Dentinal hyper sensitivity / /certified fixed orthodontic courses by Indian dental academy

INDIAN DENTAL ACADEMY
Leader in Continuing Dental Education
www.indiandentalacademy.com


Introduction

“ An enigma, because it was frequently
encountered yet poorly understood”
Johnson. R.H 1982

“Not the enigma it once was, there still
much to be discovered”
Martin Addy 2002

contents
• HISTORY
• ODONTOBLAST – DENTIN COMPLEX
• INNERVATION OF DENTIN
• DEFINITION
• DIAGNOSIS
• STRATIGIES for MANAGEMENT
• TREATMENT MODALITIES
• CONCLUSION

HISTORICAL PERSPECTIVE
• Tomes 1856, “The dentine tubes are constantly filled by fluid,
and the pulp at their inner extremities feels pressure made upon the
fluid at the exposed ends of the tubes”

• Whit (1870) “ the pain arising from the contact with sensitive
dentine cannot be conveyed by direct contact with the ultimate fibres
of the dentine nerve, but through some intermediary agent.”

• Beers (1893) “ There is no doubt, but sensitiveness is due to
the presence of the tube contents, whether nerve fibres enter or not.
Dentine is nothing but [a] passive matrix, in which lie the sources of
sensation.”


• Gysi, 1900 introduced hydrodynamic concept.

• Hopewell-Smith (1923) “Dentine is not live, nor
is it dead like enamel, it serves as an intermediate tissue
between the external enamel and the internal living pulp,
it does not generate sensations but transmits through its
tubes impulses of various kinds to the pulp.”

• Fish (1927) “there is a lymphatic fluid in the dentinal
tubule and that tubules terminate with a lymphatic
plexus, providing a continuous lymphatic flow through
the various tubules and the pulp.”


• Orban (1940) “displacement of odontoblasts…. and
pulp cells into the tubule”

• Ivory & Kramer (1952) showed aspiration of
odontoblasts

• Anderson (1958) “receptors responsible for pain
sensations were in the pulp, rather than the dentine.”

• Brännström’s (1966) hydrodynamic explanation of
dentine sensitivity


PULPO-DENTIN COMPLEX
“an oversimplication”
"odontoblast-dentin complex" and the pulp
as two distinct tissues. (Goldberg and
Lasfargues, 1995).

• “function as an integrated unit which is
generally termed the pulpo-dentin
complex.”
D.H. Pashley
• Crit Rev Oral Bio Med7(2): 104-133 (1996)


Odontoblast-dentin complex

• DENTINE MORPHOLOGY

• DYNAMICS OF DENTIN


The extent of the odontoblast
process
• “there are no supporting cells or blood
vessels, the ability of the odontoblast cell body
to support a long cytoplasmic process is in
question.” (Holland, 1976; Byers and Sugaya, 1995).

• An odontoblast process at the DEJ or CDJ
would be 3 mm or 3000 µm from the nearest
capillary, which is a very long diffusion distance.


Changes in dentin structure with depth

“area occupied by tubule lumina at the
DEJ to be approximately 1% of the total
surface area at the DEJ and 22% at the
pulp”- Pashley (1984)

• “It is clear that the water content or
wetness of dentin is not uniform, but
varies 20-fold from superficial to deep
dentin.”

Dentin permeability
Divided into two broad categories:
1. Transdentinal movement
2. Intradentinal movement

• Dentin can be regarded as both a barrier or a
permeable structure, depending upon its thickness,
age, and other variables.
• The permeability of dentin is not uniform but varies
widely.
• Highest at the pulp.
• Lowest at the DEJ

Balance between the permeation of noxious
substances across dentin and their clearance
by the pulpal circulation


• The outward fluid flow through tubules -
first line of defense against the inward
diffusion of noxious substances.

• Dentinal fluid contains plasma proteins which
can bind or agglutinate - protective role

• A second defensive reaction causes the
permeability of dentin to fall .


Control of dentin permeability
Peripheral Reductions in Dentin Permeability

• Relatively large molecules (e.g.,albumin,
globulins, fibrinogen) exits pulpal blood vessels,
gain access to extracellular spaces, and reach
the dentinal tubules (Bergenholtz et al, 1993,
1996).

Internal Reductions in Dentin Permeability

• "reactionary dentinogenesis“
• "reparative dentinogenesis".

Dynamics of Dentin


REACTIONS TO CAVITY PREPARATIONS:
FLUID SHIFTS

• Inward fluid shifts (because of frictional
heat generation on the end of a poorly
irrigated cutting bur).
• Outward fluid shifts due to evaporative
water loss (if only air cooling is used), and
slight inward fluid shifts due to osmotic
movement of cooling water into dentin
(Horiuchi and Matthews, 1973).
These fluid shifts occur in both directions at
various stages of cavity preparation.

DISRUPTION OF ODONTOBLAST LAYER
• Deep cavity preparation causes aspiration of
odontoblasts (Byers et al, 1988),
• More shallow preparation causes disruption of
junctional complexes between odontoblasts
(Ohsima, 1990),which decreases their barrier
properties.
• Loss of gap junctions interferes secretion of
collagen matrix in a synchronous. coordinated
manner, due to the loss of cell signaling between
adjacent cells.


• The proteins that make up gap junctions
are called connexins

• How long it takes odontoblasts to
reestablish the continuity of gap junctions
and to revert to tissue rather than cellular
function is unknown


PULPAL REACTIONS TO DENTIN EXPOSURE:
NERVE RESPONSES

• Sensory nerve fibers innervating dentin by
release neuropeptides such as CGRP (Gazelius et
al, 1987; Byers et al, 1988, 1992a; Heyeraas et al, 1994; Byers,
1996),

• The depletion of the neuropeptides is in
response to rapid fluid shifts produced by
evaporative, thermal, and physical forces.

• Reparative dentin is not well-innervated and
seems to form much faster than innervated
tubular dentin (Byers, 1984).

INNERVATION OF DENTIN
• Developmental

• Receptive Fields

• Modification of Nerve Activity

• Dentin Sensitivity

• Nerve Reactions to Exposure of Dentin

Developmental
• Nerves grow into the pulp early in bell stage of
tooth development.
Nerves enter the apex

Only a few nerves are given off in the root
(< 10%, Byers and Matthews, 1981),

Forms Nerve plexus of Rashkow

Terminate in predentin or dentin,

Receptive Fields
• Individual A-8 fibers have discrete receptive
areas on dentin which can be located by
probing.

• localized to a small spot on the dentin

• surface, some single nerve fibers have two or
three separate receptive areas separated from
each other by many millimeters.

Modification of Nerve Activity
• “Neurotrophic proteins such as NGF may
produce analgesic activity in chronically
inflamed teeth, making them
asymptomatic. If this is confirmed, it may
provide an explanation for the lack of
correlation between the signs of pulpal
inflammation and patient pain”
(Hargreaves et al, 1996).


Nerve Reactions to Exposure of
Dentin
• The NGF travels up the axon to the trigeminal
ganglion,where it stimulates the neuron to
increase the synthesis of more CGRP (Lindsay
et al, 1989, 1990) and, by mechanisms not yet
completely understood, to cause branching and
sprouting of nerve terminals beneath the exposed
dentin.

• increases the number of CGRP-positive nerve terminals
in the region of exposed dentin within 48 hrs, but the
response disappears within 7-10 days if there is no
further irritation.

Dentin Sensitivity
• Transducer theory

• Modulation theory

• “gate” control and vibration theory

• The hydrodynamic theory


Transducer theory
• Odontoblasts function as receptors

• Coupled to nerves ,either electrically
through gap junctions or through chemical
synapses.

• Receptors located beneath the
odontoblasts

“Gate” control / Vibration theory
• Melzack and Wall (1965) Pain
mechanisms: a new theory. Science 1965;
150: 971–979

• This theory states that pain is a function of
the balance between the information
traveling into the spinal cord through large
nerve fibers and information traveling into
the spinal cord through small nerve fibers

Large nerve fibers carry non-
nociceptive information and small nerve
fibers carry nociceptive information


• According to the gate control theory , A-β nerve
fibers, which transmit information from vibration
receptors.

• Stimulate inhibitory interneurons in the spinal
cord, which in turn act to reduce the amount of
pain signal transmitted from A-δ and C fibers
across the midline of the spinal cord and from
there to the brain.
.
Melzack R. From the gate to the neuromatrix. Pain. 1999 Aug;
Suppl 6:S121-6.


Pain Modulation theory
• Levels Theory of Pain Control

• Spinal Levels of Pain Control
Level 1 Gate Control Theory

Level 2 Central Biasing (hyperstimulation
analgesia)

Level 3 Endogenous Opiate (Pituitary level)

The hydrodynamic theory
• Gysi, 1900 introduced hydrodynamic concept.
“An attempt to explain the senstiveness of dentine” – Br
J Dent Sci: 43:865 – 8

• 1960s, Brannstrom demonstrated that pain
producing stimuli induced fluid shifts across
dentin in vitro.
• Provided experimental data to support to
develop a plausible theory.
• Brannstrom M, Linden LA, Astrom A (1967). The
hydrodynamics of the dental tubule and of pulp fluid.
Caries Res L310-312.


Hydrodynamics (Blaise Pascal 1600)
• Fluid movement

• osmotic pressure

• Volumetric changes

• Hydrostatic pressures

• Viscosity

• Velocity

Fluid movement
• The rate of this fluid flow depends upon
the hydraulic conductance of dentin and
the pulpal tissue pressure (Pashley,1990)

• hydraulic conductance of dentin suddenly
increases, permitting both a slow outward
spontaneous fluid flow (Pashley,1992)


osmotic pressure
• colloid osmotic pressure of plasma
proteins could cause negative tissue
pressures under special conditions of low
to zero pulpal blood flow. Thus, under
special conditions (intense sympathetic
stimulation or adrenergic drug-induced
vasoconstriction), dentinal fluid (and its
contents) can be "aspirated" into the pulp.
– Brown et al. (1969)

Volumetric changes
“Thermal stimuli cause more rapid volumetric
changes in dentinal fluid than in dentin itself,
resulting in an outward (cold) or inward (hot)
movement of fluid.
The reason(s) why cold stimuli are more
effective than hot stimuli is unclear.
It may be due to the fact that the resistance to
fluid movement across dentin is different when
fluid moves inward vs. outward.”
Horiuchi and Matthews (1973).

Hydrostatic pressures
• Positive hydrostatic pressures always produced
higher hydraulic conductances (and higher fluid
shifts) than negative pressures

• Positive hydrostatic pressures - inward fluid
movement - displace the odontoblasts slightly
away from the orifice .

• Negative pressures would tend to seat them
more firmly in the tubules .

• Altered hydrodynamic resistances

Positive Negative
hydrostatic www.indiandentalacademy.com
hydrostatic

Viscosity
• As dentinal fluid is cooled, its viscosity increases
significantly .

• Since dentinal fluid flow through tubules is
inversely related to viscosity , decreases in
temperature would decrease fluid flow
but increase shear stresses on
dentinal/pulpal nerves.

• Heating dentin would do the reverse.


Velocity
Fluid flow is occurring between the tubule wall and
odontoblasts and/or nerve terminals.

velocities of fluid movement - sufficient
shear forces to deform nerve terminals .

Neural elements responsible for pain may not
necessarily involve stretch sensitive ion
channels but rather simple shear forces on free
nerve endings.


DEFINITION
• Dowell 1985
• Orchardson and collins 1987

• Dentine hypersensitivity is characterized
by short, sharp pain arising from exposed
dentin in response to stimuli typically
thermal, evaporative, tactile, osmotic or
chemical and which cannot be ascribed to
any other form of dental defect or
pathology (Holland 1997)

Two processes must to cause
dentinal hypersensitivity……
• Lesion localization:
Dentin must be exposed to etiological
agents

• Lesion Initiation:
Sensitivity must be induced by tubular
exposure


Lesion localization
• Loss of periodontal tissue
Gingival recession

• Loss of Enamel
Attrition
Abrasion
Erosion
Abfraction

Lesion Initiation
• Cementum - extremely labile – offers little
protection against sensitivity. (Bevenius
1994)
• Non-sensitive dentin shows few tubules at
the surface (Absi 1987)

• Two category initiating agents:
1. Abrasive 2.Erosive

PREVALENCE AND DISTRIBUTION
• Prevalence studies to date yield limited
associations with etiological factors.

• Distribution data suggests association between
tooth cleaning ,gingival recession and
hypersensitivity.

• Bacterial plaque – negatively associated

• Plaque induced sensitivity is different from
dentin hypersensitivity

GINGIVAL RECESSION
• The exposure of root surface by an apical shift in
the position of the gingiva.


RECESSION

Mechanical Destructive
Factors Periodontal
Disease
(Tooth brushing)
(Serino, JCP, 1994)

Only buccal All tooth
surfaces are surfaces are
involved involved


• High muscle attachment and frenal pull
(Trott, 1966)

• Tooth malposition (Gorman, JP, 1967)

• Irregular tooth alignment in the dental
arch,(Stoner J,JP, 1980)

• Areas with absence or a narrow zone (width)
of attached gingiva (Tenenbaum H. JCP,
1982)


• Reduced thickness of the alveolar bone in the
buccolingual side (Wennström, JCP, 1987)

• Root prominence (Gartrell JR, 1976)

• Alveolar bone dehiscence ( Lost, JCP, 1984)

• Iatrogenic factors related to restorative and
periodontal treatment procedures (Lindhe, 1987)


• Margins of gingival restorations
(Donaldson D., JP, 1973)

• Orthodontic tooth movement (Steiner, G,
JP, 1981)

• Viruses (Prato GP, JP, 2002)


Buccal recession
maxillary molars and bicuspids

mandibular bicuspids

mandibular molars

Maxillary and mandibular incisors
• (Harald Löe, JP, 1992; The Natural History of periodontal Disease
in Man)


• Interproximal recession

• Lingual recession

It is characterized by the loss of periodontal
connective tissue fibers, along with tooth
cementum and alveolar bone.(Santarelli GA,
2001)

cervical root caries.(Anson D., 1999)

Erosion
• Defined as the chemical dissolution of
teeth by acids.
• Common site – Palatal surface of upper
anteriors (O’Brien1993)
• Caused by
1. Regurgitated gastric juice – pH 1 to 2
2. Dietary acids – pH around 3 (Smith
1994)

Gastric acid

• Gastro-esophageal reflux disease – enters
mouth passively

• Anorexia and Bulmia nervosa – enters
forcibly

• Chronic alcoholism – either passive
regurgitation or chronic vomiting

ABRASION
• The pathological wearing away of dental
hard tissue through abnomal mechanical
processes involving foreign objects or
substances repeatedly introduced in the
mouth and contacting the teeth. (Imfeld
1996)
• Soft tissue damage - tooth brush
• Hard tissue loss - tooth paste
(Sangnes 1976,Davis and Winter 1980)

Variables influencing Abrasion
• Brushing technique
vertical vs Horizontal
• Bristle Stiffness
Hard filaments retain more paste
• Brushing Force
Manual –upto 500g ,Power – upto 200g
• Time Spent

• Frequency
Excess of twice/day – encourages abrasion

Tooth Paste Abrasivity
• Diatomaceous earth
• Calcium carbonate
• Dicalcium phosphate
• Hydrated/anhydrous insoluble sodium
metaphosphate
• Silica
• Aluminium oxide
• Calcium pyrophosphate
• Alumina
• Pumice

ATTRITION
• The physiological wearing away f dental
hard tissues as a result of tooth –to –tooth
contact without the intervention of foreign
bodies (Imfeld 1996)
• 29xm/year – molars
• 15xm/year – Premolars (Lambrechs 1989)
• High bite force and bruxism
• “prerequisite for balanced occlussion”
• “considered physiological” (Begg 1954)

Associations with abfractive
lesions
• An abfraction lesion is a wedge shaped
(rarely saucer-shaped) defect at the
cervical region of a tooth.

• Tensile stress-induced microtrauma from
hyperfunction or parafunction

• High correlation between dentinal
hypersensitivity and abfraction lesions.

DENTINAL PAIN……?
• The International Association for the Study
of Pain defines pain as “unpleasant
sensory and emotional experience arising
from actual or potential tissue damage ”
– Carr DB (Ed). Vol1, Issue1, May 1993

Dentin hypersensitivity satisfies all the criteria to
be classified as a true pain syndrome, and
therefore needs to be treated accordingly.
- Dababneh RH, Br Dent J 1999;187:606-11.


• Pain is complex, subjective, and assessed only
indirectly, based on the patient’s overt
communication, both verbal and behavioural.

• Dentin hypersensitivity is a painful
condition subject to these complexities.

• “Unreported” pain does not mean
“unimportant” pain


DIAGNOSIS
• Diagnosis of exclusion

• Symptoms mimicking dentin
hypersensitivity must be ruled out

• Appropriate to rely on patients’ perception
of pain


Assessment of Hypersensitivity

• Subjective evaluation
Response based assessment

• Objective evaluation
Stimulus based assessment


Subjective evaluation
• Verbal rating scales - Keele1948

• Visual analogue scales – Ekowski 1972

• Verbal descriptor checklist – Gracely 1978

• McGill word descriptors – Melzack 1987

• Hospital anxiety and
Depression scale – Zigmond & Snaith 1983

Objective Assessment
• Mechanical stimulation
Pressure sensitive probes

• Chemical (osmotic) stimulation
Hypertonic solutions – sucrose or
CaCl2

• Electrical stimulation
Electric pulp testers

• Dehydrating (evaporative) stimuli
20.C (room temp) air blasts

• Thermal stimulation
Cold water, air ethyl chloride contact
cold probes

• Hydrostatic pressure
Fluid filtration


EXAMINE PATIENT TO EXCLUDE
• Cracked tooth syndrome
• Fractured restorations
• Chipped teeth
• Dental caries
• Gingival inflammation
• Post-restorative sensitivity
• Marginal leakage
• Pulpitis
• Palatogingival grooves


Strategies for MANAGEMENT
• Prevention

• Tubule occlusion
1. Endogeneos desensitization
2. Exogenous desensitization

• Altering tubule content

• Modifying nerve excitablity

Tubule occlusion
• Endogeneos desensitization

Promote formation of smear layer or
impermeable surface deposits

Intratubular dentin

Tertiary dentin


Tubule occlusion
Exogenous desensitization

• Block tubule orifice with barrier

• Tooth paste constituents

• Topical agents

• Restorative materials

Altering tubule content
• Viscosity of tubular fluid could be raised by
increasing its macromolecular protein
content.

• So that stimulus generates less fluid flow


Modifying nerve excitability
• Potassium ions – reduces intradental
nerve excitability
• When applied to outer dentin surface
might diffuse along the tubules and block
intradental nerve function by raising the
K+ ions concentration
• A positive pressure could be applied to
overcome the pulpal pressure, or the
pulpal pressure could be reduced

TREATMENT MODALITIES
• Home use products:
Tooth pastes containing
strontium /potassium salts

Tooth paste containing
sodium and amine fluoride

Mouth rinses containing
Aluminium lactate

In – office products
• Agents that do not polymerize
Varnishes/precipitants
Primers containing HEMA
• Agents that undergo setting or polymerization
GIC, Resin reinforced GIC/COMPOMERS
Resin primers, Bonding agents

• MOUTH GUARDS
• IONTOPHORESIS
• LASERS
• PERIODONTAL SURGERY/GRAFTING
• CROWN PLACEMENT

Varnishes/precipitants
• Shellacs
• 5% sodium fluoride varnish
• 1%NaF,0.4%SnF2,0.14%HF solutions
• 3% mono-potassium-monohydrogen
oxalate
• 6% acidic ferric oxalate
• Cacium phosphate preparations
• Calcium hydroxide


Primers containing HEMA
• 5% glutaraldehyde ,35% HEMA in water

• 35% HEMA in water


MOUTH GUARDS
• Mouthguard type appliance to deliver
potassium nitrate (Reinhart 1990)

Severe Bruxism cases - a vacuum formed
muthguard with small amount of 5% KNO3
dentrifice (Jerome 1995)


IONTOPHORESIS
• Pivati 1747
• Galvani and Volta 1821- electricity can move
different metal ions
• LeDuc 1900 – Ionotheraphy & formulated laws

• Iontophoresis is a method of electrically transporting
ionic particles into hard or soft tissue (Sausen, 1955;
Harris,1967; and Zadok et al., 1976).

• Defined as the introduction by means of direct electrical
current, of ions of soluble salts in to the tissues of the
body for therapeutic purposes
– Singh and Maibach 1994

• Fluoride, which is such an ionic particle, is
negatively-charged.

• when an electrical potential is applied, fluoride
ion would be repelled from the negative
electrode (cathode) and attracted to the positive
(anode).

• (Manning, 1961; Jensen, 1964; Murthy et al.,
1973; and Gangarosa and Park, 1978)
iontophoresis of fluoride was more effective in
reducing dentin hypersensitivity than was topical
application alone.

LASER
• Increases excitability threshold of the free
nervous terminations, causing an
analgesic effect.
• Stimulates pulp mesenchymal cells to
differ in Odontoblasts, with the purpose to
produce reparative dentin
• Both red and infrared wavelength lasers
have been effective.


Surgical methods for root
coverage
• Pedicle gingival grafts

a. Laterally positioned grafts
b. Double Papilla Flaps
c. Transpositional flaps
d. Coronally positioned flaps

• Free autogenous gingival grafts
• Connective tissue grafts or subepithelial
connective tissue grafts
• GTR
• Semilunar Coronally Positioned flaps

• Future………NANOROBOTICS…?


conclusion
While it may not be feasible to prevent dentine
exposure ,it should be possible to prevent
exposed dentin from becoming unduly
sensitive.

This requires identification and elimination of
the various factors predisposing to persistent
tubule patency.


References
• Tooth wear and sensitivity – Martin Addy
• Clinical Periodontology - Glickman
• Oral Histology – Orbans
• Oral Histology – TenCate
• ImplantPeridontology - lindhe


• DYNAMICS OF THE PULPCHDENTIN COMPLEX, D.H. Pashley, Crit Rev Oral Biol Med
7(2):104-133 (1996)
• Physiology of dentine hypersensitivity: clinical treatment, Charles Cox DMD,
• Fluoride Levels in Dentin after lontophoresis of 2% NaF, J. M. WILSON, J Dent Res 63(6):897-900,
June, 1984
• ASSESSING THE EFFICACY OF THREE DENTIFRICES IN THE TREATMENT OF
DENTINAL HYPERSENSITIVITY, G. SILVERMAN, JADA, Vol. 127, February 1996
• Cervical Dentin Hypersensitivity: Etiology & Current Treatment, THOMAS A. COLEMAN,
• Consensus-Based Recommendations for the Diagnosis and Management of
Dentin Hypersensitivity, J Can Dent Assoc 2003; 69(4):221–6
• DIAGNOSIS OF PERIODONTOCLASIA, F. V. SIMONTON,
• THE DENTIN DISC SURFACE: A PLAUSIBLE MODEL FOR DENTIN
PHYSIOLOGY AND DENTIN SENSITIVITY EVALUATION, D.G. GlLLAM, Adv Dent Res
11(4):487-501,1997
• Displacement of the contents of dentinal tubules and sensory transduction in
intradental nerves of the cat, D. Andrew and B. Matthews, J. Physiol. 2000;529;791-802
• Nanodentistry, ROBERT A. FREITAS, JADA, Vol. 131, November 2000
• Dentine hypersensitivity: new perspectives on an old problem, Martin Addy,
International Dental Journal (2002) 52, 367–375
• Transmission Electron Microscopic Characterization of Hypersensitive Human
Radicular Dentin, M. YOSHIYAMA, J Dent Res 69(6):1293-1297, June, 1990
• Scanning Electron Microscopic Characterization of Sensitive vs. Insensitive Human
Radicular Dentin, M. YOSHIYAMA, J Dent Res 68(11):1498-1502, November, 1989


THANK YOU FOR WATCHING


Dentinal hyper sensitivity / /certified fixed orthodontic courses by Indian dental academy

Recommandé

Recommandé

Contenu connexe

Tendances

Tendances (20)

En vedette

En vedette (7)

Similaire à Dentinal hyper sensitivity / /certified fixed orthodontic courses by Indian dental academy

Similaire à Dentinal hyper sensitivity / /certified fixed orthodontic courses by Indian dental academy (20)

Plus de Indian dental academy

Plus de Indian dental academy (20)

Dernier

Dernier (20)

Dentinal hyper sensitivity / /certified fixed orthodontic courses by Indian dental academy