ACUTE GINGIVAL INFECTIONS

DR.E. RAMNATH M.D.S

SENIOR LECTURER
DEPARTMENT OF PERIODONTICS
A.P.D.C.H
INTRODUCTION
Necrotizing ulcerative gingivitis (NUG) is an
inflammatory destructive disease of the gingiva, which
presents characteristic signs and symptoms.
ANUG
Is a microbial disease of the gingiva in the context of
an impaired host response.
It is characterised by the death and sloughing of
gingival tissue and presents with characteristic sign
and symptoms
NUG often undergoes a diminution in severity, leading to a
subacute stage with milder clinical symptoms.
The disease may sometimes subside spontaneously
without treatment.
Such patients generally have a history of repeated
remissions and exacerbations.
Recurrence of the condition in previously treated patients
is also frequent.
Involvement may be limited to a single tooth or group of
teeth or may be widespread throughout the mouth.
NUP
NUP
NUG can cause tissue destruction involving the
supporting structures. When bone loss occurs the
condition is called necrotizing ulcerative periodontitis
(NUP)
HISTORY
HISTORY

NUG is characterized by sudden onset, sometimes

following an episode of debilitating disease or acute
respiratory tract infection.

A change in living habits, protracted work without

adequate rest, and psychologic stress are frequent
features of the patient's history.
ORAL SIGNS
 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 gingival craters is covered by a gray,
pseudomembranous slough, demarcated from the remainder
of the gingival mucosa by a pronounced linear erythema
 ORAL SIGNS
In some instances, the lesions are denuded of the surface
pseudomembrane, exposing the gingival margin, which is
red, shiny, and hemorrhagic.

The characteristic lesions may progressively destroy the

gingiva and underlying periodontal tissues
CLINICAL SIGNS

Spontaneous gingival hemorrhage or pronounced

bleeding on the slightest stimulation are additional
characteristic
Other signs often found are fetid odor and increased
salivation.
NUG can occur in otherwise disease-free mouths or
can be superimposed on chronic gingivitis or
periodontal pockets.
However, it does not usually lead to periodontal pocket
formation because the necrotic changes involve the
junctional epithelium; a viable junctional epithelium
is needed for pocket deepening
It is rare in edentulous mouths, but isolated spherical
lesions occasionally occur on the soft palate.
ORAL SYMPTOMS
ORAL SYMPTOMS
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.
EXTRAORAL

SYSTEMIC SIGNS AND SYMPTOMS.

EXTRAORAL AND SYSTEMIC SIGNS AND 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 marked systemic
complications such as high fever, increased pulse rate,
leukocytosis, loss of appetite, and general lassitude.
EXTRAORAL AND SYSTEMIC SIGNS AND SYMPTOMS.

Systemic reactions are more severe in children.

Insomnia, constipation, gastrointestinal disorders,
headache, and mental depression

In very rare cases, severe sequelae such as noma or

gangrenous stomatitis have been described.
STAGES
STAGES
Pindborg and colleagues have described the following
stages in the progress of NUG:
(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; and
(4) bone is exposed.
 STAGES
Horning and Cohen
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 also to the attached gingiva (1%)
Stage 5: Necrosis extending into buccal or labial mucosa(6%)
Stage 6: Necrosis exposing alveolar bone (1%)
Stage 7: Necrosis perforating skin of cheek (0%)
According to Horning and Cohen,
 stage 1 is NUG,
stage 2 may be either NUG or NUP because attachment
loss may have occurred,
 stages 3 and 4 are NUP,
stages 5 and 6 are necrotizing stomatitis, and
stage 7 is noma.
Uohara 1967 similarly suggested three stages of disease:
NUG
necrotizing ulcerative mucositis
noma, also known as cancrum oris, an orofacial gangrene
MICROSCOPIC FEATURES
Listgarten" described the following four zones
MICROSCOPIC FEATURES
Listgarten" described the following four zones

Zone 1: Bacterial zone,

Zone 2: Neutrophil-rich zone
 Zone 3: Necrotic zone
Zone 4: Zone of spirochetal infiltration
MICROSCOPIC FEATURES
Listgarten" described the following four zones

Zone 1: Bacterial zone, the most superficial, consists of

varied bacteria, including a few spirochetes of the
small, medium, and large types.

Zone 2: Neutrophil-rich zone contains numerous

leukocytes, preponderantly neutrophils, with bacteria,
including many spirochetes of various types, between
the leukocytes.
MICROSCOPIC FEATURES
Zone 3: Necrotic zone consists of disintegrated tissue
cells, fibrillar material, remnants of collagen fibers,
and numerous spirochetes of the medium and large
types, with few other organisms.

Zone 4: Zone of spirochetal infiltration consists of well

preserved tissue infiltrated with medium and large
spirochetes, without other organisms.
DIAGNOSIS
DIAGNOSIS

Diagnosis is based on clinical findings of gingival pain,

ulceration, and bleeding.
 A bacterial smear is not necessary or definitive
because the bacterial picture is not appreciably
different from that in marginal gingivitis, periodontal
pockets, pericoronitis, or primary herpetic
gingivostomatitis.
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, dermatoses (pemphigus, erythema
multiforme, and lichen planus); and stomatitis
venenata.
Streptococcal gingivostomatitis
Agranulocytosis
Vincent's angina
Leukemia
AIDS
ETIOLOGY

The Role of Bacteria.

Plaut 54 and Vincent," in 1894 and 1896, respectively,
introduced the concept that NUG is caused by specific
bacteria, namely a fusiform bacillus and a spirochetal
organism.
Rosebury and colleagues described a fusospirochetal
complex consisting of T. microdentium, intermediate
spirochetes, vibrios, fusiform bacilli, and filamentous
organisms, in addition to several Borrelia species.
ROLE OF HOST RESPONSE
ROLE OF HOST RESPONSE
These bacteriologic findings have been supported by
immunologic data from Chung and colleagues.'
These investigators reported increased
immunoglobulin (IgG and IgM) antibody titers for
medium-size spirochetes and prevotella intermedia in
NUG patients compared with titers in those with
chronic gingivitis and healthy controls.
 Cogen and colleagues described a depression in host
defense mechanisms, particularly in PMN chemotaxis
and phagocytosis in NUG patients
LOCAL PREDISPOSING FACTORS.
LOCAL PREDISPOSING FACTORS.

Preexisting gingivitis, injury to the gingiva, and

smoking are important predisposing factors.
Although NUG may appear in an otherwise disease-
free mouth, it most often occurs superimposed on
preexisting chronic gingival disease and periodontal
pockets.
LOCAL PREDISPOSING FACTORS.

Deep periodontal pockets and pericoronal flaps are

particularly vulnerable areas because they offer a
favorable environment for the proliferation of
anaerobic fusiform bacilli and spirochetes.

Areas of the gingiva traumatized by opposing teeth in

malocclusion, such as the palatal surface behind the
maxillary incisors and the labial gingival surface of the
mandibular incisors, are frequent sites of NUG.
SYSTEMIC PREDISPOSING FACTORS.
NUTRITIONAL DEFICIENCY.
DEBILITATING DISEASE.
Psychosomatic Factors.
COMMUNICABILITY
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 described as
contagious. It has been demonstrated that disease
associated with the fusospirochetal bacterial complex
is transmissible
END