Periapical pathology

PRESENTED BY Dr EKTA GARG
MDS 1st YEAR
DEPARTMENT OF CONSERVATIVE DENTISTRY &
ENDODONTICS

Consists of cementum, pdl and
alveolar process.
CEMENTUM
 Mineralized, avascular connective
tissue covering the roots of the
teeth.
 Consists of 3 different types-
• Acellular afibrillar cementum
• Acellular extrinsic fiber
cementum
• Cellular intrinsic fiber
cementum

 Cemental matrix consists of growth factors such as IGF-1, FGFs, EGF,
BMPs, TGF-β and PDGF.
 These factors r shown 2 b associated with cementoblast proliferation,
migration, and differentiation during cementum wound healing.
PERIODONTAL LIGAMENT
 Soft, specialized connective tissue that connects the cementum to the
alveolar bone.
 Contains heterogenous cell populations and extracellular matrix(ECM)
 Cells include- osteoblasts, osteoclasts, fibroblasts, epithelial cell rests
of malassez, macrophages, cementoblasts, & undifferentiated
mesenchymal cells (stem cells)

 ECM consists of collagen fibers, fibronectin, elastin, other non-
collagenous proteins, & proteoglycans.
ALVEOLAR PROCESS
 Forms the bony troughs containing the roots of the teeth.
 Divided into-
• Alveolar bone proper : lines the alveolus or the bony sockets
that house the roots of the teeth.
• Supporting Alveolar bone : Cancellous(spongy) bone adjacent to
the alveolar bone proper covered by 2 outer tables of compact
bone.

 As a consequence of pathologic changes in the dental pulp, the root
canal system can harbor numerous irritants. Egress of these irritants
from infected root canals into the periradicular tissues can initiate
formation and perpetuation of PERIRADICULAR LESIONS.
 Depending on the nature and quantity of these irritants, as well as the
duration of exposure of the periradicular tissues, a variety of tissue
changes can occur.
 When the irritants are transient in nature, the inflammatory process is
short-lived and self-limiting.
 However, with an excessive amount of irritants or persistent exposure,
the nonspecific and specific immunologic reactions can cause
destruction of periradicular tissues.

 Radiographically, these lesions appear as radiolucent areas around
the portal(s) of exit of the main canal or lateral and/or accessory
canals.

 Histologically, depending on their stage of development, the lesions
contain numerous inflammatory cells such as polymorphonuclear
neutrophil leukocytes (PMNs), macrophages, lymphocytes, plasma
cells, mast cells, basophils, and eosinophils.

The interaction between the irritants
and the host defensive mechanisms
results in release of numerous
mediators that curtail progression of
infection and development of severe
local infection (osteomyelitis) and
systemic complication such as
septicemia.

IRRITANTS
 Can b divided into-
• The LIVING irritants which include microorganisms and viruses.
• The NON-LIVING irritants which include mechanical, thermal &
chemical irritants.
 Mild to moderate injuries of short duration cause REVERSIBLE tissue
damage and recovery of these tissues.
 Persistent and/or severe injuries usually cause IRREVERSIBLE
changes in the pulp and development of periradicular lesions.

Microbial Irritants
 Includes-
bacteria, bacterial toxins, bacterial fragments, and viruses
 These irritants egress apically from the root canal system into the
periradicular tissues and initiate inflammation and tissue alterations.
 A number of studies have shown that pulpal and/or periradicular
pathosis do not develop without the presence of bacterial
contamination.

 In addition to bacterial irritation, the periradicular tissues can be
mechanically irritated and inflamed.
 Physical irritation of periradicular tissues can also occur during root
canal therapy if the canals are instrumented or filled beyond their
anatomic boundaries.
 Periradicular tissues can be irritated by impact trauma,
hyperocclusion, endodontic procedures and accidents, pulp
extirpation, overinstrumentation, root perforation, and
overextension of filling materials.

 The reaction of the periradicular tissues to noxious products of
tissue necrosis, bacterial products, and antigenic agents from the
root canal has been described by FISH.
 Four well-defined zones of reaction found were-
• Zone of infection
• Zone of contamination
• Zone of irritation
• Zone of stimulation

CHIEF COMPLAINT: Pain on biting, pain wid swelling, pus discharge etc.
DENTAL HISTORY : Recurring episodes of pain, swelling wid discharge,
swelling which reduces on its own.
OBJECTIVE EXAMINATION
• Xtraoral xamination- general appearance, skin tone, facial asymmetry,
swelling, extraoral sinus, sinus tract, tender or enlarged cervical lymph
nodes.
• Intraoral xamination- examination of soft tissues nd teeth to look 4
discolouration, abrasion, caries, restoration etc.

CLINICAL PERIAPICAL TESTS
1. PERCUSSION- indicates inflammation of the peridontium.
2. PALPATION- determines how far the inflammatory process has
extended periapically.

3. PULP VITALITY-
• Thermal tests- includes heat and cold testing
• Anesthetic testing
• Test Cavity
• Electrical pulp testing
4. PERIODONTAL XAMINATION-
• Probing- determines the level of connective tissue attachment.
• Mobility- determines the status of pdl.

5. RADIOGRAPHIC XAMINATION-
• Loss of lamina dura apically
• Radiolucency at apex regardless of cone angle nd usually resembles
a hanging drop.
• Cause of pulp necrosis is usually evident.

WHO classification of periradicular tissues
CODE NUMBER CATEGORY
K04.4 Acute apical periodontitis
K04.5 Chronic apical periodontitis
(apical granuloma)
K04.6 Periapical abscess with sinus
(dentoalveolar abscess with
sinus, periodontal abscess
of pulpal origin)
to maxillary antrum
to nasal cavity

CODE NUMBER CATEGORY
K04.62 Periapical abscess with sinus to
oral cavity
Ko4.63 Periapical abscess with sinus
to skin
Ko4.7 Periapical abscess with out
sinus
Ko4.8 Radicular cyst(apical periodontal
cyst, periapical cyst)
Ko4.80 Apical & Lateral cyst
Ko4.81 Residual cyst
Ko4.82 Inflammatory Paradental cyst

GROSSMAN’S CLASSIFICATION
 Acute Periradicular disease
(a) Acute alveolar abscess
(b) Acute apical periodontitis(symptomatic periodontitis)
- Vital
- Non Vital
(c) Acute exacerbation of chronic apical periodontitis(phoenix
abscess)
 Chronic periradicular diseases
(a) Chronic apical periodontitis
- chronic alveolar abscess
- cystic apical periodontitis
(b) Persistent apical periodontitis
 Condensing osteitis
 External root resorption
 Diseases of the periradicular tissues of non-endodontic origin

WEINE’S CLASSIFICATION
 Painful pulpoperiapical pathosis
(a) Incipient acute apical periodontitis
(b) Advanced acute apical periodontitis
- Acute Periapical abscess
- Phoenix abscess
- Subacute Periapical abscess
 Non painful Periapical pathosis
(a) Condensing ostestis
(b) Incipient chronic apical periodontitis
(c) Advanced chronic apical periodontitis
- Periapical granuloma
- Chronic Periapical abscess
- Periapical cyst

INGLE’S CLASSIFICATION
 Painful pulpoperiapical pathosis
(a) Acute apical periodontitis
(b) Advanced acute apical periodontitis
- Acute apical abscess
- Phoenix abscess
- Suppurative apical periodontitis
 Non painful pulpoperiapical pathosis
(a) Condensing ostetis
(b) Chronic apical periodontitis
- Incipient
- Advanced
(c) Chronic apical periodontitis
- Periapical granuloma
- Apical cyst
- Suppurative apical periodontitis

 Painful inflammation of the peridontium
as a result of trauma, irritation, or
infection through the root canal,
regardless of whether the pulp is vital
or nonvital.
 Also referred to as symptomatic apical
periodontitis.
 Tooth is tender on percussion & pain can
be severe making closure of the teeth
difficult.

Etiology
IN VITAL TEETH-
 Abnormal occlusal contacts
 Recently inserted restoration extending beyond the occlusal plane
 Wedging of a foreign object between the teeth such as a toothpick
or food
 Traumatic blow to the teeth

IN NONVITAL TEETH-
a) Sequelae of pulpal diseases, i.e., the diffusion of bacteria & noxious
products from an inflamed or necrotic pulp.
b) Iatrogenic
• Root canal instrumentation forcing bacteria or debris
inadvertently through the apical foramen
• Forcing of irrigating irrigants or medicaments through the
apical foramen
• Extension of obturating material through the apical foramen
to impinge on periapical tissue
• Perforation of the root
• Overinstrumentation during cleaning & shaping of root canals.

Signs & Symptoms
 Tooth is tender on percussion & may b slightly sore
 Dull, throbbing & constant pain
 Tooth may feel extruded & patient would have pain on closure &
mastication.
 Negative or delayed vitality test
 Radiographically, widening of the pdl space or a small area of
rarefaction if a pulpless tooth is involved & may show normal
periradicular structures if a vital pulp is present in the tooth.

HISTOPATHOLOGY
Inflammatory rxn in pdl
Dilation of blood vessels
Initiation of inflammatory response due to presence of
polymorphonuclear leukocytes & round cells
Accumulation of serous exudate
Distension of Pdl & extrusion of tooth, slight tenderness
If continuous irritation occurs, loss of alveolar bone

Periodontitis caused
due to trauma.
Widening of pdl space caused
due to abnormal occlusal contacts
Widening caused due to
orthodontic treatment

Periodontitis caused due
to carious xposure

TREATMENT
 Determining the cause & relieving the symptoms.
 Adjustment of high points (in hyperocclusion cases).
 Removal of irritatants (in case of nonvital infected pulp)
 When the acute phase has subsided, the tooth is treated by
conservative means.

OUTCOME OF SYMPTOMATIC APICAL PERIODONTITIS
 Spontaneous healing
 Acute alveolar abscess
 “Point” and open to the exterior (fistulation and sinus tract formation)
 Lesion becomes asymptomatic and enters chronic phase.

 An acute alveolar abscess is a
localized collection of pus in the
alveolar bone at the root apex of a
tooth following death of pulp with
extension of infection through apical
foramen into periradicular tissue.
ETIOLOGY
• Trauma
• Chemical & mechanical irritation
• Bacterial invasion of dead pulp tissue.

CLINICAL FEATURES
 Tenderness of the tooth relieved by continued slight pressure on
the extruded tooth.
 Severe, throbbing pain, with swelling of the overlying soft tissue.
 No reaction to cold, heat or EPT.
 As infection progresses, swelling becomes more pronounced &
extends beyond the original site & tooth becomes more painful,
elongated & mobile.
 In case of max ant, swelling may extend to 1 or both the eyelids & in
case of mand ant, swelling may involove the lower lip & chin.

 In case of max post, cheek may swell 2 an immense size, distorting
the facial structures & in case of mand post, swelling may xtend 2 ear
or round the border of the jaw into the submaxillary region.
 SYSTEMIC REACTIONS include-
• Pt may appear pale, irritable & weakened due to pain & loss of
sleep.
• Mild cases- slight rise in temp (99-100˚C)
• Severe cases- temp above normal (102-103˚C)
• Fever often preceded or accompanies by chills.
• Intestinal stasis, manifesting orally by a coated tongue & foul
breath.
• Headache & malaise

TREATMENT
 Immediate treatment includes establishing drainage & controlling
the systemic reaction.

 LA is ineffective when injected into acutely inflamed tissue.
 Conduction anesthesia may b administered to reduce the pain.
 Hot saline rinses should b prescribed to assist drainage.
 If the swelling is extensive, soft nd fluctuant, an incision through the
soft tissue to the bone may b necessary.
 If it is hard, can b converted to soft, fluctuant state by rinsing with
hot saline solution 3-5 min at a time repeated every hr.
 Antibiotics & analgesics can b prescribed as needed.
 Finally, tooth shud b disoccluded slightly if extruded 4m its socket.

 An acute inflammatory reaction superimposed on an existing chronic
lesion, such as cyst or granuloma.
 Acute exacerbation of a chronic lesion.
ETIOLOGY
1.When state of equillibrium in granuloma /cyst is upset by:
• Influx of bacteria/necrotic products of high virulence and
antigenicity
• Lowering of host defenses
2. Mechanical irritation during RCT.

CLINICAL FEATURES
 Clinically often indistinguishable from periapical abscess.
 Initially, tooth may b tender on palpation.
 As inflammation progresses, tooth gets elevated from the socket &
becomes sensitive.
 Mucosa over the radicular area may appear red & swollen & sensitive
to palpation.
 Most commonly associated with initiation of root canal therapy.
 Do not respond to vitality testing.

 Radiographically, well defined periradicular lesion may b present.
 Histopathologically, shows areas of liquefaction necrosis with
disintegrated polymorphonuclear leukocytes & cellular debris
surrounded by macrophages, lymphocytes, plasma cells in periradicular
tissues.
 Shud b differentiated from acute alveolar abscess through pt’s
history, symptoms & clinical tests results.
TREATMENT
 Establishment of drainage
 Once symptoms subside, complete root canal treatment.

 Symptomless sequelae of acute apical
periodontitis.
 May develop and enlarge insidiously
without any subjective signs or
symptoms.
 Necrotic pulp gradually releases
noxious agents with low grade
pathogenecity or in low concentration.
 Develops after inadequate root canal
treatment.
 Synonyms- asymptomatic apical
periodontitis, periapical granuloma.

ETIOLOGY
• Death of the pulp followed by mild irritation of periapical tissue that
stimulates a productive cellular reaction.
• Some cases preceded by chronic alveolar abscess.
CLINICAL FEATURES
 Asymptomatic, discovered on routine radiographic xamination.
 No pain on percussion
 Associated tooth has a necrotic pulp therefore shud not respond to
the electrical or thermal stimuli.

HISTOLOGICAL CHARACTERIZATION
• Periradicular granuloma or cyst.
The only accurate way to distinguish these two entities is by histologic
examination.

 A growth of
granulomatous tissue
continuous with the
periodontal ligament
resulting from death of
the pulp and the
diffusion of bacteria and
bacterial toxins from
the root canal into the
surrounding periradicular
tissues through the
apical and lateral
foramina.

 Histologically, the periradicular granuloma consists predominantly of
granulation inflammatory tissue with many small capillaries,
fibroblasts, numerous connective tissue fibers, inflammatory
infiltrate, and usually a connective tissue capsule

 Occasionally, needle-like spaces (the remnants of cholesterol
crystals), foam cells, and multinucleated foreign body giant cells are
seen in these lesions.

ZONES OF WELL ESTABLISHED GRANULOMA

TREATMENT
 Root canal treatment is recommended.
 Removal of cause of inflammation is usually followed by
resorption of Granulomatous tissue & repair with
trabeculated bone.

 Pathological cavity containing fluid, semi fluid or gaseous material
not created by accumulation of pus, frequently but not always lined
by epithelium(Kramer 1974).
 Radicular cyst are generally considered to be a direct sequelae of
chronic apical periodontitis.
 Not every lesion develops into cyst.
 According to the studies 6-55% lesions are cyst.
 There are two distinct categories of radicular cyst:-
• Periapical true cyst
• Periapical pocket cyst

ETIOLOGY
 Acc to NAIR, cyst develops from dormant epithelial cell rests that
proliferate probably under the influence of inflammatory cytokines
& growth factors released by various cells residing in the lesion.
 When proliferation occurs within the body of the granuloma, it plugs
the body of the apical foramen which limits the egress of the
bacteria.
 Sometimes, epithelial plugs protrude out of the apical foramen
resulting in a pouch connected to the root & continuous with the
root canal.

Hypothesis related wid this growth-
a. Nutritional Deficient Theory-
• Periradicular inflammatory changes cause the epithelium 2
proliferate.
• As the epithelium grows into a mass of cells, the center loses
the source of nutrition from the peripheral tissues.
• This leads to necrosis in the center & a cavity is formed which
is lined by stratified squamous epithelium.
b. Abscess Theory-
• An abscess cavity is formed within the connective tissue & is
then surrounded with proliferating epithelial tissue, thereby
producing a cyst.

PRIAPICAL POCKET CYST
 Originally designated as bay cyst.
 Cyst contains an epithelial lined cavity that is
open towards the root canal of the affected
tooth.
 initiated by the accumulation of neutrophils
around the apical foramen in response to the
bacterial presence in the apical root canal.
 This forms a microabscess, that gets
enclosed by the proliferating epithelium,
forming a collar with epithelial attchment on
contacting the root tip.

PERIAPICAL TRUE CYST
 Characterized by cavities
that are completely
enclosed in epithelial lining
and are totally
independent of the root
canal of the affected
tooth.

Clinical features
• No symptoms associated with
development of a cyst except
incidental to necrosis of the pulp.
• May become large enough, however,
to become obvious as a swelling.
• Pressure of the cyst may b sufficient
to cause movement of the teeth,
owing to accumulation of cystic fluid.
• If left untreated, may continue to
grow at the expense of the max or
mand.

HISTOPATHOLOGY
• Cavity is lined by stratified
squamous epithelium.
• Surrounded by connective
tissue that is infiltrated by
lymphocytes, plasma cells, and
polymorphonuclear neutrophils.
• Contains debris and
eosinophilic material.
• Cholestrol clefts,
macrophages, & giant cells also
present in CT.

RADIOLOGICAL FEATURES:
 Classically presents as round
/ ovoid radiolucency with
sclerotic borders and
associated with pulpally
affected tooth / teeth.
 If infection supervenes, the
margins become indistinct,
making it impossible to
distinguish it from a
periapical granuloma.

TREATMENT
• The treatment of choice is root canal therapy, followed by periodic
observation.
• Surgery required when lesion fails to resolve or symptoms develop.
• Extraction in case of severe bone loss.

Periapical cyst
Radiographically, shows a
well-circumscribed radiolucent
periapical lesion with a partial
sclerotic border, measuring
more than 1 cm in diameter.
Histologically, shows the
presence of an epithelial lining
with underlying dense
fibrocellular connective tissue
stroma
Granuloma
Radiographically, shows a well-
circumscribed radiolucent periapical
lesion without a sclerotic border,
measuring less than 1 cm in size.
Histologically, shows fibrocellular
connective tissue stroma consisting of
chronic inflammatory cell infiltrate
(mainly lymphocytes and plasma cells)
and endothelium-lined blood capillaries
with red blood cells, fibroblasts, and
collagen fibers.

 Long standing, low grade
infection of the periradicular
alveolar bone.
 Characterized by presence of
an abscess draining through a
sinus tract.
 Synonyms- chronic suppurative
apical periodontitis,
asyptomatic apical abscess.

ETIOLOGY
• Source of infection is in
the root canal.
• It is a natural sequelae of
death of the pulp with
extension of the infective
process periapically, or
may result from a pre-
existing acute abscess.

CLINICAL FEATURES
• Tooth is asymptomatic or mildly
painful.
• Detected only during radiographic
examination or because of the
presence of a fistulous tract, which
can b either intraoral or extraoral.
• Exudate can also drain through
the gingival sulcus of the involved
tooth mimicking a periodontal
lesion with a pocket.
• Vitality test is negative.

RADIOGRAPHICAL EXAMINATION
 A radiograph is taken after the insertion of GP cone into the sinus
tract which often shows the involved tooth by tracing the sinus tract
to its origin.
 At times, the sinus tract is several teeth away from the cause.
 Radiograph shows diffuse area of rarefaction which fade indistinctly
into normal bone.
 The pdl is thickened.

HISTOPATHOLOGY
 Some of the periodontal fibers at the root apex are detached
or lost followed by destruction of apical periodontal ligament.
 lymphocytes & plasma cells are generally found toward the
periphery of abscessed area, with variable numbers of
polymorphonuclear leukocytes at the center.
 Fibroblast may start to form a capsule at the periphery.

TREATMENT
 Elimination of infection in root canal.
 Once this is accomplished & root canal is filled, repair
of the periradicular tissues generally take place.
 In case of smaller area of rarefaction, treatment is
similar to that of a tooth with a necrotic pulp.

 It is a rapidly spreading inflammation of the soft tissues
characterized by diffuse pus formation.
 This happens if an abscess is not able to establish drainage
through the skin surface or into oral cavity.
 Cellulitis arising from dental infection and spreading through soft
tissues of head and neck can take various forms.
 Mostly, infection spreads through tissue spaces like canine space,
infratemporal space, pharyngeal space, buccal space, submental and
submandibular space etc.
 Two dangerous forms of cellulitis are –
- Ludwig’s angina
- Cavernous sinus thrombosis

TREATMENT
• Removal of the necrotic pulp.
• Extraction of the infected tooth.
• Incision & drainage of the swelling.
• In severe cases hospitalization required.
• Antibiotics & analgesics

 Post treatment apical
periodontitis in an
endodontically treated
tooth.
ETIOLOGY
• Anatomical complexity
• Apical biofilms
• Cholestrol clefts
• Foreign body reaction to
gp
• Cellulose granuloma
• Periapical scar tissue

BACTERIOLOGY
 E. Faecalis is the most consistently reported organism that can
survive prolonged starvation & can grow as a monoinfection in
endodontically treated teeth.
 Studies have shown presence of yeast & candida albicans.
 Gram+ cocci, rods & filaments, & Propioniobacterium have also
been implicated.

Apical scar is an area at the apex of a
tooth that fails to fill in with osseous
tissue after endodontic treatment.

CHARACTERISTIC FEATURES
 Bone structures are recognized within the rarefaction.
 The periphery of the rarefaction may be irregular and
may be demarcated by a compact bone border.
 The rarefaction is often located asymmetrically around
the apex.
 The connection of the rarefaction with the periodontal
space may be angular.

 A surgical defect is that portion of bone that fails to form osseous
tissue.
 It is frequently seen periapically after root resection in which the
site is filled with dense fibrous (collagen) tissue instead of bone.
 It is an asymptomatic persistent radiolucency.
 An extraction site can also form a surgical defect.
 Approximately 75% of all surgically treated periapical
radiolucencies require 1 to 10 years or longer for complete
resolution. In the remaining 25%, complete healing does not occur.

 Condensing osteitis is a reaction of bone induced by inflammation.
 It occurs mainly at the apex of a tooth from an infected pulp.
 The infection from tooth caries reaches the pulp and progresses
to the apical tissues to produce a small periapical radiolucency
called RAREFYING OSTEITIS.
 The small rarefying osteitis may be either a periapical granuloma, a
radicular cyst or an abscess.
 The bone surrounding this rarefying osteitis becomes dense in
order to prevent further spread of the lesion. This dense
radiopacity surrounding the rarefying osteitis is called
CONDENSING OSTEITIS.

CLINICAL FEATURES
 Usually Asymptomatic
 Discovered during routine radiographic
examination.
 Pulp of the involved tooth is nonvital.

RADIOGRAPHIC EXAMINATION
• The tooth involved may exhibit a
large carious lesion or a large
restoration close to the dental
pulp.
• The lesion shows a diffuse
radiopacity surrounding a
small central radiolucency at the
apex (or apices) of a tooth.
• It is the area of dense bone with
reduced trabecular pattern.

HISTOPATHOLOGY
 Appears as an area of dense bone with reduced trabecular pattern
lined with osteoblasts.
 Chronic inflammatory cells, plasma cells, & lymphocytes are seen in the
scant bone marrow.
TREATMENT
Treatment consists of removing the infection either through tooth
extraction or root canal therapy.

CLASSIFICATION
 Types of tooth resorption includes-
• External
a. External surface resorption
b. External inflammatory root resorption
c. External replacement resorption or ankylosis
• Internal

ETIOLOGY
• Trauma
• Excessive forces
• Granuloma
• Cyst
• Central jaw tumors
• Impaction of teeth
• Bleaching
• Systemic diseases
• If no cause is evident, the disorder is called as idiopathic
resorption.

CLINICAL FEATURES
 Asymptomatic
 On complete resorption, tooth may become mobile.
 If extends into the crown, gives appearance of “pink tooth” as seen
in internal resorption.
 In case of replacement resorption or ankylosis, root is gradually
replaced by bone, renders the tooth immobile, in infraocclusion, &
with a high mettalic percussion sound.

RADIOGRAPHICAL EXAMINATION
• Concave or ragged areas on the
root surface or blunting of the
apex.
• Inflammatory root resorption
caused by the pressure of a
growing granuloma, cyst or tumor
adjacent 2 the area of
radiolucency.
• Areas of ankylosis hav a resorbed
root with no pdl space & with bone
replacing the defects.

TREATMENT
• Varies with etiology
• If extended by pulpal
disease, root canal therapy.
• If due to excessive
orthodontic forces,
treatment of choice would b
reducing those forces.
• In case of cervical root
resorption, surgical xposure
of the defect & restoration
with a suitable rest material.

 Odontogenic or
 Nonodontogenic

• Dentigerous cyst
• Lateral periodontal cyst
• Odontogenic keratocyst
• Residual cyst

Bone Pathologies: fibro-osseous lesions
 Periradicular cemental dysplasia
 Osteoblastoma
 Cementoblastoma
 Cementifying & ossifying fibroma
 Odontogenic tumours- ameloblastoma

• Central giant cell granuloma
• Nasopalatine duct cyst
• Globulomaxillary cyst
• Simple bone cyst
• Enostosis

 Establishment of proper diagnosis is of utmost importance
to carry out the effective clinical procedure for the
benefit of patient .
 Review after the treatment is also to be given importance .
 Researches done and ongoing research has thrown light on
various aspects untangling the puzzle which persisted for
long.
 So this knowledge can be used in the practice to make
endodontic treatment a success when the controversy is
going on about to pull out or salvage the tooth with implant
coming strongly on the field of dentistry.

Periapical pathology

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