ACUTE GINGIVAL

INFECTIONS
CONTENTS

 Introduction

 Primary herpetic gingivostomatitis

 Necrotizing ulcerative gingivitis (NUG)

 Pericoronitis

 Abscesses of periodontium
INTRODUCTION

 An acute lesion is of sudden onset and short duration

and is painful.

 They are manifested with severe pain along with

systemic manifestations

 Thus these lesions must be treated at the earliest

with a proper treatment protocol.
Primary herpetic gingivostomatitis
 HSV- type 1

 Infants/ children younger than 6 yrs

 Males=females

 Primary infection asymptomatic

 The virus ascends through the sensory or autonomic

nerves and persists in the neuronal ganglia that innervate
the site as a latent HSV

 Sunlight, fever, trauma, stress , after oral surgical

procedures
Secondary manifestations

 Herpes labialis

 Herpetic stomatitis

 Herpes genitalis

 Ocular herpes

 Herpetic encephalitis
 Late stage showing brownish
Early stage
crusted lesions
CLINICAL FEATURES
Intra-oral

 Diffuse, erythematous, shiny

involvement of the gingiva and
adjacent oral mucosa

 Varying degree of edema and

gingival bleeding

 Discrete spherical grey vesicles

Primary herpetic
gingivostomatitis
 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
 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

Extra-oral

 Cervical adenitis

 Fever (101ͦ -105ͦ F)

 Generalized malaise
HISTOPATHOLOGY

Virus targets epithelial cells

Ballooning degeneration (acantholysis, nuclear clearing,

nuclear enlargement)

Tzanck cells
 Fusing of infected cells

Formation of multinucleated cells and intercellular edema

Formation of intraepithelial vesicles

Rupture

Secondary inflammatory response with fibropurulent exudate

Ulcers with central portion of acute inflammation and exudation

surrounded by zone rich in engorged blood vessels
DIAGNOSIS
 Early diagnosis important (reducing symptoms and
recurrences)

 History/clinical findings

 Virus culture

 Immunologic tests using monoclonal antibodies or DNA

hybridization techniques
DIFFERENTIAL DIAGNOSIS
Erythema multiforme:

o More extensive vesicles with pseudomembrane

formation on rupture

o Tongue more involved

o Skin lesions present

o Prolonged involvement may occur for weeks

 Stevens-Johnson syndrome: rare form of EM
characterized by hemorrhagic lesions in the oral cavity,
hemorrhagic occular lesions and bullous skin lesions
Bullous lichen plannus:

 Rare & painful condition

 Large blisters on tongue & skin- rupture

undergo ulceration

 Skin lesions + oral involvement

 Prolonged indefinite course

 Linear, grey, lacelike lesions of lichen

plannus inter-spread among bullous
eruptions
Desquamative gingivitis

 Chronic condition

 Diffuse involvement of gingiva

 Varying degree of peeling of epithelium

Recurrent aphthous stomatitis

 Small well defined round shallow

ulcers, yellowish grey central
areas & red halo

 H/o previous mucosal ulcers is

dignostic, unknown etiology

 No diffuse erythematous
involvement of the gingiva, no
acute toxic symptoms
COMMUNICABILITY

 Contagious

 Most adults develop immunity due to infection during

childhood – subclinical infection

 Hence seen in infants & children

 Recent studies have demonstrated HSV in periodontal

pockets (Slots J 2000)
TREATMENT
Consists of early diagnosis & immediate initiation of antiviral
therapy.

Antivirals :

o Acyclovir suspension 15mg/kg is given 5 times daily for 7

days (Amir et al,1997)

o It reduces days of fever, pain, lesion and virus shedding

o Acyclovir does not affect normal cells but inhibits DNA
replication in HSV infected cells

o Newer antivirals like Valacyclovir and Famicyclovir can

also be used

o <3 days– antiviral

o >3 days- (immunocompetent pt) limited value

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

 Infection of fingers of health professional treating
infected patients may occur and is known as Herpetic
Whitlows
Necrotizing ulcerative gingivitis
 Necrotizing Gingivitis, Necrotizing Periodontitis and
Necrotizing Stomatitis are the most severe inflammatory
disorders caused by plaque bacteria

 They are rapidly destructive and debilitating

 A distinction between these diseases has not always been

made in the literature
 Microbial diseases affecting gingiva/ periodontium in the
context of an impaired host response

 Characterized by death and sloughing of tissues

 HISTORY

 Fourth century BC, Xenophon mentioned that Greek soldiers

were affected with “sore mouth” and foul-smelling breath

 In 1778, John Hunter described the clinical findings and

differentiated ANUG from scurvy and chronic destructive
periodontal disease

 ANUG occurred in epidemic form in the French army in the

19th century
 In 1886, Hersch, a German pathologist, discussed some of
the features associated with the disease such as enlarged
lymph nodes, fever, malaise and increased salivation

 In 1890s, Plaut and Vincent described the disease and

attributed its origin to fusiform bacilli and spirochetes
NOMENCLATURE

 Ulceromembranous gingivitis

 Acute necrotizing ulcerative gingivitis

 Trench mouth

 Vincent’s gingivostomatitis

 Phagedenic gingivitis

 Fusospirallary periodontitis

 Plaut-Vincent stomatitis
CLINICAL FEATURES

Classification

 Acute
 Subacute (Repeated remissions and exacerbations)

 Recurrent

 Single tooth, group of teeth

 Entire mouth
NUP
(long standing, severe immunosuppression)

NUS

Noma
ORAL SIGNS AND SYMPTOMS

 Punched out, craterlike depressions at the crest of the

interdental papilla

 Can extend into the marginal gingiva, attached gingiva and

oral mucosa

 Grey pseudomembranous slough

 Linear erythema

 Removing slough exposes red, hemorrhagic, shiny surface

which bleeds easily
 Fetid odor

 Metallic taste

 Increased salivation/pasty saliva

 Can be superimposed on chronic gingivitis/periodontitis

 Recession rather than pocket formation

 Constant radiating, gnawing pain that is intensified on
eating spicy and hot foods and on chewing

 Lesions extremely sensitive to touch

 Low socioeconomic groups

 Seasonal variations (Skach et al, 1970)

EXTRAORAL AND SYSTEMIC SIGNS AND
SYMPTOMS

 Local lymphadenopathy

 Fever

 Increased pulse rate, leukocytosis, loss of apetite and

general lassitude additionally seen in severe cases

 Insomnia, constipation, GI disorders, headache and

mental depression in children
OTHER SEVERE SEQUELAE

1) Fusospirochetal meningitis

2) Peritonitis

3) Pulmonary infection

4) Toxemia

5) Fatal brain abscess

6) Noma
CLINICAL COURSE

ACCORDING TO HORNING AND COHEN:

 Stage 1 : Necrosis of tip of the interdental papilla (93%).

 Stage 2 : Necrosis of entire papilla (19%)

 Stage 3 : Necrosis extending to gingival margin (21%)

 Stage 4 : Necrosis extending to attached gingiva (1%)

 Stage 5 : Necrosis extending to buccal / labial mucosa (6%)

 Stage 6 : Necrosis exposing alveolar bone (1%)

 Stage 7 : Necrosis perforating skin and check (0%)

ACCORDING TO PINDBORG:

 Stage 1: Erosion of only tip of interdental papilla

 Stage 2: Lesion extending to marginal gingiva and causing

potentially a complete loss of papilla

 Stage 3: Involving attached gingiva

 Stage 4: Exposure of bone

 HISTOPATHOLOGY

 Microscopically the lesion is acute necrotizing inflammation of

the gingiva, involving both the stratified squamous epithelium
and the underlying connective tissue

 Epithelium destroyed and replaced by meshwork of fibrin,

necrotic epithelial cells and PMN’s and various types of
microorganisms (surface pseudomembrane)

 Border: Epithelium edematous and individual cells exhibit

varying degree of hydropic degeneration along with infilteration
of PMN’s in the intercellular spaces
 Underlying connective tissue: hyperemic with numerous
engorged capillaries and dense infiltration by PMN’s (linear
erythema)

 Plasma cells at the periphery(underlying chronic condition)

 Epithelium and CT alterations decrease with increase in distance

from the necrotic area and gradually blends with the uninvolved
area
Listgarten – described four zones that blend with each other

 ZONE I - BACTERIAL ZONE- The Most superficial

zone
Consists of varied bacteria, including a few spirochetes
of small, medium and large type.

 ZONE II – NEUTROPHIL RICH ZONE - Contains

numerous leukocytes, predominantly neutrophils, with
bacteria, including many spirochetes of various types,
between the leukocytes
 ZONE III – NECROTIC ZONE- Consists of disintegrated
tissue cells, fibrillar material, remnants of collagen fibers and
numerous spirochetes of the medium and large types, with
few other organisms

 ZONE IV – SPIROCHETAL INFILTRATION ZONE-

Consists of well preserved tissue infiltrated with medium and
large spirochetes without other organisms.

Spirochetes have been found as deep as 300 microns from the

surface
ETIOLOGY

Role of bacteria

o Plaut and Vincent in 1894 and 1896, respectively

introduced the concept NUG is caused by specific
bacteria – namely a fusiform bacillus and a spirochetal
organism.

o Fusiform bacilli and a spirochetal organism are always

found in the disease.
 Rosebury and coworkers described a fusospirochetal
complex consisting of T. marcodentium, intermediate
spirochetes, vibrios, fusiform bacilli and filamentous
organisms in addition to several Borrelia species
 More recently Loesche and colleagues described a constant
flora and a variable flora

Constant flora :- Fusospirochetal organisms, P.

intermedia, A. odontolyticus and
various spirilla like Selenomonas
species.

Variable flora :- Heterogenous array of bacterial

types
 Bacteriologic findings have been supported by
immunological data presented by Chung et al who
reported increased IgG and IgM antibodies to
intermediate spirochetes, P. intermedia in NUG patients
as compared to those with chronic gingivitis and healthy
controls

 Metronidazole effective
Role of host response

 Presence of organisms insufficient to cause disease

 NUG is not produced experimentally in humans and

animals by inoculation of bacterial exudates from the
lesion

 Characteristic lesions occurs in animals when they are

under immunosupression

 Not found in well nourished individuals with fully

functional immune system
 Immunosupression essential- NUG patients displayed
depression in leukocyte chemotaxis and phagocytosis
(Cogen et al, 1983)

 Nutritional deficiency, fatigue caused by chronic sleep

deprivation, alcohol/drug abuse, psychological factors,
systemic disease

 It is hence concluded that -

The specific cause of NUG has not been established & it is

produced by a complex of bacterial organisms but requires
underlying tissue changes to facilitate the pathogenic activity
of the bacteria.
 HIV
 LOCAL PREDISPOSING FACTORS

 Pre-existing gingivitis

 Injury to the gingiva (eg: malocclusion)

 Smoking

 98% pts with NUG were smokers & frequency of the disease
increases with increasing exposure to tobacco smoke
(Pindborg et al, 1951)

 Preexisting chronic periodontitis, pericoronal flaps (favourable

environment for anaerobic fusiform bacilli and spirochetes)
SYSTEMIC PREDISPOSING FACTORS

Nutritional deficiency

 Produced in animals by giving them nutritionally deficient

diet

 Nutritional deficiencies diminishes immune responses and

alteres the periodontal structures, making them more
susceptible
Debilitating disease

 Chronic diseases( syphilis, cancer)

 Severe gastrointestinal disorders (ulcerative colitis)

 Blood dyscrasias( anemia, leukemia)

 AIDS
Psychosomatic factors

 Disease often occurs in association with stressful situations

(induction into the armed forces, school examinations)

 Hypothalamic-pituitary-adrenal axis activation resulting in

cortisol secretion and decrease in immune response
 Increase in the levels of cortisol and catecholamines
leads to reduced gingival microcirculation and salivary
flow which enhances nutrition to P.intermedia

 Depression in neutrophil and lymphocyte function leads

to bacterial invasion and tissue damage.

(Johnson and Engel 1986)

DIAGNOSIS

 Clinical findings (gingival pain,ulceration and bleeding)

 Bacterial smear not definitive

 Microscopic examination of biopsy specimen (TB,

neoplastic disease)
DIAGNOSTIC CRITERIA

By Genco, Goldman and Cohen:

 Interproximal necrosis and ulceration (punched-out papillae)

 Painful gingiva

 Bleeding (spontaneous or on slight provocation)

 Pseudomembrane (fibrin, debris)

 Fever, malaise, lymphadenopathy

 “Fetor Oris”
 Herpetic Gingivostomatitis
 Chronic Periodontitis
 Desquamative Gingivitis
 Streptococcal Gingivostomatitis
 Apthous Stomatitis
 Diptheric And Syphilitic Lesions
 Tuberculous Gingival Lesion
 Candidiasis
 Agranulocytosis
 Dermatoses (Pemphigus, Erythema Multiforme ,Lichen
Planus)
 Treatment differs
 Herpes/NUG
STREPTOCOCCAL GINGIVOSTOMATITIS

 Characterized by diffuse erythema of the gingiva and other

areas of the oral mucosa

 Necrosis of the gingival margin – not a feature of this

disease.

 No fetid odor

 Bacterial smears– streptococcal forms

 Streptococcus viridans , groupA ß-hemolytic streptococcus

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
 AGRANULOCYTOSIS

 Characterized by marked decrease in number of circulating

PMN’s

 Lesions similar to NUG

 No marked inflammation due to diminished defense mechanism

 Blood studies can be used to differentiate between NUG and

agranulocytosis
VINCENT’S ANGINA

 Fusospirochetal infection of oropharynx and throat,

distinguished from NUG, which affects marginal gingiva.
May extend to the larynx and the middle ear
NUG in Leukemia

 Not produced by leukemia per se , but due to reduced

host defense mechanism

 NUG may superimpose on gingival tissue alteration

caused by leukemia
NUG IN HIV PATIENTS

 Same clinical features

 Extremely destructive course leading to NUP

 Presenting symptom for HIV

COMMUNICABILITY

 Not contageous

 Study by King

 Kitchen facilities (controlled conditions, anaerobic

environment, do not survive on utensils)

 Occurrence in epidemic like outbreaks– due to common

predisposing factors

 Immunosupression+bacteria
NUP

 Extension of NUG or different disease entity

 No evidence

 Clinical similarities

 Until distinction can be proved/disproved, classified together

 Classification first adopted in world workshop in clinical

periodontics in 1989
 Deep interdental osseous craters

 Recession

 HIV positive patients

 Strongly associated

 Marker of immune supression and diagnosis of AIDS

 HIV-P

 Aggressive form of chronic periodontitis

TREATMENT

 Alleviation of the acute symptoms by reducing microbial load

and removal of necrotic tissue

 Treatment of chronic disease either underlying the acute

involvement or elsewhere in the oral cavity
 Alleviation of the generalized symptoms such as fever
and malaise

 Correction of the systemic conditions that contribute to

the initiation or progression of gingival changes.
SEQUENCE OF TREATMENT

FIRST VISIT
 Complete evaluation

 Comprehensive medical history with special attention to recent

illness, living conditions, dietary backgrounds, type of
employment, hours of rest, cigarette smoking, stress levels, HIV

 Examination should include general appearance, presence of

halitosis, skin lesions, vital signs, lymph nodes
o Characteristic lesions

o Oral hygiene (Pericoronal flap Pockets Local irritants)

o Only acutely involved areas

o Isolated with cotton rolls and dried

o Topical anesthetic
 Area swabbed to remove pseudo membrane with moistened
cotton pellet after 2-3 min

 Cleanse area with warm water

 Superficial calculus removed (ultrasonic scalers)

 Subgingival scaling and curettage – contraindicated

(bacteremia, extend infection to deeper tissues)
 Surgical procedures other than emergencies postponed
until pt is symptom free for 4 weeks

 Antibiotic regimen (amoxicillin 500 mg orally every 6 hrs

for 10 days) in moderate to severe cases

 Metronidazole (500mg BID 7 days)

 Emergency procedures along with systemic antibiotics

 PATIENT INSTRUCTIONS

 Patient told to rinse every two hours – glass full of equal

mixture of warm water and 3 % Hydrogen peroxide and /
or twice daily with 0.12%chlorhexidine

 Adequate rest

 Confine toothbrushing to removal of surface debris,

ultrasoft brush, bland dentrifice
 Analgesics

 Avoid tobacco, alcohol, condiments

 Report back in 1-2 days

 Motivation
SECOND VISIT

 Patient condition – usually improved. Pain is diminished

or no longer present.

 Areas still erythematous but without pseudomembrane

 Shrinkage of gingiva – expose calculus which is then

gently removed.

 Instruction same as previous visit

 THIRD VISIT

 5 days after 2nd visit

 Patient should be symptom free

 Repeat scaling and root planing

 Discontinue hydrogen peroxide mouthwash but continue CHX

mouthwash

 Patient instructed in plaque control procedures

 Councelling on nutrition, habits

SUBSEQUENT VISITS

 Tooth surfaces in the involved areas are scaled.

 Plaque control is checked and corrected if required.

 Patient should now be scheduled for treatment of chronic

disease.
GINGIVAL CHANGES WITH HEALING

 Removal of pseudo membrane – exposes red crater like

hemorrhagic depression.(loss of normal barrier function

of epithelium)

 Next day: Bulk and redness of crater margins reduced –

but surface shiny.(reduction in inflammation and

reepithelization)
 Early signs of restoration of normal gingival contour and

color. (further reduction in inflammation, reestablishment of

normal barrier function including keratinization)

 Final stage- Normal gingival contour, colour, consistency are

restored. Portions of roots exposed are covered by healthy

gingiva
ADDITIONAL TREATMENT CONSIDERATIONS

Countouring of gingiva as adjunctive procedure

 Shelf like margin

 Unesthetic, favours plaque retention

Systemic antibiotics/topical antimicrobials

 Only in pts with systemic complications and local adenopathy

 Drug therapy—adjunctive to local debridement

Supportive systemic treatment

 Copious fluid consumption

 Administration of analgesics

 Bed rest
Nutritional supplements

RATIONALE

 Lesions similar to NUG have been produced in animals –

with certain nutritional deficiencies

 Difficulty in chewing raw fruits and vegetables may lead

to selection of diet deficient in Vit B and C.

 Fewer recurrences – local treatment of NUG is

supplemented by Vit B or C.

 Supplements may be discontinued after two months

PERSISTANT OR RECURRENT CASES

 Reassessment of differential diagnosis to rule out

diseases that resemble NUG

 Underlying systemic disease causing immunosupression

(HIV)

 Inadequate local therapy (mandibular anterior area due to

pericoronal infection)

 Inadequate compliance
 Pericoronitis

 Abscesses of the periodontium

ACUTE GINGIVAL INFECTIONS-ӀӀ
 CONTENTS

 Introduction

 Primary herpetic gingivostomatitis

 Necrotizing ulcerative gingivitis/ periodontitis (NUG)

 Pericoronitis

 Abscesses of periodontium

 Conclusion

 References
Pericoronitis
 Inflammation of the gingiva in relation to the crown of
an incompletely erupted tooth

 Mandibular third molar area

Chronic Acute

Subacute
PATHOGENESIS

 Space- ideal area for

accumulation of food debris and
bacterial growth
 Interferes with
complete
Inflammatory Aggrevation
Increase in closure of
fluid and of the
bulk of the jaws or can be
cellular inflammatory
flap traumatized by
exudate involvement
contact with
opposing jaw
CLINICAL FEATURES

Chronic – no clinical signs or symptoms (chronic

inflammation and ulceration on inner surface)

Acute (trauma, occlusion, foreign body impaction)

Inflammatory involvement +systemic complications

 Red swollen suppurating lesion

 Tender

 Radiating pain to ear, throat, floor of mouth

 Foul taste

 Inability to close jaws

 Swelling of cheek, lymphadenitis, trismus

 Fever, leukocytosis, malaise

COMPLICATIONS
 Localized- pericoronal abscess

 Spread- submaxillary, posterior cervical, deep cervical

and retropharyngeal lymph nodes

 Peritonsillar abscess, cellulitis, Ludwig’s angina

Pericoronal abscess Peri-tonsillar abscess Ludwig’s angina

TREATMENT

Severity of inflammation

Retaining/extracting Systemic
involved tooth complications
Chronic pericoronitis
 Removal as a preventive measure

Acute pericoronitis
 Flushing area with warm water to remove debris and
exudate

 Swabbing with antiseptic after elevating the flap gently

 Occlusal adjustment
 Abscess drainage

 Antibiotics

 Decision to retain or extract the tooth after acute

symptoms subside
 Decision governed by likelihood of further eruption into
good functional position, bone loss distal to second
molars

 Extraction- Early extraction before root formation is

completed
 Retaining tooth- removal of pericoronal flap using
periodontal knives or electrosurgery
 Surgical procedure to remove operculum

correct

incorrect
healed site
Abscesses of the
periodontium
DEFINITION

Periodontal abscess is defined as a lesion with expressed

periodontal breakdown occuring during a limited period
of time and with easily detectable clinical symptoms, and
localized accumulation of pus within the gingival wall of
the periodontal pocket (Hafstrom et al, 1994)
 Independent disease entity (AAP world workshop, 1999)

 Represents period of active tissue breakdown due to

extension of infection into intact periodontal tissues
CLASSIFICATION

According to location (Meng et al, 1999)

 Gingival abscess

 Periodontal abscess

 Pericoronal abscess

According to clinical signs and symptoms

 Acute abscess

 Chronic abscess
According to number
 Single

 Multiple (diabetes, immunosupression)

Localized periodontal abscess in pt with

poorly controlled type 2 diabetes mellitus
According to aetiology
A) Periodontitis related abscess

1) Exacerbation of chronic lesion

Post scaling abscess

2) Post therapy periodontal abscess

a) Post scaling periodontal abscess (Dello Russo, 1985)—

calculus impaction or obstruction
b) Post surgery periodontal abscess (Garrett et al, 1997)–
foreign body reaction, incomplete removal of calculus
c) Post antibiotic periodontal abscess (no mechanical therapy,
superinfection)
B) Non periodontitis related abscess

1) Impaction of foreign body in gingival sulcus

2) Root morphology alterations– invaginated root, fissured

root, external root resorption, root tears, iatrogenic
endodontic perforations
 GINGIVAL ABSCESS

 Localized acute inflammatory lesion

that may arise from a variety of
sources such as microbial plaque
infection, trauma and foreign body
impaction

 Red, smooth, fluctuant, painful

 Marginal gingiva/interdental papilla

PERICORONAL ABSCESS

o Associated with
operculum of partially
erupted tooth

o Mandibular 3rd molars

most frequently affected
PERIODONTAL ABSCESS

 A localized purulent infection within the tissues adjacent to

the periodontal pocket that may lead to the destruction of
periodontal ligament and alveolar bone

 In patients with untreated periodontitis

 Moderate to deep pockets

 Acute exacerbation of chronic condition

 Incomplete calculus removal, antibiotic therapy,

periodontal surgery

 Occlusion due to deep tortuous pocket, tooth

morphology, debris, closely adapted pocket epithelium
 ACUTE ABSCESS
 Exacerbation of chronic condition due to increase in number or
virulence of bacteria combined with lowered tissue resistance
and lack of spontaneous drainage

 Exudation

 Sensitivity to percussion

 Pain, Mobility

 Tooth elevation in socket

 Systemic involvement
CHRONIC ABSCESS
 Forms when spreading infection has been controlled by
spontaneous drainage, host response or therapy

 No/dull pain

 Fewer/no symptoms

 Fistulous tract

 No systemic involvement
Periodontal Vs. Periapical Abscess
Periodontal Abscess
•Vital tooth
• No caries
• Pocket, bone loss
• Lateral radiolucency
• Mobility
• Percussion sensitivity variable
• Sinus tract opens via
keratinized gingiva
•Dull localized pain
Periapical Abscess
•Non-vital tooth
• Caries, restoration
• No pocket
• Apical radiolucency
• No or minimal mobility
• Percussion sensitivity
• Sinus tract opens via
alveolar mucosa
•Severe, diffuse pain
PREVALENCE

 8-14% among all dental conditions

needing emergency treatment (Ahl et
al, 1986)

 Positively correlated with pocket depth

 High prevalence in molars- 50%

(Smith and Davies, 1986)

 3rd most frequent dental emergency

PATHOGENESIS AND HISTOPATHOLOGY

 Contains bacteria, bacterial products, inflammatory cells,

tissue breakdown products and serum

 Occlusion of pocket lumen, extension of infection into

soft tissues

 Entry of bacteria into soft tissue pocket wall

 Accumulation of leukocytes,
connective tissue destruction,
bacterial encapsulation,
formation of pus

 Central area

 Rate of tissue destruction

depends on– growth and
virulence of bacteria, Ph
MICROBIOLOGY

 Polymicrobial, mainly caused by endogenous bacteria

(Tabaqhali, 1988)

 Similar to flora of chronic periodontitis

 Domination by gram negative, non-motile, strict

anaerobic, rod-shaped species

 Pg
 Pi, Tf, Fn, spirochetes (anaerobic species)

 Bifidobacterium spp, Actinomyces spp (gram positive,

strict anaerobic)

 Aa, Capnocytophaga spp, Campylobacter spp (gram

negative, facultative anaerobic)
DIAGNOSIS

 Clinical signs and radiological signs

 Ovoid elevation on lateral side of root

 Fistula, suppuration

 Pain, tenderness, swelling

 Sensitivitry to percussion
 Mobility, tooth elevation, pocket

 Bone loss

 Systemic effects

 Use of dark field microscopy ( Trope et al, 1988)

 PET (Liu, 1996)

DIFFERENTIAL DIAGNOSIS
 Periapical abscess

 Lateral periapical cyst

 Vertical root fractures

 Endo-perio abscesses

 Parrish et al (1989)- 3 cases of osteomyelitis

TREATMENT

1) Resolving acute lesion

2) Management of the resulting chronic condition

 ACUTE ABSCESS
 Drainage through pocket retraction or incision

 Scaling/ root planing

 Periodontal surgery

 Short term high dose adjunctive systemic antibiotics

 Tooth removal

 Avoid aggressive mechanical instrumentation in initial stage

 Reduce exertion

 Fluid intake

 Chlorhexidine mouthwash

 Warm saline gargles

 Analgesics/antibiotics
Chronic abscess
 SPT, surgery/ antibiotics

Gingival abscess
 Scaling/ root planing

 Drainage

 Removal of cause

 Warm saline gargles

Pericoronal abscess

 Drainage

 Irrigation to remove debris

 Warm saline gargles, antibiotics

 Analgesics

 Operculectomy/ extraction
COMPLICATIONS

A) Tooth loss

B) Dissemination of infection
1) Dissemination of bacteria inside the tissues during
therapy

2) Bacterial dissemination through blood stream due to

bacteriema from an untreated abscess
 Pulmonary actinomycosis

 Brain abscess

 Cellulitis

 Cervical necrotizing fasciitis

 Necrotizing cavernositis
CONCLUSION

 Acute gingival infections lead to severe discomfort and

may lead to life-threatening complications, and therefore
they need to be treated promptly

 Adequate patient education and motivation is necessary

as patients do not complete the treatment once the acute
phase has subsided
 REFERENCES

o Newman, Takei, Klokkevold, Carranza: Carrazanza’s Clinical

Periodontology, Saunders, 10th edition.

o Acute necrotizing ulcerative gingivitis: risk factors involving

host defense mechanisms.-- Yoji, Hidemi, Atsushi:
Periodontology 2000, Vol. 6, 1994, 116-124.

o Burkitt – Textbook of oral medicine

o Shafer –Textbook of oral pathology

o Lindhe, Lang, Karring: Clinical Periodontology and Implant
Dentistry. Blackwell Munksgaard, 5th edition.

o The Periodontal abscess– A Review: Herrera et al, JCP 2000;

27: 377-386