ABSCESS OF

THE
PERIODONTIUM
 Contents
 Introduction
 Classification
 Periodontal abscess
 Etiology
 Pathogenesisand histopathology
 Microbiology
 Diagnosis

 Treatment

 Complications and postoperative care.

 Gingival abscess
 Pericoronal abscess
 Conclusion
INTRODUCTION

 Abscess- Localised collection of pus purulent

material collected in a cavity caused by
destruction of tissues.
 Classified primarily, based on their anatomical
locations in the periodontal tissue. There are three
types:
 Gingival abscess
 Pericoronal abscess
 Periodontal abscess.
 The periodontal abscess is the most important one,
which often represents the chronic and refractory
form of the disease.

 It is a destructive process occurring in the

periodontium, resulting in localized collections of
pus, communicating with the oral cavity through
the gingival sulcus or other periodontal sites and
not arising from the tooth pulp
CLASSIFICATION
I. Depending on the location of the abscess
Gingival Abscess-- localized painful swelling affecting only the
marginal and interdental gingiva
Mainly due to impaction of foreign objects
May be present on a previously healthy gingiva
Periodontal Abscess – with similar symptoms, usually affect deeper
periodontal structures, including deep pockets, furcations and
vertical osseous defects.
Usually located beyond Mucogingival junction.
II. Depending on the course of the lesion
 Acute periodontal abscess.
• Presents with symptoms like pain, tenderness,
sensitivity to palpation and suppuration upon gentle
pressure.
 Chronic periodontal abscess.
• Normally associated with a sinus tract.
• Usually asymptomatic, can refer mild symptoms
III. According to periodontal tissue affected

 Gingival abscess - in previously healthy sites and

caused by impaction of foreign bodies.
 Periodontal abscess – either acute or chronic
developing into a periodontal pocket.
 Pericoronal abscess – in incompletely erupted
teeth.
IV Depending on the cause of acute infectious process

Periodontitis related abscess: - when the acute infection

originates from biofilm present in a deepened periodontal
pocket.
Non-periodontitis related abscess: - when the acute infection
originates from other local source, such as foreign body
impaction or alteration in root integrity.
Periodontal Abscess
DEFINITION
 A periodontal abscess is a localized purulent infection in the
periodontal tissue

(GLICKMAN)

 A localized purulent inflammation of the periodontal tissues.

It is also known as Lateral periodontal abscess or Parietal
Abscess.

(AAP GLOSSARY 1992)

PREVALENCE
 3rd most prevalent emergency infection, after acute alveolar
(14-25%) and periodontitis (10-11%).

 More likely to occur in a pre-existing periodontal pocket.

 More in molar sites (> 50%)

ETIOLOGY
 Periodontal abscesses have been either directly
associated to periodontitis or to sites without the prior
existence of a periodontal pocket.

1. Periodontal abscesses in periodontitis

(Periodontitis – Related Abscess)
 In periodontitis, a periodontal abscess represents a period
of active bone destruction (exacerbation).
 The existence of tortuous pockets, which eventually
become isolated, may favor the formation of abscesses .
The development of a periodontal abscess in periodontitis
may occur at different stages during the course of the
infection:
As an acute exacerbation of an untreated
periodontitis
During periodontal therapy
In refractory periodontitis or
During periodontal maintenance
Different mechanisms behind formation are
A. Exacerbation of chronic lesions:
Occur without any obvious external influences.

B. Post therapy periodontal abscess

 Post scaling periodontal abscess –occur immediately
after scaling or routine prophylaxis.
 due to inadequate scaling which will allow calculus to
remain in the deepest pocket area,
 Post-surgery periodontal abscess.
 Incomplete removal of sub-gingival calculus or the presence
of foreign substance. Ex-sutures, regenerative devices or
periodontal pack.
 Post-antibiotic periodontal abscess.
 Treatment with systemic antibiotics without subgingival
debridement in patients with advanced periodontitis may
also cause abscess formation.
 It is attributed to a likely change in the composition of
subgingival microbiota, leading to a super infection and
massive inflammation.
2. Periodontal abscesses in the absence of Periodontitis
 Impaction of foreign bodies. Periodontal abscesses
caused by foreign bodies, related with oral hygiene
aids, have been named "oral hygiene abscesses”.
 Perforation of the tooth wall by an endodontic
instrument
 Infection of lateral cysts.
 Local factors affecting the morphology of the root may
predispose to periodontal abscess formation
PATHOGENESIS
HISTOPATHOLOGY

 Intact Neutrophils are found surrounding a central area of soft tissue

debris and destroyed leukocytes.

 At a later stage a pyogenic membrane, composed of macrophages

and neutrophils is organized.

 The rate of destruction in the abscess will depend on the growth of

bacteria and its virulence as well as the local pH, since an acidic

environment will favor the activity of lysosomal enzymes

De Witt et al. (1985) studied biopsy punches taken from
12 abscesses. They observed, from the outside to the
inside:
(a) A normal oral epithelium and lamina propria;
(b) An acute inflammatory infiltrate;
(c) An intense foci of inflammation (neutrophil-
lymphocyte) with the surrounding connective tissue
destroyed and necrotic;
(d) A destroyed and ulcerated pocket epithelium;
(e) A central region, as a mass of granular, acidophilic,
and amorphous debris.
MICROBIOLOGY
 The most frequent type of bacteria were gram-negative
anaerobic rods and gram-positive facultative cocci. In
general, gram-negatives predominated over gram-positives
and rods over cocci.
Bacterial species with capacity of producing proteinases, such
as P. intermedia are important, since they may increase the
availability of nutrients, and thereby, increasing the number of
bacteria inside the abscess.
Culture studies of periodontal abscesses have revealed high
prevalence's of
 Porphyromonas gingivalis (55-100%),
 Prevotella intermedia (25-100%), and
 Fusobacterium nucleatum (44-65%)
Other pathogens which have been reported are
 Actinobacillus actinomycetemcomitans (25%)
 Campylobacter Rectus (80%)
 Prevotella Melaninogenica (22%)
Clinical Features
 Smooth, shiny swelling of the gingiva
 Painful, tender to palpation
 Purulent exudate
 Increased probing depth
 Mobile and/or percussion sensitive
 Tooth usually vital
DIAGNOSIS
Diagnosis should be based on
 Patients chief complaint
 Clinical signs and symptoms
 Additional information can be obtained through a careful medical
and dental history, and radiographic examination.
 Symptoms range from light discomfort to severe pain, tenderness
of the gingiva, swelling, tooth mobility, tooth elevation, sensitivity
of the tooth to palpation
 Another common finding is suppuration, either spontaneous or
after pressure on the abscess combined with rapid tissue
destruction and deep pocket formation.
 The radiographic examination may reveal a normal appearance,
or some degree of bone loss, ranging from a widening of the
periodontal space to a dramatic radiographic bone loss.
 Systemic involvement has been reported in some severe cases,
including fever, malaise, leukocytosis and regional
lymphadenopathy.
Van Winkelhoff et al (1985) established 4 diagnostic criteria
 Association of pocket of >/= 6 mm,
 Presence of bleeding on probing,
 Evidence of radiographic bone loss &
 Absence of periapical lesion.
DIFFERENTIAL DIAGNOSIS
 Gingival abscess
 Periapical abscess
 Lateral periodontal cyst
 Pericoronitis
 Vertical root fracture
 Osteomyelitis
 Eosinophilic granuloma
Periodontal abscess Gingival abscess

Involves supporting periodontal Confined to marginal and / or

structure interdental gingiva.

Often occurs in the course of Occurs in previously disease free

chronic destructive periodontitis areas.

X-ray- bone loss present Acute inflammatory response to

forcing of foreign material into the
gingiva. No bone loss

Pocket present No pockets

Periodontal abscess Gingival abscess

Pain – diffuse. Pain – dull

May affect the entire side of the localized.

face.

Affected by thermal changes Not affected by thermal changes.

Periodontal cyst (non-infected)

No inflammatory signs

More common in mandibular canine – premolar region
On radiograph well defined oval radiolucency on the lateral
surface of the root, with chronic border, < 1 cm in diameter.
Microscopically thin, non-keratinized stratified squamous
epithelia with focal epithelial thickening.
Inflammatory cells seen if secondarily infected.
Treatment – Enucleation.
 Pericoronitis
 Usually seen in incompletely erupted tooth
 Commonly associated with mandibular 3rd molar.

 Osteomyelitis
 Rapid diffuse bone destruction may occur with in a few days
 Deeper pain being only symptom.
 Radiograph – indistinct trabecular and disappearance of lamina
dura
 As infections increases, lymphadenopathy, fever and malaise
are more common.
 Eosinophilic granuloma
 Diagnosed by the rapid bone destruction after periodontal
therapy
 Biopsy.
 Vertical root fracture
 Loupes or operating microscopes assist in visualization of
cracks/fractures
 The bite test, Transillumination with fiber optic light and use
of dyes helps in detecting the suspected fracture
TREATMENT
Treatment of acute periodontal abscess usually involves two
stages
 Management of the acute lesion.
 The appropriate treatment of the original and / or residual
lesion, once the acute situations has been controlled.
The purpose of treatment of acute periodontal abscess is
 Alleviate pain,
 Control the spread of infection, and
 To establish drainage.
Protocol recommended.
 Incision and drainage (closed or open approach)
 Scaling and Root planning
 Compression and debridement of soft tissue wall.
 Use of different systemically administered antibiotics
 Periodontal surgery
 Tooth extraction.
Antibiotic administration
 Metronidazole – 200 mg, tid, 5 days –Smith and
Davies(1986)
 Tetracycline – 1 gm / day – 2weeks -Hafstrom(1994)
 Azithromycin, 500mg, OD, 3 days – Herrera D
 Amoxicillin + Clavulanate, 500 + 125 mg, tid, 8days -
Herrera D
allergy
Chronic periodontal Abscess
Surgical therapy
 Gingivectomy
 Flap procedures
COMPLICATIONS
 Tooth Loss
 Bacteraemia related with an untreated abscess
 Sickle cell crisis in patient with sickle cell anemia:
Gingival Abscess
Alocalized purulent infection that involves the
marginal gingiva or interdental papilla
 Etiology
 Acute inflammatory response to foreign substances
forced into the gingiva
 Clinical Features
 Localized swelling of marginal gingiva or papilla
 A red, smooth, shiny surface
 May be painful and appear pointed
 Purulent exudate may be present
 No previous periodontal disease
For the treatment of Gingival Abscess, the protocol should
include the following:
 Elimination of the foreign object, through careful
debridement (Abrams 1983)
 Drainage through the sulcus with a probe or light scaling,
 Rinsing with warm saline and follow-up after 24-48 hours
Pericoronal Abscess
 A localized purulent infection within the tissue surrounding
the crown of a partially erupted tooth.
 Most common adjacent to mandibular third molars in young
adults; usually caused by impaction of debris under the soft
tissue flap
Pericoronal Abscess
 Clinical Features

• Operculum (soft tissue flap)

• Localized red, swollen tissue
• Area painful to touch
• Tissue trauma from opposing tooth common
• Purulent exudate, trismus, lymphadenopathy,
fever, and malaise may be present
 Treatment Options

• Debride/irrigate under pericoronal flap

• Tissue recontouring (removing tissue flap)
• Extraction of involved and/or opposing tooth
• Antimicrobials (local and/or systemic as needed)
• Culture and sensitivity
• Follow-up
Treatment
 The acute pericoronal abscess is properly
anaesthetized
 Drainage is established –lifting the soft
tissue operculum with periodontal probe or
currette
 If the underlying debris is accessible, It
must be removed-followed gentle irrigation
 Systemic antibiotics are given-
swelling,regional lymphadenopathy.
 The patient is then instructed to rinse with
warm water for every 2 hours and reassesed
for 24 hours.
 Analgesics also prescribed-discomfort.
CONCLUSION
 Proper management depends on thorough
knowledge of the proper etiology and ability of
clinician to identify the same…
 Proper treatment protocols to be followed to
establish proper drainage and to maintain…