Sandbox: Reddy

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aravind Kuchkuntla, M.B.B.S[2]

Synonyms and keywords: Vincent’s disease, fusospirochetal gingivitis, trench mouth, acute ulcerative gingivitis, necrotizing gingivitis, acute necrotizing ulcerative gingivitis, ANUG

Historical Perspective

• The first description of NUG was recorded in Xenophon's troops in fourth century B.C, with features of painful decaying between the teeth.
• In 1894, Plaut described NUG for the first time.
• In 1896, Vincent described the pathogenesis of NUG as an endogenous, opportunistic fusospirochetal infection. He used topical iodine applications and rinses of boric acid solution for treatment.
• From 1900 to 1920 oxidising agents such as chromic acid were used for the treatment of NUG.
• In 1930, Hirschfeld proposed that debridement and use of sodium perborate rinses were useful for the treatment of NUG till the inflammation reduced.
• In 1949, Schluger treated his patients with deep and thorough curettage, followed by hydrogen peroxide and water rinses for six to eight weeks.
• In 1968, Goldhaber reported that periodic scalings and rinses with hydrogen peroxide helped with maintaining good oral hygiene.
• In 1984, Stevens described the triad of criteria for the diagnosis of NUG, which include acute necrosis and ulceration of the interdental papillae, pain, and bleeding.

Classification

There is no classification for NUG.

Pathophysiology

Pathogenesis

• Pathogenesis of NUG is unclear and is explained in relation to the presence of predisposing factors.
• The presence of predisposing factors such as, acute stress, pre-existing gingivitis, immunosuppression, corticosteriod use, poor oral hygiene result in bacterial overgrowth and followed by invasion.
• The overgrowth of bacteria results in the formation of a plaque. A plaque is a biofilm which begins to form within 24 hours if it is not regularly removed. This biofilm once formed can minimize the effect of host defense and antibiotic penetration promoting bacterial overgrowth.
• Invasion of the bacteria into the gingiva results in NUG.
• Necrotizing ulcerative gingivitis causes necrosis of the gingival crest which is described as "punched out" ulcerated papillae resulting in gingival bleeding and pain.
• NUG affects the interdental and marginal soft tissue and has minimal osseous involvement when compared to periodontitis.

Microscopic Pathology

• The features characteristic of NUG on microscopic examination include neutrophil rich, necrotic, and spirochetal infiltration zones are unique to NUG.
• The biopsy of the gingiva under the electron microscopy examination demonstrate four zones and include:
  • Bacterial zone: This zone demonstrates many different morphological types of high bacterial load, including the presence of spirochetes.
  • Neutrophil rich zone: Below the bacterial zone, a neutrophil rich zone is demonstrated.
  • Necrotic zone: This zone demonstrates disintegrated cells, with the presence of spirochetes and fusiform bacteria.
  • Spirochete infilteration zone: The zone demonstrates tissues infiltrated by spirochetes which are present in high number. Absence of other other bacteria is characteristic.

Causes

NUG is a polybacterial infection and the exact causative organisms are not identified, however the following organisms have been identified in most of the patients. The following is a list of organisms are associated with NUG, the presence of these organisms does not always help to make the diagnosis of NUG.

• Prevotella intermedia
• Fusobacterium species
• Treponema species - T. vincentii and T. buccalis
• Selenomonas species

Risk Factors

The following risk factors predispose patients to develop NUG:

• Acute psychological stress
• Immunosuppression
• Smoking
• Malnutrition
• Pre-existing gingivitis
• Trauma
• Poor oral hygiene
• Alcohol consumption

Epidemiology and Demographics

Age

• Trench mouth mostly impacts individuals who are 35 years of age or younger.
• In particular, trench mouth seems to affect teenagers most.

Developed Countries

• In developed countries, trench mouth occurs mostly in young adults.

Developing Countries

• In developing countries, trench mouth may occur in children of low socioeconomic status, usually occurring with malnutrition (especially inadequate protein intake) and shortly after the onset of viral infections, such as measles.

Natural History, Complications and Prognosis

Natural History

In the early stages some patients may complain of a feeling of tightness around the teeth. If three signs are present, the diagnosis of trench mouth can be assumed. These include:

• Severe gingival pain
• Profuse gingival bleeding that requires little or no provocation
• Ulcerated interdental papillae with necrotic slough.

Complications

• Destruction of gingival papillae
• Interdental gingival crater formation in the anterior gingiva is disfiguring.
• Recurrence
• Loss of teeth
• Pain
• Periodontitis
• Spread of infection

Prognosis

Untreated, the infection can lead to rapid destruction of the periodontium and can spread, as necrotizing stomatitis or noma, into neighbouring tissues in the cheeks, lips or the bones of the jaw. As stated, the condition can occur and be especially dangerous in people with weakened immune systems. This progression to noma is possible in malnourished susceptible individuals, with severe disfigurement possible.

Diagnosis

History and Symptoms

To make the diagnosis of NUG the traid of interdental necrosis, bleeding, and pain must be present. Absence of any one of the features rules out the diagnosis of NUG.

More common symptoms

• Pain is the presenting symptom in all the patients.
• Gingival bleeding

Less common symptoms

• Lymphadenopathy
• Bad breath-halitosis
• Fever
• Malaise
• Red or swollen gums
• Pain when eating or swallowing
• A gray film/gray residue on gums
• Crater-like sores (ulcers)
• Loss of gum tissue in between the teeth

Vital Signs

• Fever

HEENT

Oral examination findings suggesting NUG include:

• Interdental gingival necrotic ulcers, which appear like punched out lesions
• Bleeding gums with minimal pressure
• Red or swollen gums
• A gray film on gums
• Crater-like (ulcers)
• Lymphadenopathy
• Halitosis

Treatment

Medical Therapy

• Medical therapy is not a definitive treatment option, it is used to in addition with gingivoplasty, scaling or curettage procedures.
• Chlorhexidine gluconate, a topical chemotherapeutic agent has shown to improve outcomes after surgical treatment.
• Periodic chlorhexidine rinses are used during the period of wound healing of the damaged gingiva after scaling or curettage procedures.
• Antiboiotic therapy with penicillin or metronidazole for a period of 7 to 10 days is recommended to control bacterial growth.

Surgical Therapy

• Debridement of the plaque by scaling and root planing, periodic curettage and gingivoplasty are the primary treatment options for NUG.
• Repeated curettage and good plaque control can result in regeneration of destroyed papillae. It is an effective treatment option, but is associated with recurrence as the patients fail to adhere the repeated follow-up visits once the symptoms resolve.
• In patients with anterior gingival involvement scaling and planing is a good option for treatment as it has a good esthetic result compared to gingivoplasty. Scaling and root planing should be done periodically to stimulate the regeneration of the interdental papillae and to reduce the need for gingivoplasty. Therapy must be continued for a period of 9 months and the success rates of gingival regeneration are variable.
• Repeated episodes of NUG can result in gingival deformities, to avoid this complication gingivoplasty can be done for adequate plaque control and recreate physiologic gingival form and contour.