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ACUTE
GINGIVAL
INFECTIONS
Dr.Pradnya Wagh
CONTENTS:
 Introduction
 Classification
 Acute necrotizing ulcerative gingivitis.
 Terminology
 History
 Definition
 Clinical features
 Oral symptoms
 Classification
 Histopathology
 Etiology
 Epidemiology and Prevalence
 Diagnosis
 Differential diagnosis
 Treatment.
 Necrotizing ulcerative periodontitis.
 Acute herpetic gingivostomatitis
 Clinical features
 Oral symptoms
 History
 Histopathology
 Diagnosis
 Differential diagnosis
 Pericoronitis
 Definition
 Types
 Etiology
 Clinical features
 Acute pericoronitis
 Complications
 Treatment
 Tuberculosis
 Syphillis
 Traumatic injuries
 Herpangina
 Hand foot and mouth disease
 Glandular fever
 Measles
 Candidiasis
 Gingival abscess
 Apthous Stomatitis
 Erythema multiforme
 Conclusion
 References
INTRODUCTION
CLASSIFICATION OF VARIOUS ACUTE GINGIVAL LESIONS:
According to Manson R
a.Traumatic lesions of gingiva:
• Physical injury
• Chemical injury
b.Viral infections:
• Acute herpetic gingivostomatitis
• Herpangina
• Hand, foot and mouth diseases
• Measles
• Herpes varicella/zoster virus infection
• Glandular fever
c.Bacterial infections:
• Acute necrotizing ulcerative gingivitis
• Tuberculosis
• Syphilis
d.Fungal diseases:
• Candidiasis.
e.Gingival abscess
f. Apthous ulceration
g.Erythema multiforme.
h.Drug allergy and contact hypersensitivity
ACUTE NECROTIZING ULCERATIVE GINGIVITIS
(ANUG): (Bacterial)
TERMINOLOGIES:
 Trench mouth,
 Vincent's stomatitis,
 Vincent’s infection,
 Plaut-Vincents stomatitis,
 Stomatitis ulcerosa.
 ANUG is a microbial disease of gingiva in the
context of an impaired immune response.
 Maybe localized or generalized.
HISTORY
 Xenophen (401 B.C)-sore ulcerated and foul smell.
 Hirschfeld and Hunter(1778)- Made first clinical
differential diagnosis between ANUG ,periodontoclasia
and oral symptoms of scurvy.
 Plaut and Vincent (1890) described the disease.
DEFINITION:
Non–contagious anaerobic infection
associated with overwhelming proliferation of
Borrelia vincenti and fusiform bacteria.
-Laskaris and Scully
Necrotizing ulcerative gingivitis(NUG)is an
inflammatory destructive disease of the gingiva,
which presents characteristic signs and symptoms.
-Carranza and Klokkevold
CLINICAL FEATURES:
 Schluger(1943) provided pathognomonic signs
of ANUG:
 Painful ulceration and engorgement of the
interdental papillae(punched out inverted
papillae). These craters are covered by greyish
pseudo membranous slough, which is
demarcated from the remaining of the mucosa
by a pronounced linear erythema.
 The ulcerations of necrotizing ulcerative
gingivitis could be of two types, lateral
ulceration and necrosis, deep ulceration and
necrosis .
 Pseudo membrane- easily removed exposing raw
bleeding tissue.
 Pronounced tendency to gingival bleeding.
 Halitosis.
 Sialorrhoea.
 Fever, Malaise and lymphadenopathy.
 Other sites of involvement:Occational spread to
contiguous or adjacent tissues.
ORAL SYMPTOMS
1.The lesions are extremely sensitive to touch.
2.Complains of a constant radiating, gnawing pain that is
intensified by eating spicy or hot foods and chewing.
3. There is a metallic foul taste, and the patient is
conscious of an excessive amount of “pasty saliva”.
EXTRAORAL SIGNS AND SYMPTOMS
 Mild to Moderate stages- local lymphadenopathy,
elevated temperature.
 Severe -Marked systemic complications such as
high fever, increased pulse rate, leukocytosis,
loss of appetite and general lassitude are
common.
 Systemic reactions -more severe in children.
Insomnia, constipation, gastrointestinal
disorders,headache,and mental depression also
accompany.
Walter.D.Shields (1977) conducted a study of some of the
contributing factors for ANUG in army population and
divided signs and symptoms into primary and
secondary.
PRIMARY SIGNS:
1.Gingival bleeding
2.Pain
3.Interdental ulceration and necrosis especially in the
mandibular anteriors with resultant blunting and
cratering.
SECONDARY SIGNS:
1.Pseudomembrane.
2.Fetid Odor.
3.Bad Taste.
4.Elevated Temperature And Malaise.
5.Wooden Sensation In The Mouth.
6.Lymphadenopathy.
 ANUG in malnourished, debilitated and
immunocompromised patients may extend onto the oral
mucosa and skin resulting in cancrum oris
(noma;gangrenous stomatitis).
Anaerobes- porphyromonas species and Fusobacterium
necrophorum-implicated .
Spreading necrosis penetrates buccal
mucosa Gangrene
Oro-cutaneous fistula and
scarring.
 Fusospirochetal meningitis, peritonitis,
toxemia, and fatal brain abscess.
 Goldhaber and Giddon (1964) –stated that most
significant criteria in diagnosis of ANUG are :
 Interproximal necrosis and ulceration.
 History of soreness and bleeding in the area.
CLASSIFICATION:
 According to Pindborg J(1951)-classified into 3 forms
 Acute
 Subacute
 Chronic
(Now considered a misidentification of recurrence
of the disease).
Pindborg (1967) proposed following stages:
Stage 1:Only tip of the papilla was affected.
Stage 2:Marginal gingiva involved with punched out papillae.
Stage 3:Attached gingiva was also involved.
Stage 4:Bone was exposed.
Horning and Cohen(1995) extended the staging of these
oral necrotizing diseases as follows:
 Stage 1: Necrosis of the tip of the interdental papilla
(93%)
 Stage 2: Necrosis of the entire papilla (19%)
 Stage 3: Necrosis extending to the gingival margin
(21%).
 Stage 4: Necrosis extending also to the attached
gingiva(1%).
 Stage 5: Necrosis extending into buccal or labial
mucosa (6%).
 Stage 6: Necrosis exposing alveolar bone (1%).
 Stage 7: Necrosis perforating skin of cheek (0%).
STAGE 1
STAGE 2
STAGE 3
STAGE 4
STAGE 5
STAGE 6
STAGE 7
Uohora (1967)
suggested three stages of the disease:
• Stage 1:ANUG
• Stage 2:Necrotizing ulcerative mucositis.
• Stage 3:Cancrum oris (noma).
HISTOPATHOLOGY:
Listgarten and colleagues (1965)described four zones
namely:
1. Zone I—Bacterial zone: It is the most superficial zone,
consists of varied bacteria, including a few spirochetes
of the small, medium-sized and large types.
2. Zone II—Neutrophil-rich zone: Contains numerous
leukocytes predominantly neutrophils with bacteria
including spirochetes of various types.
3. Zone III—Necrotic zone: Consists of a dead tissue cells,
remnants of connective tissue fragments, and numerous
spirochetes.
4. Zone IV—Zone of spirochetal infiltration: Consists of a
well preserved tissue infiltrated with spirochetes of
intermediate and large-sized without other organisms.
ETIOLOGY:
1.ROLE OF BACTERIA
 Plaut and Vincent introduced the concept that
acute necrotizing ulcerative gingivitis is caused
by a specific bacteria namely, a fusiform
bacillus and a spirochetal organisms.
 More recently Loesche and colleagues described
a constant and a variable flora associated with
ANUG.
 Constant flora is composed of Fusospirochetal
organisms and also Bacteroides intermedius.
The Variable flora consists of a heterogeneous
array of bacterial types .
 Caused by specific bacteria fusiform bacillus and
spirochetal organism .
 Rosebury described,
 a fusospirochetal complex consisting of treponema
microdentium.
 Intermediate spirochetes
 Vibrios
 Fusiform bacilli
 Filamentous organisms
 Borrelia species.
Loesche described
 predominant constant flora
 Variable flora
2.ROLE OF HOST RESPONSE
 Regardless of whether specific bacteria are
implicated in the etiology of NUG,the presence of
these organism is insufficient to cause the disease.
 NUG has been associated with physical and emotional
stress and decreased resistance to infection.
 Plaut and Vincent = specific
bacteria
 Rosebury = Fusospirochetal
complex
 Loesche et al = Constant flora
and variable flora
 All the predisposing factors for NUG are associated
with immunosuppression.
 Immunodeficiency may be related to varying levels of
nutritional deficiency,
 fatigue caused by chronic sleep deprivation,
 other health habits
 Psychological factors or systemic disease.
3.LOCAL PREDISPOSING FACTORS
 Pre existing gingivitis
 Injury to the gingiva
 Smoking
 most often occurs superimposed on pre existing
chronic gingival disease and periodontal pockets.
 Deep periodontal pockets
 Pericoronal flaps
 Areas of the gingiva traumatized by opposing teeth in
malocclusion may predispose to NUG
 Pindborg reported that 98 % of his patients with NUG
were smokers and that the frequency of this disease
increases with an increasing exposure to tobacco
smoke.
4.SYSTEMIC PREDISPOSING FACTORS.
 NUG is not found in a well nourished individual with a
fully functional immune system.
 Immunodeficiency may be related to varying levels of
nutritional deficiency.
 Fatigue caused by chronic sleep deficiency.
 Other health habits.
 Systemic disease.
5.NUTRITIONAL DEFICIENCY
 A poor diet has been cited as a predisposing factor in
NUG.
 Nutritional deficiencies accentuate the severity of
the pathologic changes .
6.DEBILIATING DISEASE
 May predispose patients to the development of NUG
such systemic disturbances include chronic
diseases,severe GIT disorders,blood dyscrasias.
7.PSYCHOSOMATIC FACTORS.
 Important in the etiology of NUG
 Disease often occurs in association with stressful
situations
 Psychological disturbances
 Decreased adrenocortical secretion
 Alterations in digital and gingival capillary responses
suggesting increased autonomic nervous activity.
EPIDEMIOLOGY AND PREVALENCE
 NUG occurs at all ages.
 Highest incidence 20-30 years and 15-20 years.
 Not common in children.
 Reported in children from low socio economic groups.
 NUG is more common in children with DOWN
SYNDROME than in other children and deficiencies.
 COMMUNICABILITY
 PHGS is contagious
 Usually occurs in infants and children.
 Signifies a capacity for the maintenance of
infection by natural modes of spread such as
direct contact through drinking
water,food,via airborne route or by means of
arthropod vectors.
 A disease that is communicable is called
contagious.
 TRANSMISSIBILITY
 Denotes a capacity for the maintenance of an
infectious agent in successive passages
through a susceptible animal host.
DIAGNOSIS
 Diagnosis is based on clinical findings
 A bacterial smear may be used to corroborate
the clinical diagnosis, but it is not necessary
nor definitive because the bacterial picture is
not appreciably different from the other
conditions (Gingivitis, periodontal pockets etc).
DIFFERENTIAL DIAGNOSIS include:
a. Gonococcal stomatitis.
b. Agranulocytosis.
c. Vincent’s angina.
d. Desquamative gingivitis.
e. Acute necrotizing ulcerative gingivitis in
leukaemia.
f. Acute necrotizing ulcerative gingivitis in
AIDS.
g. Streptococcal gingivostomatitis.
TREATMENT:
The treatment of NUG consists of
(1) Alleviation of the acute inflammation plus
treatment of chronic disease either
underlying the acute involvement or else
where in the oral cavity,
(2) Alleviation of generalized toxic symptoms
such as fever and malaise, and
(3) Correction of systemic conditions that
contribute to the initiation or progress of
the gingival changes.
Treatment for:
1. Non-ambulatory patient: With symptoms of
generalized systemic complications.
2. Ambulatory patient: With no serious systemic
complications.
TREATMENT FOR NON-AMBULATORY PATIENTS
Day 1:
 Local treatment limited to gently removing the necrotic pseudomembrane
with a pellet of cotton saturated with hydrogen peroxide (H2O2)
 Advised bed rest and rinse the mouth every 2 hours with a diluted 3
percent hydrogen peroxide .
 Systemic antibiotics like penicillin or metronidazole can be prescribed.
Day 2:
 If condition is improved, proceed to the treatment described for
ambulatory patients. If there is no improvement at the end of the 24
hours, a bedside visit should be made. The treatment again includes gently
swab the area with hydrogen peroxide, instructions of the previous day are
repeated.
Day 3:
 Most cases, the condition will be improved, start the treatment for
ambulatory patients.
TREATMENT FOR AMBULATORY PATIENTS
 First visit: Cotton pellet to remove pseudomembrane
and non-attached surface debris .
 Superficial calculus is removed with ultrasonic scalars.
 Patients with moderate or severe necrotizing ulcerative
gingivitis and local lymphadenopathy, -Antibiotic
regime - Penicillin 500 mg thrice daily, Penicillin-
sensitive patients erythromycin or metronidazole 200
mg or 400 mg twice daily for seven days.
 Sub-gingival scaling and curettage are contraindicated.
INSTRUCTIONS TO THE PATIENT:
 1. Avoid smoking and alcohol.
 2. Rinse with 3 percent hydrogen peroxide and warm
water for every two hours.
 3. Confine toothbrushing to the removal of surface
debris with a bland dentifrice, use of interdental aids
and chlorhexidine mouth rinse are recommended.
Second visit:
 Scalers and curettes are added to the instrumentarium,
shrinkage of the gingiva may expose previously covered
calculus which is gently removed. Same instructions are
reinforced.
Third visit:
 Scaling and root planing are repeated, plaque control
instructions are given. Hydrogen peroxide rinses are
discontinued.
Fourth visit:
 Oral hygiene instructions are reinforced and thorough
scaling and root planing are performed.
Fifth visit:
 Appointments are fixed for treatment of chronic
gingivitis, periodontal pockets and pericoronal flaps,
and for the elimination of all local irritants. Patient is
placed on maintenance programme.
FURTHER TREATMENT CONSIDERATIONS
1. Gingivoplasty.
2. Role of drugs (escharotic drugs and silver
nitrate hydrogen peroxide, sodium perborate).
3. Systemic antibiotics—only in patients with toxic
systemic complications.
4. Supportive systemic treatment—copious fluid
consumption and administration of analgesics
and adequate bed rest.
5. Nutritional supplements—vitamin B/C
supplements.
NECROTIZING ULCERATIVE PERIODONTITIS
An infection characterized by necrosis of gingival tissues,
periodontal ligament, and alveolar bone.
Types
1. AIDS type NUP
1ST form
2. Non AIDS type NUP
2nd form
 1st form – evolves from a previous onset of NUG
 2nd form – superinfection of chronic gingivitis or periodontitis.
. Non AIDS type NUP:
Clinical features
Absence of deep pockets with deep interdental osseous craters.
AIDS type NUP
 Very aggressive, extensive tissue damage and
destruction
 Necrosis and exposure of the alveolar bone
 severe loss of attachment, formation of
interproximal craters
 May involve buccal vestibule and palate
MANAGEMENT
 Emergency treatment – broad spectrum
antibiotic cover
 Comprehensive treatment - SRP
 Alternative treatment – maintenance of oral
hygiene, mouth rinse, interdental cleaning
aids.
ACUTE HERPETIC GINGIVOSTOMATITIS (AHG)
(Viral)
 It is a viral infection of the oral mucous membrane
caused by HSV (Herpes simplex virus). It occurs most
frequently in infants and children younger than 6 years
of age but is also seen in adults.
CLINICAL FEATURES:
ORAL SIGNS
1.Diffuse, shiny erythematous, involvement of the gingiva
with edema and gingival bleeding.
2.Initial stage-appears as discrete, spherical, gray vesicles
dispersed in different areas, e.g. labial and buccal
mucosa, soft palate, pharynx and tongue.
After 24hours the vesicles rupture and form painful
small ulcers with a red, elevated, halo-like margins and
a depressed yellow and greyish white central portion.
3. Diffuse, edematous, erythematous enlargement of the
gingiva with a tendency towards bleeding is seen
(primary herpes occuring without ulceration).
4. The course of the disease is 7 to 10 days. It may appear
in a localized form following operative procedures in
the oral cavity and by placement of cotton rolls or by
vigorous application of digital pressure.
Scarring does not occur in the areas of healed
ulcerations.
 Disease is accompanied by generalized ‘’soreness’’ of the oral
cavity,which interferes with eating,drinking,and oral hygiene.
 The ruptured vesicles are focal sites of pain.
 In infants,the disease is marked by irritability and refusal to
take food.
ORAL SYMPTOMS
1. Generalized soreness of the oral cavity
2. The ruptured vesicles are sensitive to touch,
thermal changes and foods.
EXTRAORAL AND SYSTEMIC SIGNS AND SYMPTOMS
 Involvement of the lips, face (Herpes labialis,
“cold sore”) with vesicles and surface scale
formation .
 Cervical adenitis,fever as high as 101degree F to
105 degree F(38 degree C to 40.6 degree C),and
generalised malaise are common.
HISTORY
 The condition frequently occurs after an episode of
febrile diseases such as pneumonia, meningitis,
influenza and typhoid. It also tends to occur during
periods of anxiety, strain or exhaustion.
 The location of virus is in the gasserian ganglion. The
virus may descend to the lip through the trigeminal
nerve.
 Is the result of an acute infection by HSV and has an
acute onset.
HISTOPATHOLOGY
 Vesicles rupture to form a discrete ulceration-central portion
of acute inflammation (ulceration) and purulent exudate,
surrounded by a zone rich in engorged blood vessels.
 Microscopic picture of the vesicle - extra- and intracellular
edema and degeneration of the epithelial cells.
 The cell cytoplasm -liquified and clear. Later the nucleus
also degenerates.
 The vesicle formation results from fragmentation of the
degenerated epithelial cells.
 Round -eosinophilic inclusion bodies in the nuclei of
epithelial cells-Lipschutz’s bodies.
 Connective tissue is infiltrated by plasma cells. Smear
obtained is Tzanks smear and the stain used is Giemsa’s
stain.
 Ballooning degeneration that consists of acantholysis,nuclear
clearing, and nuclear enlargement.These cells are called
TZANCK cells.
 Intaepithelial vesicles rupture and develop  secondary
inflammation.
 Results in discrete ulcerations.
DIAGNOSIS
 Patients history and clinical findings.
 Confirmatory tests-
 Direct smear
 Inoculation of the virus - tissue culture.
 Serological studies: Its role is still uncertain.
DIFFERENTIAL DIAGNOSIS
1. Acute necrotizing ulcerative gingivitis
2. Erythema multiforme
3. Steven’s-Johnson syndrome
4. Lichen planus
5. Desquamative gingivitis
6. Apthous stomatitis (canker sores).
PERICORONITIS
DEFINITION
 It is an acute infection which refers to inflammation of
gingiva and surrounding soft tissues of an incompletely
erupted tooth.
 It occurs most frequently in the mandibular third molar
area.
 TYPES
Acute,
sub-acute or
chronic.
ETIOLOGY
 Partially erupted or impacted mandibular third molar.
 Space between the crown of the tooth and the
overlying gingival flap (operculum)
 Acute inflammatory involvement is a constant
possibility
 May be exacerbated by trauma, occlusion,or a foreign
body trapped underneath the tissue flap (e.g,popcorn
husk, nut fragment).
CLINICAL FEATURES
Signs and Symptoms:
 Markedly red, edematous suppurating lesion ,extremely
tender with radiating pain to the ear, throat and floor
of the mouth.
 Foul taste
 Inability to close the jaws.
 Swelling of the cheek in the region of the angle of the
jaw is seen.
ACUTE PERICORONITIS :
 Varying degrees of involvement of pericoronal
flap as well as with systemic complications.
 An influx of inflammatory fluid and cellular
exudates results in an increase in bulk of the
flap which interferes with complete closure of
the jaws. The flap is traumatized by contact
with the opposing jaw and inflammatory
involvement is aggravated.
 Lymphadenitis, toxic systemic complications-
fever, leukocytosis and malaise.
COMPLICATIONS :
• Involvement may become localized-pericoronal
abscess.
• Occurrence in a partly-erupted vital tooth- cyst
formation.
• Spread posteriorly -oropharyngeal area and
medially into the base of the tongue- difficulty
in swallowing.
• Involvement of the submaxillary, cervical, deep
cervical and retro pharyngeal lymph node.
• Peritonsillar abscess formation, cellulitis and
Ludwig’s angina occur infrequently.
TREATMENT
• Severity of the inflammation.
• The systemic complications and,
The advisability of, retaining the involved tooth.
OPERCULECTOMY -
 Periodontal knife or
 Electro surgery
 Radiosurgical loop
SYPHILLIS (Bacterial)
 Treponema pallidum is the microaerophilic
spirochete that causes syphilis, a chronic
systemic venereal disease with multiple clinical
presentations
 Primary syphilis manifest as a solitary ulcer.
Secondary
 mucous patches manifest as oval-to-
crescenteric erosions or shallow ulcers of about
1 cm diameter, covered by a grey mucoid
exudate and with an erythematous border
TUBERCULOSIS (Bacterial)
 TB is a chronic infectious granulomatous disease
caused by bacteria. It usually is acquired by inhaling
droplets contaminated by Mycobacterium tuberculosis
 Typical lesion seen on the gingiva is an indurate
chronic non healing ulcer that is painful
TRAUMATIC INJURIES
• Traumatic injuries involving the
oral cavity may typically lead to
the formation of surface
ulcerations.
• The injuries may result from
events such as accidentally
biting oneself while talking,
sleeping, or secondary to
mastication.
 Other forms of mechanical trauma, as well as
chemical, electrical, or thermal insults, may
also be involved. In addition, fractured,
carious, malposed, or malformed teeth, as
well as the premature eruption of teeth, can
contribute to the formation of surface
ulcerations.
 Poorly maintained and ill-fitting dental
prosthetic appliances may also cause trauma.
 The treatment of ulcerated lesions varies
depending upon size, duration, and location.
 With ulcerations induced by mechanical trauma
or thermal burns from food, remove the obvious
cause. These lesions typically resolve within 10-
14 days.
 Ulcerations associated with chemical injuries
will resolve. The best treatment for chemical
injuries is preventing exposure to the caustic
materials.
 With electrical burns, verify status and
administer the vaccine if necessary. Patients
with oral electrical burns are usually treated at
burn centers.
 Antibiotics, usually penicillin, may be
administered to prevent secondary infection,
especially if the lesions are severe and deeply
seated. Most traumatic ulcers resolve without
the need for antibiotic treatment.
 Treatment modalities for minor ulcerations
include the following:
 Removal of the irritants or cause
 Use of a soft mouth guard
 Use of sedative mouth rinses
 Consumption of a soft, bland diet
 Use of warm sodium chloride rinses
 Application of topical corticosteroids
 Application of topical anesthetics
SELF-INFLICTED INJURY
 Abrasive toothbrushing
 Chewing on sticks
 Self-induced wounds
 Tattooing
ETIOLOGY:
 Mostly from abrasive toothbrushing, usually over-
vigorous horizontal brushing.
 Children - fingernail.
 Gingival recession -induced by oral jewelry - tongue
studs.
 Gingival damage maybe seen in:
Learning disability.
Syndromes with
pain insensitivity:
- Congenital
indifference to pain.
 CLINICAL FEATURES:
Damage to the gingival margin or other areas
accessible to the dominant hand usually .
Gingival Involvement - Uncommon
 DIAGNOSIS- is from history and clinical features.
DIFFERENTIAL DIAGNOSIS
 Neoplasm
 Aphthae
 Systemic disease
Infections
Hematological disease
Gastrointestinal disease
Mucocutaneous disease
TREATMENT
Psychotherapy
Protective splints
HERPANGINA (Viral)
 Herpangina is a viral illness characterized by ulcers and
lesions (sores) inside the mouth, sore throat, and fever.
 Herpangina is caused by a virus, the common viruses
which cause the disease are
 Coxsachie virus
 echovirus
TREATMENT
 The goal of treatment for herpangina is to help
decrease the severity of the symptoms. Since it is
a viral infection, antibiotics are ineffective.
Treatment may include:
 increased fluid intake
 acetaminophen for any fever
 Proper hand washing is essential in helping to
prevent the disease from being spread to other
children.
HAND FOOT AND MOUTH DISEASE(Viral)
 Hand-foot-and-mouth disease (HFMD) is
an acute viral illness that presents as a
vesicular eruption in the mouth.
 HFMD can also involve the hands, feet, buttocks, and/or
genitalia. Coxsackievirus A type 16 (CV A16) is the
etiologic agent involved in most cases of HFMD, but the
illness is also associated with coxsackievirus A5, A7, A9,
A10, B2, and B5 strains.
 Enterovirus 71 (EV-71) has also caused outbreaks of HFMD
TREATMENT
 The treatment of hand-foot-and-mouth disease (HFMD) is
supportive.
 Ensure adequate fluid intake to prevent dehydration.
 Cold liquids are generally preferable.Spicy or acidic
substances may cause discomfort.
 Intravenous hydration may be necessary if the patient has
moderate-to-severe dehydration or if discomfort precludes
oral intake. Fever may be treated with antipyretics. Pain
may be treated with standard doses of acetaminophen or
ibuprofen. Direct analgesia may also be applied to the oral
cavity via mouthwashes or sprays.
GLANDULAR FEVER (Viral)
 Infectious mononucleosis, also known as kissing
disease,is a disease caused by the Epstein-Barr
(EB) virus.
ORAL MANIFESTATIONS
 There are apparently no specific oral manifestations of this
condition, although secondary lesions do occur.
 These are in the form of acute gingivitis and stomatitis.
There is an appearance of a white or grey membrane in
various areas, palatal petechiae and occasional oral ulcers.
 The occurrence of palatal petechiae is an early clinical
diagnostic sign of infectious mononucleosis.
 Research shows that a few patients with hemorrhagic
tendency exhibited oronasopharyngeal bleeding, including
bleeding from the gingiva.
TREATMENT
 There is no specific treatment for this disease.
 Various antibiotics have been used without great success.
 Bed rest and adequate diet are probably as good as any
other therapy. The disease generally runs its course in two
or three weeks and there are rarely any complications.
MEASLES(Viral)
 Measles, also known as rubeola, is an acute, infectious,
highly contagious disease that frequently occurs in
children.
 The measles virus is a paramyxovirus.
 Koplik spots are pathognomonic for measles. They are located
on the buccal mucosa in the premolar and/or molar area. The
intraoral lesions may persist for several days and begin to
slough with the onset of the rash.
 Koplik spots consist of bluish-gray specks against an
erythematous background. They have been compared to
grains of sand. As few as 1 spot and as many as 50 spots may
occur. The lesions are plaquelike or nodular and oval or
round.
TREATMENT
 Is symptomatic
 Antivirals may be given
CANDIDIASIS (Fungal)
 “Oral thrush,” a fungal disease of the oral mucosa and
tongue, is caused most often by Candida albicans,
although there have been reports of increased incidence
of non-albicans species.
 In the absence of other known causes of immune
suppression, oral thrush in an adult is highly suggestive
of HIV infection.
CLINICAL FEATURES
 Patient complains of white patches on oral mucosa,
smooth red areas, burning or painful mouth areas,
changes in taste sensation, sensitivity to spicy foods,
and decreased appetite.
 Erythematous candidiasis tends to be symptomatic
with complains of oral burning, most often while
eating salty or spicy foods or drinking acidic beverages.
 Pseudomembranous candidiasis appears as creamy
white curd-like plaques on the buccal mucosa,
tongue, and other mucosal surfaces that will wipe
away, leaving a red or bleeding underlying surface.
Lesions may be as small as 1-2 mm in size, or
extensive plaques covering the entire hard palate.
 Erythematous candidiasis presents as a flat red,
subtle lesion or lesions either on the dorsal surface
of the tongue and/or the hard/soft palates. The
tongue may have depapillated red mucosal areas on
its dorsal surface
TREATMENT
 Topical therapies are recommended for mild to
moderate cases of intraoral candidiasis.
 Treatment with fluconazole can result in selective
growth of non-albicans species, and should only be
implemented when necessitated by more severe
disease.
 Patient education
 GINGIVAL ABSCESS
DEFINITIONS
 When an abscess is confined to the marginal gingiva, it
has been termed as gingival abscess (McFall, 1964;
O’Brien 1970).
 Abscess localized in the gingiva, caused by injury to the
outer surface of the gingiva and not involving the
supporting structures is called a gingival abscess
(Carranza – 9th Edition).
ETIOLOGY
 Forceful impaction of a foreign object into the
gingiva /gingival sulcus.
 Example: - pop-corn kernel .
 CLINICAL FEATURES
Since it develops within a few days to a week, the
patients may be able to recall particular food items
or incidents of trauma associated with the
development of the abscess.
 Involves the gingival margin and extend to the
mucogingival Junction or be solely localized to
the gingival unit.
 Occur in previously healthy periodontium.
 Little or no calcified deposits on the root surface.
 Red, smooth, shiny surface
 May be painful and appear pointed.
 Purulent exudates may be present
DIFFERENTIAL DIAGNOSIS for gingival abscess
 Periodontal abscess
 Gingival cyst in adults
 Pericoronal abscess
 More common in older age (40 years)
 With or without bony involvement
 Mandibular canine premolar region most
commonly involved.
 Histological feature: lined with a thin, non-keratinized
squamous epithelium
 Treatment: - local surgical excision.
TREATMENT
 Elimination of the foreign object
 Thorough careful debridement.
 Drainage through the sulcus with a probe / light scaling /
incision through fluctuant area with # 11 blade covered
with gauze pad.
 Rinsing with warm saline every 2 hours.
 Follow up after 24-48 hrs.
 If the residual size of the lesion is too great. It is removed
surgically.
APHTHOUS STOMATITIS :
CLINICAL FEATURES
 Characterized by discrete spherical vesicles
that rupture after 1 or 2 days and form
depressed spherical ulcers. The ulcers consist
of a saucer like red or greyish red central
portion and an elevated rim at the periphery.
 Site-Mucobuccal fold, the floor of the mouth -
most common.
 Painful lesion ,Single lesion or multiple.
 Onset –childhood or adolescence.
 The duration of each lesion is 7 to 10 days.
May occur in the following forms:
 Occasional aphthae: Single lesions-occurs occasionally-
months to years.
 Acute aphthae: Acute episode-persist for weeks; Seen
in children and adults with acute gastrointestinal
disorders.
 Chronic recurrent aphthae: One or more oral lesions -
recurrent condition- many years.
There are three distinct clinical patterns of aphthae:
• Minor - small ulcers (< 4 mm) on mobile mucosae,
healing within 14 days, no scarring.
• Major - large ulcers (may be > 1 cm), any site including
dorsum of tongue and hard palate, healing within 1-3
months, with scarring .
• Herpetiform ulcers - multiple minute ulcers that
coalesce to produce ragged ulcers.
ETIOLOGY:
 Unknown (Herpes simplex virus was suspected to be the
cause but antibody and tissue culture studies
discourage this opinion).
 Changes in cell mediated immunity.
 Cross reactivity with Streptococcus Sanguis.
 Predisposing factors include hormonal disturbances,
allergic phenomena, gastro intestinal disorders and
psychosomatic factors.
TREATMENT:
A. Local applications: Using 8 percent zinc chloride,
Talbot’s iodine,phenol, riboflavin, thiamine, etc.
 Chlortetracycline (aureomycin)-mouthwash ,topically
in a 3% ointment or administered systemically in the
form of 250 mg capsules.
B. Palliative treatment:
Plaque ,food debris and superficial calculus are
removed to reduce gingival inflammation.
 Relief in pain -dicyclomine hydrochloride—a
topical anaesthetic mouth wash(0.5%)-diluted
1:1 with water.
C. Supportive treatment: Copious fluid intake,
Systemic antibiotic therapy- for management of
toxic systemic complications.
For relief of pain-aspirin (systemically
administered).
ERYTHEMA MULTIFORME
 Erythema multiforme (EM) is an acute self-limited
eruption characterized by a distinctive clinical
eruption, the hallmark of which is the iris or target
lesion.
 EM may present within a wide spectrum of severity.
 EM minor represents a localized eruption of the skin
with mild or no mucosal involvement, corresponding
to the initial description of Von Hebra.
 EM major and Stevens-Johnson syndrome (SJS) are
more severe mucosal and skin diseases and are
potentially life-threatening disorders.
 Oral lesions are the most common, with the lips, the
palate, and the gingiva often affected.
 More severe erosions of at least 2 mucosal surfaces are
seen in EM major and are characterized by a
hemorrhagic crusting of the lips and ulceration of the
nonkeratinized mucosa.
TREATMENT
 Symptomatic treatment, including oral antihistamines,
analgesics, local skin care, and soothing mouthwashes, is
of great importance.
 Topical steroids may be considered.
CONCLUSION
 Acute gingival problems require an accurate diagnosis, so
that appropriate emergency care can be provided to
relieve the patient's symptoms of pain.
 Careful follow-up of the affected areas is essential for the
avoidance of recurrent problems, which can lead to further
soft and/or hard tissue destruction.
REFERENCES:
 Textbook of clinical periodontology-Carranza -
9th edition.
 Periodontal manifestations of local and
systemic diseases –G.Laskaris and C.Scully.
 Loesche WJ,Syed S A, Langhom BE. The
bacteriology of acute necrotizing ulcerative
gingivitis. J Periodontol 1982;53:223.
 Martin Dunitz:Periodontal and gingival diseases
in children and adolescents.
 Yoji Murayama, Hidemi Kurihara, Thomas E. Van
Dyke. Acute necrotizing ulcerative gingivitis,
risk factors involving host defense mechanisms,
Periodontol 2000:1994.
 Periodontol 2000:vol 34; Diagnostics.
 J Periodontol 1986;vol 57:pg:141-150.
 Annals of periodontology: ANUG;vol 4 :pg:65-
73.
 Drugs,diseases and the periodontium:Seymour
and Heasman.
 J Clin Periodontol 2000;vol 27:pg 377-386.

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Acute Gingival Infections Guide by Dr. Pradnya Wagh

  • 2. CONTENTS:  Introduction  Classification  Acute necrotizing ulcerative gingivitis.  Terminology  History  Definition  Clinical features  Oral symptoms  Classification  Histopathology  Etiology  Epidemiology and Prevalence  Diagnosis  Differential diagnosis  Treatment.  Necrotizing ulcerative periodontitis.
  • 3.  Acute herpetic gingivostomatitis  Clinical features  Oral symptoms  History  Histopathology  Diagnosis  Differential diagnosis  Pericoronitis  Definition  Types  Etiology  Clinical features  Acute pericoronitis  Complications  Treatment  Tuberculosis  Syphillis
  • 4.  Traumatic injuries  Herpangina  Hand foot and mouth disease  Glandular fever  Measles  Candidiasis  Gingival abscess  Apthous Stomatitis  Erythema multiforme  Conclusion  References
  • 6. CLASSIFICATION OF VARIOUS ACUTE GINGIVAL LESIONS: According to Manson R a.Traumatic lesions of gingiva: • Physical injury • Chemical injury b.Viral infections: • Acute herpetic gingivostomatitis • Herpangina • Hand, foot and mouth diseases • Measles • Herpes varicella/zoster virus infection • Glandular fever
  • 7. c.Bacterial infections: • Acute necrotizing ulcerative gingivitis • Tuberculosis • Syphilis d.Fungal diseases: • Candidiasis. e.Gingival abscess f. Apthous ulceration g.Erythema multiforme. h.Drug allergy and contact hypersensitivity
  • 8. ACUTE NECROTIZING ULCERATIVE GINGIVITIS (ANUG): (Bacterial) TERMINOLOGIES:  Trench mouth,  Vincent's stomatitis,  Vincent’s infection,  Plaut-Vincents stomatitis,  Stomatitis ulcerosa.  ANUG is a microbial disease of gingiva in the context of an impaired immune response.  Maybe localized or generalized.
  • 9. HISTORY  Xenophen (401 B.C)-sore ulcerated and foul smell.  Hirschfeld and Hunter(1778)- Made first clinical differential diagnosis between ANUG ,periodontoclasia and oral symptoms of scurvy.  Plaut and Vincent (1890) described the disease.
  • 10. DEFINITION: Non–contagious anaerobic infection associated with overwhelming proliferation of Borrelia vincenti and fusiform bacteria. -Laskaris and Scully Necrotizing ulcerative gingivitis(NUG)is an inflammatory destructive disease of the gingiva, which presents characteristic signs and symptoms. -Carranza and Klokkevold
  • 11. CLINICAL FEATURES:  Schluger(1943) provided pathognomonic signs of ANUG:  Painful ulceration and engorgement of the interdental papillae(punched out inverted papillae). These craters are covered by greyish pseudo membranous slough, which is demarcated from the remaining of the mucosa by a pronounced linear erythema.  The ulcerations of necrotizing ulcerative gingivitis could be of two types, lateral ulceration and necrosis, deep ulceration and necrosis .
  • 12.  Pseudo membrane- easily removed exposing raw bleeding tissue.  Pronounced tendency to gingival bleeding.  Halitosis.  Sialorrhoea.  Fever, Malaise and lymphadenopathy.  Other sites of involvement:Occational spread to contiguous or adjacent tissues.
  • 13. ORAL SYMPTOMS 1.The lesions are extremely sensitive to touch. 2.Complains of a constant radiating, gnawing pain that is intensified by eating spicy or hot foods and chewing. 3. There is a metallic foul taste, and the patient is conscious of an excessive amount of “pasty saliva”.
  • 14. EXTRAORAL SIGNS AND SYMPTOMS  Mild to Moderate stages- local lymphadenopathy, elevated temperature.  Severe -Marked systemic complications such as high fever, increased pulse rate, leukocytosis, loss of appetite and general lassitude are common.  Systemic reactions -more severe in children. Insomnia, constipation, gastrointestinal disorders,headache,and mental depression also accompany.
  • 15. Walter.D.Shields (1977) conducted a study of some of the contributing factors for ANUG in army population and divided signs and symptoms into primary and secondary. PRIMARY SIGNS: 1.Gingival bleeding 2.Pain 3.Interdental ulceration and necrosis especially in the mandibular anteriors with resultant blunting and cratering.
  • 16.
  • 17.
  • 18. SECONDARY SIGNS: 1.Pseudomembrane. 2.Fetid Odor. 3.Bad Taste. 4.Elevated Temperature And Malaise. 5.Wooden Sensation In The Mouth. 6.Lymphadenopathy.
  • 19.  ANUG in malnourished, debilitated and immunocompromised patients may extend onto the oral mucosa and skin resulting in cancrum oris (noma;gangrenous stomatitis). Anaerobes- porphyromonas species and Fusobacterium necrophorum-implicated .
  • 20. Spreading necrosis penetrates buccal mucosa Gangrene Oro-cutaneous fistula and scarring.  Fusospirochetal meningitis, peritonitis, toxemia, and fatal brain abscess.
  • 21.  Goldhaber and Giddon (1964) –stated that most significant criteria in diagnosis of ANUG are :  Interproximal necrosis and ulceration.  History of soreness and bleeding in the area.
  • 22. CLASSIFICATION:  According to Pindborg J(1951)-classified into 3 forms  Acute  Subacute  Chronic (Now considered a misidentification of recurrence of the disease).
  • 23. Pindborg (1967) proposed following stages: Stage 1:Only tip of the papilla was affected. Stage 2:Marginal gingiva involved with punched out papillae. Stage 3:Attached gingiva was also involved. Stage 4:Bone was exposed.
  • 24. Horning and Cohen(1995) extended the staging of these oral necrotizing diseases as follows:  Stage 1: Necrosis of the tip of the interdental papilla (93%)  Stage 2: Necrosis of the entire papilla (19%)  Stage 3: Necrosis extending to the gingival margin (21%).  Stage 4: Necrosis extending also to the attached gingiva(1%).  Stage 5: Necrosis extending into buccal or labial mucosa (6%).  Stage 6: Necrosis exposing alveolar bone (1%).  Stage 7: Necrosis perforating skin of cheek (0%).
  • 27. Uohora (1967) suggested three stages of the disease: • Stage 1:ANUG • Stage 2:Necrotizing ulcerative mucositis. • Stage 3:Cancrum oris (noma).
  • 28. HISTOPATHOLOGY: Listgarten and colleagues (1965)described four zones namely: 1. Zone I—Bacterial zone: It is the most superficial zone, consists of varied bacteria, including a few spirochetes of the small, medium-sized and large types. 2. Zone II—Neutrophil-rich zone: Contains numerous leukocytes predominantly neutrophils with bacteria including spirochetes of various types.
  • 29. 3. Zone III—Necrotic zone: Consists of a dead tissue cells, remnants of connective tissue fragments, and numerous spirochetes. 4. Zone IV—Zone of spirochetal infiltration: Consists of a well preserved tissue infiltrated with spirochetes of intermediate and large-sized without other organisms.
  • 30. ETIOLOGY: 1.ROLE OF BACTERIA  Plaut and Vincent introduced the concept that acute necrotizing ulcerative gingivitis is caused by a specific bacteria namely, a fusiform bacillus and a spirochetal organisms.  More recently Loesche and colleagues described a constant and a variable flora associated with ANUG.  Constant flora is composed of Fusospirochetal organisms and also Bacteroides intermedius. The Variable flora consists of a heterogeneous array of bacterial types .
  • 31.  Caused by specific bacteria fusiform bacillus and spirochetal organism .  Rosebury described,  a fusospirochetal complex consisting of treponema microdentium.  Intermediate spirochetes  Vibrios  Fusiform bacilli  Filamentous organisms  Borrelia species.
  • 32. Loesche described  predominant constant flora  Variable flora 2.ROLE OF HOST RESPONSE  Regardless of whether specific bacteria are implicated in the etiology of NUG,the presence of these organism is insufficient to cause the disease.  NUG has been associated with physical and emotional stress and decreased resistance to infection.
  • 33.  Plaut and Vincent = specific bacteria  Rosebury = Fusospirochetal complex  Loesche et al = Constant flora and variable flora
  • 34.  All the predisposing factors for NUG are associated with immunosuppression.  Immunodeficiency may be related to varying levels of nutritional deficiency,  fatigue caused by chronic sleep deprivation,  other health habits  Psychological factors or systemic disease.
  • 35. 3.LOCAL PREDISPOSING FACTORS  Pre existing gingivitis  Injury to the gingiva  Smoking  most often occurs superimposed on pre existing chronic gingival disease and periodontal pockets.  Deep periodontal pockets  Pericoronal flaps  Areas of the gingiva traumatized by opposing teeth in malocclusion may predispose to NUG  Pindborg reported that 98 % of his patients with NUG were smokers and that the frequency of this disease increases with an increasing exposure to tobacco smoke.
  • 36. 4.SYSTEMIC PREDISPOSING FACTORS.  NUG is not found in a well nourished individual with a fully functional immune system.  Immunodeficiency may be related to varying levels of nutritional deficiency.  Fatigue caused by chronic sleep deficiency.  Other health habits.  Systemic disease.
  • 37. 5.NUTRITIONAL DEFICIENCY  A poor diet has been cited as a predisposing factor in NUG.  Nutritional deficiencies accentuate the severity of the pathologic changes . 6.DEBILIATING DISEASE  May predispose patients to the development of NUG such systemic disturbances include chronic diseases,severe GIT disorders,blood dyscrasias.
  • 38. 7.PSYCHOSOMATIC FACTORS.  Important in the etiology of NUG  Disease often occurs in association with stressful situations  Psychological disturbances  Decreased adrenocortical secretion  Alterations in digital and gingival capillary responses suggesting increased autonomic nervous activity.
  • 39. EPIDEMIOLOGY AND PREVALENCE  NUG occurs at all ages.  Highest incidence 20-30 years and 15-20 years.  Not common in children.  Reported in children from low socio economic groups.  NUG is more common in children with DOWN SYNDROME than in other children and deficiencies.
  • 40.  COMMUNICABILITY  PHGS is contagious  Usually occurs in infants and children.  Signifies a capacity for the maintenance of infection by natural modes of spread such as direct contact through drinking water,food,via airborne route or by means of arthropod vectors.  A disease that is communicable is called contagious.  TRANSMISSIBILITY  Denotes a capacity for the maintenance of an infectious agent in successive passages through a susceptible animal host.
  • 41. DIAGNOSIS  Diagnosis is based on clinical findings  A bacterial smear may be used to corroborate the clinical diagnosis, but it is not necessary nor definitive because the bacterial picture is not appreciably different from the other conditions (Gingivitis, periodontal pockets etc).
  • 42. DIFFERENTIAL DIAGNOSIS include: a. Gonococcal stomatitis. b. Agranulocytosis. c. Vincent’s angina. d. Desquamative gingivitis. e. Acute necrotizing ulcerative gingivitis in leukaemia. f. Acute necrotizing ulcerative gingivitis in AIDS. g. Streptococcal gingivostomatitis.
  • 43.
  • 44.
  • 45.
  • 46. TREATMENT: The treatment of NUG consists of (1) Alleviation of the acute inflammation plus treatment of chronic disease either underlying the acute involvement or else where in the oral cavity, (2) Alleviation of generalized toxic symptoms such as fever and malaise, and (3) Correction of systemic conditions that contribute to the initiation or progress of the gingival changes.
  • 47. Treatment for: 1. Non-ambulatory patient: With symptoms of generalized systemic complications. 2. Ambulatory patient: With no serious systemic complications.
  • 48. TREATMENT FOR NON-AMBULATORY PATIENTS Day 1:  Local treatment limited to gently removing the necrotic pseudomembrane with a pellet of cotton saturated with hydrogen peroxide (H2O2)  Advised bed rest and rinse the mouth every 2 hours with a diluted 3 percent hydrogen peroxide .  Systemic antibiotics like penicillin or metronidazole can be prescribed. Day 2:  If condition is improved, proceed to the treatment described for ambulatory patients. If there is no improvement at the end of the 24 hours, a bedside visit should be made. The treatment again includes gently swab the area with hydrogen peroxide, instructions of the previous day are repeated. Day 3:  Most cases, the condition will be improved, start the treatment for ambulatory patients.
  • 49. TREATMENT FOR AMBULATORY PATIENTS  First visit: Cotton pellet to remove pseudomembrane and non-attached surface debris .  Superficial calculus is removed with ultrasonic scalars.  Patients with moderate or severe necrotizing ulcerative gingivitis and local lymphadenopathy, -Antibiotic regime - Penicillin 500 mg thrice daily, Penicillin- sensitive patients erythromycin or metronidazole 200 mg or 400 mg twice daily for seven days.  Sub-gingival scaling and curettage are contraindicated.
  • 50. INSTRUCTIONS TO THE PATIENT:  1. Avoid smoking and alcohol.  2. Rinse with 3 percent hydrogen peroxide and warm water for every two hours.  3. Confine toothbrushing to the removal of surface debris with a bland dentifrice, use of interdental aids and chlorhexidine mouth rinse are recommended. Second visit:  Scalers and curettes are added to the instrumentarium, shrinkage of the gingiva may expose previously covered calculus which is gently removed. Same instructions are reinforced. Third visit:  Scaling and root planing are repeated, plaque control instructions are given. Hydrogen peroxide rinses are discontinued.
  • 51. Fourth visit:  Oral hygiene instructions are reinforced and thorough scaling and root planing are performed. Fifth visit:  Appointments are fixed for treatment of chronic gingivitis, periodontal pockets and pericoronal flaps, and for the elimination of all local irritants. Patient is placed on maintenance programme.
  • 52. FURTHER TREATMENT CONSIDERATIONS 1. Gingivoplasty. 2. Role of drugs (escharotic drugs and silver nitrate hydrogen peroxide, sodium perborate). 3. Systemic antibiotics—only in patients with toxic systemic complications. 4. Supportive systemic treatment—copious fluid consumption and administration of analgesics and adequate bed rest. 5. Nutritional supplements—vitamin B/C supplements.
  • 53. NECROTIZING ULCERATIVE PERIODONTITIS An infection characterized by necrosis of gingival tissues, periodontal ligament, and alveolar bone. Types 1. AIDS type NUP 1ST form 2. Non AIDS type NUP 2nd form  1st form – evolves from a previous onset of NUG  2nd form – superinfection of chronic gingivitis or periodontitis.
  • 54. . Non AIDS type NUP: Clinical features Absence of deep pockets with deep interdental osseous craters.
  • 55. AIDS type NUP  Very aggressive, extensive tissue damage and destruction  Necrosis and exposure of the alveolar bone  severe loss of attachment, formation of interproximal craters  May involve buccal vestibule and palate MANAGEMENT  Emergency treatment – broad spectrum antibiotic cover  Comprehensive treatment - SRP  Alternative treatment – maintenance of oral hygiene, mouth rinse, interdental cleaning aids.
  • 56. ACUTE HERPETIC GINGIVOSTOMATITIS (AHG) (Viral)  It is a viral infection of the oral mucous membrane caused by HSV (Herpes simplex virus). It occurs most frequently in infants and children younger than 6 years of age but is also seen in adults. CLINICAL FEATURES: ORAL SIGNS 1.Diffuse, shiny erythematous, involvement of the gingiva with edema and gingival bleeding. 2.Initial stage-appears as discrete, spherical, gray vesicles dispersed in different areas, e.g. labial and buccal mucosa, soft palate, pharynx and tongue. After 24hours the vesicles rupture and form painful small ulcers with a red, elevated, halo-like margins and a depressed yellow and greyish white central portion.
  • 57. 3. Diffuse, edematous, erythematous enlargement of the gingiva with a tendency towards bleeding is seen (primary herpes occuring without ulceration). 4. The course of the disease is 7 to 10 days. It may appear in a localized form following operative procedures in the oral cavity and by placement of cotton rolls or by vigorous application of digital pressure. Scarring does not occur in the areas of healed ulcerations.
  • 58.  Disease is accompanied by generalized ‘’soreness’’ of the oral cavity,which interferes with eating,drinking,and oral hygiene.  The ruptured vesicles are focal sites of pain.  In infants,the disease is marked by irritability and refusal to take food.
  • 59.
  • 60. ORAL SYMPTOMS 1. Generalized soreness of the oral cavity 2. The ruptured vesicles are sensitive to touch, thermal changes and foods. EXTRAORAL AND SYSTEMIC SIGNS AND SYMPTOMS  Involvement of the lips, face (Herpes labialis, “cold sore”) with vesicles and surface scale formation .  Cervical adenitis,fever as high as 101degree F to 105 degree F(38 degree C to 40.6 degree C),and generalised malaise are common.
  • 61. HISTORY  The condition frequently occurs after an episode of febrile diseases such as pneumonia, meningitis, influenza and typhoid. It also tends to occur during periods of anxiety, strain or exhaustion.  The location of virus is in the gasserian ganglion. The virus may descend to the lip through the trigeminal nerve.  Is the result of an acute infection by HSV and has an acute onset.
  • 62. HISTOPATHOLOGY  Vesicles rupture to form a discrete ulceration-central portion of acute inflammation (ulceration) and purulent exudate, surrounded by a zone rich in engorged blood vessels.  Microscopic picture of the vesicle - extra- and intracellular edema and degeneration of the epithelial cells.  The cell cytoplasm -liquified and clear. Later the nucleus also degenerates.  The vesicle formation results from fragmentation of the degenerated epithelial cells.  Round -eosinophilic inclusion bodies in the nuclei of epithelial cells-Lipschutz’s bodies.  Connective tissue is infiltrated by plasma cells. Smear obtained is Tzanks smear and the stain used is Giemsa’s stain.
  • 63.  Ballooning degeneration that consists of acantholysis,nuclear clearing, and nuclear enlargement.These cells are called TZANCK cells.  Intaepithelial vesicles rupture and develop  secondary inflammation.  Results in discrete ulcerations.
  • 64. DIAGNOSIS  Patients history and clinical findings.  Confirmatory tests-  Direct smear  Inoculation of the virus - tissue culture.  Serological studies: Its role is still uncertain.
  • 65. DIFFERENTIAL DIAGNOSIS 1. Acute necrotizing ulcerative gingivitis 2. Erythema multiforme 3. Steven’s-Johnson syndrome 4. Lichen planus 5. Desquamative gingivitis 6. Apthous stomatitis (canker sores).
  • 66. PERICORONITIS DEFINITION  It is an acute infection which refers to inflammation of gingiva and surrounding soft tissues of an incompletely erupted tooth.  It occurs most frequently in the mandibular third molar area.  TYPES Acute, sub-acute or chronic.
  • 67. ETIOLOGY  Partially erupted or impacted mandibular third molar.  Space between the crown of the tooth and the overlying gingival flap (operculum)  Acute inflammatory involvement is a constant possibility  May be exacerbated by trauma, occlusion,or a foreign body trapped underneath the tissue flap (e.g,popcorn husk, nut fragment).
  • 68. CLINICAL FEATURES Signs and Symptoms:  Markedly red, edematous suppurating lesion ,extremely tender with radiating pain to the ear, throat and floor of the mouth.  Foul taste  Inability to close the jaws.  Swelling of the cheek in the region of the angle of the jaw is seen.
  • 69. ACUTE PERICORONITIS :  Varying degrees of involvement of pericoronal flap as well as with systemic complications.  An influx of inflammatory fluid and cellular exudates results in an increase in bulk of the flap which interferes with complete closure of the jaws. The flap is traumatized by contact with the opposing jaw and inflammatory involvement is aggravated.  Lymphadenitis, toxic systemic complications- fever, leukocytosis and malaise.
  • 70.
  • 71. COMPLICATIONS : • Involvement may become localized-pericoronal abscess. • Occurrence in a partly-erupted vital tooth- cyst formation. • Spread posteriorly -oropharyngeal area and medially into the base of the tongue- difficulty in swallowing. • Involvement of the submaxillary, cervical, deep cervical and retro pharyngeal lymph node. • Peritonsillar abscess formation, cellulitis and Ludwig’s angina occur infrequently.
  • 72. TREATMENT • Severity of the inflammation. • The systemic complications and, The advisability of, retaining the involved tooth. OPERCULECTOMY -  Periodontal knife or  Electro surgery  Radiosurgical loop
  • 73.
  • 74. SYPHILLIS (Bacterial)  Treponema pallidum is the microaerophilic spirochete that causes syphilis, a chronic systemic venereal disease with multiple clinical presentations  Primary syphilis manifest as a solitary ulcer. Secondary  mucous patches manifest as oval-to- crescenteric erosions or shallow ulcers of about 1 cm diameter, covered by a grey mucoid exudate and with an erythematous border
  • 75. TUBERCULOSIS (Bacterial)  TB is a chronic infectious granulomatous disease caused by bacteria. It usually is acquired by inhaling droplets contaminated by Mycobacterium tuberculosis  Typical lesion seen on the gingiva is an indurate chronic non healing ulcer that is painful
  • 76. TRAUMATIC INJURIES • Traumatic injuries involving the oral cavity may typically lead to the formation of surface ulcerations. • The injuries may result from events such as accidentally biting oneself while talking, sleeping, or secondary to mastication.
  • 77.  Other forms of mechanical trauma, as well as chemical, electrical, or thermal insults, may also be involved. In addition, fractured, carious, malposed, or malformed teeth, as well as the premature eruption of teeth, can contribute to the formation of surface ulcerations.  Poorly maintained and ill-fitting dental prosthetic appliances may also cause trauma.
  • 78.  The treatment of ulcerated lesions varies depending upon size, duration, and location.  With ulcerations induced by mechanical trauma or thermal burns from food, remove the obvious cause. These lesions typically resolve within 10- 14 days.  Ulcerations associated with chemical injuries will resolve. The best treatment for chemical injuries is preventing exposure to the caustic materials.  With electrical burns, verify status and administer the vaccine if necessary. Patients with oral electrical burns are usually treated at burn centers.
  • 79.  Antibiotics, usually penicillin, may be administered to prevent secondary infection, especially if the lesions are severe and deeply seated. Most traumatic ulcers resolve without the need for antibiotic treatment.  Treatment modalities for minor ulcerations include the following:  Removal of the irritants or cause  Use of a soft mouth guard  Use of sedative mouth rinses  Consumption of a soft, bland diet  Use of warm sodium chloride rinses  Application of topical corticosteroids  Application of topical anesthetics
  • 80. SELF-INFLICTED INJURY  Abrasive toothbrushing  Chewing on sticks  Self-induced wounds  Tattooing
  • 81. ETIOLOGY:  Mostly from abrasive toothbrushing, usually over- vigorous horizontal brushing.  Children - fingernail.  Gingival recession -induced by oral jewelry - tongue studs.  Gingival damage maybe seen in: Learning disability. Syndromes with pain insensitivity: - Congenital indifference to pain.
  • 82.  CLINICAL FEATURES: Damage to the gingival margin or other areas accessible to the dominant hand usually . Gingival Involvement - Uncommon  DIAGNOSIS- is from history and clinical features.
  • 83.
  • 84. DIFFERENTIAL DIAGNOSIS  Neoplasm  Aphthae  Systemic disease Infections Hematological disease Gastrointestinal disease Mucocutaneous disease TREATMENT Psychotherapy Protective splints
  • 85. HERPANGINA (Viral)  Herpangina is a viral illness characterized by ulcers and lesions (sores) inside the mouth, sore throat, and fever.  Herpangina is caused by a virus, the common viruses which cause the disease are  Coxsachie virus  echovirus
  • 86. TREATMENT  The goal of treatment for herpangina is to help decrease the severity of the symptoms. Since it is a viral infection, antibiotics are ineffective. Treatment may include:  increased fluid intake  acetaminophen for any fever  Proper hand washing is essential in helping to prevent the disease from being spread to other children.
  • 87. HAND FOOT AND MOUTH DISEASE(Viral)  Hand-foot-and-mouth disease (HFMD) is an acute viral illness that presents as a vesicular eruption in the mouth.  HFMD can also involve the hands, feet, buttocks, and/or genitalia. Coxsackievirus A type 16 (CV A16) is the etiologic agent involved in most cases of HFMD, but the illness is also associated with coxsackievirus A5, A7, A9, A10, B2, and B5 strains.  Enterovirus 71 (EV-71) has also caused outbreaks of HFMD
  • 88. TREATMENT  The treatment of hand-foot-and-mouth disease (HFMD) is supportive.  Ensure adequate fluid intake to prevent dehydration.  Cold liquids are generally preferable.Spicy or acidic substances may cause discomfort.  Intravenous hydration may be necessary if the patient has moderate-to-severe dehydration or if discomfort precludes oral intake. Fever may be treated with antipyretics. Pain may be treated with standard doses of acetaminophen or ibuprofen. Direct analgesia may also be applied to the oral cavity via mouthwashes or sprays.
  • 89. GLANDULAR FEVER (Viral)  Infectious mononucleosis, also known as kissing disease,is a disease caused by the Epstein-Barr (EB) virus.
  • 90. ORAL MANIFESTATIONS  There are apparently no specific oral manifestations of this condition, although secondary lesions do occur.  These are in the form of acute gingivitis and stomatitis. There is an appearance of a white or grey membrane in various areas, palatal petechiae and occasional oral ulcers.  The occurrence of palatal petechiae is an early clinical diagnostic sign of infectious mononucleosis.  Research shows that a few patients with hemorrhagic tendency exhibited oronasopharyngeal bleeding, including bleeding from the gingiva.
  • 91. TREATMENT  There is no specific treatment for this disease.  Various antibiotics have been used without great success.  Bed rest and adequate diet are probably as good as any other therapy. The disease generally runs its course in two or three weeks and there are rarely any complications.
  • 92. MEASLES(Viral)  Measles, also known as rubeola, is an acute, infectious, highly contagious disease that frequently occurs in children.  The measles virus is a paramyxovirus.
  • 93.  Koplik spots are pathognomonic for measles. They are located on the buccal mucosa in the premolar and/or molar area. The intraoral lesions may persist for several days and begin to slough with the onset of the rash.  Koplik spots consist of bluish-gray specks against an erythematous background. They have been compared to grains of sand. As few as 1 spot and as many as 50 spots may occur. The lesions are plaquelike or nodular and oval or round.
  • 94. TREATMENT  Is symptomatic  Antivirals may be given
  • 95. CANDIDIASIS (Fungal)  “Oral thrush,” a fungal disease of the oral mucosa and tongue, is caused most often by Candida albicans, although there have been reports of increased incidence of non-albicans species.  In the absence of other known causes of immune suppression, oral thrush in an adult is highly suggestive of HIV infection.
  • 96. CLINICAL FEATURES  Patient complains of white patches on oral mucosa, smooth red areas, burning or painful mouth areas, changes in taste sensation, sensitivity to spicy foods, and decreased appetite.  Erythematous candidiasis tends to be symptomatic with complains of oral burning, most often while eating salty or spicy foods or drinking acidic beverages.
  • 97.  Pseudomembranous candidiasis appears as creamy white curd-like plaques on the buccal mucosa, tongue, and other mucosal surfaces that will wipe away, leaving a red or bleeding underlying surface. Lesions may be as small as 1-2 mm in size, or extensive plaques covering the entire hard palate.  Erythematous candidiasis presents as a flat red, subtle lesion or lesions either on the dorsal surface of the tongue and/or the hard/soft palates. The tongue may have depapillated red mucosal areas on its dorsal surface
  • 98. TREATMENT  Topical therapies are recommended for mild to moderate cases of intraoral candidiasis.  Treatment with fluconazole can result in selective growth of non-albicans species, and should only be implemented when necessitated by more severe disease.  Patient education
  • 99.  GINGIVAL ABSCESS DEFINITIONS  When an abscess is confined to the marginal gingiva, it has been termed as gingival abscess (McFall, 1964; O’Brien 1970).  Abscess localized in the gingiva, caused by injury to the outer surface of the gingiva and not involving the supporting structures is called a gingival abscess (Carranza – 9th Edition). ETIOLOGY  Forceful impaction of a foreign object into the gingiva /gingival sulcus.  Example: - pop-corn kernel .
  • 100.  CLINICAL FEATURES Since it develops within a few days to a week, the patients may be able to recall particular food items or incidents of trauma associated with the development of the abscess.  Involves the gingival margin and extend to the mucogingival Junction or be solely localized to the gingival unit.  Occur in previously healthy periodontium.  Little or no calcified deposits on the root surface.  Red, smooth, shiny surface  May be painful and appear pointed.  Purulent exudates may be present
  • 101. DIFFERENTIAL DIAGNOSIS for gingival abscess  Periodontal abscess  Gingival cyst in adults  Pericoronal abscess  More common in older age (40 years)  With or without bony involvement  Mandibular canine premolar region most commonly involved.  Histological feature: lined with a thin, non-keratinized squamous epithelium  Treatment: - local surgical excision.
  • 102. TREATMENT  Elimination of the foreign object  Thorough careful debridement.  Drainage through the sulcus with a probe / light scaling / incision through fluctuant area with # 11 blade covered with gauze pad.  Rinsing with warm saline every 2 hours.  Follow up after 24-48 hrs.  If the residual size of the lesion is too great. It is removed surgically.
  • 103. APHTHOUS STOMATITIS : CLINICAL FEATURES  Characterized by discrete spherical vesicles that rupture after 1 or 2 days and form depressed spherical ulcers. The ulcers consist of a saucer like red or greyish red central portion and an elevated rim at the periphery.  Site-Mucobuccal fold, the floor of the mouth - most common.  Painful lesion ,Single lesion or multiple.  Onset –childhood or adolescence.  The duration of each lesion is 7 to 10 days.
  • 104. May occur in the following forms:  Occasional aphthae: Single lesions-occurs occasionally- months to years.  Acute aphthae: Acute episode-persist for weeks; Seen in children and adults with acute gastrointestinal disorders.  Chronic recurrent aphthae: One or more oral lesions - recurrent condition- many years.
  • 105. There are three distinct clinical patterns of aphthae: • Minor - small ulcers (< 4 mm) on mobile mucosae, healing within 14 days, no scarring. • Major - large ulcers (may be > 1 cm), any site including dorsum of tongue and hard palate, healing within 1-3 months, with scarring . • Herpetiform ulcers - multiple minute ulcers that coalesce to produce ragged ulcers.
  • 106.
  • 107. ETIOLOGY:  Unknown (Herpes simplex virus was suspected to be the cause but antibody and tissue culture studies discourage this opinion).  Changes in cell mediated immunity.  Cross reactivity with Streptococcus Sanguis.  Predisposing factors include hormonal disturbances, allergic phenomena, gastro intestinal disorders and psychosomatic factors.
  • 108. TREATMENT: A. Local applications: Using 8 percent zinc chloride, Talbot’s iodine,phenol, riboflavin, thiamine, etc.  Chlortetracycline (aureomycin)-mouthwash ,topically in a 3% ointment or administered systemically in the form of 250 mg capsules.
  • 109. B. Palliative treatment: Plaque ,food debris and superficial calculus are removed to reduce gingival inflammation.  Relief in pain -dicyclomine hydrochloride—a topical anaesthetic mouth wash(0.5%)-diluted 1:1 with water. C. Supportive treatment: Copious fluid intake, Systemic antibiotic therapy- for management of toxic systemic complications. For relief of pain-aspirin (systemically administered).
  • 110. ERYTHEMA MULTIFORME  Erythema multiforme (EM) is an acute self-limited eruption characterized by a distinctive clinical eruption, the hallmark of which is the iris or target lesion.  EM may present within a wide spectrum of severity.  EM minor represents a localized eruption of the skin with mild or no mucosal involvement, corresponding to the initial description of Von Hebra.  EM major and Stevens-Johnson syndrome (SJS) are more severe mucosal and skin diseases and are potentially life-threatening disorders.
  • 111.  Oral lesions are the most common, with the lips, the palate, and the gingiva often affected.  More severe erosions of at least 2 mucosal surfaces are seen in EM major and are characterized by a hemorrhagic crusting of the lips and ulceration of the nonkeratinized mucosa.
  • 112. TREATMENT  Symptomatic treatment, including oral antihistamines, analgesics, local skin care, and soothing mouthwashes, is of great importance.  Topical steroids may be considered.
  • 114.  Acute gingival problems require an accurate diagnosis, so that appropriate emergency care can be provided to relieve the patient's symptoms of pain.  Careful follow-up of the affected areas is essential for the avoidance of recurrent problems, which can lead to further soft and/or hard tissue destruction.
  • 115. REFERENCES:  Textbook of clinical periodontology-Carranza - 9th edition.  Periodontal manifestations of local and systemic diseases –G.Laskaris and C.Scully.  Loesche WJ,Syed S A, Langhom BE. The bacteriology of acute necrotizing ulcerative gingivitis. J Periodontol 1982;53:223.  Martin Dunitz:Periodontal and gingival diseases in children and adolescents.
  • 116.  Yoji Murayama, Hidemi Kurihara, Thomas E. Van Dyke. Acute necrotizing ulcerative gingivitis, risk factors involving host defense mechanisms, Periodontol 2000:1994.  Periodontol 2000:vol 34; Diagnostics.  J Periodontol 1986;vol 57:pg:141-150.  Annals of periodontology: ANUG;vol 4 :pg:65- 73.  Drugs,diseases and the periodontium:Seymour and Heasman.  J Clin Periodontol 2000;vol 27:pg 377-386.