Trench mouth

Trench mouth or necrotizing ulcerative gingivitis(NUG) is an acute necrotic condition affecting the interdental region resulting in pain, bleeding and loss of teeth. The presence of the triad: pain, bleeding and necrotic ulcer is required for the diagnosis, and absence of any one of the criteria rules out the diagnosis of NUG. The pathogenesis of NUG is unclear but is related to the presence of predisposing factors such as acute stress, immunosuppression, malnutrition and poor oral hygiene. These predispose to the formation of a dental plaque, resulting in overgrowth of the bacteria in the interdental area. Invasion of the bacteria into the tissue causes NUG. It is a clinical diagnosis and must be differentiated from herpetic gingivostomatitis. Treatment is primarily by scaling and root planing or gingivoplasty based on the individual patient presentation. The prognosis is variable from patient to patient and recurrence is common in most patients. If left untreated it can progress to necrotizing ulcerative periodontitis or noma. Prevention is by maintaining good oral hygiene with brushing and oral rinsing with oral chlorhexidine.

• The first description of NUG was recorded in Xenophon’s troops in fourth century B.C, with features of painful decaying between the teeth.^[1]
• In 1894, Plaut described NUG for the first time.^[2]
• 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.^[3]
• 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.

There is no classification for NUG.

• Pathogenesis of NUG is unclear and is explained in relation to the presence of predisposing factors.^[4]
• 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.^[5]
• 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.^[6]
• 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.^[3]
• NUG affects the interdental and marginal soft tissue and has minimal osseous involvement when compared to periodontitis.

• The features characteristic of NUG on microscopic examination include neutrophil rich, necrotic, and spirochetal infiltration zones are unique to NUG.^[1]
• The biopsy of the gingiva under the electron microscopy examination demonstrate four zones and include:^{[7] [8]}
  • 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.

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.^[4][9][2]

• Prevotella intermedia^[10][11]
• Fusobacterium species
• Treponema species – T. vincentii and T. buccalis
• Selenomonas species

NUG must be differentiated from the following diseases which have similar presentation:^[12]

The following risk factors predispose patients to develop NUG:^[18][19]

• Acute psychological stress^[20]
• Immunosuppression^[21][22]
• Smoking
• Malnutrition
• Pre-existing gingivitis
• Trauma
• Poor oral hygiene^[23]
• Alcohol consumption

• It is difficult to conduct epidemiological studies on NUG due to the variability of descriptions of the disease.^[24][25][26]

• NUG is common in individuals younger than 35 years of age.^[27]

• In developed countries, NUG occurs mostly in young adults.^[28]

• 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.^[28]

In the early stages some patients may complain of a feeling of tightness around the teeth. The presence of the following triad suggests NUG:^{[29] [30][31]}

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

• Destruction of gingival papillae
• Interdental gingival crater formation in the anterior gingiva is disfiguring.
• Noma^[32]
• Recurrence
• Loss of teeth^[33]
• Pain
• Periodontitis

Prognosis of NUG is variable with treatment, majority of the patients have good response to the treatment and few do not respond to the treatment. In patients with treatment, recurrence is common affecting the outcome. In patients with immunosuppresion, the prognosis is poor and it progresses to noma.^[4][5]

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.^[30][34]

• Pain, always the presenting symptom^[35][36]
• Gingival bleeding

• Lymphadenopathy^[30][37]
• 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

Oral examination in patients with NUG is significant for the presence of interdental necrosis with the presence of ulcers and halitosis.

• Fever

Oral examination findings suggesting NUG include:^[36][38]

• 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

NUG is primarily a clinical diagnosis therefore laboratory investigation for confirmation of the diagnosis is not done.^[3]

• X-Rays are useful to look for the extent of osseus involvement of the infection.^[37]

• Medical therapy is not a definitive treatment option, it is used as adjunct to gingivoplasty, scaling or curettage procedures.^[39]
• Chlorhexidine gluconate, a topical chemotherapeutic agent has shown to improve outcomes after surgical treatment.^[40]
• Periodic chlorhexidine rinses are used during the period of wound healing of the damaged gingiva after scaling or curettage procedures.
• Antibiotic therapy with penicillin or metronidazole for a period of 7 to 10 days is recommended to control bacterial growth.^[41]

For any signs of systemic involvement, the recommended antibiotics that can provide rapid relief include:^[42]

• Amoxicillin, 250 mg 3x daily for 7 days ± Metronidazole, 250 mg 3x daily for 7 days

If debridement is delayed one of the following regimen is followed:^[43]

• Amoxicillin 500 mg every 8 hours for 3 days
• Erythromycin 250 mg every 6 hours for 3 days
• Tetracycline 250 mg every 6 hours for 3 days

• Debridement of the plaque by scaling and root planing, periodic curettage and gingivoplasty are the primary treatment options for NUG.^[44]
• 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 attend repeated follow-up visits once the acute symptoms resolve.^[42]
• 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.^[45]
• 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.^[42]

Effective measures of primary prevention strategies for trench mouth include:

• Good general health
• Good nutrition
• Good oral hygiene with thorough tooth brushing and flossing. Antiseptic mouthwash such as chlorhexidine 0.12% decreases bacterial count and is effective when used in combination with good mouth care.
• Mechanisms to cope with stress
• Smoking cessation

• Regular follow up and with the physician for the duration of the treatment, reduces recurrence.

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