desensitizing agents for a continuous period of atleast 2 weeks.
22. STRONTIUM CHLORIDE
(10%)
â˘In-vitro studies: Slightly reduces dentinal
fluid flow, the occurrence thought to be
produced by abrasive filler occluding the
tubule orifice
â˘Skurnick: Decreased sensitivity in 93% cases
â˘Anderson and Matthews: ineffective
POTASSIUM NITRATE
⢠Greenhill and Pashley: ineffective in in-vitro
study even at 30% conc.
â˘Others: 5% effective
â˘Hodash,1974: effective at 1-15%
concentration
â˘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
â˘Powerful protein precipitate
â˘Greenhill and Pashley: Silver nitrate either
alone or in combination with formalin ppt
silver chloride and elemental silver
â˘May cause pulpal inflammation
â˘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. BrännstrÜm M, à strÜm 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;137:990â998.
5. Porto IC, Andrade AK, Montes MA. Diagnosis and treatment of dentinal hypersensitivity. J
Oral Sci. 2009;51:323â332.
6. Miglani S, Aggarwal V, Ahuja B. Dentin hypersensitivity: Recent trends in management. J
Conserv Dent. 2010;13:218â224.
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:3Aâ13A
10. Cummins D. Dentin hypersensitivity: from diagnosis to a breakthrough therapy for
everyday sensitivity relief. J Clin Dent. 2009;20:1â9.
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
Known as common cold of dentistry, toothbrush disease
2 process to occur for hypersensitivity: lesionlocalisation and lesion initiation
Poiseuilleâs equation: inversely proportional to length
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
Successive increase of 5 centinewtons till pain is felt
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
Corticosteroids: Induce remineralisation leading to tubular occlusion
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