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2. DENTINAL HYPERSENSITIVITY
Presented by,
Dr. Farah naaz

3. contents
• Introduction
• History
• Definition
• Epidemiology
• Relevant anatomy
• Etiopathogenesis
• Theories of DHS
• Management of DHS
• Treatment
• Conclussion
• References

4. Introduction

5. History
• 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)

6. Definition
• “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).

7. • 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).

8. Prevalence
• The prevalence distribution and appearance of
the disease have been reported differently in
different studies.
• These differences are due to the differences in
populations, habits, dietaries, and methods of
investigation

9. Epidemiology
FEMALE
CANINE
PREMOLAR
Affects the buccal
aspect of cervical
area
Age group
30-40

10. Etiopathogenesis
• Dentin is sensitive to stimuli due to the lesion
extension of odontoblastic process and
formation of dentin-pulp complex

11. Dentin-pulp complex
• Odontoblast and its processes
• Dentinal tubules
• Sclerosed dentin
• Neurovascular bundle

12. Odontoblast and its processes
• ectomesenchymal differentiation
• the dental papilla
• formation of dentin.
• extend into the dentin.
• more in the coronal dentin
• entire length of the tubule

13. Dentinal tubules
• channels via which the odontoblastic processes
traverse.
• the entire length
• diffusion of nutrients
• sigmoid shape
• Straight
• course of the odontoblast.
• majorly in the root dentin

14. Sclerosed dentin
• continuous deposition of peritubular dentin.
• Mineral deposition within the tubules without
dentin formation
• mineralisation of the odontoblastic processes
• These ultimately reduce permeability of the
dentin

15. Neurovascular supply
• A plexus( of Raschkow) of nerve exist in the
coronal part of the crown.
• short distance into the dentinal tubules hence,
called intra-tubular nerves.
• myelinated (A-fibers) and unmyelinated (C-
fibers).

16. Pathogenesis
• Two phases are involved in the pathogenesis
of dentin hypersensitivity;
• Lesion localisation
• Lesion initiation

17. Lesion localisation
• Gingival recession exposing dentin
• Exposer of radicular dentin.
• apical to the cement–enamel junction
• which is then rapidly lost.

18. causes
• thin alveolar cortex,
• Periodontitis and management of the condition
• dehiscence and fenestration of alveolar bone,
• self-inflicted injury
• prosthodontics treatment

19. • not age-related.
• horizontal bone loss due to osteoporosis .
• healthy and diseased periodontium and high
and low standards of oral hygiene

20. • Periodontal disease and periodontal treatment
result in compensatory remodelling of the
supporting tissues around the tooth after tissue
destruction, leading to an apical shift of the
soft tissue margin and often results in root
sensitivity, occurring in approximately half of
patients following scaling and root planning

21. • Gunnsolley et al. demonstrating a strong
association between smoking and both
attachment loss and recession in subjects who
have minimal or no periodontal disease.

22. • Rugg-Gunn et al. showed the brushing cycle
was in the order of about 1 min; however, the
tooth surfaces did not receive equal brushing
time; the first site receiving the most attention
and the last the least.

23. • Loss of hard tissue exposing dentin
• loss of hard tissue exposing dentin. Above the
cemental–enamel junction (CEJ),
• development of non-carious cervical lesions
(NCCL) are important factors for dentin
exposure at the gingival margin

24. • Aubry et al. evaluated in a recent study
archaeological samples from France and found
no NCCLs in 3,927 teeth from 259 individuals.
• reported that the risk of NCCL was higher for
women and increased with age. Premolars
were the most affected tooth type.

25. causes
• abrasion, erosion and possibly microfractures
(abfraction).
• Wood et al. concluded that an abfraction lesion
is more likely due to abrasion and erosion
only.
• Abrasion, the physical wear as a result of
mechanical processes

26. Lesion Initiation
• Toothpaste detergents also chemically
“abrade” dentin probably by dissolution of the
collagen matrix

27. • Erosion is defined as chemical wear as the
result of extrinsic or intrinsic acid or chelators
acting on plaque-free tooth surfaces

28. extrinsic and intrinsic causes
• acidic food and beverages
• gastric juices, possibly caused by, for example,
reflux disease, eating disorders, chronic
alcoholism and pregnancy.

29. • Abfraction (fatigue wear) means physical wear
as a result tensile or shear stress in the
cemento–enamel region provoking
microfractures in enamel and dentin.

30. • Grippo and Simring stated that toothpaste
abrasion in a corrosive (erosive) environment
increases loss of tooth structure due to tensile
forces concentrated at the cervical area of
teeth.

31. • It has also been postulated that lack of Hunter
Schreger-bands in the cervical region
contributes to the development of abfraction
lesions

32. • V-shaped lesion develop as a result of erosion
and abrasion rather than from abfraction.
• Sharply defined margins could be caused by
abfraction and/or abrasion due to excessive
tooth brushing,
• dish-shaped broader and shallow lesions could
be caused by erosion.

33. • Attrition may play a role in some cases of
occlusal dentin hypersensitivity, due to
parafunctional habits like bruxism

34. ENAMEL
LOSS

35. Theories
• Four theories :
• the transducer,
• Direct Neural
• Odontoblastic and
• Hydrodynamic theories.

36. Transducer Theory
stimulus
impulse transmitted to
the nerve endings in
the inner dentin.
no neurotransmitter
vesicles in the
odontoblast process to
facilitate the synapse

37. Odontoblastic theory
The theory assumed that odontoblast
extend to the periphery.
Stimuli
Excite the process or body of
odontoblast.
The membrane of odontoblasts come
into close apposition with that of the
nerve ending in the pulp or in D.T.
The odontoblast transmets the
excitation of these nerve endings

38. Direct Neural theory
Activation to initial excitation
of these nerve ending in
dentinal tubules
nerve signals are conducted
along the parent primary
afferent nerve fibers.
Dental nerve branch.
brain

39. Hydrodynamic Theory
• Fish in 1927s observed the interstitial fluid of
the dentin and pulp, referring to it as the
"dental lymph." He postulated that the flow of
this fluid could take place in either an outward
or inward direction depending on the pressure
variations in the surrounding tissue.

40. • According to the hydrodynamic theory, as put
forth by Brannstrom and Astrom," a
dentinalgia results from a stimulus causing
minute changes in the fluid movement within
the dentinal tubules.

41. • This may subsequently deform the odontoblast
or its process and hence cause an elicitation of
pain via the intimately associated "mechano-
receptor-like" nerve endings.

42. Hydrodynamic theory
• Stimuli
• Displacement of fluid that
exists in the dentinal
tubules
• Activates the nerve
endings present in the
dentin or pulp

44. Management of DHS
• EXAMINATION
• INVESTIGATION
• DIAGNOSIS
• TREATMENT
• TRADITIONAL METHOD
• CURRENT TRENDS IN TREATMENT

45. EXAMINATION
• Evidence of tooth wear lesion (attrition,
abrasion, erosion)
• Gingival recession

47. 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;

48. • Air jet
• Cold water jet
• Electrical devices
• Dental explorer
• Periodontal probe
• Radiographs
• Caries diagnostic devices
• Percussion testing
• Assessment of occlusion
• Bite stress tests

50. 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

51. Prevention Factors
• proper tooth brushing with technique,
• highly abrasive tooth powder or pastes
• brushing with excessive pressure
• Avoid brushing immediately after taking
acidic drinks
• polishing exposed dentin

52. • Avoid over-instrumenting the root surfaces
during scaling and root planing, particularly in
the cervical area of the tooth.
• Avoid violating the biologic width during
restoration placement, as this may cause
recession.
• .

53. • 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

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

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

56. CLASSIFICATION OF
DESENSITIZING AGENTS
I. Mode of administration
At home desensitizing agents
In-office treatment
II. On the basis of mechanism of action
Nerve desensitization
• Potassium nitrate

57. Protein precipitation
• Gluteraldehyde
• Silver nitrate
• Zinc chloride
• Strontium chloride hexahydrate
Plugging dentinal tubules
• Sodium fluoride
• Stannous fluoride
• Strontium chloride
• Potassium oxalate

58. • Calcium phosphate
• Calcium carbonate
• Bio active glasses (SiO2–P2O5–CaO–Na2O)
Dentine adhesive sealers
• Fluoride varnishes
• Oxalic acid and resin
• Glass ionomer cements
• Composites
• Dentin bonding agents

59. Lasers
• Neodymium:yttrium aluminum garnet (Nd–
YAG) laser
• GaAlAs (galium–aluminium–arsenide laser)
• Erbium–YAG laser
Homeopathic medication
• Propolis

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

61. Traditional treatment methods
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.

62. • 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.

63. • 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

64. 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.

65. 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.

66. 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

67. 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

68. Anti-inflammatory
• Topical application 0.5% solution of
prednisolone on exposed root surface will
induce remineralisation leading to tubular
occlusion.

69. • 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.

71. Current trends in treatment of
DHS
• Arginine-base product Pro-Arginine™
• Laser
• Bio-glass
• Casein phosphopeptide
• nanodentistry

72. 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

73. • 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.
• phosphate, calcium and carbonate

74. Occlusion of dentinal tubules by
the Pro-Argin technology

75. • 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).

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

77. 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.

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

79. 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.

80. 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.

81. • 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).
•

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

83. • 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.

84. 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.

85. References
• Carranza 10th edition
• Jan lindhe 4th edition
• University of Washington, Seattle, WA,
Private Practice Dentist and Northwest
PRECEDENT Dentist-Investigator, Albany,
OR, Private Practice Dentist and Northwest
PRECEDENT Dentist-Investigator, Spokane,
• Orban’s twelth edition.

86. • Christian R. Gernhardt. How valid and
applicable are current diagnostic criteria and
assessment methods for dentin
hypersensitivity? An overview. Clin Oral
Invest (2013) 17.
• Mikkilineni M, Rao AS, Tummala M, Elkanti
S. Nanodentistry: New buzz in dentistry. Eur J
Gen Dent 2013;2:109-13

88. Gate Control Theory and
Vibration
• When the dentin is irritated, for example, by
cavity preparation, all of the pulpal nerves
become activated from the vibrations.
• The larger myelinated fibers may
accommodate to the sensations.
• The smaller C-fibers may tend to be
maintained and not adjust to the stimulus.

90. • Thus, as the low intensity "pain gates" from
the larger fibers are closed,
• the high-intensity "pain gates" from the
smaller fibers are enhanced.
• "Pain gates" may be opened by some stimuli,
such as anxiety, and may be closed by
distracting stimuli such as "audio-analgesia"