Pulp and Periapical Diseases

PULP AND PERIAPICAL
DISEASES-2
INDIAN DENTAL ACADEMY
Leader in continuing Dental Education
www.indiandentalacademy.com

OBJECTIVES
 At the end of the lecture student should know the
– etiology. Clinical features, histological features and
treatment of focal irreversible pulpitis
– etiology. Clinical features, histological features and
treatment of chronic hyperplastic pulpitis
–etiology. Clinical features, histological features and
treatment of pulp necrosis
–etiology. Clinical features, histological features and
treatment of gangrenous necrosis of pulp
–pathophysiology of periodontal diseases
– etilogy. Clinical features, histological features and
treatment of periapical abscess

• It is persistent inflammatory condition of the pulp,
symptomatic or asymptomatic caused by a
noxious stimulus.
• Acute irreversible pulpitis exhibits pain usually
caused by hot or cold stimulus, or pain that occurs
spontaneously. The pain persist for several minutes
to hours.
Irreversible Pulpitis

Pain Symptoms in Irreversible
Pulpitis• Spontaneous
• Dull
• More than 20 min duration
• lingering after removal of the thermal stimulus
• Affected by body position
• Often difficult to localize

Acute pulpitis – Tooth exhibiting a focal
area of intrapulpal hemorrhage and acute
pulpitis resulting from overheating during
crown preparation.
Extensive acute inflammation of dental
pulp-frequent immediate sequela of
Acute pulpitis

Clinical features
• Large carious lesion / defective restoration with
‘recurrent caries’.
• Severe pain elicited by thermal change specially cold.
• Pain persists even after removal of thermal stimulus.
• Pain poorly localized.

• Pain increases in severity with extent of disease
(lancinating /throbbing)
• Intensity increases with lying down position.
• Application of heat causes an acute exacerbation of pain
• Response to electric pulp tester: at low level of current
( lower pain threshold /greater sensitivity)
Severity of pain depends upon the close & open pulpitis.

Histopathology
• No odontoblastic layer can be
identified, but individual odontoblasts
are in their normal position.
• Some odontoblastic nuclei have been
displaced into the dentinal tubules.
• The cells in the subodontoblastic
region are well delimited to the
exposed dentinal tubules and they
comprise neutrophilic and
mononuclear leucocytes as well as
fibroblasts and undifferntiated cells.
• Many capillaries are present.

Histopathology – Infection has penetrated
to the pulp, part of the pulp has been
destroyed, and an abscess has formed
containing a bead of pus
A focal area of acute inflammation
( pulpal abscess ) in a tooth with
advanced recurrent caries

Vacuolization of the odontoblasts

• No Odontoblasts are recognizable.
• Marked inflammatory cell infiltration in subodontoblastic
layer www.indiandentalacademy.com

Chronic Hyerplastic Pulpitis
( Pulp Polyp):-
• It is a productive pulpal inflammation due
to an extensive carious exposure of a
young pulp.
• This is characterized by the development
of granulation tissue covered at times
with epithelium and resulting from long-
standing, low-grade irritation.

• It occurs in young pulp, involves teeth with large open carious
lesion most commonly deciduous molar and the first
permanent molar.
• It appears as a pinkish-red globule of tissue protruding from
the pulp chamber and often filling the entire cavity
• It is symptomless, except during mastication, when pressure of the
food bolus may cause
• Discomfort.

Histopathology
• A mass of granulation tissue protruding from the
crown of a fractured or carious tooth
• The fibrovascular stroma - numerous small,
delicate vascular channels and a prominent
lymphocytes, plasma cells, and neutrophils.
• Although the surface may be ulcerated, it is
covered by stratified squamous epithelium that
resembles oral mucosa in approximately 50% of
these inflammatory hyperplastic lesions.

The source of this epithelium:
• From the engraftment of desquamated oral epithelial
cells
• The migration of the epithelium from the adjacent
gingival tissues.
• Rubbing of buccal mucosa

In more mature lesions that are covered with squamous
epithelium, the granulation tissue is replaced by fibrous
connective tissue with minimal inflammation and foci of
dystrophic calcification.
Treatment -- root canal therapy or extraction of the tooth.
Prognosis is excellent. No risk for recurrence exists once
definitive treatment has been rendered.

Pulp Necrosis:- Necrosis or death of pulp tissue is a
sequela of acute and chronic inflammation of the pulp
or an immediate
arrest of circulation by traumatic injury.
• It may be partial or total ,depending on the extent of
pulp tissue involvement.

Gangrenous necrosis of pulp- Necrosis of pulp due to ischemia
with superimposed bacterial infection.
• It is caused by saprophytic organism that invade the tissue
• A type of gangrene known as dry gangrene, sometimes
occurs when the pulp dies for some unexplained reason.
• This condition may be due to some traumatic injury or
infract.

Infection in dental pulp
Established
Spread through root canals
Periapical region

PULPITIS
Acute Chronic
APICAL PERIODONTITIS
Acute Chronic
PERIAPICAL ABSCESS PERIAPICAL GRANULOMA
Acute chronic APICAL PERIODONTAL CYST
OSTEOMYELITIS
Acute Chronic
Focal Diffuse
PERIOSTITIS
CELLULITIS ABSCESSwww.indiandentalacademy.com

Acute Periapical Condition
• Young tooth with open tubules
• Rampant caries
• Closed acute pulpitis
• Presence of highly virulent microorganisms
• Weakened host defense system

Acute apical periodontitis
• Progress of acute pulpitis (H/O previous pulpitis)
• Painful condition (no thermal stimulation)

Clinical Features
• Intense pain
• Fever with malaise
• Tooth is elevated in the socket
• Contact with opposite tooth produces pain

• Slight widening of periodontal ligament space
Radiographic Features

Histopathological features
• Inflammation of pdl characterised by vascular dilatation
& inflammatory cell infiltration.
• Localized around the root apex.
• Progresses to resorption of surrounding bone.
• Abscess may form if associated with bacterial infection-
acute periapical abscess

Chronic apical Periodontitis
/Periapical Granuloma
• Sequele of Pulpitis progresses to periapical lesion/acute
periapical periodontitis.
• Can transform to periapical abscess
• Can transform to periapical cyst

Clinical features
• Tooth is usually nonvital
• Tender on purcussion
• Tooth is slightly elevated in the socket
• Mild pain on biting
• Sensitivity
• May be asymptomatic

Radiographic features
Thickening of the pdl at root apex.
Occasional root resorption

Radiolucent area of variable size, usually well
circumscribed.

Sometimes a zone of sclerotic bone surrounding the lesion

Histopathological features
• Outer fibrous tissue
• Central zone of granulation tissue
• Center contain macrophages with
foamy cytoplasm
• Cholesterol crystals surrounded
by multinucleated giant cells

Presence of epithelium.
• Originates from cell rest of Malassez Or
• Respiratory epithelium of maxillary sinus
• Oral epithelium growing in fistulous tract
• Oral epithelium proliferating apically from a periodontal
pocket, bifurcation,or trifurcation involvement.

Giant- cell hyalin angiopathy
(Dunlap & Barker)
• Inflammatory cell infiltration
• Foreign body giant cells
• Rushton bodies

Pulse granuloma
(King & Mincer & coworkers)
• Fragments of foreign material, resembling vegetable
matter ,legumes

Periapical Abscess/Dento-alveolar
Abscess/Alveolar Abscess
• Acute or chronic suppurative process
• Progress of acute periapical Periodontitis / Periapical
granuloma
• Painful condition

Phoenix abscess
• Acute exacerbation of a chronic periapical lesion, as a
result of
1. Carious pulp infection
2. Necrosis of the pulp due to traumatic injury
3. Irritation to periapical tissues by mechanical
manipulation /chemicals in endodontics.

Clinical Features
Acute periapical abscess
• Intense pain
• Fever with malaise
• Tooth is elevated in the socket
• Contact with opposite tooth produces pain

Clinical Features
Chronic periapical abscess
• Symptom less

• Loss of lamina dura
• Extend into surrounding medullary bone
• Leads to increased radiolucency
Radiographic Features

Histopathological Features
• Central area of disintegrating PMNL.
• Lymphocytes , plasma cells, necrotic material, &
bacterial colonies.

Treatment & prognosis
• Drainage
• If untreated-
1. Osteomyelitis
2. Cellulitis
3. Bacteremia
4. Fistulous tract
5. Cavernous sinus thrombosis

Summary
1.focal reversible pulpitis
2.focal irreversible pulpitis
3.chronic hyperplastic pulpitis
4.pulp necrosis
5.gangrenous necrosis of pulp
6. pathophysiology of periodontal diseases
7. etilogy. Clinical features, histological features and
treatment of acute periapical conditions, periapical
abscess and periapical granuloma

BIBLIOGRAPHY
 Text book of oral pathology Shafer's, 5 & 6th
edition
 Color Atlas of Oral Diseases Cawson, R. 2nd
edition
 Oral and Maxillofacial Pathology Neville, Brad W. 2nd
 Lucas’s Pathology Of Tumor’s of the Oral Tissues
Cawson, R. A., Bennie, W. H 5th
edition

Pulp and Periapical Diseases

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