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THE DENTAL PULP
AND ITS CLINICAL
CONSIDERATIONS
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CONTENTSCONTENTS
 IntroductionIntroduction
 DevelopmentDevelopment
 HistologyHistology
 Functions of the pulpFunctions of the pulp
 Theories of pain mechanismTheories of pain mechanism
 Physiologic changes in pulpPhysiologic changes in pulp
-aging-aging
-calcification-calcification

 Pulp in clinical scenarioPulp in clinical scenario
-Reaction to caries-Reaction to caries
-Iatrogenic pulp testing-Iatrogenic pulp testing
-Dentistogenic pulpitis-Dentistogenic pulpitis
-Depth of cavity preparation-Depth of cavity preparation
-Extensiveness of preparation-Extensiveness of preparation
-Pinledge preparation-Pinledge preparation
-Speed of rotation-Speed of rotation
-Dry cavity preparation-Dry cavity preparation
-Nature of cutting instrument-Nature of cutting instrument
-Size of wheels and burs-Size of wheels and burs
-Hand instruments-Hand instruments
-Coolants-Coolants
-Polishing of restorations-Polishing of restorations
-Traumatic occlusion-Traumatic occlusion

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 Chemical irritants to the pulpChemical irritants to the pulp
-Dentin sterilizing agent-Dentin sterilizing agent
-Restorative materials-Restorative materials
 Radiant irritantsRadiant irritants
-X- irradiation-X- irradiation
-Laser-Laser
Agents for pulp protectionAgents for pulp protection
Management of deep carious lesionManagement of deep carious lesion
Revascularization of pulpRevascularization of pulp
ConclusionConclusion

DENTAL PULPDENTAL PULP

INTRODUCTIONINTRODUCTION
 The dental pulp is a soft connective tissue that occupies theThe dental pulp is a soft connective tissue that occupies the
centre of each tooth.centre of each tooth.
 Their shape conforms to the respective toothTheir shape conforms to the respective tooth
 Each pulp organ occupies the pulp chamber and is circumscribedEach pulp organ occupies the pulp chamber and is circumscribed
by the dentin and lined peripherally by a cellular layer ofby the dentin and lined peripherally by a cellular layer of
odontoblasts adjacent to the dentin.odontoblasts adjacent to the dentin.
 Every person normally has 52 pulp organsEvery person normally has 52 pulp organs

 Total volume of all the permanent teeth pulp -0.38ccTotal volume of all the permanent teeth pulp -0.38cc
mean volume of a single adult human pulp is 0.02cc.mean volume of a single adult human pulp is 0.02cc.
Molar pulps are 3 - 4 times larger than incisor pulpsMolar pulps are 3 - 4 times larger than incisor pulps
(Orbans,11(Orbans,11thth
edition).edition).
 Pulp and dentin are integrally connected in the sensePulp and dentin are integrally connected in the sense
that physiologic and pathologic reactions of one of thethat physiologic and pathologic reactions of one of the
tissue will also affect the other. They have the sametissue will also affect the other. They have the same
embryonic origin and remain in an intimateembryonic origin and remain in an intimate
relationship throughout the life of the vital tooth.relationship throughout the life of the vital tooth.

Development of the pulpDevelopment of the pulp
 About the eighth week of fetal life in the cap stage of toothAbout the eighth week of fetal life in the cap stage of tooth
formation, the formation of the dental papilla is seenformation, the formation of the dental papilla is seen
((Seltzer and Bender,3Seltzer and Bender,3rdrd
edition).edition).
 This is a condensation of ectomesenchymal connective tissueThis is a condensation of ectomesenchymal connective tissue
under the inner dental epithelium, which will become the futureunder the inner dental epithelium, which will become the future
dental pulp.dental pulp.
 The cells in the dental papilla at first are large and rounded orThe cells in the dental papilla at first are large and rounded or
polyhedral, with pale cytoplasm and large nuclei. As the pulppolyhedral, with pale cytoplasm and large nuclei. As the pulp
matures, the cells take on a spindle shape.matures, the cells take on a spindle shape.

 Metachromatic ground substance (acidMetachromatic ground substance (acid
mucopolysaccharides) is present in great abundancemucopolysaccharides) is present in great abundance
(Fulmer 1972)(Fulmer 1972)
 In addition, glycogen deposits of considerable sizeIn addition, glycogen deposits of considerable size
accumulate in the cytoplasm of undifferentiatedaccumulate in the cytoplasm of undifferentiated
mesenchymal cells but not in the fibroblasts ormesenchymal cells but not in the fibroblasts or
odontoblasts (Russel 1967).odontoblasts (Russel 1967).
 The glycogen may provide the energy for subsequentThe glycogen may provide the energy for subsequent
protein synthesis of the fibroblasts of the dental pulp.protein synthesis of the fibroblasts of the dental pulp.
 The changes in the dental papilla occur concomitantlyThe changes in the dental papilla occur concomitantly
with the development of the epithelial enamel organ.with the development of the epithelial enamel organ.

Histology of dental pulpHistology of dental pulp -- Layers and cells ofLayers and cells of
the pulpthe pulp
 An intact vital pulp may be removed from the root canal in oneAn intact vital pulp may be removed from the root canal in one
piece , on examination, it is found to be a firm, cohesive, andpiece , on examination, it is found to be a firm, cohesive, and
resilient unit, maintaining its original shape.resilient unit, maintaining its original shape.
 This is possible because the pulp is composed principally of aThis is possible because the pulp is composed principally of a
gelatin-like material called ground substance, which is reinforcedgelatin-like material called ground substance, which is reinforced
throughout by irregularly arranged and interlaced collagen fibersthroughout by irregularly arranged and interlaced collagen fibers
and fiber bundles.and fiber bundles.
 Embedded in this stroma are the cells, blood vessels, and nerveEmbedded in this stroma are the cells, blood vessels, and nerve
fibers that make up the loose connective tissue categorized asfibers that make up the loose connective tissue categorized as
the dental pulp organ.the dental pulp organ.

 The dental pulp has a rich circulatory force that,.by virtue of theThe dental pulp has a rich circulatory force that,.by virtue of the
dynamics of fluid interchange between capillaries and tissue,dynamics of fluid interchange between capillaries and tissue,
establishes and maintains an extravascular hydrostatic pressureestablishes and maintains an extravascular hydrostatic pressure
within this chamberwithin this chamber
 The intrapulpal pressure, which has been measured to be aboutThe intrapulpal pressure, which has been measured to be about
10 mm Hg (5-20 mm Hg)10 mm Hg (5-20 mm Hg)
 no consistent effective collateral circulation exists to overcome ano consistent effective collateral circulation exists to overcome a
severe irritant force,severe irritant force,
(QIJ 2001;32 :427-446)(QIJ 2001;32 :427-446)

ZONES OF THE PULPZONES OF THE PULP

The dental pulp may be subdivided into fourThe dental pulp may be subdivided into four
zoneszones
 CENTRAL ZONE orCENTRAL ZONE or PULP PROPERPULP PROPER
 It isIt is a core of loose connective tissue (stroma)a core of loose connective tissue (stroma)
containing the larger nerves and blood vesselscontaining the larger nerves and blood vessels
that begin to arborize toward the peripheralthat begin to arborize toward the peripheral
pulpal areas.pulpal areas.

 CELL RICH ZONECELL RICH ZONE
 Outlining the central zone is an area richly populatedOutlining the central zone is an area richly populated
with reserve (undifferentiated mesenchymal) cells andwith reserve (undifferentiated mesenchymal) cells and
fibroblasts.fibroblasts.
 ThisThis cell-rich zonecell-rich zone serves as a reservoir for replacementserves as a reservoir for replacement
of destroyed dentin-producing cells (odontoblasts).of destroyed dentin-producing cells (odontoblasts).
 Although most frequently observed in the coronal pulp,Although most frequently observed in the coronal pulp,
this zone can also exist in the radicular pulp.this zone can also exist in the radicular pulp.

 SUBDENTINOBLASTIC ZONESUBDENTINOBLASTIC ZONE
Peripheral to the cell-rich zone is thePeripheral to the cell-rich zone is the
subdentinoblastic zone of the pulp, or zone of Weil.subdentinoblastic zone of the pulp, or zone of Weil.
 This area appears to be relatively free of cellsThis area appears to be relatively free of cells
and is often referred to as theand is often referred to as the cell-free or cell-poorcell-free or cell-poor
zonezone
 This zone may diminish in size or temporarilyThis zone may diminish in size or temporarily
disappear when dentin formation is occurring atdisappear when dentin formation is occurring at
a rapid ratea rapid rate

 DENTINOBLASTIC ZONEDENTINOBLASTIC ZONE
 Dentinoblastic zone, where the nerve fibres terminateDentinoblastic zone, where the nerve fibres terminate
as filaments, beads, or varicosities.as filaments, beads, or varicosities.
 Many of the nerve fibers (10% to 20%) terminate inMany of the nerve fibers (10% to 20%) terminate in
the tubules of the predentin and inner mature dentin.the tubules of the predentin and inner mature dentin.
 The combined dentinoblastic layer andThe combined dentinoblastic layer and
subdentinoblastic free nerve network form a sensorysubdentinoblastic free nerve network form a sensory
complex (peripheral sensory units) that completelycomplex (peripheral sensory units) that completely
envelops or encapsulates the central pulp core.envelops or encapsulates the central pulp core.

Cells of the dental pulpCells of the dental pulp
 Formative cells – odontoblasts , fibroblastsFormative cells – odontoblasts , fibroblasts
 Defense cells – histiocytes , lymphocytesDefense cells – histiocytes , lymphocytes
 Reserve cells – undifferentiated mesenchymalReserve cells – undifferentiated mesenchymal
cellscells

FibroblastsFibroblasts
 The principal cell distributed throughout theThe principal cell distributed throughout the
pulp, is abundant in the cell-rich zone.pulp, is abundant in the cell-rich zone.
 It produces gelatinous intercellular matrix, inIt produces gelatinous intercellular matrix, in
which all pulpal components are embedded, aswhich all pulpal components are embedded, as
well as collagen fibers that reinforce the matrixwell as collagen fibers that reinforce the matrix

 Young fibroblasts may undergo mitosis andYoung fibroblasts may undergo mitosis and
differentiate into replacement odontooblasts .differentiate into replacement odontooblasts .
 The shape of the fibroblasts varies fromThe shape of the fibroblasts varies from
fusiform (cigar shaped) with long, slender,fusiform (cigar shaped) with long, slender,
protoplasmic processes to stellate (star shaped)protoplasmic processes to stellate (star shaped)
with shorter numerous branches.with shorter numerous branches.

 The health state of the fibroblasts reflects' theThe health state of the fibroblasts reflects' the
age and vitality of the pulp and consequently theage and vitality of the pulp and consequently the
potential of the pulp to respond favorably topotential of the pulp to respond favorably to
deleterious changes in its environment.deleterious changes in its environment.
 As a result of the aging process, whether itAs a result of the aging process, whether it
occurs in a natural sequence or is accelerated byoccurs in a natural sequence or is accelerated by
caries, abrasion, or pulp capping, there is acaries, abrasion, or pulp capping, there is a
diminution in the size and number of thesediminution in the size and number of these
cells .cells .

Reserve cellsReserve cells
 found principally along capillaries and in the cell-found principally along capillaries and in the cell-
rich zone, is a primitive undifferentiated cell thatrich zone, is a primitive undifferentiated cell that
forms a reserve of pluripotential cells.forms a reserve of pluripotential cells.
 Such cells have the capacity to differentiate intoSuch cells have the capacity to differentiate into
various cell types as the need arises.various cell types as the need arises.

HistiocytesHistiocytes
 The histiocyte (tissue macrophage) is anotherThe histiocyte (tissue macrophage) is another
type of defense cell found in the connectivetype of defense cell found in the connective
tissue of the pulp .tissue of the pulp .
 When activated, histiocytes migrate to theWhen activated, histiocytes migrate to the
inflammatory site and become phagocytesinflammatory site and become phagocytes
(macrophages) that engulf bacteria, foreign(macrophages) that engulf bacteria, foreign
bodies, and dead cells.bodies, and dead cells.

DentinoblastDentinoblast
 The dentinoblast (odontoblast) is a highly specializedThe dentinoblast (odontoblast) is a highly specialized
connective tissue cell of the dental pulp, it is "special"connective tissue cell of the dental pulp, it is "special"
because of the unique role it plays in both dentin and pulpbecause of the unique role it plays in both dentin and pulp
function.function.
 The dentinoblasts form a palisade arrangement at theThe dentinoblasts form a palisade arrangement at the
pulp periphery.pulp periphery.

 The size and shape of these cells vary ranging from highThe size and shape of these cells vary ranging from high
columnar in the pulp chamber, to low columnar and cuboidal incolumnar in the pulp chamber, to low columnar and cuboidal in
the cervical or midroot area, to flattened at the apex.the cervical or midroot area, to flattened at the apex.
 The intercellular spaces between the dentinoblast may vary fromThe intercellular spaces between the dentinoblast may vary from
200 to 300 A *.200 to 300 A *.
 Their lengths vary from 8 to 25 or more microns, with diametersTheir lengths vary from 8 to 25 or more microns, with diameters
ranging from 3 to 8 microns.ranging from 3 to 8 microns.
 The dentinoblasts not only are in close physical contact with eachThe dentinoblasts not only are in close physical contact with each
other, but also communicate via numerous junctional complexes,other, but also communicate via numerous junctional complexes,
so that if one dentinoblast is injured, others are immediatelyso that if one dentinoblast is injured, others are immediately
affected.affected.

 the dentinoblastic layer is demarcated from thethe dentinoblastic layer is demarcated from the
predentin by a heavily stained (hyperchromatic)predentin by a heavily stained (hyperchromatic)
line called the pulpodentinal membrane.line called the pulpodentinal membrane.
 Disruption of this pulpodentinal (pseudo)Disruption of this pulpodentinal (pseudo)
membrane or the palisade arrangement of themembrane or the palisade arrangement of the
dentinoblasts is microscopic evidence ofdentinoblasts is microscopic evidence of
pathologic change.pathologic change.

 Junctional complexes have been observed in the pulp, whichJunctional complexes have been observed in the pulp, which
Seltzer and Bender have classified asSeltzer and Bender have classified as..
 Impermeable junctionsImpermeable junctions - The tight junction, or zonula- The tight junction, or zonula
occludens, is so classified because of the fusion of adjacentoccludens, is so classified because of the fusion of adjacent
plasma membranes.plasma membranes.
 Adhering junctionsAdhering junctions: Under light microscopy, adhering: Under light microscopy, adhering
junctions were referred to as intercellular bridges.junctions were referred to as intercellular bridges.
 Communicating junctions:Communicating junctions: Communicating junctions, or gapCommunicating junctions, or gap
junctions (nexus-type junctions), are sites of cell-to-celljunctions (nexus-type junctions), are sites of cell-to-cell
communication between adjacent dentinoblasts and betweencommunication between adjacent dentinoblasts and between
dentinoblasts and fibroblasts of the subdentinoblastic layer.dentinoblasts and fibroblasts of the subdentinoblastic layer.

The dentinal tubules and the dentinoblasticThe dentinal tubules and the dentinoblastic
process:process:
 TheThe dentinoblastic processdentinoblastic process is a direct extension of the cell bodyis a direct extension of the cell body
 The cytoplasm of the dentinoblastic process, unlike the cellThe cytoplasm of the dentinoblastic process, unlike the cell
body, is usually devoid of major cytoplasmic organellesbody, is usually devoid of major cytoplasmic organelles
 The predominant structures in the dentinoblastic process areThe predominant structures in the dentinoblastic process are
microtubules (200 to 250 A * diameter)microtubules (200 to 250 A * diameter)

 The dentinoblastic processes are bathed by intercellularThe dentinoblastic processes are bathed by intercellular
fluid from the dental pulp (dentinal lymph).fluid from the dental pulp (dentinal lymph).
 TheThe dentinal fluiddentinal fluid is attracted into the tubules byis attracted into the tubules by
capillary actioncapillary action
 Tanaka, using lanthanum tracers, confirmed thatTanaka, using lanthanum tracers, confirmed that
dentinal fluid emanates from terminal capillaries anddentinal fluid emanates from terminal capillaries and
diffuses to the dentinoenamel junction throughdiffuses to the dentinoenamel junction through
peridentinoblastic spacesperidentinoblastic spaces
 The dentinoblasts are not nerve cells by origin orThe dentinoblasts are not nerve cells by origin or
function, but their cell bodies and processes are in closefunction, but their cell bodies and processes are in close
contact with the nerve terminalscontact with the nerve terminals

 Thus, when injured or deformed, they may produceThus, when injured or deformed, they may produce
stimuli that are perceived by the free endings in contactstimuli that are perceived by the free endings in contact
with any part of the dentinoblastwith any part of the dentinoblast
 One such stimulus may be the release of aOne such stimulus may be the release of a
neurotransmitter substance by the dentinoblast, whichneurotransmitter substance by the dentinoblast, which
alters the permeability of the free nerve endingsalters the permeability of the free nerve endings
(producing an action potential).(producing an action potential).
 Another stimulus may also be in the form of aAnother stimulus may also be in the form of a
mechanical deformation of the dentinoblast (cell bodymechanical deformation of the dentinoblast (cell body
or process), that acts by converting mechanical energyor process), that acts by converting mechanical energy
into electrical energyinto electrical energy

 TheThe intercellular component of the pulpintercellular component of the pulp areare
-the collagen fibers,-the collagen fibers,
-the amorphous ground substance matrix and-the amorphous ground substance matrix and
-the intercellular tissue fluid-the intercellular tissue fluid
 Pulpal collagen, produced by both denti-Pulpal collagen, produced by both denti-
noblasts and fibroblasts, is a mixture of Types I and IIInoblasts and fibroblasts, is a mixture of Types I and III
at a ratio of 55:45at a ratio of 55:45
 The principal chemical components that give the formThe principal chemical components that give the form
and properties to the ground substance are complexand properties to the ground substance are complex
protein carbohydrate compounds calledprotein carbohydrate compounds called
mucopolysaccharides, also referred to asmucopolysaccharides, also referred to as
glycosaminoglycans (GAGs) or proteoglycansglycosaminoglycans (GAGs) or proteoglycans

 The ground substance is hydrophilic; The water is not free water,The ground substance is hydrophilic; The water is not free water,
as observed in tissue fluid, but is bound in a colloidal or gel stateas observed in tissue fluid, but is bound in a colloidal or gel state
 Any change in the nature or quality of the ground substance (i.e.,Any change in the nature or quality of the ground substance (i.e.,
the state of polymerization) directly influences the spread ofthe state of polymerization) directly influences the spread of
inflammation and infection.inflammation and infection.
 The viscosity of the gelated ground substance reinforced withThe viscosity of the gelated ground substance reinforced with
collagen fibers acts as a barrier against the spread of micro-collagen fibers acts as a barrier against the spread of micro-
organisms and toxic substances.organisms and toxic substances.

 However, organisms such as the hemolyticHowever, organisms such as the hemolytic
streptococcus can elaborate spreading factorstreptococcus can elaborate spreading factor
(hyaluronidase) that may dissolve the barrier and allow(hyaluronidase) that may dissolve the barrier and allow
a faster invasion.a faster invasion.
 Chemical mediators, (e.g., proteolytic enzymes,Chemical mediators, (e.g., proteolytic enzymes,
hyaluronidase), edema, and heat may alter the quality ofhyaluronidase), edema, and heat may alter the quality of
the ground substance (hydrolytic agents)the ground substance (hydrolytic agents)
 Pressure from increased tissue fluid and temperaturePressure from increased tissue fluid and temperature
rise during inflammation collapses the thin-walled veinsrise during inflammation collapses the thin-walled veins
and venules, causing a vascular stasis and ischemia andand venules, causing a vascular stasis and ischemia and
resulting in local cellular deathresulting in local cellular death
(Orban’s 11(Orban’s 11thth
edition)edition)

Functions of the pulpFunctions of the pulp
 The dental pulp carries out the four basicThe dental pulp carries out the four basic
functions ascribed to all loose connective tissues:functions ascribed to all loose connective tissues:

formativeformative
 nutritivenutritive
 nervousnervous
 defensivedefensive

I. Formative functionI. Formative function
 Dentin formation occurs throughout the life of theDentin formation occurs throughout the life of the
toothtooth
 The initial or primary dentin is tubular and regularlyThe initial or primary dentin is tubular and regularly
arranged because the odontoblasts are not crowded andarranged because the odontoblasts are not crowded and
the tooth is under minimal functional strainthe tooth is under minimal functional strain
 As more functional stresses are placed on the tooth,As more functional stresses are placed on the tooth,
dentin formation increases to such an extent that theredentin formation increases to such an extent that there
is encroachment on the pulp cavity.is encroachment on the pulp cavity.


 As the odontoblasts secrete the dentinal matrixAs the odontoblasts secrete the dentinal matrix
and retreat toward the pulp center, they becomeand retreat toward the pulp center, they become
crowded and their direction is altered.crowded and their direction is altered.
 The dentin produced is wavier and containsThe dentin produced is wavier and contains
fewer tubules per unit area.fewer tubules per unit area.
 This type of dentin is appropriatelyThis type of dentin is appropriately calledcalled
functional, or secondaryfunctional, or secondary dentindentin

 Operative procedures, caries, severe attritionalOperative procedures, caries, severe attritional
stimulation (abrasion), and erosion produce initial rapidstimulation (abrasion), and erosion produce initial rapid
formation of dentin.formation of dentin.
 Mjor considers it a specialized type of scar tissue formedMjor considers it a specialized type of scar tissue formed
in response to a local lesion. The tubules are irregular orin response to a local lesion. The tubules are irregular or
frequently are absent. This tertiary type of dentin isfrequently are absent. This tertiary type of dentin is
usually called reparative, irregular, or defensive, but moreusually called reparative, irregular, or defensive, but more
accurately has been termed irritation dentin by Langelandaccurately has been termed irritation dentin by Langeland
 Tertiary dentin formed by surviving primaryTertiary dentin formed by surviving primary
odontoblasts following a mild stimulus is called theodontoblasts following a mild stimulus is called the
reactionary dentinreactionary dentin
 Dentin formed by a new generation of odontoblast isDentin formed by a new generation of odontoblast is
called reparative dentin.called reparative dentin.

II. Nutritive functionII. Nutritive function
 The dental pulp must maintain theThe dental pulp must maintain the
vitality of the dentinvitality of the dentin by providingby providing
oxygen and nutrients to theoxygen and nutrients to the
dentinoblasts and their processes, asdentinoblasts and their processes, as
well as providing a continuing sourcewell as providing a continuing source
of dentinal fluidof dentinal fluid
 Fulfillment of the nutritive functionFulfillment of the nutritive function
is made possible by the richis made possible by the rich
peripheral capillary networkperipheral capillary network
(terminal capillary network, or TCN)(terminal capillary network, or TCN)
and its numerous projections intoand its numerous projections into
the dentinoblastic zonethe dentinoblastic zone

III. Nervous functionIII. Nervous function

 The dental pulp requires a nerve supply to provide itsThe dental pulp requires a nerve supply to provide its
primary but related functions: vasomotor control andprimary but related functions: vasomotor control and
defensedefense
 Vasomotor innervation controls the movements of theVasomotor innervation controls the movements of the
muscular layer in the wall of the blood vessels, whichmuscular layer in the wall of the blood vessels, which
results in expansion (vasodilation) or contractionresults in expansion (vasodilation) or contraction
(vasoconstriction).(vasoconstriction).
 Such control regulates the blood volume and rate ofSuch control regulates the blood volume and rate of
blood flow of a particular arteriole that in turn affectsblood flow of a particular arteriole that in turn affects
the fluid interchange between tissue and capillaries andthe fluid interchange between tissue and capillaries and
influences the intensity of the intrapulpal pressureinfluences the intensity of the intrapulpal pressure

Two types of nerve cells (neurons)Two types of nerve cells (neurons)
are associated with the dental pulp:are associated with the dental pulp:
I. The afferent (sensory) neuron is called aI. The afferent (sensory) neuron is called a
pseudounipolar neuron with two processes.pseudounipolar neuron with two processes.
 The peripheral process (dendrite) originates inThe peripheral process (dendrite) originates in
the dental pulp, and its terminals are thethe dental pulp, and its terminals are the
receptors at the pulp peripheryreceptors at the pulp periphery
 The cell body is located in the semilunarThe cell body is located in the semilunar
ganglion of the trigeminal nerveganglion of the trigeminal nerve

 The second process (axon) proceeds to the CNS,The second process (axon) proceeds to the CNS,
where it terminates (synapses) in an island of graywhere it terminates (synapses) in an island of gray
matter (nucleus) called the spinal nucleus of the fifthmatter (nucleus) called the spinal nucleus of the fifth
cranial nervecranial nerve
 A second order neuron decussates (crosses to theA second order neuron decussates (crosses to the
other side) and carries the impulse to the thalamus,other side) and carries the impulse to the thalamus,
synapsing with the third-order neuron (whichsynapsing with the third-order neuron (which
terminates in the postcentral gyrus of the cerebralterminates in the postcentral gyrus of the cerebral
cortex.cortex.

II. The efferent system of nerve cells from theII. The efferent system of nerve cells from the
CNS to the dental pulp are multipolar neuronsCNS to the dental pulp are multipolar neurons
 They have many incoming shorter processesThey have many incoming shorter processes
(dendrites) and one outgoing process (axon) of(dendrites) and one outgoing process (axon) of
varying lengthsvarying lengths

The nerve impulse depends on a change in theThe nerve impulse depends on a change in the
permeability of the neuronal membrane and thepermeability of the neuronal membrane and the
sodium-potassium pumps of the cellsodium-potassium pumps of the cell
The sequential steps in this phenomenon are :The sequential steps in this phenomenon are :
 Stimulation increases the permeability of the axonStimulation increases the permeability of the axon
membrane to Na+, permitting their movement intomembrane to Na+, permitting their movement into
the axon. As a result, a momentary depolarizationthe axon. As a result, a momentary depolarization
occurs at the point of stimulation.occurs at the point of stimulation.
 Stimulus to the next segment on the membraneStimulus to the next segment on the membrane

 As the impulse moves away, the membrane isAs the impulse moves away, the membrane is
recharged by the outward migration of K+.recharged by the outward migration of K+.
 Subsequently the sodium pump expels Na +Subsequently the sodium pump expels Na +
into the extracellular fluid while the potassiuminto the extracellular fluid while the potassium
pumps returns K+ to the intracellular fluid.pumps returns K+ to the intracellular fluid.
 The resting potential is now restored locallyThe resting potential is now restored locally
because the membrane is once again positivebecause the membrane is once again positive
on the outside and negative on the inside ofon the outside and negative on the inside of
the axon membrane.the axon membrane.

 The actual speed with which a nerve impulseThe actual speed with which a nerve impulse
passes along a neuron varies directly with thepasses along a neuron varies directly with the
diameter of the axon: the larger the diameter, thediameter of the axon: the larger the diameter, the
faster the conduction.faster the conduction.
 Fibers having the largest diameter are classified asFibers having the largest diameter are classified as
A fibers, those with the smallest diameter as CA fibers, those with the smallest diameter as C
fibers, and those of the intermediate size as Bfibers, and those of the intermediate size as B
fibers.fibers.

 The A fibers are myelinated and subdivided into theThe A fibers are myelinated and subdivided into the
larger-diameter A-alpha and A-beta, the intermediate A-larger-diameter A-alpha and A-beta, the intermediate A-
gamma, and the small A-delta fibers.gamma, and the small A-delta fibers.
 The A-beta and A-gamma fibers carry touch, pressure,The A-beta and A-gamma fibers carry touch, pressure,
and proprioceptive impulses at a speed as high as 70and proprioceptive impulses at a speed as high as 70
m/sec. The A-delta fibers carry pain (nociceptive)m/sec. The A-delta fibers carry pain (nociceptive)
sensations at a speed ranging between 2 to 30 m/sec.sensations at a speed ranging between 2 to 30 m/sec.

 The afferent sensory C fibers are unmyelinatedThe afferent sensory C fibers are unmyelinated
and carry pain sensations at a slower speed (0.5and carry pain sensations at a slower speed (0.5
to 1.0 m/ sec) because of their lack of myelinto 1.0 m/ sec) because of their lack of myelin
and smaller diameter.and smaller diameter.
 Unmyelinated C fibers average three to fourUnmyelinated C fibers average three to four
times the number of myelinated A fiberstimes the number of myelinated A fibers
(Johnsen). However, not all the C fibers are(Johnsen). However, not all the C fibers are
sensory; approximately 10% are sympatheticsensory; approximately 10% are sympathetic
(Holland).(Holland).

 It has been postulated that the A-delta fibers produce theIt has been postulated that the A-delta fibers produce the
initial momentary sharp pain response to external stimuliinitial momentary sharp pain response to external stimuli
because of their peripheral location, low threshold ofbecause of their peripheral location, low threshold of
excitability, and greater conduction speed.excitability, and greater conduction speed.
 On the other hand, continuous, constant, or throbbingOn the other hand, continuous, constant, or throbbing
pain is a result of sustained smaller C fiber activity; thesepain is a result of sustained smaller C fiber activity; these
C fibers have a much higher threshold of excitability.C fibers have a much higher threshold of excitability.
 It should be noted that A-delta fibers could be stimulatedIt should be noted that A-delta fibers could be stimulated
without injuring the tissues, whereas C fiber stimulationwithout injuring the tissues, whereas C fiber stimulation
is associated with tissue damage and the inflammatoryis associated with tissue damage and the inflammatory
process.process.

CLINICAL RELEVANCECLINICAL RELEVANCE
 Note that only the A-delta fibers are activated by theNote that only the A-delta fibers are activated by the
frequently used electric and cold "vitality" tests.frequently used electric and cold "vitality" tests.
 This may explain why these tests are not reliable on theThis may explain why these tests are not reliable on the
immature teeth of young patients.immature teeth of young patients.
 These teeth contain significantly fewer A-delta fibersThese teeth contain significantly fewer A-delta fibers
than mature teeth because myelinated nerves do notthan mature teeth because myelinated nerves do not
reach their maximal development and penetration intoreach their maximal development and penetration into
the pulp until the apex completes its development.the pulp until the apex completes its development.

Theories of pain mechanism:Theories of pain mechanism:
 Three of many theories attempting to explain theThree of many theories attempting to explain the
mechanism of pain transmission aremechanism of pain transmission are
 The specificity theoryThe specificity theory (advanced by Von Frey in(advanced by Von Frey in
1894) states that different sensory fibers mediate1894) states that different sensory fibers mediate
different sensory modalities such as pain, heat, cold,different sensory modalities such as pain, heat, cold,
touch, and pressure. The receptors for pain are specifictouch, and pressure. The receptors for pain are specific
and are mostly unmyelinated free nerve endings. Whenand are mostly unmyelinated free nerve endings. When
stimulated, these fibers transmit impulses along specificstimulated, these fibers transmit impulses along specific
pathways.pathways.

 The pattern theoryThe pattern theory proposes that pain beproposes that pain be
generated by nonspecific receptors. It assumesgenerated by nonspecific receptors. It assumes
that all nerve fiber endings are alike and that thethat all nerve fiber endings are alike and that the
pattern for pain is produced by a more intensepattern for pain is produced by a more intense
stimulation than for the other sensations.stimulation than for the other sensations.
 The summation of the pain impulses produce aThe summation of the pain impulses produce a
pattern that the brain receives and recognizes thepattern that the brain receives and recognizes the
mechanism is a subject of controversy.mechanism is a subject of controversy.

Gate controlGate control
 A gating mechanism located in a specific areaA gating mechanism located in a specific area
of gray matter in the spinal cord is called theof gray matter in the spinal cord is called the
substantia gelatinosa.substantia gelatinosa.
 This gating mechanism receives painfulThis gating mechanism receives painful
(sensory or afferent) impulses from peripheral(sensory or afferent) impulses from peripheral
nerves and permits their passage to the brainnerves and permits their passage to the brain
by opening the gate, or prevents their passageby opening the gate, or prevents their passage
by closing the gate.by closing the gate.

 Whether the gate opens or closes depends onWhether the gate opens or closes depends on
(a) the speed (velocity) of the impulse (the larger the(a) the speed (velocity) of the impulse (the larger the
fiber, the greater the velocity),fiber, the greater the velocity),
(b) the interaction between noxious (nociceptive) pain(b) the interaction between noxious (nociceptive) pain
stimuli transmitted along smaller-diameter fibers, andstimuli transmitted along smaller-diameter fibers, and
(c) those stimuli of touch and pressure(c) those stimuli of touch and pressure
(mechanoreceptors) that are transmitted along the(mechanoreceptors) that are transmitted along the
larger diameter fibers.larger diameter fibers.
 Descending central control from intrinsic brainDescending central control from intrinsic brain
mechanisms modulates the gating mechanism.mechanisms modulates the gating mechanism.

Dentin innervation:Dentin innervation:
 The theory of dentin innervation states thatThe theory of dentin innervation states that
there are nerve fibers within the dentinal tubulesthere are nerve fibers within the dentinal tubules
that, when injured, initiate the nerve impulsethat, when injured, initiate the nerve impulse
(action potential).(action potential).
 However, the extent of observable nerve fiberHowever, the extent of observable nerve fiber
penetration has been limited to the predentinpenetration has been limited to the predentin
and inner dentinal zones.and inner dentinal zones.

Relative studiesRelative studies
 Johnsen cited a number of investigators whoJohnsen cited a number of investigators who
have estimated that more than 40% of thehave estimated that more than 40% of the
dentinal tubules in the areas of the pulp hornsdentinal tubules in the areas of the pulp horns
have innervated tubules.have innervated tubules.
 This number diminishes rapidly coronoapically:This number diminishes rapidly coronoapically:
4% to 8% (mid crown),4% to 8% (mid crown), 0.2%0.2% to 1% (cervicalto 1% (cervical
area), andarea), and 0.02%0.02% toto 0.2%0.2% (mid root).(mid root).

 Experimental evidence by investigators (e.g., NiirhiExperimental evidence by investigators (e.g., Niirhi
et aI, Brannstrom and Astrom, Anderson andet aI, Brannstrom and Astrom, Anderson and
Naylor) suggests that nerve fibers are not present inNaylor) suggests that nerve fibers are not present in
peripheral tubules. Such evidence includes:peripheral tubules. Such evidence includes:
 Algogenic (pain-producing) substances such as KCI,Algogenic (pain-producing) substances such as KCI,
bradykinin, acetylcholine, and histamine , do notbradykinin, acetylcholine, and histamine , do not
produce pain when applied to exposed peripheralproduce pain when applied to exposed peripheral
dentin.dentin.
 Hypertonic NaCI solution, capable of depolarizingHypertonic NaCI solution, capable of depolarizing
nerve membranes in the deeper layers of dentin ornerve membranes in the deeper layers of dentin or
the exposed pulp, will not initiate a nerve impulsethe exposed pulp, will not initiate a nerve impulse
when applied to peripheral dentin:when applied to peripheral dentin:
Contradictory reportsContradictory reports

WHY IS DEJ MORE SENSITIVEWHY IS DEJ MORE SENSITIVE
 Yamada's electrophysiologic studies on dentin inYamada's electrophysiologic studies on dentin in
dogs revealed that the dentinoenamel junctiondogs revealed that the dentinoenamel junction
produced more action potentials than in theproduced more action potentials than in the
deeper cavity preparationsdeeper cavity preparations
 dentinoenamel junctional area contains adentinoenamel junctional area contains a
multiplicity of terminal arborizations of themultiplicity of terminal arborizations of the
dentinal tubules and therefore a greater surfacedentinal tubules and therefore a greater surface
area to stimulatearea to stimulate

 Holland demonstrated a greater number of tubules inHolland demonstrated a greater number of tubules in
the predentin and inner dentinal layer. The numberthe predentin and inner dentinal layer. The number
diminished to about one-third in the middle zone ofdiminished to about one-third in the middle zone of
calcified dentin, rising again in the periphery because ofcalcified dentin, rising again in the periphery because of
the terminal branching.the terminal branching.
 These observations by both Yamada and Holland showThese observations by both Yamada and Holland show
that dentin sensitivity is greatest at the periphery,that dentin sensitivity is greatest at the periphery,
decreases in the middle third, and increases again in thedecreases in the middle third, and increases again in the
inner zones, closest to the pulp.inner zones, closest to the pulp.

The dentinoblasts are more vulnerable to injury thanThe dentinoblasts are more vulnerable to injury than
any other pulp cells. When irritated or injured, theyany other pulp cells. When irritated or injured, they
contribute to one or more defense functions of thecontribute to one or more defense functions of the
pulpodentinal complex.pulpodentinal complex.
 Dentinal pain - hypersensitivity.Dentinal pain - hypersensitivity.
 The smear layerThe smear layer
 Tubular sclerosisTubular sclerosis
 Irritation (reparative) dentin formationIrritation (reparative) dentin formation
 Inflammation of the subjacent connective tissueInflammation of the subjacent connective tissue

 If the injury is mild and of short duration, theIf the injury is mild and of short duration, the
response may be limited to- the dentinal tubulesresponse may be limited to- the dentinal tubules
and the dentinoblasts in the form ofand the dentinoblasts in the form of scleroticsclerotic
and/orand/or irritation dentin.irritation dentin.
 As the severity of the irritant increases, theAs the severity of the irritant increases, the
underlying pulp tissue responds with progressiveunderlying pulp tissue responds with progressive
inflammation, first in the subdentinoblastic zoneinflammation, first in the subdentinoblastic zone
and ultimately in the central zone.and ultimately in the central zone.

The smear layer:The smear layer:
 Scaling, abrasion, attrition, caries, and cavityScaling, abrasion, attrition, caries, and cavity
preparation (cutting, grinding) leave microcrystallinepreparation (cutting, grinding) leave microcrystalline
debris or a smear layer that extends slightly into thedebris or a smear layer that extends slightly into the
dentinal tubules (smear plugs), covers the dentinaldentinal tubules (smear plugs), covers the dentinal
surface, and is usually several microns in thickness.surface, and is usually several microns in thickness.
 This debris is mixed with saliva, water, and/or dentinalThis debris is mixed with saliva, water, and/or dentinal
fluidfluid
 Such a closure of the dentin wound reduces bothSuch a closure of the dentin wound reduces both
sensitivity and permeability. In a way this is a defensesensitivity and permeability. In a way this is a defense
mechanism.mechanism.

Tubular sclerosis:Tubular sclerosis:
 PProduced by milder or moderately irritating agents such as slowlyroduced by milder or moderately irritating agents such as slowly
progressing caries, mild acute injury of cavity preparation,progressing caries, mild acute injury of cavity preparation,
abrasion, erosion, attrition, and age changes.abrasion, erosion, attrition, and age changes.
 It is the cumulative effect of several factors: continuingIt is the cumulative effect of several factors: continuing
peritubular dentin formation by the dentinoblastic processesperitubular dentin formation by the dentinoblastic processes
(physiologic sclerosis)(physiologic sclerosis) andand intratubular calcification (pathologic sclerosis).intratubular calcification (pathologic sclerosis).
 Considered a defense mechanism of the pulpodentinal complexConsidered a defense mechanism of the pulpodentinal complex
because its formation alters the permeability of the tubules,because its formation alters the permeability of the tubules,
blocking the access of irritants to the pulp.blocking the access of irritants to the pulp.

Peritubular dentin (physiologic sclerosis)Peritubular dentin (physiologic sclerosis)
 It is calcified secretion of the dentinoblasticIt is calcified secretion of the dentinoblastic
process.process.
 These products, formed in the endoplasmicThese products, formed in the endoplasmic
reticulum of the dentinoblast cell body, passreticulum of the dentinoblast cell body, pass
through the Golgi complex and now appear inthrough the Golgi complex and now appear in
the vesicles of the dentinoblastic process to bethe vesicles of the dentinoblastic process to be
released as peritubular dentin matrix.released as peritubular dentin matrix.

 The sparsity of organic matrix and the highThe sparsity of organic matrix and the high
concentration of calcium salts in the dentinconcentration of calcium salts in the dentin
environment permit the peritubular dentin to beenvironment permit the peritubular dentin to be
more highly mineralized than the intertubularmore highly mineralized than the intertubular
dentin.dentin.
 As a result of both peritubular dentin formation andAs a result of both peritubular dentin formation and
intratubular calcification, the tubules become narrowerintratubular calcification, the tubules become narrower
and may ultimately close completely (sclerosis).and may ultimately close completely (sclerosis).

Intratubular calcification (pathologic sclerosis)Intratubular calcification (pathologic sclerosis)
 It is a physicochemical process caused by theIt is a physicochemical process caused by the
precipitation of mineral salts within the dentinalprecipitation of mineral salts within the dentinal
tubules and is therefore fundamentally differenttubules and is therefore fundamentally different
from peritubular dentin.from peritubular dentin.
 This type of calcification is found in theThis type of calcification is found in the
translucent zone of carious dentin and in thetranslucent zone of carious dentin and in the
dentin of severe attrition, erosion, and abrasion.dentin of severe attrition, erosion, and abrasion.

 Frank et al. identified the intratubular deposits asFrank et al. identified the intratubular deposits as
hydroxyapatite crystals (needle shaped) andhydroxyapatite crystals (needle shaped) and
Whitlockite crystals (rhomboidal).Whitlockite crystals (rhomboidal).
 A hypothesis for another source of pathologicA hypothesis for another source of pathologic
sclerosis is the precipitation of the calciumsclerosis is the precipitation of the calcium
phosphate salts from the supersaturated dentinalphosphate salts from the supersaturated dentinal
fluid, which may obliterate the dentinal tubulesfluid, which may obliterate the dentinal tubules
by being deposited in or around degeneratingby being deposited in or around degenerating
dentinoblastic processes..dentinoblastic processes..

Irritation dentin formationIrritation dentin formation
 It may be referred to as defensive dentinIt may be referred to as defensive dentin
because it is a means of pulpodentinal defense.because it is a means of pulpodentinal defense.
 The tubular structure of this rapid formingThe tubular structure of this rapid forming
dentin can be erratic.dentin can be erratic.
 The tubules are frequently twisted and lessThe tubules are frequently twisted and less
numerous than in regular dentin and at times arenumerous than in regular dentin and at times are
completely absent.completely absent.

 This dentinal barrier helps block irritants fromThis dentinal barrier helps block irritants from
the exterior but also prevents reinnervation ofthe exterior but also prevents reinnervation of
injured dentin by sprouting pulpal nerve fibers.injured dentin by sprouting pulpal nerve fibers.
 Adjacent surviving dentin with intact dentinalAdjacent surviving dentin with intact dentinal
tubules may become heavily innervated in thetubules may become heavily innervated in the
repair process.repair process.

Inflammation.Inflammation.
 Mild and moderate injury to the dentinoblasticMild and moderate injury to the dentinoblastic
processes may produce tubular sclerosis andprocesses may produce tubular sclerosis and
irritation dentin.irritation dentin.
 But prolonged and/or severe irritation canBut prolonged and/or severe irritation can
irreversibly affect the plasma membrane and theirreversibly affect the plasma membrane and the
nucleus of the dentinoblasts, thus initiating thenucleus of the dentinoblasts, thus initiating the
first step toward an inflammatory responsefirst step toward an inflammatory response
(pulpitis).(pulpitis).

 For example, the irritation of deep cavity lessFor example, the irritation of deep cavity less
than 2 mm from the pulp may be intensified by:than 2 mm from the pulp may be intensified by:
 1. Inadequate water coolants1. Inadequate water coolants
 2. Acid cements2. Acid cements
 3. Inadequate insulation of metal fillings3. Inadequate insulation of metal fillings
 4. Micro leakage of restorations4. Micro leakage of restorations

Five facets of inflammationFive facets of inflammation
 Nature of the inflammatory responseNature of the inflammatory response
 Role of the dentinoblastRole of the dentinoblast
 Primary factors that initiate the inflammatoryPrimary factors that initiate the inflammatory
responseresponse
 Types of inflammationTypes of inflammation
 Immunologic considerationsImmunologic considerations

Nature of the inflammatory responseNature of the inflammatory response
 TheThe exudative (acute) responseexudative (acute) response is the initial immediateis the initial immediate
response of the pulpal or periapical tissue to anyresponse of the pulpal or periapical tissue to any
irritant-mechanical, chemical, thermal, or microbial.irritant-mechanical, chemical, thermal, or microbial.
 This emergency action to overcome and neutralize theThis emergency action to overcome and neutralize the
injurious agent is characterized by an inflammatoryinjurious agent is characterized by an inflammatory
edema to dilute and detoxify and by the infiltration ofedema to dilute and detoxify and by the infiltration of
white cells to ingest and immobilize the irritant.white cells to ingest and immobilize the irritant.
 The dominant cells in this phase are theThe dominant cells in this phase are the
polymorphonuclear leukocytes (neutrophils).polymorphonuclear leukocytes (neutrophils).

 TheThe proliferative (chronic) responseproliferative (chronic) response is a secondary or delayedis a secondary or delayed
action.action.
 Its presence depends on the ability of the exudativeIts presence depends on the ability of the exudative
(acute) forces to decrease the toxicity of the irritant.(acute) forces to decrease the toxicity of the irritant.
 It is an attempt of the connective tissue components ofIt is an attempt of the connective tissue components of
the pulp and periapex to form new cells (fibroblasts),the pulp and periapex to form new cells (fibroblasts),
blood vessels (angioblasts), and fibers.blood vessels (angioblasts), and fibers.
 Pulpal and periapical nerve fibers proliferate inPulpal and periapical nerve fibers proliferate in
response to acute pulpal injury.response to acute pulpal injury.

 Sprouting of these nerve fibers occurs in pulpal areasSprouting of these nerve fibers occurs in pulpal areas
subjacent to the injury site but also in correspondingsubjacent to the injury site but also in corresponding
periapical before apical progression of pathosisperiapical before apical progression of pathosis
 These elements constituteThese elements constitute granulation tissuegranulation tissue whosewhose
function is to repair and replace the damaged tissuefunction is to repair and replace the damaged tissue
 Granulomatous tissue is therefore not only a healingGranulomatous tissue is therefore not only a healing
tissue,tissue, but a defense tissue as well, wherebut a defense tissue as well, where
organisms are destroyed, not nurtured.organisms are destroyed, not nurtured.

Role of the dentinoblastRole of the dentinoblast
 The following sequence of changes can be observedThe following sequence of changes can be observed
as the dentinoblastic injury increases progressively:as the dentinoblastic injury increases progressively:
 Increased permeability of the dentinal tubuleIncreased permeability of the dentinal tubule because of thebecause of the
destructive effect of the injury to the dentinoblastdestructive effect of the injury to the dentinoblast
and its process. Microorganisms and chemicaland its process. Microorganisms and chemical
irritants now have easier access to the pulp.irritants now have easier access to the pulp.
 Disturbance of the pulpodentinal membrane.Disturbance of the pulpodentinal membrane. This is not aThis is not a
true membrane but a three dimensional illusiontrue membrane but a three dimensional illusion
caused by the junctional complexes. Thecaused by the junctional complexes. The
disturbance is a reflection of the aggregatedisturbance is a reflection of the aggregate
breakdown of the dentinoblastsbreakdown of the dentinoblasts

 Disruption of the palisaded dentinoblastic layer.Disruption of the palisaded dentinoblastic layer.
 Aspiration of many of the dentinoblastic nucleiAspiration of many of the dentinoblastic nuclei intointo
the dentinal tubules (also referred to asthe dentinal tubules (also referred to as
displacementdisplacement oror migration).migration). This phenomenonThis phenomenon
may be due to the outward flow of tubularmay be due to the outward flow of tubular
fluid (Brannstrom) as a result of dry frictionalfluid (Brannstrom) as a result of dry frictional
heat, air blast, etc.heat, air blast, etc.
 Irreversible dentinoblastic injury,Irreversible dentinoblastic injury, which results inwhich results in
the release of thethe release of the tissue injury factors.tissue injury factors.

 Inflammatory changesInflammatory changes in the dentinoblastic zone.in the dentinoblastic zone.
These includeThese include
dilation of capillaries and the resultant stasis of theirdilation of capillaries and the resultant stasis of their
blood flow.blood flow.
Autolysis can also occur if oxygen and metabolitesAutolysis can also occur if oxygen and metabolites
are denied because of congestion of nearby bloodare denied because of congestion of nearby blood
vessels (within 2 to 4 minutes). The subsequentvessels (within 2 to 4 minutes). The subsequent
effect of such severe injuries is the furthereffect of such severe injuries is the further
disruption of the palisade arrangement of the cellsdisruption of the palisade arrangement of the cells
and the accumulation of edematous fluid within theand the accumulation of edematous fluid within the
tissue gaps createdtissue gaps created (vacuolization).(vacuolization).

 Subdentinoblastic inflammatory changesSubdentinoblastic inflammatory changes
vasodilation, leukocytic infiltration, edema.vasodilation, leukocytic infiltration, edema.
 Central zone inflammationCentral zone inflammation reflects thereflects the
circumferential and apical progression ofcircumferential and apical progression of
irreversible total pulpitisirreversible total pulpitis

Physiologic changes in the pulpPhysiologic changes in the pulp
 AgingAging --Atrophy and fibrosisAtrophy and fibrosis causes a lot ofcauses a lot of
changes in the pulp.changes in the pulp.
 ItIt tries to ward off the irritants by increasing itstries to ward off the irritants by increasing its
fibrillar content and decreasing the cellularfibrillar content and decreasing the cellular
content.content.

 With age, there is an increase in length and diameter toWith age, there is an increase in length and diameter to
form mature collagen fibers.form mature collagen fibers.
 These larger collagen fibers are made up of bundles ofThese larger collagen fibers are made up of bundles of
several to a few dozen fibrils.several to a few dozen fibrils.
 The number and size of the cytoplasmic organellesThe number and size of the cytoplasmic organelles
decrease.decrease.
 Atherosclerotic plaques appear in the pulpal vessels.Atherosclerotic plaques appear in the pulpal vessels.
(Orban’s, 11(Orban’s, 11thth
edition)edition)

 A study by Bernick and Nedelman demonstrated that inA study by Bernick and Nedelman demonstrated that in
the aging process the following occurred:the aging process the following occurred:
 Progressive reduction in the size of the pulp chamberProgressive reduction in the size of the pulp chamber
 Progressive deposition of calcium masses that originateProgressive deposition of calcium masses that originate
in the root pulp and progress into the coronal pulpin the root pulp and progress into the coronal pulp
 Decrease in the nerves and blood vessels of the coronalDecrease in the nerves and blood vessels of the coronal
pulp because of the calcification in these structurespulp because of the calcification in these structures
 Persistence of the connective tissue sheaths of thePersistence of the connective tissue sheaths of the
affected blood vessels and nerves, giving the pulp aaffected blood vessels and nerves, giving the pulp a
fibrotic appearancefibrotic appearance

CalcificationsCalcifications
 These are found in both healthy and aging pulps,These are found in both healthy and aging pulps,
although their incidence increases with agealthough their incidence increases with age
 Willman found calcifications in 87% of. 164 teethWillman found calcifications in 87% of. 164 teeth
selected at random. Many of the calcifications (15%)selected at random. Many of the calcifications (15%)
were not seen on a radiograph.were not seen on a radiograph.
 Hill reported calcifications in 66% of all teeth inHill reported calcifications in 66% of all teeth in
individuals between 10 and 20 years of age and 90%individuals between 10 and 20 years of age and 90%
between 50 and 70 years of age.between 50 and 70 years of age.

 Dystrophic calcificationDystrophic calcification is a deposition of calcium salts inis a deposition of calcium salts in
dead or degenerating tissue. It may be due to localdead or degenerating tissue. It may be due to local
alkalinity of the destroyed tissue that attracts the salts.alkalinity of the destroyed tissue that attracts the salts.
This mineralization thus may occur in minute areas ofThis mineralization thus may occur in minute areas of
young pulp tissue affected by minor circulatoryyoung pulp tissue affected by minor circulatory
disturbance.disturbance.
 Diffuse calcificationsDiffuse calcifications are generally observed in the rootare generally observed in the root
canal but may also be seen in the pulp chamber.canal but may also be seen in the pulp chamber.
 The larger, well-outlined dentic1es develop moreThe larger, well-outlined dentic1es develop more
frequently in the pulp chamber.frequently in the pulp chamber.

 Pulp denticles, are classified according to location (free,Pulp denticles, are classified according to location (free,
embedded, or attached) and according to structure (true or false).embedded, or attached) and according to structure (true or false).
 Free denticlesFree denticles,, lying free in the chamber, may become attachedlying free in the chamber, may become attached
or embedded as more dentin is laid down around them.or embedded as more dentin is laid down around them.
 True denticlesTrue denticles are not dystrophic structures, since they areare not dystrophic structures, since they are
composed of dentin and formed by detached dentinoblasts orcomposed of dentin and formed by detached dentinoblasts or
fragments of Hertwig's sheath, which may stimulatefragments of Hertwig's sheath, which may stimulate
undifferentiated cells to assume dentinoblastic activity.undifferentiated cells to assume dentinoblastic activity.
 False denticlesFalse denticles are formed when a degenerating tissue structureare formed when a degenerating tissue structure
serves as a nidus for deposition of concentric layers of calcifiedserves as a nidus for deposition of concentric layers of calcified
tissue.tissue.

Pulp in clinical scenarioPulp in clinical scenario
REACTION TO CARIOUS LESIONREACTION TO CARIOUS LESION
 The initial ports of entry to the pulp for bacteria,The initial ports of entry to the pulp for bacteria,
bacterial antigens, toxic, and allergenicbacterial antigens, toxic, and allergenic
components are the dentinal tubules.components are the dentinal tubules.
 The pulp subjacent to deep caries lesions showsThe pulp subjacent to deep caries lesions shows
the presence of chronic inflammatory exudate,the presence of chronic inflammatory exudate,
including lymphocytes, macrophages, and plasmaincluding lymphocytes, macrophages, and plasma
cells.cells.
 Formation of tertiary dentin usually takes place onFormation of tertiary dentin usually takes place on
the pulpal aspect of the affected tubules.the pulpal aspect of the affected tubules.

 The localized increase in dentin thickness is oftenThe localized increase in dentin thickness is often
accompanied by a reduced odontoblastic layer in theaccompanied by a reduced odontoblastic layer in the
affected area.affected area.
 The depth of bacterial penetration into the dentin hasThe depth of bacterial penetration into the dentin has
been claimed to be decisive for the degree ofbeen claimed to be decisive for the degree of
inflammatory reactioninflammatory reaction
 The pulpal reactions are well localized to the affectedThe pulpal reactions are well localized to the affected
dentindentin
 increased tissue fluid pressure associated with pulpalincreased tissue fluid pressure associated with pulpal
inflammation.inflammation.
 cellular proliferation in the cell-free zone was notedcellular proliferation in the cell-free zone was noted

IATROGENIC PULP TESTINGIATROGENIC PULP TESTING
 According to Van Hassel, intrapulpal pressure variationsAccording to Van Hassel, intrapulpal pressure variations
provide much of the pain phenomena associated with pulpitis.provide much of the pain phenomena associated with pulpitis.
 He suggests further that heat and cold are two distinctlyHe suggests further that heat and cold are two distinctly
different diagnostic tools because they represent two differentdifferent diagnostic tools because they represent two different
phenomenaphenomena
1.1. Heat stimulationHeat stimulation
 Heat causes vasodilation and subsequent increases in intrapulpalHeat causes vasodilation and subsequent increases in intrapulpal
pressure. If the threshold of the sensory structures is reached,pressure. If the threshold of the sensory structures is reached,
pain is produced.pain is produced.
 Intrapulpal pressure rises directly and predictably as heat isIntrapulpal pressure rises directly and predictably as heat is
applied to the tooth.applied to the tooth.

 In an intact pulp a specific pulpal temperatureIn an intact pulp a specific pulpal temperature
must be reached before there is pain from heat.must be reached before there is pain from heat.
Therefore application of heat to normal teethTherefore application of heat to normal teeth
gives a delayed response.gives a delayed response.
 In a tooth with an inflamed pulp an increasedIn a tooth with an inflamed pulp an increased
intrapulpal pressure already exists; therefore oneintrapulpal pressure already exists; therefore one
would expect an immediate painful response towould expect an immediate painful response to
gradual or sudden heat increase.gradual or sudden heat increase.

Cold stimulationCold stimulation
 The response to cold of a tooth with a normal or intact pulp isThe response to cold of a tooth with a normal or intact pulp is
immediate. Since cold decreases intrapulpal pressure, pain fromimmediate. Since cold decreases intrapulpal pressure, pain from
this source cannot be caused by increased pressure.this source cannot be caused by increased pressure.
 Brannstrom attributes the pain from cold to a hydrodynamicsBrannstrom attributes the pain from cold to a hydrodynamics
mechanism.mechanism.
 The contraction of the fluid results in a rapid outward flow ofThe contraction of the fluid results in a rapid outward flow of
fluid in the dentinal tubules and the subjacent pulpal tissue.fluid in the dentinal tubules and the subjacent pulpal tissue.
 Such a movement deforms intratubular and peripheral (A-delta)Such a movement deforms intratubular and peripheral (A-delta)
nerve membranes, which activates an action potential.nerve membranes, which activates an action potential.

 In advanced acute pulpitis (advanced acute pulpalgia) whenIn advanced acute pulpitis (advanced acute pulpalgia) when
coronal necrosis is present in varying degrees, cold may notcoronal necrosis is present in varying degrees, cold may not
exacerbate the painful symptoms.exacerbate the painful symptoms.
 If the peripheral coronal A-delta receptor units are not viable,If the peripheral coronal A-delta receptor units are not viable,
they cannot be activated by fluid movement.they cannot be activated by fluid movement.
 Instead, cold relieves the pain immediately because theInstead, cold relieves the pain immediately because the
vasoconstrictor effect reduces the blood volume.vasoconstrictor effect reduces the blood volume.
 This in turn lowers the intrapulpal pressure to a subthresholdThis in turn lowers the intrapulpal pressure to a subthreshold
level for still viable C fibers.level for still viable C fibers.
 Removal of the cold results in the return to pain within 30 to 60Removal of the cold results in the return to pain within 30 to 60
seconds as the intrapulpal pressure returns to its formerseconds as the intrapulpal pressure returns to its former
suprathreshold level.suprathreshold level.

DENTISTOGENIC" (IATROGENIC) PULPITISDENTISTOGENIC" (IATROGENIC) PULPITIS
 Some commonly used operative procedures endangerSome commonly used operative procedures endanger
the health of the tooth more than do the diseasethe health of the tooth more than do the disease
processes they are intended to correct.processes they are intended to correct.
 Decay, in many instances, is much less harmful than theDecay, in many instances, is much less harmful than the
operative procedure used to treat itoperative procedure used to treat it
 Pulp inflammation for which the dentists ownPulp inflammation for which the dentists own
procedures are responsible may well be designatedprocedures are responsible may well be designated
"dentistogenic pulpitis""dentistogenic pulpitis"

DEPTH OF CAVITYDEPTH OF CAVITY
PREPARATIONSPREPARATIONS
 Cavity preparation causes an increased rate of dentinCavity preparation causes an increased rate of dentin
collagen turnover (Hoppenbrouwers et aI, 1982) andcollagen turnover (Hoppenbrouwers et aI, 1982) and
some odontoblastic cell damage (Kawahara andsome odontoblastic cell damage (Kawahara and
Yamagami, 1970).Yamagami, 1970).
 The deeper a cavity is cut and, therefore, the closer theThe deeper a cavity is cut and, therefore, the closer the
odontoblastic nucleus is approached, the more severe isodontoblastic nucleus is approached, the more severe is
the injury to the odontoblast.the injury to the odontoblast.
 A superficial cavity preparation that cuts theA superficial cavity preparation that cuts the
odontoblastic processes close to the dentinoenamelodontoblastic processes close to the dentinoenamel
junction usually produces only mild irritationjunction usually produces only mild irritation

 As the cavity depth is increased, and with theAs the cavity depth is increased, and with the
cutting of the odontoblastic processes, there iscutting of the odontoblastic processes, there is
an increase in irritation, with a consequentan increase in irritation, with a consequent
increase in the rate of production of reparativeincrease in the rate of production of reparative
dentindentin
 It was found that about 45,000 tubules per mmIt was found that about 45,000 tubules per mm22
near the pulp, in the middle dentin, there werenear the pulp, in the middle dentin, there were
29,500 tubules per mm29,500 tubules per mm22
and at the periphery, theand at the periphery, the
number of tubules decreased to 20,000/mmnumber of tubules decreased to 20,000/mm22

 The closer the dentin preparation is to the pulp,The closer the dentin preparation is to the pulp,
the greater the number of dentinal tubules perthe greater the number of dentinal tubules per
unit surface area.unit surface area.
 Closer to the pulp, there is also an increase inCloser to the pulp, there is also an increase in
the diameter of each tubule.the diameter of each tubule.
Both of these factors contribute to an increaseBoth of these factors contribute to an increase
in diffusional surface area in dentin.in diffusional surface area in dentin.

 When not more than 0.5 mm of dentin remain between the baseWhen not more than 0.5 mm of dentin remain between the base
of a cavity and the pulp, each decrease of 0.1 mm producesof a cavity and the pulp, each decrease of 0.1 mm produces
progressively more severe pulp inflammation in low-speedprogressively more severe pulp inflammation in low-speed
preparations without coolant.preparations without coolant.
 When low-speed preparations are made with proper coolingWhen low-speed preparations are made with proper cooling
devices, the floor of the preparation can be brought much closerdevices, the floor of the preparation can be brought much closer
to the pulp (0.3 mm) with less danger of severe inflammatoryto the pulp (0.3 mm) with less danger of severe inflammatory
response.response.
 With high-speed preparations also (200,000 rpm and more), theWith high-speed preparations also (200,000 rpm and more), the
damage is less severe, provided adequate cooling is delivered atdamage is less severe, provided adequate cooling is delivered at
the interface between the bur and the dentinthe interface between the bur and the dentin
(Seltzer and Bender,3(Seltzer and Bender,3rdrd
edition)edition)

EFFECTIVE DEPTHEFFECTIVE DEPTH
 The effective depth is the area of minimumThe effective depth is the area of minimum
thickness of sound dentin separating the pulpalthickness of sound dentin separating the pulpal
tissue from the carious lesiontissue from the carious lesion
 2mm or more, healthy reparative reaction2mm or more, healthy reparative reaction
 0.8 – 2mm, unhealthy reparative reation0.8 – 2mm, unhealthy reparative reation
 0.3 – 0.8mm, pulpal destucton0.3 – 0.8mm, pulpal destucton
(Marzouk, Indian edition 2006)(Marzouk, Indian edition 2006)

EXTENSIVENESS OFEXTENSIVENESS OF
PREPARATIONPREPARATION
 The extensiveness of the preparation has an influenceThe extensiveness of the preparation has an influence
on the amount of heat generatedon the amount of heat generated
 Class 1 and Class 5 cavity preparations produced aClass 1 and Class 5 cavity preparations produced a
much lower heat reaction than did mesioocclusodistalmuch lower heat reaction than did mesioocclusodistal
(MOD) or full crown preparations.(MOD) or full crown preparations.
 Full crown shoulder preparations are more harmful toFull crown shoulder preparations are more harmful to
the pulp than are shoulderless ones, because, in thethe pulp than are shoulderless ones, because, in the
former, the preparations are much deeper into theformer, the preparations are much deeper into the
dentin and closer to the pulpdentin and closer to the pulp

PINLEDGE PREPARATIONSPINLEDGE PREPARATIONS
 In pinledge the use of high-speed instruments shouldIn pinledge the use of high-speed instruments should
be avoided because the coolant is prevented frombe avoided because the coolant is prevented from
reaching the depth of the preparationreaching the depth of the preparation
 The insertion of pins introduces the hazard of dentinalThe insertion of pins introduces the hazard of dentinal
fractures or unnoticed pulp exposures.fractures or unnoticed pulp exposures.
 Moreover, the deep insertion of the pin can increaseMoreover, the deep insertion of the pin can increase
pulpal irritation of an already chronically inflamed pulppulpal irritation of an already chronically inflamed pulp

 To mitigate the extra irritation from the pins, theTo mitigate the extra irritation from the pins, the
application of calcium hydroxide in the preapplication of calcium hydroxide in the pre
pared holes has been advocatedpared holes has been advocated
(Suzuki et al,1973).(Suzuki et al,1973).
 The response to pin insertion was minimal ifThe response to pin insertion was minimal if
some remaining dentin was present.some remaining dentin was present.
 However, dentinal cracks and slightHowever, dentinal cracks and slight
inflammatory changes persisted for few days.inflammatory changes persisted for few days.

SPEED OF ROTATIONSPEED OF ROTATION
 When dentin is cut by rotary instruments at variousWhen dentin is cut by rotary instruments at various
speeds, an odontoblastic reaction will occur; the injuryspeeds, an odontoblastic reaction will occur; the injury
varies in degree only.varies in degree only.
 The greatest amount of odontoblastic damage occurs atThe greatest amount of odontoblastic damage occurs at
speeds up to 50,000 rpm with both belt-driven andspeeds up to 50,000 rpm with both belt-driven and
turbine-driven instruments.turbine-driven instruments.
 The least amount of damage occurs at speeds ofThe least amount of damage occurs at speeds of
150,000 to 250,000 rpm, provided that a coolant is used150,000 to 250,000 rpm, provided that a coolant is used
properly.properly.

 Marsland and Shovelton (1957) and LangelandMarsland and Shovelton (1957) and Langeland
(1961) reported that very low speeds (300-500(1961) reported that very low speeds (300-500
rpm) produced an absence of, or a reduction in,rpm) produced an absence of, or a reduction in,
odontoblastic reactionsodontoblastic reactions
 Without the use of a coolant, there is no safeWithout the use of a coolant, there is no safe
speed.speed.
 However, with sharp burs at 3000 to 5000 rpm,However, with sharp burs at 3000 to 5000 rpm,
without coolant, there is less damage than atwithout coolant, there is less damage than at
ultra-high speeds without coolantultra-high speeds without coolant
(Riethe, 1969)(Riethe, 1969)

 With the increase of speeds of rotation of cuttingWith the increase of speeds of rotation of cutting
instruments, not only is greater heat generated but thereinstruments, not only is greater heat generated but there
is also an increase in vibrations, which affects the pulp.is also an increase in vibrations, which affects the pulp.
 Searles (1967) has pointed out that mechanical vibrationSearles (1967) has pointed out that mechanical vibration
during high speed drilling may be responsible forduring high speed drilling may be responsible for
protein denaturation of the odontoblasts.protein denaturation of the odontoblasts.
 The denaturation causes morphologic changes leadingThe denaturation causes morphologic changes leading
to destruction of the odontoblasts.to destruction of the odontoblasts.
(Seltzer and Bender, 3(Seltzer and Bender, 3rdrd
edition)edition)

DRY CAVITY PEPARATIONDRY CAVITY PEPARATION
 It has been found that dry cavity preparationIt has been found that dry cavity preparation
causes greater trauma to the pulp thancauses greater trauma to the pulp than
preparation under water spraypreparation under water spray
(Cotton et at 1965)(Cotton et at 1965)
 Prolonged dehydration with air causesProlonged dehydration with air causes
odontoblastic displacement and pulpal oedema,odontoblastic displacement and pulpal oedema,
a condition that cannot be reversed bya condition that cannot be reversed by
moistening the dentin after cavity preparation.moistening the dentin after cavity preparation.

 Pulpal temperatures above 46° C causedPulpal temperatures above 46° C caused
irreversible changes stasis and thrombosis in theirreversible changes stasis and thrombosis in the
pulp blood vessels.pulp blood vessels.
(Pohto and Scheinin,1958)(Pohto and Scheinin,1958)
 Intrapulpal pressure is also affected by excessiveIntrapulpal pressure is also affected by excessive
heat generation causing a rise due to release ofheat generation causing a rise due to release of
various amines leading to persistentvarious amines leading to persistent
vasodilatation.vasodilatation.

NATURE OF CUTTINGNATURE OF CUTTING
INSTRUMENTINSTRUMENT
 Marsland and Shoelton (1957) and Weiss et al (1963)Marsland and Shoelton (1957) and Weiss et al (1963)
demonstrated that thermal damage was greater withdemonstrated that thermal damage was greater with
steel burs than with carbide burs.steel burs than with carbide burs.
 With proper cooling, carbide burs produce negligibleWith proper cooling, carbide burs produce negligible
pulp damage.pulp damage.
 Even with proper coolant, diamond instruments areEven with proper coolant, diamond instruments are
capable of producing damage to pulp, but this may becapable of producing damage to pulp, but this may be
related to additional pressurerelated to additional pressure
(Shovelton and Marsland, 1958)(Shovelton and Marsland, 1958)

SIZE OF WHEELS AND BURSSIZE OF WHEELS AND BURS
 The size of wheels and burs that are used is significant.The size of wheels and burs that are used is significant.
 The larger sizes produce greater pulp damage, owing toThe larger sizes produce greater pulp damage, owing to
increased heat generation and a greater area is cut at theincreased heat generation and a greater area is cut at the
same time.same time.
 The coolant cannot get to the tooth as readily, resultingThe coolant cannot get to the tooth as readily, resulting
in more severe reactionsin more severe reactions
 Less severe reactions are seen when smaller instrumentsLess severe reactions are seen when smaller instruments
are employed.are employed.

HAND INSTRUMENTSHAND INSTRUMENTS
 It has been noted that damage to pulp seemed toIt has been noted that damage to pulp seemed to
be more severe with the use of handbe more severe with the use of hand
instruments.instruments.
(Massler,JOE 1959)(Massler,JOE 1959)
 Pressure introduced With the use of handPressure introduced With the use of hand
instruments is responsible for the pulpalinstruments is responsible for the pulpal
damage.damage.

COOLANTSCOOLANTS
 There is less likelihood of pulp damage when water isThere is less likelihood of pulp damage when water is
used as the coolantused as the coolant
(Zach and Cohen, 1962).(Zach and Cohen, 1962).
 Zach and Cohen (1962; 1965) and Marsland andZach and Cohen (1962; 1965) and Marsland and
Shovelton (1970) found that the immediate damage toShovelton (1970) found that the immediate damage to
the dental pulp was greater in air-cooled than in waterthe dental pulp was greater in air-cooled than in water
cooled teeth, up to 15 days postoperatively.cooled teeth, up to 15 days postoperatively.
 Furthermore, up to 7 weeks, repair processes wereFurthermore, up to 7 weeks, repair processes were
more advanced in the pulp of the water-cooledmore advanced in the pulp of the water-cooled
specimens.specimens.

 Furthermore, with water cooling, the rate of removal ofFurthermore, with water cooling, the rate of removal of
debris is improveddebris is improved
(Lloyd et al, 1978).(Lloyd et al, 1978).
 Kim et al (1983) observed the pulpal microvasculatureKim et al (1983) observed the pulpal microvasculature
that were subjected to full crown preparations boththat were subjected to full crown preparations both
with and without water spray.with and without water spray.
 The pulpal blood flow was reduced by 12% in the toothThe pulpal blood flow was reduced by 12% in the tooth
prepared with water spray. After 1 hour, the blood flowprepared with water spray. After 1 hour, the blood flow
returned to within 7% of the control.returned to within 7% of the control.
 Without water spray, there was a 44% reduction ofWithout water spray, there was a 44% reduction of
blood flow. After 1 hour, the pulpal blood flow wasblood flow. After 1 hour, the pulpal blood flow was
even further decreased.even further decreased.

 To be effective, the water should be deliveredTo be effective, the water should be delivered
directly at the point of contact between the burdirectly at the point of contact between the bur
and the toothand the tooth
 High-speed cutting should be done with a brushHigh-speed cutting should be done with a brush
stroke similar to that employed by a painterstroke similar to that employed by a painter
using water colors. In this way, the bur and theusing water colors. In this way, the bur and the
tooth can be covered simultaneously by thetooth can be covered simultaneously by the
coolant.coolant.

 The temperature of the water cooling used duringThe temperature of the water cooling used during
cavity preparation apparently has little significant effectcavity preparation apparently has little significant effect
on the pulp.on the pulp.
 Croft and Stanley (1966) found no significantCroft and Stanley (1966) found no significant
histopathologic differences between three groups ofhistopathologic differences between three groups of
teeth in which cavity preparations were made withteeth in which cavity preparations were made with
different coolant temperatures ranging from 12.5°Cdifferent coolant temperatures ranging from 12.5°C
(54.5°F) to 18°C (64.4°F).(54.5°F) to 18°C (64.4°F).
 Frank et al (1972) found that even subfreezingFrank et al (1972) found that even subfreezing
temperatures produced only a transient fall intemperatures produced only a transient fall in
intrapulpal blood pressure, a condition that was quicklyintrapulpal blood pressure, a condition that was quickly
reversible.reversible.

POLISHING OF RESTORATIONSPOLISHING OF RESTORATIONS
 Polishing of restorations without takingPolishing of restorations without taking
precautions for dissipation of heat is dangerousprecautions for dissipation of heat is dangerous
to the pulpto the pulp
(Aplin et al, 1967).(Aplin et al, 1967).
 A significant elevation in temperature occurs asA significant elevation in temperature occurs as
a result of friction.a result of friction.www.indiandentalacademy.com

 Sandpaper discs or rubber cups, run dry at high speeds,Sandpaper discs or rubber cups, run dry at high speeds,
can generate sufficient heat to damage the pulp.can generate sufficient heat to damage the pulp.
 The generated heat can also cause enamel to fractureThe generated heat can also cause enamel to fracture
(Brown et al,IEJ 1978).(Brown et al,IEJ 1978).
 Therefore, polishing instruments should be runTherefore, polishing instruments should be run
intermittently at low speeds, or in conjunction withintermittently at low speeds, or in conjunction with
coolants in order to reduce heat generationcoolants in order to reduce heat generation
(Christensen and Dilts, 1968).(Christensen and Dilts, 1968).

TRAUMATIC OCCLUSIONTRAUMATIC OCCLUSION
 Clinical observations have led to the postulation thatClinical observations have led to the postulation that
excessive occlusal forces may cause pulp changes suchexcessive occlusal forces may cause pulp changes such
as increased pulp stones, pulpitis, and necrosisas increased pulp stones, pulpitis, and necrosis
(Natkin and Ingle, 1963; Ramfjord and Ash, 1966).(Natkin and Ingle, 1963; Ramfjord and Ash, 1966).
 Landay et al (1970) found that light occlusal forcesLanday et al (1970) found that light occlusal forces
produced by the placement of high amalgamproduced by the placement of high amalgam
restorations had not caused significant pulpal changesrestorations had not caused significant pulpal changes
over short periods (up to 6 months).over short periods (up to 6 months).

 subsequently concentrations of macrophagessubsequently concentrations of macrophages
and lymphocytes became evident in the pulps ofand lymphocytes became evident in the pulps of
the traumatized teeth.the traumatized teeth.
 In addition, there were disruptions of theIn addition, there were disruptions of the
odontoblastic layer and deposition of reparativeodontoblastic layer and deposition of reparative
dentin on the floor of the pulp chamber and indentin on the floor of the pulp chamber and in
the root canals.the root canals.

CHEMICAL IRRITANTS TO THECHEMICAL IRRITANTS TO THE
PULPPULP
 DENTIN STERILIZING AGENTS – used toDENTIN STERILIZING AGENTS – used to
destroy bacteria in the dentinal tubules in deepdestroy bacteria in the dentinal tubules in deep
carious lesions.carious lesions.
1. Phenol – it increased, rather than decreasing the1. Phenol – it increased, rather than decreasing the
permeability of dentinal tubules, thereforepermeability of dentinal tubules, therefore
greater pulpal damage.greater pulpal damage.
(Martin, 1951)(Martin, 1951)

2. Silver nitrate – silver salts diffuse rapidly2. Silver nitrate – silver salts diffuse rapidly
through the dentinal tubules and regardless ofthrough the dentinal tubules and regardless of
the depth of the cavity eventually reach the pulpthe depth of the cavity eventually reach the pulp
tissue resulting in an inflammatory reaction.tissue resulting in an inflammatory reaction.
3. Camphorated parachlorophenol and penicillin-3. Camphorated parachlorophenol and penicillin-
combination of both is an effective in deepcombination of both is an effective in deep
cavities but cause pulpal inflammation.cavities but cause pulpal inflammation.
(Langeland,JOE 1981)(Langeland,JOE 1981)

4. Eugenol – when mixed loosely with zinc oxide inhibits4. Eugenol – when mixed loosely with zinc oxide inhibits
the action potential in the nerve fibers thus reducingthe action potential in the nerve fibers thus reducing
pain associated with pulpal inflammation (anodynepain associated with pulpal inflammation (anodyne
effect).effect).
(Trowbridge et al,JOE 1982)(Trowbridge et al,JOE 1982)
- When placed on exposed pulp, a marked inflammatoryWhen placed on exposed pulp, a marked inflammatory
reaction is seen.reaction is seen.
- The presence of an intervening layer of dentin isThe presence of an intervening layer of dentin is
necessary to prevent an inflammatory response.necessary to prevent an inflammatory response.

SILICATE CEMENTSILICATE CEMENT
 Severe pulp irritantSevere pulp irritant
 The pH at the time of insertion is about 2.0 andThe pH at the time of insertion is about 2.0 and
remains below 7 even after a month.remains below 7 even after a month.
ZINC PHOSPHATE CEMENTZINC PHOSPHATE CEMENT
 Pulp response is moderate.Pulp response is moderate.
 Three minutes after mixing the pH is about 3.0Three minutes after mixing the pH is about 3.0
 It approaches neutrality in 24 to 48 hours.It approaches neutrality in 24 to 48 hours.

 Thickness of dentine as great as 1.5mm can beThickness of dentine as great as 1.5mm can be
penetrated by the acid.penetrated by the acid.
 Thus very thin mixes should be avoided as theyThus very thin mixes should be avoided as they
are more acidic.are more acidic.
ZINC OXIDE EUGENOL CEMENTZINC OXIDE EUGENOL CEMENT
 The pH is 6.6 to 8.0, thus they are the leastThe pH is 6.6 to 8.0, thus they are the least
irritating of all the cements.irritating of all the cements.

GLASS IONOMER CEMENTGLASS IONOMER CEMENT
 Pulpal response is mild.Pulpal response is mild.
ZINC POLYCARBOXYLATE CEMENTZINC POLYCARBOXYLATE CEMENT
 Pulpal response is mildPulpal response is mild
 The pH of set cement is 5.0 to 6.0The pH of set cement is 5.0 to 6.0
 Penetration of polyacrylic acid into the dentinalPenetration of polyacrylic acid into the dentinal
tubules is less because of the high moleculartubules is less because of the high molecular
weight and larger size.weight and larger size.

CALCIUM HYDROXIDE CEMENTCALCIUM HYDROXIDE CEMENT
 Alkaline in nature with pH of 9.2 to 11.7Alkaline in nature with pH of 9.2 to 11.7
 This high alkalinity is responsible for theThis high alkalinity is responsible for the
reparative dentin formationreparative dentin formation

ACID ETCHINGACID ETCHING
-It does not cause any irreversible damage to the pulp-It does not cause any irreversible damage to the pulp
-It only causes early inflammatory reaction which subsides-It only causes early inflammatory reaction which subsides
(Nakabayashi-hybridisation of dental tissues)(Nakabayashi-hybridisation of dental tissues)
COMPOSITESCOMPOSITES
-Adequately cured composites are relatively biocompatible-Adequately cured composites are relatively biocompatible
- Inadequately curing results in leaching out ofInadequately curing results in leaching out of
components that induce long term pulpal inflammationcomponents that induce long term pulpal inflammation
(Phillip’s,11(Phillip’s,11thth
edition)edition)

EFFECT OF RADIANTEFFECT OF RADIANT
IRRITATIONSIRRITATIONS
 X- IRRADIATIONX- IRRADIATION
In the pulps of irradiated teeth during the formative stageIn the pulps of irradiated teeth during the formative stage
- Odontoblasts are injuredOdontoblasts are injured
- Pulp cells become necroticPulp cells become necrotic
- Osteodentin is formedOsteodentin is formed
In pulps of fully formed teeth, relative to dosage, theIn pulps of fully formed teeth, relative to dosage, the
odontoblasts appear to be extremely radioresistantodontoblasts appear to be extremely radioresistant
(Kineldorf et al, 1963)(Kineldorf et al, 1963)

 LASER BEAMLASER BEAM
Laser damage to pulp varies with intensity of theLaser damage to pulp varies with intensity of the
energy.energy.
- 20 joules of energy produced mild inflammatory20 joules of energy produced mild inflammatory
response in a period of 3 daysresponse in a period of 3 days
- 40 joules of energy produced degenerative40 joules of energy produced degenerative
changes in the cells, fibers and ground substancechanges in the cells, fibers and ground substance
of the pulp.of the pulp.
(Jesionowski,(Jesionowski,
1970)1970) www.indiandentalacademy.com

AGENTS FOR PULP PROTECTIONAGENTS FOR PULP PROTECTION
 CAVITY LINERSCAVITY LINERS
-form a coating on the tooth surface by-form a coating on the tooth surface by
evaporation of the solvents thereby reducingevaporation of the solvents thereby reducing
pulpal irritationpulpal irritation
-no thermal insulation-no thermal insulation
-applied in two or three coats-applied in two or three coats
eg : copal or rosin, or synthetic resins dissolved ineg : copal or rosin, or synthetic resins dissolved in
acetone, ether or chloroform.acetone, ether or chloroform.

 CAVITY LINERSCAVITY LINERS
-seals the dentin from the influx of-seals the dentin from the influx of
microorganisms and other restorative irritantsmicroorganisms and other restorative irritants
-reparative dentin formation(calcium hydroxide-reparative dentin formation(calcium hydroxide
liner)liner)
Eg : calcium hydroxide,Type IV ZOE cement,Eg : calcium hydroxide,Type IV ZOE cement,
Type III GICType III GIC

 CAVITY BASESCAVITY BASES
- Protects the pulp against thermal, galvanic, andProtects the pulp against thermal, galvanic, and
chemical injurychemical injury
- Applied in a thikness of 0.75mm below theApplied in a thikness of 0.75mm below the
restorationrestoration
Eg : zinc phosphate, ZOE cement, calciumEg : zinc phosphate, ZOE cement, calcium
hydroxide, glass ionomerhydroxide, glass ionomer
(Phillip’s,11(Phillip’s,11thth
edition)edition)

MANAGEMENT OF DEEPMANAGEMENT OF DEEP
CARIOUS LESIONSCARIOUS LESIONS
 DEEP CARIES MANAGEMENT;DEEP CARIES MANAGEMENT;
 INDIRECT PULP CAPPINGINDIRECT PULP CAPPING
 DIRECT PULP CAPPINGDIRECT PULP CAPPING
 PARTIAL PULPOTOMYPARTIAL PULPOTOMY
 PULPOTOMYPULPOTOMY
 CONCEPT OF REVASCULARIZATIONCONCEPT OF REVASCULARIZATION

FACTORS TO BE ASSESEDFACTORS TO BE ASSESED
BEFORE DCMBEFORE DCM
 Type of decayType of decay –more acute the decay process, less–more acute the decay process, less
effective the defense mechanism, thus greater tendencyeffective the defense mechanism, thus greater tendency
of destructive reaction in the pulp-dentin complex.of destructive reaction in the pulp-dentin complex.
 Duration of decayDuration of decay
–– longer duration of acute decay, greater pulp tissuelonger duration of acute decay, greater pulp tissue
destruction due to high diffusion of irritants throughdestruction due to high diffusion of irritants through
the dentinal tubulesthe dentinal tubules
- longer duration of chronic decay, greater chances of- longer duration of chronic decay, greater chances of
repair, provided the pulp is not directly involved.repair, provided the pulp is not directly involved.

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