DISEASES OF

PERIRADICULAR TISSUES

Presented by :sucheta kapil

MDS 1st year
 NORMAL PERIRADICULAR TISSUE
Periradicular tissue consists of:
• Cementum
• Periodontal ligament
• Alveolar process
 SEQUELAE OF PERIRADICULAR
DISEASES
PULPAL INFLAMMATION/PULPAL
INFECTION

IRREVERSIBLE PULPITIS/NECROSIS

Symptomatic apical Asyptomatic apical

periodontitis Periodontitis

Chr. Ap.Abscess Phnoenix Radicular Cond.

Abscess Cyst Ostitits
cellulitis Acute apical
abscess

Periapical True Periapical Pocket

Cyst Cyst
 Clinical classification of diseases of
periradicular tissues
1. Symtomatic periradicular diseases
a. Symtomatic apical periodontitis
I. Vital tooth
II. Nonvital tooth
b. Acute alveolar abscess
c. Acute execerbation of asymptomatic apical
periodontitis/phoenix abscess
2. Asymptomatic periradicular diseases
a) Asymptomatic apical periodontitis
b) Ch. Alveolar abscess
c) Radicular cyst
d) Condensing ostitis
3. External root resorption
4. Persistent apical periodontitis
5. Diseases of periradicular tissues of
nonendodontic origin
 WHO 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
• K04.63periapical abscess with sinus to skin
• K04.7periapical abscess without sinus
• K04.8 radicular cyst
• K04.80 apical and lateral cyst
• K04.82 inflammatory paradental cyst
Symptomatic periradicular diseases
• Symptomatic apical periodontitis
• Definition :It is a painful inflammation of periodontium as a
result of trauma, irritation, or infection through the root canal
regardless of whether the pulp is vital or non-vital, producing
clinical symptoms including painful response to biting and
percussion.
Causes of symptomatic apical periodontitis in
vital teeth

• Abnormal occlusal contacts

• Recently inserted restoration extending
beyond the occlusal plane
• Wedging of foreign object b/w the teeth e.g.
tooth picks or food
• Traumatic blow to teeth
causes in vital teeth
 Causes of symtomatic apical periodontitis in
nonvital teeth
• Iatrogenic causes like:
• Sequaelae of pulpal diseases
1. Root canal instumentation forcing bacteria
and debris through apical foramen
2. Forcing of irritating irrigants or medicaments
through apical foramen
3. Extremation of obturation material through
the apical foramen to impinge on
periradicular tissue
4 Perforation of the root
5 Overinstumentation during shaping and
cleaning of root canals
causes in nonvital teeth
Symptoms of periradicular diseases
• Pain and tenderness of the tooth
 diagnosis
• Clinically Pain on percussion is the classical
diagnostic feature of the symtomatic apical
periodontitis
• Radiographically
• Radiographic changes are dependent on the
pulp vitality status of the involved tooth.
• In nonvital teeth : 1. slight widening of apical
periodontal ligament space
• 2 . Loss of apical lamina dura
• In vital tooth : no radiographic changes with
normal
 Differential diagnosis
• Differential diagnosis should be made b/w
symtomatic apical periodontitis and acute
alveolar abscess
• Acute alveolar abscess represents further
stage in development of disease with
breakdown of periradicular tissue
 bacteriology
• Pulp and periradicular tissues may be sterile if
periodontitis is due to
1 Blow
2 Occlusal trauma
3 Chemical or mechanical irritation during
endodontic treatment
4 Bacteria and toxic products are present in root
canal forced through apical foramen and may
irritate the apical periodontal tissues
 Histopathology
• Inflammatory reaction occurs in apical
periodontal ligament.
• Blood vessels are dilated, PMN leucocytes are
present.
• An accumulation of serous exudate extends
the PDL and extrude the tooth slightly
• If irritation is severe and continued osteoclasts
may become active and may breakdown the
periradicular bone and may lead to next stage
namely acute alveolar abscess
 treatment
• Treatment of symtomatic apical periodontitis
consists of determining the cause and
relieving the symptoms
• It is important to determine whether apical
periodontitis is associated with vital or
nonvital tooth
 In vital teeth
• Adjustment of high points in case of
hyperocclusion

In nonvital teeth
• Removal of irritants is the immediate line of
treatment
 prognosis
• Prognosis of the tooth is generally favourable
in case of symtomatic apical periodontitis
 Acute alveolar abscess
• Definition an acute alveolar abscess is an
inflammatory reaction to pulpal infection and
necrosis characterized by rapid onset, spontaneous
pain, tenderness of the tooth to pressure,pus
formation and eventual swelling of associated
tissues
• Synonyms acute abscess, acute apical
abscess,dentoalveolar abscess,acute periapical
abscess and acute radicular abscess
 cause

Chemical
or
Trauma Mechanica
l irritation

Bacterial
invasion of dead
pulp tissue
symptoms
 symptoms
• First symptom may be a mere tenderness of the
tooth that may be relieved by continued slight
pressure on extruded tooth to push it back into
the alveolus
• Later the patient has severe throbbing pain with
attendant swelling of the overlying tissue
• As the infection progresses swelling becomes
more pronounced and extends beyond the
original site
• The tooth becomes more elongated and
mobile.
• If left untreated the infection may progress to
chronic apical abscess wherein the contained
pus may break through to form a sinus tract
usually opening in the labial or buccal mucosa.
• It may further progress to ostitis, periostitis,
cellulitis or osteomyelitis.
 diagnosis
• The diagnosis is made quickly and accurately
from clinical examination and from the
subjective history given by the patient
• In early stages it may be difficult to locate the
tooth because of the absence of clinical signs
and the presence of diffuse annoying pain
.
• The tooth is easily located when the infection
has progressed to the point of periodontitis
and extrusion of tooth.
• The diagnosis may be confirmed by means of
electric pulp test and by thermal test.
• The affected tooth is necrotic and does not
respond to electric current or to application of
cold.
• An acute alveolar abscess is painful and
rapidly progressing Sequelae of symptomatic
apical periodontitis.
Radiographically A slight widening of the
apical periodontal ligament space and loss of
the apical lamina dura of the involved pulpless
tooth may be the only radiographic changes
that are seen.
 Differential diagnosis
• Acute alveolar abscess should be
differentiated from periodontal abscess
• A periodontal abscess is an accumulation of
pus along the root surface of the tooth that
originates from infection in the supporting
structures of the tooth.
• It is associated with a periodontal pocket and
is manifested by swelling and mild pain.
• The swelling is usually located opposite to
midsection of the root and gingival border,
rather than root apex or beyond it
• A periodontal abscess is generally associated
with vital rather than with pulpless teeth
• In acute alveolar abscess pulp is nonvital
• Test for pulp vitality are useful in establishing a
correct diagnosis
 bacteriology
• In abscess the concentration of
microorganisms is large
• Streptococci and staphylococci are generally
recovered
• Purulent material drained from root canal may
be sterile because it will consist chiefly of dead
leucocytes and dead bacteria
 histopathology
• Infiltration of PMNS and rapid accumulation of
inflammatory exudate in response to an active
infection distends the PDL and thereby
elongate the tooth.
• If the process continues, the PDL fibres will
separate and the tooth will become mobile
 treatment
• Emergency treatment
• Establish drainage
• Control systemic reaction
• Hot saline rinses
• Endodontic treatment
 prognosis
• Prognosis for the tooth is generally
favourable,depending on degree of local
involvement and amount of tissue destruction
• In most cases tooth can be saved by
endodontic treatment
 Phoenix abscess
• Definition : this condition is an acute
inflammatory reaction superimposed on an
existing asymptomatic apical periodontitis.
• Synonyms: exacerbating apical periodontitis
and phoenix abscess
• It is an acute inflammatory reaction
superimposed on an existing asymptomatic
apical periodontitis
• Asymptomatic apical periodontitis is in a state
of equilibrium, the periradicular tissues are
asymptomatic
• Noxious stimuli from diseased pulp can cause
acute inflammatory response in these dormant
lesions
• Lowering of body’s defense due to influx of
bacterial toxins from canal or irritation during
instrumentation can trigger acute response
 symptoms
• Initially , the tooth may be tender to
percussion.
• As the inflammation progresses the tooth gets
elevated from its socket and becomes
sensitive
• The mucosa over the radicular area may
appear red and swollen and is sensitive to
palpation
 diagnosis
• The radiograph shows well defined periradicular
lesion.
• Patient gives history of trauma that lead to tooth
discolouration over a time period.
• Lack of response to vitality tests diagnose a necrotic
pulp
• A tooth can respond to vitality test because of fluid in
root canal or in multirooted teeth on rare occasions.
 Differential diagnosis
• Phoenix abscess causes symptoms similar to
acute alveolar abscess
• Treatment of both lesions is same.
• So differential diagnosis is not needed.
• This tooth can be distinguished from a tooth
with painful pulpitis with pulp vitality test.
 bacteriology
• The periradicular lesions are usually devoid of
bacteria, except for transient bacteria
 histopathology
• Area of liquefaction necrosis with
disintegrating PMNs and cellular debris are
observed
• These areas are surrounded by infiltration of
macrophages and some lymphocytes and
plasma cells
 treatment
• Treatment is same as that of acute alveolar
abscess i.e.
• Emergency
• Establish drainage
• Warm saline rinses
• Endodontic treatment
 prognosis
• Prognosis of the tooth is good once the
symptoms have subsided
 Asymptomatic periradicular diseases
A. Asymptomatic apical periodontis/Periapical
granuloma
DEFINITION :Asymptomatic apical periodontitis is the
symptomless Sequelae of symptomatic apical
periodontitis and is characterized radiographically
by periradicular radiolucent changes and
histologically by the lesion dominated with
macrophages,lymphocytes,and plasma cells.
 causes
Asymptomatic apical periodontitis (AAP) may
be preceded by SAP or by an apical abscess.
• Inadequate root canal treatment may also
cause the development of these lesions.
• Mostly follows pulp necrosis – followed by
continued mild infection or irritation of the
periradicular tissues that stimulate productive
cellular reaction.
• If AAP perforates the cortical plate of the
bone, palpation of superimposed tissues may
cause discomfort.
• The associated tooth has a necrotic pulp and
therefore does not respond to electrical or
thermal stimuli.
 Radiographic Features
• Periradicular radioluceny
• Changes range from widening
of the periodontal ligament and
resorption of the lamina dura
to destruction of apical bone
resulting in a well-demarcated
radiolucency
 diagnosis
• The diagnosis is generally made by routine
radiographic examination.
• The area of rarefaction is well defined with
lack of continuity of lamina dura.
• An exact diagnosis can be made only by
microscopic examination.
 Differential diagnosis
• AAP can not be differentiated from other
periradicular diseases unless the tissue is
examined histologically.
 histopathology
• Granulomatous tissue, which replaces the
alveolar bone and periodontal ligament, may
vary in diameter from fraction of mm to a
centimetre or even larger.
• It is composed of rich vascular network,
fibroblasts derived from PDL and moderate
infiltration of lymphocytes and plasma cells
• Macrophages and foreign body giant cells may
also be present
 bacteriology
• The periapical tissue is sterile in most cases,
even though microorganisms may be present
in the root canal.
 treatment
• Root canal therapy is the treatment of AAP.
• Removal of the cause of inflammation is
usually followed by resorption of
granulomatous tissue and repair with
trabeculated bone.
 Chronic alveolar abscess
• DEFINITION A chronic alveolar abscess is a
long standing ,low grade infection of the
periradicular alveolar bone generally
symptomless and characterized by presence of
an abscess draining through a sinus tract.
• Synonyms chronic suppurative apical
periodontitis, suppurative periradicular
periodontitis, chronic apical abscess chronic
periapical abscess
 Causes
• Chronic alveolar abscess is the natural
sequaelae of death of pulp with extension of
the infective process periapically.
• It may also result from a pre-existing acute
abscess.
 symptoms
• Usually asymptomatic. If the sinus tract drainage becomes
blocked, however, varying levels of pain and swelling will be
experienced
• Often diagnosed during
routine radiographic
examination or by the
presence of a sinus tract
• The sinus usually
prevents exacerbation or
swelling by providing continued drainage of the periradicular
lesion
• The sinus tract may be partially lined with
epithelium or the inner surface composed of
inflamed connective tissue
• The sinus tract arises and persists because of
irritants from the pulp.
• sinus tracts, whether lined or not, resolve
following root canal treatment removing the
etiology.
• Patient gives history of sudden sharp pain that
subsided and has not recurred or a history of
traumatic injury.
 diagnosis

Radiographic- Diffuse area of bone

rarefaction- fade indistinctly into normal bone
 widened PDL.

 When drainage is intermittent, discharge is

preceded by swelling, pressure from
contained pus is sufficient to rupture the thin
wall of soft tissue, pus is discharged through
the opening.
• Opening usually present opposite the root
apex on labial or buccal mucosa
 histopathology
• Some of the PDL fibres are detached or lost
followed by destruction of apical PDL.
• Apical cementum may also become affected.
• Lymphocytes and plasma cells are generally
found towards the periphery of the abscessed
area.
• Mononuclear cells may also be present .
 treatment
• Endodontic treatment.
• Once the root canal is filled repair of
periradicular tissue takes place
 Apical abscess
• An abscess is a localized collection of pus in a
cavity formed by the disintegration of tissues.
• Based on the degree of exudate formation
and its discharge, the severity of pain, and the
presence or absence of systemic signs and
symptoms, apical abscesses can be
 symptomatic (acute)
 asymptomatic (chronic)
 Radicular cyst
• DEFINITION: A cyst is a close cavity or sac
internally lined with epithelium, which is filled
with fluid or semisolid material
• Cysts of jaw are divided into :
1. Odontogenic
2. Nonodontogenic
3. nonepithelial
• ODONTOGENIC CYSTS :Arise from
odontogenic epithelium and are classified as:
A. Follicular :Arising from follicle or enamel
organ.
B. Radicular :Arising from cell rests of malassez.
• NONODONTOGENIC CYSTS : Are classified as:
A. Fissural :Arising from epithilial remnants
entrapped in the fusion of facial processes
B. Nasoplantine :Arising from the remnants of
Nasoplantine duct.
• Pseudo cysts or nonepithilial cysts:
A. Idiopathic bone cavities
B. Aneurismal bone cyst
C. Traumatic cyst
• RADICULAR CYST: radicular cyst is a slowly
growing epithilial sac at the the apex of the
tooth that lines a pathologic cavity in the
alveolar bone
• The lumen of the cyst is filled with a low
concentration of proteinaceous fluid.
causes
histopathology
 Incidence of periapical cyst
• Periapical cysts are the most common jaw cysts,
comprise 52-68% of all jaw cysts
• Higher prevalence in males and in third decade of
life
• More common in maxilla
• Maxilla- anterior region
• Mandible- premolar region
• Prevalence of cysts among periapical lesions 6-55%
( only 15% are true periapical cysts)
• In 1980 Simon-
2 distinct types of
radicular cysts
 Cavities completely
enclosed in epithelial
lining.
 Epithelium lined cavities that are open to root canals (bay
cysts or pocket cysts) a pocket cyst can be diagnosed only
when cut root apexes and altered soft tissue are examined
 Ingle- 9% apical true cysts and 6% periapical pocket cysts
True cysts are located in granulomas and there is no
connection between their cavity and that of the root canal
space.
 pathogenesis
• Periapical true cyst- it is a chronic inflammatory lesion at the
per apex that contains an epithelium lined closed
pathological cavity
• Sequel of apical granuloma
• Only 10% of periapical lesions change into true radicular
cysts
3 phases of formation
 Phase 1- dormant cell rests of malassez proliferate due to
the effect of inflammation, under influence of bacterial
antigens, epidermal growth factors, cell mediators,
metabolites released by various cells in the periapical lesion
 Phase 2- Epithelium lined cavity formed

2 theories regarding the formation of the cavity

Nutritional deficiency abscess theory

theory
 Nutritional deficiency theory
• Epithelial proliferation results in an epithelial mass
that is too large for nutrients to reach its core resulting
in necrosis and liquefaction
• Central cells are far away from the source of nutrition
• Undergo necrosis and liquefactive degeneration
• Neutrophils are attracted at this site
• Such microcavities containing degenerating epithelial
cells, infiltrating mobile cells and tissue fluid coalesce
to form the cyst cavity lined by stratified epithelium
 Abscess theory

• The tissue liquefaction occurred first at the

central part of an abscess that was later lined
by locally proliferating epithelium.
• It postulates that proliferating epithelium lines
an abscess cavity formed by tissue necrosis and
lysis because of the innate nature of the
epithelial cells to cover exposed connective
tissue surfaces.
 Phase 3- cyst grows by osmosis
Presence of necrotic tissue in the cyst lumen attracts
neutrophils which extravasate and transmigrate
through the epithelial lining into the cyst cavity.

The lytic products of the dying cells in the lumen

release large no. of molecules.

The osmotic pressure of the cyst fluid rises higher

than that of the tissue fluid.
 Tissue fluid diffuses into the cyst cavity to raise the
intraluminal hydrostatic pressure above the a capillary
pressure.

The increased intracyst pressure lead to bone

resorption and expansion of the cyst

Molecular mechanism of cyst expansion

The T lymphocytes and macrophages in the cyst may
provide a continuous source of bone resorptive
metabolites and cytokines. Presence of MMP 1 and
MMP- 2 are present in cyst wall
• The peripheral pocket cyst is an epithelium lined
pathologic cavity that is open to the root canal of the
affected tooth. It was originally designated as bay
cyst.

• The micro luminal space becomes enclosed in a

stratified squamous epithelium that grows and forms
an epithelial collar around the root tip

• The epithelial collar forms an epithelial attachment to

the root surface that seals off the infected root canal
and the micro cystic lumen from the periapical area
 Microorganism in the apical foramen attract
neutrophils by chemo taxis into the micro lumen

The lumen acts as a “death trap” for the

neutrophils

Accumulation of the necrotic tissue and

microbial products, the lumen enlarges and
forms a diverticulum of the root canal space into
the periapical area.
 diagnosis
• Proposed radiographic features-
size of lesion (larger is cyst) but not supported
histologically
Presence of radio opaque rim (no correlation
histologically)
• Periapical lesions cannot be radiographically differentiated
into cystic and non-cystic lesions- Albeit et al
• Histological serial sectioning of the lesions in tooth is the
only reliable diagnostic method after surgical removal of
the root tip with the attached periapical lesion
 management
• About 85-90% of cysts heal after non surgical endodontic
treatment
• Prevalence of true radicular cysts is less than 10%
• The true cysts are self sustaining as the lesion is no longer
dependant on the presence or absence of root canal
infection so less likely to resolve after non surgical
treatment
• So apical surgery should be considered when orthograde
re treatment has failed to heal the periapical radiolucency
• Pocket cysts especially the smaller ones heal after RCT
 Condensing ostitis/chronic focal scelerosing
osteomelitis

• It is a diffuse radio opaque lesion believed to

represent a localized bony reaction to a low
grade inflammatory stimulus, usually seen at
the apex of a tooth in which there has been a
long standing pulpal pathosis (Grossman)
• local bony reaction to a low grade
inflammatory stimulus
• It is a diffuse radio opaque lesion believed to
represent a localized bony reaction to a low
grade inflammatory stimulus, usually seen at
the apex of a tooth in which there has been a
long standing pulpal pathosis (Grossman)
• local bony reaction to a low grade
inflammatory stimulus
• The tooth associated with condensing ostitis
may be asymptomatic or sensitive to stimuli.
• Depending on the pulpal status, the tooth may
or may not respond to electrical and thermal
stimuli.
• The radiographic appearance of condensing
ostitis, a well-circumscribed radiopaque area
• The radiopacity may or
may not respond to
endodontic treatment
 histopathology
• Dense bone with reduced trabecular pattern
lined with osteoblasts
• Chronic inflammatory cells, plasma cells and
lymphocytes are seen in the scant bone
marrow
 External root resorption
• External resorption is a lytic process occurring
in the cementum and dentine of the roots of
the teeth
 classification
• External tooth resorption has been classified into three types
based on clinical and histological features namely:
1. External surface resorption
2. External inflammatory root resorption
3. External replacement resorption or ankyolosis
 causes
• Due to trauma
• Excessive forces
• Granuloma
• Cysts
• Central jaw tumours
• Reimplantation of teeth
• Bleaching of teeth
• Impaction of teeth
• Systemic diseases
• Resorption due to unknown cause is called IDIOPATHIC
RESORPTION
 histopathology
• It is the result of osteoclastic activity on the
root surface of the involve tooth
• Microscopically there are small areas of
cementum resorption replaced by connective
tissue or repaired by new cementum.
• Large areas of resorption may be replaced by
osseous tissues
• Or scooped out areas of resorption replaced by
inflammatory or neoplastic tissues
 symptoms
• Throughout its development external root resorption
is asymptomatic
• When the root is completely resorbed the tooth may
become mobile.
• If the external root resorption extends into the crown
then it will give the appearance of PINK TOOTH like
seen in internal resorption
• In replacement resorption tooth becomes immobile,
in infraocclusion and with a high metallic percussion
sound.
 diagnosis
• Small areas of external root resorption can not
be seen radiographically and can be detected
histologically.
• On radiographs external inflammatory root
resorption appears as concave or ragged areas
or blunting of the apex
 treatment
• Treatment of external root resorption varies
with etiological factor.
• If it is caused by extension of pulpal disease
into the supporting tissue ,root canal therapy
will usually will stop the resorptive process
• Resorption caused by excessive forces from
orthodontic treatment can be stopped by
reducing those forces.
• Intervention in form of surgical procedure of
the defect and restoration with suitable
restorative material is the treatment of choice
before the resorptive defect invades the pulp
space
 Persistent apical periodontitis
• Persistent apical periodontitis is a post-
treatment apical periodontitis in an
endodontically treated tooth
 causes
• Nair had highlighted certain extraradicular factors
that contribute to persistent apical periodontitis:
A. Apical bio films/periapical plaque
B. Actinomycosis infection
C. Cholesterol crystals
D. Forgien body reaction to gutta percha
E. Cellulose granuloma
F. Periapical scar tissue
 Diseases of periradicular tissues of non
endodontic origin
 Lesions of nonendodontic origin with vital
pulps include:
• Cementoma/periapical cementum dysplasia
• Cementoblastoma
• Odontogenic cysts
• Fissural cysts
• Central giant cell granuloma
• Metastatic malignant tumors or
ameloblastoma are aggressive lesions that
produce excessive bone loss, mobility of teeth,
extensive root resorption and loss of pulp
vitality. These lesions can be differentiated
from endodontic lesions by their
aggressiveness
 Nonmicrobial endodontic disease
• Microbial infection is not the only etiologic factor
of apical radiolucencies persisting post-treatment
• Nonmicrobial aspects of the disease are
generally associated with asymptomatic
persistent periapical radiolucencies also known
as endodontic failures
• Persistent apical periodontitis is a post treatment
apical periodontitis in an endodontically treated
tooth
Nonmicrobial factors are
 True cystic lesions
 Extruded root canal fillings of other materials
that cause a foreign body reaction
 Accumulation of endogenous cholesterol
crystals that irritate periapical tissue
 Scar tissue healing of lesion
 Foreign bodies
• Foreign materials trapped in the periapical
tissue can induce tissue reaction
• Root canal filling materials, other endodontic
materials, food particles can initiate a foreign
body reaction and can cause periapical
radiolucency
• Leaching zinc oxide from GP cones is cytotoxic
in vitro, tissue irritating in vivo and associated
with inflammatory reaction
• The accumulation of macrophages around the
fine particles of GP impairs healing
• May induce a foreign body reaction and
activate macrophages which release
proinflammatory cytokines and cause bone
resorption
• Commercial GP becomes contaminated with
tissue irritating substances can initiate a
foreign body reaction at the periapex
 Oral pulse granuloma
• Foreign body reaction to particles of vegetable
food- legume seeds like peas, beans, pulses that
get lodged in oral tissues
• Also called giant cell hyaline angiopathy,
vegetable granuloma and food induced
granuloma
• Periapical pulse granuloma are associated with
teeth grossly damaged by caries and with
history of endodontic treatment
• Cellulose in plants induces granuloma
• Abundance of giant cells and inflammatory
cells
• Extremely rare
 Cellulose granuloma
• Foreign body reaction to particles of vegetable food- legume
seeds like peas, beans, pulses that get lodged in oral tissues
• Also called giant cell hyaline angiopathy, vegetable
granuloma and food induced granuloma
• Periapical pulse granuloma are associated with teeth grossly
damaged by caries and with history of endodontic
treatment
• Cellulose in plants induces granuloma
• Abundance of giant cells and inflammatory cells
• Extremely rare
 Other foreign materials
• Endodontic sealers, amalgam, calcium salts
(from Ca(OH)₂ extruded periapically)
• Etiological significance of these materials in
producing periapical lesions is not seen
 Periapical scar healing
• Periapical scar usually develops because
precursors of soft connective tissue colonize both
the root tip and periapical tissue
• Tooth is completely asymptomatic
• Radiolucency with intact lamina dura and a well
obturated root canal
• This occurs before the appropriate cells having
potential to restore various structural components
of the apical periodontium are able to do so
 references
• Ingle’s Endodontics 6. John I Ingle, Leif K Bakland,
J Craig Baumgartner
• Cohen’s Pathways of the Pulp
• Grossman’s Endodontic Practice- 13th edition
• Ramachandran Nair, P. N., G. Pajarola, and H. E.
Schroeder(1996) Types and incidence of human
periapical lesions obtained with extracted teeth.
Oral Surgery, Oral Medicine, Oral Pathology, Oral
Radiology, and Endodontology 81, 93-102.