DISEASES OF

THE PULP

Prepared by:
Dr. Rea Corpuz
Pulp

 formative organ of tooth

 builds primary dentin

during development of tooth

 secondary dentin after

tooth eruption

 reparative dentin in response

to stimulation as long as
odontoblast remain vital
Pulpitis

 most common cause of

dental pain

 loss of teeth in younger

persons

 usual cause is caries

penetrating the dentin
 Pulpitis

UNTREATED

Death of pulp

Spread of Infection through

apical foramina into periapical
tissues

Causes Periapical Periodontitis

Causes of Pulpal
Inflammation
 (1) Mechanical Cause

 (2) Thermal Cause

 (3) Chemical Cause

 (4) Bacterial Cause

Causes of Pulpal
Inflammation
 (1) Mechanical Cause

 traumatic accident

 iatrogenic damage for

dental procedure

 atrrition

 abrasion
Causes of Pulpal
Inflammation
 (2) Thermal Cause

 uninsulated metallic
restoration

 during cavity preparation

 polishing
Causes of Pulpal
Inflammation
 (3) Chemical Cause

 arise from erosion

 or inappropriate use
of acidic dental material
Causes of Pulpal
Inflammation
 (4) Bacterial Cause

 can damage pulp

through toxins secreted
by bacteria from caries
Classification

 (1) Based on Severity of

Inflammation

 (2) According to Involvement

(1) Based on Severity
of Inflammation

 (1) Reversible Pulpitis

 (2) Irreversible Pulpitis

 (3) Pulp Degeneration

 (4) Pulp Necrosis

(1) Based on Severity
of Inflammation

 (1) Reversible Pulpitis

 Symptomatic (acute)
 Aysptomatic (chronic)

 (2) Irreversible Pulpitis

 Acute
• Abnormally responsive to cold
• Abnormally responsive to heat
(1) Based on Severity
of Inflammation

 (2) Irreversible Pulpitis

 Chronic
• Asymptomatic with
pulp exposure
• Hyperplastic
• Internal resorption
(1) Based on Severity
of Inflammation
 (3) Pulp Degeneration

 Calcific

 (4) Pulp Necrosis

(2) According to
Involvement
 (1) According to Involvement

 (2) According to Severity

 (3) According to presence or

absence of direct
communication
between dental pulp +
oral environment
(2) According to
Involvement
 (1) According to Involvement

 Focal or Subtotal or
Partial Pulpitis

 Total or Generalized
Pulpitis
(2) According to
Involvement

 (2) According to Severity

 Acute
 Chronic
(2) According to
Involvement

 (3) According to presence or

absence of direct
communication
between dental pulp +
oral environment

 Pulpitis Aperts (open pulpitis)

 Pulpitis Clausa (closed pulpitis)

Reversible Pulpitis

 mild to moderate inflammatory

condition of pulp

 caused by noxious stimuli

 pulp is capable of returning

to un-inflammed state

 following removal of stimuli

Reversible Pulpitis

 Causes

 agent capable of
injuring pulp like:

• trauma
• disturbed occlusal
relationship
• thermal shock
Reversible Pulpitis

 Clinical Features

 sharp pain lasting for

a moment

 often brought on by cold

than hot food or beverages
and by cold air
Reversible Pulpitis

 Clinical Features

 does not continue

when the cause has been
removed

 tooth responds to electric

pulp testing at lower
current
Reversible Pulpitis

 Management

 prevention

 periodic care

 early insertion of filling

if a cavity has developed

 removal of noxious
stimuli
Focal Reversible
Pulpitis
earliest form

 also known as pulp hyperemia

 excessive accumulation of
blood within pulp tissue

 leads to vascular congestion

Focal Reversible
Pulpitis
 Clinical Features

 sensitive to thermal
changes

 particularly to cold

 application of ice or cold

fluids to tooth result in pain
Focal Reversible
Pulpitis
 Clinical Features

 disappears upon removal

of thermal irritant or
restoration of normal
temperature

 responds to electrical test

stimulant at lower level
of current
Focal Reversible
Pulpitis
 Clinical Features

 indicates lower pain

threshold than that of
adjacent normal
teeth
Focal Reversible
Pulpitis
 Clinical Features

 teeth show:

• deep carious lesion

• large metallic restoration

• restoration with defective

margins
Focal Reversible
Pulpitis
 Management

 removal of irritants
before the pulp is
severely damaged
Irreversible Pulpitis

 persistent inflammatory
condition of pulp

 may be symptomatic or
asymptomatic

 caused by noxious stimulus

Irreversible Pulpitis

 Causes

 bacteria involvement of
pulp through caries

 chemical

 thermal

 mechanical injury
Irreversible Pulpitis

 Clinical Features

Early Stage

 paroxysm of pain
caused by:

• sudden temperature
changes like cold,
sweet, acid foodstuffs
Irreversible Pulpitis

 Clinical Features

Early Stage

 pain often continues

when cause has been
removed

 may come and go

spontaneously
Irreversible Pulpitis

 Clinical Features

Early Stage

 pain

• sharp
• piercing
• shooting
• generally severe
Irreversible Pulpitis

 Clinical Features

Early Stage

 pain

• bending over exacerbates pain which

• lying down is due to change in
• change of position intrapulpal pressure
Irreversible Pulpitis

 Clinical Features

Late Stage

 pain

• more severe as if tooth is under

• throbbing constant pressure
Irreversible Pulpitis
 Clinical Features

Late Stage

 pain

• patient is often awake

at night due to pain

• increased by heat and

sometimes relieved by cold,
although continued application
of cold may intensify pain
Irreversible Pulpitis
 Management

 complete removal of pulp

or pulpectomy

 placement of intracanal
medicament

 to act as disinfectant or
obtundent
• cresatin
• eugenol
• formocresol
Clinical Difference

Reversible Pulpitis Irreversible Pulpitis

 pain is generally traceable  more severe
to a stimulus  lasts longer
 cold water  pain may come
 air without
any apparent stimulus
Acute Pulpitis

 extensive acute inflammation

of pulp

 frequent sequel of focal

reversible pulpitis
Acute Pulpitis

 Causes

 tooth with large carious

lesion

 defective restoration
where there has been
recurrent caries

 pulp exposure due to

faulty cavity preparation
Acute Pulpitis

 Clinical Features

 severe pain is elicited by

thermal changes

 pain persists even after

thermal stimulus
disappears or been
removed
Acute Pulpitis

 Clinical Features

 may be continuous

 intensity may be increased

when patient lies down

 application of heat may

may cause acute
exacerbation of pain
Acute Pulpitis

 Clinical Features

 tooth reacts to electric

pulp vitality tester at a
lower level of current
than adjacent normal
teeth
Acute Pulpitis

 Clinical Features

 pressure increases
because of lack of
escape of inflammatory
exudate

 rapid spread of inflammation

through pulp with pain
+ necrosis
Acute Pulpitis

 Management

 early stages of pulpotomy

(removal of coronal pulp)

 placing material that

favors calcification such
as:
• calcium hydroxide
over entrance of
root canals
Acute Pulpitis

 Management

 root canal filing with

inert material like
gutta percha should be
done
Chronic Pulpitis

 may develop with or

without episodes of
acute pulpitis

 many pulps under large

carious cavities die painlessly

 1st indication is then

development of periapical
periodontitis, either with pain
or seen by chance in radiograph
Chronic Pulpitis

 Clinical Features

 dull aching type

 more often intermittent

than continuous
Chronic Pulpitis

 Management

 root canal therapy

 followed by crown
restoration
Chronic Hyperplastic
Pulpitis
 also called as pulp polyp
or pulpitis aperta

 essentially an excessive
exuberant proliferation
of chronically inflammed
dental pulp tissue
Chronic Hyperplastic
Pulpitis
 pulpal inflammation due
to an extensive carious
exposure of a young pulp

 development of granulation
tissue

 covered at times by epithelium

 resulting from long standing

low grade infection
Chronic Hyperplastic
Pulpitis
 Causes

 slow progressive
exposure of pulp

 bacterial infection
Chronic Hyperplastic
Pulpitis
 Clinical Features

 most commonly involved

are deciduous molars +
1st permanent molar

• excellent blood supply

• large root opening
Chronic Hyperplastic
Pulpitis
 Clinical Features

 asymptomatic

 seen only in teeth of children

+ young adults
Chronic Hyperplastic
Pulpitis
 Clinical Features

 polypoid tissue appears

• fleshy
• reddish pulpal mass filling
most of pulp chamber
or cavity
• or even extend beyond
confines of tooth
Chronic Hyperplastic
Pulpitis
 Clinical Features

 polypoid tissue appears

• sometimes, if mass is
large enough
• interferes with closure
of mouth
Chronic Hyperplastic
Pulpitis
 Clinical Features

 polypoid tissue appears

• may cause discomfort

during mastication
• due to pressure of food
bolus
Chronic Hyperplastic
Pulpitis
 Clinical Features

 polypoid tissue appears

• tissue easily bleeds

because of rich network
of blood vessels

• tooth may respond or

not at all to thermal test
Chronic Hyperplastic
Pulpitis
 Management

 elimination of polypoid tissue

 followed by extirpation of pulp

 hyperplastic tissue bleeeding

can be controlled by pressure

 extraction of tooth can also

be done
Necrosis

 death of pulp

 may be partial or total

depending on whether part
or the entire pulp is
involved
Necrosis

 Causes

 sequeala of inflammation

 can also occur following

trauma

• pulp is destroyed before

an inflammatory reaction
Necrosis

 Types

 (1) Coagulation Necrosis

 (2) Liquefaction Necrosis

Necrosis

 Types

 (1) Coagulation Necrosis

• soluble portion of
tissue is precipitated
• or converted into a solid
material
Necrosis

 Types

 (1) Coagulation Necrosis

• tissue is converted into

tissue mass consisting
chiefly of coagulated

 proteins
 fats
 water
Necrosis

 Types

 (2) Liquefaction Necrosis

• results when proteolytic

enzymes convert the
tissue into softened mass
liquid or amorphous debris
Necrosis

 Clinical Features

 no painful symptoms

 discoloration of tooth

• 1st indication that the pulp

is dead
Necrosis

 Clinical Features

 history of pain lasting from

a few minutes to a few
hours followed by
complete + sudden
cessation of pain
Necrosis

 Management

 preparation + obturation of
root canals
References:
 Books
 Cawson, R.A: Cawson’s Essentials of Oral
Oral Pathology and Oral Medicine,
8th Edition
• (page 60)
 Ghom, Ali & Mhaske, Shubhangi: Textbook of
Oral Pathology
• (pages 420-425)