ORAL AND MAXILLOFACIAL

PATHOLOGY I
DEN 7326
Dr. Victoria Woo

September 17, 2019

Pulp and periapical diseases I
 Overview
Pulpal diseases Periapical diseases
• Pulpitis (self review) • Periapical granuloma
1. Reversible pulpitis Periapical scar
2. Irreversible pulpitis • Periapical abscess
3. Chronic hyperplastic • Periapical cyst
pulpitis
• Secondary and
Tertiary dentin
• Pulpal calcifications
 Pulpitis
• Dental pulp confined within dental hard tissue
- dentin provides mechanical support, acts as barrier to oral
bacteria
• Unique response to inflammation in two respects:
1. Breach in dentin barrier inflammation, increase in pulpal
volume in confined space
2. Inflammatory response intrinsically impaired because sole
source of vascularity through apical foramen, no collateral blood
supply
• Bacterial involvement of pulp can spread to normally sterile apical bone
 Pulpitis
• Inflammation of the pulp
• Etiology:
Inflammatory response of pulp to noxious stimuli
Overall aims of inflammatory response:
1. Eliminate invasive organisms
2. Remove cellular debris
3. Limit tissue damage

During inflammation, inflammatory mediators cause vasodilation,

increased blood flow, and edema localized increase in pulpal
volume, pressure
 Pulpitis
• Etiology (cont’d):
Pulp chamber a confined space
Increase in pulpal pressure compression of vasculature
localized necrosis and ischemia of pulpal tissues

Pulpal healing occurs in most cases

If insult severe enough, healing mechanism
overwhelmed generalized pulpal necrosis
 Pulpitis
• Etiology (cont’d):
4 types of noxious stimuli
1. Mechanical damage
2. Thermal injury
3. Chemical irritation
4. Bacterial damage
 Pulpitis
• Etiology (cont’d):
4 types of noxious stimuli
1. Mechanical damage
- traumatic (accidents)
- iatrogenic (dental procedures)
- physiologic (attrition, abrasion)
 Pulpitis
• Etiology (cont’d):
4 types of noxious stimuli
1. Mechanical damage
2. Thermal injury
- heat conduction through metallic
restorations, dental procedures, exothermic
reactions from dental materials
 Pulpitis
• Etiology (cont’d):
4 types of noxious stimuli
1. Mechanical damage
2. Thermal injury
3. Chemical irritation
- erosion, acidic dental materials
 Pulpitis
• Etiology (cont’d):
4 types of noxious stimuli
1. Mechanical damage
2. Thermal injury
3. Chemical irritation
4. Bacterial damage
- direct damage from caries, indirect
damage (vascular transport of bacteria)
 Pulpitis
• 3 main types of pulpitis:
1. Reversible pulpitis
2. Irreversible pulpitis
3. Chronic hyperplastic pulpitis (“pulp polyp”)
 Pulpitis
• 3 main types of pulpitis
1. Reversible pulpitis
** Frank invasion by bacteria
2. Irreversible pulpitis
3. Pulpal necrosis
4. Chronic hyperplastic pulpitis (“pulp polyp”)
 Pulpitis
Reversible pulpitis
• Lower level of pulpal inflammation
• Pulp able to return to normal state of health after
stimulus removed

• Gender and age: No predilection

• Site: Any tooth
 Pulpitis
Reversible pulpitis
• Clinical features:
Onset of pain: Sudden
Duration of pain: Short
Stimulus: Cold, sweet or sour foods
Pain occurs with stimulus, subsides shortly
after removal
EPT response: responds at lower levels vs. cntrl
No mobility, no sensitivity to percussion
• May progress to irreversible pulpitis
 Pulpitis
Irreversible pulpitis
• Higher level of pulpal inflammation
• Pulp unable to return to normal state; irreversible
damage

• Gender and age: No predilection

• Site: Any tooth
 Pulpitis
Irreversible pulpitis
• Clinical features:
Onset of pain: Sudden; severe, sharp
Duration of pain: Long
Stimulus: May be spontaneous
Cold, heat, sweet or sour foods
Pain lingers after removal
May be worse in supine position, at night
EPT response: Early - lower levels
Late - higher levels or no response
+ Mobility or sensitivity to percussion
May be asymptomatic
 Pulpitis
Irreversible pulpitis (cont’d)
• Clinical features (cont’d):
Early - pain can be localized to tooth
- with progression, more difficult to
identify offending tooth
- pain involve quadrant, other arches

Later - heat increases pain, cold relieves pain

- symptoms may resolve with drainage
 Pulpitis
Pulpal necrosis
• Clinical features:
Pain varies
No response to EPT, thermal tests
 Pulpitis
Chronic hyperplastic pulpitis (“pulp polyp”)
• Etiology:
Mechanical damage, bacterial damage
loss of dentinal roof, exposure of pulp
Hyperplastic granulation tissue
Apex open - reduces chance of pulpal necrosis

• Gender: No predilection
• Age: Children, young adults
• Site: Primary or permanent molars (large pulps)
 Pulpitis
Chronic hyperplastic pulpitis (“pulp polyp”)
• Clinical features:
Pink to red
Nodular growth from pulp chamber
Mostly asymptomatic
Courtesy of Dr. David Zegarelli,
Columbia University Medical Center
Courtesy of Dr. Jerry Bouquot,
University of Texas at Houston
Courtesy of Dr. David Zegarelli,
Columbia University Medical Center
Courtesy of Dr. Nicholas Delisle,
UNLV
 Pulpitis
• Histology:
Most cases not examined histopathologically
Histologic findings may not correlate with clinical
severity
Reversible pulpitis
- hyperemia, edema
- scattered inflammatory cells

Oral and Maxillofacial Pathology, 4th ed., Neville et al.

 Pulpitis
• Histology:
Irreversible pulpitis
- vessel congestion
- necrosis with
acute inflammatory cells Oral and Maxillofacial Pathology, 4th ed., Neville et al.

- surrounding and deeper

pulpal CT - fibrosis, chronic
inflammation
 Pulpitis
• Histology:
Chronic hyperplastic
pulpitis
- granulation tissue = fibrous
connective tissue that is:
1. inflamed
2. well-vascularized
- stratified squamous
epithelium + ulceration
- deeper pulp - fibrosis,
chronic inflammation Oral and Maxillofacial Pathology, 4th ed., Neville et al.

- apical tissue normal

 Pulpitis
• Diagnosis:
Dependent on:
1. Clinical presentation (onset of pain, duration of pain)
2. Response to thermal stimuli
3. Response to EPT
4. Response to percussion

** Predictive value of vitality testing not optimal

Fairly reliable in confirming vitality, less reliable in
confirming necrosis
 Cold Heat EPT Percussion
EARLY 0
+ +/- May vary from control.
Discomfort – lasts seconds Usually not uncomfortable Not very useful Because PDL not involved
Reversible
pulpitis
EARLY
+++ ++ + , ++
↕↕
Irreversible Pain lingers Lingering dull pain
LATE
Level of PDL involved

pulpitis

RELIEVES
PAIN
+++ +/- ++
Partial Very sensitive to hot liquids Variable response Level of PDL involved

necrosis

0 +/- 0 ++++
Highest reading (80) w/o
Total response

necrosis
RELIEVES EARLY
+++++ +++++
Focal PAIN

reversible
pulpitis
 Pulpitis
• Diagnosis:
Dependent on:
1. Clinical presentation (onset of pain, duration of pain)
2. Response to thermal stimuli
3. Response to EPT
4. Response to percussion
• Other conditions can have similar presentation
- myofascial pain, trigeminal neuralgia, atypical facial
neuralgia, migraines, nasal or sinus pathology, angina
pectoris
 Pulpitis
• Treatment:
Reversible pulpitis
Removal of noxious stimulus/irritant
Prognosis good with early intervention
Re-test for vitality in 3 months

Irreversible pulpitis
Chronic hyperplastic pulpitis
Extraction of tooth OR
Endodontic therapy
 Secondary and Tertiary dentin
• Dentin deposited throughout life

• Primary dentin - dentin deposited before

completion of crown
Secondary dentin - dentin deposited after
completion of crown
Tertiary dentin - dentin deposited in response to
focal injury

• Progressive reduction in size of pulp chamber

and canals with age
 Secondary and Tertiary dentin
(Physiologic) Secondary dentin

• Etiology:
Aging, occlusal forces
May be accelerated in rare conditions - e.g. progeria
• Gender:
M slightly >F
Association with calcification-related diseases
- e.g. arthritis, gout, kidney stones, gall stones,
atherosclerosis, hypertension
 Secondary and Tertiary dentin
(Physiologic) Secondary dentin

• Age: Increases after age 35 to 40

• Site:
Any tooth
Generally proceeds from coronal to apical
Posterior teeth - primarily involves pulpal floor >
roof > sidewalls
 Secondary and Tertiary dentin
Tertiary dentin
• AKA: reactionary dentin; reparative dentin; irregular dentin

• Etiology:
Odontoblasts stimulated by focal injury
- e.g. attrition, abrasion, erosion, fracture, caries, periodontal
disease, injury from dental procedures or materials
 Secondary and Tertiary dentin
Tertiary dentin
• Etiology (cont’d)
Mild damage - primary odontoblasts survive, deposit
reactionary dentin
More severe damage - primary odontoblasts die
- release of growth factors formation of
secondary odontoblasts deposit reparative
dentin
If injury severe enough, early obliteration of pulp
chamber and canal
- known as calcific metamorphosis
 Secondary and Tertiary dentin
• Clinical features:
Reduced tooth sensitivity
Reduced susceptibility to caries, dental trauma
Impact on dental procedures
- reduced susceptibility to mechanical trauma
- reduced incidence of pulp exposures
- difficulty in endodontics (e.g. perforation)

Calcific metamorphosis - opaque, yellow discoloration

of tooth
- usually apparent ~1 year after trauma (early as 3
months)
Calcific metamorphosis

http://cudental.creighton.edu/htm/p_misc.htm
 Secondary and Tertiary dentin
• Radiographic features:
Progressive decrease in size of pulp chamber and
canals

Calcific metamorphosis
- early obliteration of pulp chamber and canals
 http://cudental.creighton.edu/htm/p_misc.htm

Calcific metamorphosis
 Secondary and Tertiary dentin
• Histology:
Secondary dentin
- regular dentin tubules
- line of demarcation between 1o
and 2o dentin

Tertiary dentin
- depends on severity of stimulus Primary dentin
- acellular dentin, irregular or
disorganized dentinal tubules

Secondary dentin
 Secondary and Tertiary dentin
• Treatment:
Secondary dentin
No treatment necessary
Tertiary dentin
Address etiology (e.g. caries)
Calcific metamorphosis
If periapical pathology and/or nonvital:
Endo or extraction
PA surgery
If vital: Careful monitoring, periodic follow-up
Bleaching, veneers or full coverage for esthetics
 Pulpal calcifications
• 3 types of pulpal calcifications:
1. Denticles
2. Pulp stones
3. Diffuse linear calcifications
 Pulpal calcifications
• Increased incidence in:
1. Teeth with long-standing chronic pulpitis
2. Teeth exposed to chronic pulpal irritants (e.g.
attrition, abrasion, erosion, caries periodontitis)
3. Older teeth
4. Patients with dentin dysplasia type II, pulpal
dysplasia, Ehlers-Danlos, end-stage renal
disease, others
 Pulpal calcifications
Denticles
• Etiology:
Epithelial remnants in pulp induce odontoblastic
differentiation of mesenchymal cells
Odontoblasts deposit dentin (round, ovoid)

• Site: Root canal, pulp chamber adjacent to

furcation areas of multirooted teeth
 Pulpal calcifications
Pulp stones
• Etiology:
Calcification around nidus of pulp tissue
- concentric, round

• Site: Coronal portions of pulp chamber

 Pulpal calcifications
Diffuse linear calcifications
• Etiology:
Calcification that occur parallel to neurovascular
elements
- fine, fibrillar

• Site: Pulp chamber or canals

 Pulpal calcifications
• Clinical features (all 3 types):
May cause difficulty in endodontics
Otherwise, clinically insignificant

Rarely, may interfere with root formation early

periodontal bone loss, tooth loss
Isolated; associated with several conditions
- dentin dysplasia (DD) II, pulpal dysplasia, tumoral
calcinosis, calcinosis universalis, Ehlers-Danlos
syndrome
 Pulpal calcifications
• Radiographic features:
All pulpal calcifications initially free bodies in pulp,
may eventually become attached or
embedded in dentinal walls
Denticles, pulp stones
- round/ovoid radiopacity in pulp chamber or
root canal
Diffuse linear calcifications
- no radiographic changes
 Pulp stones

Courtesy of Dr. Russell Warburton,

UNC
 Pulpal calcifications
• Histology:
Denticles
- aggregates of dentin
- attached or embedded
Pulp stones
Pulp stones Oral and Maxillofacial Pathology, 4th
- mass of calcification ed., Neville et al.

- lamellar/concentric
pattern
Diffuse linear calc.
- fine, linear calcification
- along neurovasculature
Diffuse linear calc.
 Pulp stone
Courtesy of Dr. Scott Chavez, Pulpal necrosis
UNLV
 Pulpal calcifications
• Treatment:
No treatment necessary upon radiographic
recognition
 Periapical granuloma
• AKA: Chronic apical periodontitis
• Mass of granulation tissue at apex of nonvital tooth

• Etiology:
Microbial infection of root canal spread of toxins
to apical area of tooth, defensive response
Mostly bacterial, rarely fungal or viral
 Periapical granuloma
• Evolution of periapical granuloma
1. Microbial invasion of pulp, canal, apical bone
2. Acute inflammatory phase (acute apical
periodontitis)
- rad: no radiographic alterations
- hist: neutrophils predominate
3. Neutrophils activate osteoclasts bone
resorption
 Periapical granuloma
• Evolution of periapical granuloma (cont’d)
4. Chronic inflammatory phase (chronic apical
periodontitis)
- rad: periapical radiolucency
- hist: chronic inflammatory cells predominate
5. Activate activate fibroblasts and endothelial
cells fibrosis and granulation tissue
(periapical granuloma)
 Periapical granuloma
• May:
1. Arise after quiescence of a periapical abscess OR
2. Initial manifestation of periapical pathology

• Not static - may develop into periapical cyst, may

develop secondary acute inflammatory changes
(phoenix abscess)

• Gender and age: No predilection

• Site: Any tooth
 Periapical granuloma
• Clinical features:
Early - similar to irreversible pulpitis
Dull, throbbing pain that lingers
Tooth nonvital - no response to thermal tests, EPT
May be sensitive to percussion
Later
Most are asymptomatic
Pain and sensitivity if acute exacerbation
Tooth nonvital - no response to thermal tests, EPT
Typically, no mobility or percussion sensitivity
 Periapical granuloma
• Radiographic features:
Size: <2cm; >2cm is usually a periapical cyst
Shape: Round, ovoid
Density: Radiolucent
Borders: Well- or ill-defined
Location: At apex of (periapical to) nonvital tooth
Tooth may have evidence of previous endo.
Effect on adjacent structures: Loss apical lamina
dura; + Root resorption

** Periapical granulomas, abscesses and cysts

can appear radiographically identical **
 Periapical granuloma
• Histology:
- granulation tissue with mixed
inflammatory cells (mostly
lymphocytes, plasma cells,
neutrophils)
- + histiocytes
- + cholesterol clefts, giant cells,
hemosiderin
- + RCT filling material
- + small collections of PMNs
(focal abscess formation)

** No epithelial lining **
- no lining = PA granuloma
- lining present = PA cyst
Oral and Maxillofacial Pathology, 4th ed.,
Neville et al.
Foamy histiocytes
Cholesterol clefts
RCT filling material
 Periapical granuloma
• Treatment:
Treatment of offending tooth
- endodontic therapy; apicoectomy
- extraction and apical curettage
* Submission of all apical soft tissue to pathology *
- PA granulomas can mimic other pathologic
processes (neoplastic, systemic, etc.)
- histopathologic interpretation necessary to rule
out other pathology
 Periapical granuloma
• Treatment (cont’d):
Analgesics for pain
Antibiotics if cellulitis, systemic symptoms

If not treated, some will become periapical cysts +

acute exacerbations (abscess)
 Periapical granuloma
• Treatment (cont’d):
Periodic follow-up at 1 and 2-years (at minimum)
- some recommend follow-up at 1, 3, and 6 months
- assess lesional changes (size), bone healing
- many reasons for non-healing periapical radiolucency
e.g. failure of therapy (e.g. inadequate endo, poor coronal
restoration), cyst formation, persistent pulpal infection,
extraradicular infection, periapical foreign material, perio
disease, perforation of mx sinus, scar formation, other
pathology
Endo failures may require retreatment or PA surgery
Re-biopsy if lesion persistent, enlarging, or non-
healing to rule out other pathology
Heal with normal bone, fill with scar tissue (PA scar)
 Periapical granuloma
• Treatment (cont’d):
Periodic follow-up at 1 and 2-years (at minimum)
- some recommend follow-up at 1, 3, and 6 months
- assess lesional changes (size), bone healing
- many reasons for non-healing periapical radiolucency
e.g. failure of therapy (e.g. inadequate endo, poor coronal
restoration), cyst formation, persistent pulpal infection,
extraradicular infection, periapical foreign material, perio
disease, perforation of mx sinus, scar formation, other
pathology
Endo failures may require retreatment or PA surgery
Re-biopsy if lesion persistent, enlarging, or non-
healing to rule out other pathology
Heal with normal bone, fill with scar tissue (PA scar)
 Periapical scar
• Etiology:
Same as PA granuloma
Healing defect
- bony defect created by PA granuloma fills with
scar tissue
- may occur post-endo, post-extraction, post-
apical surgery
- most common when there is loss of facial and
lingual cortical plates

• Gender and age: No predilection

• Site: Any tooth
 Periapical scar
• Clinical features:
Most are asymptomatic
If associated with a tooth, tooth nonvital
- no response to thermal tests, EPT
No mobility or percussion sensitivity

• Radiographic features:
Same as PA granuloma
Density: Radiolucent
Borders: Well- or ill-defined
Location: At apex of (periapical to) nonvital
tooth, tooth with endo, no tooth
Color Atlas of Clinical Oral Pathology,
2nd ed., Neville et al.
Oral and Maxillofacial Pathology, 2nd ed., Neville et al.
 Periapical scar
• Histology:
- dense fibrous connective
tissue (scar tissue)
- + mild chronic inflammatory
infiltrate
- + RCT filling material

** No epithelial lining **
 Periapical scar
• Treatment:
Tooth usually already treated or extracted
Biopsy to confirm diagnosis
Periodic follow-up per PA granuloma
 Periapical abscess
• Periapical abscess = accumulation of acute
inflammatory cells at apex of nonvital tooth
• Acute apical periodontitis = acute inflammation
of periodontal ligament without frank abscess
- trauma, high occlusal contacts, wedging by foreign
object, nonvital tooth
- may or may not proceed to periapical abscess
• Etiology:
Microbial infection of root canal (caries, iatrogenic,
trauma) spread of toxins to apical area of
tooth, defensive response abscess formation
 Periapical abscess
• May be:
1. Initial manifestation of periapical pathology OR
2. Acute exacerbation of chronic PA pathology
(“phoenix abscess”)

• Gender: No predilection
• Age: No predilection
• Site: Any tooth
 Periapical abscess
• Clinical features:
May be symptomatic or asymptomatic
Becomes symptomatic upon accumulation of
purulent exudate in bone
Tenderness; intense pain later
Tooth nonvital - no response to thermal tests, EPT
Tooth sensitive to percussion; extruded
+ Systemic symptoms (headache, malaise, fever,
chills, lymphadenopathy)
 Periapical abscess
• Clinical features (cont’d):
Spread through medullary spaces (osteomyelitis)
Perforation, spread to soft tissues, skin (cellulitis)
Drainage through oral mucosa, skin (sinus, fistulous
tract)
- swelling at opening of fistula (parulis, “gum boil”)
- drainage often buccal except mx lateral incisors,
palatal roots of mx molars, mn 2nd and 3rd molars
- relief of symptoms on drainage, recurrence of
symptoms on closure of fistula
Courtesy of Dr. David Zegarelli,
Columbia U.
Cellulitis
Cutaneous fistulous tract
 Fistula/parulis

Courtesy of Dr. Peggy Chuang,

UNLV
 Fistula/parulis

Fistula/parulis
Chronic hyperplastic pulpitis
 Periapical abscess
• Radiographic features:
Often no radiographic changes
- insufficient time for significant bone destruction
Thickening of apical pdl space
+ Ill-defined apical radiolucency
Phoenix abscess
Outline of initial chronic lesion + new areas of bone
loss
 Periapical abscess
• Histology:
** Most cases not examined
histopathologically
- sheets of PMNs (neutrophils)
- other inflammatory cells,
histiocytes
- necrotic material
- cellular debris
- bacterial debris

Fistulous tract, parulis

- granulation tissue, PMNs
 Periapical abscess
• Treatment:
1. Incision and drainage
- alleviation of symptoms in ~48 hrs
2. Treatment of offending tooth (exo or endo)

Analgesics (NSAIDs) for pain

Antibiotics if cellulitis, systemic symptoms,
immunocompromised state (DM, AIDS, HIV, corticosteroid
use, chemotherapy)
Surgical removal of fistulous tract, parulis
 Periapical abscess
• Treatment (cont’d):
If not treated, most will progress to periapical
granuloma and/or periapical cyst
Severe, untreated cellulitis can lead to serious
complications:
- cavernous sinus thrombosis
- mediastinitis
- necrotizing fasciitis
- cerebral abscess
• Cyst = Epithelial-lined cavity

Periapical cyst
• AKA: Radicular cyst, apical periodontal cyst
• Etiology:
Inflammation of pulpal or periodontal origin
- stimulation of epithelium at apex of nonvital tooth
- epithelium desquamates into cyst lumen increase in
protein content fluid influx in lumen to equalize
osmotic pressure slow enlargement
May be preceded by periapical granuloma
• Origin of epithelium: rests of Malassez, crevicular
epithelium, sinus lining, epithelial lining of fistulous
tracts
 Periapical cyst
• Gender and age: No predilection

• Site: Any tooth

 Periapical cyst
• 3 clinical variants:
1. Periapical cyst
- periapical pocket cyst, periapical true cyst
- apex of nonvital tooth
2. Lateral radicular cyst
- lateral aspect of nonvital tooth
- necrosis of lateral canal, periodontitis
3. Residual periapical cyst
- site of previously infected tooth that has
been extracted
 Periapical cyst
• 3 clinical variants:
1. Periapical cyst
- periapical pocket cyst, periapical true cyst
- apex of nonvital tooth
2. Lateral radicular cyst
- lateral aspect of nonvital tooth
- necrosis of lateral canal, periodontitis
3. Residual periapical cyst
- site of previously infected tooth that has been
extracted, apical tissue not curetted
- may resolve, may persist
 Periapical cyst
• Clinical features:
Mostly asymptomatic
Pain if acute exacerbation
Mild swelling
If cyst associated with tooth, tooth nonvital
- no response to thermal tests and EPT, unless
multiple canals

Periapical cyst, lateral radicular cyst - evaluate

periodontal status, tooth vitality prior to surgical
exploration
Courtesy of Dr. David Zegarelli,
Columbia U.
 Periapical cyst
• Radiographic features:
Shape: Round to ovoid; unilocular; generally >2cm
Density: Radiolucent
Residual (older) - radiolucent w/ central opacities
Borders: Well- or ill-defined
Typically non-corticated
Location: Periapical - apex; lateral - lateral aspect;
residual - no tooth
Effect on adjacent structures: Loss of lamina
dura; root resorption common
** Periapical granulomas, abscesses and cysts
can appear radiographically identical **
Courtesy of Dr. David Zegarelli,
Columbia U. Periapical cysts
Periapical cyst
Periapical cyst
Oral and Maxillofacial Pathology, Periapical cyst
4th ed., Neville et al.
Lateral radicular cysts
Residual
periapical cysts
• Histology:
Periapical cyst
Epithelial lining
- stratified squamous, rarely
pseudostratified squamous
- + mucous cells, ciliated cells
- + Rushton bodies 1. Lumen
Cyst wall 2. Epithelial lining
- fibrous connective tissue 3. Cyst wall
- acute, chronic, or mixed
inflammation
- + cholesterol clefts, giant cells,
hemosiderin deposits, foamy
histiocytes, RCT material, hyaline
bodies
Lumen
- cellular debris, fluid
Courtesy of Dr. David Zegarelli,
Columbia U.
Cholesterol clefts
Rushton bodies (epithelium)
Hyaline bodies (conn. tissue)
 Periapical cyst
• Treatment:
Periapical cyst, lateral radicular cyst
Same as periapical granuloma
Treatment of offending tooth (endo or exo, perio)
Enucleation of cyst - * submit tissue for histo exam *
NSAIDs, antibiotics if indicated
Follow-up at 1 and 2-years (at minimum)
- re-treat failures; re-biopsy if persistent, enlarging or
non-healing lesion to r/o other path
Typically do not recur; may heal with PA scar
 Periapical cyst
• Treatment (cont’d):
Residual periapical cyst
Excise and submit for histologic examination
- can mimic a variety of pathologies
- rule out other pathologic processes
• Development of squamous cell carcinoma in PA
cyst has been described
- need for histologic examination of apical tissue
and follow-up
- re-biopsy of apical lesion persistent, enlarging
or changing; non-healing