CHAPTER 19

ACUTE GINGIVAL INFECTIONS
NECROTIZING ULCERATIVE GINGIVITIS :
CLASSIFICATION :
1. Acute.
2. Subacute.
· The disease sometimes subside spontaneously without treatment, such patients have history
of repeated remissions and exacerbations.
· Ìnvolvement may be limited to a group of teeth or may be wide spread throughout mouth.
· NUG can cause tissue destruction involving the supporting structures. When bone loss
occurs the condition is called necrotizing uIcerative periodontitis.
HISTORY :
. NUG is characterized by sudden onset, sometimes following an episode of debilitating
disease or acute respiratory tract infection.
2. A change in living habits, protracted work without adequate rest, and psychologic stress.
ORAL SIGNS :
. Characteristic lesions are punched out, crater like depressions of the interdental papillae.
2. These lesions extend to marginal gingiva and rarely to attached gingiva and oral mucosa.
3. The surface is covered by a pseudomembranous slough, demarcated from the remainder of
the gingival mucosa by a pronounced linear erythema.
4. Ìn some instances, the lesions are denuded of the surface pseudomembrane, exposing the
gingival margin, which is red, shiny, and hemorrhagic.
5. The characteristic lesions progressively destroy the gingiva and underlying periodontal
tissues.
. Spontaneous gingival hemorrhage or pronounced bleeding on the slightest stimulation.
7. Other signs often found are fetid odor and increased salivation.
8. NUG can occur in otherwise disease free mouths or can be superimposed on chronic
gingivitis or periodontal pockets.
9. Does not lead to pocket formation because necrotic changes involve junctional epithelium, a
viable junctional epithelium is needed for pocket deepening.
. Rare in edentulous mouth, but isolated spherical lesions occasionally occur on the soft
palate.
ORAL SYMPTOMS :
. Lesions are extremely sensitive to touch.
2. Patient complaints of constant radiating, gnawing pain, that is intensified by eating spicy or
hot foods and chewing.
3. A metallic foul taste, and the patient is conscious of an excessive amount of " pasty ¨ saliva.
ACUTE NECROTIZING ULCERATIVE GINGIVITIS
ACUTE NECROTIZING ULCERATIVE GINGIVITIS
ACUTE NECROTIZING ULCERATIVE GINGIVITIS
EXTRAORAL AND SYSTEMIC SIGNS AND SYMPTOMS :
. Patients are ambulatory and have a minimum of systemic complications.
2. Local lympadenopathy and a slight elevation in temperature are common features of mild
and moderate stages of disease.
3. Ìn severe cases, systemic complications such as high fever, increased pulse rate,
leucocytosis, loss of appetite, and general lassitude.
4. Systemic complications are more severe in children.
5. Ìnsomnia, constipation, gastrointestinal disorders, headache, and mental depression
sometimes accompany the condition.
CLINICAL COURSE :
. Ìf left untreated NUG leads to NUP with a progressive destruction of the periodontium and
denudation of the root, accompanied by increase in the severity of toxic systemic
complications.
· Pindborg and coIIeagues described the foIIowing stages in the progress of NUG:
. Only the tip of 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.
· Horning and Cohen extended the staging of these oraI necrotizing diseases as
foIIows:
STAGE Ì : Necrosis of the tip of interdental papilla (93%).
STAGE ÌÌ : Necrosis of the entire papilla (9%).
STAGE ÌÌÌ : Necrosis extending to the gingival margin (2%).
STAGE ÌV : Necrosis also extending to the attached gingiva (%).
STAGE V : Necrosis extending into buccal or labial mucosa (%).
STAGE VÌ : Necrosis exposing alveolar bone(%).
STAGE VÌÌ : Necrosis perforating skin of cheek(%).
According to Horning and Cohen, stage is NUG, stage 2 may be either NUG or NUP
because of attachment loss may have occurred, stage 3 and stage 4 are NUP, stage 5 and
are necrotizing stomatitis, and stage 7 is noma.
HISTOPATHOLOGY :
. The surface epithelium is destroyed and is replaced by a meshwork of fibrin, necrotic
epithelial cells, polymorphonuclear neutrophils (PMNs).
2. At immediate border of necrotic pseudomembrane, epithelium is edematous and individual
cells exhibit varying degree of hydropic degeneration.
3. Connective tissue is hyperemic, with numerous engorged capillaries and a dense infiltration
of PMNs.
4. Numerous plasma cells may appear in the periphery of the infiltrate.
BACTERIAL FLORA :
· Predominantly spirochetes and fusiform bacilli.
· These two are seen with other oral spirochetes, vibrios, streptococci, and filamentous
organisms.
DIAGNOSIS :
· Based on clinical findings of gingival pain, ulceration, and bleeding.
DIFFERENTIAL DIAGNOSIS :
· Herpetic gingivostomatitis, chronic periodontitis, desquamative gingivitis, gonococcal
gingivostomatitis, diphtheritic and syphilitic lesions, tuberculous gingival lesions,
candidiasis,and stomatitis venenata.
LOCAL PREDISPOSING FACTORS :
. Preexisting gingivitis, injury to gingiva and smoking.
2. Deep periodontal pockets and pericoronal flaps are vulnerable sites.
3. Areas of the gingiva traumatized by opposing teeth in malocclusion, such as palatal surface
behind maxillary incisors and labial gingival surface of mandibular incisors are frequent sites
of NUG.
SYSTEMIC PREDISPOSING FACTORS :
1. NutritionaI deficiency :
a) Bacteria proliferate only when the tissues were altered by the deficiency.
b) A poor diet has been mentioned as a predisposing factor in NUG.
c) Nutritional deficiencies (eg., vitamin C, vitamin B2) accentuate the severity of the pathologic
changes.
2. DebiIitating disease :
a) Debilitating systemic disease may predispose the development of NUG.
b) Systemic diseases are, syphilis and cancer, severe gastrointestinal disorders such as
ulcerative colitis, blood dyscrasias such as leukemias and anaemia, AÌDS.
PSYCHOSOMATIC FACTORS :
. Psychologic factors play important role in the etiology of NUG.
2. NUG often occurs in association with stress situations.
3. Psychological disturbances, as well as increased adrenocortical secretion, are common in
patients with the disease.
PRIMARY HERPETIC GINGIVOSTOMATITIS :
. Ìt an infection of the oral cavity caused by herpes simplex virus type Ì (HSV- ).
2. Occurs in infants and children younger than yrs of age, but also seen in adolescents and
adults.
3. Occurs with equal frequency in male and females.
4. After the primary infection, the virus ascends through sensory and autonomic nerves and
persists in neuronal ganglia that innervate the site as latent HSV.
CLINICAL FEATURES :
ORAL SIGNS :
. A diffuse, erythematous, shiny involvement of the gingiva and the adjacent oral mucosa, with
varying degree of edema and gingival bleeding.
2. Ìn 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.
3. After 24hrs the vesicles rupture and form painful, small ulcers with a red, elevated, halolike
margin and a depressed, yellowish- or grayish- white central portion.
4. These occur either in widely separated areas or in clusters.
5. Occasionally, primary herpetic gingivitis may occur without vesiculation.
. Diffuse, erythematous, shiny discoloration and edematous enlargement of the gingiva with a
tendency to bleed.
7. The course of disease is limited to 7 to days.
8. Diffuse gingival erythema and edema persists for several days after ulcerative lesions have
healed. Scarring does not occur in the areas of healed ulcerations.
ACUTE HERPETIC GINGIVOSTOMATITIS
ORAL SYMPTOMS :
. Generalized "soreness¨ of the oral cavity, which interferes with eating and drinking.
2. The ruptured vesicles are the focal sites of pain and sensitive to touch, thermal changes,
foods such as condiments and fruit juices.
3. Ìn infants the disease is marked by irritability and refusal to take food.
EXTRAORAL AND SYSTEMIC SIGNS AND SYMPTOMS :
· Cervical adenitis, fever as high as to 5 (38.3C to 4.C), and generalized malaise
are common.
HISTORY :
. Recent acute infection is a common feature of the history.
2. Often occurs during and immediately after an episode of such febrile diseases as
pneumonia, meningitis, influenza, and typhoid.
3. Also occurs during periods of anxiety, strain, or exhaustion.
4. A history of exposure to patients with herpetic infection of oral cavity or lips, often occurs in
early stage of infectious mononucleosis.
HISTOPATHOLOGY :
. The epithelial cells shows " baIIooning degeneration " consisting of acantholysis, nuclear
clearing and nuclear enlargement.
2. These cells are called Tzanck ceIIs.
3. Ìnfected cells fuse, forming multinucleated cells, and intercellular edema leads to formation
of an intraepithelial vesicles that rupture and develop a secondary inflammatory response
with a fibropurulent exudate.
4. Discrete ulcerations results from rupture of vesicles have a central portion of acute
inflammation, with degrees of purulent exudate, surrounded by a zone rich in engorged
blood vessels.
DIAGNOSIS :
. Established from patient's history and the clinical findings.
2. A virus culture and immunologic tests using monoclonal antibodies or DNA hybridization
techniques are used.
DIFFERENTIAL DIAGNOSIS :
· Should be differentiated from NUG, erythema multiforme, stevens- johnson syndrome,
bullous lichen planus, desquamative gingivitis, and recurrent aphthous stomatitis.
COMMUNICABILITY :
. Ìt is contagious.
2. Adults have developed immunity to HSV as the result of infection during childhood therefore
occurs in infants and children.
3. Secondary herpetic infection of skin, such as herpes labialis, does recur.
PERICORONITIS :
. Ìnflammation of the gingiva in relation to the crown of an incompletely erupted tooth.
2. Occurs most often in mandibular third molar area.
3. Pericoronitis may be acute, subacute, or chronic.
CLINICAL FEATURES :
. Partially erupted or impacted mandibular third molar is the most common site of pericoronitis.
2. 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.
ACUTE PERICORONITIS :
. Ìs an inflammation of pericoronal flap and adjacent structures as well as systemic
complications.
2. The inflammatory fluid and cellular exudate increase the bulk of the flap, which then may
interfere with complete closure of the jaw, aggravating the inflammatory involvement.
CLINICAL FEATURES :
. Red, swollen, suppurating lesion that is exquisitely tender.
2. Pain radiating to the ear, throat, and floor of mouth.
3. Patient is extremely uncomfortable because of a foul taste and an inability to close the jaws,
in addition to the pain.
4. Swelling of the cheek in the region of the angle of the jaw and lymphadenitis.
5. Patient may also have toxic systemic complications such as fever, leukocytosis, and
malaise.
COMPLICATIONS :
. May spread posteriorly into the oropharyngeal area and medially to the base of the tongue,
making it difficult for the patient to swallow.
2. Depending on the severity and extent of the infection, there is involvement of the
submaxillary, posterior cervical, deep cervical and retropharyngeal lymph nodes.
3. Peritonsillar abscess formation, cellulitis and ludwig's angina are infrequent but potential
sequelae of acute pericoronitis.

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