ORAL INFECTION

1. ACUTE GINGIVAL
INFECTIONS
Comunicación y Gerencia
PRESENTED BY:
DR. NAVNEET SINGH
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2. TYPES
 Necrotizing Ulcerative Gingivitis
 Primary Herpetic Gingivostomatis
 Pericoronitis

3. ACUTE NECROTIZING
ULCERATIVE GINGIVITIS
 NUG (necrotizing ulcerative gingivitis) is
a progressive painful infection with ulceration,
swelling and sloughing off of dead tissue from
the mouth and throat due to the spread of
infection from the gums.
 This condition is also called Vincent's
angina after the French physician Vincent
(1862-1950). The word "angina" comes from
the Latin "angere" meaning "to choke or
throttle”

4. SYNONYMS
 As with most poorly understood diseases, Vincent's
angina goes by many other names including
 acute membranous gingivitis,
 fusospirillary gingivitis,
 fusospirillosis,
 fusospirochetal gingivitis,
 necrotizing gingivitis,
 ulcerative gingivitis,
 Vincent's gingivitis,
 Vincent's infection, and
 Vincent's stomatitis.

5. HISTORICAL PERSPECTIVE
 This disease entity has been described as far back as the days
of Hippocrates.
 Xenophon in 401 BC -- observed that many of his soldiers, on
their retreat from Persia, were plagued with sore, ulcerated and
foul-smelling mouths
 John Hunter, in 1778, --made the first clinical differential
diagnosis between gingival lesions now recognized as ANUG &
the oral symptoms of Scurvy.
 Bergeron, who, while serving with French troops in 1859, also
described a similar disease with both acute and chronic forms.
 Hirschfeld further noted ,in 1886, added the diagnostic
features of ropy saliva, enlarged sub-maxillary lymph glands,
fever and malaise

6. Contd..
 Plaut and Vincent are those who independently, in
the 1890's, first came to recognize the fusiform-
spirochete nature of this disease.
 Indeed, it is Vincent whose name is most clearly
associated with this form of gingivitis, formerly
known widely as Vincent's infection.
 Jean Henri Vincent spent part of his career as a
physician in France's Military Medical Service. By
1892, he came to recognize the ulceromembranous
condition which later bore his name.

7. Acute or chronic?
To be or not to be..
 While most authors agreed on the presence of these
predominant signs, there is a widespread difference of opinion
on variations in the extent and degree of severity of the disease
 Pindborg has designated the terms incipient, sub-acute, acute
and chronic ulceromembranous gingivitis to denote different
forms of the disease, based on extent of destruction.
 Beust et al.also classify the disease as having acute, subacute
and chronic stages.
 Kristoffersen and Lie suggest that as acute symptoms
subside, a condition they call chronic necrotizing gingivitis may
occur in untreated or in undertreated patients
 Hooper and Seymour suggested that the presence of
lymphocytes and plasma cells indicates that the NUG lesion is
superimposed on a chronic marginal gingivitis lesion, since
plasma cells are the predominant cell type in chronic gingivitis
but would not be expected in an acute lesion.

8.  There may also be some risk that in attempting to
categorize too rigidly on the basis of gradation of
symptoms, the dentist may fail to properly diagnose
NUG in patients who do not manifest all of the
symptoms of a particular category.
 Schluger has suggested that necrotizing ulcerative
gingivitis should be subdivided into mild acute, acute
and recurrent acute categories. Such a classification
provides simplicity, is descriptive and allows for
recognition of individual differences in severity.
 Acute Necrotizing Ulcerative Gingitivitis (ANUG), is
now classified as Necrotizing Periodontal Disease
according to the 1999 American Academy of
Periodontics classification system

9. EPIDEMIOLOGY
 ANUG was well known in Europe and North America
some centuries ago. These Western Countries
reported ANUG especially among military personnel.
 With the advent of antibiotics and with improved
nutritional status, the incidence has decreased and
even become extinct in developed countries
 In marked contrast,the disease is still frequently seen
in developing countries, especially in Sub- Saharan
Africa where it occurs almost exclusively among poor
children usually between the ages of 3 years and 10
years from low socio-economic backgrounds. Similar
observations have also been reported in India

10. Contd..
 However, with the HIV infection so
widespread, ANUG has become widely
recognized as a lesion which is strongly
pathognomonic of the infection.
 Reports of the prevalence of ANUG among
HIV infected patients vary between 4.3%-
16.0%
 Suggested incidence of ANUG is increasing
with a prevalence as high as 23% .

11. Etiology
 The precise etiology of ANUG is
unknown, however, it is believed to be
a polymicrobial infection with the
implicated organisms being normal
commensals of the oral cavity.
However, when the local resistance of
the human gingival area becomes
reduced, the organisms then become
pathogenic.

12.  Vincent and Plaut were the first to recognize
the fusiform-spirochete nature of NUG
 This evidence of the fusiform-spirochete
component of the disease was reinforced by
other light microscopic evidence and later
through electron microscopic evaluation.
 However, the significant role of these
organisms became doubtful as these bacterial
forms were present in the oral cavity of
periodontally healthy individuals as well.
Microbiology

13.  More light was shed on the bacterial nature of NUG
by Loesche et al. when they did quantitative cultures
of plaque samples from NUG sites under anaerobic
conditions. A partial characteristic of the microbial
analysis was done, and they determined the
cultivated flora contained a “constant portion” and a
“variable portion.” The constant portion contains a
limited number of bacterial types which is believed to
be pathogenic for NUG.
 These include Treponema species and the spirilla –
like selenomonas species. The variable portion of the
flora contained a heterogenous array of various
bacterial types

15.  Listgarten in 1965 provided electron
microscopic data confirming the invasion of
spirochetes in the ulcerated lesions could be
broadly grouped into four zones of increasing
depth from the tissue surface:
(1) bacterial zone,
(2) neutrophil-rich zone,
(3) necrotic zone and
(4) the zone of spirochete infiltration.

16. Immune system
 Necrotizing ulcerative gingivitis (NUG) is a microbial disease of
the gingiva in the context of an impaired host response.
 Cogen et al.reported a study of NUG patients who showed a
marked depression of the polymorphonuclear leukocytes (PMN)
responsiveness in both chemotaxis and phagocytosis.
 Cogen's research group also found reduced proliferation of
peripheral blood lymphocytes from NUG patients. While the
biological reason for, and significance of, reduced PMN
suggested that stress-induced elevated levels of cortisol in NUG
patients may produce these alterations in leukocyte function.
 Rowland et al. study showed reduced level of IgG and IgM
NUG patients,also suggesting impaired immune functions in
these patients.
 Evidence to support alterations in immune function as an
etiological factor in NUG is the reported high incidence of NUG
in HIV positive patients.

17. Malnutrition
 Enwonwu et al tried to explain the possible interrelationship
between NUG, protein-energy malnutrition, and immunological
competence.
 Malnutrition impairs innate and adaptive defense mechanisms in
the host with an associated dysfunction of the cytokine system.
 Also, in protein energy malnutrition tissue integrity is markedly
affected resulting in increased permeability of mucosa surfaces
to oral microbes and their products.
 Malnutrition does not only affect the integrity of the epithelium,
which is the first defense barrier against infection, but also
affects the number and depresses the protective function of the
PMN against periodontal disease.

18.  Decreased dietary protein resulting from malnutrition also
results in impairment of glycolytic activity,which is required to
give energy to PMN for phagocytosis. Also, energy required by
the epithelial cells for rapid turn over every 3-6 days and by the
periodontal collagen for metabolism and rapid remodeling is
impaired
 Ascorbic acid (Vitamin C), is necessary for optimum phagocytic
function of PMNs at a serum level of 0.7mg%, has been found
to be extremely low in malnourished chidren.This results in
impaired PMN function. Vitamin A has also been found deficient
in these malnourished children, and this can cause progressive
damage to mucosal tissues.
 Minerals such as zinc and folic acid have been found deficient in
malnutrition. Folic acid is known to be important for the
synthesis of purines, pyrimidines, and deoxyribonucleic acid
and, thus, its deficiency adversely affects the integrity of the
rapidly renewing epithelial cells

19. The Role of Stress
 Stress could be in the form of emotional stress, which
is often seen among military cadets, in harsh physical
conditions, and in stressful living endemic contagious
diseases, especially measles.
 Stress is believed to predispose to ANUG by causing
an elevation in adrenocortical secretion.
 It also causes the release of substanceP, a peptide
hormone which suppresses both specific and non
specific immunity. It also affects patients’ moods
resulting in changes in oral hygiene and nutrition.

20. Smoking
 Predisposing factor to ANUG
 Pindborg and Goldhaber found 98% of their
patients were smokers.
 Kardachi and Clarke cite reports that local
and systemic catecholamines are released in
response to nicotine and hypothesized the
effect of cathecolamine super-imposed on
psychological and physiological stress could
cause a reduction in gingival papillary flow
and, thus, cause papillary necrosis.

21. Clinical Features
 NUG is usually identified as an acute disease. NUG
often undergoes a diminution in severity without
treatment, leading to a subacute stage with milder
clinical symptoms. Thus, patients may have a history
of repeated remissions and exacerbations.
 NUG can cause tissue destruction involving the
periodontal attachment apparatus, especially in
patients with long standing disease or severe
immunosuppression. When bone loss occurs, the
condition is called necrotizing ulcerative periodontitis
(NUP)

22. Oral Signs
 Characteristic lesions are punched out,
craterlike depressions at the crest of the
interdental papillae, extending to the
marginal gingiva and rarely to the attached
gingiva and oral mucosa.
 The surface of the gingival craters is covered
by a gray, pseudomembranous slough,
demarcated from the remainder of the
gingival mucosa by a pronounced linear
erythema.
 In some cases the lesions are denuded of the
surface pseudomembrane, exposing the
gingival margin, which is red, shiny &
hemorrhagic.

23.  Spontaneous gingival hemorrhage or
pronounced bleeding after slightest
stimulation are additional characteristic
clinical signs.
 Other signs often found are fetid odor
and increased salivation.
 NUG can be superimposed on chronic
gingivitis or periodontal pockets.
However, NUG or NUP does not usually
lead to periodontal pocket formation
because the necrotic changes involve
the marginal gingival causing recession
rather than pocket formation.

24.  The 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.

25. Extra oral and Systemic
Signs and Symptoms
 Patients are usually ambulatory and have a minimum of
systemic symptoms.
 Local lymphadenopathy and a slight elevation in temperature
are common features of the mild and moderate stages of the
disease.
 In severe cases there may be high fever, increased pulse rate,
leukocytosis, loss of appetite, and general lassitude.
 Insomnia, constipation, gastrointestinal disorders, headache,
and mental depression sometimes accompany the condition.
 In very rare cases, severe sequelae such as gangrenous
stomatitis and noma have been described

26. Clinical Course
 Clinical Course can vary. If untreated NUG
may lead to NUP with a progressive
destruction of the periodontium & gingival
recession, accompanied by an increase in the
severity of systemic complications.
 Pindborg et al 1966 have described these
stages in the progress of NUG
 (1) Erosion of only the tip of the interdental
papilla
 (2) The lesion extending to marginal gingiva
and causing a further erosion of the papilla
and potentially a complete loss of the papilla
 (3) The attached gingiva also being affected;
 (4) Exposure of bone.

28.  Horning & Cohen 1995 extended the staging of these
oral necrotizing diseases as follows-
 Stage 1: Necrosis of the tip of the interdental papilla
(93%)
 Stage 2: Necrosis of the entire papilla (19%)
 Stage 3: Necrosis extending to the gingival margin
(21%)
 Stage 4: Necrosis extending to the attached gingival
(1%)
 Stage 5: Necrosis extending to buccal mucosa (6%)
 Stage 6: Necrosis exposing alveolar bone (1%)
 Stage 7: Necrosis perforating skin of cheek (0%)

29.  According to Horning and Cohen,
stage 1 -NUG,
stage 2 -NUG /NUP because attachment
loss may have occurred,
stages 3 &4- NUP,
stages 5 &6 -necrotizing stomatitis,
stage 7 - noma.

30. DIFFERENTIAL DIAGNOSIS
 NUG should be differentiated from other conditions that
resemble it in some respects such as:
 Herpetic gingivostomatitis
 Chronic periodontitis;
 Desquamative gingivitis
 Streptococcal gingivostomatitis;
 Aphthous stomatitis;
 Gonococcal gingivostomatitis;
 Diphtheritic and syphilitic lesions;
 Tuberculous gingival lesion;
 Candidiasis,
 Agranulocytosis,
 Dermatosis
 Stomatitis venenata

31. Streptococcal
gingivostomatitis
 It is a rare condition characterized by diffuse
erythema of the gingiva and other areas of the oral
mucosa. In some cases it is confined as a marginal
erythema with marginal hemorrhage. Necrosis of
the gingival margin is not a feature of this disease,
and there is no notably fetid odor. Bacterial smears
show a preponderance of streptococcal forms,
which were identified as Streptococcus viridans, but
more recent studies report it to be group A β-
hemolytic streptococcus.

32.  Aganulocytosis is charaterized by a marked
decrease in the number of circulating PMNs,
lesions of the throat & other mucous
membranes & ulceration & necrosis of the
gingiva which may resemble that of NUG.
 The oral condition in agranulocytosis is
primarily necrotizing. Because of the
diminished innate defense mechanisms in
Aganulocytosis, the clinical picture is not
marked by the severe inflammatory reaction
seen in NUG.
 Blood studies serve to differentiate between
NUG & the gingival necrosis in Aganulocytosis.

36.  A distinction must be made between
"communicability" and "transmissibility" when
referring to the characteristics of disease. The
term transmissible denotes a capacity for the
maintenance of an infectious agent in
successive passages through a susceptible
animal hosts' The term communicable
signifies a capacity for the maintenance of
infection by natural modes of spread, such as
direct contact through drinking water, food,
and eating utensils; via the airborne route; or
by means of arthropod vectors. A disease
that is communicable is describes. It has
been demonstrated that disease associated
with the fusospirochetal bacterial complex is
transmissible; however, it has not been
shown to be communicable or contagious.

37. PRIMARY HERPETIC
GINGIVOSTOMATITIS
 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, but it is also seen in adolescents and
adults.
 It occurs with equal frequency in male and female patients. In
most persons, however, the primary infection is asymptomatic.
 These secondary manifestations include herpes labialis, herpetic
stomatitis, herpes genitalis, ocular lesions,and herpetic
encephalitis.

38. CLINICAL FEATURES
 Oral Signs: Primary herpetic gingivostomatitis 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, which may occur on the
gingiva, labial and buccal mucosa soft palate, pharynx, sub-
lingual mucosa, and tongue.
 After 24 hours, the vesicles rupture an form painful, small ulcers
with a red, elevated, halo-like margin in a depressed, yellowish
or grayish white central portion.
 These occur either in widely separated areas or in clusters,
where confluence occurs.

39.  Oral Symptoms. The disease is accompanied by
generalized "soreness" of the oral cavity, which
interferes with eating and drinking.
 The ruptured vesicles are the focal sites of pain and
are particularly sensitive touch, thermal changes,
foods such as condiments and fruit juices, and the
action of coarse foods.
 In infants the disease is marked by irritability and
refusal to take food.
 Extraoral and Systemic Signs and Symptoms:.
Cervical adenitis, fever as high as 101° F to 105° F
(38.3° C to 40.6° C), and generalized malaise are
common.

41.  HISTORY:
 Primary herpetic gingivostomatitis is the
result of an acute infection by HSV and has
an acute onset.
 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

42. Diagnosis
 It is critical to arrive at a diagnosis as early as
possible in primary herpetic infections.
 Treatment with antiviral medications can
dramatically alter the course of the disease,
reducing symptoms and potentially reducing
recurrences.
 The diagnosis is usually established from the
patient's history and the clinical findings.

44.  Differential Diagnosis
 Primary herpetic gingivostomatitis should be differentiated from
several conditions.
 NUG can be differentiated in different ways.
 Erythema multiforme can be differentiated because its vesicles
are general more extensive than those in primary herpetic
gingivostomatitis and on rupture demonstrate a tendency
toward pseudomembrane formation
 In addition, the tongue is usually very involved in erythema
multiforme, with infection of the ruptured vesicles resulting in
varying degrees of ulceration.
 Oral involvement in erythema multiforme may be accompanied
by skin lesions. The duration of erythema multiforme may be
comparable with that of primary herpetic gingivostomatitis, but
prolonged involvement may occur for weeks.

45.  Bullous lichen planus is a very rare and painful
condition. It is characterized by large blisters on the
tongue and cheek that rupture and undergo
ulceration.Patches of liner, gray, lacelike lesions of
lichen planus are often interspersed among the
bullous eruptions. Lichen planus involvement of the
skin may coexist with the oral lesions and facilitate
differential diagnosis.
 Desquamative gingivitis is characterized by diffuse
involvement of the gingiva, with varying degrees of
peeling of the epithelial surface and exposure of the
underlying tissue. It is a chronic condition.

46.  Lesions of recurrent aphthous stomatitis (RAS) range
from occasional small (0.5-1 cm in diameter), well-
defined, round or ovoid, shallow ulcers with a
yellowish gray central area surrounded by an
erythematous halo, which persists for weeks and heal
with scaring. The cause is unknown, although
immunopathologic mechanisms appear to play a role.
 RAS is a different clinical entity from primary herpetic
gingivostomatitis. Diffuse erythematous involvement
of the gingiva and acute toxic systemic symptoms do
not occur in RAS. A history of previous episodes of
painful mucosal ulcerations suggests RAS rather than
primary HSV

48.  PERICORONITIS
 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
mandibullar third molar area.
Pericoronitis may be acute, subacute, or
chronic.

49. Clinical Features
 The partially erupted or impacted mandibular third molar is the
most common site of pericoronitis.
 The space between the crown of the tooth and the overlying
gingival flap (operculum) is an ideal area for the accumulation
and of food debris bacterial growth.
 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 mouth the mouth.
 The patient is extremely uncomfortable because of 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
complications, such as fever, leucocytosis, and malaise.

51.  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.