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

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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

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* 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

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There is no classification for NUG.

## Pathophysiology

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### Pathogenesis

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* 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.

### Microscopic Pathology

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* 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

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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

## Differential Diagnosis

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

Disease  | Clinical Features  | Diagosis  | Treatment

|
|
|

Primary herpetic gingivoestomatitis[13] |

* Pin-head vesicles rupture to form painful irregular ulcerations covered by yellow-grey membrane
* Severe pain
* Submandibular lymphadenopathy
* Halitosis
* It involves buccal mucosa, tongue, posterior pharynx, and gingival and palatal mucosa

* Tzanck test demonstrates multinucleated epithelial giant cells[14]
* Viral culture is the gold standard for diagnosis
* Direct immunofluorescence

* Valacyclovir
* Famciclovir

Gonococcal or streptococcal stomatitis[15] |

* Severe gingival inflammation and pain

* Bacterial cultures
* Gram stain

* Periodontal therapy (scaling, root planning, curettage)
* Antibiotics

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

* Topical corticosteroids

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

* Endodontic therapy
* Root canal therapy

## Risk Factors

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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

## Epidemiology and Demographics

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### Incidence and Prevalence

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

### Age

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

### Developed Countries

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

### Developing Countries

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* 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

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### Natural History

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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.

### Complications

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

### Prognosis

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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

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### History and Symptoms

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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

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

#### Less common symptoms

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* 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

### Physical Examination

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

### Vital Signs

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* Fever

### HEENT

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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

### Laboratory Findings

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

#### Dental X-Ray

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

## Treatment

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### Medical Therapy

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* 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

### Surgical Therapy

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* 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]

## Prevention

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### Primary Prevention

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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

### Secondary Prevention

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

## References

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1. ↑ 1.0 1.1 Hampp EG (1945). "Vincent's Infection-A Wartime Disease: Observations on the Oral Spirochetal Flora Present in Vincent's Infection". Am J Public Health Nations Health. 35 (5): 441–50. PMC 1625444. PMID 18016160.
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.CS1 maint: Multiple names: authors list (link)
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.
7. ↑ LISTGARTEN MA (1965). "ELECTRON MICROSCOPIC OBSERVATIONS ON THE BACTERIAL FLORA OF ACUTE NECROTIZING ULCERATIVE GINGIVITIS". J Periodontol. 36: 328–39. doi:10.1902/jop.1965.36.4.328. PMID 14326701.
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.
10. ↑ Loesche WJ, Syed SA, Laughon BE, Stoll J (1982). "The bacteriology of acute necrotizing ulcerative gingivitis". J Periodontol. 53 (4): 223–30. doi:10.1902/jop.1982.53.4.223. PMID 6122728.CS1 maint: Multiple names: authors list (link)
11. ↑ Gmür R, Wyss C, Xue Y, Thurnheer T, Guggenheim B (2004). "Gingival crevice microbiota from Chinese patients with gingivitis or necrotizing ulcerative gingivitis". Eur J Oral Sci. 112 (1): 33–41. PMID 14871191.CS1 maint: Multiple names: authors list (link)
12. ↑ Keine KC, Kuga MC, Pereira KF, Diniz AC, Tonetto MR, Galoza MO; et al. (2015). "Differential Diagnosis and Treatment Proposal for Acute Endodontic Infection". J Contemp Dent Pract. 16 (12): 977–83. PMID 27018033.CS1 maint: Explicit use of et al. (link) CS1 maint: Multiple names: authors list (link)
13. ↑ Kolokotronis, A.; Doumas, S. (2006). "Herpes simplex virus infection, with particular reference to the progression and complications of primary herpetic gingivostomatitis". Clinical Microbiology and Infection. 12 (3): 202–211. doi:10.1111/j.1469-0691.2005.01336.x. ISSN 1198-743X.
14. ↑ Chauvin PJ, Ajar AH (2002). "Acute herpetic gingivostomatitis in adults: a review of 13 cases, including diagnosis and management". J Can Dent Assoc. 68 (4): 247–51. PMID 12626280.
15. ↑ Ciçek Y, Ozgöz M, Canakçi V, Orbak R (2004). "Streptococcal gingivitis: a report of case with a description of a unique gingival prosthesis". J Contemp Dent Pract. 5 (3): 150–7. PMID 15318266.CS1 maint: Multiple names: authors list (link)
16. ↑ Vijayakar HN, Shah PP, Desai AB, Ghonasgi SR, Gawankar RJ (2014). "Chronic desquamative gingivitis in siblings: A report of two cases". J Indian Soc Periodontol. 18 (3): 385–9. doi:10.4103/0972-124X.134585. PMC 4095635. PMID 25024556.CS1 maint: Multiple names: authors list (link)
17. ↑ Laudenbach, Joel M.; Simon, Ziv (2014). "Common Dental and Periodontal Diseases". Medical Clinics of North America. 98 (6): 1239–1260. doi:10.1016/j.mcna.2014.08.002. ISSN 0025-7125.
18. ↑ Murayama Y, Kurihara H, Nagai A, Dompkowski D, Van Dyke TE (1994). "Acute necrotizing ulcerative gingivitis: risk factors involving host defense mechanisms". Periodontol 2000. 6: 116–24. PMID 9673175.CS1 maint: Multiple names: authors list (link)
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.CS1 maint: Multiple names: authors list (link)
22. ↑ Shangase L, Feller L, Blignaut E (2004). "Necrotising ulcerative gingivitis/periodontitis as indicators of HIV-infection". SADJ. 59 (3): 105–8. PMID 15214212.CS1 maint: Multiple names: authors list (link)
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.
24. ↑ Dean HT, Singleton DE (1945). "Vincent's Infection-A Wartime Disease: Preliminary Considerations on the Epidemiology of Ulcerative Gingivostomatitis". Am J Public Health Nations Health. 35 (5): 433–40. PMC 1625430. PMID 18016159.
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.CS1 maint: Multiple names: authors list (link)
26. ↑ Dufty J, Gkranias N, Petrie A, McCormick R, Elmer T, Donos N (2016). "Prevalence and treatment of necrotizing ulcerative gingivitis (NUG) in the British Armed Forces: a case-control study". Clin Oral Investig. doi:10.1007/s00784-016-1979-9. PMID 27830369.CS1 maint: Multiple names: authors list (link)
27. ↑ Stevens AW, Cogen RB, Cohen-Cole S, Freeman A (1984). "Demographic and clinical data associated with acute necrotizing ulcerative gingivitis in a dental school population (ANUG-demographic and clinical data)". J Clin Periodontol. 11 (8): 487–93. PMID 6592176.CS1 maint: Multiple names: authors list (link)
28. ↑ 28.0 28.1 Lindhe, Jan; Lang, Niklaus & Karring, Thorkild (2008), Clinical Periodontology and Implant Dentistry (5 ed.), Hoboken, New Jersey: Wiley-Blackwell
29. ↑ Karring, Thorkild (2008). Clinical Periodontology and Implant Dentistry. New Jersey: Wiley-Blackwell. ISBN 978-1405160995.
30. ↑ 30.0 30.1 30.2 Sangani I, Watt E, Cross D (2013). "Necrotizing ulcerative gingivitis and the orthodontic patient: a case series". J Orthod. 40 (1): 77–80. doi:10.1179/1465313312Y.0000000037. PMID 23524550.CS1 maint: Multiple names: authors list (link)
31. ↑ Horning GM (1996). "Necotizing gingivostomatitis: NUG to noma". Compend Contin Educ Dent. 17 (10): 951–4, 956, 957-8 passim, quiz 964. PMID 9533316.
32. ↑ Osuji OO (1990). "Necrotizing ulcerative gingivitis and cancrum oris (noma) in Ibadan, Nigeria". J Periodontol. 61 (12): 769–72. doi:10.1902/jop.1990.61.12.769. PMID 2269918.
33. ↑ MacCarthy, Denise; Claffey, Noel (1991). "Acute necrotizing ulcerative gingivitis is associated with attachment loss". Journal of Clinical Periodontology. 18 (10): 776–779. doi:10.1111/j.1600-051X.1991.tb00071.x. ISSN 0303-6979.
34. ↑ Campbell CM, Stout BM, Deas DE (2011). "Necrotizing ulcerative gingivitis: a discussion of four dissimilar presentations". Tex Dent J. 128 (10): 1041–51. PMID 22206178.CS1 maint: Multiple names: authors list (link)
35. ↑ FRANKL SN (1960). "Herpetic gingivostomatitis and necrotizing ulcerative gingivitis in the child and adolescent". Clin Proc Child Hosp Dist Columbia. 16: 282–5. PMID 13701428.
36. ↑ 36.0 36.1 Jiménez LM, Duque FL, Baer PN, Jiménez SB (2005). "Necrotizing ulcerative periodontal diseases in children and young adults in Medellín, Colombia, 1965--2000". J Int Acad Periodontol. 7 (2): 55–63. PMID 15912925.CS1 maint: Multiple names: authors list (link)
37. ↑ 37.0 37.1 Novak MJ (1999). "Necrotizing ulcerative periodontitis". Ann Periodontol. 4 (1): 74–8. doi:10.1902/annals.1999.4.1.74. PMID 10863377.
38. ↑ Bermejo-Fenoll A, Sánchez-Pérez A (2004). "Necrotising periodontal diseases". Med Oral Patol Oral Cir Bucal. 9 Suppl: 114–9, 108–14. PMID 15580128.
39. ↑ "Parameter on acute periodontal diseases. American Academy of Periodontology". J. Periodontol. 71 (5 Suppl): 863–6. 2000. doi:10.1902/jop.2000.71.5-S.863. PMID 10875694.
40. ↑ Horning GM, Cohen ME (1995). "Necrotizing ulcerative gingivitis, periodontitis, and stomatitis: clinical staging and predisposing factors". J Periodontol. 66 (11): 990–8. doi:10.1902/jop.1995.66.11.990. PMID 8558402.
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.
42. ↑ 42.0 42.1 42.2 Rowland RW (1999). "Necrotizing ulcerative gingivitis". Ann Periodontol. 4 (1): 65–73, discussion 78. doi:10.1902/annals.1999.4.1.65. PMID 10863376.
43. ↑ "Acute Necrotizing Ulcerative Gingivitis (ANUG) - Dental Disorders - Merck Manuals Professional Edition". Retrieved October 25, 2016.
44. ↑ "Managing Patients with Necrotizing Ulcerative Gingivitis".
45. ↑ Axelsson, P.; Lindhe, J.; Nystrom, B. (1991). "On the prevention of caries and periodontal disease. Results of a 15-year longitudinal study in adults". Journal of Clinical Periodontology. 18 (3): 182–189. doi:10.1111/j.1600-051X.1991.tb01131.x. ISSN 0303-6979.

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