PULPAL PATHOLOGY AND ITS

SEQUELAE

Presenter

Dr. Ravi Acharya

PG Resident

Dept. Of Conservative Dentistry and Endodontics

B.P.Koirala Institute of Health Sciences

Dharan, Nepal

"The pulp lives for the dentin and the

dentin lives by the grace of the pulp.

Few marriages in nature are marked by

a greater affinity."

Alfred L. Ogilvie

CONTENTS

• Response of the pulp to dental caries

• Immune response in the dental pulp

• Hard tissue response to irritation

• Histologic changes in acute inflammation

• Histologic changes in the chronic inflammation

• Haemodynamic changes in the pulp during

caries

• Neural changes during pulpal inflammation

• Antiinflammatory and antinociceptive

mechanisms in the dental pulp

• Less common pulpal responses

• Factors limiting the pulps response

• Iatrogenic effects on the dental pulp

• Systemic factors

• Pulpal sequelae to impact trauma

The causes of pulp inflammation, necrosis, and dystrophy are:

I. Bacterial

A. Coronal ingress

1. Caries

2. Fracture

a. Complete

b. Incomplete (cracks, infraction)

3. Nonfracture trauma

4. Anomalous tract

a. Dens invaginatus (dens in dente)

b. Dens evaginatus

c. Radicular lingual groove (palatogingival

groove)

B. Radicular ingress

1. Caries

2. Retrogenic infection

a. Periodontal pocket

b. Periodontal abscess

3. Hematogenic

II. Traumatic

A. Acute

1. Coronal fracture

2. Radicular fracture

3. Vascular stasis

4. Luxation

5. Avulsion

B. Chronic

1. Adolescent female bruxism

2. Traumatism

3. Attrition or abrasion

4. Erosion

III. Iatral

A. Cavity preparation

1. Heat of preparation

2. Depth of preparation

3. Dehydration

4. Pulp horn extensions

5. Pulp hemorrhage

6. Pulp exposure

7. Pin insertion

8. Impression taking

B. Restoration

1. Insertion

2. Fracture

a. Complete

b. Incomplete

3. Force of cementing

4. Heat of polishing

C. Intentional extirpation and root canal filling

D. Orthodontic movement

E. Periodontal curettage

F. Electrosurgery

G. Laser burn

H. Periradicular curettage

I. Rhinoplasty

J. Osteotomy

K. Intubation for general anesthesia

IV. Chemical

A. Restorative materials

1. Cements

2. Plastics

3. Etching agents

4. Cavity liners

5. Dentin bonding agents

6. Tubule blockage agents

B. Disinfectants

1. Silver nitrate

2. Phenol

3. Sodium fluoride

C. Desiccants

1. Alcohol

2. Ether

3. Others

V. Idiopathic

A. Aging

B. Internal resorption

C. External resorption

D.Hereditary hypophosphatemia

E. Sickle cell anemia

F. Herpes zoster infection

G.Human immunodeficiency virus (HIV) and

acquired immune deficiency syndrome (AIDS)

RESPONSE OF THE PULP TO DENTAL

CARIES

• Bacteria are responsible for most pulpal disease.

• Kakehashi et al. proved that exposed pulps in

gnotobiotic (germ free) rats did not become

inflamed while similarly exposed pulps in rats with

a full oral flora did.

• The response of the pulp may vary depending on

whether the caries process progresses rapidly

(acute caries) or slowly (chronic caries), or is

completely inactive (arrested caries).

• Conditions for growth and availability of

nutrients are quite different in enamel caries than

in dentinal caries

• Products of bacterial metabolism, notably

organic acids and proteolytic enzymes, destroy

enamel and dentin.

• Relatively large bacterial product, bacterial

endotoxin, is able to diffuse through dentinal

tubules to the pulp chamber .

• Bacterial antigens diffusing from the lesion to the

pulp through the dentinal tubules are captured

and processed by APCs, which leads to the

activation of the immune system.

• Deep penetration of dentin by bacteria results in

acute inflammation and eventually infection and

necrosis of the pulp.

• The first reaction of odontoblasts to superficial

caries lesions in enamel is a marked reduction in

the cytoplasm: nucleus ratio, suggesting an altered

metabolism.

• In active lesions, primary odontoblasts are

involved in the formation of reactionary dentin.

• However, even before the appearance of

inflammatory changes, the size and number of

odontoblasts decrease, at which time their

metabolic activity is reduced while cellular

proliferative activity in the cell-free zone of the

pulp increases.

• Although normally tall columnar cells,

odontoblasts adversely affected by caries become

flat to cuboidal in shape.

• The boundary zone between primary and

reparative dentin is atubular and lacks continuity

of tubules.

• Electron microscopic examination of the

odontoblasts beneath a superficial caries lesion

revealed cellular injury in the form of ballooning

degeneration of mitochondria and a reduction in

the number and size of other cytoplasmic

organelles.

• Eventually, the primary odontoblasts die, usually

followed by proliferation of replacement

odontoblasts and reparative dentin formation.

•Bacteria infect some tubules

long before others are infected.

• The distribution of infected tubules is not

uniform, as neighboring uninfected tubules are

frequently found interspersed among infected

tubules.

•At the completion of cavity or

crown preparation, some infected

tubules may not have been

eliminated.

• Basic reactions that tend to protect the pulp

against caries includes:

1. Decrease in the permeability of the dentin due to

dentinal sclerosis,

2. Formation of new dentin (tertiary dentin),

3. Effectiveness of inflammatory and immunologic

reactions.

Dentinal Sclerosis:

• It develops at the periphery of almost all caries

lesions.

• Most common response to caries.

• In dentinal sclerosis, the dentinal tubules

become partly or completely filled with mineral

deposits consisting of both hydroxyapatite and

whitlockite crystals.

• Dentinal sclerosis reduces the permeability of

dentin, thus shielding the pulp from irritation.

• In order for sclerosis to occur, vital odontoblast

processes must be present within the tubules.

• In highly active caries lesions, odontoblast

may die before sclerosis has occurred.

• Disintegration of odontoblast processes

within the tubules results in a dead tract.

Tertiary dentin:

• There are two types of tertiary dentin based upon

the cell type responsible for dentin production:

1. Reactionary Dentin

2. Reparative Dentin

• Compared with primary dentin, reparative dentin

is less tubular and less well calcified.

• At times no tubules are formed; this type of

tertiary dentin has been characterized as a form of

fibrodentin.

• If the pulp is inflamed or has undergone

degenerative changes, the quality of the dentin is

more variable.

•An example of a poor

quality dentin is “Swiss

cheese” appearance of

dentin.

•The holes represent soft

tissue that was trapped in

the matrix and

subsequently underwent

necrosis.

Hard tissue response to irritation

Irritational dentin

• An odontoblast that is mildly stimulated

may form dentin that closely resembles

normal physiologic dentin.

• Since odontoblasts are incapable of

mitosis, they must be replaced by

underlying cells that mature from dividing

undifferentiated precursors or by

redifferentiation of fibroblasts.

• These new cells are atypical, frequently

without a process, and thus form an

atypical irregular structure called irritation

or reparative dentin.

• Its formation occurs independently of the

presence of inflammation and may form on

the walls of an irreversibly damaged pulp.

• Continued irritation dentin formation may

depend on persistent injurious stimuli; such

a condition is neither desirable nor

reparative.

• Anything that exposes or contacts dentin

has the potential to stimulate formation

of underlying irritation dentin.

• The morphology of irritation dentin has

been studied, but little is known of its

functions.

• Some attribute protective properties to this

tissue and therefore recommend methods

or materials to stimulate its formation.

• Others doubt its ability to protect the

underlying pulp.

• They have demonstrated its permeability,

permitting passage of chemicals and

bacteria and other substances.

• The presence of irritation dentin delays, but

does not prevent, the eventual penetration

of caries into the pulp.

BACTERIA AND THEIR BY-PRODUCT

CAN REACH THE PULP FROM OTHER

SOURCES

1. Anomalous Crown Morphology, Fractures,

and Cracks

Fig: Palatogingival GrooveClassification of invaginated teeth

2. Periodontal Disease

Saglie R et al: Scanning electron

microscopic depiction of the inside of

an ulcerated and infected pocket. Area

1 (right border) is the surface view of

lining epithelium. C, epithelial cell.

Dotted line demarcates the cut

surface of the epithelium (Area 2).

The basement lamina (BL) separates

the epithelium from connective tissue

(Area 3), which contains collagen

fibers (CF) and connective tissue cells

(CC). Bacteria (top arrow) enter a

hole (H) in the epithelium (left by a

desquamated cell) and travel through a

“tunnel” to emerge into connective

tissue through the hole. Abundant

cocci, rods, and filaments are seen

alongside the hole on the basement

lamina. Filaments and cocci are then

seen perforating the basement

membrane (double arrow) to

penetrate connective tissue and

reach blood and/or lymph vessels.

3.Blood Stream (Anachoresis)

ANTIGEN RECOGNITION IN THE

DENTAL PULP

• All three antigen-presenting cell types

expressing the type II major histocompatibility

complex (MHC) surface proteins,

macrophages, dendritic cells, and B

lymphocytes, are present and active in the

pulp's response to bacteria and toxins.

• In a normal healthy pulp, macrophages are

present in a resting form, as monocytcs.

• Macrophages require stimulation by bacteria or

cytokines before they express type II MHC

molecules.

• At rest they are found predominantly around

blood vessels though a few are distributed

throughout the tissue.

• Dendritic cells form a network throughout the

pulp concentrating around blood vessels and the

odontoblast layer.

• Some of the dendritic cells in the odontoblast

layer extend their processes into the dentinal

tubules.

• They constantly express the MHC molecules on

their surface without provocation.

• The number of dendritic cells increases in the

pulp when it becomes inflamed and they

accumulate beneath the carious lesion.

• B cells have been reported in the normal pulp but

are rather rare.

• Their role in the initial stages of antigen

recognition and presentation in the pulp is

unclear.

• Occasional T cells are found in normal pulp and

may be activated by antigen presenting cells

locally.

• In the pulp, there is a close anatomic relationship

between nerve fibers and dendritic cells, and

both increase in parallel when the pulp is

inflamed.

• The sympathetic nervous system has recently

been shown to have a modulating influence on

pulpal inflammation.

• The sympathetic system inhibits the production

of proinflammatory cytokines, although

stimulating the production of antiinflammatory

cytokines.

• In addition, T

lymphocytes and other

leukocytes produce anti

nociceptive molecules

such as β-endorphin and

somatostatin during

inflammation which

reduce the excitability of

pain fibers.

• Odontoblasts are the first cells to encounter an

antigen diffusing along the dentinal tubules.

• Odontoblasts respond differentially to the toxins

produced by gram-positive and gram negative

bacteria.

• Odontoblasts express microbial pattern

recognition receptors in situ, allowing

differential responses to gram-positive and

gram-negative bacteria.

• Pro-inflammatory cytokines and innate immune

responses in decayed teeth may result from TLR

signaling.

Veerayutthwilai O, Byers MR, Pharn TTT, et al. Differential regulation of immune

responses by odontoblasts. OralMicrobiol lmmunol 2007;22:5--1 3.

The Process of Antigen Recognition

• Dendritic cells and macrophages bind to and

phagocytize antigen that is then processed

intracellularly, bound to MHC molecules, and

moved to the cell membrane for recognition by T

cells.

• B cells bind antigen to specific cell surface

receptors.

• All the antigen-presenting cell types enter the

blood stream and carry the surface molecules

to the lymph nodes where T cell activation

takes place, though some may occur locally.

• The T cells respond not to the antigen itself but

to the modified complex in the cell membrane

of the antigen- presenting cells.

• Being stationary, the odontoblast does not

participate directly in the activation of T cells

but, presumably, activates dendritic cells.

HISTOLOGIC CHANGES IN ACUTE

INFLAMMATION

• Cariogenic bacteria in the dental plaque produce

a mixture of acids and enzymes that dissolve the

mineral elements of enamel and dentin and then

digest the organic matrix.

• The initial removal of mineral makes the enamel

more permeable and the bacterial toxins will

diffuse well ahead of cavitation.

• Once the dentin is reached, the toxins and, much

later, the bacteria themselves will travel along the

dentinal tubules.

• Clearly, variations in the composition and

thickness of enamel and dentin, and particularly

the patency of the dentinal tubules, will determine

the rate at which these toxins reach the pulp.

• In vital teeth, this

movement will be

opposed by the outward

flow of dentinal fluid.

• Toxins, however, reach

the pulp at a very early

stage relative to surface

changes.

HISTOLOGIC CHANGES IN CHRONIC

INFLAMMATION

• The immediate

"inflammatory" phase

of the immune

response begins very

shortly after the

antigen arrives in the

tissue.

• If the body has been exposed to the antigen on a

previous occasion, the production of specific

antibodies begins very quickly (within a few

hours).

• If antigen not encountered before, it takes

several days for the production of antibodies.

• At this stage, the pulpal response is

characterized by the presence of the

lymphocytes.

• If the carious lesion is not treated, however, the

increasing quantity of irritants will eventually

cause irreversible changes.

•These are at first limited

in size and may even form

a "pulpal abscess.“

• This local necrosis, unless checked, will

progress gradually throughout the tissue and

into the periradicular tissues.

• The progress of tissue damage in the pulp is

determined by the presence and spread of

bacterial toxins and is not due to the

"strangulation" of blood vessels.

Suppuration and Necrosis

• Exposure of the pulp to caries often results in

suppurative inflammation, depending upon the

nature of the invasive bacteria.

• The generation of chemotaxins by pyogenic

bacteria produces a massive accumulation of

neutrophils.

• HOCL produced from neutrophil destroys

bacteria by halogenation and lipid peroxidation.

• The ability to avoid phagocytosis is of key

importance in the virulence of pyogenic bacteria.

• Because of certain antiphagocytic virulence factors,

it is difficult for neutrophils to kill pyogenic

bacteria, and as a result more and more neutrophils

are mobilized in an attempt to overwhelm the

invading organisms.

• As bacteria invade deep into the dentin, neutrophils

begin to accumulate adjacent to the dentinal tubules.

• Because bacteria in the tubules are virtually

unassailable by host defenses, there is a constant

supply of chemotaxins to mobilize neutrophils.

• If the number of neutrophils reaches a critical

mass, an abscess, a walled-off area of suppuration,

will develop.

• The death of neutrophils in situ gives rise to

purulence, formed chiefly by autolysis of

neutrophils by their own lysosomal enzymes.

• As this process continues, an abscess cavity is

formed.

• Tissue necrosis develops when neutrophils release

activated oxygen metabolites and proteases.

• It results in liquefaction necrosis.

• As the caries exposure enlarges and an ever-

increasing number of bacteria enter the pulp, the

defending forces are eventually overwhelmed

• Therefore, when blood flow can no longer meet the

demand for inflammatory elements, the

inflammatory response can no longer be sustained

and bacteria may grow unopposed within the pulp

chamber.

• This ultimately leads to total pulp necrosis.

• Exposure of the pulp to caries does not invariably

result in suppuration.

• In the absence of a sufficient number of pyogenic

bacteria, a localized area of necrosis may develop.

• The body responds to this necrotic debris by

attempting to produce reparative dentin.

• Exposure of the pulp may also trigger extensive

fibrosis of the pulp.

Chronic ulcerative pulpitis

• The histologic term ulcerative is actually a

misnomer in these cases because no surface

epithelium is involved.

• This condition is the result of local excavation of

the surface of the pulp resulting from liquefaction

necrosis of pulp tissue.

• Excavation is likely to occur when drainage of

inflammatory exudate is established through a

pathway of decomposed dentin.

•The inflammation remains

localized and asymptomatic

because drainage prevents a

buildup of pressure.

Chronic hyperplastic pulpitis

• Occurs most often in primary and immature

permanent teeth with incompletely formed roots.

• At this stage of development, numerous blood

vessels enter the pulp through the wide apical

foramen.

• Histologically characterized by proliferation of

small vessels and fibroblasts and a chronic

inflammatory cell infiltrate.

• The lesion acquires a stratified squamous covering,

presumably because of grafting of vital

desquamated epithelial cells from the oral mucosa.

• Chronic hyperplastic pulpitis develops when carious

pulp exposure creates a large open cavity.

• This opening establishes a pathway for drainage of

the inflammatory exudate.

• When drainage is established, acute inflammation

subsides and chronic inflammatory tissue

proliferates through the opening created by the

exposure to form a polyp.

HEMODYNAMIC CHANGES IN THE PULP

DURING CARIES

Blood Flow

• Using plaque extract to initiate inflammation in a

rat incisor model, a 40% increase in blood flow

in a "moderately inflamed" pulp but a 35%

reduction in a "partially necrotic" pulp was

reported.

Kim S, Liu M, Simchon 5, Dorscher-Kim JE. Effects of selected inflammatory mediators on blood

flow and vascular permeability in the dental pulp. Proc Finn Dent Soc t 992;88 (Suppl 1):387-92.

• The application of Lippolysaccharide to the pulp

resulted, after 10 minutes, in a reduction in blood

flow that continued for the 3-hour duration of the

experiments. This was interpreted as a limited

ability of the pulp to respond.

Blelsa A, Berggreen E, Fristad I, et al. Cytokine signalling in rat pulp interstitial fluid and transcapillary fluid

exchange during lipopolysaccharide-induced acute inflammation. J PhysioI 2006;573:225-36.

Interstitial Fluid Pressure

• The healthy dental pulp has an interstitial

pressure of 5 to 10 mm Hg.

• One of the key changes during inflammation is

the movement of fluid from within the

capillaries into the interstitial space.

• Increasing the amount of fluid in a rigid chamber

leads to an increase in pressure. It was assumed,

for a long time, that such a pressure rise in the

pulp would cause compression of the blood

vessels leading to vascular stasis and necrosis.

• It was even suggested that this pressure change

could lead to strangulation of the vessels at the

apex causing necrosis in areas of the pulp not

directly affected by the bacterial toxins.

• Necrosis occurs beneath persisting carious

lesions only when bacterial toxins, spreading

throughout the pulp, poison cells directly.

NEURAL CHANGES DURING PULPAL

INFLAMMATION

• Sympathetic nerves control blood flow by constricting

precapillary sphincters and by interaction with other

elements of inflammation.

• It inhibits the production of proinflammatory cytokines,

stimulating the production of anti-inflammatory

cytokines and is involved in the recruitment of

inflammatory cells to the area.

• Has an inhibitory effect on odontocasts and stimulate

reparative dentin production.

• Afferent sensory fibers from the trigeminal

system plays an important role in response to

toxins and injury.

• They release substance P and Calcitonin Growth

Related Protein (CGRP).

• They both causes vasodilatation and increase

capillary permeability.

• In injured pulps, there is an increased expression

of nerve growth factor (NGF) and its receptors.

• A concomitant sprouting of the afferent terminals

and increased presence of substance P and CGRP

also takes place.

• Pulpal injury and inflammation are also

associated with neural changes outside the pulp

itself.

• In the trigeminal ganglion after pulpal injury the

expression of various neuropeptides increases.

• There are also detectable changes in the

supporting cells of the ganglion.

• Most significant from a clinical point of view are

changes in the nucleus related to central

sensitization.

• This may help explain the variable presentation of

pulpitis in terms of pain.

ANTI-INFLAMMATORY AND

ANTINOCICEPTIVE MECHANISMS IN THE

DENTAL PULP

• Neuroimmune interactions control pain

through the activation of opioid receptors on

sensory nerves by immune derived opioid

peptides.

• Opoid receptors are present on pulpal nerves.

• On exposure to stress, opioid peptides are

released, bind to opoid receptors on peripheral

sensory neurons, and induce endogenous

antinociception.

LESS COMMON PULPAL RESPONSES:

CALCIFICATION AND RESORPTION

• Calcification of the pulp

takes a variety of forms.

Discrete pulp stones occur

in a large proportion of the

population.

• The vast majority of pulp

stones are found in molars.

• Pulp stones are more common in patients with

atheromatous cardiovascular disease.

• A higher incidence of pulpal mineralization is

associated with some genetic disorders such as

Ehlers-Danlos syndrome and amelogenesis

imperfecta.

• A generalized, more diffuse mineralization of

the pulp may occur after trauma and is one of

several good reasons for follow-up radiographs.

• Internal resorption has

been considered an

alternative sequelae to

trauma.

WHEN THE PULPAL RESPONSE

SUCCEEDS: REPAIR AND REGENERATION

• The immune response, including inflammation,

is only one part of the pulp's total response to

toxins or injury.

• When effective, it neutralizes and removes any

foreign material and allows and probably

initiates the second part, recovery, repair, and

regeneration.

• When no cells are killed,

the original odontoblasts

can form reactionary

(tertiary) dentin.

• When the odontoblasts are

killed, new dentin-forming

cells develop from stem

cells (undifferentiated

mesenchymal cells) and

form reparative (tertiary)

dentin.

• The repair of larger areas of damage is more

variable and depends on the nature of any

clinical intervention.

ENCOURAGING A SUCCESSFUL

RESPONSE

• Most of our strategies for encouraging pulpal

repair involve removal of the irritant and

diseased tissue and the prevention of further

injury.

FACTORS LIMITING THE PULP'S

RESPONSE

• The only significant factor that limits the pulp's

ability respond to injury is age.

• The older pulp has a reduced number of cells,

innervation, and vascularity, but the immune

response remains active.

IATROGENIC EFFECTS ON THE DENTAL

PULP-Local Anesthetics

• Local anesthetics reduce pulpal blood flow by

approximately half when they contain

vasoconstrictors.

• It is important to remember that when preparing

a cavity in an anesthetized tooth the pulp is in a

suboptimal condition to respond.

Cavity/Crown Preparation

Heat: Cutting Dentin

The amount of heat produced is determined by:

1. Sharpness of the bur

2. Amount of pressure exerted on the bur

3. Length of time the cutting instruments

contacts tooth structure.

The two cooling methods most frequently

applied are:

1. Air cooling

2. Water cooling

Damage has been observed in pulps of teeth cut

with air-cooling only.

• Dentin is a good insulator of heat unless the

thickness of dentin between preparation and

pulp is less than 1.0 mm.

• The “blushing” of dentin is due to frictional heat

resulting in vascular injury in the pulp.

The safest way to prepare tooth structure is to

use:

1. Ultrahigh speeds of rotation (100,000-

250,000 rpm),

2. Efficient water-cooling system,

3. Light pressure,

4. Intermittent cutting

• The close proximity of

the pulp to the external

surface of the tooth,

particularly at the furcal

plane area, where tooth

preparation for full

coverage of

periodontally involved

teeth is so critical, has

been emphasized by

Sproles.

Heat: Laser Beams

• Laser irradiation can generate a large increase in

temperature within dentin and pulp tissue.

• Proper power setting, time of application, and

use of water spray will mitigate the temperature

increase to levels below the heat threshold of

pulp damage.

Pins

• Pulp damage may result from pinhole preparation

or pin placement.

• Coolants do not reach the depth of the pin

preparation.

• During preparation, there is always the risk of pulp

exposure.

• Furthermore, friction locked pins often

produce micro-fractures that may extend to the

pulp, subjecting the pulp to irritation and the

effects of microleakage.

Cavity Cleansing

• A prolonged blast of compressed air aimed

onto freshly exposed vital dentin will cause a

rapid outward movement of fluid in patent

dentinal tubules.

Activates strong capillary forces

Causes rapid outward flow of dentinal

fluid

Stimulates nociceptors also causes

odontoblast displacement

Removal of fluid from the tubules by blast of air

Etching Dentin/Smear Layer

• Microleakage is increased if the smear layer

remains, whereas dentin permeability is

increased if the smear layer is removed.

Impressions And Temporary Crowns

• Modeling compound may be damaging because

of the combination of heat and pressure.

• Rubber base and hydrocolloid materials do not

injure the pulp.

• The heat generated during the exothermic

polymerization of autopolymerizing resins may

also injure the pulp.

• Cooling is strongly recommended when

provisional crowns are fabricated directly.

• The temporary crown/cement should be in

place for a short period of time.

• Microleakage around temporary crowns is a

common cause of postoperative sensitivity.

Crown Cementation

• During the cementation of crowns, inlays, and

bridges, strong hydraulic forces may be exerted

on the pulp as cement compresses the fluid in the

dentinal tubules.

• In deep preparations, this can result in a

separation of the odontoblast layer from the

predentin.

• Vents in the casting will allow cement to escape

and facilitate seating.

Dental Materials

Microleakage

• The most important characteristic of any

restorative material, in determining its effect on

the pulp, is its ability to form a seal that prevents

the leakage of bacteria and their products onto

dentin and then into the pulp.

Cytotoxicity

• Certain restorative materials are composed of

chemicals having the potential to irritate the

pulp.

• When placed in a cavity, the intervening dentin

usually neutralizes or prevents leachable

ingredients from reaching the pulp in a high

concentration to cause injury.

• The thickness and permeability of dentin

between a material and the pulp affect the

response to the material.

• In addition, the penetration of some materials

through dentin may be limited by the outward

flow of fluid through the tubules that will be

increased if the pulp is inflamed.

Heat upon Setting

• Temperature increases during setting procedures

may be over l0°C but can be limited to 2 to 3°C

with care.

• Cooling techniques include the use of air/water

cooling and removing the temporary upon initial

polymerization.

• The most exothermic luting material is ZnOP

cement.

• However, during setting, an intrapulpal

temperature increase of only 2°C was recorded.

Heat of this magnitude is not sufficient to injure

the pulp.

Desiccation by Hygroscopy

• Some hygroscopic materials may potentially

cause injury by withdrawing fluid from dentin.

• Moisture absorbed by materials is probably much

less than that removed from dentin during cavity

drying, a procedure that produces an insignificant

amount of pulpal inflammation.

SPECIFIC MATERIALS –

Zinc Oxide- Eugenol

• Eugenol, is toxic when placed in direct contact

with tissue.

• When included in cements to temporize crown

preparation, some eugenol does reach the pulp,

but the amounts are small and unrelated to

RDT.

Zinc Phosphate Cement

• The phosphoric acid liquid phase was formerly

thought to injure the pulp.

• However, recent studies have shown that this is

not the case.

• Researchers reported that ZnOP is more likely

to produce pulpal sensitivity at the time of

cementation and 2 weeks after cementation

than glass ionomer. However, 3 months after

cementation, there is no difference in

sensitivity.

Polycarboxylate Cement

• When placed in cavities or used as a luting

cement, zinc polycarboxylate does not irritate the

pulp.

• In cementing well-fitting crowns and inlays,

neither polycarboxylate nor ZnOP cements

contract enough to permit the ingress of bacteria.

Restorative Resins

• The first adhesive bonding and resin composite

systems contracted during polymerization

resulting in gross microleakage and bacterial

contamination of the cavity.

• With recently developed hydrophilic adhesive

bonding composite systems, the problem of

marginal leakage appears to have been

diminished.

Glass Ionomer Cements

• A photo-activated RMGI showed minimal to no

cytotoxicity in vitro tests.

• In vivo tests demonstrated only minimal pulp

reactions when RMGI was evaluated in non

human usage models.

•Recent studies have

demonstrated that

pulpotomy is successful

when restored with an

RMGI Adhesive Resin

Systems or adhesive.

•RMGI has been used as a

definitive restorative agent

to decrease microleakage.

Amalgam

• There is shrinkage during setting, which results in

microleakage.

• This decreases as corrosion products accumulate

between restoration and cavity walls and can be

reduced by the use of liners.

• Amalgam is the only restorative material in which

the marginal seal improves with time.

MTA

• The most promising material is mineral trioxide

aggregate (MTA) because of its superior

characteristics as a direct pulp-capping agent

compared with Ca(OH)2 controls in several

animal models.

• Results show reparative dentin bridge formation

in the majority of samples with minimal

inflammatory cell response.

Histologic section from a

nonhuman primate pulp that

was direct capped with Dycal

for 24 months. The dentin

bridge contains a tunnel defect

running from the restoration

interface to the dental pulp,

Histologic section of a nonhuman primate

pulp that was direct capped with MTA for

5 months. A new dentin bridge is seen

midfield directly below the MTA particles

with new odontoblastoid cells along the

pulp interface. The deeper pulp is free of

operative debris chips and inflammation

POLISHING RESTORATIONS

• Polishing glass ionomer and composite

restorations does not cause an increased

temperature at the pulp-dentin interface.

• Polishing amalgam restoration produce

temperatures that may be damaging.

• When polishing an amalgam restoration with

continuous pressure and no water coolant, it is

recommended to not exceed 4,000 rpm.

• With use of coolant, light pressure, and

intermittent contact during polishing, there is a

low likelihood of heat-generated pulp damage.

POST-RESTORATIVE HYPERSENSITIVITY

• If pain is prolonged, a preexisting pulpitis may

have been exacerbated.

• If delayed, the cause may be microleakage of

bacterial toxins under a poorly sealed

temporary restoration.

• If pain evoked is by biting on a recently restored

tooth, an intracoronal restoration may be

exerting a strong shearing force on the dentin

walls of the preparation.

• Hyperocclusion from an extra-coronal

restoration is not injurious to the pulp but may

cause a transient hypersensitivity.

VITAL TOOTH BLEACHING

• Can cause mild pulpitis which is

reversed within 2 weeks.

VITALITY TESTING

• Heat and cold testing within normal

clinical parameters does not damage the

dental pulp.

ORTHODONTICS

• Orthodontic tooth movement of a routine nature

does not cause clinically significant changes in

the dental pulp.

• The heavy forces used to reposition impacted

canines frequently lead to pulp necrosis or

calcific metamorphosis.

A, Radiograph of canine intruded by trauma. B, Effect of hypoxia on

pulp owing to intrusion.Myelinated nerve showing vacuolization

of axon (closed arrow), disruption and smudging of myelin sheath

(open arrow), and loss of cellular detail. C, Loss of cellular

detail in the nucleus (N) and cytoplasm (C). Cell clumping in nucleus and

loss of organelles with rupture of lysosome (arrow) in cytoplasm.

• Bracket removal by use of an electrothermal

device (ETD) does not cause gross damage or

necrosis of dental pulp.

• There may be limited peripheral disruption of

odontoblasts with slight inflammation.

ULTRASONIC SCALING

• Ultrasonic scaling of roots requires

prolonged contact of the ultrasonic

device, and the potential for pulp damage

exists.

• Proper water cooling of both ultrasonic

and sonic scalers will prevent excessive

heat production in the pulp.

SYSTEMIC FACTOR

Hereditary Hypophosphatemia

• It is characterized dentally by the abnormally

large pulps and incomplete calcification of the

dentin.

• The pulps in these teeth appear to be fragile and

succumb to minor irritating stimuli.

SYSTEMIC FACTOR

• Sickle cell anemia

• Herpes zooster infection

• HIV and AIDS

PULPAL SEQUELAE TO IMPACT

TRAUMA

It can be categorized as

1. Repair

2. Calcification

3. Resorption

4. Necrosis

• The response depends on type, duration,

severity and suceptibility of the pulp to injury.

The result maybe:

1. Adaptation

2. Reversible injury

3. Death

Radiograph of max central

incisor. The pulp chamber and

canal are obliterated with

irritational dentin.

A, Radiograph of a maxillary left central

incisor. The canal is large because the trauma

stopped root development when the pulp

became necrotic. There is inflammatory

resorption of the apex. B, After endodontic

therapy.

CONCLUSION

• Exposure of dentin through attrition, trauma, or

caries produces profound pulpal reactions that

tend to reduce dentin permeability and stimulate

formation of additional dentin.

• These reactions are brought about by changes in

fibroblasts, nerves, blood vessels, odontoblasts,

leukocytes, and the immune system.

• Recent discoveries of the effects of nerves on

pulpal blood vessels and vice versa have

produced a new appreciation for the interaction

of these two systems in response to stimuli

applied to dentin.

• The special features of the dental pulp, including

restricted vascularity, enclosure in dentin, and

susceptability to bacterial infection or trauma,

play an important role in defining the

inflammatory and healing potential of this tissue

References

• Ingle’s Endodontics,5th and 6th edition

• Dental Pulp, Seltzer and Benders

• Cohen’s Pathways Of the Pulp,9th edition

• Essentials of Endodontics, Vimal K Sikri

• Textbook of Endodontics, Nisha Garg, 2nd

Edition