Perio-Endo Interrelation

Dr.
Abd El Rahman El Mekkawi

Lecturer of Endodontics
Acting Head of Endodontic Department
sinaiuniversity.net
abdelrahman.osama@su.edu.eg
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Endo-Perio lesions
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Anatomic Considerations:
● There is an intimate relationship between the periodontium and pulpal tissues
● As the tooth develops and the root is formed, 3 main avenues (physical
pathways) for communication are created:
1. Apical Foramen
2. Lateral Canals
3. Accessory Canals
4. Dentinal Tubules
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Pathway for exchange of noxious agents
between endodontic and periodontal tissue.

Apical foramen:
Average size of apical foramen of the maxillary teeth in the
adult is 0.4 mm
 Mandibular teeth 0.3 mm
 Sometimes it is found on the lateral side of the apex

although the root itself is not curved.
 Frequently there are two or more foramina separated

by a portion of dentin and cementum or by cementum
only.

Apical Foramen:
● It is the principal and the most direct
route of communication between the
pulp and periodontium
● Bacterial and inflammatory byproducts

may exit readily through the apical
foramen to cause periapical pathosis
● The apex may also serve as a portal of

entry of inflammatory byproducts from
deep periodontal pockets to the pulp
● It is a two way pathway from the pulp to the PDL, and from the PDL to the pulp
Furcation of root creates communication between roots Canal system and

periodontium
Apical Foramen:
SEM of the apical third of a root. Note the opening of an accessory canal at
ninety degrees from the main canal
They are not centered on the apex because there are lateral canals

Lateral and Accessory Canals
Leading from the radicular pulp laterally through the root

dentin to the periodontal tissue.
 May be seen anywhere along the root but are most

numerous in the apical third of the root.
 Clinically significant in spread of infection, either from

the pulp to the periodontal ligament or vice versa.
Dentin Tubules:
● Exposed dentinal tubules in areas of
denuded cementum may serve as
communication pathways between the
pulp and PDL
● In the root, dentinal tubules extend from the pulp to the cemento-
dentinal junction. They range in size from 1 to 3 microns in
diameter (bacteria and their toxins are smaller in size)

Scanning electron micrograph of dentinal tubules
● The tubules may be denuded
of their cementum coverage as
a result of perio disease,
surgical procedures or
developmentally when the
cementum and enamel do not
meet at the CEJ thus leaving
areas of exposed dentin

● Patients experiencing
cervical dentin
hypersensitivity are
examples of such a
phenomenon

Additional Avenues of communication between the Pulp
and the Periodontium (pathological pathways)
● Perforations – these may result from extensive carious

lesions, resorption, or from operator error
● Vertical root fractures – these can produce deep periodontal
pocketing and localized destruction of alveolar bone. The
fracture site provides a portal of entry for irritants from the
root canal to the PDL
● Developmental malformations – such as palatogingival grooves of
maxillary incisors. These usually begin in the central fossa, cross the
cingulum, and extend apically with varying distances
• Resorption will cause a poor prognosis

PULPAL DISEASE - Etiologic Factors:
The major causes of pulpal inflammation are:
(1) instrumentation during periodontal, restorative, or prosthetic
dentistry;
(2) the progression of dental caries;
(3) direct, local trauma such as tooth fracture.
The extent of inflammation of the pulp and the signs and symptoms
that result vary with the severity of the insult and the ability of the
host to ameliorate the inflammation that results

Route of entry of Bacteria:

The root canal can be considered a highly controlled limited environment :
Niche 1 – coronal segment:
High oxygen tension
Nutrients available from the oral cavity
Microorganisms directly exposed to treatment action
Niche 2 – main canal
Low oxygen tension.
Reduced amount of nutrients from the oral cavity.
Microorganisms are directly exposed to treatment actions.
Niche 3 – apical segment
Very low oxygen tension.
Nutrients available from the periapical tissues.
Microorganisms probably less affected by treatment measures.
Pulpal infection is a poly-microbial process. Although a correlation between causation

and any species of bacteria is not currently possible
The organisms cultured are predominantly gram-negative anaerobes.

Classification of Pulpal Disease:
● Reversible pulpitis
● Irreversible pulpitis
● Hyperplastic pulpitis
● Pulpal necrosis
Effect Of Pulpal Diseases On The Periodontium

● Pulpal infection may cause a tissue destructive process which may progress from apical
region to the gingival margin, termed as “retrograde periodontitis”
● Commonly, the areas of bone resorption are seen at apex, furcation areas and on the lateral
surface of the root.
● Inflammatory lesions may also form from a root canal infection through lateral and
accessory canals present on the lateral surface of root and furcation areas.
Effect Of Periodontal Diseases On Pulpal Tissue
● The pathogenic bacteria and inflammatory products of periodontal diseases may

enter into the root canal system via accessory canals, lateral canals, apical
foramen, dentinal tubules or iatrogenic errors.
● Though ;Irreversible pulpitis or pulpal necrosis is not the common occurrence.

● As periodontal disease extends
from gingival sulcus towards
apex, the auxiliary canals get
affected which results in pulpal
inflammation.
● It becomes more serious if these

canals get exposed to oral cavity
because of loss of periodontal
tissues by extensive pocket depth.

Periodontal therapy also affects the pulp:
● Periodontal instruments like

ultrasonic scalers, vibrators, curettes
may cause harm to the pulp
specially when the remaining dentin
thickness is smaller than 2 mm.
● Also the chemicals and
medicaments used during
periodontal therapy may cause
pulpal damage.

● Minor injury such as periodontal root planning or the conservative
preparation of a tooth for a restoration may lead to pulpal
symptoms.
● A transient hypersensitivity to thermal stimuli is the most common

symptom noted.
● The application of a thermal stimulus results in a brief, painful

response that varies in intensity from mild to severe. The response
rapidly disappears after removal of the stimulus.

Etiology Of Endodontic Periodontal Problems
● Bacterial plaque “bio-film”: is the primary etiologic agent in both periodontitis and
endodontic lesions.
1.Bacterial plaque:
A. a., F. nucleatum, P. intermedia, P. gingivalis and spirochetes sometimes C. albicans, herpes
simplex, cytomegalo virus and E.B.V.

2.Foreign bodies like amalgam filling, root canal filling material, dentin or cementum chips and
calculus deposits can irritate pulp and periodontium.

3. Contributing factors:
• Malposed teeth causing trauma.
• Presence of extra canals in teeth.
• Cervical enamel projections into furcation of multirooted teeth.

• Large number of accessory and the lateral canals.
• Trauma combined with gingival inflammation.
• Vertical root fracture.

• Crown fracture.
• Root resorption.
• Perforations
• Systemic factors such as diabetes.

Internal resorption
External resorption

Effects on the Periodontium:
Classification of Periradicular Lesions
● Acute apical periodontitis
● Chronic apical periodontitis
● Condensing osteitis
● Acute apical abscess
● Chronic apical abscess

Reversible Pulpitis/Hyperemia/ Hyperactive Pulpalgia:
 Is mild-to-moderate inflammatory condition of the pulp, caused by
noxious stimuli in which the pulp is capable of returning to the normal
state following removal of stimuli “less than the pain threshold of the
pulp organ”.
 Pain:
- It is sharp but of brief duration (lasting for a moment ) .
- Not spontaneous & does not continue (stops immediately) when irritant is
removed.
- It is usually caused by cold, sweet and sour stimuli.
Acute Pulpitis / Irreversible Pulpitis / Hot Tooth
 Is a severe inflammatory process of the pulp that does not resolve even if the
cause is removed, where the pulp is incapable of healing & slowly or rapidly
becomes necrotic.

Stages of irreversible pulpitis:
I) Early (Incipient) stage :
- Hot  pain inc., due to inc. vasodilatation & inc. pressure on C fibres (Hot
Tooth)
- Cold  pain increase due to hydrodynamic theory ( movement of fluids in
dentinal tubule ) result in stimulation of A fibers.
II) Advanced ( Late ) stage :

As the pulpal inflammation progresses, heat intensifies the response because it
has expansible effect on blood vessels. Cold tends to relieve pain because of its
contractile effect on vessels, reducing the intrapulpal pressure.
2- Signs & symptoms:
Severe or sharp, lancinating, throbbing pain, characterized by:
A) Sudden, rapid onset.
B) Spontaneous.
C) Caused by an irritant, but lingers for some time after the removal of the
cause.
D) Pain exacerbated on bending down or lying down due to increase of
intrapulpal blood pressure.
E) Diffuse or referred pain, because pulp has only sensory nerve endings, while
pain localization requires the presence of both sensory & pro-prio-ceptors.
Innervation of Pulp
A-delta nerve fibers C-nerve fibers
1- At the odontoblastic layer, They send 1- More resistant to hypoxic conditions or

free nerve endings into dentinal tubules. compromised blood flow.
2- Fast conduction velocities 2- Slow conduction velocities
3- Pain is localized, Sharp, quick, 3- Pain is not localized, Dull, throbbing

pricking and disappears quickly on and lingering.
removal of stimulus.
A-delta nerve fibers C-nerve fibers
4- Electrical pulp tester stimulates A delta 4- Stimulated by intense cold or hot

fibers first because of their lower stimuli or mechanical stimulation
threshold. because of their high threshold.
5- 20 % of pulp nerve fibers. 5- 80 % of pulp nerve fibers. responsible

for pain occurring during instrumentation

Classification of Pulpoperiapical Pathosis
I- Symptomatic
a) Acute apical periodontitis b) Acute apical periodontitis

(incipient / early stage) (advanced/ late stage)
1- Acute periapical 2- phoenix 3- Subacute

abscess
periapical
abscess
abscess

II- Asymptomatic
a) Chronic apical periodontitis b) Chronic apical periodontitis

(incipient / early stage) (advanced / late stage)
1- Chronic 2- Periapical 3- Periapical 4- Condensing
periapical granuloma cyst osteitis
abscess

I- Symptomatic Pulpoperiapical Disease
Distention of periodontal ligament & extrusion of tooth with slight tenderness  Biting
on the tooth relieves pain, due to blood driven away of dilated blood vessel & decreases
pressure .
If irritation continues inc Accumulation of inflammatory exudate  Edema

& White blood cell infiltration Blood flow is slow  Congestion & stasis
results  Hypoxia periapical tissue cells  Necrosis  inc Pus formation
Agglutination of the extra-vasated fluid & pus  pain on biting  Pus
stimulates osteoclastic activity  Loss of alveolar bone  Penetration of the
cortical bone Swelling  Acute periapical abscess .

A) Acute apical periodontitis (incipient stage):
a) mild to moderate pain.
b) pain is localised, due to the presence of proprioceptors in the periodontal
ligament.
B) Acute apical periodontitis (advanced stage):

Same as in the incipient stage, except for the throbbing pain which
increases:
- on biting on the tooth.
- At night.
C) Acute periapical abscess :
1- Visual examination and history:
a) Redness & hotness of the mucosa opposite to the periapical region of
the affected tooth.
b) Swelling of the oral mucosa & skin is noticed later.
a) Severe throbbing pain increases on biting or at night.

b) Feeling of fullness or elongation of the tooth.
c) The patient suffers from fever, malaise or loss of appetite.

- The most intense pain occurs, as the pus penetrates the
outer plate of bone & begins to raise the periosteum.
- Once the periosteum & the mucosa rupture, due to:
- Pressure of the suppurutive material
- Operator’s scalp
- The pain subsides & will not return unless the drainage
is blocked.

D) Recrudescent periapical abscess (phoenix) :
Etiology :
Chronic periradicular lesions such as granulomas are
asymptomatic due to state of equilibrium. Lowered body
defenses together with influx of necrotic products,
bacteria and their toxins from diseased pulp to
periapical tissue may trigger an acute inflammatory
response.
Diagnosis:
All steps are similar to acute periapical abscess, EXCEPT FOR a large
well defined radiolucent area.
II- Asymptomatic Pulpoperiapical Disease
1) Chronic apical periodontitis :
a) Chronic periapical abscess:
This long standing low grade inflammatory

reaction of the periapical C.T. to pulpal irritants, is
characterised by the formation of pus draining
through the stroma of a sinus tract.
 It develops from chronic apical periodontitis or
acute periapical abscess, that found a pathway for
drainage through the mucosa.

b) Periapical granuloma:
Definition :
It is usually described as a mass of
chronically inflamed granulation tissue
found at the apex of nonvital tooth.
 All diagnostic features are the same as in
chronic periapical abscess exept :
- Radiographically : Well-defined radiolucent
area surrounded by radio-opaque margin.
- Clinically : no sinus tract is present.

c) Periapical cyst:
Definition :
A periapical granuloma with a central fluid-filled epithelial lined cavity.
Pathogenesis:
Stimulation of Epithelial rests of Mallassez in the periapical granuloma
epithelial cells proliferate  form large mass of cells  central cells
deprived from blood supply  undergo liquefaction necrosis  definite
central cavity develops, containing fluid & a number of cells in different
stages of degeneration  cystic growth by bone resorption as it
stimulates U.M.C. to osteoclast  around the cyst there is a thick layer of
bone (condensing osteitis).
d) Condensing osteitis: (pulpoperiapical osteosclerosis) :
It is a productive response of the periapical bone to a low grade long
standing pulpal irritation.
 Characterized by ↑ density of bone, not because ↑ concentration of
minerals, but because of osteoblastic hyperactivity.
 So ↑ bone formation at apex in expense of bone marrow space, which ↓.
Radiographically: Appears radio-opaque.

Classification Of Endodontic Periodontal Lesions
Weine: Based on etiology and treatment plan:
● Clinical and radiography : simulated periodontal involvement But has pulpal
inflammation and necrosis.
● Tooth has both concomitantly.
● Tooth has no pulpal problem but need endodontic for periodontal healing.
● Clinical and radiography simulated pulp involvement but has periodontal disease.
Ingle:
● Primary endodontic
● Primary periodontal
● Combined: a- primary endodontic, secondary periodontics.
● b- Primary periodontics, secondary endodontic.
● c- True.

Simon:
primary endo.
● Primary endo, secondary perio
● Primary perio
● Primary perio secondary endo
● Concomitant
● True.

Kim:
● Endo Group:
● A- No Lesion.
● B- Lesion at apical ¼ “small part”.
● C- Lesion at apical ½ “large part”.
● Endo-Perio Group:
● D- Class B with perio pocket.
● E- Class B with periodontal communication.
● F- Total buccal fenestration.
Grossman:
Type I: Lesions requiring endodontic treatment only, e.g.
a. Tooth with necrotic pulp reaching periodontium.
b. Root perforations
c. Root fractures
d. Chronic periapical abscess with sinus tract
e. Replants
f. Transplants
g. Teeth requiring hemisection.

Type II: Lesion that require periodontal treatment only.
For example:-
a. Occlusal trauma causing reversible pulpitis
b. Suprabony or infrabony pockets caused during periodontal treatment resulting in pulpal
inflammation.
Type III: Lesions that require combined endodontic and periodontal treatment. It includes:-
a. Any lesion of type I which result in irreversible reaction to periodontium requiring
periodontal treatment.
b. Any lesion of Type II which results in irreversible damage to pulp tissue requiring endodontic
therapy.

Theoretic pathways of osseous lesion formation
(according to Origin):
1. Primary endodontic lesions.
2. Primary endodontic lesion with secondary periodontal involvement.
3. Primary periodontal lesions.
4. Primary periodontal lesion with secondary endodontic involvement.
5. Combined lesions.

1) Primary endodontic lesions:
Clinically:
1. Caries , restoration
2. Tenderness to percussion
3. Increased mobility
4. The suppurative process may drain coronally through the periodontal ligament into the gingival
sulcus causing single narrow probing defect (pseudo-pocket) and causing:
A. Swelling the marginal gingiva.
B. Sinus tract that can be traced with Gutta-percha down to tooth apex or
lateral canal.
C. In multi-rooted teeth the sinus tract can drain into the furcation area
1) Primary endodontic lesions
5) No increase in probing depth elsewhere around the tooth  only single
narrow probing defect.
6) Few or no plaque or calculus
7) Negative pulp test.
Radiographically:
Apical Radiolucency
Treatment:
Only Root canal treatment
Prognosis:
Good if proper root canal treatment is done.

2) Primary periodontal lesion:
● Periodontal disease has a progressive nature, it starts in the sulcus and
migrates to the apex as accumulation of plaque and calculus produce
inflammation, causing loss of surrounding alveolar bone and surrounding
periodontal soft tissues. This leads to loss of clinical attachment and
formation of periodontal abscess during the acute phase of destruction.
Clinically:
1. Intact teeth with various degrees of mobility.
2. Accumulation of plaque and calculus.
3. Positive pulp test.
4. Probing reveals pocket formation.
5. Tenderness to percussion

2) Primary periodontal lesion
Radiographically:
Widespread vertical and horizontal bone loss
along root surfaces at various levels
Treatment:
Long term periodontal treatment.
Prognosis:
Depends on the extent of periodontal disease
and patient’s ability to follow and maintain
long term therapy.
3)Primary endodontic lesion with secondary
periodontal involvement
● When a lesion of endodontic origin is not treated, destruction of
periapical alveolar bone will progress into the inter-radicular area
causing breakdown of hard and soft tissues.
Clinically:
1) The affected tooth with necrotic pulp or failed root canal treatment.
2) As drainage persists through the gingival sulcus:
 accumulation of plaque and calculus
 Presence of probing defects around the affected tooth.

2)Primary endodontic lesion with secondary periodontal
involvement
Radiographically:
Periradicular and Angular bone defects
Treatment:
Both, root canal and periodontal treatment are required.
Prognosis:
If root canal treatment is properly done, then the prognosis depends on:
a) severity of periodontal involvement.
b) efficacy of periodontal treatment.
4) Primary periodontal lesion with secondary endodontic
involvement
● Prolonged periodontal pathosis can permit bacteria or bacterial byproducts to invade the
pulpal tissues starting a sequence of pulpal pathosis.
● These lesions may be indistinguishable from primary endodontic lesions with secondary
periodontal involvement.
Clinically:
1. Teeth with deep pockets, extensive periodontal disease and possible history of past
periodontal therapy.
2. When pulp becomes involved, pain increases and clinical signs and symptoms of pulpal
diseases may appear (acute pulpitis with acute apical periodontitis).
3. In long standing cases, patient may be asymptomatic.

4) Primary periodontal lesion with secondary
endodontic involvement
Radiographically:
Similar to primary endodontic lesions with secondary periodontal
involvement.
Treatment:
Both, root canal treatment and periodontal treatment are required.
Prognosis:
Depends on continuing periodontal treatment subsequent to endodontic
treatment.
5) Combined lesions
● In and around the same tooth, pulpal and periodontal diseases may occur
independently
 if both diseases do not communicate with no evidence either disease state
has influenced the other : Concomitant pulp and periodontal lesions.
 if each disease progress until they merge: True combined lesions.
● Clinically:
1. Necrotic pulp or failed root canal treatment.
2. Accumulation of plaque and calculus, periodontal disease in other areas.

5) Combined lesions
Radiographically:
 Crestal bone loss of periodontal disease and an independent periradicular
lesion of pulpal origin Concomitant pulp and periodontal lesions.
 Crestal bone loss of periodontal disease continuous with periradicular
lesion of pulpal origin True combined lesions.
Treatment:
Requires both root canal and periodontal treatments.
Prognosis :
Depends on severity of periodontal disease.

Concomitant pulp and True combined lesion
periodontal lesion
Diagnosis:
● The correct diagnosis of the periodontal endodontic lesions is of
fundamental importance to determine the treatment and
prognosis
● A thorough clinical and radiographic examination is imperative

for developing a diagnosis

Diagnosis:
● Data Collected must include:
○ Peri-apical radiographs
○ pulp vitality testing: cold, EPT, cavity test
○ percussion
○ palpation
○ pocket probing
○ sinus tract tracking
○ cracked tooth testing: trans-illumination, staining

Radiographs showing endo-perio lesion with bone resorption.
Tracking sinus or fistula:
Tracking the fistula may aid the clinician to differentiate the source .

Differential Diagnosis:
Pulp Perio
Clinical
Etiology Pulp infection Perio infection
Extension Apical to coronal coronal to apical
Pain Acute Dull diffused
Vitality Non vital vital
Restoration deep -----
Plaque – Calculus ----- Generalized
Inflammation acute chronic
Pocket Single, narrow Multiple, wide

Pulp Perio
Radiography
Pattern Localized Generalized
Bone loss Wide apical Wide coronal
Vertical loss No Yes
Periapical bone radiolucent Not affected
Histological
Junction epithelium No migration Apical migration
Granulation tissue Apical – minimum Coronal – large
Gingiva normal Recession

THANK YOU
For any questions feel free

to contact me by mail
Abdelrahman.osama@su.edu.eg
Dr. Abd El Rahman El Mekkawi
Lecturer of endodontics
Acting Head of Endodontic Department
www.su.edu.eg

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Dr.

Abd El Rahman El Mekkawi

abdelrahman.osama@su.edu.eg info@su.edu.eg www.su.edu.eg

abdelrahman.osama@su.edu.eg info@su.edu.eg www.su.edu.eg

 Mandibular teeth 0.3 mm

 Sometimes it is found on the lateral side of the apex

 Frequently there are two or more foramina separated

abdelrahman.osama@su.edu.eg info@su.edu.eg www.su.edu.eg

● Bacterial and inflammatory byproducts

● The apex may also serve as a portal of

Furcation of root creates communication between roots Canal system and

abdelrahman.osama@su.edu.eg info@su.edu.eg www.su.edu.eg

Leading from the radicular pulp laterally through the root

 May be seen anywhere along the root but are most

 Clinically significant in spread of infection, either from

abdelrahman.osama@su.edu.eg info@su.edu.eg www.su.edu.eg

abdelrahman.osama@su.edu.eg info@su.edu.eg www.su.edu.eg

abdelrahman.osama@su.edu.eg info@su.edu.eg www.su.edu.eg

● Perforations – these may result from extensive carious

abdelrahman.osama@su.edu.eg info@su.edu.eg www.su.edu.eg

abdelrahman.osama@su.edu.eg info@su.edu.eg www.su.edu.eg

abdelrahman.osama@su.edu.eg info@su.edu.eg www.su.edu.eg

Pulpal infection is a poly-microbial process. Although a correlation between causation

The organisms cultured are predominantly gram-negative anaerobes.

abdelrahman.osama@su.edu.eg info@su.edu.eg www.su.edu.eg

Effect Of Pulpal Diseases On The Periodontium

● The pathogenic bacteria and inflammatory products of periodontal diseases may

abdelrahman.osama@su.edu.eg info@su.edu.eg www.su.edu.eg

● It becomes more serious if these

abdelrahman.osama@su.edu.eg info@su.edu.eg www.su.edu.eg

● Periodontal instruments like

abdelrahman.osama@su.edu.eg info@su.edu.eg www.su.edu.eg

● A transient hypersensitivity to thermal stimuli is the most common

● The application of a thermal stimulus results in a brief, painful

abdelrahman.osama@su.edu.eg info@su.edu.eg www.su.edu.eg

abdelrahman.osama@su.edu.eg info@su.edu.eg www.su.edu.eg

abdelrahman.osama@su.edu.eg info@su.edu.eg www.su.edu.eg

abdelrahman.osama@su.edu.eg info@su.edu.eg www.su.edu.eg

abdelrahman.osama@su.edu.eg info@su.edu.eg www.su.edu.eg

abdelrahman.osama@su.edu.eg info@su.edu.eg www.su.edu.eg

abdelrahman.osama@su.edu.eg info@su.edu.eg www.su.edu.eg

abdelrahman.osama@su.edu.eg info@su.edu.eg www.su.edu.eg

abdelrahman.osama@su.edu.eg info@su.edu.eg www.su.edu.eg

II) Advanced ( Late ) stage :

1- At the odontoblastic layer, They send 1- More resistant to hypoxic conditions or

2- Fast conduction velocities 2- Slow conduction velocities

3- Pain is localized, Sharp, quick, 3- Pain is not localized, Dull, throbbing

4- Electrical pulp tester stimulates A delta 4- Stimulated by intense cold or hot

5- 20 % of pulp nerve fibers. 5- 80 % of pulp nerve fibers. responsible

abdelrahman.osama@su.edu.eg info@su.edu.eg www.su.edu.eg

a) Acute apical periodontitis b) Acute apical periodontitis

1- Acute periapical 2- phoenix 3- Subacute

abdelrahman.osama@su.edu.eg info@su.edu.eg www.su.edu.eg

a) Chronic apical periodontitis b) Chronic apical periodontitis

1- Chronic 2- Periapical 3- Periapical 4- Condensing

periapical granuloma cyst osteitis

abdelrahman.osama@su.edu.eg info@su.edu.eg www.su.edu.eg

If irritation continues inc Accumulation of inflammatory exudate  Edema

abdelrahman.osama@su.edu.eg info@su.edu.eg www.su.edu.eg

B) Acute apical periodontitis (advanced stage):

a) Severe throbbing pain increases on biting or at night.

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