INFORMATIVE

1. Dr Aghimien osaronse
University of Benin School of Dentistry. Nigeria
DENTIN HYPERSENSITIVITY AND
CURRENT TRENDS IN
MANAGEMENT

2. outline
Introduction
Definition of dentin hypersensitivity DHS
Epidemiology
Relevant anatomy: dentin-pulp complex
Odontoblast and its processes
Dentinal tubules
Sclerosed dentin
Neurovascular bundle
Etiopathogenesis
lesion localisation
lesion initiation

3. Theories of DHS
neural
nerve transduction
hydrodynamic
Management of DHS
o diagnosis;
history
examination
differential diagnosis
investigation/tools
definitive diagnosis
o prevention/removal of predisposing factors

4. o Treatment
classification of treatment options
traditional method
current trends in treatment
• Arginine-base product Pro-Arginine™
• Laser
• Bio-glass
• Casein phosphopeptide
• nanodentistry
CONCLUSSION
REFERENCES

5. introduction
Dentin hypersensitivity is said to be one of most
painful and chronic dental condition. Previously
described as an enigma because it was poorly
understood. It has a higher prevalence among
periodontally compromised patients, 60%–98%
(Von Troil et al, 2002).

7. Definition
As defined by an international workshop on DH:
“Dentine hypersensitivity is characterized by short,
sharp pain arising from exposed dentine in response
to stimuli, typically thermal, evaporative, tactile,
osmotic or chemical and which cannot be ascribed to
any other dental defect or pathology”( Holland et al,
1997).

8. • Dentine Hypersensitivity is a transient
tooth pain, characterized by a short,
sharp pain arising from exposed
dentine in response to a stimulus that
cannot be attributed to any other form
of dental defect or pathology(Andy M,
2002).

9. Epidemiology
It occurs in patients 30 to 40 years old, but
it can occur in patients significantly
younger or older.
 female are more commonly affected than
males.
Canines and premolars are more affected

10. OOOCH….

11. Dentin-pulp complex
The close relation (embryologically, histologically and
functionally) between them warrant their discussion as a
unit.
Relevant anatomic consideration as it relates to this
discussion would be considered. These include;
Odontoblast and its processes
Dentinal tubules
Sclerosed dentin
Neurovascular bundle

12. Odontoblast and its processes
They are formed from the ectomesenchymal
differentiation of cells of the dental papilla
and are responsible for the formation of
dentin.
Their processes extend into the dentin.
They are more in the coronal dentin than the
root dentin
The processes tend to traverse the entire
length of the tubule

13. Dentinal tubules
They are channels via which the odontoblastic
processes traverse.
They extend the entire length of the dentin
permitting diffusion of nutrients through out the
dentin
They run a sigmoid shape in the coronal dentin but
straight in the root dentin, this is determine by the
course of the odontoblast.
Dentinal tubules branch majorly in the root dentin
than in coronal dentin.

14. Dentinal fluid
The odontoblastic processes are surrounded by
dentinal fluid inside the tubules.
The dentinal fluid forms around 22% of total
volume of dentin.
It is an ultrafiltrate of blood from the pulp via
dentinal tubules and forms a communication
medium between the pulp (via the odontoblastic
layer) and outer regions of the dentin.

15. Sclerosed dentin
Results from
continuous deposition of peritubular
dentin.
Mineral deposition within the tubules
without dentin formation
mineralisation of the odontoblastic
processes and intra-tubular collagen fibrils.
These ultimately reduce permeability of
the dentin thereby prolonging the pulp
vitality

16. Neurovascular supply
A plexus( of Raschkow) of nerve exist in
the coronal part of the crown. No plexus
exist in the root area as they are supply by
ascending branched.
 the nerve further extend for a short
distance into the dentinal tubules hence,
called intra-tubular nerves.

17. Within the dentinal tubules there are two
types of nerve fibers, myelinated (A-fibers)
and unmyelinated (C-fibers). The A-fibers are
responsible for the sensation of dentinal
hypersensitivity, perceived as pain in response
to all stimuli.
 it is said that the density of the intra-tubular
nerve varies as high as one for every two
tubules

18. Etiopathogenesis
Regardless of the cause it is important to
state that apart from been expose, the
dentinal tubule should be patent for
sensitivity to occur.
Two phases are involved in the
pathogenesis of dentin hypersensitivity;
Lesion localisation
Lesion initiation

19. Lesion localisation
This involves the exposure of the dentin a as result
of various mechanical or chemical processes;
1. Attrition due to bruxism
2. Erosion
3. Abfraction
4. Abrasion
5. Pocket reduction surgery
6. Tooth preparation for crown
7. Excessive flossing
8. Secondary to periodontal diseases

20. This involves the actual mechanism that results
in the sensitivity felt by the patient. It is on this
ground that different theories have been
postulated as to how the response is brought
about.
1. Direct innervation/neural theory
2. Odontoblastic receptor theory
3. Hydrodynamic/fluid movement
theory/Brannstrom 1964

21. Neural theory
It explains that the nerve is the primary receptor
that excites the action potential.
But;
Newly erupted teeth are sensitive even when the
plexus of nerves and intra-tubular nerve are not
yet establish
Is the outer layer of the dentin directly
innervated?

22. Odontoblastic receptor theory
Odontoblast was postulated as the receptor. It was assume
that the odontoblast is of same neural crest origin as the
nerve hence, it should retain the ability to transduce and
propagate impulses.
But;
No organise junction exist between the axon and the
odontoblastic process
Membrane potential of the odontoblastic process is too
low to permit transduction

23. Consistent with the odontoblastic theory
are;
Odontoblastic process traverse the entire
length of the tubule
There is the possibility of gap junction
between the odontoblast.

24. Hydrodynamic theory
Fluid movement within the tubule distort the
pulpal environment and is sense by the free
nerve ending of the Raschkow plexus. The
wider tubules increase the fluid movement and
thus the pain response.
The profuse branching of the tubules at the
dentin-enamel junction explains the increase
sensitivity felt.
The response of pulpal nerves, mainly A delta
intra-dentinal afferent fibers, depends upon the
pressure applied, i.e. intensity of stimuli.

25. It has been noted that stimuli which tend to
move the fluid away from the pulp–dentine
complex produce more pain.
These stimuli include cooling, drying,
evaporation and application of hypertonic
chemical substances.

27. Management of DHS
DIAGNOSIS;
HISTORY
EXAMINATION
INVESTIGATION
TREATMENT
TRADITIONAL METHOD
CURRENT TRENDS IN TREATMENT

28. IMPORTANT STEPS TO FOLLOW
1. Correct diagnosis of dentin hypersensitivity including
a patient’s history screening and a brief clinical
examination
2. Identification of etiologic and predisposing factors
3. Differential diagnosis, to exclude all other dental
conditions
4. If present, treatment of all conditions with symptoms
similar to dentin hypersensitivity
5. Removal or minimization of etiologic and
predisposing factors

29. Occur in females than males; this is in
keeping with their dietary practices
Middle age group of 30-40 years are
commonly affected
Pain is described as sharp, short lasting
irrespective of the stimuli and usually of
chronic duration History of excessive tooth
brushing, flossing and oral habit should be
checked.

30. Past dental treatment like vital tooth
bleaching, periodontal procedures 54%–
55% (Howard E. S, 2009).
Medical condition that results in tooth
wear lesion bulemics and gastrointestinal
reflux disease
Social practices involving intake of acidic
foods and drinks(quantity and frequency)

31. EXAMINATION
Evidence of tooth wear lesion (attrition, abrasion,
erosion)
Gingival recession

32. Exposed root surfaces

33. Recession and attrition

34. investigations
• It is important to note that DHS is a diagnosis of
exclusion hence, effort should be made to rule out other
conditions that would mimic this presentation. The
following diagnostic tools could help;
1. Air jet
2. Cold water jet
3. Electrical devices
4. Dental explorer
5. Periodontal probe
6. Radiographs
7. Caries diagnostic devices
8. Percussion testing
9. Assessment of occlusion
10. Bite stress tests

35. Differentials
Bite stress test, transillumination could help diagnosis a
fracture
Percussion test could exclude pulpitis and periodontal
involvement
Radiographs or other caries detecting devices exclude
caries(root)
Occlusion assessment could rule out traumatic occlusion
from high restoration

36. Differential diagnosis
Cracked tooth syndrome
Fractured restorations
Restorations left in traumatic occlusion
Chipped teeth
Dental caries, root caries
Postoperative sensitivity
Pulpal response to restorative treatment or
certain materials
Marginal leakage of restorations
Pulpitis, pulpal status
Vital bleaching procedures

37. Definitive diagnosis
A simple clinical method of diagnosing
DHS includes a jet of air or using an
exploratory probe on the exposed
dentin, in a mesio-distal direction,

38. Prevention/eliminate
predisposing factors
1) Ensure proper toothbrush consistency,
ensure proper brushing technique, highly
abrasive tooth powder or pastes should be
avoided.
2) Avoid over-brushing with excessive
pressure or for an extended period of time or
excessive flossing
3) Avoid brushing immediately after taking
acidic drinks
4) Avoid over-polishing exposed dentin during
stain removal.

39. Prevention cont’d
5) Avoid over-instrumenting the root
surfaces during scaling and root planing,
particularly in the cervical area of the tooth.
6) Avoid violating the biologic width during
restoration placement, as this may cause
recession.
7) Patient with gastrointestinal reflux disease
should be properly managed by the
physician and fabrication of occlusal splint
to cover the affected areas, to prevent their
contact with the acids.

40. Treatment of DHS
• Classification of treatment options
• Ideal properties of a desensitizing
agent
• Traditional methods of treatment
• Current trends in treatment

41. Two main group of products are
available;
To occlude or plug the tubules
Nerve desensitisers

42. CLASSIFICATION OF DESENSITIZING AGENTS
1. Base on mode of administration:
at-home
in-office
2. Base on mode of action
Nerve desensitization
Protein precipitation
Plugging dentinal tubules
Dentine adhesive sealers
Lasers
Homeopathic medication
3.’’ Others’’
gingival graft

43. 1. Mode of administration
At home desensitizing agents
In-office treatment
2. On the basis of mechanism of action
A. Nerve desensitization
Potassium nitrate
B. Protein precipitation
Gluteraldehyde
Silver nitrate
Zinc chloride
Strontium chloride hexahydrate

44. C. Plugging dentinal tubules
STROTIUM ACETATE…..SENSODYNE RAPID ACTION
Sodium fluoride
Stannous fluoride
Potassium oxalate
Calcium phosphate
Calcium carbonate
Bio active glasses (SiO –P O –CaO–Na O)
D. Dentine adhesive sealers
Fluoride varnishes
Oxalic acid and resin
Glass ionomer cements
Composites
Dentin bonding agents

45. E. Periodontal soft tissue grafting.
F. Anti-inflammatory
corticosteroids
G. Crown placement and restorative materials
H. Lasers
 Neodymium:yttrium aluminum garnet (Nd-
YAG) laser
 GaAlAs (galium-aluminium-arsenide laser)
 Erbium-YAG laser
 He:Ne laser
I. Homeopathic medication
Propolis

46. Ideal properties of a desensitizing agent
(Grossman et al, 1965)
1. Rapidly acting with long-term effects,
2. non-irritant to pulp,
3. painless
4. easy to apply, and
5. Should not stain the tooth.

47. Traditional treatment
methods
A. Adhesive composite resin, GIC and dentin
bonding agents;
 Indicated when the exposed sensitive root
surface has surface loss due to abrasion, erosion
and/or abfraction leaving a notching of the root.
 The adhesive resins can seal the dentinal
tubules effectively by forming a hybrid layer.
 Newer bonding agents modify the smear layer
and incorporate it into the hybrid layer.

48.  Hydroxyethyl methacrylate (HEMA),
forms deep resinous tags and occludes the
dentinal tubules. 5% of Gluteraldehyde
could be added to 35% of HEMA causing
coagulation of the proteins inside the
dentinal tubules

49. B. Fluoride varnish:(e.g. sodium
fluoride, stannous fluoride)
Fluorides decrease the dentinal
permeability by precipitation of calcium
fluoride crystals inside the dentinal tubules.
5% sodium fluoride varnish painted over
exposed root surfaces is effective treatment
of DHS.

50. C. oxalate.
 precipitates and occlude the open dentinal
tubules.
 Oxalate reacts with the calcium ions of dentine
and forms calcium oxalate crystals inside the
dentinal tubules as well as on the dentinal surface.
 Topical application of 3% potassium oxalate can
reduce DHS post periodontal surgery.
 Avoid using with tray for a long time as it can
cause gastric irritation.

51. D. desensitizing dentifrices.
 desensitizing ingredient in toothpastes is potassium
nitrate.
 It acts by penetrating the A-fibres of the nerves
reducing its excitabilty.
 for a potassium nitrate toothpaste it must contain
5% potassium nitrate.
It takes up to two weeks to show any effectiveness

52. Others.
Gingival graft;
This is indicated when recession is progressive,
aesthetic is a major concern and when the treatment is
not responding to convention treatment, including
coronally reposition flaps, lateral sliding graft, free
gingival and connective tissue graft
Anti-inflammatory
Topical application 0.5% solution of prednisolone
on exposed root surface will induce remineralisation
leading to tubular occlusion.

53. Fluoride Iontophoresis can also be
used, a technique that utilizes a low galvanic
current to accelerate ionic exchanges and
precipitation of insoluble calcium with
fluoride gels to occlude the open tubules.

54. Current trends in treatment of
DHS
a. Arginine-base product Pro-
Arginine™
b. Laser
c. Bio-glass
d. Casein phosphopeptide
e. nanodentistry

55. Arginine-base product
Utilizes arginine, an amino acid; bicarbonate, a pH
buffer; and calcium carbonate, a source of calcium.
Mechanism of action is based upon the role that saliva
plays in naturally reducing dentinal hypersensitivity
Arginine at a neutral pH is positively charged and bind
to the negatively charged tubules thereby attracting a
calcium-rich layer from the saliva to infiltrate and block
the dentinal tubules.
The dentin plug contained high amounts of phosphate,
calcium and carbonate and also significantly reduced the
flow of dentinal fluid in the tubules.

56. A slow speed hand piece is use to apply the paste
on the exposed tubule.
 It provides instant relief from discomfort that
lasted 4 weeks after a single application with
71.7% reduction in sensitivity measured by air-
blast and an 84.2% reduction by the “scratch”
test immediately following application
(Kleinberg I.S, 2002).
Significant relieve is experienced when applied
before dental procedure.

57. Occlusion of dentinal tubules by
the Pro-Argin™ technology

58. Laser
MECHANISM OF ACTION
a. Occlusion of dentinal tubules e.g. Nd-YAG
b. Alteration of nerve transmission. GaAlAs
c. Coagulation of proteins within the dentinal tubules
and blockage of fluid movement.
d. deposition of insoluble salts into the exposed
dentinal tubules: Er: YAG laser
LASER can be carried out alone or in association with
surface treatment.

59. Casein phosphopeptide–amorphous
calcium phosphate CCP-ACP
The phosphoseryl sequences within the
casein phosphopeptide get attached to the
ACP which maintain a supersaturated
solution of bioavailable calcium and
phosphates.
The stabilised CCP-ACP is able to
remineralised subsurface enamel lesion which
is also important in treatment of dentine
sensitivity.

60. ACP can be used to control bleaching
sensitivity when incorporated into
bleaching gels.
Direct application on teeth by brushing
could relieve sensitivity.

61. Bioglass (NovaMin)
e.g. calcium sodium phosphosilicate bioactive
glass e.g. NovaMinR
Has silica as the main component, acting as a
nucleation site for the precipitation of calcium
and phosphate.
Upon its application an apatite layer is formed
which occlude the tubule.
Relieve should be expected after 6 weeks of
home used.

62. THE PLACE OF
NANODENTISTRY
Nanodentistry will make possible the
maintenance of comprehensive oral health by
employing nanomaterials, biotechnology,
including tissue engineering, and ultimately
dental nanorobotics(robots at the nanoscale.).
These nanorobots will be able to bring about a
variety of functions as they exert precise control
over matter.

63. In the area dentine sensitivity nanorobots
could selectively and precisely occlude
selected tubules in minutes, offering patients
a quick and permanent cure (Mallanagouda
et al., 2008; Jhaver, 2005; Freitas, 2005).
isn’t this wonderful?

64. Dentin hypersensitivity is always a diagnosis
of exclusion, it is confirmed only after all
possible other conditions have been
diagnostically eliminated

65. The importance of implementing
preventative strategies in identifying and
eliminating predisposing factors in
particularly erosive factors (e.g. dietary
acids) cannot be ignored if you as the
practitioner is going to treat this
troublesome, stubborn and recalcitrant
clinical condition successfully.

66. Conclusion
Depending on the severity of dentinal
hypersensitivity, clinical management may
include both in-office and self-applied at-
home therapies, including recent and novel
technologies that have been introduced.
The least invasive, most cost-effective
treatment is the use of an effective
desensitizing toothpaste.

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