Cyst

Periapical Abscess
(Dento-Alveolar abscess, Alveolar Abscess)

An abscess is a collection of pus that has built up within the tissue of the body.
 Acute or chronic suppurative process of the dental periapical region.
 Developed from acute periodontitis / periapical granuloma.
 Acute exacerbation of chronic lesion → Phoenix Abscess
Etiology:
 Traumatic injury
 pulp necrosis
 irritation of periapical tissues
Clinical freatures:
 Common findings of inflammation:heat, redness, swelling and pain
 Tenderness of tooth (relives after pressure application)
 Extreme painful tooth extrude from socket
 Systemic manifestations like lymphadenitis & fever may present when confined to
periapical region
 Rapid extension to adjacent bone marrow spaces produces acute osteomyelitis or
dentoalveolar abscess.
Radiographic features:
 Slight thickening of PDL space
 Radiolucent area at apex of root.
Treatment:
 Drainage of abscess by opening pulp chamber or extraction
 Root canal treatment
If untreated, causes osteomyelitis, cellulites & bacteremia & formation of fistulous tract
opening to oral mucosa.
Acute exacerbation of a chronic lesion / Phoenix abscess

An acute inflammatory reaction superimposed on an existing chronic lesion such as a
cyst or granuloma
Etiology
 Periradicular disease
 (Flair-up)Bacteria released from root canals during instrumentation may trigger
acute response
Symptoms:
 At onset, tooth is tender to touch
 As inflammation progresses tooth may be elevated in its socket and may become
sensitive.
 Mucosa appears red and swollen over the radicular area
Diagnosis:
 Common findings of inflammation:heat, redness, swelling and pain
 Most commonly associated with the initiation of RCT
 History of trauma
 Well-defined periradicular lesion
Treatment:
 Drainage and debriment
 Root Canal Treatment
Chronic Apical Periodontitis

(Periapical Granuloma)
 A growth of granulomatous tissue continuous with the Periodontal ligament due to
the pulp death and the diffusion of bacterial toxins from the root canals into
surrounding periradicular tissue through the apical and lateral canals
 Low- grade infection
 Most common sequelae of pulpitis or apical periodontitis.
 If acute (exudative) left untreated → chronic (proliferative).
 Term is not accurate since it doesn’t shows true granulomatous inflammation
microscopically.
 Presence of lateral or accessory root canals opening
on the lateral surface of the root give rise to
lateral granuloma
Etiology
 Pulp death
 Irritation of the periapical tissue which stimulates a productive cellular response
Clinical features:
 Non vital tooth
 slightly tender on percussion.
 Mild pain on chewing
 Slightly socket enlargement
 Sensitivity is due to hyperemia, edema and inflammation of PDL. In many cases,
asymptomatic.
 Fully developed granuloma
 No perforation of bone and oral mucosa forming fistulous tract unless undergoes
acute exacerbation.
 Thickening of PDL at root apex.
 As bone resorption and proliferation of granulation tissue appears to be radiolucent
area.
 Thin radiopaque line /zone of sclerotic bone outlining lesion
 Root resorption ( long standing lesions)
Treatment:
 Extraction
 RCT with / without apicoetomy
If untreated → apical periodontal cyst formation.

Radicular cyst/ Periapical cyst/apical periodontal cyst/root end cyst or
dental cyst
 Most common inflammatory and
odontogenic cysts
 Arises from the epithelial residues in
the periodontal ligament as a result of
periapical periodontitis following pulp
necrosis
Periapical Cyst:
Radicular cyst that is present at root apex
Lateral Radicular Cyst:
Radicular cyst that is present at the opening of lateral accessory root canals
Residual Cyst:
Radicular cyst that remains even after extraction of offending tooth
Etiology:
 Infection leads to pulp necrosis
 Inflammation stimulates the epithelial rests of melassez(in apical periodontal
ligament) which results in periapical granuloma formation(infected/sterile) then
epithelium undegoes necrosis(lack of blood supply) then cyst is developed
Bay Cyst:
Island of squamous epithelium which have developed from the odontogenic rests of
Malassez can also be found in a periapical granuloma without cystic transformation.
Pathogenesis:
It’s consists of three phases:
1. Initiation
2. Cyst formation
3. Enlargement
 The phase of initiation

Epithelial linings of this cyst is derived from the epithelial cell rests of Malassez in
the periodontal ligament.
Epithelium may also be derived from:
1. Respiratory epithelium of the maxillary sinus
2. Oral epithelium growing in through a fistulous tract
3. Oral epithelium proliferating apically from a periodontal pocket or bifurcation
or trifurcation involvement by periodontal disease also with apical
proliferation.
 Phase of cyst formation (2 concepts)
1. Epithelium proliferates and covers the bare connective tissue surface of an
abscess cavity or a cavity which may occur as a result of connective tissue
breakdown by proteolytic enzyme activity.
2. More widely supported theory→ cyst cavity forms within a proliferating
epithelial mass in an apical granuloma by degeneration and death of cells in
the centre
The proliferating epithelial masses show considerable intercellular oedema.
These intercellular accumulations of fluid coalesce to form microcysts
containing epithelial and inflammatory cells.
 Growth and enlargement of the radicular cyst
1. According to Toller:
osmosis is responsible for size increasing
Lytic products of the epithelial and inflammatory cells in the cyst cavity provided
the greater numbers of smaller molecules which raised the osmotic pressure of the
cyst fluid.
2. According to Harris and Toller (1975):
Epithelial proliferation continues as long as there is inflammation
3. According to Harris and Goldhaber (1973):
Cyst growth must accompanied by degradation of adjacent connective tissues
and bone resorption.
The synthesis of prostaglandins, their bone resorbing capacity and their
possible role in the enlargement of jaw cysts. (Harris et al 1973)
Collagenases also contribute to breakdown of the connective tissues and
collagenolytic activity→ Expansion
Clinical features:
 Peak in 3rd, 4th and 5th decade
 More in males
 Most common cystic lesion of jaws
 Primarily symptomless
 Diagnostic criteria(non vital tooth)
 Rare in deciduous teeth.
 At first the enlargement is bony hard but as the cyst increases in size, the covering
bone becomes very thin despite subperiosteal bone deposition and the swelling
then exhibits ‘egg shell crackling’
 Occasionally, a sinus may lead from the cyst cavity to the oral mucosa.
 Round / ovoid well- defined radiolucency with sclerotic borders and associated
with pulpally affected tooth.
 Rarely induce resorption of affected teeth
 The outer cortical plates of the maxilla or mandible may expand in a curved or
circular shape
 Cysts may displace the affected tooth or themandibular alveolar nerve canal in an
inferior direction.
Treatment:
 Extraction of the involved tooth + Curettage of the periapical tissue.
 Root canal treatment + Apicocectomy.
https://www.slideshare.net/DRKALPAJYOTI/pulp-and-periapical-lesions-of-the-tooth-
ppt
https://www.slideshare.net/ashokkangeyam/periapical-diseases
https://pocketdentistry.com/21-cysts/

Cyst

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Periapical Abscess

(Dento-Alveolar abscess, Alveolar Abscess)

Acute exacerbation of a chronic lesion / Phoenix abscess

Chronic Apical Periodontitis

 The phase of initiation

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