I.A.AYISHA TALAT BDS FINAL YEAR SEM2

1. GOOD MORNING
I.A.AYISHA TALAT

2. ACUTE GINGIVAL
INFECTIONS
1.ANUG
2.Primary herpetic
gingivostomatitis
3.Pericoronitis
● acute lesions is of sudden onset
and short duration and is painful.
● They are manifested with severe
pain along with systemic
manifestations.
● Thus these lesions must be treted
at earliest with a proper treatment
protocol.

3. Acute Necrotizing Ulcerative Gingivitis
● Microbial disease of the gingiva in
context of an impaired host
response and is characterized by
necrosis and sloughing of the
gingival tissue.
● Vincents infections, acute
ulceromembranous gingivitis,
trench mouth, ulcerative gingivitis,
Vincents stomatitis, plaut Vincent
stomatitis, stomatitis ulcerosa, fedid
stomatitis, fusospirillary gingivitis
and putrid stomatitis.

4. HISTORY
● In 4th century BC Xenophon mentioned that Greek soldiers were affected with
“sore mouth” and “foul smelling breath”.
● In 1778 John Hunter described the clinical features and differentiation of ANUG
with scury and chronic destructive periodontal disease.
● Occured in epidemic form in the french army in 19th century.
● In 1886 Hersch german pathologist said that the features were associated with
lymphadenopathy, fever, malaise, hypersalivation.
● In 1890 Plaut and Vincent describes the disease was originated to Fusiform
bacilli and Spirochetes.

5. CLINICAL FEATURES
● Acute disease and can undergo
diminution in severity without treatment
leading to subacute stage.
● Involve single or group of teeth and can
cause tissue destruction involving
periodontal attachment apparatus in
severe immunosuppression patients.
● When bone loss occurs the condition is
called as necrotizing ulcerative
periodontitis (NUP)

6. ETIOLOGY
1. ROLE OF BACTERIA :
● Plaut 1894 and Vincent 1896 introduced the concept NUG is caused by specific
bacteria namely fusiform bacillus and Spirochete.
● Rosebury and co described a fusospiral complex consisting of T.macrodentium,
intermediate Spirochetes, vibrios, fusiform bacilli, filamentous organisms to
several Borrelia species.
● Loesche and co described a constant
flora and a variable flora.
● Treatment with METRONIDAZOLE
reduced Treponema species, prevotella
intermedia and fusobacterium.

7. 2.ROLE OF HOST RESPONSE :
● Presence of organisms insufficient to cause disease.
● Insufficient host response.
● Seen in immunosuppressed patients.
● NUG patients displayed depression in leukocyte chemotaxis and phagocytosis
● Leads to immunodeficiency related to nutritional deficiencies, fatigue, health
habits such as alcohol or drug abuse.
Thus specific cause of NUG has not been established but complex bacterial
organisms and requires underlying tissue changes to facilitate pathogenic activity
of bacteria.
3.LOCAL PREDISPOSING FACTORS :
● Pre existing gingivitis, injury to gingiva (malocclusions)
● Smoking
● Pre existing chronic periodontitis, periodontal flaps

8. 4.SYSTEMIC FACTORS :
● Nutritional deficiencies dimishes immune response and alters the periodontal
structures making it more susceptible.
● Debilitating diseases such as chronic disease (syphilis, cancer), GIT disorders,
blood dyscrasias, AIDS.
● Stress ( Hypothalamus-pituitary-adrenal axis activation resulting in cortisol
secretion and decrease in immune response.
● Increased level of cortisols and catecholamines leads to reduced gingival
microbes and salivary flow which enhanced nutrition to P.intermedia.
● Decrease in neutrophils and lymphocytes functions lead to bacterial invasion and
tissue damage.

9. ORAL SIGNS AND SYMPTOMS
● Punched out craterlike depression at the
crest of the interdental papilla.
● Can extend into marginal and attached
gingiva and oral mucosa.
● Surface of crater is covered by gray
pseudomembranous slough demarcated
from linear erythema.
● Removing slough exposes red
hemorrhagic shiny surface which bleeds
easily.
● Sensitive to touch, radiating gnawing pain
intensified by eating spicy or got food and
chewing.

10. ● Metallic foul taste and pasty saliva.
● Usually ambulatory
● Local lymphadenopathy, increase temperature, high fever, increase pulse rate,
leukocytosis, loss of appetite, insomnia,constipation,headache,depression.
Clinical course :

12. BACTERIA ~ANUG

13. TREATMENT:
● Alleviate acute symptoms by reducing microbial load and removalmof necrotic
tissues.
● Treatment of chroic disease either underlying the acute involvement or elsewhere in
the oral cavity.
● Alleviate generalized symptoms such as fever and malaise.
● Correction of the systemic conditions that contribute to initiation or progrssion.

17. Primary Herpetic Gingivostomatitis
● an infection of the oral cavity caused by
HSV Type 1.
● Infants and children <6yrs of age.
● Males = Females
● Asymptomatic infections.
● PRIMARY INFECTION : Virus ascends
through the sensory or autonomic nerves
and persists in the ganglia that innervates
the site as a latent HSV.
● SECONDARY INFECTION : Sunlight,
trauma, fever, stress which are månifested
as H.labialis, H.stomatitis, H.genitalis etc.

18. ORAL SIGNS AND SYMPTOMS:
● Diffuse erythematous shiny involvement
of gingiva and adjacent oral mucosa.
● Edema and gingival bleeding.
● Dicrete spherical grey vesicles.
● Rupture of vesicles and formation of ulcers
after 24hrs.
● Ulcer - small, painful,red, elevated, halo
like margin with depressed yellowish grey
white central portion.
● Widely spread or clustered
● Heals within 7- 10 days with no scarring.
● Soreness, difficulty in eating,drinking,
irritability and refuse to take food in

20. TREATMENT:

22. Pericoronitis
● Inflammation of the gingiva in relation to
the crown of an incompletly erupted tooth.
● Most often in the mandibular third molar
area.
● Acute, subacute, chronic.

23. CLINICAL FEATURES:
● Operculum - The space between crown of
the tooth and the overlying gongival flap is
an ideal area for the accumulation of food
debris and bacterial growth.
● Gingival flap is often chronically inflamed
infected and ulcerated and exacerbated by
trauma, occlusion or foreign body trapped in
the space.
● Acute pericoronitis is identified by
inflammatory involvement of flap and
adjacent structures as well as systemic
complications.

25. ● Red, swollen, suppurating lesions that is
tender with radiating pain to ear, throat,
floor of mouth.
● Patient becomes uncomfortable due to
pain, foul taste, inability to close jaws,
swelling in cheek, lymphadenitis,
trismus, fever, malaise, leukocytosis.
● Pericoronal abscess
● Peritonsillar abscess sequelae of acute
● Cellulitis pericoronitis
● Ludwigs angina
Complications:

26. TREATMENT: