periodontal abscess

1. ABSCESS OFTHE
PERIODONTIUM

2. CONTENTS
 Introduction
 Abscess of the periodontium
 Periodontal abscess
 O Definition
 O Prevalence
 O Classification
 O Etiology
 O Clinical features

3. O Pathogenesis and histopathology
O Microbiology
O Diagnosis
O Differential Diagnosis
O Treatment
O Complications and postoperative care.
 Gingival abscess
 Pericoronal abscess
 Conclusion
 References

4. INTRODUCTION
 Abscess- Localised collection of pus purulent material
collected in a cavity caused by destruction of tissues. (GPT)
 Abscesses of the periodontium have been classified primarily,
based on their anatomical locations in the periodontal tissue.
There are three types:
 O Gingival abscess
 O Pericoronal abscess
 O Periodontal abscess.

5. The abscesses of the periodontium, the
periodontal abscess is the most important one, which
often represents the chronic and refractory form of the
disease.
O 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

7. Periodontal Abscess
O A localized purulent infection within the tissues
adjacent to the periodontal pocket that may lead to the
destruction of periodontal ligament and alveolar bone

8. O An acute, destructive process in the periodontium
resulting in localized collection of pus communicating
with the oral cavity through the gingival sulcus or other
periodontal sites & not arising from the tooth pulp.
(RANNY 1977)

10. CLASSIFICATION
I) Depending on the location of the abscess
(Gillette and Van House-1980, AhI et al
1986)

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.

11. 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

12. III. Depending on the number
(Topell et al 1990)
 Single periodontal abscess – related to local factors,
which contribute to the closure of the drainage of a
periodontal pocket.
 Multiple periodontal abscess
O Seen in uncontrolled diabetes mellitus,
O medically compromised patients,
O in patients with untreated periodontitis after systemic
antibiotic therapy for non-oral reasons .

13. IV. 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.




14. V.
Depending on the cause of
acute infectious process


(Lindhe)
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.

15. VI. Based on
location of abscess
 Abscess in the supporting periodontal tissues along
the lateral aspect of the root, sinus tract present.
 Abscess in the soft tissue wall of a deep periodontal
pocket.

16. ETIOLOGY
O Periodontal abscesses have been either directly
associated to periodontitis or to sites without the
prior existence of a periodontal pocket.
O
O
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, with cul-de-sac,
which eventually become isolated, may favor the
formation of abscesses .

17. O The marginal closure of a periodontal pocket, may lead
to an extension of the infection into the surrounding
periodontal tissues due to the pressure of the
suppuration inside the closed pocket.
O The fibrin secretions leading to the local accumulation
of pus may favor the closure of the gingival margin to
the tooth surface.
O Changes in the composition of the microflora, bacterial
virulence, or in host defenses (Kareha et al. 1981)
could also make the pocket lumen inefficient to drain
the increased suppuration.

18. O The development of a periodontal abscess in
periodontitis may occur at different stages during the
course of the infection:
O As an acute exacerbation of an untreated periodontitis
(Dello Russo 1985)
O During periodontal therapy (Dello Russo 1985,
Carranza 1990)
O In refractory periodontitis (Fine 1994) or
O During periodontal maintenance (Chace & Low 1993,
McLeod et al. 1997)

19. Different mechanisms
behind formation are
Occur without any obvious external influences.
B. Post therapy periodontal abscess

O
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,

20. O while the resolution of the inflammation at the coronal
pocket area will occlude the normal drainage and then
cause the abscess formation.
O When the periodontal abscess occurs immediately after
scaling or after a routine prophylaxis, it has been related
to the dislodging of calculus fragments, which can be
pushed into the tissues.

21.  Post-surgery periodontalabscess.
O Incomplete removal of sub gingival calculus or the
presence of foreign substance. Ex-sutures, regenerative
devices or periodontal pack.
O clinical study on guided tissue regeneration reported
that 10 out of 80 controls (non-resorbable barrier) and 4
out of 82 tests (bio-absorbable barrier) showed abscess
formation or suppuration at the treated sites.
(Garrett et al 1997)

22.  Post-antibiotic periodontalabscess.
O Treatment with systemic antibiotics without subgingival
debridement in patients with advanced periodontitis
may also cause abscess formation.
O It is Attributed to a likely change in the composition of
subgingival microbiota, leading to a super infection and
massive inflammation.

23. O Topell et al (1990) reported on the
development of multiple abscess (4-10) in 10
untreated periodontal patients who received
systemic antibiotic therapy. (Penicillin,
tetracycline) for non-oral infections.
O Helovuo et al. (1993) studied 72 patients with untreated
periodontitis, who were followed for 12 weeks, after
intake of systemic antibiotics for non-oral reasons.
Patients were divided into 3 groups according to the
antibiotic used,

24. O 10 out of 24 patients (42%) in the penicillin group
developed abscesses within the next 4 weeks.
O The number of abscesses ranged between 1-10. No
abscesses were detected in the erythromycin or the
control groups.
O Koller-Benz et al. (1992) showed that after initiation of
nifedipine therapy, 8 abscesses appeared in 5 days.
O The nifedipine therapy was discontinued, and the
abscesses resolved. 3 weeks later the treatment was
resumed, and after 2 weeks another abscess was
detected.

25. 2. Periodontal abscesses in the
absence of Periodontitis
O
O
O
O
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 (Carranza 1990)
Infection of lateral cysts (Kareha et al. 1981)
Local factors affecting the morphology of the root
may predispose to periodontal abscess formation

26. PATHOGENESIS AND
HISTOPATHOLOGY
O The entry of bacteria into the soft tissue pocket wall
could be the first event to initiate the periodontal
abscess.
O Inflammatory cells are then attracted by chemotactic
factors released by the bacteria, and
O The concomitant inflammatory reaction leads to
destruction of the connective tissues, the encapsulation
of the bacterial infection and the production of pus.

27. O Histologically, the intact Neutrophils are found
surrounding a central area of soft tissue debris and
destroyed leukocytes.
O At a later stage a pyogenic membrane, composed of
macrophages and neutrophils is organized.
O 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 favour the activity
of lysosomal enzymes

30. MICROBIOLOGY
O 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.
O The periodontal abscess microbiota is usually
indistinguishable from the microflora found in the
subgingival plaque in adult periodontitis.
O The microflora from abscesses and deep pockets was
similar and harbored higher proportions of pathogens
when compared to the microflora of shallow pockets.

31. Microbiology






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%)

32. O 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

35. DIAGNOSIS
Diagnosis should be based on
O Patients chief complaint
O Clinical signs and symptoms
O Additional information can be obtained through a
careful medical and dental history, and radiographic
examination.
O Symptoms range from light discomfort to severe pain,
tenderness of the gingiva, swelling, tooth mobility,
tooth elevation, sensitivity of the tooth to palpation

36. O Another common finding is suppuration, either
spontaneous or after pressure on the abscess combined
with rapid tissue destruction and deep pocket formation.
O 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.
O Systemic involvement has been reported in some severe
cases, including fever, malaise, leukocytosis and
regional lymphadenopathy.

37. O Other recommended additional diagnostic tools: include
the use of Dark-Field Microscopical examination of
the abscess microflora in order to exclude an
endodontic origin, due to the higher percentage of
spirochetes in periodontal abscesses.
O Positron Emission Tomography and a Fluorine-18-
Fluoromisonidazole marker for detection of
periodontal abscesses and other anaerobic infections in
the mouth. Results from the clinical study showed that
100% of periodontal abscesses were found with this
procedure.

38. Periodontal abscess
Gingival
abscess
Involves supporting periodontal
structure
Often occurs in the course of
chronic destructive periodontitis
X-ray- bone loss present
Confined to marginal and / or
interdental gingiva.
Occurs in previously disease free
areas.
Acute inflammatory response to
forcing of foreign material into the
gingiva. No bone lossPocket present No pockets

39. Periodontal abscess
Gingival
abscess
localized.
Pain – diffuse.
May affect the entire side of the
face.
Affected by thermal changes Not affected by thermal changes.

40. Periodontal abscess
Periapical
abscess
Associated with deep restoration,
caries or Tooth wear
Non-vital
Associated with preexisting
periodontal pockets, caries or
both.
Pulp test- vital.
Swelling generalized and located
around the involved tooth and
gingival margin, seldom with a
fistulous tract.
Swelling localized often with
fistulous tract opening in the
apical area.

41. Periodontal abscess Periapical abscess
Pain - severe, throbbing, last for
long, deep, unable to locate the
offending tooth
Severe than periodontal abscess.
Pain – dull, constant, less severe,
localized and patient usually can
locate the offending tooth
Pain associated with the
movement or percussion is not as
severe as with a pulpal disease
Lateral radiolucency
Apical radiolucency

42. Periodontal abscess Periapical abscess
Angular bone defects,
Furcation involvement
Endodontic filling or
Endodontic or post perforations
Responds dramatically well to
sub gingival debridement.
Responds poorly or not at all to
periodontal therapeutic
interventions

43. TREATMENT
Treatment of acute periodontal abscess usually
involves two stages
O Management of the acute lesion.
O 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
O Alleviate pain,
O Control the spread of infection, and
O To establish drainage.

44. O Incision and drainage (closed or open approach)
O Scaling and Root planning
O Compression and debridement of soft tissue wall.
O Use of different systemically administered
antibiotics
O Tooth extraction.

45. Incision and
drainage
O Through the pocket (Closed approach)
O Incision from the outer surface (Open approach)
Closed approach
O Anesthesia
O Flat instrument /probe – carefully introduced into the
pocket.
O Distend the pocket wall for drainage.
O Further drain and gently curettage the mass of tissue
internally.

46. Open approach
O Vertical incision through the most fluctuant part of the
swelling, extending to an area just apical to the abscess.
O Curette the granulomatous tissue internally.
O External aspect of the abscess is gently pushed to drain
the remaining pus.
O Saline irrigation
O Approximate to wound margin
O No sutures required.

47. Antibiotic administration
O Metronidazole – 200 mg, tid, 5 days
O Azithromycin, 500mg, OD, 3 days.
O Amoxicillin + Clavulanate, 500 + 125 mg, tid, 8days.

49. Chronic periodontal Abscess
Surgical therapy
O Gingivectomy
O Flap procedures
O Mainly in abscess associated with deep vertical defects,
where the resolution of the abscess may only be
achieved by a surgical operation.
O Objective : To eliminate the remaining calculus and to
obtain drainage at the same time.

50. For the treatment of Gingival Abscess, the protocol
should include the following:
O Elimination of the foreign object, through careful
debridement (Abrams 1983)
O Drainage through the sulcus with a probe or light
scaling,
O Rinsing with warm saline and follow-up after 24-48
hours

51. COMPLICATIONS
 Tooth Loss
O Suggested as the main cause for extraction in the
maintenance phase.
O History of repeated abscess formation is considered as a
“hopeless” prognosis for the tooth.
O In a retrospective study, 45% of teeth with periodontal
abscesses in a maintenance population were extracted
(McLeod et al. 1997)

52.  Dissemination of theinfection
Two possibilities have been described:
I. The dissemination of the bacteria during therapy
(bacteraemia); or
II. Bacteraemia related with an untreated abscess.
The Dissemination of the bacteria during therapy
O Suzuki & Delisle (1984) related a case of pulmonary
actinomycosis due to a periodontal abscesses, which was
ultra-sonically scaled. it was suggested that during
treatment, Actinomyces sp. from the subgingival
microflora had passed to the lungs.

53. O Gallaguer et al. (1981) described a healthy patient with
a periodontal abscess who was treated with drainage
and curettage, but without systemic antibiotic.
O 2 weeks later a brain abscess was diagnosed,
Microbiology of the lesions demonstrated, among other
bacteria, Bacteroides melaninogenicus and other
bacteroides, species.

54. II.Bacteraemia related with an untreated abscess.
O Cellulitis in breast cancer patients has been claimed to
follow gingivitis or an abscess (Manian 1997)
O due to transient bacteraemia and reduced host defenses
(radiation therapy and axillary dissection). The breast
and the upper extremities are particularly susceptible to
infections of oral origin (Manian 1997)
O periodontal abscess is also associated with the
development of a cervical necrotizing fascitis. it is
frequently associated with oropharyngeal infections.

55. Gingival Abscess
O A localized purulent infection that involves the
marginal gingiva or interdental papilla

56. Gingival Abscess

57. O Etiology
O Acute inflammatory response to foreign substances
forced into the gingiva
O Clinical Features
O Localized swelling of marginal gingiva or papilla
O A red, smooth, shiny surface
O May be painful and appear pointed
O Purulent exudate may be present
O No previous periodontal disease

58. O Treatment
O Elimination of foreign object
O Drainage through sulcus with probe or light scaling
O Follow-up after 24-48 hours

59. Pericoronal
Abscess
O A localized purulent infection within the tissue
surrounding the crown of a partially erupted tooth.
O Most common adjacent to mandibular third molars in
young adults; usually caused by impaction of debris
under the soft tissue flap

60. Pericoronal
Abscess

61. O 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

62. O 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

63. O The treatment of pericoronal abscess is aimed at
 Managemant of acute abcess,followed by
 Resolution of the chronic condition.

64. O The acute pericoronal abscess is properly anaesthetized
O Drinage is established –lifting the soft tissue operculum
with periodontal probe or currette
O If the underlying debris is accessible, It must be
removed-followed gentle irrigation

65. O Systemic antibiotics are given- swelling,regional
lymphadenopathy.
O The patient is then instructed to rinse with warm water
for every 2 hours and reassesed for 24 hours.
O Analgesics also prescribed-discomfort.

66. O Acute phase has been controlled, the partially erupted
teeth may be definitely treated with ;
O Surgical excision of the overlying gingiva
O Removal of the offending tooth.