Transcript Acute gingival infections

Acute gingival infections
Logien Al Ghazal
27/10/2015
•Acute Gingival Infections
1. Necrotizing Ulcerative Gingivitis
2. Clinical Features
3. Relation of Bacteria to Characteristic Lesion
4. Diagnosis
5. Etiology
6. Communicability
• Primary Herpetic Gingivostomatitis
1. Clinical Features
2. Diagnosis
3. Differential Diagnosis
4. Communicability
•
Pericoronitis
1. Clinical Features
2. Complications
Nomenclature:
Necrotizing gingivitis (NG), necrotizing periodontitis (NP), and necrotizing
stomatitis (NS)
In cases with loss of attachment is NP.
Progression to include tissue beyond the mucogingival junction is
characteristic of necrotizing stomatitis.
The necrotizing periodontal diseases have had several names, including
ulceromembranous gingivitis, acute necrotizing ulcerative gingivitis (ANUG).
Vincent’s gingivitis or Vincent’s gingivostomatitis.
Necrotizing gingivostomatitis, and trench mouth.
Necrotizing stomatitis or cancrum oris.
Characteristics:
1. Are the most severe inflammatory periodontal disorders caused by plaque
bacteria.
2. The necrotizing diseases usually run an acute course and therefore the term
acute is often included in the diagnoses.
3. They are rapidly destructive and debilitating.
4. The disease may sometimes subside spontaneously without treatment.
5. Such patients generally have a history of repeated remissions and
exacerbations.
6. Recurrence of the condition in previously treated patients is also frequent.
7. Involvement may be limited to a single tooth or group of teeth or may be
widespread throughout the mouth.
Clinical features
A. Symptoms:
•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.
•Psychological stress are frequent features of the patient's history.
A. Symptoms
•Lesions are extremely sensitive to touch.
•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.
B. 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.
• In some instances, the lesions are denuded of the surface pseudomembrane,
exposing the gingival margin, which is red, shiny, and hemorrhagic.
B. Oral Signs
• The characteristic lesions may progressively destroy the gingiva and
underlying periodontal tissues.
•Spontaneous gingival hemorrhage or pronounced bleeding on the
slightest stimulation are additional characteristic.
•Other signs often found are fetid odor and increased salivation.
Extraoral and Systemic Signs and Symptoms
•Patients are usually ambulatory and have a minimum of systemic complications.
• 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.
• Systemic reactions are more severe in children. Insomnia, constipation,
gastrointestinal disorders, headache, and mental depression sometimes accompany
the condition.
Clinical stages of the disease
The clinical course is indefinite.
NUG can occur in otherwise disease-free mouths or can be superimposed on
chronic gingivitis or periodontal pockets.
It is rare in edentulous mouths, but isolated spherical lesions occasionally
occur on the soft palate.
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.
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
4. bone is exposed.
(Pindborg et al 1966)
Relation of Bacteria to the Characteristic Lesion
.
Etiology: Causing agents are fusiform bacilli, and spirochetes
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.
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 wellpreserved tissue infiltrated with
medium and large spirochetes, without other organisms.
Diagnosis
.
Diagnosis is based on clinical findings of gingival pain, ulceration, and bleeding
A bacterial smear is not necessary or definitive.
Bacterial studies are useful, however, in the differential diagnosis of NUG and specific
infections of the oral cavity such as diphtheria, thrush, actinomycosis, and streptococcal
stomatitis, tuberculosis or from neoplastic disease.
Differential Diagnosis
•Pericoronitis.
• Primary herpetic gingivostomatitis such as herpetic gingivostomatitis
•chronic periodontitis.
• Desquamative gingivitis.
•Streptococcal gingivostomatitis.
•Aphthous stomatitis
•Gonococcal gingivostomatitis.
•Diphtheritic lesions.
•Syphilitic lesions.
• Tuberculous gingival lesions.
•Candidiasis
•Agranulocytosis.
•Dermatoses :pemphigus, erythema multiforme, and lichen Planus.
•Stomatitis venenata.
Necrotizing Ulcerative
Gingivitis
Primary Herpetic
Gingivostomatitis
Etiology: Interaction between host and
bacteria, most probably
fusospirochetes.
Specific viral etiology
Necrotizing condition
Punched out gingival margin;
pseudomembrane that
peels off, leaving raw areas.
Marginal gingiva affected;
other oral tissues rarely affected.
Uncommon in children
No definite duration
No demonstrated immunity
Contagion not demonstrated
Diffuse erythema and vesicular
eruption ,Vesicles rupture and leave
slightly depressed oval or
spherical ulcer.
Diffuse involvement of gingiva, may
include buccal mucosa
and lips.
Occurs more frequently in children
Duration of 7 to 10 days
An acute episode results in some
degree of immunity
Contagious
Necrotizing Ulcerative
Gingivitis
Etiology: interaction between
host and bacteria, possibly
fusospirochetes
Diphtheria
Secondary Stage of
Syphilis
(Mucous Patch)
Specific bacterial etiology:
Corynebacterium diphtheriae.
Specific bacterial etiology:
Treponema pallidum.
Rarely affects marginal gingiva
Membrane removal difficult.
Rarely affects marginal gingiva
Membrane not detachable.
Painful condition.
Less painful
Throat, fauces, tonsils affected.
Minimal pain
Any part of mouth affected
Serologic findings abnormal
Serologic findings normal
Serologic findings normal
(Wassermann, Kahn, Venereal
Disease Research Laboratory
[VDRL])
Immunity not conferred
Immunity conferred by an attack
Immunity not conferred
Doubtful contagiousness.
Contagious
Only direct contact will
communicate
disease
Antibiotic therapy relieves
symptoms
Antibiotic treatment has little
effect
Antibiotic therapy has excellent
results
Affects marginal gingiva
Membrane removal easy.
Differential Diagnosis
Streptococcal gingivostomatitis: is a rare condition characterized by a diffuse
erythema of the gingiva and other areas of the oral mucosa, marginal erythema with
marginal hemorrhage.
Agranulocytosis is characterized by a marked decrease in the number of circulating
PMNs, lesions of the throat, and other mucous membranes, as well as ulceration and
necrosis of the gingiva, which may resemble that of NUG. Blood studies serve to
differentiate between NUG and the gingival necrosis in agranulocytosis.
Vincent's angina is a fusospirochetal infection of the oropharynx and throat,
The process may extend to the larynx and middle ear.
Differential Diagnosis
NUG in leukemia is not produced by leukemia per se but may be the result of a reduction
in host defense mechanisms seen with leukemia. Generalized diffuse discoloration and
edema of the attached gingiva may indicate systemic disorder.
NUG in acquired immunodeficiency syndrome (AIDS) has the same clinical features,
although it follows a very destructive course leading to NUP with the
loss of soft tissue, bone, and the formation of bony sequestra.
Predisposing Factors
Local:
•Preexisting gingivitis.
•Injury to the gingiva.
•Smoking.
Systemic Predisposing Factors
•Nutritional deficiencies such as vitamin C.
•Systemic disturbances are chronic diseases such as syphilis and cancer.
Gastrointestinal disorders such as ulcerative colitis.
•Blood dyscrasias such as the leukemias and anemia, and acquired
immunodeficiency syndrome (AIDS).
Psychosomatic Factors
Anxiety, depression, stress.
Communicability
Transmissible denotes a capacity for the maintenance of an infectious agent in
successive passages through a susceptible animal hosts.
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.
NUP OR NUG is transmissible.
PRIMARY HERPETIC GINGIVOSTOMATITIS
Characteristics:
Etiology : 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
•But it is also seen in adolescents and adults.
•frequency male = female patients.
•Primary infection is asymptomatic.
Characteristics:
•After the primary infection, the virus ascends through sensory and autonomic
nerves and persists in neuronal ganglia that innervate the site as latent HSV.
•Stimuli for secondary infections: such as sunlight, trauma, fever, or stress.
•These secondary manifestations include herpes labialis herpes genitalis, ocular
herpes, and herpetic encephalitis.
Clinical Features
Oral Signs:
•The condition 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 mucosae, soft palate,
pharynx, sublingual mucosa, and tongue.
•After approximately 24 hours the vesicles rupture and form painful, small ulcers with
a red, elevated, halolike margin and a depressed, yellowish- or grayish-white central
portion.
•These occur either in widely separated areas or in clusters.
•Occasionally, primary herpetic gingivitis may occur without vesiculation.
Diffuse, erythematous, shiny discoloration and edematous enlargement of the
gingivae with a tendency toward bleeding make up the clinical picture.
•The course of the disease is limited to 7 to 10 days.
•The diffuse gingival erythema and edema that appear early in the disease persist
for several days after the ulcerative lesions have healed.
•Scarring does not occur in the areas of healed ulcerations.
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
to 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.
•Generalized malaise are common.
Diagnosis
The diagnosis is usually established from the patient's history and the clinical findings.
Recent acute infection is a common feature of the history of patients with primary herpetic
gingivostomatitis.
The condition often occurs during and immediately after febrile diseases as pneumonia,
meningitis, influenza, and typhoid.
 It also tends to occur during periods of anxiety, strain, or exhaustion, as well as during
menstruation.
A history of exposure to patients with herpetic infection of the oral cavity or lips may also be
elicited.
Often occurs in the early stage of infectious mononucleosis.
Differential Diagnosis
•Erythema multi forme.
•Stevens-Johnson syndrome.
•Bullous lichen planus.
•Desquamative gingivitis.
•recurrent aphthous stomatitis.
Communicability
Primary herpetic gingivostomatitis is contagious
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 mandibular third molar area.
Pericoronitis may be acute, subacute, or chronic.
Clinical symptoms and signs
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 is an ideal area
for the accumulation of food debris and bacterial growth.
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.
The patient may also have toxic systemic complications such as fever, leukocytosis, and
malaise.