acute gingival infections

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

Early stage Late stage showing brownish 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 vesiclesPrimary 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 (101 ͦ -105 ͦ 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

Acute

Subacute

Chronic

PATHOGENESIS Space- ideal area for

accumulation of food debris and bacterial growth

Inflammatory fluid and cellular exudate

Increase in bulk of the

flap

Interferes with complete closure of

jaws or can be traumatized by

contact with opposing jaw

Aggrevation of the

inflammatory involvement

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

Systemic complications

Retaining/extracting involved tooth

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

incorrect

correct

healed site

Surgical procedure to remove operculum

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 aetiologyA) Periodontitis related abscess

1) Exacerbation of chronic lesion

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)

Post scaling abscess

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

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

Periodontal Abscess

•Vital tooth

• No caries

• Pocket, bone loss

• Lateral radiolucency

• Mobility

• Percussion sensitivity variable

• Sinus tract opens via

keratinized gingiva

•Dull localized 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

TREATMENT1) 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

COMPLICATIONSA) Tooth loss

B) Dissemination of infection1) 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

REFERENCESo 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