PERIAPICAL PATHOLOGIES

NAMRATA SENGUPTA
MDS(II)
GUIDED BY: Dr. SACHIN SARODE
PRESENTED ON: 28th May, 2021
 Periapicallesions are among the most frequently diagnosed apical odontogenic
pathologies in human teeth.

 The condition is generally described as apical periodontitis. 

 It is viewed as a dynamic encounter between microbial factors and host defenses

at the interface between infected radicular pulp and periodontal ligament that
results in local inflammation, resorption of hard tissues, destruction of other
periapical tissues, and eventual formation of various histopathological categories
of apical periodontitis, commonly referred to as periapical lesions. 
Aetiology
• Non-treated pulpal disease

• Trauma (hyperocclusion)

• Irrigants
• Instrumentation
Symptoms of periapical pathosis

Clinical Radiological
Generally
examination: symptoms
• Anamnesis: • Vitality test: • Loss of lamina
• acute: pain, usually negative dura
swelling
• chronic: mild or
no symptoms
DISEASES OF THE PERIAPICAL TISSUE

• Acute Apical periodontitis

Apical periodontitis • Chronic Apical periodontitis (periapical granuloma)

• Periapical Cyst
Apical periodontal cyst

• Chronic
Periapical Abscess • Phoenix Abscess

• Acute
Osteomyelitis • Chronic
• Garre’s
DISEASES OF THE PERIAPICAL TISSUE

• Acute alveolar abscess

I. Acute periradicular • Acute apical periodontitis
diseases • Vital
• Non vital

II. Chronic • Chronic alveolar abscess

periradicular diseases • Periapical Granuloma
with areas of • Periapical cyst
rarefaction
Acute Apical Periodontitis:
 Painful inflammation of the periodontium as a result of trauma,
irritation, or infection through the root canal, regardless of whether
the pulp is vital or non vital.
 Symptoms:

- The symptoms of acute apical periodontitis are pain and tenderness of

the tooth.
- The tooth may be extruded, making closure painful.
Treatment:

o Treatment of acute apical periodontitis consists of determining the

cause and relieving the symptoms. It is particularly important to
determine whether apical periodontitis is associated with a vital or a
pulpless tooth. When the acute phase has subsided, the tooth is
treated by conservative means.
Periapical Granuloma
Also known as chronic apical periodontitis
Low grade infection

A granuloma is 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.

Involved tooth non vital

On percussion: slightly tender or dull sound

Mild pain on biting or chewing

Tooth feels elongated
 Pathogenesis

 Essentially localized mass of chronic granulation tissue formed in response to

infection
 Cause is due to apical spread of infection
 Spread along the lateral or accessory canals: lateral granuloma
 Diagnosis
 An exact diagnosis can be made only by microscopic examination, however.
 The involved tooth is generally non tender to percussion, and is not mobile.
 The mucosa over the root apex may or may not be tender to palpation.
 The tooth does not respond to thermal or electric pulp tests.
 The patient may give a history of pulpalgia that subsided.
 Radiographic features

 The presence of a granuloma, which is symptomless, is generally discovered by

routine radiographic examination.
 Thickening of the periodontal ligament at the root apex
 Granuloma appears as a radiolucent area attached to the root apex
 The area of rarefaction is well defined, with lack of continuity of the lamina dura.
 In long standing lesions thin radiopaque sclerotic bone line is seen
 Histopathology

 Characterized by chronic inflammation and increased vascularity

 Predominantly macrophages, lymphocytes, and plasma cells
 Abundant new capillaries with swollen endothelial cells
 Proliferation of fibroblasts and delicate collagen fibrils
 Russellbodies: eosinophilic immunoglobulin secretions both within
plasma cells and extracellularly

 Foam cells: large number of phagocytes which have ingested lipid

material

 Abundant mast cells may also be found

RUSSELL BODIES
MACROPHAGES
 Deposits of hemosiderin and cholesterol are often present

 Cholesterol clefts clear needle like spaces or clefts owing to loss of

cholesterol in processing

 Invariably associated with foreign body type giant cells

 Sometimes epithelial rests of Malassez

 Treatment

 Root canal therapy with apicectomy

 Extraction of involved tooth
 If left untreated may transform to apical periodontal cyst
Periapical Cyst

Most common odontogenic cyst, caused by

inflammatory processes.

All PCs are associated with non-vital teeth and identified at the apices of teeth.
Either carious process or trauma triggers the residual epithelial remnants at the
periapical region and stimulates and proliferates the remnants, leading to cyst
formation.

These cysts are well identified through radiological

investigations.
Pathogenesis of cyst

Inflammation stimulates keratinocyte growty factor

Acts on epithelial rests

Causes epithelial proliferation Necrosis of central cells

Cyst formation results

Stages in cyst formation

 Phase of initiation
 Phase of cyst formation
 Phase of enlargement
 Clinical features
 Most are asymptomatic
 No symptoms associated with the development of a cyst, except those incidental to necrosis of the pulp.

 Tooth non vital

 A cyst may become large enough, however to become obvious as a swelling.
 Pressure of the cyst may be sufficient to cause movement of the affected Teeth. Teeth may also become
mobile.
 In long standing cases may undergo an acute exacerbation of the inflammatory process and develop
rapidly in to an abscess that may than proceed to a cellulitis.

 Pulp testing and radiography are compulsory for diagnosing PC.

 Teeth associated with PCs must be nonvital and do not respond to thermal or electric pulp testing
methods.
 Generally radiolucent lesion with radiopaque border
 Initially bony hard swelling then thinning of bone and later erosion of bone—fluctuation
 DIAGNOSTIC MODALITIES

 Pulp testing, radiographs, and histopathologic evaluation are helpful

in achieving an accurate diagnosis.
 Radiologically recognized by well-defined, well-circumscribed,
unilocular radiolucency that is closely associated with the apex of the
affected tooth.
 Loss of lamina dura and a faint or thin radiopaque line (sclerotic
border) that encircles the cystic region are also important
radiographic markers for securing a diagnosis.
Histopathology

Cystic Lining: non-keratinized, stratified squamous epithelium

Inflammatory hyperplasia of the epithelium shows a characteristic arcading
and forking pattern.

Surrounded by inflamed connective tissue stroma.

The connective tissue stroma may show Russel and Rushton bodies.

Rushton body: hyaline body: they are tiny, linear arc shaped, amorphous,
eosinophilic and brittle
 Connective tissue wall: compressed collagen bundles that often
appear compressed
 Variable number of fibroblasts and blood vessels
 Characteristic chronic inflammatory infiltrate adjacent to epithelium
in connective tissue
 At times: cholesterol clefts and dystrophic calcifications
 CHOLESTEROL CLEFTS &
CRYSTALS
 Cholesterol is a steroid alcohol found in all tissue types. It is the main component of cell
membranes.
 Cholesterol crystals can be found in odontogenic cysts, especially radicular cysts. The
cystic fluid with cholesterol crystals is gold- or straw-coloured clinically and is crystalline
diamond (rhomboid) in shape when viewed under a microscope.
 If a tissue with cholesterol crystal is stained with H & E, needle-shaped clefts, also
called cholesterol clefts, are revealed.
 The prevalence of cholesterol crystals was reported in the range of 18%–44% (Nair et
al. 1998) being higher in inflammatory odontogenic cysts and lower in non-
inflammatory cysts.
 The inflammatory process is likely to have an important role in the formation of
cholesterol crystal.
Cholesterol crystals showing typical rectangular shaped
crystals with notched corner under light microscope.
CHOLESTEROL CLEFTS
 Cystic lumen: watery, straw coloured, blood tinged fluid to semi
solid materials
 Low protein concentration
 At times: cholesterol and keratin
 Rarely blood
 Treatment

 Similar to granuloma
 PCs are usually managed with conventional root canal treatment with
periapical surgery; that is, apicoectomy (removal of tooth apex).
 Extraction with curettage is another mode of treatment.
 Inadequate curettage may lead to persistent radiolucent cavity
(residual cyst).
 If thoroughly removed: no recurrence
 If untreated: increases in size and more bone resorption
 Periapical Abscess
 Acute or chronic suppurative process of dental periapical region
 Cause: pulpal infection spreads periapically

or trauma or other injury

 Presents features of acute inflammation of periapical region
 Tooth tenderness , relieved by pressure application
  The terms dental abscess, dentoalveolar abscess, and odontogenic abscess are often
used synonymously to describe abscesses formed in the tissues around the tooth.
 Acute apical abscess is the most common form of dental abscess and is caused by
infection of the root canal of the tooth. It is usually localized intraorally, but in
some cases the apical abscess may spread and result in severe complications or
even mortality.
Chronic Alveolar Abscess (Chronic suppurative apical periodontitis)

 A chronic alveolar abscess is a long-standing, low-grade infection of the

periradicular alveolar bone. The source of the infection is in the root canal.
 Detected only during routine radiographic examination or because of the
presence of sinus tract.
 The sinus tract usually prevents exacerbation or swelling by providing
continual drainage of the periradicular lesion.
 A radiograph taken after the insertion of a gutta-percha cone into the sinus
tract often shows the involved tooth by tracing the sinus tract to its origin.
 Tooth becomes extremely painful and extrudes from the socket
 Trismus may occur.
 Systemic manifestations may also develop, including fever,
lymphadenopathy, malaise, headache, and nausea.

 May extend to bone causing osteomyelitis and swelling

 Chronic lesion: no clinical features, mild well circumscribed area

 Radiographically slight thickening of periodontal ligament

 Studies using culture and advanced molecular microbiology methods
for microbial identification in apical abscesses have demonstrated a
multispecies community conspicuously dominated by anaerobic
bacteria.
 Species/phylotypes commonly found in these infections belong to the
genera Fusobacterium, Parvimonas, Prevotella, Porphyromonas, Dia
lister, Streptococcus and Treponema.
 Histopathology

 Area of suppuration, with central areas of disintegration

 Surrounding leukocytes, lymphocytes, cellular debris, necrotic

materials and bacterial colonies
 Blood vessels in periodontal ligament and bone marrow dilated
 Serous exudate
 Treatment
 Treatment of acute apical abscesses involves incision for drainage and
root canal treatment or extraction of the involved tooth to remove the
source of infection
 Either pulp drainage or extraction
 Adjunctive systemic antibiotics are not necessary in most cases of
localized and uncomplicated apical abscesses
 Analgesics may be prescribed for pain control. 
 If untreated serious complications like osteomyelitis, cellulitis and
bacteremia
 Cavernous thrombosis has been reported
Acute Exacerbation of a Chronic Lesion:
(Phoenix abscess)

 An acute inflammatory reaction superimposed on an existing chronic

lesion, such as a cyst or granuloma.

 Symptoms:
- At the onset, the tooth may be tender to the touch. As inflammation
progresses, the tooth may be elevated in its socket and may become
sensitive.
- The mucosa over the radicular area may be sensitive to palpation and
may appear red and swollen.
 OSTEOMYELITIS

 Defined as the inflammation of the bone and the bone marrow.

 Osteitis : inflammation of the bone only.
 Predisposing factors: chronic systemic disease,

immunocompromised status, decreased vasculature ,host defense

mechanism
Suppurative

 Acute Suppurative and

 Chronic Suppurative osteomyelitis
 Chronic Suppurative osteomyelitis further classified into

1) primary
2) secondary
Non suppurative

 Chronic sclerosing Focal

Diffuse

 Garre’s osteomyelitis
 Actinomycotic osteomyelitis
 Radiation osteomyelitis
Acute Osteomyelitis

 Insufficient time for body to react to infection hence leads to acute

osteomyelitis.
 Seen in less than one month of duration.
 Fever ,leukocytosis and lymphadenopathy.
 Sensitivity and soft tissue swelling of the affected area.
 Radiograph shows a ill-defined radiolucency.
 Acute osteomyelitis
 suppurative inflammation in marrow spaces  compression of blood
vessels  bone necrosis  sequestrum
  subperiostal area  perforation  fistulas to skin and oral mucosa

 complications: fracture
 chronic osteomyelitis
 Histopathology

 Submitted section for biopsy predominantly consists of necrotic bone

and is diagnosed as sequestrum.
 Necrotic bone shows loss of osteocytes leading to emptying lacunae.
 Peripheral resorption and bacterial colonisation.
 Abundant PMNL cells in haversian canals and peripheral bone

Treatment :drainage and antibiotics.

PHOTOMICROGRAPH OF BONE SEQUESTRUM
Chronic Osteomyelitis
 Exists when defensive response leads to formation of granulation
tissue which subsequently forms dense scar tissue in an attempt to
wall off the infection.
 The encircled dead space acts as a reservoir for microbes hence
antibiotics do not reach the site leading to severe infection.
 Ifacute does not resolve then chronic occurs or may be “de novo”
 Swelling pain and sinus formation.
 Tooth loss or pathological fractures
 Acute exacerbations or remissions seen
Radiological features
 Patchy ragged and ill defined radiolucency which contain central
radiopaque sequestra
 Chronic suppurative osteomyelitis –MOTHEATEN appearance
 Subperiosteal new bone formation leads to—ONION PEEL
appearance.
Histopathology
 Chronically inflamed fibrous tissue
 Scattered sequestra and abscess formation
 Empty lacunae with resorption bays
 Chronic inflammatory cells

Treatment : IV antibiotics
Chronic diffuse sclerosing osteomyelitis
 Seen in adults, mandible
 Increased radiopacity develops around the sites of chronic infection
 Restricted to a single site but may be multifocal
 Pain and swelling are not typical
Pathogenesis
 Bacteria spread through cancellous bone with preforation of cortex
 At this site the periosteum is elevated from cortical surface with
localised deposition of periosteal new bone
Diagnosis and treatment
 For a definitive should diagnosis, microbial culture should be
positive and antibiotics given should be appropriate

 Treatment – antibiotics – patient should be kept under observation

Chronic focal sclerosing osteomyelitis (condensing
osteitis)
 Localised areas of bone sclerosis associated with apices of teeth with
pulpitis – from large carious lesions or pulpal necrosis
 Seen in children and young adults
 Classically, localised area of increased radiopacity – adjacent to root
apex of a tooth with thickened PDL space
Panoramic radiograph showing an apical Panoramic radiograph showing two COLs at
and interradiculer COL at right right mandibular second premolar and left
mandibular first molar mandibular first molar

Altun O, Dedeoğlu N, Umar E, Yolcu Ü, Acar AH. Condensing osteitis lesions in Eastern Anatolian Turkish population. Oral Surg Oral Med
Oral Radiol. 2014 May;2(2):17-20.
Treatment
 Endodontic treatment or extraction of the involved tooth
Garre’s osteomyelitis
 Unique type of osteomyelitis
 Caused by less virulent bacteria
 Radiographically, localised thickening of periosteum and deposition of laminated
subperiosteal bone
 Garre’s osteomyelitis is a well-documented pathologic entity in the dental literature.
 Because the majority of the reported cases are sequel to an odontogenic infection due to
caries, the disease is most often associated with a deep carious lesion and peirapical
pathology
Etiology
1. Dental caries
2. Secondary to periodontal infection
3. Fractures

4. Malignant tumors
Clinical features
 Seen in younger individuals
 Hard swelling, generally affecting the mandible
 Radiographically, radiopacity with occasional radiolucency
 Cortex is thickened with new bone formation
 Periosteum shows development of several rows of reactive vital bone
parallel to each other
Histopathology
 Lesional tissue shows formation of highly dense connective tissue –
occupying bone marrow
 Reactive woven bone formation seen in parallel rows
 No sequestration
 Less inflammatory cells
Histolopathology of the biopsied tissue reveals reactive bone
formation together with findings of chronic inflammation .
Treatment
 Endodontic treatment or extraction of the involved tooth
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