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Indian Dental Academy Guide to Acute Gingival Lesions
1. INDIAN DENTAL ACADEMY
Leader in Continuing Dental Education
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2. An Acute Lesion Is Of Sudden Onset And
Short Duration And Can Be Painful. A Less
Severe Phase Of Acute Condition Is Termed
As Subacute. There Are Various Acute
Gingival Lesions, The Most Commonly
Occurring Ones Are :
*Necrotizing Ulcerative Gingivitis
*Primary Herpetic Gingivostomatitis
*Pericoronitis/Pericoronal Abcess
*Acute gingival Abcess
*Acute periodontal Abcess
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3. Necrotizing Ulcerative
Gingivitis (Nug)
• Is An Inflammatory Destructive Disease Of
The Gingiva, Which Presents Characteristic
Signs And Symptoms.
• Classification
*Acute → Most Common Form Of Occurrence
*Subacute → With Milder Clinical Features
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4. ANUG
• Clinical Features
• History : Sudden Onset
• May Follow Debilitating Disease Or
Acute Respiratory Tract Infection.
• Psychological And Physical Stress.
• May Have A History Of Repeated
Remissions And Exacerbations
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5. Oral Signs
• Characteristic Lesions Are Punched Out,
Crater-like Depression At The Crest Of
Interdental Papillae.
• May Extend Upto Marginal Gingiva Or
Rarely To Attached Gingiva And Mucous
Membrane.
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7. Gingival Crater Is Covered By Gray,
Pseudomembranous, Slough, Demarcated From
The Remainder Of The Gingival Mucosa By A
Pronounced Linear Erythema.
At Times The Pseudomembrane May Be
Denuded Exposing The Gingival Margin, Which
Red, Shiny And Hemorrhagic.
Spontaneous Gingival Hemorrhage Or
Pronounced Bleeding On Slightest Stimulation Is
Characteristic Feature.
Fetid Odor
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Increased Salivation
8. Oral Symptoms :
• Extremely Sensitive To Touch.
• Constant Radiating, Gnawing Pain,
Which Aggravates On Eating Spicy Or
Hot Foods.
• Metallic Foul Taste
• Excessive Amount Of ‘Pasty’ Saliva
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9. Extra-oral Or Systemic Signs
‘N’ Symptoms
• Local Lymphadenopathy
• Slight Elevation Of Temperature
• In Severe Cases.
• High Fever
• Increased Pulse Rate
• Leukocytosis
• Loss Of Appetitie
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10. • General lassitude
• Insomnia, constipation, GI disorder
headache and mental depression.
Sometimes accompany the condition.
• In severe cases Noma or gangrenous
stomatitis may be seen
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11. Horning and Conene staging
• 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
(%)
• Stage 5 : Necrosis extending to buccal / labial
mucosa (6)
• Stage 6 : Necrosis exposing alveolar bone (1%)
• Stage 7 : Necrosis perforating skin and check (0%)
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12. HISTOPATHOLOGY :
• Microscopic appearance is non-specific,
involving stratified squamous epithelium
and underlying connective tissue.
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13. Relation of Bacteria
• Light microscopy and electron microscopy shows
presence of cocci-, fusifom bacilli and spirochetes .
• Listgarten described the following four zones which
blend with each other and may not be present in
every case.
• Zone 1 : Bacterial Zone
The Most superficial
Consists of varied bacteria, including a few
spirochetes of small, medium and large types.
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14. Zone 2 : Neutrophil - Rich Zone
Contains Numerous Leukocytes,
Predominantly Neutrophils, With Bacteria,
Including Many Spirochetes Of Various
Types, Between The Leukocytes.
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15. Zone 3 : 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
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16. • Zone 4 : Zone Of Spirochetal
Infiltration
• Consists Of Well Preserved Tissue
Infiltrated With Medium And Large
Spirochetes Without Other
Organisms.
• Spirochetis Have Been Found As Deep
As 300 Microns From The Surface
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17. DIAGNOSIS :
• Clinical features
• Microscopic examination of a biopsy
specimen is not sufficiently specific to be
diagnostic.
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19. • Etiology
• Bacterias Involved
• Treponema
• Fusioform Bacillus
• Local Predisposing Factors
• Injury To Gingiva
• Smoking
• Deep Periodontal Pockets And Periocoronal Flaps.
• Systemic Predisposing Factors :
• Nutritional Deficiency Eg. : Vit. C, Vit. B2
• Debilitating Disease
• Chronic Diseases Like Syphititis Etc.
• Cancers
• Gastrointestinal Disorders Like Ulcerative Collitis
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• Blood Dysplasia Such As Leukemia And Anaemia
20. • Psychosomatic Factors
• Psycho logic Factors Appears To Be An
Important Etiologic Factor In NUG
• Chone-cole And Colleagues Suggested That
A Psychiatric Disturbance (Eg. : Trait
Anxiety, Depression And Pshchopathic
Deviance) And The Impact Of Negative Life
Events (Stress) May Lead To Activation Of
The Hypothalmic Pituitary Adrenal Axis.
This Results In Elevation Of Serum And
Urine Cortisol Levels ,Lymphocytes And
PNM Function That May Predispose To
NUG.
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21. • Communicability
• The Occurrence Of The Disease In
Epidemic - Like Outbreak Does Not
Necessity Mean That It Is Contagious. The
Affected Group May Be Affiliated By The
Disease Because Of Common
Predisposing Factors
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22. • RX OF ACUTE NECROTIZING
ULCERATIVE GINGIVITIS.
• First visit
• A detailed history of the patient must be
recorded along with a through clinical
examination of the patient.
• The involved area are isolated and then
clamed. The pseudomembrane and debris
are removed where a local anesthetic may
be used.
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23. Ultrasonic scaling is done to remove the calculus
subgingival scaling curettage are contraindicated
because of possibility of extending the infection to
deeper tissues.
Patient is adviced to rinse mouth twice with equal
mixture of warm water to 3% hydrogen peroxide and
twice daily rinse with 12% chlorhexidine.
Antibodies : penicillin 500 mg every 6 hrs.
or (erythromycin 500 mg every 6 hrs.)
along with metronidazole 500 mg twice daily for 7
days.
Patient is also advised to avoid tobacoo, alcohol and
condiments.
Patient recalled after 1-2 days
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24. • Second visit
• Patient condition reevaluated : There is
usually marked improvement.
• Scaling and root planning are repeated.
• Hydrogen peroxide rinse is discontinued
after 2-3 weeks.
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25. • Subsequent visit :
• The tooth surface is scaled & smoothned
and plaque control by patient is checked
and corrected if necessary.
• Appointments are scheduled for the Rx of
the gingivitis, periodontal pockets, and
pericoronal flaps as well as for elimination
of all forms of local irritation.
GIGIVOPLASTY IS DONE IF THE LOST GINGIVAL
ARCHITECTURE IS NOT REGAINED
AFTER NONSURGICAL THERAPY
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26. • PRIMARY HERPETIC
GINGIVOSTOMATITIS
• Caused by herpes simplex virus type I
• Occurs commonly in children and
infants younger than 6 yrs. of age, but
is also seen in adolescents and adults.
• Males - females
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27. • It Is Usually Asymptomatic. After Primary
Infection, The Virus Ascends Through
Sensory And Autonomic Nerves And
Persists In Neuronal Ganglia That Innervate
The Site As Latent HSV.
• Secondary Manifestations Occur As A
Result Of Various Stimuli Such As
Sunlight, Trauma Fever Or Stress.
• Secondary Manifestations Include Herpes
Labials Herpes Genitals, Ocular Herpes And
Herpetic Encephalitis.
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28. • CLINICAL FEATURES :
• Oral signs :
• Diffuse, erythematous shiny involvement of gingiva
and adjacent oral mucosa.
• Varying degree of edema and gingival bleeding.
• In initial stage → discrete spherical gray
vesicles are seen
• on gingiva, labial and buccal mucosa, soft
• palate, pharynx tongue etc.,
• After about 24 hrs vesicles repture forming painful
ulcers with red, elevated, halo like margin and a
depressed, yellowish or grayish white central
portion.
• Course of disease limited to 7 to 10 day
• Scarring dos not occur in areas of healed
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ulcerations.
30. • Oral symptoms
• Generalized soreness
• Inability to eat and drink
• Painful and sensitive to touch, thermal changes,
foods such as condiments and fruit juices and
action of coarse foods.
• Extra oral & systemic signs and symptoms
• Cervical adentis
• Fever →101o to 105o (38.3oc to 40.6o c)
• Generalized malaise
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31. • History
• Recurrent acute infection
• Episode may occur after febrile disease as
pneumonia, meningitis, influenza typhoid.
• It also tends to occurring during periods of
anxiety, stress or exhaustion as well as
during menstruation.
• Also occur during early stage of infections
mononucleosis
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32. • HISTOPATHOLOGY :
• The virus target the epithelial cells which
show ‘ballooning degeneration’ consisting of
acantholysis nuclear cleaning and nuclear
enlargement. These cells are called Tzank
cells
• Infected cells fuse forming multinucleated
cells and intercellular edema that leads to
formation of an intra epithelial vesicles that
rupture and develop a secondary
inflammatory response with a fibropurulent
exudate.
• Discrete ulcerations resulting from rupture
of the vesicles have a central portion of
acute inflammation, with varying degree of
purulent exudate, surrounded by a zone
rich in engorged blood vessels.
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33. • DIAGNOSIS :
• Patient’s history
• Clinical findings
• Virus culture
• Immunologic list using monoclonal
antibodies or DNA hybridization
techniques
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35. • COMMUNICABILITY :
• It is contagious
• Most adults develop immunity due to
infection during childhood
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36. • Rx OF ACUTE HERPETIC GINGIVOSTOMATITIS
• Various medications have been used to treat
herpetic gingivostomatitis with little success, these
included local application and also escharotics,
vitamins, radiation and antibiotics and also
acyclovirs.
• Rx consist of palliative measures alone.
• Removal of plaque, food debris and superficial
calculus to reduce gingival inflammation.
• Tropical application of local anesthetics for
symptomatic relief eg : lidocaine hydrochloride
• Else asprin or a NSAID agent can be given
systematically.
• Application of local antibiotics to prevent
opportunistic infection especially in immuno-
compromised patients.
• The patient must be informed that the disease is
contagious thus precautions must be taken.
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37. • PERICORONITIS
• Periocoronitis refers to inflammation of gingiva in
relation to the crown of an incompletely erupted
tooth.
• Occurs most commonly in mandibular III molar
area.
• TYPES :
• Acute
• Subacute
• Chronic
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39. • CLINICAL FEATURES :
• Space between crown and overlying gingival
flap shows accumulation of food debris and
bacteria; causing inflammation.
• Inflammatory fluid and cellular exudate
increase the bulk of the flap, which then
may interefere with complete closure of
jaws or can be traumatized by contact with
opposing jaw, aggregate the inflammatory
involvement.
• Clinically it is seen as a markedly red,
swollen, suppurating lesion that is
exquisitely tender, with radiating pain to
the ear, throat and floor of the mouth.
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40. Patients is extremely uncomfortable because of a foul
taste and an inability to close the jaws, in addition to
pain.
Swelling of check in the region of angle of jaw and
lymphadenitis are seen.
Patient may also have toxic systemic symptoms such
as fever, leukocytosis and malaise.
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41. • COMPLICATIONS :
• Pericoronal abscess formation
• May spread pericoronal into the oropharangeal
area and medialy to base of tongue, making it
difficult for patient to swallow.
• Depending of severity these may be the
involvement of submaxillary, posterior cervical,
deep cercial and retropharyngeal lymph nodes.
• Peritondillar absecess formation, cellulitis and
ludwig’s angina are infrequent but potential
sequelre of acute periocoronitis
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42. • Rx of acute pericoronitis
• Rx depends on severity of inflammation, the
systemic complications and the advisability of
retaining the involved tooth
• Persistant symptom free periocoronal flaps
should be removed as a preventive measure
against subsequent acute involvement
• Specific Rx
• Gently flushing the area with warm water to
removed debris and exudate
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43. • Swabbing with antiseptic after elevating the
flap gently from the tooth with a scaler
• Then the dentist has to decide whether the
tooth is to be retained or extracted.
• If it is decided to retain tooth, the periocoronal
flap is removed using periodontal knives on
electro surgery.
• After removal of the flap, a periodontal pack is
applied which is removed after I week.
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