clinical features and classification of acute gingival infections

1. ACUTE GINGIVAL
INFECTIONS
Dr.D.Navya,MDS

2. Acute gingival diseases include-
– Necrotizing Ulcerative Gingivitis.
– Primary Herpetic Gingivostomatitis.
– Pericoronitis.

3. Necrotizing Ulcerative Gingivitis (NUG)

4.  NUG is a microbial disease of the gingiva in the context
of an impaired most response.
 It is characterized by the death and sloughing of gingival
tissue and presents with characteristic signs and
symptoms.
Clinical Features
 NUG is usually identified as an acute disease, and may
be limited to a single tooth or group of teeth or may be
widespread throughout the mouth.
 When bone loss also occurs, it is called Necrotizing
Ulcerative Periodontitis (NUP).

5.  NUG is characterized by sudden onset of symptoms,
sometimes following an episode of debilitating disease
or acute respiratory tract infection.
Oral Signs:
 Characteristic lesions are punched-out, craterlike
depressions at the crest of the interdental papillae,
subsequently extending to the marginal gingiva and
rarely to the attached gingiva and oral mucosa.
 The surface of the craters is covered by a gray,
pseudomembranous slough, demarcated from the
remainder of the gingival mucosa by a pronounced
linear erythema.

6.  In some cases the lesions are denuded of the surface
pseudomembrane, exposing the gingival margin, which
is red, shiny and hemorrhagic.
 Spontaneous bleeding, fetid odour, and increased
salivation are additional clinical signs.
Oral Symptoms:
 Lesions are extremely sensitive to touch, and the patient
often complains of a constant radiating, gnawing pain
that is intensified by eating spicy or hot foods and
chewing.
 There is a “metallic” foul taste, and the patient is
conscious of an excessive amount of “pasty” saliva.

7. Necrotizing Ulcerative Gingivitis…

8. Extraoral Systemic Signs and Symptoms:
 Patients are usually ambulatory and have a minimum of
systemic symptoms.
 Local lymphadenopathy and a slight elevation in
temperature are seen in mild and moderate forms of the
disease.
 In severe forms, there may be high fever, increased
pulse rate, leukocytosis, loss of appetite, and general
lassitude.
Clinical Course:
 If untreated, NUG may lead to NUP with a progressive
destruction of the periodontium and gingival recession.

9.  Pindborg et al have described these stages in the
progress of NUG-
1. Erosion of only the tip of the interdental papillae.
2. Lesion extending to marginal gingiva and
causing a further erosion of the papilla and
potentially a complete loss of the papilla.
3. Attached gingiva also being affected.
4. Exposure of bone.

10. Severe sequelae of necrotizing gingivitis in children
with severe malnutrition…

11. Histopathology
 Microscopically, the NUG lesion is acute necrotizing
inflammation of the gingival margin, involving both the
stratified squamous epithelium and the connective
tissue.
 The surface epithelium is destroyed and replaced by a
meshwork of fibrin, necrotic epithelial cells, PMNs and
various microorganisms. This is the zone that appears
clinically as the surface pseudomembrane.
 The underlying connective tissue is extremely
hyperemic, with numerous engorged capillaries and a
dense infiltration of PMNs. This acutely inflamed zone
appears clinically as the linear erythema beneath the
pseudomembrane.

12. Survey section of interdental papilla in NUG…

13. Relation of Bacteria to Characteristic Lesion
 The layer between the necrotic and the living tissue is
found to have enormous numbers of fusiform bacilli and
spirochetes.
 Spirochetes have been found as deep as 300 microns
from the surface.
Diagnosis
 Diagnosis is based on clinical findings of gingival pain,
ulceration, and bleeding; a bacterial smear is not
definitive of necessary.

14. Bacterial smear from lesion in NUG…

15.  Microscopic examination of a biopsy specimen is not
sufficiently specific to be diagnostic.
 Microscopy can be used to differentiate NUG from
specific infections such as tuberculosis or from
neoplastic disease, but it does not differentiate between
NUG and other necrotizing conditions of non specific
origin.
 NUG should be differentiated from other conditions that
resemble it in some respects such as herpetic
gingivostomatitis, chronic periodontitis, desquamative
gingivitis, streptococcal gingivostomatitis, tuberculous
gingival lesion, agranulocytosis, candidiasis etc.

16. Differentiation between NUG and Primary
Herpetic Gingivostomatitis…

17. Differentiation among NUG, Chronic Desquamative
Gingivitis, and Chronic Periodontal Disease…

18. Differentiating among NUG, Diphtheria, and
Secondary stage of Syphilis…

19. Etiology
– Role of Bacteria.
– Role of the Host Response.
– Local Predisposing Factors.
– Systemic Predisposing Factors.
• Nutritional Deficiency.
• Debilitating Disease.
– Psychosomatic Factors.

20. Epidemiology and Prevalence
 NUG often occurs in groups in an epidemic pattern.
 NUG occurs at all ages with the highest incidence
reported between ages 20 and 30 years and ages 15 and
20 years.
 It is not common in children in the US, Canada, and
Europe,, but is prevalent in children from low
socioeconomic groups in underdeveloped countries.
 NUG is more common in children with Down syndrome
than in other children with mental deficiencies.

21. Communicability
 The tem communicable signifies a capacity for the
maintenance of infection by natural modes of spread.
 A disease that is communicable is described as
contagious.
 NUG has not been shown to be communicable or
contagious.
 The occurrence of NUG in epidemic-like outbreaks does
not mean it is contagious. It may be because of common
predisposing factors in the afflicted groups rather than
because of its spread from person to person.

22. Primary Herpetic Gingivostomatitis

23.  Primary herpetic gingivostomatitis is an 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 and occurs with equal frequency in male
and female patients.
 In most persons however, the primary infection is
asymptomatic.
 As part of the primary infection, the virus ascends
through sensory and autonomic nerves, where it persists
as latent HSV in neuronal ganglia that innervate the site.
 Secondary manifestations result from various stimuli.

24. Clinical features
Oral Signs:
 It appears as a diffuse, erythematous, shiny involvement
of the gingiva and the adjacent oral mucosa, with
varying degrees of edema and gingival bleeding.
 In its initial stage, it is characterized by the presence of
discrete, spherical gray vesicles.
 After approximately 24 hours, the vesicles rupture and
form painful, small ulcers with a red, elevated, halo-like
margin and a depressed, yellowish or grayish white
central portion.
 The course of the disease is limited to 7 to 10 days;
scarring does not occur in the areas of healed
ulcerations.

25. Recurrent intra-oral herpetic vesicles in the palate (Left)
and in the gingiva (Right)…

26. Recurrent herpes vesicles in the lip…

27. Primary herpetic gingivostomatitis in a 12-year old
boy…

28. Involvement of the lip, gingiva, and tongue in
primary herpetic gingivostomatitis…

29. Oral Symptoms:
 The disease is accompanied by generalized soreness of
the oral cavity, which interferes with eating and drinking.
 The ruptures vesicles are the focal sites of pain and are
particularly sensitive to touch, thermal changes, foods
such as condiments and fruit juices, and the action of
coarse foods.
Extraoral and Systemic Signs and Symptoms:
 Cervical adenitis, high fever, and generalized malaise are
common.
History:
 Primary herpetic gingivostomatitis is the result of an
acute infection by HSV and has an acute onset.

30. Histopathology
 The virus targets the epithelial cells, which show
ballooning degeneration consisting of acantholysis,
nuclear clearing, and nuclear enlargement.
 These cells are called ‘Tzanck cells’. Infected cells fuse,
forming multinucleated cells, and intercellular edema
leads to formation of intraepithelial vesicles that rupture.
 Discrete ulcerations resulting from the rupture of the
vesicles have a central portion of acute inflammation,
with varying degrees of purulent exudate, surrounded by
a zone rich in engorged blood vessels.

31. Biopsy showing intraepithelial viral vesicles,, containing
fluid and debris, with large number of viruses and
virally altered epithelial cells…

32. Aphthous lesion in the lip…

33. Diagnosis
 The diagnosis is usually established from the patient’s
history and the clinical findings.
 Material may be obtained from the lesions and submitted
to the laboratory for confirmation tests, including virus
culture and immunologic tests using monoclonal
antibodies or DNA hybridization techniques.
 This should not delay treatment if strong clinical
evidence exists for primary gingivostomatitis.

34. Differential Diagnosis
 Primary herpetic gingivostomatitis should be
differentiated from several conditions such as-
– Erythema multiformae.
– Stevens-Johnson syndrome.
– Bullous lichen planus.
– Desquamative gingivitis.
– Lesions of recurrent aphthous stomatitis.

35. Communicability
 Primary herpetic gingivostomatitis is contagious.
 Most adults have developed immunity to HSV as the
result of infection during childhood, which in most cases
is subclinical.
 For this reason, acute herpetic gingivostomatitis usually
occurs in infants and children.

36. Pericoronitis

37.  The term “Pericoronitis” refers to inflammation of the
gingiva in relation to the crown of an incompletely
erupted tooth.
 It occurs most often in the mandibular third molar area.
 Pericoronitis may be acute, sub-acute, or chronic.

38. Clinical Features
 The space between the crown of the impacted tooth and
the overlying gingival epithelium (operculum) is an ideal
area for the accumulation of food debris and bacterial
growth.
 Acute inflammatory involvement is a constant possibility
and may be exacerbated by trauma, occlusion, or a
foreign body trapped underneath the tissue flap.
 Inflammatory fluid and cellular exudate increase the bulk
of the flap, which then may interfere with complete
closure of the jaws and can be traumatized by contact
with the opposing jaw, aggravating the inflammatory
involvement.

39.  The resultant clinical picture is that of a red, swollen,
suppurating lesion that is exquisitely tender, with
radiating pains to the ear, throat and floor of the mouth.
 The patient is extremely uncomfortable because of a foul
taste and an inability to close the jaws, in addition to the
pain.
 Swelling of the cheek in the region of the angle of the
jaw and lymphadenitis are common findings; trismus
may also be a presenting complaint.
 The patient may also have systemic complications such
as fever, leukocytosis, and malaise.

40. Inflamed coronal flap
covering disto-occlusal
surface of impacted
mandibular third molar…

41. Complications
 The involvement may be localized in the form of a
pericoronal abscess.
 It may spread posteriorly into the oropharyngeal area
and medially to the base of the tongue, making it
difficult for the patient to swallow.
 Depending on the extent and severity of the infection,
there is involvement of the sub-maxillary, posterior
cervical, deep cervical, and retropharyngeal lymph
nodes.
 Peritonsillar abscess formation, cellulitis, and Ludwig’s
angina are infrequent but potential sequelae.