It was my final year presentation on Acute gingival infections and desquamative gingivitis.

1. ACUTE GINGIVAL
INFECTIONS AND
DESQUAMATIVE
GINGIVITIS
REBEKAH. M. JAMES
FINAL YEAR PART 1.

2. CONTENTS
NECROTIZING ULCERATIVE GINGIVITIS
•Historical background
•Clinical features
•Clinical course
•Histopathology
•Relation of bacteria
•Diagnosis
•Differential diagnosis
•Etiology
•Management.

3. PRIMARY HERPETIC GINGIVOSTOMATITIS
Pathogenesis
Clinical features
Histopathology
Diagnosis
Differential diagnosis
Management

4. PERICORONITIS
Clinical features
Complications
Management.
DESQUAMATIVE GINGIVITIS
Classification
Clinical features
Diagnosis
management

5. ACUTE GINGIVAL INFECTIONS
Necrotizing
Ulcerative
Gingivitis
Primary Herpetic
Gingivostomatitis
Pericoronitis

6. NECROTIZING
ULCERATIVE GINGIVITIS
•It is an microbial disease of the gingiva.
•Characterised by the necrosis and sloughing of gingival tissues.
•Presents with characteristic signs and symptoms.
Results from impaired host response to a pathogenic microflora.
Vincents infection,
Acute
ulceromembraneous
gingivitis,
Trench mouth,
Ulcerative gingivitis,
Vincents stomatitis,
Stomatis ulcerosa,
Fedid stomatitis,
Fusospirillary gingivitis,
Putid stomatitis,
Plaut-Vincents stomatitis.

7. HISTORICAL BACKGROUND
Xenophon-recognised in 4th century(sore mouth and foul smelling breath)
John Hunter-differentiated from scury and chronic destructive periodontal disease
and described the clinical findings.
Hersch-LN enlargement, fever, malaise and increase salivation.
Plaut and Vincent-described and attributed its origin to fusiform bacilli and
spirochete.

8. ETIOLOGY
Role of bacteria-fusiform bacillus and spirochetal organism.
Role of host response.
Local predisposing factors like pre existing gingivitis, injury to gingiva, smoking.
Systemic predisposing factors like immunodeficiency, diabetes, debilitating
infections, alcohol or drug abuse.
Psychosomatic factors.

9. CLINICAL FEATURES
Acute disease, sudden onset.
Undergoes a diminution in severity without treatment-subacute stage with milder
clinical symptoms
Repeated remissions and exacerbations.
Recur in previously treated patients also.
Single or multiple teeth involvement or widespread involvement throughout the
mouth.
When bone loss Necrotizing ulcerative periodontitis(NUP).
In long standing disease or immunosuppression cases.

11. HISTORY
oAfter an episode of debilitating disease or acute resp tract infection,
oChange in living habits,
oProtracted work without adequate rest,
oPoor nutrition,
oTobacco use,
oPsychological stress.

12. ORAL SIGNS
•Punched out, crater like depressions at the crest of interdental papilla that subsequently
extend to marginal gingiva and rarely to the attached gingiva and oral mucosa.
•The surface - gray, pseudomembrane slough, ie, demarcated from the remainder of the
gingival mucosa by linear erythema.
•Some cases, it is denuded of the surface pseudomembrane, thereby exposing the gingival
margin, which is
•red, shiny and haemorrhagic.
•Destroy the gingiva and the underlying periodontal tissues.
•Spontaneous gingival haemorrhage or pronounced bleeding after slightest stimulation.
•Fetid odour and salivation

14. Can occur in disease free mouths.
NUG or NUP usually doesn't lead to formation of periodontal pocket because the
necrotic changes involve the junctional epithelium.
Rare in edentulous mouth, but isolated spherical lesion occur in soft palate.

15. ORAL SYMPTOMS
Extremely sensitive to touch.
Constant radiating, gnawing pain ie, intensifying by eating spicy or hot food and
chewing.
Metallic foul taste.
Excessive amount of “pasty” saliva.

16. EXTRAORAL & SYSTEMIC SIGNS
AND SYMPTOMS
Local lymphadenopathy and
 a slight elevation in temperature.
High fever, increased pulse rate,
Leucocytosis, loss of apetite,
And general lassitude.
Systemic reactions are more severe in children. Insomnia, constipation, GI disorders,
headache, mental depression.
Gangrenous stomatitis and noma.
MILD TO MODERATE CASE
SEVERE CASE
VERY RARE CASE

17. CLINICAL COURSE
By Pindborg and coworkers-
1) Erosion of the tip of the interdental papilla.
2) The lesion involving all of the papilla and also involving the marginal gingiva
3) The attached gingiva also get involved.
4) Exposure of the bone with complete loss of interdental papilla, marginal gingiva
and the attached gingiva.

19. STAGE 1-Necrosis of the tip of the interdental
papilla.
STAGE 2-Necrosis of the entire papilla.
STAGE 7-Necrosis perforating skin of the
cheek.
STAGE 6-Necrosis exposing alveolar bone.
STAGE 5-Necrosis involving the buccal and labial
mucosa.
STAGE 4-Necrosis of the attached gingiva.
STAGE 3-Necrosis extending to the marginal
gingiva.
According
to
HORNING
AND
COHEN

20. HISTOPATHOLOGY
Nonspecific.
Involves both stratified squamous epithelium and the underlying connective
tissue.
The surface epithelium is destroyed and replaced by a meshwork of fibrin, necrotic
epithelial cells, PMN’s and various types of microorganisms (surface
pseudomembrane).
The epithelium is edematous and individual cells show hydropic degeneration in
varying degrees.
Infiltration of PMN’s in the intercellular spaces.

21. The underlying connective tissue is hyperemic, with numerous engorged
capillaries and a dense infiltration of PMN’s(linear erythema).
Numerous plasma cells may appear in the periphery of the infiltrate, and is
clinically seen as area of established chronic gingivitis

22. RELATION OF BACTERIA
1. Zone I—Bacterial zone: 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 many spirochetes
of various types between the leukocytes.
3. Zone III—Necrotic zone: Consists of a disintegrated tissue cells,
fibrillar material, remnants of collagen fibers, and numerous
spirochetes with few other organisms.
4. Zone IV—Zone of spirochetal infiltration: Consists of a well
preserved tissue infiltrated with intermediate and large-sized
spirochetes without other organisms.
LISGARTE
N

23. DIFFERENTIAL DIAGNOSIS
Stomatitis
venenata
Dermatosis
Agranulocytosis
Candidiasis
Tuberculous
gingival lesions
Diphteric &
syphilitic lesions
Gonococcal
gingivostomatitis
Apthous
stomatitis
Desquamative
gingivitis
Chronic
periodontitis
Herpetic
gingivostomatitis

24. DIAGNOSIS
CLINICAL FINDINGS-
Gingival pain
Ulcerations
And bleeding.
The bacterial smear is not necessary or definitive.
The microscopic examination of a biopsy specimen is not sufficiently specific to be
diagnostic.

25. TREATMENT 2.Treatment of
chronic disease
either underlying
the acute
involvement or
elsewhere in the
oral cavity.
1.Alleviation of the
acute inflammation by
reducing the microbial
load & removal of
necrotic tissue.
3.Alleviation of
generalised
symptoms such as
fever and malaise.
4.Correction of
systemic conditions
or factors that
contribute to the
initiation or
progression of the
gingival changes.

26. FIRST VISIT
•A topical anesthetic is applied .
•After 2-3 min the area is gently swabbed with a moistened cotton pellet with
hydrogen peroxide to remove the pseudomenbrane and non-attached surface
debris.
•Bleeding may be profuse.
•After the area is cleansed with warm water, the superficial calculus is removed.
Ultra sonics are very useful.
•Subgingival scaling and curettage
•Amoxicillin 500mg orally every 6hr – 10 days

27. SECOND VISIT
1-2 days after the first visit.
Evaluation of the patient.
Scaling is done if necessary.

28. THIRD VISIT
5 days after the second visit.
Evaluation of the patient.
Plaque control procedures.

29. INSTRUCTIONS TO THE PATIENT
Avoid tobacco, alcohol usage.
Rinse with equal amount of h2o2 and warm water every 2 hr or twice daily with
0.12%chlorhexidine.
Get adequate rest.
Confine toothbrushing with ultra soft brush or bland dentrifice.
NSAID’s

30. PRIMARY HERPETIC
GINGIVOSTOMATITIS
Is an infection of the oral cavity caused by herpes simplex virus(HSV) type 1.
It occurs most often among infants and children who are less than 6 years, but also
seen in adolescents and adults.
There is no sex predilection.
Primary infection is asymptomatic.
It is contagious

31. PATHOGENESIS
As a part of primary infection, virus ascends through the sensory and autonomic
nerves.
Where it persists as latent HSV in neuronal ganglia.
Secondary manifestations-sunlight, trauma, stress, fever.
Herpes labialis, herpetic stomatitis, herpes genitalis, herpetic encephalitis.

32. CLINICAL FEATURES
Appears as a diffuse, erythematous, shiny involvement of the gingiva and the adjacent
oral mucosa, with varying degree of oedema and gingival bleeding.
During the initial stages, a presence of discrete, spherical grey vesicles, which may
occur on the gingiva, the labial and buccal mucosa, the soft palate, the pharynx, the
sublingual mucosa and the tongue.
After 24hrs the vesicle rupture and form painful small ulcers with red, elevated, halo-
like margins and depressed yellowish or greyish-white central portions.
The course of disease is 7-10 days. Scarring does not occur in the areas of healed
ulcerations.

33. ORAL SYMPTOMS
Generalised ‘soreness’ of the oral cavity which interferes with eating, drinking, and
oral hygiene.
Sensitive to touch and thermal changes.
In infants it is marked by irritability and refusal to take food.

34. EXTRAORAL & SYSTEMIC SIGNS
AND SYMPTOMS
Cervical adenitis, fever (101-105F) and generalised malaise.

35. HISTOPATHOLOGY
•The virus targets epithelial cells which show ballooning
degeneration that consists of
oAcantholysis
oNuclear clearing
oAnd nuclear enlargement.
•These cells are known as Tzank’s cells.
•Infected cells fuse to form multinucleated cells, and
intercellular oedema leads to formation of intraepithelial
vesicles that rupture and develop a secondary inflammatory
response with fibropurulent exudate.

36. DIFFERENTIAL DIAGNOSIS
DIFFERENT
IAL
DIAGNOSIS
NUG
Erythema
multiforme
Recurrent
apthous
stomatitis
Stevens
Johnson
Syndrome

37. DIAGNOSIS
Patients history
Clinical findings.
Virus culture and immunological tests.

38. TREATMENT
oCan be treated with topical lignocaine for pain relieve.
oAcyclovir at 15 mg/kg five times a day for 5-7 days.
oAn NSAID( Ibuprofen) reduce fever and pain.

39. PERICORONITIS
“Pericoronitis” means inflammation of the gingiva in relation to the crown of an
incompletely erupted tooth.
Mandibular third molar region
Acute, subacute or chronic.

40. CLINICAL FEATURES
•Common site.
•Operculum is an ideal area of accumulation of food debris and bacterial growth.
•Gingival flap often will be chronically inflamed and infected and will be ulcerated along its
inner surface.
•Inflammatory process is exacerbated by trauma, occlusion or a foreign body trapped
underneath.
•Clinically seen as red, swollen suppurating lesion ie, exquisitely tender with radiating pain to
the ear, throat and the floor of the mouth.
•Extremely painful, foul taste and inability to close the jaws.
•Swelling of the cheek of the angle of the jaw and lymphadenitis
•Trismus
•Fever, leucocytosis and malaise

42. COMPLICATIONS
oPericoronal abscess(posteriorly-
oropharyngeal area & medially-base of
tongue. Difficultly in swallowing.
oBased on severity, LN are involved
oPeritonsillar abscess formation, cellulitis,
Ludwigs angina- Rare

43. TREATMENT
The treatment of pericoronitis depends on severity of the inflammation ,systemic complications,
and the advisability of retaining the involved tooth.
First Visit:
The area is gently flushed with warm water to remove superficial debris and exudate followed by
application of topical anesthetic agent after gently elevating the flap. The flap is reflected with a
scaler and the underlying debris is also removed and the area is flushed with warm water.
The occlusion is evaluated.
Antiobiotics is prescribed in severe cases.
Instructions to the patient include hourly rinses with a solution of teaspoonful of salt in a glass of
warm water, rest, copious fluid intake and administration of systemic antibiotics.
 If the gingival flap is swollen and fluctuant-an antero-posterior incision to establish drainage is
made with a No. 15 bard parker blade.

44. In the next visit, determination is made as to whether the tooth is to be retained or
extracted. If it is decided to retain tooth ,necessary surgical procedures are
performed using periodontal knife or electrosurgery.
 Under anesthesia, a wedge shaped incision is made to section a tissue that
includes gingival flap with tissue distal to involved tooth as well. After the tissue is
removed, periodontal pack is placed.
If not the tooth is extracted under LA.

46. DESQUAMATIVE GINGIVITIS
Unusual disorder.
Different names and different etiological factors like nutritional deficiencies,
degeneration, hormonal derangements, and so on.
Tomes and Tomes – 1894.
Goodby-mentioned it in his book.
Prinz-chronic diffuse desquamative gingivitis.
Schour and Massler-gingivosis.

47. •Unusual, unique, nonplaque associated gingivitis characterized by intense diffuse
erythema and desquamation of the surface epithelium.
•It is often associated with ulceration of the marginal and attached gingiva.
•It is not a specific disease entity by a clinical manifestation of a variety of conditions.

48. CLASSIFICATION
 Lichen Planus
 Cicatricial
pemphigoid
 Bulous
pemphigoid
 Pemphigus
vulgaris
 Psoriasis
 Dermatitis
herptiformis
 Eryhtema
multiformae
 Lupus
erythematosus
 Estrogen
deficiency in
females(menopaus
e, following
hysterectomy,
oophorectomy)
 Testosterone
defeciency in
males
 Tuberculosis
 Chronic
candidiasis
 Histoplasmosis
DRUG REACTIONS
(Lichenoid Reactions)
 Toxic-
antimetabolites
 Allergic-
barbiturate,
antibiotics, and
certain dental
materials.
OTHERS
 Crohn disease
 Chronic ulcerative
stomatitis
 Plasma cell
gingivitis
 Graft versus host
disease.
DERMATOSES
ENDOCRINAL
IMBALANCE
CHRONIC
INFECTIONS IDIOPATHIC
BASED ON ETIOLOGICAL
FACTORS

49. CLINICAL FEATURES
1.5-2.5% of population with female predilection.
3-4th decade of life but seen in younger generation also.
Mostly asymptomatic.
Symptomatic-burning sensation, to severe pain.
50%-gingiva rest to intraoral and dermatological involvement.
Pemphigus vulgaris-systemic impact also.

50. MILD FORM-
1.Diffuse erythema
2.Painless
3.Blanching
4.Intolerance to hot and spicy food
MODERATE FORM-
1.Patchy distribution of bright red and gray areas.
2.Smooth, shiny, soft gingiva
3.Burning sensation and sensitivity to temperature.
4.Auspitz sign
5.Brushing is highly discomforting.
6.Inhalation of air is painful. Intolerance to spicy, citrus
and drinks.
SEVERE FORM-
1.Wide areas of oral cavity involved.
2.Surface epithelium appears shredded.
3.Blowing of air cause a bubble in gingival epithelium.
4.Very painful.

51. MANAGEMENT
1.A meticulous
history
2.Careful
clinical
examination
3.Opinion
from a
dermatologist
if necessary
4.Biopsy and
other
investigations
5.Local and
systemic
therapy

52. CLINICAL HISTORY
I. Regarding the symptoms associated with the condition as well as its historical
aspect.
II. Regarding the previous therapy to alleviate the condition should also be
documented.

53. CLINICAL EXAMINATION
Recognise the pattern of distribution of the lesion(focal
or multifocal, with or without confinement to the gingival
tissues)
Nikolsky’s sign-vesiculobullous disorder. With a pledget of
wet cotton roll, the lesion may be gently scrapped to see
any peeling of the surface epithelium.
The handle of mouth mirror or periodontal probe may
gently pressed on the lesion to observe any blanching.
Examination of the skin and eyes.

54. BIOPSY
oIncisional biopsy.
oIt is done best after initial scaling and debridement.
oBuffered formalin (10%) is used to fix the tissues
oMichel’s buffer is used to transport solution for immunofluorescence assessment.

55. MICROSCOPIC EXAMINATION
Sections of approximately 5 micrometer of formalin fixed, paraffin embeded tissue
stained with conventional H&E are obtained for light microscopy examination.

56. IMMUNOFLURESCENCE
For direct-unfixed frozen sections are incubated with a variety of fluorescein
labelled, antihuman serum (anti Ig G, anti I g A, antifebrin and anti C3)
For indirect-unfixed frozen sections of oral or oesophageal mucosa from an animal
such as monkey are first incubated with the patient’s serum to allow for the
attachment of any serum antibodies to the mucosal tissue.
The tissue is then incubated with fluorescein labelled antihuman serum.
Immunofluorescence tests are positive if a fluorescent signal is observed in the
epithelium, its associated basement membrane, or the underlying connective
tissue.

57. SUPPORTIVE MEASURES
1. maximal emphasis provide for optimal oral hygiene.
2. a super soft toothbrush with gentle brushing is ideal.
3. caustic mouthwashes should be avoided.
4. dietary changes recommended with avoidance of spicy foods.
5. good nutritional diet is vital.
6. lifestyle changes should be enforced.
7. smoking and alcohol consumption should be avoided.

58. MEDICATIONS
Topical steroids- triamcenalone acetonide, beclomethasone.
•Systemic corticosteroids like prednisolone, beclomethasone.
•Systemic tetracycline
•Topical cyclosporine
•Dapsone
•Cyclosporine
•Azothioprine
•Methotrezate
•Topical tacrolimus
•Cyclophosphamide.
 PHOTOPHERESIS
 PLASMAPHERESIS
 FREE GINGIVAL
GRAFT
 LASER APPLICATION

59. REFERENCE
1. CARRANZA’S clinical periodontology-Second South Asia Edition.
2. Internet