This document provides an overview of dentinal hypersensitivity. It defines dentinal hypersensitivity as pain from exposed dentin in response to stimuli like heat, cold, sweet or tactile sensations. The hydrodynamic theory is discussed, which proposes that fluid movement in dentinal tubules stimulates nerve endings and causes pain. Natural defenses against sensitivity like reparative dentin formation and methods of measuring sensitivity like air or tactile tests are also summarized. Causes of exposed dentin like erosion, abrasion, or periodontal procedures are described as common etiologies of dentinal hypersensitivity.

1. Dr .Nikhat Fatima. PG
Dept. of Periodontics.

2. Overview
 Definition
 Pulp –Dentin complex.
 Etiology
 Stimuli that elicit pain response.
 Hydrodynamic theory.
 Natural defense mechanisms
 Methods of measuring sensitivity.
 Treatment of sensitivity.
 Conclusion

3. Definition
 Characteristic pain arises from exposed dentine
typically in response to a variety of stimuli ,thermal,
evaporative, tactile, osmotic or chemical which
cannot be ascribed to any other form of dental
defect or disease.
Canadian Advisory Board on Dentine
Hypersensitivity in 2003.

5.  The relative frequency of sensitivity of
different teeth has been reported as follows
 Premolars ( 38%)
 Incisors (26%)
 Canines (24%)
 Molars (12%)

6. Prevalence
 Dentinal hypersensitivity has been shown to
peak in 20 to 30 year olds and then rise again
when in their 50’s. The condition generally
involves the facial surfaces of teeth near the
cervical aspect

7. Pulp –Dentin complex
 Many investigators believe pulp-dentine complex
as a single tissue.
 According to Pashley , pulp lives for dentin and
dentin lives by the grace of the pulp.
 Dentin is formed by cells called odontoblasts,
and they are considered part of dentin and pulp
because their cell bodies are in the pulp cavity ,
but their slender cytoplasmic processes extend
into tubules in the mineralized dentin.

8.  Dentine is considered as living tissue
and reacts to physiologic and
pathologic stimuli, and forms,
secondary dentin, sclerotic dentin,
reparative dentin and dead tracts.

9. Anatomy and histology of dentin
 The dentin provides the bulk and general form
of the tooth and it is characterized as a hard
tissue with tubules throughout its thickness.

10. The formation of primary dentin continues
until the tooth becomes functional (Linde &
Goldberg 1993) or until the root apex is
closed (Torneck 1994).
Thereafter dentin formation proceeds as
secondary dentinogenesis, which continues
at a slower rate than the primary
dentinogenesis during the life-time of the
individual.

11. Structure of dentine
Approximately 70% inorganic material
mainly of hydroxyapatite, 20% organic
material - type I collagen with
glycoproteins, proteoglycans,
phosphoproteins and plasma proteins
and 10% water.

12. It is characterized by closely packed
dentinal tubules that surround its entire
thickness and contain the cytoplasmic
extensions of odontoblasts. The cell
bodies of odontoblasts are aligned along
the aspect of the dentine, where they
also form the peripheral boundary of the
dental pulp.

13. Contents of tubule
Odontoblast and its process, nerves are
also found in some tubules.
Fluid that is assumed to be present
which might be equivalent to serum.
It is thought that apart from collagen and
nerve fibrils, the fluid might contain
proteoglycans, tenascin, the serum
protein albumin, transferrin and type V
collagen.

14. Odontoblasts and process
Odontoblast cells
Odontoblast process
Dentin Pulp

16. Dentinal tubules

17. Types of Dentin
Dentin
Primary
physiologic
dentin
Secondary physiologic
dentin
Tertiary dentin or
reparative dentin or
reactionary dentin or
irregular secondary dentin
Mantle
dentin
Circumpulpal
dentin
Peritubular
dentin
Intertubular
dentin

18. Primary dentin: is the dentin formed in a tooth before the completion
of the apical foramen of the root. Primary dentin is noted for its
regular pattern of tubules.
Secondary dentin: is the dentin that is formed after the completion of
the apical foramen and continues to form throughout the life of the
tooth.
Peritubular (intratubular) dentin: dentin that creates the wall of the
dentinal tubule.
Types of Dentin

19. Primary
physiological
dentin
Secondary
physiological
dentin

20. Primary
physiological
dentin
Secondary
physiological
dentin
Tertiary
dentin

21. Intertubular dentin: dentin found between the tubules.
Mantle dentin: the first predentin that forms and matures
within the tooth.
Circumpulpal dentin: the layer of dentin around the outer
pulpal wall.

22. Dentinal tubules
Peritubular dentin Intertubular dentin

23. P
U
L
P
Mature dentine: Varieties
MANTLE DENTINE just
below DEJ coarser fibrils
PRIMARY (CIRCUMPULPAL)
DENTINE - main mass of dentine
TERTIARY DENTINE - slow
increment to pulpal surface
REPARATIVE DENTINE -
response to caries/erosion

24.  Tertiary dentin (reactionary or reparative
or irregular secondary dentin) is the
outcome of odontoblastic response to
irritation occurring mainly during
secondary dentinogenesis and is
caused by dental abrasion, attrition,
cavity preparation, erosion or dental
caries (Torneck 1994).

25.  Lesot et al. (1993) defines reactionary dentin to
be the result of irritation of post-mitotic
odontoblasts, whereas reparative dentin is formed
by odontoblasts or odontoblast-like cells which
differentiate from pulp cells after the cell death of
primary odontoblasts (Magloire et al. 1992,
Magloire et al. 1996).

26. Age and Functional Changes in Dentine
 Primary dentine changes:
•Transparent or Sclerotic dentine.
• Dead tracts.
• ↓ permeability and sensitivity

27. Transparent (Sclerotic Dentin)
 The affected area has occluded dentinal
tubules, so the dentin will have uniform
refractive index. This area of dentin appears
translucent by transmitted light.

28. Dental caries
Sclerotic dentin

29. Dead Tracts
 Severe stimulation to dentin leads to
destruction of the odontoblastic process and
odontoblasts. This leads to empty and wide
dentinal tubules. These areas appear black
with transmitted light. Under the dead tracts
from the pulpal surface , reparative dentine
will be formed.

30. Dead Tracts

31. Primary
physiological
dentin
Secondary
physiological
dentin
Tertiary
dentin
Dead tracts

32. Dentine permeability
 It is constant interchange of fluid between
dentine & pulp. It differs from one person to
another and from one area to other.
 Trowbridge observed that degree of noxious
stimuli toward the pulp are directly related to
the absence or presence of a dense dentin
barrier.
 Most permeable would be dead tract dentin
(empty tubules) , followed by primary dentin.
Irritation dentin is considerably less
permeable.

33. Factors governing dentinal
permeability
 Types of dentine
 Type & nature of diffusions
 Degree of mineralization
 Dentine exposed during tooth preparation
 Effective depth
 Induced stresses
 Hydraulic pressure
 Deficient resistance and retention form
 Micro leakage
 Cracks & micro cracks in dentine & enamel
 Types of intermediary base or restorative material
 Desiccation

34. Pain mechanism theories
 Number of theories have been proposed over
the years to explain the pain mechanism of
dentinal hypersensitivity.
 An early hypothesis was the dentinal receptor
mechanism theory which suggests that
dentine hypersensitivity is caused by the
direct stimulation of sensory nerve endings in
dentine. This theory was discarded as no
neural cells exist in the sensory portion of the
outer dentine.

35. Current flow theory
 Sicher postulated that the oral cavity is
positively charged and pulp is negatively charged
(Personal communication 1958) .
 Any electrolyte such as salt or fruit acid , upsets
this ionic balance, and the resultant current
stimulates the nerve endings to the odontoblasts.
 The sensation disappears as soon as the
electrolyte is diluted away or removed.

36. Odontoblast transducer mechanism
 The odontoblast transducer mechanism
proposed by Rapp et al suggested that
odontoblasts act as receptor cells, mediating
changes in the membrane potential of the
odontoblasts via synaptic junctions with
nerves. However the evidence for the
odontoblast transducer mechanism theory is
generally lacking and inconclusive.

37. Hydrodynamic theory
 Brannstrom (1960) It is based on the
observation that fluid within the dentinal
tubules can flow in either an outward or
inward direction depending on the pressure
variations in the surrounding tissues. The
rapid movement of fluid in the open dentinal
tubules may subsequently deform the
odontoblast or its process and therefore elicit
the transmission of a pain causing stimulus.

38.  This theory of hydrodynamics helps explain
the reason why so many different stimuli can
elicit the same pain response.

39.  Dentinal tubules normally are filled with
odontoblastic process and dentinal fluid , a
transudate of plasma. Pulpal fluid has a
slight positive pressure that forces fluid
outward toward any breach in the external
seal. The tubules become fluid- filled
channels from the cut surface directly to the
pulp.

40.  Depiction of Brannstrom’s Theory.

43.  The dentinal tubules in the sensitive areas are
microscopically to be wider and more numerous
than in non sensitive areas.
The condition generally involves the facial
surfaces of teeth near the cervical aspect.

44. Innervation of dentin
 Trigeminal nerve supplies the pulp, with
innervation from myelinated fibers ( A-β and
A-δ) and nonmylinated C fibers.
 It is proposed that the larger myelinated fibers
(A-β and some A-δ) can respond to stimuli
that displace the fluid in the dentinal tubule
through a hydrodynamic mechanism, such as
tactile, evaporative , osmotic or thermal
challenges, to elicit short, sharp, stabbing
pain that typically lasts for only a few
seconds.

47. Classification
 Dentine hypersensitivity sufferers can readily
be divided into 2 groups.
1. Those who have sharp, shooting pain.
2. Those who have dull, aching pain

48.  The poorly localized, dull , burning ache
is thought to be caused by unmyelinated
nerves, C-fibers and some of the slowest
A-δ fibres.

49. Pulp in dentine hypersensitivity.
 The status of the pulp in dentine hypersensitivity
is not known , although symptoms would suggest
minor inflammation as a result of the length of
time that symptoms persist without developing
into a true pulpitis.
 It has been suggested that when the pain
continues as a throbbing ache then a true pulpitis
is present.

50. Etiology
 The etiology of dentinal sensitivity is
multifactorial.
 Gingival recession
 Abrasion
 Erosion
 Periodontal therapy
 Defective restorations
 Caries

51.  Gingival recession is a common finding both in
populations with high standards of oral hygiene
as well as in populations with poor oral hygiene.
 The overzealous tooth brushing leads to gingival
recession. And gingival recession due to
periodontitis exhibits dentinal hypersensitivity,
and these 2 etiologies result in the same pain
condition, however they should be treated
differently in terms of prevention, etiology and
research. Recession linked to periodontal disease
is often termed root sensitivity.

52.  Prevention should focus on improving tooth
brushing skills and investigating the abrasive
nature of the tooth paste which play a role in
etiology of recession.
 Prevention , early recognition and treatment of
periodontal disease should be a priority and
stringent efforts should be made to control the
periodontal diseases.

53. Abrasion and erosion
 Enamel is highly susceptible to acid erosion,
which is most aggressive type of wear
compared with abrasion and attrition.
 The acid is derived from gastric or sources that
are dietary in origin like carbonated drinks, wine,
herbal teas will remove smear layer and expose
tubules.
 In summary, evidence strongly suggests that
dentine hypersensitivity lesions can be localized
through dentine exposure by the effects of tooth
brushing and gingival recession , by erosion
alone or by combined erosion/ abrasion.

54. Periodontal procedures
 Periodontal therapy may create or increase
the exposure of root surfaces.
 The root surface is covered with cementum
which is softer than calculus and often it is
removed by hand or ultrasonic instruments,
exposing the dentinal surface.

55.  Dentine once it has been exposed and
traumatized , over time develops a reparative
dentin and thus becomes less susceptible to the
debriding stimulus.
 However, after periodontal surgery, which
results in apically positioned gingival tissues in
conjunction with root debridement , dentine is
newly exposed and the root becomes acutely
sensitive to stimuli until reparative dentin can
form.

56. “Catch 22”-equation
 The hypersensitive dentine is painful to brush
and floss and therefore avoided by the
patient.
 The bacterial plaque that then forms causes
greater sensitivity , so the area is avoided all
the more during home care, which in turn
leads to more plaque and greater sensitivity.

57. Restorations and caries
 Dental caries or crown preparations have
resulted in dental sensitivity.
 The postoperative sensitivity may be avoided
if a varnish and base material are placed
beneath restoration and crown preparation.
 The varnish helps seal the dentinal tubules
and the base provides additional insulation
from the restorative material.

58. Natural defense mechanism
 To protect itself from irritating stimuli dentine
produces reparative dentine, sclerotic dentine.
 This process is evidenced by mineralization in
the peritubular dentin that blocks the patent
tubule and prevent passage of painful
impulses.
 The majority of treatments for dentinal
sensitivity attempt in some way to block fluid
flow in the tubule.

59. Diagnosis of Dentinal Hypersensitivity
 An air-water syringe (thermal testing)
 Dental explorer (touch testing)
 Bite stress tests
 Percussion testing
 Other thermal tests, including an ice cube and
occlusal assessment.

60. Tactile method
 The simplest tactile method used to test for
hypersensitivity is to lightly pass a sharp explorer
over the sensitive area of tooth (usually along the
CEJ).
Patient response is graded on a scale.
0 - No pain felt
1 - Slight pain or discomfort
2 - Severe pain
3 - Severe pain that lasts after the stimulus
is removed

61. Smith and Ash scratch device
 A device with a 15 mm (0.26 gauge) stainless
steel wire with a tip ground to a fine point &
movable across the highest arc curve of facial
surface of the sensitive tooth under test.
Pressure in wire is increased with adjustment
screw incrementally in ¼ or 1/3 of mm until
subject is able to feel a pain sensation. At that
point , the scratching force expressed in mm is
taken as threshold value. If no pain is felt tooth
is considered as Non sensitive.

62. Force sensitive electronic probe by Yeaple
 Used for measurement of periodontal pocket
at fixed pressure. In dentinal hypersensitivity
test, probe force can be increased in steps of
5 gm until the subject experience discomfort,
that point is taken as pain threshold.
If maximum force of 70 gm is reached with no
discomfort tooth is scored non sensitive

64. Thermal
 A simple thermal method for testing is directing a burst of air at
room temperature from a dental syringe on to the test tooth.
Room air is cooler than teeth and cooling by this means is
easily detected as pain if tooth is sensitive.
Air stimulation has been standardized in number of studies as a
one second blast from the air syringe of a dental unit, where its
temperature is set generally between 65° and 70° F and a
pressure 60 psi. (the air is directed at right angles to test
surface with adjacent teeth usually isolated by operators
fingers).
0 - No discomfort
1 - Discomfort but no severe pain
2 - Severe pain-during application
3 - Pain persists even after removal of stimuli.

65.  Devices that involve electrical cooling or heating of direct
contact metal probes have been used in a number of
Hypersensitivity studies.
The tip diameter of these probes is usually small enough to
permit placement in the cervical area of a tooth.
One such device developed by Smith and Ash, the
temperature of the probe tip was measured with a thermistor
embedded in the tip.
A flow of current in one direction was used to cool the probe
tip from room temperature to 12°C, current flow in the other
direction heated the tip to 82°C.

66.  Intensity of the current to the probe from a power
supply controlled the temperature. The initial
temperature (standard) 37.5°C
For cold stimulation 1°C is reduced and the tip is
placed in contact with tooth, for heat stimulation it is
increased in 1°C increments and placed in contact with
tooth. Temperature at which pain could be felt is
recorded. The subject rated sensation as no pain or
pain and recorded as 0 or 1 respectively.

69. Differential diagnosis
 Dental caries
 A cracked or chipped tooth
 A fractured restoration
 Gingival inflammation
 Post restorative sensitivity
 Marginal leakage
 pulpitis

70. Clinical management of
dentin hypersensitivity

76. Treatment of sensitivity

77.  Pattisson and Pattison listed the following possible
mechanism of action for desensitizing agents.
 Precipitating or denaturing organic material at the
exposed end of the (odontoblastic process) tubule.
Depositing an inorganic salt at the supposed end of the
dentinal tubules.
 Stimulating secondary dentin formation with in the pulp.
Suppressing pulpal inflammation.
Desensitizing agents
(at -office procedure)

78.  Myjor suggests that the treatment should be
aimed towards a reduction in the permeability
of the dentin rather than towards an attempt to
stimulate secondary dentin.
Treatment through tubules occlusion:
Several therapeutic approaches to tubule
occlusion have been developed with promise
as dentin desensitizing agents.

79.  There are variety of physiochemical mechanisms
that can lead to such reduction in permeability and
sensitivity of dentin
 Formation of calculus over sensitive tubules.
 Formation of intra tubular crystals from salivary mineral
 Intratubular crystals from dentinal fluid
 Progressive formation of peritubular dentin
 Invasion of tubules by bacteria
 Formation of caries crystals
 Formation of intratubular collagen plugs
 Leakage of plasma proteins up into tubules
 Formation of smear layer by brushing, tooth pick etc.
 Formation of irritation dentin
 Resin impregnation or covering
 Topical application of calcium hydroxide, sodium fluoride.

80.  The concept of tubule occlusion as a method of
dentin desensitization is logical extension of
Hydrodynamic theory.
But not all agents that decrease dentin sensitivity
do so by occluding dentinal tubules.

81.  This is because there are 2 mechanisms of
action of desensitizing agents.
 One involves blocking fluid movements by
occluding dental tubules.
The other involves blocking pulpal nerve activity
by altering the excitability of sensory nerves.

82. Fluorides
Sodium fluoride:
Clinical investigations have shown fluoride tooth
paste and concentration of fluoride solutions are
highly efficient especially with iontophoric
technique.
Fluoride was first proposed as a desensitizing
agent by Lukomsky in 1941.

83.  The use 2% sodium fluoride following
pretreatment with, 10% strontium chloride
was observed to have an additive effect in
reducing sensitivity (Gedalia et al 1978)
although sodium fluoride alone was still
significantly effective.

84. Stannous fluoride
 It has been demonstrated that aqueous solutions
of stannous fluoride in low concentration will
effectively control Dentin hypersensitivity (Miller et
al 1949).
 Two concepts have been put forward for the
mechanism of action of stannous fluoride.
That it acts as an enzyme to inactivate the
odontoblastic process. (Kutsches 1967).

85.  That it induces high mineral content which
creates a calcific barrier on the dentin surface
(Furseth 1970).
In view of the questionable importance of the
odontoblast process in pain transmission the
former suggested mode of action appears
unlikely.
As with sodium fluoride the formation of a calcific
barrier blocking tubular openings is perhaps the
more probable effect.

86. Strontium
 A possible explanation for the mechanism of
action of strontium ion in suppressing Dentin
Hypersensitivity had been advanced by
Gutentag.

87.  He proposed that because calcium has been
shown to establish excitable neural membranes
by modifying their permeability to Na+ and K+ the
effect was more pronounced and long lasting
with strontium.
As a result effects in Dentin Hypersensitivity
were attributed to a blockage of the organic
matrix of the tooth (Powlowska 1956).

88. Calcium hydroxide
 Calcium hydroxide has been a popular agent for
the treatment of dentin hypersensitivity for many
years particularly after root planing.
The exact mechanism of action is unknown, but
evidence suggests that it may block dentinal
tubules or promote peritubular dentin formation.
 Increasing the concentration of calcium ions
around nerve fibers can result in decreased nerve
excitability and thus suppresses nerve activity.

89. Potassium nitrate
 The desensitizing effectiveness of potassium
nitrate used in professional hands has been
reported by Hodosh in 1974 and Green et al
1977.

90.  Tarbet et al (1980) demonstrated for the first
time that the daily use of 5% potassium
nitrate delivered in low abrasive toothpaste
constituted a highly effective home therapy
regime for patients with Dentin
hypersensitivity.
Penetration of K+ ions into pulp, there by
sensory nerves are prevented to repolarise
after depolarization.

91. Formaldehyde
 The use of a dentifrice containing formalin was
reported by Fitzgerald (1956) who noted excellent
results in most of patients seeking relief from
cervical hypersensitivity.
However, Smith and Ash 1964 using as more
objective method of evaluating responses to
thermal and mechanical stimuli, found no
significant alteration of Hypersensitivity after use of
dentifrices containing formalin.

92. Resin and adhesive
 The rationale for the use being the possibility
of sealing dentinal tubules.
Results of studies were promising and have
demonstrated an immediate and long lasting
blockage of sensitivity on most surfaces for
between 1 month and 1 year.
Doereig and Jensen (1985) have used light
cure dentin bonding agents out of 12
participants with hypersensitivity, 74%
reported no pain three months after
placement of this agent.

93. Oxalates
 Oxalates have been used popularly as
desensitizing agent, they are relatively
inexpensive, easy to apply and well tolerated
by the patients.
6% Ferric oxalate 30% potassium oxalate and
3% Monohydrogen monopotassium oxalate
solutions are used as desensitizing agents.
The oxalate ions react with calcium ions in the
dentinal fluid to form insoluble calcium oxalate
crystals that are deposited within the tubules.

94. Corticosteroids
 Myjor and Ferseth have reported that application of
corticosteroids preparation to dentin caused
complete obliteration of tubules thus decreasing
dentin permeability.
 Bowers and Elliot concluded that 1.2% solution
containing 25% by weight the parachlorophenol,
25% metacrystal acetate, 49% gumcomphor, 1%
prednisolone was effective in treatment of
sensitivity due to incisal or occlusal fracture,
periodontal surgery, occlusal adjustment and post
scaling after root planing.

95. Iontophoresis
 Iontophoresis is a method of facilitating the transfer
of ions by means of an electrical potential into soft
or hard tissues of the body for therapeutic
purposes.
The object of fluoride Iontophoresis is to drive
fluoride ions more deeply into the tubules than can
not achieved with topical application of fluoride
alone.

96.  It is hypothesized that fluoride Iontophoresis
may increase the concentration and depths of
penetration of calcium fluoride there by
occluding the tubules and reducing the
conduction of hydrodynamically mediated
stimuli.

97.  Iontophoresis is not a simple procedure it involves
the placement of a negative electrode to dentin
and a positive electrode to the patients face or
forearm. Although iontophoresis has gained some
popularity, its effectiveness needs to be
demonstrated in well-controlled clinical studies,
these devices are expensive and somewhat
difficult to use.

98. Lasers
 Types used : Argon, Co2, Ho:YAG, Nd:YAG, erbium
YAG etc. These systems have become available
which are tailored specifically for dental surgery
using fibre optic delivery to a hand piece, smaller
than a conventional rotary dental instrument.
The availability of laser would potentially satisfy all
the requirements of a desensitizing agent.
 However question whether laser may be thermally
damaging to vital tooth structure has been raised by
some investigators.

99. Action
 Blocks the tubules probably
by fusion of crystals
(Hydroxyapatite), as low
intensity defocused beam is
used.
Side effects :
Tubules may act as optical
fibers causing damage to the
pulp

100. Burnishing
 Burnishing of dentin with tooth pick or orange
wood stick will create a partial smear layer on
dentin surface, there by occluding the orifices
of dentinal tubules.

101. At -home treatments
 Now, most desensitizing
toothpastes contain a
potassium salt such as
potassium nitrate, potassium
chloride or potassium citrate.

102. Toothpaste application
 Practitioners should educate patients on how
to use dentifrices and monitor their tooth
brushing techniques. Dentifrices should be
applied by tooth brushing. There is no
evidence to suggest that finger application of
the paste increases effectiveness. Many
patients habitually rinse their mouths with
water after tooth brushing. Rinsing with water
may cause the active agent to be diluted and
cleared from the mouth and, thus, reduce the
efficacy of the caries-reducing effect of
fluoride toothpaste.

103. Mouthwashes and chewing gums
 Studies have found that
mouthwashes containing
potassium nitrate and sodium
fluoride, potassium (Gillam DG,
Bulman) citrate or sodium
fluoride(Yates R, West N,) or a
mixture of fluorides can reduce
dentine sensitivity.

104.  In only one of these studies,
however, was the effect of the
active mouthwash significantly
greater than that of the control
product. Another study
(Krahwinkel T,) concluded that a
chewing gum containing
potassium chloride significantly
reduced dentine sensitivity but
the study did not include a control
group.

106. Conclusion
 Patients should be informed of all the possible steps
that may be necessary to eliminate their
hypersensitivity. The first step should be to identify
and eliminate the cause. The next is to rectify the
recession or seal the exposed dentinal tubules from
the oral environment.
 If the patient is thoroughly informed of all the
possible steps then they become a partner in the
treatment process, identifying for the dentist when
they want to proceed to the next step. This
minimizes frustration on the patient's part and
facilitates the process by which the dentist solves the
problem

107. References
 Endodontics –John. I .Ingle
 Orban’s oral histology and embryology
 Art and science of operative dentistry –sturdevant.
 Dental hygiene- Daniel and Harfst
 Periodontology 2000- vol-48. 2008
 J Clin Periodontol 2004;31:885–9

108. Thank you