acute gingival infections Necrotizing Ulcerative Gingivitis Primary Herpetic Gingivostomatitis Pericoronitis symptoms clinical feature diagnosis and treatment

2. ACUTE GINGIVAL INFECTIONS
Necrotizing Ulcerative Gingivitis
Primary Herpetic Gingivostomatitis
Pericoronitis

3. Necrotizing Ulcerative Gingivitis
 It is a microbial disease of the gingiva in the context of
an impaired host response.
 It is characterized by the death and sloughing of
gingival tissue and presents with characteristic signs
and symptoms.

4.  Nomenclature
 Ulceromembranous gingivitis, acute necrotizing
ulcerative gingivitis, Vincent’s gingivitis, Vincent’s
gingivostomatitis, necrotizing gingivostomatitis, trench
mouth
 Epidemiology & prevalence
 Endemic pattern
 in developing countries
 0.02 to 0.08% or lesser in industrialized countries
 54 to 58% in India??
 More in HIV+ve patients

5. Clinical features
 Classification
 Acute
 Subacute
 NUP- When bone loss occurs
 History
 Sudden onset
 Debilitating disease
 Change in living habits, stress, poor nutrition, tobacco use

6. Oral signs
 Characteristic punched out, crater like depression at
the crest of the interdental papilla
 A gray pseudomembraneous slough with a linear
erythema
 Spontaneous gingival hemorrhage or pronounced
bleeding on slightest stimulation
 Can occur in a disease free mouths or be
superimposed on chronic gingivitis/ periodontitis
 Oral hygiene is generally very poor

7. Oral symptoms
 Fetid odor
 Extremely painful to touch
 Constant radiating, gnawing pain
 Metallic foul taste
 Excessive amounts of ‘pasty’ saliva

8. Extraoral signs and symptoms
 Patients may or may not have systemic complications
 Local lymphadenopathy
 High fever, increased pulse rate, leucocytosis, loss of
appetite & general lassitude

9. Clinical course
 Indefinite course & may progress to NUP till noma
 Pindborg classified NUG into following stages:
(1) Only the tip of the interdental papilla is affected
(2) The lesion extends to marginal gingiva and causes
punched-out papilla
(3) The attached gingiva is also affected
(4) Bone is exposed

10. Horning & Cohen classified as follows
 Stage 1: Necrosis of tip of interdental papilla (93%)
 Stage 2: Necrosis of entire papilla (19%)
 Stage 3: Necrosis till gingival margin (21%)
 Stage 4: Necrosis till attached gingiva (1%)
 Stage 5: Necrosis till labial or buccal mucosa (6%)
 Stage 6: Necrosis till alveolar bone (1%)
 Stage 7: Necrosis till skin of cheek (0%)

17. Histopathology
 Nonspecific acute necrotizing inflammation
 Surface epithelium is destroyed & replaced by fibrin, necrotic cells,
PMNs & various microorganisms
 Underlying connective tissue is hyperemic with numerous engorged
capillaries & PMNs
 Plasma cells & monocytes are found in deeper tissues

18.  Predominately spirochetes & fusiform
bacteria
 Spirochetal organisms form a light staining,
conspicuous, interlacing network
 Electron microscopy classifies spirochetes
into
 Small spirochetes (7 to 39%)
 Medium spirochetes (43.9 to 90%)
 Large spirochetes ( 0 to 20%)
 Bacteriology different in HIV +ve & -ve
individuals
 Trepenoma, selenomonas,
fusobacterium, melaninogenicus, P. intermedia
in HIV +ve individuals
 Borrelia, Gram +ve cocci, β hemolytic
streptococci, C albicans in HIV –ve individuals
Bacterial flora

19. Relation of bacteria to Characteristic lesion
Listgarten described four zones:
 Zone 1: Bacterial zone
 Zone 2: Neutrophil rich zone
 Zone 3: Necrotic zone
 Zone 4: Zone of spirocheteal infiltration

20. Diagnosis
Clinical findings
 Interproximal necrosis & ulceration
 Painful gingiva
 Bleeding
 Microscopic examination may not be
sufficiently specific to be diagnostic

21. Differential diagnosis
 Streptococcal / gonococcal gingivostomatitis
 Desquamative gingivitis
 Apthous stomatitis
 Tuberculosis
 Candidiasis
 Agranulocytosis
 Vincent’s angina
 NUG in leukemia
 Stomatitis venenata

25. Etiology
 Role of bacteria
 Combination of fusiform & spirocheteal organisms
 Role of Host response
 Local predisposing factors
 Preexisting gingivitis/ periodontitis, smoking, injury to gingiva
 Systemic predisposing factors
 Nutritional deficiency
 Diet, vitamins
 Debilitating disease
 HIV
 Psychosomatic factors
 Stress
Communicability

26. Treatment
(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
(3) Correction of systemic conditions that contribute
to the initiation or progress of the gingival
changes.

27. Sequence of Treatment
First visit
 History & examination
 Pseudomembrane removed under topical anesthesia with
cotton pellets.
 Area is cleansed with warm water
 Superficial scaling
 Rinses with hydrogen peroxide or chlorhexidine
 Antibiotics & analgesics
 Patient instructions
 Avoid smoking & alcohol
 Avoid physical exertion
 Avoid brushing over the area

28. Second visit
 1 to 2 days after first visit
 Gentle scaling
 Same instructions
Third visit
 5 days after second visit
 Scaling & root planing
Subsequent visits
 Rechecking & scaling of the areas

29. Additional Treatment Considerations
Contouring of gingiva
Systemic antibiotics and topical
antimicrobials
Supportive systemic treatment
Nutritional supplements

30. Persistent or Recurrent Cases
Reassessment of differential
diagnosis
Underlying systemic disease
causing immunosuppression
Inadequate local therapy
Inadequate compliance

31. Primary Herpetic Gingivostomatitis
 Caused by HSV- I
 Common in infants & children > 6 years of age
 Can occur in older individuals
 Asymptomatic in many persons
 No sex predilection
 Persists in neuronal ganglion after primary
infection
 Secondary manifestations occurs as a result of
various stimuli like sunlight, trauma, fever or
stress

32. Clinical features
Oral signs
 Diffuse erythematous, shiny involvement of gingiva &
adjacent oral mucosa
 Accompanied with varying degree of edema & gingival
bleeding
 Discrete, spherical grey vesicles on gingiva, labial & buccal
mucosa, soft palate, pharynx, sublingual mucosa & tongue are
seen in the initial stage
 They rupture & form painful small ulcers with red elevated
halo like margin & a depressed yellowish or greyish white
central area
 Course of disease is limited to 7 to 10 days
 Heals without scarring

35. Oral symptoms
 Generalized soreness of the mouth
 Pain is present and lesions are sensitive to touch, thermal
changes, foods
Extra oral signs
 Cervical adenitis, fever (101 - 105° F), malaise
 History
 History of exposure to a patient
 History of febrile diseases like pneumonia, meningitis,
influenza & typhoid
 It also occurs in the early stages of infectious mononucleosis.

36. Histopathology
 Epithelial cells are targeted
 Cells shows ballooning degeneration consisting of acantholysis,
nuclear clearing & nuclear enlargement
( Tzanck cells)
 Infected cells fuse & form multinucleated cells & intercellular edema
 This inturn leads to the formation of intraepithelial vesicles that
ruptures & develop a secondary inflammatory response with a
fibropurulent exudate
 Discrete ulcerations results from rupture of vesicles having a central
area of inflammation with a purulent exudate, surrounded by a zone
rich in blood vessels

37. Diagnosis
 History & clinical findings
 Conformatory tests include viral culture, immunologic
tests
Differential diagnosis
 Erythema multiforme
 Stevens Johnson syndrome
 Bullous lichen planus
 Desquamative gingivitis
 Recurrent aphthous stomatitis
Communicability
 Highly contagious

38. Treatment
 Usually self limiting disease
 Rarely specific
 Treatment consists of palliative measures to
make the patient comfortable, untill the disease
runs its course.
 Scaling is done to reduce inflammation
 Lidocaine hydrochloride mouth washes are
given before food
 NSAIDS can be administered
 Antibiotics is some times recommended
 Copious fluid intake is necessary
 Herpetic whitlow

39. Pericoronitis
 Refers to inflammation of the gingiva in relation to the
crown of an incompletely erupted tooth
 Occurs most commonly in the mandibular third molar
area
 may be acute, subacute or chronic

40. Clinical features
 Partially erupted or impacted third molars is the most
common site
 There is accumulation of food and bacterial growth
between the space of tooth and overlying gingiva
 Inflammatory fluid & cellular exudate increase the bulk
of the flap, which interferes with closure of mouth thus
aggravating the inflammatory process
 Finally there is a markedly red, swollen, suppurating
lesion which is extremely tender with radiating pain
 There is a foul taste & trismus
 Swelling & lymphadenitis are seen with systemic
complications

43. Complications
Pericoronal abscess
Peritonsillar abscess, cellulitis &
Ludwig’s angina

44. Treatment
 All pericoronal flaps can be removed as a preventive
measure
 In acute conditions
 Flush the area with warm water
 Swabbing with antiseptic solution
 Antibiotics are prescribed
 Drainage is done in abscess
 In chronic conditions
 Decide whether to extract the tooth or save it
 Pericoronal flap is removed by blade or electrosurgery