PULP & PERIAPICAL PATHOSIS

INTRODUCTION

Inflammation of pulp and periapical tissue is

one of the most common diseases encountered in our
day to day practice.

To give proper and effective treatment one has to

diagnose correctly. Arriving at a correct diagnosis
requires knowledge, skill, art and experience;
knowledge of the diseases and their symptoms, skill
to apply proper test procedures, the art to correlate
the facts and experiences to reach proper conclusions.
 PULPAL PATHOSIS

“ The pulp lives for the dentin and the

dentin lives by the grace of the pulp. Few
marriages in nature are marked by a greater
affinity.” - Alfred L. Ogilvie
ETIOLOGY OF PULPAL DISEASES
According to Ingle,
I. BACTERIAL

a) CORONAL INGRESS

1. Caries
2. Fracture
3. Non fracture trauma
4. Developmental Anomalies

b) RADICULAR INGRESS

1. Caries
2. Retrogenic infection – periodontal pocket & abscess
3. Hematogenic
2. TRAUMATIC

a) ACUTE
1. Coronal fracture
2. Radicular fracture
3. Vascular stasis
4. Luxation
5. Avulsion

b) CHRONIC
1. Adolescent female bruxism
2. Traumatism
3. Attrition or abrasion
4. Erosion
3. IATROGENIC

 Cavity preparation

 Restorations

 Periodontal curettage

 Orthodontic movement

 Electrosurgery

 Laser burn

 Rinoplasty

 Osteotomy
4. CHEMICAL
 Restorative materials

 Disinfectants

 Desiccants
5. IDIOPATHIC
 Aging.

 Internal resorption.

 External resorption.

 Sickle cell anaemia.

 Herpes zoster infection.

 HIV

Endodontics 5th edition John I. Ingle

According to Grossman
 PHYSICAL

a) MECHANICAL

a) Trauma

b) Pathological wear

c) Cracked tooth syndrome

d) Barometric changes

b) THERMAL

a) Heat from cavity preparation

b) Exothermic heat from the setting of cement

c) Conduction of temperature through deep fillings

d) Frictional heat caused by polishing of restoration

c) ELECTRICAL

a) Galvanic Current

 CHEMICAL

a) Phosphoric acid, acrylic monomer

b) erosion

 BACTERIAL

a) Toxins associated with caries

b) Direct invasion of pulp from caries or trauma

c) Anachoreses
 PULPAL PATHOPHYSIOLOGY
irritation to clinical crown

initial localized pulpal inflammation

insult
increased local tissue pressure

venous collapse stasis ischemia local necrosis

localized
effect
release of intracellular inflammatory agents

Circumferential vascular disturbance

Mechanism Increased tissue pressure

Of spread
Necrosis of additional tissue

Total pulpitis
CLASSIFICATION OF PULPAL DISEASES
According to Grossman

I] PULPITIS

a) REVERSIBLE
1. Acute (symptomatic)
2. Chronic (asymptomatic)

b) IRREVERSIBLE
1. Acute

- Abnormally responsive to cold

- Abnormally responsive to heat

2. Chronic

- Asymptomatic with pulp exposure

- Hyperplastic pulpitis
- Internal resorption
II] PULP DEGENERATION

Calcific (Radiographic diagnosis)

Others (Histopathologic diagnosis)

III] PULP NECROSIS

According to Cohen:

 Reversible pulpitis

 Irreversible pulpitis

 Asymptomatic Irreversible pulpitis

 Symptomatic irreversible

 Hyperplastic pulpitis

 Internal resorption

 Pulp necrosis
According toWeine

A) INFLAMMATORY CHANGES

HYPERALGIA

 Hypersensitive dentin.
 Hyperemia.

PAINFUL PULPITIS

 Acute pulpalgia (acute pulpitis)

 Chronic pulpalgia (subacute pulpitis)

NON PAINFUL PULPITIS

 Cronic Ulcerative Pulpitis

 Chronic Pulpitis
 Hyperplastic pulpitis.
B) ADDITIONAL PULP CHANGES

 Necrosis

 Retrogressive changes

 Internal Resorption
 According to SELTZER (HISTOLOGIC CLASSIFICATION)

• Intact - uninflammed pulp

• Atrophic pulp
• Acute pulpitis
• Intact pulp with scattered chronic inflammatory cells (transitional stage)
• Chronic partial pulpitis
- with partial liqufeaction necrosis
-with partial coagulation necrosis
• Chronic total pulpitis
- with partial liqufeaction necrosis
• Total pulp necrosis
 ACCORDING TO F.J. HARTY

A simple classification based on the state of the pulp.

◦ Normal pulp.

◦ Reversible pulpitis.

◦ Irreversible pulpitis.

◦ Pulp necrosis.
 SHAFER’S Classification

1.According to involvement

a) Partial
b) Total

2. According to severity

a) Acute
b) Chronic

3. According to presence or absence of direct communication between

the dental pulp and oral environment

a) Pulpitis aperta
b) Pulpitis Clausa
 REVERSIBLE PULPITIS

A mild to moderate inflammatory condition of

pulp caused by noxious stimuli in which pulp is
capable of returning to the uninflamed state following
removal of the stimuli. Also, referred as “PULP
HYPERAEMIA”.
ETIOLOGY

1. Trauma

2. Thermal shock

3. Excessive dehydration

4. Galvanism

5. Chemical stimulus

6. Bacteria

7. Circulatory disturbances

8. Local vascular congestion

Symptoms
 Sharp pain lasting for a moment

 More often brought on by cold than hot food

 Does not occur spontaneously

 Does not continue when stimulus has been removed

 Teeth are not tender on percussion

Histopathology
 Hyperaemia - mild to moderate inflammatory changes are limited to the
area of involved dentinal tubules

 Reparative dentin, dilated blood vessels, disruption of odontoblast layer

 Extravasation of edema fluid
 Immunologically competent chronic inflammatory cells
 Presence of acute inflammatory cells
DIAGNOSIS

1. Pain: Sharp pain, lasts for a few seconds

Cold, sweet or sour causes pain

2. Visual examination & history:

Examine for caries, restorations, fractures or traumatic occlusion

History of past dental treatment

3. Clinical tests:

Cold test is excellent way to locate pain

Normal to percussion, palpation and mobility

4. Radiographically : No changes

5. Vitality test:

More readily response to cold stimulation than normal teeth

EPT requires minimal current to initiate positive response
Treatment
- Prevention
- Removal of the noxious stimuli
- Check for vitality
- Periodic care to prevent caries
- Proper insulation of the restoration
- Desensitization

Prognosis
 Good - if irritant is removed earlier
 Otherwise condition may develop to Irreversible pulpitis
 IRREVERSIBLE PULPITIS

A persistent inflammatory condition of the pulp,

symptomatic or asymptomatic, caused by noxious stimulus.

 May be
Acute or chronic

ETIOLOGY

 Caries
 Chemical, thermal and mechanical injuries
 Sequelae of reversible pulpitis
 HISTOPATHOLOGY
Both acute and chronic inflammatory stages are seen

dentin Chronic inflammatory

response

inflammatory changes will increase

Caries not removed
in severity

Post capillary venules

become congested
Attract Acute
PMNL’s Inflammatory
Affect circulation - Necrosis reaction

PMNL ‘s
Die & release
lysosomal lysis
Phagocytosis by PMNL ‘s enzymes

Chronic ulcerative Carious process

microabscess pus
pulpitis continues
SYMPTOMS OF IRREVERSIBLE PULPITIS

 Early stages – Pain can be spontaneous in nature

which is sharp, piercing, intermittent or continuous in
nature.
 Pain exacerbated on bending down or lying down
 Presence of referred pain
 Later stages  Pain is more severe, boring, throbbing
in nature.
 Diagnosis

 Deep cavity extending to the pulp.

 Decay under filling.
 Greyish scum like layer.
 An odor of decomposition.
 Probing into the area is not painful.
 Deep probing will result in pain & haemorrhage.
History-
-May reveal previous symptoms or a traumatic experience

Radiographic examination:
-May not show anything of significance.
-It may disclose an interproximal cavity or caries under a filling

Percussion:
-Tenderness
Vitality test:

Thermal test:
As pulpal inflammation progresses, heat will intensify the responses.
Cold will tend to relieve the pain in advanced stages of pulpits.

Electric test:
Early stages – response to less current.
Later (Necrotic tissue)- more current is required.

Treatment:

Pulpectomy.
Surgical removal should be considered if the tooth is unrestorable.
 POTENTIALLY REVERSIBLE PROBABLY IRREVERSIBLE

Pain Sharp, Momentary : dissipates readily Continuous, throbbing : Persists

after removal of stimulus minutes to hours
Stimulus Requires external stimulus Spontaneous : dead or injured
(cold, heat, sweet) tissue in chambers or canal.
Intermittent : Spontaneous pain
of short duration.
History Recent dental procedure, cervical Extensive restoration, pulp
abrasion capping, deep caries, trauma
Electric test Premature response Premature, delayed or mixed
response
Referred pain Negative Common

Lying down Negative Increases pain

Color Negative May be present due to tissue lysis

& intrapulpal haemorrhage.
Radiograph Restoration ,caries, periodontal Deep restoration, caries
pocket, cupping of alveolar crest
Periapex - Normal Periapex – widening of PDL

Endodontic Therapy Franklin S. Wein 6th edition

CHRONIC HYPERPLASTIC PULPITIS (Pulp Polyp)

Chronic hyperplastic pulpitis is a productive pulpal inflammation

due to an extensive carious exposure of a young pulp.

Characterized by - development of granulation tissue, covered at

times with epithelium and resulting from long standing, low

grade irritation.
ETIOLOGY

 Slow, progressive carious exposure.

 Pulp polyp develops in a tooth with large, open cavity having

a young resistant pulp & a chronic low grade stimulus

 Mechanical irritation & bacterial infection provide stimulus.

Symptoms

It is asymptomatic, except during mastication.

HISTOPATHOLOGY

 Budding capillaries, proliferating fibroblasts & inflammatory cells

are seen.

 Presence of granulation tissue – which is young vascular

connective tissue containing PMNL’s, lymphocytes & plasma
cells.

 Collagenous fibres -rooted in

deeper tissue of pulp chamber.

 Sensory nerve fibres are almost

absent near surface.

 Surface is usually covered by

stratified squamous epithelium.
DIAGNOSIS

- Appearance of polyp tissue clinically, characteristic of a fleshy,

reddish, pulpal mass which fills most of pulp chamber.

- Radiographically- a large open cavity with direct access to the pulp

chamber.

- Thermal tests- Feeble or no response

- EPT : More current than normal may be required to elicit a response

Differential Diagnosis
- Proliferating gingival tissue (Gingival Polyp)
 TREATMENT

• Elimination of polyp tissue with a sharp curette or spoon excavator,

followed by extirpation of the pulp, provided the tooth can be
restored.

• Bleeding can be controlled with pressure.

• pulpectomy can be completed in a single visit.

CHRONIC PULPITIS (CLOSED FORM)

 Occur from operative procedures, trauma or periodontal lesions

extending apically to the foramina of lateral canals

 Excessive orthodontic movement may affect the vascular supply to

the pulp producing localized areas of necrosis

 Depending on the strength and duration of the inciting irritant,

pulpitis may be chronic from onset or become chronic after the acute
responses have subsided

 Exacerbation – additional operative procedures

 Minimal pulpal damage – resolution may occur

 CHRONIC PULPITIS (ULCERATIVE OR OPEN FORM)

 Is a chronic inflammation of the cariously exposed pulp

characterized by the formation of an abscess at the point of
exposure (ulcer).

 Terms used are - Pulpal chronic abscess or pulpal granuloma.

 The abscess is surrounded by granulomatous tissue

 Can be partial or total.

 INTERNAL RESORPTION

An idiopathic, slow or fast progressive resorptive process occurring

in dentin of the pulp chamber or root canals of teeth.

Synonyms: Internal granuloma, Odontoclastoma,

Pink tooth of mummary
ETIOLOGY:
Unknown, but patient often has a history of trauma.

TYPES- ( James L. Gutmann 1999)

• Root canal replacement resorption (Metaplastic resorption)
• Internal inflammatory resorption

(Quintessence Int ,1999 :vol 30)

MECHANISM OF INTERNAL RESORPTION

Pulp inflammation due to infection

Alteration or loss of pre- dentin and odontoblastic layer

Undifferentiated mesenchymal cells come in contact

with mineralized dentin

Differentiate into dentinoclasts

Resorption results
SYMPTOMS
- Asymptomatic.
- In the crown, it is manifested as a reddish area called “pink spot”
representing the granulation tissue showing through the resorbed area
of crown.

HISTOPATHOLOGY:

• Shows Osteoclastic activity.

• Resorptive lacunae may be filled in by osteoid tissues
• Presence of granulation tissue, multinucleated giant
cells ,dentinoclasts, chronic inflammatory cells.
• Metaplasia of pulp i.e. transformation to another tissue
DIAGNOSIS

- Recognized during routine radiographic examination

- Affects either crown or root or both.
- It is slow & progressive or develops rapidly to perforate the
tooth .
- Most commonly involved - maxillary anterior teeth.

RADIOGRAPHICALLY

- Pulp chamber / root canal with a round or ovoid radiolucent area.

DIFFERENTIAL DIAGNOSIS

- External resorption
TREATMENT

- Extirpation of pulp, stops the internal resorptive process.

- Routine endodontic treatment is indicated, but in advanced
cases -calcium hydroxide paste dressing
- Repair is completed when calcific barrier is present.
- Later the canal with its defect is obturated with plasticized gutta
percha.

PROGNOSIS
Is favourable, before perforation occurs.
RETROGRESSIVE PULP CHANGES (PULP DEGENERATION)

Pulp degeneration is induced by attrition, abrasion, trauma,

operative procedures, caries, pulp capping and reversible pulpitis.
Generally present in older people .
May occur in the following forms

Atrophy Fibrosis Calcifications

ATROPHIC DEGENERATION

- Is observed histopathologically in pulps of older people.

- Fewer stellate cells are present
- Intercellular fluid is increased.
- Pulp tissue is less sensitive than normal.
- No clinical diagnosis exists.

FIBROUS DEGENERATION
- Is characterized by replacement of cellular elements by fibrous
connective tissue.
- Pulp has a characteristic appearance of a leathery fibre.
- Reduction in size of pulp chamber.
- Decrease in nerve supply or blood supply.
- There are no distinguishing symptoms.
CALCIFICATIONS

 Here a part of pulp tissue is replaced by calcific material, i.e. pulp

stones or denticles are formed, either within pulp chamber or
root canal.
3 types
-Dystrophic, Diffuse, Denticles / pulp stones

DYSTROPHIC CALCIFICATIONS

 Occur by deposition of calcium salts in dead or degenerated

tissue

 Occur in minute areas of young pulp affected by minor

circulatory disturbances, in blood clot or around a single
degenerated cell.

 It can also begin in the connective tissue walls of blood vessels

and nerves and follow their course
DIFFUSE CALCIFICATIONS

 Generally observed in root canals

 The deposits become long, thin and fibrillar on fusing
DENTICLES / PULP STONES

 True denticles are composed of dentin and formed by

detached dentinoblasts or fragments of Hertwig’s sheath which
may stimulate undifferentiated cells to assume dentinoblastic
activity.
 False denticles are formed when a degenerating tissue structure
serves as a nidus for deposition of concentric layers of calcified
tissue

Pulp stones are considered harmless, although

referred pain in few patients has been reported.
 DENTICLES

size location
structure

free
true false
Local diffused attached
embedded
 NECROSIS OF PULP

Necrosis or death of the 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.

ETIOLOGY

1) As a Sequelae to inflammation
2) Bacteria, trauma and chemical irritation.: causing an ischaemic
infarction & resulting in dry gangrenous necrotic pulp.
 TWO TYPES

LIQUEFACTION NECROSIS COAGULATION NECROSIS

Tissue converted into softened mass Tissue converted into solid mass
Good blood supply. Less blood supply to the area.
Inflammatory exudate. Cheesy consistency.
SYMPTOMS :

- No painful symptoms.
- Discolouration of tooth is first indication that pulp is dead.
- Dull or opaque appearance of the crown – lack of normal
translucency
- Grayish or brownish discoloration may cause tooth to lack its
usual brilliance and luster

HISTOPATHOLOGY

- Necrotic pulp tissue, cellular debris and microorganisms are

seen
- Periapical tissue may be normal or slight evidence of
inflammation of apical PDL
 POISONOUS INTERMEDIATE & END PRODUCTS
FOUND IN NECROSIS

1. Intermediate proteolytic products that emit foul odour

a. Indole and Skatole
b. Putriscine and Cadaverine
c. Indican

2. End products
Hydrogen sulphide, ammonia, water, carbon dioxide & fatty
acids

3. Exotoxins
4. Endotoxins
5. Foreign bacterial protein
DIAGNOSIS

- Pain is absent with total necrosis

 Swelling - negative
 Mobility - negative
 Tenderness to percusion - negative
 Radiographic findings are normal except if there is apical
periodontitis.
 No response to vitality tests.
 Sometimes positive electric test as result of liquefaction necrosis.
 Discoloration - as result of haemolysis of RBC s or
decomposition of pulp tissue (grey/ brown)

TREATMENT - Root Canal Therapy

 PERIAPICAL LESIONS

 As a consequence of pathologic changes in dental pulp, the root

canal can harbor numerous irritants.

 Egress of these irritants into the periapical tissues can initiate

periradicular lesions.

 Depending on the nature and quality of these irritants as well as

the duration of exposure of the periradicular tissues, a variety of tissue
changes can occur.
INTERRELATIONSHIPS OF PERIAPICAL INFECTION

Pulpitis
Acute chronic

Apical perodontitis
acute chronic

Periapical Abscess Periapical Granuloma

acute chronic
Periodontal cyst

Osteomyelitis
acute chronic

focal diffuse

Periostitis

Cellulitis Abscess
 CLASSIFICATION
According to GROSSMAN

1 ) ACUTE PERIRADICULAR DISEASES

 Acute alveolar abscess
 Acute apical periodontitis
- Vital
- Nonvital

2) CHRONIC PERIRADICULAR DISEASES WITH AREAS OF RAREFACTION

 Chronic alveolar abscess
 Granuloma
 Cyst

3) CONDENSING OSTEITIS

4) EXTERNAL ROOT RESORPTION

5) DISEASES OF PERIRADICULAR TISSUES OF NONENDODONTIC

ORIGIN
INGLE’S CLASSIFICATION

Based on the clinical signs and symptoms, as well as radiographic

findings

-Three main clinical groups

• Symptomatic apical periodontitis

• Asymptomatic apical periodontitis
• Apical abscess
WEINE’S CLASSIFICATION
PULPOPERIAPICAL DISEASE:

1] PAINFUL PULPOPERIAPICAL PATHOSES

a) Incipient acute periapical periodontitis

b) Advanced acute periapical periodontitis

i. Acute periapical abscess
ii. Recrudescent abscess
iii. Subacute periapical abscess

2] NON PAINFUL PULPOPERIAPICAL PATHOSES

a) Pulpoperiapical osteosclerosis

b) Incipient chronic periapical periodontitis

c) Advanced chronic periapical periodontitis

i. Periapical granuloma
ii. Chronic periapical abscess
iii. Periapical cyst
WHO (1995) Classification:

K04.4 -Acute apical periodontitis

K04.5 -Chronic apical periodontitis (Apical granuloma)
K04.6 -Periapical abscess with sinus
K04.60 -Periapical abscess with sinus to maxillary antrum
K04.61 -Periapical abscess with sinus to nasal cavity
K04.62 -Periapical abscess with sinus to oral cavity
K04.63 -Periapical abscess with sinus to skin
K04.7 -Periapical abscess without sinus
K04.8 -Radicular cyst (Apical periodontal cyst, Periapical cyst)
K04.80 -Apical and lateral cyst
K04.81 -Residual cyst
K04.82 -Inflammatory paradental cyst
 ACUTE ALVEOLAR ABSCESS

(Synonyms: Acute periapical abscess, Acute dentoalveolar abscess )

Definition
Localised collection of pus in the alveolar bone at the root apex
of tooth following death of pulp, with extension of infection
through apical foramen into periradicular tissues.

Etiology
Bacterial invasion , trauma, chemical or mechanical irritation.
HISTOPATHOLOGY
PMN’S infiltration
Accumulation of inflammatory exudates
Distention of PDL
Prosses continues, PDL separates
Mobile tooth
Bone resorption at apex
Liquefaction necrosis containing PMN’S ,debris,
cell remnants & purulent exudates
SYMPTOMS

 First symptom - tenderness

 Later - patient has severe throbbing pain with swelling of the

overlying soft tissue

 As the infection progresses, swelling becomes more pronounced and

extends beyond the original site

 Tooth becomes more painful, elongated and mobile

 If untreated - progresses to osteitis, periostitis, cellulitis

or osteomyelitis

 Sinus tract - opens to buccal mucosa

 When Maxillary anterior teeth - swelling of upper lip
and chin (extend both eyelids)
 When Maxillary posterior teeth - the Cheek may
swell.
 Mandibular posterior teeth- swelling extends around
border of jaw into submaxillary region or ear.
Gutta-percha is placed in the sinus tract - points to involved tooth:

SINUS TRACT TRACING

 General Systemic reaction is seen ( Septic products)

 Patient appears - Pale, Irritable & Weakened from pain and
loss of sleep
DIAGNOSIS

 Early stage - difficult to locate tooth.

 Once infection progresses to process of periodontitis & extrusion,

a radiographic evaluation shows thickening of periodontal
ligament space & breakdown of bone

 Electric test & thermal tests: No response

 Tooth is tender on percussion
 Apical mucosa is tender on palpation
 Tooth may be mobile & extruded.

DIFFERENTIAL DIAGNOSIS

Periodontal abscess & Irreversible pulpitis

Treatment:

Establish drainage & control systemic infection.

ON FIRST VISIT : Tooth is left open for drainage.
Thorough instrumentation & irrigation
before medicating and sealing.
Once the swelling and pain subsides
endodontic treatment is done.

If diffuse swelling : Antibiotic coverage is

prescribed along with hot mouth rinse, Once area
is localised, incision and drainage is instituted
 ACUTE APICAL PERIODONTITIS

A painful inflammation of periodontium as a result of trauma, irritation

or infection through root canal regardless of pulp is vital or non-vital.

HISTOPATHOLOGIC CLASSIFICATION: (P.N.R Nair)

1) Acute apical periodontitis ( PMN’s) : Primary & secondary
2) Chronic apical periodontitis ( Lymphocytes, macrophages, plasma cells)
3) Cystic apical periodontitis - True cyst, Pocket cyst (bay cyst)
APICAL PERIODONTITIS:
ETIOLOGY

 Occlusal trauma
 Wedging of foreign object between teeth
 Non-vital tooth as a sequelae to pulpal dieseases.
 Iatrogenic: during over instrumentation & extrusion of
irritating medicaments
 Perforation of root

SYMPTOMS

- Pain and tenderness

- Tooth may be slightly sore, when percussed.

HISTOPATHOLOGY

 Inflammatory reaction in apical periodontal ligament

 Blood vessels are dilated, PMNL’s are present
 Cholestrol clefts are the commom finding.
 Accumulation of serous exudate distends the periodontal ligament
 Osteoclasts are seen.
DIAGNOSIS

 Tooth is tender to percussion

 Symptoms are due to Overinstrumentation, Irritating medicament
or Overfilling
 Radiographically: thickened periodontal ligament or small area of
rarefaction

TREATMENT

 Endodontic therapy
 Postoperative pain is controlled analgesics & antibiotics
 Hyper-occlusion relieve the occlusion.
 ACUTE EXACERBATION OF A CHRONIC LESION
(PHOENIX ABSCESS)

An acute inflammatory reaction superimposed on an existing chronic

lesion, such as a cyst or granuloma

ETIOLOGY

1. Noxious stimuli from a diseased pulp with chronic periradicular

disease.
2. Because of influx of necrotic products or bacteria and their toxins, the
dormant lesions may become reactive & cause an acute inflammatory
response.
3. Lowering of the body's defenses in the presence of bacteria - may also
trigger an acute inflammatory response.
4. Mechanical irritation during root canal instrumentation

SYMPTOMS

 Tooth - tender to touch & elevated in its socket

 Mucosa - sensitive to palpation & appears red & swollen
HISTOPATHOLOGY :

Liquefaction necrosis with disintegrating PMNL & cellular debris

(pus), surrounded by infiltration of macrophages, lymphocytes &

plasma cells

DIAGNOSIS

History of patient
vitality tests Lack of response

RADIOGRAPHICALLY :- Large area of radiolucency at the apex.

DIFFERENTIAL DIAGNOSIS :

Acute alveolar abscess, Acute irreversible pulpitis

TREATMENT
 Establishment of drainage
 Once symptoms subside - RCT
 CHRONIC ALVEOLAR ABSCESS
(Chronic Suppurative Apical Periodontitis)

DEFINITION
A chronic alveolar abscess is a long-standing, low-grade
infection of the periradicular alveolar bone.

ETIOLOGY
1. Death of the pulp with extension of the infective process
periapically
2. A pre-existing acute abscess
SIGNS & SYMPTOMS

- Asymptomatic

- Detected either by the presence

of sinus tract or on routine
radiograph.

- If the sinus tract drainage becomes blocked – pain & swelling

- Range of sensitivity to percussion & palpation – depends on

the sinus tract is open, draining or closed .

A radiograph with a gutta-percha cone into the sinus tract

often shows involved tooth by tracing the sinus tract to its
origin.
DIAGNOSIS

 Chronic abscess may be painless or mildly painful.

 First sign - osseous breakdown (radiographically) seen
during routine examination.
 Patient may give the history of sudden sharp pain which
subsided & has not reoccurred.
 Clinically -A large carious exposure, composite, acrylic or
metallic restoration or discolouration of crown of tooth.

RADIOGRAPHICALLY
 A diffuse area of bone rarefaction
 Periodontal ligament is thickened.
 Vitality tests – Negative
HISTOPATHOLOGY

 Periodontal fibers at root apex are detached / lost.

 Apical cementum may be affected.
 Lymphocytes , plasma cells at the periphery & PMNL’s at the center
 Fibroblasts - form a capsule at periphery.

TREATMENT

 Endodontic thearpy.
 The sinus tract ultimately heals by granulation
 When sinus tract does not heal while the tooth is under endodontic
treatment, it is curetted with a small spoon excavator.
 PERIAPICAL GRANULOMA

A growth of granulomatous tissue continuous with the periodontal

ligament resulting from death of pulp & diffusion of bacteria and
bacterial toxins from root canal into the surrounding periradicular
tissues through apical and lateral foramina.

ETIOLOGY
 Sequelae of pulpitis
CLINICAL FEATURES

 Mild pain / Sensitive to percussion

 Tooth slightly elongated
 Sinus tract – may or may not present
 Vitality test –negative
 History of subsided pulpalgia
 Mucosa- May or may not be tender to
palpation
 No mobility

DIAGNOSIS

RADIOGRAPHICALLY:

Well defined radiolucency, with lack of continuity of the lamina dura.

Diameter – Varies from a fraction of a millimeter to a centimeter or
even larger.
ZONES OF A WELL-ESTABLISHED GRANULOMA
(FISH’S ZONES)
 KRONFELD’S MOUNTAIN PASS CONCEPT

Kronfeld :
Granuloma is not an environment in which bacteria live but one
in which they are destroyed.

Bacteria (zone I) –
compares bacteria in the root canals with an army entrenched
behind high and inaccessible mountains

Foramina : Mountain passes.

Granulomatous (proliferative) tissue :

mobilized army defending plains (periapex) from invaders.

Major battle (b/w invaders + WBC’s) - acute inflammation (zone II)

Local destruction created by battle is repaired (granulation tissue

- zone III) and the environment returns to the normal pattern.
HISTOPATHOLOGY

 Granulomatous tissue replaces alveolar bone & periodontal ligament.

 Consists of - rich vascular network, fibroblasts, lymphocytes , plasma
cells,PMN’S & fibrous capsule.
 Macrophages & giant cells.
 Macrophages containing lipid material & cholesterol
 Alveolar bone shows resorption (osteoclasts).
 Epithelium derived from cell rests of Malassez .

TREATMENT
Root canal treatment / surgery
RADICULAR CYST

Is a slowly growing epithelial sac at the apex of a tooth that

lines a pathologic cavity in the alveolar bone. The lumen contains a
low-concentration of proteinaceous fluid.

ETIOLOGY
Physical, chemical or bacterial injury (death of pulp), followed by
stimulation of epithelial cell rests of Malassez.

SYMPTOMS:
 No symptoms, except those seen in necrosis of pulp.
 A cyst may become large enough, to be obvious as a swelling.
 Teeth are mobile.
 Left untreated - continues to grow at expense of
maxilla or mandible.
FORMATION OF RADICULAR CYST
Caries / trauma

Death of dental pulp

Inflammation in apical area of bone

Periapical granuloma formation

Stimulation of epithelial rests of malassez

Proliferation of epithelium

Periapical cyst formation

DIAGNOSIS

 Location : Common in maxillary / males/ 3rd decade

 Electrical or Thermal tests – no response

 Radiographically - Loss of continuity of lamina dura

with an area of rarefaction .
Radiolucent area - round in outline except where it
approximates adjacent teeth it may be flattened &
oval shaped.

 Larger than granuloma & may include more than one

tooth

 Electrophoretic analysis( polyacrylamide gel) :

Intense albumin pattern in cysts
HISTOPATHOLOGY:

 Cavity lined by stratified squamous epithelium.

 Connective tissue is infiltrated by lymphocytes,
plasma cells, PMNL,cholesterol clefts, macrophages, & giant cells.
 Cystic cavity contains cellular debris and pale eosinophilic fluid.

According to PNR Nair, two types of radicular cysts:

(1) Those containing cavities completely enclosed in epithelial lining-
true cyst &
(2) Those containing epithelium-lined cavities that are open to the root
canals - periapical pocket cysts (bay cyst)

DIFFERENTIAL DIAGNOSIS

Periapical granuloma , Globulomaxillary cyst.

TRUE CYST POCKET CYST
TREATMENT

True cyst : Root canal treatment of the affected tooth, together

with surgical enucleation may be attempted.

Pocket cyst : Conventional RCT, followed by periodic observation.

 CHRONIC PERIRADICULAR DISEASE WITH AREA OF
CONDENSATION

CONDENSING OSTEITIS

Condensing osteitis is the response to a low-grade, chronic

inflammation of periradicular area as a result of a mild irritation
through the root canal.
Characterized as a localized overproduction of apical bone.

ETIOLOGY

Mild irritation from pulpal disease - stimulates osteoblastic

activity

SYMPTOMS

Usually asymptomatic , discovered during routine radiographic

examination.
DIAGNOSIS

 Radiographically: a well-circumscribed radioopaque area

surrounding the affected teeth.
 Mandibular posterior teeth - frequently affected.
 Tooth may or may not respond to electrical and thermal stimuli

HISTOPATHOLOGY

An area of dense bone with trabecular borders

lined with osteoblasts

Chronic inflammatory cells, plasma cells

and lymphocytes are also seen in the scant bone marrow.

TREATMENT

Endodontic treatment.
 EXTERNAL RESORPTION
CLASSIFICATION (BY JAMES L. GUTMANN ET AL IN 1999)

1. External surface resorption

2. External inflammatory root resorption
3. Dentoalveolar ankylosis
4. Replacement resorption

1) EXTERNAL SURFACE RESORPTION

 Spontaneous destruction & repair of root surface

 It is a normal physiologic response to minor injuries
 Mechanical damage to the cementum –Localized area of
resorption - Repair
 Complete periodontal healing & root surface healing in 14 days
 Symptomless, cannot be detected in routine radiographs
 Does not require any treatment.
QI vol 30: (1), 1999.
2) EXTERNAL INFLAMMATORY ROOT RESORPTION

Injury or irritation to periodontal tissues where inflammation is beyond

repair.

ETIOLOGY

 Trauma
 Orthodontic tooth movement - excessive forces.
 Trauma from occlusion
 Periodontal pathology
 Avulsion & Luxation injuries

CLINICAL FEATURES

 H/o trauma
 Necrotic pulp / irreversible pulpitis
 Tooth mobility
 Percussion sensitivity
 If resorption communicates with gingival sulcus- leads to pocket
formation
RADIOGRAPHIC FEATURES

Bowl like radiolucency with ragged irregular area on the

root surface and loss of tooth structure and alveolar
bone.

TREATMENT

Endodontic treatment with calcium hydroxide intracanal

medication.
3) DENTOALVEOLAR ANKYLOSIS

Union of tooth & bone with no intervening periodontal ligament &

connective tissue

ETIOLOGY

Trauma, Intrusive luxation, Reimplantation of avulsed tooth (damage to

PL cells & cementum)

CLINICAL FEATURES

 Lack of mobility , Lack of mesial drift

 Dull metallic sound on percussion
 Infraocclusion
RADIOGRAPHIC FEATURES

Moth eaten appearance with irregular border

Absence of periodontal ligament & lamina dura

TREATMENT OF ANKYLOSIS
No treatment
Gradual loss of tooth – finally gets mobile & exfoliates

4) REPLACEMENT RESORPTION
Similar to ankylosis, but there is the presence of an intervening
inflamed connective tissue.
NONENDODONTIC PERIRADICULAR LESIONS

ODONTOGENIC CYSTS
Dentigerous cyst
Lateral periodontal cyst
Odontogenic keratocyst
Residual apical cyst

NON- ODONTOGENIC LESIONS

Central giant cell granuloma
Nasopalatine duct cyst
Simple bone cyst
Globulomaxillary cyst
Enostosis
BONY PATHOLOGY
 Fibro-osseous lesions
 Osteoblastoma & cementoma
 Cementifying & ossifying fibroma

ODONTOGENIC TUMOURS
 Ameloblastoma

MALIGNANCIES
• Sarcoma
• Carcinoma
Conclusion:

Periapical shadows are the daily bread of the

general dentist.

The clinician should possess a thorough working

knowledge and skill necessary to establish a
suitable working diagnosis in each case.

It requires practice to gain skill and so the

clinician must approach each periapical shadow in
a logical fashion and follow it through, step by
step, until the end point is reached.
References:

1.Endodontics (4th & 5th edition) – John I. Ingle

2.Pathways of pulp (9th edition)- S Cohen and Burns

3.Shafers - A text book of oral pathology (4th edition)

4.Endodontic Practice (11th Edition) – Louis I. Grossman

5.Endodontic Therapy (4th & 5th edition) – Franklin S. Weine

6.Endodontics in clinical practice (4rd edition) – F.J. Harty

7.Endodontics (3rd edition) – K Gulabivala

8. Colour atlas & Text of Endodontics (2nd edition) –
Christopher J K Stock
9. Problem solving in Endodontics – James L Gutman

10. The Dental pulp (3rd edition) – Seltzer

11. Oral & Maxillofacial Pathology- Brad W Neville

HANK YOU