Trench mouth

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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, NUG, Necrotizing ulcerative gingivitis, Plaut-Vincent angina

Overview

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.

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.[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.

Classification

There is no classification for NUG.

Pathophysiology

Pathogenesis

Microscopic Pathology

  • 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.

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.[4][9][2]

Differential Diagnosis

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

Disease Clinical Features Diagosis Treatment
Primary herpetic gingivoestomatitis[13]
Gonococcal or streptococcal stomatitis[15]
  • Severe gingival inflammation and pain
Chronic Desquamative gingivitis [16]
  • Desquamation and ulceration of free and attached gingiva
  • Presents with pain and redness of the gingiva
  • Common cause is Lichen planus
  • Biopsy shows tooth rete pegs, hyperkeratosis, and a dense sub-epithelial lymphocytic infiltrate
Periodontal abscess[17]
  • Pain
  • Swelling of the gingival tissue typically localized to 1 or 2 teeth
  • Erythema and discharge from the gingival sulcus or through a fistula can be seen on examination
  • Clinical diagnosis

Risk Factors

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

Epidemiology and Demographics

Incidence and Prevalence

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

Age

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

Developed Countries

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

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.[28]

Natural History, Complications and Prognosis

Natural History

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]

Complications

Prognosis

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]

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.[30][34]

More common symptoms

Less common symptoms

Physical Examination

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

Vital Signs

HEENT

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

Laboratory Findings

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

Dental X-Ray

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

Treatment

Medical Therapy

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

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

Surgical Therapy

Prevention

Primary Prevention

Effective measures of primary prevention strategies for trench mouth include:

Secondary Prevention

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

References

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  2. 2.0 2.1 Socransky SS, Haffajee AD (1994). "Evidence of bacterial etiology: a historical perspective". Periodontol 2000. 5: 7–25. PMID 9673160.
  3. 3.0 3.1 3.2 Herrera D, Alonso B, de Arriba L, Santa Cruz I, Serrano C, Sanz M (2014). "Acute periodontal lesions". Periodontol 2000. 65 (1): 149–77. doi:10.1111/prd.12022. PMID 24738591.
  4. 4.0 4.1 4.2 Johnson BD, Engel D (1986). "Acute necrotizing ulcerative gingivitis. A review of diagnosis, etiology and treatment". J Periodontol. 57 (3): 141–50. doi:10.1902/jop.1986.57.3.141. PMID 3514841.
  5. 5.0 5.1 Mizrahi Y (2014). "[NUG--necrotizing ulcerative gingivitis: a review]". Refuat Hapeh Vehashinayim (1993). 31 (3): 41–7, 62. PMID 25219100.
  6. Lovegrove JM (2004). "Dental plaque revisited: bacteria associated with periodontal disease". J N Z Soc Periodontol (87): 7–21. PMID 15143484.
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  8. Cobb, Charles M.; Ferguson, Brett L.; Keselyak, Nancy T.; Holt, Lorie A.; MacNeill, Simon R.; Rapley, John W. (2003). "A TEM/SEM study of the microbial plaque overlying the necrotic gingival papillae of HIV-seropositive, necrotizing ulcerative periodontitis". Journal of Periodontal Research. 38 (2): 147–155. doi:10.1034/j.1600-0765.2003.02011.x. ISSN 0022-3484.
  9. Ryan, Michael E. (1983). "Acute Necrotizing Ulcerative Gingivitis in Children With Cancer". Archives of Pediatrics & Adolescent Medicine. 137 (6): 592. doi:10.1001/archpedi.1983.02140320068015. ISSN 1072-4710.
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  19. Shields WD (1977). "Acute necrotizing ulcerative gingivitis. A study of some of the contributing factors and their validity in an Army population". J Periodontol. 48 (6): 346–9. doi:10.1902/jop.1977.48.6.346. PMID 266582.
  20. Reners, M; Brecx, M (2007). "Stress and periodontal disease". International Journal of Dental Hygiene. 5 (4): 199–204. doi:10.1111/j.1601-5037.2007.00267.x. ISSN 1601-5029.
  21. Thompson SH, Charles GA, Craig DB (1992). "Correlation of oral disease with the Walter Reed staging scheme for HIV-1-seropositive patients". Oral Surg Oral Med Oral Pathol. 73 (3): 289–92. PMID 1532056.
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  23. Taiwo JO (1993). "Oral hygiene status and necrotizing ulcerative gingivitis in Nigerian children". J Periodontol. 64 (11): 1071–4. doi:10.1902/jop.1993.64.11.1071. PMID 8295093.
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  25. Lopez R, Fernandez O, Jara G, Baelum V (2002). "Epidemiology of necrotizing ulcerative gingival lesions in adolescents". J Periodontal Res. 37 (6): 439–44. PMID 12472838.
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  28. 28.0 28.1 Lindhe, Jan; Lang, Niklaus & Karring, Thorkild (2008), Clinical Periodontology and Implant Dentistry (5 ed.), Hoboken, New Jersey: Wiley-Blackwell
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  41. Loesche, W.J. (1999). "The Antimicrobial Treatment of Periodontal Disease: Changing the Treatment Paradigm". Critical Reviews in Oral Biology & Medicine. 10 (3): 245–275. doi:10.1177/10454411990100030101. ISSN 1045-4411.
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