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dentin hypersensitivity.ppt
1. Hypersensitivity theories ,causes and
management
Dr Huma Iftekhar
Assistant Professor
Department Of Conservative Dentistry & Endodontics
Amu,Aligarh
5. Clinicians see dentin hypersensitivity as
an exaggerated response to routine
stimulation the teeth.
Patients respond to dentin
hypersensitivity when drying a tooth with an
air spray or scratching a tooth with the tip of
an explorer.
Some patients complain of pain when
brushing their teeth or flossing
6. In normal function dentinal tubules sclerose
and become plugged. When dentin is cut or
abraded, the mineralized matrix produces
debris that spreads over the dentin surface
to form a smear layer.
Loss of this smear layer, and the unplugging
of the dentinal tubules, contributes to
dentinal hypersensitivity
7. Risk factors
Root surfaces exposed to the physical action of tooth brushing
with and without toothpaste can be predisposing factor in
removing smear layer and unplugging of dentinal tubules
Due to poor oral hygiene techniques leaving bacterial plaque
on tooth surfaces & acidic byproducts of plaque leads to
opening of dentinal tubules
Also excellent oral hygiene techniques with highly abrasive
dentifrice leads to dentinal exposure
Exposure of oral cavity to acids eg ingestion of chlorinated
water , bulimia and GI reflux disease and brushing
immediately after ingestion of acidic foods
8. causes
Dentinal hypersensitivity is due to
combination of factors
a) Enamel or cementum which covers
the dentinal surface may be removed
or denuded as a result of attrition,
abrasion or erosion
b) In some individuals cementum and
enamel which normally covers the
dentine do not meet and result in
dentine exposure as a result of
developmental anomaly
9. DH is more frequently encountered in
patients with periodontitis, and transient
hypersensitivity may occur after
periodontal procedures such as deep
scaling, root planing or gingival surgery.
Hypersensitivity also may occur after
tooth whitening and restorative
procedures.
10. In Bleaching chemicals such as carbamide
peroxide or hydrogen peroxide can rapidly
penetrate through enamel and into dentin
creating the symptoms of dentin
hypersensitivity.
In addition, many patients compound the
risk with over-treatment in their eagerness
for quick results a major contributing factor
11. The incidence of DH varies from 4 to 74%
These variations are likely due to
differences in the populations studied
and the methods of investigation .
Theincidence of DH is between
60 - 98 % in patients with periodontitis.
A majority of patients, however do not
seek treatment to desensitize their teeth
because they do not perceive DH to be a
severe oral health problem.
12. DISTRIBUTION
Affects patients mostly of 30-40 years
Affects women more commonly than men,
though sex difference is rarely significant
Most commonly affected are canine and first
premolar , followed by incisors and second
premolars (fisher at al 1992)
Buccal aspect of cervical area is the commonly
affected site
13. Histology of dentin
Dentin is a porous, mineralized connective tissue
with an organic matrix of collagenous proteins and
an inorganic component, hydroxylapatite.
Dentin contains a microscopic structure called
dentinal tubules, which are micro-canals that
radiate outward through the dentin from the pulp
cavity to the surface cemented border. These canals
have different configurations and diameters in
different teeth
14. For human dentin, one square millimetre of dentin
contains 30,000 tubules, depending on depth. Each
tubule contains a Tomes fibber (cytoplast cell
process) and an odontoblast that communicates
with the pulp. Within the dentinal tubules there are
two types of nerve fibers, myelinated (A delta
fibers) and unmyelinated (C-fibers)
The A delta-fibers are responsible for the sensation
of dentinal hypersensitivity.
16. Two phases of development of dentinal hypersensitivity
First dentin has to be exposed (lesion
localization)
Dentinal tubules must be
opened(lesion initiation)
most common clinical cause for exposed
dentinal tubules is gingival recession
17. Gingival recession is also implicated as
major contributing factor
CAUSES OF GINGIVAL RECESSION
Inadequate attached gingiva
Prominent roots
Tooth brush abrasion
Periodontal surgeries
Excessive tooth cleaning
Excessive tooth flossing
18. Abrasion and erosion may be
implicated here, but acid erosion
seems to be the predominant factor.
20. Theories of dentinal hypersensitivity
Odontoblastic receptor theory
Direct innervation theory
Hydrodynamic theory
21. Odontoblastic receptor theory
According to this theory, odontoblastic
processes are exposed on the dentine
surface and can be excited by a variety of
chemical and mechanical stimuli. As a
result of such stimulation
neurotransmitters are released and
impulses are transmitted towards the
nerve endings.
22. To date no neurotransmitters have
been found to be produced or released
by odontoblastic processes.
Drawback
23. Direct innervation theory
This theory postulates that direct
mechanical stimulation of exposed nerve
endings at the DEJ is responsible for
dentinal hypersensitivity
Major shortcoming of this theory is that
there is insufficient evidence to prove that
outer dentin that is most preone to be
sensitive is well innervated.
24. Drawback
This theory is still considered
theoretical with little solid evidence
to support it
25. Hydrodynamic theory
By far the most widely accepted theory
for dentinal hypersensitivity is the
hydrodynamic theory initially
proposed by Gysi and scientifically
validated by Barnstorm and co-
workers in 1967.
26. This theory postulates
that fluids within the
dentinal tubules are
disturbed either by
temperature, physical or
osmotic changes and
that these fluid changes
or movements stimulate
a baroreceptor which
leads to neural
discharge.
27. The sensations of hot and cold, for example, cause
fluid to move in opposite directions.
Heat causes expansion of the dentin tubule,
evoking a relatively slow inward movement of fluid
and is therefore not commonly identified as a
significant pain stimulus.
Cold stimuli cause contraction of the tubules
resulting in a rapid outward flow, and are generally
reported as most problematic for sufferers
28. The changes to
the dentinal surface
due to the physical
stimulus lead to
stimulation of the
A-type nerve fibers
surrounding the
odontoblasts.
It has been
reported that non-
sensitive teeth have
fewer exposed
dentinal tubules
than sensitive
teeth.
31. History, examination and diagnosis
A diagnosis of DH should be determined
only when the practitioner has considered
differential diagnoses after conducting a
methodical history and examination of the
patient
DH is defined as a transient tooth pain
arising in response to stimulation. The other
causes of transient tooth pain must be
excluded for a diagnosis of DH to be made.
32. Treatment of DH is a challenge
for both patients and dentist
Its difficult to measure/compare
different patient pain
Its difficult for the patient to change
their habit
33. Gingival recession with exposed root
surfaces
Facial
surface
Palatal
surface
Enamel loss with exposed dentin due to erosion
34. Treatment strategies
Plug the dentinal tubules
preventing fluid flow
Desensitize the nerve
make it less responsive to stimulation
35. Treatment
Treatments can be self-administered by the patient
at home or be applied by a dental professional in the
dental office.
At-home methods tend to be simple and
inexpensive and can treat simultaneously generalized
DH affecting many teeth.
In-office treatments are more complex and
generally target DH localized to one or a few teeth.
These various treatment options can be graded by
their complexity
36. TREATMENT CONT…
Evidence suggests that many professionals do not
consider the preventive aspects of DH.
The development of a sound treatment plan for
any oral health condition should consider causative
factors.
Similarly, any treatment plan for DH should
include identifying and eliminating predisposing
etiologic factors such as endogenous or exogenous
acids and toothbrush trauma.
37. At home treatments
Desensitizing toothpastes/dentifrices.
The first desensitizing toothpastes to appear on the
market claimed either to occlude dentinal tubules
(those that contained strontium salts and fluorides)
or destroy vital elements within the tubules (those
that contained formaldehyde).
Now, most desensitizing toothpastes contain a
potassium salt such as potassium nitrate, potassium
chloride or potassium citrate
38. Potassium salts:
Toothpastes containing potassium nitrate have
been used since 1980. Since then, pastes
containing potassium chloride or potassium
citrate have been made available.
Potassium ions are thought to diffuse along
dentinal tubules and decrease the
excitability of intradental nerves by altering
their membrane potential
39. Toothpaste application. Practitioners
should educate patients on how to use
dentifrices and monitor their toothbrushing
techniques
There is no evidence to suggest that finger
application of the paste increases its
effectiveness
40. Studies have found that mouthwashes containing
potassium nitrate and sodium fluoride, potassium
citrate or sodium fluoride or a mixture of fluorides
can reduce DH.
Another study concluded that a chewing gum
containing potassium chloride significantly reduced
DH
DH severity should be reassessed two to four
weeks after commencement of treatment to
determine the effectiveness of the first level of
desensitizing treatment If at-home care fails to
reduce DH compared with baseline levels, the next
level of treatment, an in-office method should be
started.
41. In office treatment
Desensitizing agents intended for at-home use by
patients generally are simple to administer. Dental
professionals can deliver a wider range of more
complex and more potent desensitizing treatment.
Topically applied desensitizing agents. Before
the discovery of local anesthetics, dentists would
use toxic chemicals such as silver nitrate, zinc
chloride, potash and arsenic compounds to obtund
dentin. Now, less toxic materials are used for
desensitization
42. Fluoride Fluorides such as sodium
fluoride and stannous fluoride can reduce
dentin sensitivity. Fluorides decrease the
permeability of dentin in vitro, possibly by
precipitation of insoluble calcium fluoride
within the tubules.
43. Potassium nitrate Potassium nitrate,
which usually is applied via a desensitizing
toothpaste, also can reduce dentin
sensitivity when applied topically in an
aqueous solution or an adhesive gel.
44. Oxalate In 1981, Greenhill and Pashley reported
that 30 percent potassium oxalate caused 98%
reduction in dentin permeability in vitro. Since
then, numerous oxalate-based desensitizing
products have become available
They occlude tubules and reduces DH
Some studies indicated that oxalates significantly
reduced sensitivity, while others reported that the
effects of oxalate did not differ significantly from
those of a placebo.
45. Calcium phosphates
Calcium phosphates may reduce dentin
sensitivity effectively. Calcium phosphates
occlude dentinal tubules in vitro and
decreases dentin permeability
46. Adhesives and resins Because many topical
desensitizing agents do not adhere to the dentin
surface, their effects are temporary. Stronger and
more adhesive materials offer improved and longer-
lasting desensitization.
In the 1970s, Brannstrom and colleagues suggested
using resin impregnation to desensitize dentin.
Current DH treatments involve using adhesives,
including varnishes, bonding agents and restorative
materials.
47. Ionto-phoresis
This procedure uses electricity to enhance
diffusion of ions into the tissues. Dental
iontophoresis is used most often in
conjunction with fluoride pastes or solutions
and reportedly reduces DH.
48. Lasers
The effectiveness of lasers for treating DH varies
from 5 to 100 percent, depending on the type of
laser and the treatment parameters. Studies have
reported that the neodymium:yttrium-aluminum-
garnet (YAG) laser, the erbium:YAG laser and
galium-aluminium-arsenidelow level laser all
reduce DH
Lasers represent a more expensive and complex
treatment modality
49. Currently, the mechanism of the laser treatment in
treating DH is unclear although according to
Pashley it may be through the coagulation and
precipitation of plasma proteins in dentinal fluid or
through alteration of the intradental nerve activity
McCarthy et al also suggested that reduction of DH
may be as a result of creating an altered surface
layer on the root physically occluding the tubules
(smear layer creation)
50. Miscellaneous treatments
A large number of reports support alternative
approaches for tooth desensitization. Although
these reports are not truly evidence-based, they may
apply to some clinical situations. For example,
periodontal surgery involving coronally positioned
flaps reportedly eliminates DH in extensively
exposed root dentin. If the DH is associated with an
abfraction lesion, occlusal adjustment may be
effective.
51. Initiate treatment of dentin hypersensitivity
Educate patient to risk factors
Recommendations for removal of excessive dietry acids
Recommendations for tooth brushing before eating
Less frequent and less aggressive tooth brushing
Follow up
Do dentin hypersensitivity continue
No No
further
treatme
nt
yes
Apply desensitizing agents in considerations
with cost effectiveness and techniques
52. Desensitizing tooth
pastes
Topical in office agents
Does hypersensitivity continue
Follow up
Mucogingival surgery
Restoration
Pulpal treatment
No
Maintain current treatment
Review regularly
Review diagnosis
Continue DH treatment
Continue patient education
yes
53. Suggestions for patients:
• Avoid gingival recession due to poor plaque
removal
• Avoid using large amounts of dentifrice during
brushing
• Avoid medium or hard bristle toothbrushes
• Avoid brushing teeth immediately after the
ingestion of acidic foods
• Avoid over brushing with excessive pressure or
for an extended period of time
• Avoid excessive flossing or improper use of other
inter proximal cleaning devices
• Avoid ‘picking’ or scratching at the gumline or
using toothpicks inappropriately.
54. Suggestions for professionals:
• Avoid over-instrumenting the root
surfaces during scaling and root planing ,
particularly in the cervical area of the
tooth
• Avoid over-polishing exposed dentin
during stain removal
• Avoid violating the biologic width
during restoration placement as this may
cause recession
• Avoid burning the gingival tissues
during in-office bleaching and advise
patients to be careful when using home
bleaching products.
55. CONCLUSION
Dental professionals need to understand the causes
of dentin hypersensitivity. A patient should be
evaluated based upon risk factors that may be
present.
Once a diagnosis has been made and the factors
have been identified a treatment plan can be
outlined to the patient for the treatment of dentin
hypersensitivity.
As part of the routine dental examination ,Dental
professionals should include in their patient
questions during every recall appointment whether
there are any sensitive teeth.
56. Depending on severity of the condition, clinical
management of dentin hypersensitivity may include
both in-office and self-applied at-home therapies.
In most circumstances, the least invasive, most
cost-effective treatment is the recommendation.
For individual teeth that are hypersensitive, an in-
office treatment can provide the patient with pain
relief.
Once a tooth is predisposed to dentin
hypersensitivity it needs to be re evaluated