1.

Identify normal structure of dental pulp

2. Define pulp inflammation
3. Classify pulp diseases
4. Discuss the etiology of pulp diseases
5. Describe the pathogenesis of pulp diseases
6. Describe the clinical and pathological changes in
pulp diseases
 Normal histology of the pulp
Pulp is a mesenchymal tissue
I- Extracellular matrix
• Fibrous Matrix: Collagen type I, III,
Nerves (myelinated, unmyelinated),
Blood vessels and lymphatic
channels
• Ground Substance: Glycoproteins,
Proteoglycans
II- Cells
Synthetic: Odontoblasts, Fibroblasts
Undifferentiated Mesenchymal Cells
(UMC)
Defense cells: Histiocytes, lymphocytes,
eosinophils, mast cells.
 Specific features of the pulp

1. Soft tissue enclosed within rigid calcified walls.

2. Nerves & Vessels, enter through a small apical foramen.
3. Lack of collateral circulation.
 Healing is limited
 Thrombosis is likely to occur
4. Biopsy & direct application of medication are impossible.
5. Response to sudden temperature changes
6. Pain is the only sign of inflammation
7. Pain is difficult to localize and may be referred
8. Pain is little affected by analgesics
9. Pain is not provoked by percussion or pressure
10. Pulp can die painlessly
Pulpitis:
• It is the inflammation of the pulp regardless of the

presence of infectious agents (SEPTIC or ASEPTIC).

• It is the most common cause of dental pain and loss of teeth.

• Pulpitis, if untreated is followed by death of the pulp and spread

of infection through the apical foramina into the periapical tissues
leading to periapical periodontitis
Etiology of Pulpitis (Pulp irritants):

I- Living irritants (microbial)

II- Non-living irritants:

Physical:

Mechanical, Thermal, Electrical, Irradiation.

Chemical:

Acids, alkalis, poisons.

I-Living irritants
How can microorganisms get into the pulp?
1) Through an open cavity: due to dental caries, trauma, operative
dental procedures.
2) Via the gingival crevice : and by invasion along the Periodontal
ligament
3) By extension of periapical infection from adjacent infected teeth.
4) Through the blood stream during bacteremia or septicemia
(Hematogenous infection) if the pulp is inflamed (Anachoretic
Pulpitis)
II-Non-living irritants
Mechanical Irritation
• Accidental: Fracture of a tooth crown or root
• Odontoiatrogenic: dentist responsibility
 Accidental pulp exposure
 Grinding of tooth structure
 Rapid separation of teeth
 Use of modern high-speed instruments
 Traumatic occlusion
Aerodontalgia (Barotrauma):
• It is a dental pain seen in aircrews flying at high altitudes in
unpressurized aircrafts and in divers following deep sea diving.
• Aerodentalgia is an exacerbating factor, not a direct cause of pulpitis
Thermal irritation:
 Teeth respond to sudden temperature changes. The range of
response extends from 20oC to 45oC.
Odontoiatrogenic: dentist responsibility
 Excessive heat generated by bur or stone during grinding
and cavity or crown preparation of teeth.
 Large metallic fillings without an efficient lining.
 Prolonged cooling of teeth with ethyl chloride.
 Rapid polishing of teeth or restorations.
 Prolonged contact of thermal pulp testers whether hot or
cold, to deep cavities.
 Direct contact of a very hot cauterizing loop to the crown.
Electrical irritation: (Galvanic Current)
When metal fillings of different electromotive potential (gold vs.
amalgam) are placed so that they occasionally come in contact with
each other, an intermittent electrical current may be set up which is
of sufficient intensity to irritate the pulp.
Chemical Irritation
Produced by drugs, saliva and various ingredients in food:
• Use of too strong drugs for drying the cavities, such as alcohol or
chloroform.
• Improper mixing and use of Zinc phosphate cement or silicate
cement.
 Classification of Pulp Diseases
Pulp diseases (Pulpitis) can be classified according to:
I- Type of inflammation
• Reversible Pulpitis (Pulp Hyperemia).
• Irreversible Pulpitis
• Acute Pulpitis
• Chronic Pulpitis
II- Extent of pulp involvement
• Partial or Subtotal Pulpitis
• Total or Generalized Pulpitis
III- Communication between pulp and oral environment.
• Open Pulpitis: there is direct communication
• Closed Pulpitis: no communication
Factors influence the outcome (extent-spread)of pulpitis

1. Nature of irritant (being acute or chronic).

2. Duration & severity of irritant. (e.g. virulence
of microorganisms).
3. Host defense.
4. Local anatomy of the pulp chamber.
5. Pre-existing state of the pulp.
6. Apical blood flow.
 Focal Reversible Pulpitis (Pulp Hyperemia)
Clinical Features:
• Early, mild & transient pulp inflammation

• Sensitivity to thermal changes especially cold

• Pain is temporary & disappear within seconds after removal of

stimulus.

• Inflammation is localized to the pulpal end of dentinal tubules.

• The pulp is capable to return to normal condition after removal

of stimuli
• Teeth usually show:
 deep carious lesions
 large metallic restorations without adequate isolation
 restorations with defective margins.
• The pulp response to low level of electric current than normal.
• No sensitivity to percussion
• The pain can be easily localized
• The pain does not affected by changes of body position
• Reactionary dentine: is laid down to protect the pulp from further
injury.
• The tooth remains without symptoms until it is stimulated again.
Histological Features:
• Dilatation of the pulp blood vessels.
• Interstitial edema due to leakage of
inflammatory fluid exudates (IFE)
• Migration of leukocytes to the site
of irritation
• Thrombosis of blood inside the
blood vessels may occur due to
pressure of IFE, hemoconcentration
and slow rate of blood stream and
increased viscosity
 Irreversible pulpitis
It is a higher level of inflammation (Severe), in which the pulp
damaged is permanent and beyond the point of recovery
(Not recovered even after removal of the irritant)
Clinical Features:
1. Obvious invasion by bacteria is often the cross – over point
from reversible to irreversible pulpitis.
2. It exhibits a wide spectrum of acute & chronic inflammatory
change.
3. Pain is spontaneously initiated, or precipitated by thermal
changes especially cold, but it persists after removal of the
stimulus.
4. Pain lasts for a prolonged period of time.
6. Duration of pain is increased with heat application & in laying
down (recumbent position) keeping the patient awake at night.
7. Intensity of pain:
In Acute Pulpitis:
 In early stage: Severe and short (10-15 min.).
 Later: The pain becomes more severe, throbbing or lancinating
which is continuous (may be for several days) when greater
proportion of the pulp is involved with intrapulpal abscess
formation.
 If pulpal drainage occurs the symptoms are rapidly reduce or
may resolve only to return if the drainage ceases
 The tooth responds to electric pulp testing at lower level of
current.
 In Chronic Pulpitis:
• Pain is Dull aching and intermittent lasts for long time (1-2
hrs)
• The tooth responds to electric pulp testing at higher level
due to degeneration of nerve tissue.
• The pain cannot be localized (may be referred).
• Mobility & sensitivity to percussion are absent (no spread
to apical area).
 Pathogenesis:
• It always starts as a localized area of inflammation
• The inflammation extends throughout the pulp, if not
treated.
• In multirooted teeth, the inflammation may extend to the
apex of one root before the whole pulp chamber is involved.
• In Irreversible pulpitis: Reactionary dentine may laid down
protects the pulp from further injury.
Histopathology of Acute pulpitis:
• Dilatation of B.V. (hyperemia)
• Increase blood flow.
• Edema :due to increased in
permeability of distended B.V and
IFE.
• Progressive infiltration by
neutrophils leads to release of
lysosomal enzymes lead to localized
suppuration & pulp abscess.
• Destruction of odontoblasts.
Localized acute pulpitis Diffuse acute pulpitis
(Pulp abscess)
 Irritation of the Pulp

Dilatation of BV

Leakage of inflammatory fluid exudate

Edema that press against the wall of B.V

Thrombosis & collapse of veins

Local hypoxia & anorexia

localized necrosis.
If untreated (chemical mediators-released from necrotic tissue) further
inflammation & edema --- the end-result is total necrosis.
 Histopathology of chronic pulpitis

• Low level of continuous irritation.

• Chronic inflammatory cells
infiltration (lymphocytes, plasma
cells, macrophages)
• Areas of suppuration (abscess) may
be walled off leading to temporary
cessation of spread of suppuration.
• Destruction of odontoblasts
• Granulation tissue formation.
 Chronic Open Ulcerative Pulpitis
• There is wide communication
between pulp and oral cavity
• No or irregular pain.
• The entire pulp tissue is vital
but replaced by granulation
tissue.
• It is infiltrated with chronic
inflammatory cells.
 Chronic open hyperplastic pulpitis
(pulp polyp)
Due to excessive, proliferation of chronically
inflamed dental pulp.
Clinical Features
• It appears as reddish or pinkish soft tissue
mass protruded from the large open pulp
chamber & fills the carious cavity.
• It affects children & young adult (high
resistance) deciduous molars & 1st permanent
molar (wide apical foramen)
• It affects teeth with large open cavity &
with low grade infection.
• It is insensitive (painless) on gentle probing
• It may or may not bleed.
Histopathology
• A mass of hyper-plastic granulation tissue
formed of delicate connective tissue fibers
and small capillaries and chronic
inflammatory cells (lymphocytes, plasma
cells, macrophages).
• PNL may be seen superficially.
• This granulation tissue may become
epithelialized.
• Source of epithelium
 Grafting of oral epithelial cells present in
saliva
 Cells from cell layer released by trauma or
from gingival sulcus
Gingival polyp: hyperplastic gingival mass more
sensitive, more bleeding, continuous with gingiva.
 Pulp calcifications
Pulp stones (denticles):
• They are calcified bodies with organic
matrix
• They occur mostly in the coronal pulp.
• They increase in number & size with age.
• They become more numerous after
operative procedures
• Asymptomatic, but sometimes result in a
neuralgic pain.
• When large, they may be recognized on
radiographs.
• It may present in the pulp as
1. Free
2. Attached (Adherent)
3. Interstitial (Embedded)
True pulp stones
Contain tubules (scanty & irregular) & may have an
outer layer of predentine & adjacent odontoblasts.
False pulp stones:
Composed of concentric layers of calcified material
with no tubular structure.
Dystrophic calcifications
• It consists of granules of amorphous calcified
material.
• It may be scattered along collagen fibers or
aggregated into larger masses.
• Most commonly found in the root canals.

Dystrophic calcifications & pulp stones may obstruct

endodontic therapy.
 Pulp obliteration

• It may follow traumatic injury to apical blood vessels (not

sufficient to cause necrosis).

• Seen in dentinogenesis imperfecta & dentine dysplasia .

 Pulp necrosis
Etiology
1. As sequalae of Pulpitis
2. Traumatic injury to apical blood vessel, cutting off
blood Supply to the pulp.
3. Sickle cell anemia (sickled erythrocytes block the pulp
microcirculation).
Types of necrosis
• Coagulative necrosis: due to ischemia.
• Liquefactive necrosis: pulpitis lead to breakdown of
inflammatory cells (pus formation).
• Gangrenous necrosis: infected by putrefactive bacteria
lead to foul odor.
Clinical features
• Stoppage of pain: because the nerve fibers degenerate.
However, pulp death following pulpitis may occur with no
previous history of pain.
• Discoloration: due to break down products of RBC's that enter
the dental tubules. (loss of translucency) (darker).
• Brittleness: leads to cracks & fracture: due to dehydration of
dentine.
Histopathological features: The pulp tissues break up into debris
(structureless tissue) which contains free fats & fatty acids.
Sequalae of pulp necrosis
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