The document discusses acute periodontal infections including abscesses, pericoronitis, and herpetic gingivostomatitis. It describes the clinical features, causes, microbiology, diagnosis and treatment of each condition. Abscesses are classified as gingival, periodontal or pericoronal depending on their location. Pericoronitis is inflammation around an unerupted tooth, usually due to food debris trapped under the gums. Herpetic gingivostomatitis is caused by the herpes simplex virus and presents as diffuse gingival swelling and vesicles that rupture, leaving painful ulcers. Prompt diagnosis and treatment including drainage, debridement and antibiotics are important to resolve the infections

2. Introduction
 Acute infections are of sudden onset,
limited duration & with well defined
features in contrast with chronic
lesions.
 Associated with Pain.
 Early diagnosis & prompt treatment is
necessary to prevent rapid destructions of
periodontal tissues.

3. Acute Periodontal Infections
 Abscess in the Periodontium
 Pericoronitis
 Herpetic gingivostomatitis
 Bacterial acute infections ( e.g. Streptococcal
gingivostomatitis, Gonococcal stomatitis )
 NUG

4.  An abscess is a cavity containing pus and
surrounded by inflamed tissue, formed as a
result of a localized infection.
 Periodontal abscess : 8-14% among all
dental emergency condition
- ( Ahl et al 1986, Galego-Feal et al, 1996)

5.  Classification proposed by Meng (1999),
which was included in the revised
classification system of periodontal
diseases, developed by AAP-
International Workshop for a
Classification of Periodontal Diseases
and Conditions (1999):
 Gingival abscess
 Periodontal abscess
 Pericoronal abscess

6.  Gingival abscess : A localized, painful, rapidly
expanding lesion involving the marginal gingiva or
interdental papilla, sometimes in a previously
disease-free area.
 Periodontal abscess : A localized accumulation of
pus within the gingival wall of a periodontal pocket
resulting in the destruction of the collagen fibre
attachment and the loss of nearby alveolar bone.
 Pericoronal abscess : Localized accumulation of
pus within the overlying gingival flap surrounding the
crown of an incompletely erupted tooth.

7. Gingival Abscess:
Etiology:
Acute inflammatory response to foreign substances forced
into the gingiva
Impaction of foreign bodies (such as a piece of dental floss,
a popcorn kernel, a piece of a toothpick, fishbone.
Clinical Features:
 Localized swelling involving marginal gingiva or
interdental papilla
 A red, smooth, shiny surface
 May be painful and appear pointed
 Purulent exudate may be present
 No previous periodontal disease

8. Treatment
 Treatment of gingival abscess is aimed at
reversal of the acute phase and removal
of the cause.
1. Topical or local anaesthesia by infiltration
is administered.
2. When possible, SRP to establish
drainage and remove microbial deposits.
3. In acute cases, the fluctuant area is
incised with a #15 scalpel blade and
exudate may be expressed by gentle
digital pressure.

9. 4. Any foreign material is removed.
5. The area is irrigated with warm saline water and covered with
moist gauze under light pressure.
6. Once bleeding has stopped, patient is dismissed with
instructions to rinse with warm saline water every 2 hrs.
7. After 24 hrs, the area is reassessed, and if resolution is
sufficient, scaling not previously completed is undertaken.
8. If the lesion is large or poorly accessible, surgical access
may be required.

10. Periodontal Abscess

11. Periodontal Abscess
- also known as a lateral abscess or parietal
abscess.
Definition: ‘A lesion with an expressed periodontal breakdown occurring
during a limited period of time, and with easily detectable clinical symptoms,
including a localized accumulation of pus located within the gingival wall of
the periodontal pocket’
- Herrera D, J Clin Periodontol 2000
 Etiology based Classification:
 Periodontitis related abscess: acute infections due to
bacteria present at the subgingival biofilm in a deepened
periodontal pocket
 Non-periodontitis related abscess: foreign body impaction,
alteration in the root integrity leading to bacterial
colonisation

12.  Course of the lesion :
 Acute abscess : Pain, Tenderness, sensitivity to palpation and
suppuration.
 Chronic abscess : normally associated with a sinus tract and it is
usually asymptomatic or mild symptoms
 Acute Chronic
 Number of abscesses:
 Single periodontal abscess is usually associated with local factors,
which contribute to the closure of the drainage of a periodontal pocket.
 Multiple periodontal abscesses have been reported in uncontrolled
diabetes mellitus, in medically compromised patients and in patients
with untreated periodontitis after systemic antibiotic therapy for non-oral
reasons.

13.  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

14.  Pathogenic mechanisms related to abscess formation in the periodontium:
 A) Exacerbation of a chronic lesion: obstruction of a deepened pocket, mostly
in spiral tortuous pocket.
- An untreated periodontitis patient
- Recurrent infection during SPT
 B) Post-scaling Periodontal Abscess:
 Dello Russo 1985: Shrinkage of gingival tissue post-scaling – small fragment of remaining
calculus – obstructing the pocket entrance – abscess
 Small fragment of calculus – forced into deeper previously non-inflammed tissue
 C) Post-surgery periodontal abscess: Garrett et al 1997
Presence of fragments of suture or periodontal pack within the periodontal
tissue following the surgical procedure
 D) Post- antibiotic periodontal abscess: Helovuo et al 1989, Topoll et al 1990
Systemic antibiotic with out appropriate subgingival debridement - subgingival
biofilm protected from the action of the antibiotic – acute infection – abscess
E) Non-periodontitis related abscess formation:
- Foreign body : oral hygiene devices ( bristle of tooth brush, tooth pick fragments)
- Orthodontic appliances
- Food particles, nails
F) Anatomic Factors: Invaginated roots, presence of fissures, iartrogenic endodontic
perforations

15.  Microbiology of Periodontal abscess:
 Microbiota of periodontal abscesses is not different from the
microbiota of chronic periodontitis lesions.
 It is polymicrobial and dominated by nonmotile, gram-negative,
strictly anaerobic, rod-shaped species.
 Among these bacteria, P. gingivalis is probably the most virulent
and relevant microorganism
 Other strict anaerobes - Prevotella intermedia, Prevotella
melaninogenica, Fusobacterium nucleatum, Tannerella forsythia,
Treponema spp. Parvimonas micra, Actinomyces spp. and
Bifidobacterium spp.
 Facultative anaerobic gram-negative bacteria, Campylobacter
spp., Capnocytophaga spp. and Aggregatibacter
actinomycetemcomitans , as well as gram-negative enteric rods
.

16.  Diagnosis:
 Clinical feature
 Signs & Symptoms
 Clinical findings- deep periodontal pocket, BOP, Suppuration,
Mobility ( occasional)
 Radiology:
○ No R/F or just widened PDL spaces in acute cases
○ Evident bone loss, furcation involvement in acute exacerbation of
chronic cases
 Differential diagnosis:
 PA abscess, PA cyst, Endo – perio lesions
 Rare cases : Osteomyelitis in periodontitis patients,
SCC, Metastatic tumor of head – neck region, Pyogenic
granuloma

17.  Treatment
 A) Management of acute condition:
 Establish drainage – localised abscess
○ Via sulcus is the preferred method
○ Surgical access for debridement - Incision and
drainage
○ Removal of foreign body
○ Extraction : poor prognosis in SPT
 Local / Systemic Antibiotics – diffuse involvement
 B) Management of Residual lesion in CP patients

18. Antibiotic of choice:
 Herrera et al in 2000 - Amoxicillin + Clav. Acid ( 500 + 125 mg ) .
TDPC * 8 Days
And Azithromycin ( 500 mg * OD * 3 Days)
 Smith & Davies (1986) – Metronidazole ( 200 mg * TDPC * 5 Days)
 Hafstrom et al 1994 – Tetracycline therapy for 2 weeks
 Eguchi et al 2008 – Saline + 2% Minocycline hydrochloride ointment
 Antibiotics although showed reduction in pain, edema , suppuration.
Incision, Drainage and Debridement is always the First line of
treatment, unless there is diffuse involvement

19.  Complications:
 Tooth loss : Chace & Low – 1993 : Abscess – main
cause of extraction during SPT
 Dissemination of the infection :
 Suzuki & Delisle 1984 : Pulomonary actinomycosis
 Gallaguer et al 1981 : Brain abscess
 It has been suggested that the risk of bacteremia during
abscess drainage may be reduced if a needle aspirate of
the abscess contents is obtained before the procedure
- Flood TR et al, 1990, Roberts GJ et al 1990

20. Pericoronitis
 It was first described by GUNNELL in1844
 Corona means crown in latin. Pericoronitis - Inflammation of tissues surrounding the
crown of the tooth
 Definition:
 An inflammatory condition of the gingiva in relation to the crown of an incompletely
erupted tooth. (Carranza, 12th Edition)
 It is an inflammation of gingiva & contiguous tissues about crown of an incompletely
erupted tooth. (Orban)
C/F:
1. The partially erupted or impacted Mandibular third molar is the most common
site. Maxillary Third molar, Mandibular First, Second Molars are also affected.
2. The space between the crown of the tooth and operculum (i.e. overlying gingival
flap) harbours food debris and promotes bacterial growth due its relative
inaccessibility to the cleansing measures.
3. The operculum, even in patients without any symptoms is chronically inflamed
with ulcerations in the inner aspect
4. Acute inflammation is a constant possibility, which is exacerbated by the
factors like, trauma, occlusion from the opposing teeth or foreign body
impaction

21.  It is identified by varying degrees of inflammatory
involvement of the pericoronal flap & adjacent
structures as well as by systemic complications.
 The inflammatory fluid & cellular exudate
increases the bulk of the flap, which may interferes
with complete closure of the jaw & traumatized by
contact with the opposing jaw.
 There is red, swollen, suppurating lesion that is
tender, with severe throbbing intermittent pain,
exaggerated by chewing & interfering with sleep.
 Pain radiates to ear, throat & floor of mouth.
 Foul taste, halitosis, & inability to close the mouth.

22. Subacute Stage
 Continuous dull ache, radiates
infrequently
 Stiffness of jaws, intraoral
swelling, unpleasant taste.
 Causes less systemic upset
 Trismus might be present

23. Complications:
 Involvement may be localised in form of
pericoronal abcess
 Posteriorly spread to oropharynx
 Medially to the base of the tongue, thereby
causing difficulty in swallowing
 Involvement of submaxillary, posterior &
deep cervical, retropharyngeal lymphnodes
 Peritonsilar abcess, cellulits & Ludwig’s
Angina are infrequent complications.

24.  Treatment:
 Treatment depends on severity of the inflammation,
systemic complications, Extraction or Non extraction
 Persistent asymptomatic pericoronal flap should also
be removed as a preventive measure
 Gentle flushing with warm water to remove debris
and exudate
 Swabbing with antiseptic after elevating the flap with
a scaler
 Evaluation of the occlusion of the opposing tooth and
adjustments if necessary.
 Antibiotics, in case of diffuse microbial infiltration.
 In case of fluctuant abscess drainage should be
accomplished by incision.
 Post treatment monitoring is necessary to ensure
the resolution of the acute phase. Extraction of the
impacted tooth, if necessary.

25.  Resection of some or all pericoronal tissue (operculectomy) depending on
tooth position in the jaw & soft tissue relationships, reduces the chances of
recurrent infection. Not only the Occlusal flap, the distal flap should also
be removed, to make the area cleansable and free from pocket distally.
 Operculectomy – surgical removal of operculum. It can be done using hand
instruments, or electrosurgery or LASER.

26. Herpetic Gingivostomatitis

27. HERPES SIMPLEX VIRUS
 Herpes simplex Virus is a DNA virus & is a member of the
human herpes virus family (HHV) family known as
herpetoviridae.
TYPES
 Type 1 – HSV 1 – Oral manifestation
 Type 2 – HSV 2 – Ano-genital infections
Other members of HHV family includes
 Varicella zoster virus ( HHV 3)
 Epstein barr virus ( HHV 4)
 Cytomegalo virus ( HHV 5)
 Others – HHV 6, HHV 7, HHV 8

28.  HSV- type 1
 Infants/ children younger than 6 yrs
 Male = Female
 Primary infection asymptomatic
 Virus – penetrates neural ending – retrograde
transmission through the sensory or autonomic
nerves – smmoth ER (200-300mm/day) –
Trigeminal ganglia – Latent virus
 Sunlight, fever, trauma, stress , after oral
surgical procedures

29. Secondary manifestations
 Herpes labialis
 Herpetic stomatitis
 Herpes genitalis
 Ocular herpes
 Herpetic encephalitis

30. Early stage
After few days Late stage
showing brownish crusted
lesions
Vermillion border and skin adjacent to it is affected, where the
neural endings form cluster
The lesion heals after about 2 weeks

31. Clinical features
 Diffuse, erythematous, shiny involvement of
the gingiva and adjacent oral mucosa
 Varying degree of edema and gingival
bleeding
 Discrete spherical grey vesicles
 Rupture of vesicles and formation of ulcers
after 24 hrs
 Ulcers– small , painful, red, elevated, halo-
like margin with depressed yellowish/
greyish white central portion
 Widely spread/clusters
 7-10 days
 No scarring
Primary herpetic gingivostomatitis

32.  Soreness, difficulty in eating and drinking
 Ruptured vesicles sensitive to touch, thermal
changes, foods such as condiments and fruit
juices
 Infants show irritability and refusal to take
food

33. Extra-oral
 Cervical adenitis
 Fever (101ͦ -105ͦ F)
 Generalized malaise

34. Histopathology
 Tzanck cells: Virus targeted epithelial cells
- Ballooning degeneration (acantholysis,
nuclear clearing, nuclear enlargement)
 Lipschutz bodies: There is presence of
intranuclear inclusion bodies.
 Peri inclusion halo: Nucleolar
fragmentation occurs with the
condensation of chromatin around the
periphery of the nucleus.
 Intracellular edema - intraepithelial
vesicles - vesicle ruptures
 Lesion demonstrate a surface
fibrinopurulent membrane.
 There is secondary infiltration by
inflammatory cells in subadjacent
connective tissue.

35. Diagnosis
 Early diagnosis important
 History/clinical findings
 PCR : Rapid & Reliable
 Blood sample showing high antibody titer against HSV (
diagnostically evident only in case of primary infection, as the
titer remains high through the the rest of the life)
 Virus culture
 Immunologic tests using monoclonal antibodies or DNA
hybridization techniques

36. Differential Diagnosis
Recurrent Aphthous stomatitis
 Small well defined round shallow ulcers,
yellowish grey central areas & red halo
 H/o previous mucosal ulcers is diagnostic,
unknown etiology
 Apthous does not affect keratinised mucosa,
only lining mucosa is affected
 No diffuse erythematous involvement of the
gingiva, no acute toxic symptoms

37. Communicability
 Contagious : Viral shedding
 Recent studies have demonstrated HSV in
periodontal pockets (Slots J 2000)
Herpetic Whitlows : Infection of fingers of health professional
treating infected patients may occur

38. Treatment
Consists of early diagnosis & immediate initiation of antiviral
therapy.
o Diagnosis within 3 days of Primary HGS – Antiviral
o More than 3 days - (immunocompetent patient) - Limited value
Antivirals :
o Acyclovir suspension 15mg/kg is given 5 times daily for 7 days
(Amir et al,1997)
 Valacyclovir or Famiciclovir alternative DOC

39. Rationale of using Anti-viral
Drug
 Immuno-deficeient patints with long term therapy
with acyclovir – Resistance – Alternate DOC
( Westheim et al, 1987)
 Patient with recurrent herpes infection – prophylactic
use of antiviral – prior to any dental treatment ( Miller
et al, 2004 )
Acyclovir Placebo
Fever 1 Day 3 Days
New Extra oral
lesions
0 5.5
Difficulty in eating 4 Days 7 Days
Viral shedding 1 Day 5 Dyas
* Amir et al 1997

40. Palliative measures:
o Removal of food debris, plaque and supra gingival calculus
o NSAID (FEVER AND PAIN)
o Extensive periodontal therapy to be postponed
o Local /systemic antibiotics to prevent opportunistic infection especially in immuno-
compromised patients
o The patient must be informed that the disease is contagious, thus precautions must be taken
(vesicles –highest viral titer)
Supportive measures:
o Copious fluid intake
o Nutritional supplements
o Topical anesthetics while eating

41. Streptococcal gingivostomatitis
 Characterized by diffuse erythema of the
gingiva and other areas of the oral mucosa
 Bacterial smears– streptococcal forms
 Streptococcus viridans , groupA ß-hemolytic
streptococcus

42. Gonococcal Stomatitis
 Caused by Neisseria gonorrhoeae
 Mucosa is covered with a grayish membrane that sloughs
off in areas to expose an underlying raw bleeding surface
 Most common in new born due to transmission through
maternal passages

43. Agranulocytosis
 Characterized by marked decrease in number of circulating PMN’s
 No marked inflammation due to diminished defense mechanism
 Lesions similar to NUG
 Blood studies can be used to differentiate between NUG and
agranulocytosis

44. Vincent’s angina
 Fusospirochetal infection of oropharynx and
throat, which affects marginal gingiva. May
extend to the larynx and the middle ear

45. Next Seminar……
 NUG
 NUP
 NUP as a manifestation of systemic disease