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ACUTE GINGIVAL LESIONS
1. INTRODUCTION
2. CLASSIFICATION:-
- Manson’s classification
3. VARIOUS TYPES OF ACUTE GINGIVAL LESIONS
- epidemiology and prevalence
- etiology
- Predisposing factors
- Clinical features
- Histopathology
- Treatment
4. SUMMARY
5. REFERENCES:-
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INTRODUCTION
Acute lesions are by definition of sudden onset limited duration
and with well defined clinical features, by contrast with chronic
gingivitis which frequently not painful, Acute gingival lesions are
usually easier to diagnose. There are some pathological conditions
that can affect other parts of oral Mucosa, as well as gingivae, which
is impossible to classify because a etiology is uncertain e.g. erythema
Multiforme, or because they may be chronic with Acute episodes e.g.
fungal conditions, syphilis, T.B. may occasionally involve the gingiva
but lesions are widespread involving many parts of mouth.
ACUTE NECROTISING ULCERATIVE GINGIVITIS
SYNONYMS
- ulcero membranous gingivitis
- ANUG.
- Vincent’s gingivitis
- Vincent’s gingivo stomatitis.
- Necrotising gingivostomatitis.
- Trench Mouth (Pickard 1973, Johnson and Engel 1986, Noming
and Cohen 1995)
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Vincent first described the mixed fusospirochetal microbiota of the so
called ‘Vincent’s Angina’ characterized by Necrotic Areas in the
tonsils (Vincent 1989)
Acute Necrotising ulcerative gingivitis is a distinct and specific
disease. This disease entity has been described as far back as the
days of Hippocrates is known by many synonyms such as Trench
Mouth, Vincent’s Disease and Vincent’s gingivo stomatitis. With the
advent of Antibiotics and with improved Nutritional status the
incidence has decreased and even become extinct in developed
countries. However with the increasing incidence of severe immune
deficiency states such as AIDS the lesion has become more well
recognized and often encountered in developed countries.
In developing countries ANUG remains a commonly diagnosed
clinical lesions. This is because of the existing poor nutritional status;
stressful living conditions, poor oral hygiene. In recent years there
has been increasing recognition for the need to further study ANUG;
particularly in a view of its contribution to the incidence of cancrum
oris – which has been described as a “neglected third world disease”
children in sub- Saharan Africa.
History:- ANUG is a condition that was described as far back as the
4th century B.C by Xenophon. It was 1st described among Greek
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soldiers and was characterized by sore mouth and foul smelling
breath.
- John Hunter in 1778 described the clinical features of the
condition and differentiated it from scorbutic gingivitis
- ANUG was seen as epidemic in the French army during the 19 th
century.
- In 1890 plant and Vincent attributed its origin to fusiform Bacilli
and Spirochetes. Terms included Trench mouth, Vincent’s
infection, Vincents stomatitis, spirochetal gingivitis, ulcerative
gingivitis, acute ulcero membranous gingivitis.
Epidemiology and Prevalence:-
- ANUG often occurs in groups in an epidemic pattern.
- Prevalence of NUG appears to have been rather low in U.S.A.
and Europe before 1914. During the World I and II numerous
‘epidemics’ broke out among the Allied troops, but German
soldiers did not seem to have been similarly affected.
- In a study conducted at a dental clinic in Prague, Czech
Republic, following incidence of NUG was reported
0.08% - Between 15 & 19
0.05% - Between 20 & 24
0.02% - Between 25 & 29 (skach et al 1970)
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- NUG occurs in all ages with highest incidence reported between
20 and 30 (Smith et al 1932) and ages 15 and 20 (Skach et al
1970)
- It has been reported in children from low socio economic groups
in underdeveloped countries (Jimener et al 1975)
- NUG is more common in children with down syndrome than in
children with mental deficiencies (Brown et al 1973)
- During World war II upto 14% of the Danish military personnel
encountered NPD (Puidborg 1951)
- In 1960’s NPD was found in 2.5% of 326 U.S students during the
1st college year, but over the next year more students became
affected, with a total of 6.7% demonstrating the disease during
the 1st 2 college years (Gidson 1964)
CLASSIFICATION
According to Manson
a) Traumatic lesions of gingiva
- Physical Injury
- Chemical Injury
b) vlral Infections
- Acute herpetic gingivo stomatitis.
- Herpangina (a disease caused by Cox sackie)
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- Hand foot and Mouth Diseases.
- Measles.
- Herpes varicella/zoster virus infections
- Glandular fever.
c) Bacterial Infections:-
- ANUG
- Tuberculosis
- Syphilis.
d) Fungal Diseases
- Candidiasis.
e) Gingival abscess
f) Apthous ulceration.
g) erythema Multiforme.
h) Drug allergy and contact hypersensitivity.
Pathogenic potential of microorganism:-
Bacteria can invade epithelium (Heylings et al 1967).
Spirochetes can invade the vital connective tissue (listgarten 1965).
The pathogenic potential is further substantiated by the fact that both
fuso bacteria and spirochetes can liberate endotoxins (Mergenhagen
et 1961, Hofslad 1970) This may be by Direct or Indirect effect.
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Indirectly – endotoxcins can contribute to tissue damage in several
ways –
1. They can function as Antigens and elicit Immune Response.
2. They can activate complement directly through the alternative
pathway and thereby liberate chemotoxin, but they also can
activate macrophages, B & T lymphocytes and influence the
hosts immune reactions by interfering with cytokine produced
by these cells.
Definition:-
1. Necrotizing ulcerative gingivitis is inflammatory destructive of the
gingiva, which presents characteristic signs and symptoms.
2. ANUG is a disease with rapid onset characterized by painful,
necrotic, ulcerative gingival lesions.
a) Etiology:-
i) The Role of Bacteria:-
- NUG is caused by specific Bacteria, namely a fusiform Bacillus
and spirochaetal organism (Plaut 1894 & Vincent 1896)
- Rosebury (1950) and colleagues described a fuso spirochetal
complex consisting of T.Microdentium, intermediate spirochetes,
vibrios, fusiform Bacilli, filamentous organisms, in addition to
several Borellia species.
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- Loesche et al 1982 described a predomint flora and variable
flora associated ANUG. Constant flora is composed of provotella
intermedia, in addition to fuso bacteria, treponemas and
selenomonas species.
The variable flora consists of heterogeneous ray of Bacterial
types.
- Chung et al 1983 found increased Immunoglobulin (IgE and IgM)
antibody titers for intermediated size spirochetes and prevotella
intermedia compared with titers in those with chronic gingivitis
and healthy controls.
- Cogen et al 1983 described a depression in host defense
mechanism, particularly in PMN chemotaxis and phagocytosis.
ii) Local predisposing factors:-
- Pre-existing gingivitis:- It may also occur in disease free
mouths. It always occurs superimposed on preexisting chronic
gingival Disease and periodontal pockets.Deep periodontal
pockets and pericoronal flaps are particularly vulnerable areas
because they offer a favorable environment for the proliferation
of anaerobic fusiform Bacilli and spirochetes hence called
Incubation Zones.
- Areas of gingiva traumatized by opposing teeth in malocclusion,
such as palatal surface behind the maxillary incisors and labial
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gingival surface of the mandibular incisors are frequent sites of
NUG.
- Pindborg et al 1951 & Goldhaber 1957 reported that 98% of the
patients with NUG were smokers and that the frequency of this
disease increase with an increasing exposure to tobacco smoke.
b) Debilitaling Disease:-
This may predispose the development of NUG. These disease
include chronic diseases such as syphilis and cancer, severe GIT
disturbances like ulcerative colitis. Blood dyscrasias like leukemia
(Bregman et al 1992) AND aids (Drinkard et 1991, Glick 1994,
Horning 1995)
- Nutritional deficiency resulting from debilitating disease may be
an additional predisposing factor.
Mechanism:-
Psychosomatic factors:
- The disease often occurs in association with stress situations
e.g. induction into armed forces or school examination (Giddon
et al 1964) as well as increased adrenocortical secretion.
(Shannon et al 1964) are common in ANUG patients.
Mechanism of Action:- According to cohen-cole et al 1983. Cohen
and coworkers have suggested that a psychiatric disturbance may
lead to activation of the hypothalamic pituitary adrenal axis. This
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results in elevation of serum and urine cortisol levels, which is
associated with a depression of lymphocyte and
polymorphonuclear leukocytes function that may predispose to
acute necrotizing ulcerative gingivitis.
Other Mechanism:-(Kardachi & Clarke 1974) – stress could reduce
Blood flow to the gingiva arteriorles, stimulated by the sympathetic
Nervous system CLINICAL FEATURES:- It often occurs as an acute
episode; it under goes a diminution in severity leading to sub Acute
stage with milder clinical symptoms.
- Disease may subside spontaneously without treatment. Such
patients generally have history of repeated remissions and
exacerbations. Recurrence in this is frequent.
Oral Signs:-
- lesions are punched out crater like depression at the crest of the
interdental papillae, subsequently extending into marginal
gingival and rarely to attached gingiva and oral mucosa.
- Surface of gingival craters in covered by a gray
pseudomembranous slough, demarcated from the remainder of
the gingival mucosa by a pronounced linear erythema
- In some instance, the lesions are demarcated of the surface
pseudomembrane, exposing the gingival margin, which is red,
shiny and haemorrhagic.
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- Spontaneous gingival hemorrhage or pronounced bleeding on
the slightest stimulation.
- Fetid odor
- Increased Salivation.
Symptoms:-
- Lesions are sensitive to touch.
- Constant radiating, gnawing pain which is intensified by eating
spicy or hot foods and chewing.
- Metallic foul taste,
- Pasty saliva.
Extraoral and systemic signs and symptoms:-
- Local lymphadenopathy.
- Slight elevation in temperature.
- Marked systemic complications like high fever, increased pulse
rate, leucocytosis, loss of appetite and general lassitude.
- Insomnia.
- Constipation
- GIT disorders.
- Headache
- Mental depression.
- In rare cases, severe sequel such noma or gangrenous
stomatitis have been described (enwon et al 1972)
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CLINICAL COURSE:-If untreated, NUG may lead to NUP with a
progressive destruction of the periodontium and denudation of the
roots.
A) Pindborg et al 1966 have described the following stages in
progress of NUG.
i. only the tip of the interdental papilla affected.
ii. lesion extends to marginal gingiva and causes punched out
papilla
iii. Attached gingiva is affected
iv. Bone is exposed.
B) Horning and cohen et al 1995 extended the staging of these oral
necrotizing disease as follows.
Stage 1 – Necrosis of tip of the interdental papilla 93%
Stage 2 – Necrosis of the entire papilla (19%)
Stage 3 – Necrosis extending to 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 check (0%)
Stage 1 is NUG
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Stage 2 may be either NUG or NUP because attachments loss have
occurred.
Stage 3 & 4 are NUP
Stage 5 & 6 are necrotizing stomatitis.
Stage 7 is Noma.
Histopathology:-
- it involves both stratified squamous epithelium and underlying
connective tissue.
- The surface epithelium is destroyed and is replaced by a
meshwork of fibrin, necrotic epithelial cells, PMN’s and various
types of microorganisms.
- The underlying connective tissue is markedly hyperemic, with
numerous (excess of blood in a part) engorged capillaries and
a dense infiltration of PMN’s.
Relation of Bacteria to lesions:-
List garden – 1965 described the following 4 zones which blend with
each other and may not all be present in every case.
Zone 1 :- Bacterial Zone, the most superficial, consists of varied
Bacteria, including a few spirochetes of the small, medium and large
types.
Zone 2:- Neutrophil Rich zone contains numerous leukocytes many
spirochetes of various types, between the leucocytes.
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Zone 3:- Necrotic Zone consists of disintegrated tissue , fibrillar
material, remnants of collagen, and numerous spirochetes of the
medium and large types with few other organisms.
Zone 4 :- Zone of spirochetal Infiltration:-
Consists of well preserved tissue infiltrated with medium and large
spirochetes, without other organisms.
Bacterial flora showed that swears from the lesions present scattered
Bacteria, predominantly spirochetes and fusiform Bacilli,
desquamated epithelial cells and occasional PMN’s.
electron microscopic study showed that spirochetes may be classified
into small (7% to 39% of the total spirochetes),Medium (43.9% to
90%) and large (0 to 20%). (Listgarten et al 1967). It was also
suggested that medium sized spirochetes are present in greater
numbers in pooled scrapings from lesions of NUG and are found in
greater percentage in deeper portion of the lesions.
Treatment:
1. Non Ambulatory patient – With symptoms of generalized
systemic complications.
2. Ambulatory patient – With no serious systemic complications
1. Treatment for Non Ambulatory Patients
Day 1
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a. Local treatment limited to gently removing the necrotic
pseudomembrane with a pellet of cotton saturated with
hydrogen peroxide [H2O2.]
b. Advised bed rest and rinse the mouth every 2 hours with a
diluted 3% hydrogen peroxide [H2O2.]
c. Systemic antibiotics like penicillin or metronidazole can be
prescribed.
Day 2
a. 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 include again gently swab the area with hydrogen
peroxide, instructions of the previous day are repeated.
Day 3
a. Most cases, the condition will be improved, start the
treatment for ambulatory patients.
2. Treatment for Ambulatory Patients
1 st visit
A topical anesthetic is applied and after 2 or 3 minutes the
areas are gently swabbed with a cotton pellet to remove
pseudomembrane and non attached surface debris. After the
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area is cleansed with warm water the superficial calculus is
removed with ultrasonic scalers. Patients with moderate or
severe necrotizing ulcerative gingivitis and local
lymphadenopathy, are placed on antibiotic regime of penicillin
500 mg thrice daily, for penicillin sensitive patients
erythromycin or metronidazole 200mg or 400mg twice daily for
seven days.
Sub gingival scaling and curettage are contraindicated at this
time because of possibility of extending the infection to deeper
tissues.
Instruction to the patient :
1. Avoid smoking, alcohol.
2. Rinse with 3% hydrogen peroxide and warm water for every two
hours.
3. Confine tooth brushing to the removal of surface debris with a
bland dentifrice, use of interdental aids and chlorhexidine
mouth rinse are recommended.
2 nd 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.
3 rd Visit
Scaling and root planing are repeated, plaque control
instructions are given. Hydrogen peroxide rinses are discontinued.
4 th Visit
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Oral hygiene instructions are reinforced and thorough scaling
and root planing are performed.
5 th 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 consideration:-
1. Gingivoplasty:- If teeth are irregularly aligned healing
sometimes results in formation of shelf like gingival margin,
which favors the retention of plaque and recurrence of gingival
Inflammation. This can be eliminated by gingivoplasty or
electro surgery.
2. Surgical procedures:- Tooth extraction or periodontal surgery
should be postponed until 4 weeks after the acute signs and
symptoms of NUG have subsided. If emergency Rx is required
prophylactic chemotherapy with systemic penicillin.
3. Role of drugs:- Escharotic drugs such as phenol, silver nitrate
and tannic acid should not be used. They are Nercotizing
Agents that alleviate the painful symptoms by destroying the
nerve endings in the gingiva. They also destroy the young cells
necessary for repair and delay healing. Their repeated use
results in loss of gingival tissues.
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4. Systemic Antibiotics:- Only in patients with toxic systemic
complications.
5. Supportive systemic treatment:-
- copious fluid consumption
- Analgesics
- Bed rest.
6. Nutritional supplements:-
- Vitamin B and C.
Primary Herpetic Gingivo Stomatitis.
It is a viral infection of the oral cavity caused by the herpes
simplex virus type 1 (HSV 1). It occurs most often in infants and
children younger than 6 years of age (Scott et al 1941) but it is also
seen in adolescents and adults. It occurs with equal frequency in
male and female patients.
C/F
Oral signs:-
- It appears as a diffuse, shiny erythematous involvement of the
gingiva and the adjacent oral mucosa with varying degrees of
edema and gingival Bleeding.
- In its initial stage it may appear as discrete, spherical gray
vesicles dispersed in different areas. E.g. labial and Buccal
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Mucosa, soft palate, pharynx and tongue. After approximately
24 hours the vesicles rupture and form painful small ulcers with
a red, elevated halo like margin and a depressed yellow, and
grayish white central portion.
- Diffuse, edematous, erythematous enlargement of the gingiva
with a tendency towards bleeding is seen.
- Course of the disease is 7-10 days. The diffuse gingival
erythema and edema that appear early in me disease persist for
several days after ulcerative lesions have healed. Scarring does
not occur in the areas of healed ulceration.
Oral symptoms:-
- Generalized soreness of the oral cavity which interferes with
eating and drinking.
- The ruptured vesicles are sensitive to touch, thermal changes
and foods.
Extra Oral and systemic signs and symptoms:-
- Involvement of the lips, face (herpes labialis, cold sore) with
vesicles and surface scale formation may accompany the intra
oral disease.
- Cervical Adenitis, fever as high as 101 – 105 F and generalized
malaise are common.
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History:-
The condition frequently occurs after a episode of febrile
disease such as pneumonia, meningitis, influenza and typhoid. It also
tends to occur during periods of anxiety, strain or exhaustion.
Location of the virus is in the gasserian ganglion. The virus may
descend to the lip through the trigeminal nerve, which may explain
why the location of the blister on the lip is usually seen.
Histopathologic:-
- Epithelium of gingiva is thinned out or atrophied due to
Balloning degeneration. The virus targets the epithelial cells.
Balloning degeneration consists of acantholysis, nuclear clearing
and nuclear enlargement. These cells are called Tzanck cells
- Vesicles formed rupture to form a discrete ulceration, which
appears to have a central portion of acute inflammation
characterized by ulceration and varying degrees of purulent
exudates, surrounded by a zone rich in engorged blood vessels.
- Vesicles characterized by extra and intra cellular edema and
degeneration of epithelial cells.
- Smear taken from fluid shows under election microscope the
presence of intra nuclear virus particles - Lip schutz Bodies.
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There are round esinophilic inclusion Bodies are found in nuclei
of epithelial cells.
Diagnosis:-
- Patients history and clinical findings. Laboratory diagnosis include
a. Direct smear :- Material is obtained from the base of the lesions
and smeared and stained. Presence of multi nuclear giant cells,
containing intra nuclear eosinophilic inclusion Bodies. However
this cannot distinguish from other infections like CMV, varicella
zooster virus.
b. Innoculation of the virus from a suspected site, to tissue
culture.
c. Virus can be determined by an election microscopic
examination and specific HSV Antigens can be detected in cells
from the lesions by Immuno florescence.
Treatment Various medications have been used in the
treatment of this condition including;
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Local applications – using 8% zinc chloride, Talbot’s iodine, phenol,
riboflavin, thiamine etc. Chlortetracycline (aureomycin) has
been successfully used as a mouthwash applied topically in a 3%
ointment or administered systemically in the form of 250mg
capsules
Palliative treatment – makes the patient comfortable until the
disease runs its course (7-10 days).
Plaque food debris and superficial calculus are removed to reduce
gingival inflammation.
Relief in pain is obtained with diclonine hydrochloride – a topical
anesthetic mouth wash, which is available in a 0.5% solution that
maybe diluted 1:1 with water.
Supportive treatment : Copious fluid intake and systemic
antibiotic therapy for management of toxic systemic
complications. For relief of pain, systemically administered aspirin
is usually sufficient.
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.
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Types - Acute, sub acute or chronic.
Clinical features:
Signs and symptoms : Include markedly red, edematous
suppurating lesion that is extremely tender with radiating pain to
the ear, the throat and floor of the mouth.The patient is extremely
uncomfortable because of the foul taste and inability to close the
jaws . In addition to the pain, swelling of the cheek in the region of
the angle of the jaw is seen.
Acute pericoronitis: It is identified by 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 is a common finding; the patient may also have
toxic systemic complications such as fever, leukocytosis and malaise.
Complications
The involvement may become localized, in the form of
pericoronal abscess.
If it occurs in a partly erupted vital tooth it may give rise to
cyst formation.
It may spread posteriorly into the oropharyngeal area and
medially into the base of the tongue, making it difficult for the
patient to swallow.
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Depending on the severity there is involvement of the
submaxillary, cervical, deep cervical and retropharygeal lymph
node.
Peritonsillar abscess formation, cellulitis and Ludwig’s angina
are infrequent but nevertheless potential sequelae of acute
pericoronitis.
Treatment:The treatment of pericoronitis depends on:
Severity of the inflammation .
The systemic complications and ,
The advisability of, retaining the involved tooth .
First visit
1. The area is gently flushed with warm water to remove
superficial debris and exudate followed by application of topical
anesthetic agent.
2. The flap is reflected with a scaler and the underlying debris is
also removed and the area is flushed with warm water.
3. Instructions to the patient include hourly rinses with a solution
of a tea spoonful of salt in a glass of warm water, rest, copious
fluid intake and administration of systemic antibiotics, if toxic
symptoms are present.If the gingival flap is swollen and
fluctuant an anteroposterior incision to establish drainage is
made with a No. 15 bard parker blade, followed by insertion of
¼ inch gauze wick.
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In the next visit, determination is made as to whether the
tooth is to be retained or extracted . This decision is governed by
the likelihood of further eruption into a good functional position.
If it is decided to retain the tooth, the necessary surgical
procedures are performed using a periodontal knife or electro
surgery. Under anesthesia, a wedge shaped incision is made to
section a tissue that includes the gingival flap with the tissue
distal to the involved tooth as well. After the tissue is removed, a
periodontal pack is placed.
SUMMARY:-
1. Acute gingival lesions are classified as acute necrotizing
ulcerative gingivitis (ANUG) primary herpetic gingivostomatitis,
and pericoronitis.
2. ANUG is an inflammatory, destructive disease of the gingiva,
which presents with characteristic signs and symptoms.
3. Oral lesions are characterized by punched-out, crater like
depressions at the crest of the Interdental papillae,
subsequently involving marginal gingiva and rarely attached
gingiva.These craters are covered by greyish
pseudomembraneus slough.Patients with ANUG complain of a
constant radiating, gnawing pain and metallic taste with
excessive amount of pasty saliva.
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4. Etiological factors responsible for ANUG are divided into :
- Role of bacteria (fusospirochetal complex)
- Local predisposing factors like pre existing gingivitis, injury to
the gingiva and smoking.
- Systemic predisposing factors like nutritional deficiency,
debilitating diseases and psychosomatic factors
5. Primary herpetic gingivostomatitis is a viral infection
characterized by diffuse erythema and vesicular eruptions.
6. Pericoronitis is an acute infection, which refers to inflammation
of the gingiva and the surrounding soft tissues of an
incompletely erupted tooth. (Mostly in mandibular III molar
area).
REFERENCES
1. J.D. Manson & Bmeley, Outline of Periodontitis, Third Edition
2. Yoji Murayama, Hidemikurihara and Thomas E. Van Dyke,
Acute Necrotizing Ulcerative Gingivitis, Risk Factors involving
Host Defense Mechanisms, Periodontol 2000, Vol. 6, 1994.
3. Loesche WJ, Syed SA, Langhorn BE. The bacteriology of
acute necrotizing ulcerative gingivitis. J. Periodontol, 1982: 53:
223.
4. Carranza and Newman, Clinical Periodontology W.B.
Saunders, 9th Edition.