Pulp diseases

• The dental pulp is a delicate connective tissue interspersed with tiny blood vessels,
lymphatics, myelinated nerve and unmyelinated and undifferentiated connective
tissue.
Etiology of pulp disease
In the dental pulp, inflammation is the response to an injury (an irritant),
just as it is in any other organ. If the irritant or injury is severe, the result is instead
necrosis of these cells.
Etiological factors (pulp irritants)
(1)Dental caries
• It is the most frequent form of injury to pulp
• Pulp irritation starts before the leading microorganisms in the carious dentine reach
the pulp showing that the initial pulp reactions follow the diffusion of bacterial
irritants through dentinal tubules.
(2)Bacterial invasion to the pulp in absence of dental caries
• Direct invasion of the pulp as a result of:
(i) Tooth fracture →exposed pulp to oral fluids and microorganisms.
(ii) Attrition, abrasion or restorative traumatic procedures leads to pulp exposure.
• Indirect bacterial invasion i.e. without pulp exposure
(iii) Periodontitis and periodontal pockets through pulp canals.
(vi) Anachoretic pulpitis → it is the shift of bacteria from blood to the pulp in case of
bacteremia.
NB: Anachoresis means the shift of bacteria from blood to a tissue in cases of
bacteremia.
(3) Chemical irritants
• Chemical irritants may be directly applied to an exposed pulp, or may diffuse
through the dentinal tubules after the insertion of a restorative material as cements
(zinc phosphate cement) with in adequate powder/liquid ratio.
• Chemical related damage can arise from erosion.
(4) Thermal irritants
• Frictional heat evolved during dental procedures of cavity preparation and polishing
causes significant pulp irritation so the importance of adequate coolants can’t be
overemphasized.
• Large metallic restorations, particularly where there is inadequate lining material,
may also transmit thermal changes to the pulp.
• Exothermic chemical reactions of dental materials.
(5) Mechanical or traumatic irritants: Mechanical sources of irritation include:
• Direct blow or trauma to tooth i.e. accidental trauma.
• Trauma during cavity or crown preparation.
• Attrition and abrasion.
(7) Electro-galvanic current: It is generated by direct contact between two opposite
dissimilar metallic restorations in presence of saliva → electro-galvanic current →
irritation and damage of pulpal and periodontal tissues.

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(6) Aerodontalgia (Aero= air/dont=tooth/algia=pain or ache)
Definition: Pain within tooth due to presence of air bubbles. This dental pain
simulates pulpitis.
• It was reported during World War II in flying persons at high attitudes.
• Generally, it was observed in recently filled teeth of individuals exposed to sudden
and high pressure changes such as astronauts, pilots and divers
• This pain has been attributed to formation of nitrogen gas bubbles in the pulp tissue
or vessels which result in pressure on dental nerve.
Classification of pulp diseases
• Pulp diseases of an inflammatory nature (pulpitis) have been classified in a variety
of ways:
(A) Simple classification of pulpitis into
 Acute
 Chronic
(B) Depending on extend of pulpal inflammation acute and chronic pulpitis may
be divided into
 Partial (subtotal) focal: The inflammation is confined to a portion of the pulp
usually a portion of the coronal pulp such as the pulp horn.
 Total (generalized): Most of the pulp is diseased.
(C) Classification based on the presence or absence of direct communication
between the dental pulp and oral cavity
 Opened pulpitis → pulp exposed to oral environment.
 Closed pulpitis →pulp still enclosed with dentine i.e not exposed to oral
environment
Pulpitis
Definition: Inflammation of the pulp
• All the principles of inflammation that apply to any other body organ apply to
lesions of the dental pulp.
Dental pulp has some unique features
• It is enclosed (encased) by hard tissues (dentin & enamel) that doesn't allow for the
usual swelling associated with the exudates of acute inflammatory process.
• There is no collateral circulation to maintain vitality when the primary blood supply
is compromised.
• Biopsy and direct application of medication are impossible without causing necrosis
of the entire pulp.
• Pain is the only sign that can be used to determine the severity of pulpal
inflammation.
Microscopical changes of inflammation
Acute inflammation
The inflamed tissue reveals the following morphological changes:
(1) Vasodilatation of blood vessels at area of inflammation.
(2) Increased vascular permeability due to contraction or destruction of endothelial
cells → escape of fluids outside the vessel through dilated pores between the
endothelial cells → oedema & exudates.
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(3) Increased viscosity of blood as a result of escape of large amount of fluid portion
of the blood fluids into the tissue spaces → haemoconcentration →↓blood flow
(hemostasis).
(4) Margination of neutrophils and monocytes at inner wall of blood vessels.
(5) Diapedesis of some PMNLs (acute inflammatory cells).
(6) Some red cells may be extravasated under the effect of hydrostatic pressure
through the defect left by the emigrated leucocytes.
NB: Until now, there is no tissue damage i.e. can be reversed
(7) Heavy infiltration with PMNLs which may release proteolytic enzymes leading to
digestion of tissue debris (necrotic tissue) & dead and living PMNLs &
microorganisms & their toxins → pus.
(8) If pus is surrounded with dense zone of acute inflammatory cells it will be called
acute abscess.
Chronic inflammation
• Chronic inflammation is an inflammatory process in which lymphocytes, plasma
cells and macrophages predominate. It is accompanied by formation of granulation
tissue resulting in fibrosis.
• The inflamed tissue reveals the following morphological changes:
(1) Vasodilatation of the blood vessels (less marked than acute).
(2) Oedema & exudates (less marked than acute).
(3) Haemoconcentration & hemostasis.
(4) Chronic inflammatory cells infiltrate which consists of lymphocytes,
(main cells of chronic inflammation) plasma cells, macrophages and foreign body
multinucleated giant cells (formed by fusion of macrophages).
(5) Formation of granulation tissue and fibrosis as an attempt for tissue repair.
• Granulation tissue consists of proliferating fibroblasts & collagen fibers & newly
formed capillaries and chronic inflammatory cells (lymphocytes, plasma cells and
macrophages).
• The previously mentioned morphological changes are the same which are observed
in different types of pulpitis
• Moreover, irreversible pulpitis (acute & chronic) revealed edematous changes of
odontoblasts (wheat sheaving of odontoblasts).
• Pus may be formed within chronic inflammation → central cavity containing pus
surrounded with heavy zone of chronic inflammatory cells (chronic abscess).
Different types of pulpitis
I- Acute focal reversible pulpitis (pulp hyperemia)
II- Acute closed pulpitis (Acute pulp abscess)
III- Acute opened pulpitis
VI- Chronic closed pulpitis (chronic pulp abscess)
V- Chronic opened pulpitis: It includes
Chronic opened
Chronic opened hyperplastic pulpitis (pulp polyp)

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 Acute reversible pulpitis Acute closed pulpitis
comparison Acute opened pulpitis
(pulp hyperemia) (acute pulp abscess)

Definition & etiology • It is acute mild inflammatory pulpal reaction • This is inflammatory response may occur as a progression of focal reversible pulpitis,
typically follows carious destruction of a tooth or or it may represent an acute exacerbation of already established chronic pulpitis
placement of large metallic filling.

• Mild to moderate intermittent pain of short • Sever, continuous, long standing throbbing, • Mild to moderate pain due to
Nature of duration lancinating pain which increased or diminished pressure as inflammatory
pain • No pain without stimulation precipitated at recumbent or lay down position products are directly drained within
• pain subsides within seconds after removal of the & commonly keeping the patient awake oral cavity.
stimulus
Clinical picture

• Although hot stimuli may initiate pain, the • Pain is elicited by thermal changes. • Pain is increased by thermal
Thermal
affected tooth responds most to cold stimuli as a • In later stages, heat ↑ the pain, however cold changes but with less extent. i.e.
stimuli
result of decreased drainage due to may produce relief reduced pain with thermal stimuli
vasoconstriction of the lymph vessels.
Electric
pulp tester • The affected tooth responds at lower level of current than adjacent normal teeth indicating increased sensitivity of the pulp.

Other • Sweet, sour food and beverages also may cause pain with different extents as they produce high osmotic pressure leading to hydrostatic
stimuli movement of fluids within dentinal tubules
• Tooth mobility and sensitivity to percussion are absent except in cases of spread of inflammation to the apical area.

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 (1) Vasodilatation of blood vessels. (1) Vasodilatation of blood vessels
(2)↑vascular permeability →exudate & edema (2) ↑vascular permeability → exudate &edema
(3) Haemoconcentration & hemostasis. (3) Haemoconcentration & hemostasis
(4) Margination of neutrophils & monocytes at inner (4) Margination of neutrophils & monocytes at inner wall of blood vessels
wall of blood vessels (5) Diapedesis of some PMNLs
(5) Diapedesis of some PMNLs (6) Extravasation of RBCs
(6) Extravasation of RBCs (7) Heavy infiltration with PMNLs which may release proteolytic enzymes
Microscopical leading to digestion of tissue debris ( necrotic tissue ) & dead and living PMNLs
morphological & microorganisms & their toxins → pus.
Changes (8) If pus is surrounded with dense zone of acute inflammatory cells →
acute pulp abscess.
(9) edematous changes of odontoblasts which may result in production of wheat
sheath appearance of degenerated odontoblasts.

NB: Acute opened pulpitis revealed the following:

o broken dentin and exposed pulp
o no abscess formation as pus is directly drained within oral cavity through
the broken dentine

• Removal of the irritant • Endodontic treatment is the first choice.

Treatment
• Carious tooth → filling • If endodontic treatment isn't indicated, tooth extraction will be the required
• Defective restoration → replacement treatment.

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 Comparison Chronic closed pulpitis (chronic pulp abscess) Chronic opened pulpitis

Definition & • It is an inflammatory reaction that results from long term of low grade injury or occasionally from quiescence of an acute process.
etiology
Nature of
pain • Spontaneous attacks of intermittent mild to moderate dull aching pain. • Pain is not a feature in most of cases due to nerve degeneration.

Thermal
• Pain is increased by thermal changes but with less extent i.e. reduced • Nearly no effect.
stimuli
pain with thermal stimuli.
Clinical picture

Electric
• The affected tooth responds at lower level of current than adjacent • Respond at higher level than normal due to nerve degeneration and
pulp tester
normal teeth indicating increased sensitivity of the pulp. elevated pain threshold.

• Sweet, sour food and beverages also may cause pain with different extents as they produce high osmotic pressure leading to hydrostatic
Other
movement of fluids within dentinal tubules.
stimuli
• Tooth mobility and sensitivity to percussion are absent except in cases of spread of inflammation to the apical area.

(1) Vasodilatation of the blood vessels (less marked than acute).

(2) Edema & exudates (less marked than acute).

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 (3) Haemoconcentration & hemostasis.
(4) Chronic inflammatory cells infiltrate which consists of lymphocytes, plasma cells, macrophages and foreign body multinucleated giant cells.
(5) Formation of granulation tissue and fibrosis as an attempt for tissue repair.
It consists of proliferating fibroblasts & collagen fibers & newly formed capillaries and chronic inflammatory cells (lymphocytes, plasma cells
and macrophages).
(6) Edematous changes of odontoblasts which may result in production of wheat sheath appearance of degenerated odontoblasts.
Microscopical
(7) Pus may be formed within chronic inflammation → central cavity containing pus surrounded with heavy zone of chronic inflammatory cells
morphological
chronic abscess.
Changes
NB: Chronic opened pulpitis revealed the following:
o broken dentin and exposed pulp
o no abscess formation as pus is directly drained within oral cavity through the broken dentine.

• Pulpectomy i.e. Endodontic treatment is the first choice.

Treatment
• If endodontic treatment isn't indicated, tooth extraction will be the required treatment.

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Chronic opened hyperplastic pulpitis (pulp polyp)
• It is a special form of chronic opened pulpitis characterized by excessive formation
of granulation tissue that extrudes from the pulp champer and often fills the entire
dental cavity. It occurs either as a chronic lesion from the onset or as a chronic stage
of a previously acute pulpitis.
Clinical features
Age: Children and young adults
Site: Deciduous molars & first permanent molars as they have high blood supply
through their wide apical foramina. High blood supply is coupled with high tissue
resistance and reactivity in young persons, accounts for the unusual proliferative
property of the pulp tissue.
Size: Small or large Surface: Smooth Shape: Rounded or ovoid
Pain: painless because the hyperplastic pulpal tissue contains few nerves as well as
nerve degeneration
Bleeding: May or may not depending on degree of vascularity
Color: Pinkish white or reddish depending on the presence or absence of surface
epithelium.
Histopathology
1- Vasodilatation of blood vessels.
2- Edema & exudate (less marked).
3- Granulation tissue consists of proliferating fibroblasts & collagen fibers & newly
formed capillaries and chronic inflammatory cells (lymphocytes, plasma cells and
macrophages).
4- Granulation tissue may be covered with non-keratinized stratified squamous
epithelium with rete processes which may be derived from:
Desquamated epithelial cells in saliva
Rubbing of the polyp against cheek mucosa
NB: Pulp polyp may be non epitheliated i.e. not covered with epithelium.
Treatment: Endodontic treatment is the first choice.
• If endodontic treatment isn't indicated, tooth extraction will be the required
treatment.
Pulp necrosis
• Pulp necrosis may follow either pulpitis (acute or chronic) or a traumatic injury to
apical blood vessels cutting the blood supply to the pulp.
• Ischemia may cause coagulative necrosis of the pulp
• Pulpitis may result in liquefaction necrosis which may become infected by
putrefactive bacteria from caries → pulp gangrene
• Pulp gangrene → it is a necrotic pulp tissue with superimposed bacterial infection. It
is the end result of pulpitis
Clinically
• Painless with no response to thermal changes as well as to electric pulp tester.
• Discoloration of the affected tooth due to hemolysis of red blood cells.
Histopathology: Structureless mass of necrotic pulp tissue i.e. no cells, no fibers, no
vessels

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Treatment
• Endodontic treatment is the first choice.
• If endodontic treatment isn't indicated, tooth extraction will be the required treatment.
Pulp calcification (pulp stone or denticles)
Definition: They are calcified deposits within the pulp
Types
According to structure
I-True pulp stones
• It contains organic matrix with dentinal tubules and may have an outer layer of
predentine and adjacent odontoblasts.
• It results from formation of irregular type of dentine by undifferentiated mesenchymal
cells due to the effect of remnants of epithelial root sheath of Hertwig.
• Mostly, they are small in size.
II-False pulp stones
• It consists of amorphous concentric layers of calcified material with no tubular structure.
• It occurs at area of hemorrhage or degenerated cells forming the nidus of deposition of
concentric layers of calcification.
• Mostly, they are larger than true stones (large in size).
According to location
I-Free pulp stones: Completely surrounded by pulp tissue (i.e within pulp)
II-Attached pulp stones: Partially surrounded by pulp tissue and dentine
III-Embedded pulp stones: completely surrounded by dentine
NB:
• Pulp stones may be either diffuse (linear) or focal.
• They increase in number and size with age.
• They produce no symptoms.
X-rays
• Radio-opaque enlargements within the pulp champer or canal.
Complications
• They may be problematic during endodontic treatment of teeth
Age changes in the pulp
1- Decreased pulp size gradually with age due to continued production of secondary
dentine
2- Decreased vascularity
3- Reduction in cellularity
4- Increased collagen fiber content
NB: These changes may impair the response of the tissue to injury and its healing
potential

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Sequalae of pulp diseases
• Once the infection has become established in dental pulp the spread of infection through
root canal and into perapical region occur.

Pulpitis
Chronic
Acute

Periapical Periodontitis
Acute Chronic

Periapical Granuloma
Periapical Abcess

Acute Chronic

Periapical Cyst

Osteomyelitis
Acute Chronic

Periostitis

Cellulitis Skin abscess

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