Acute necrotizing ulcerative gingivitis

Acute necrotizing ulcerative gingivitis also known as ANUG, necrotizing ulcerative gingivitis (NUG), Vincent’s disease, fusospirochetal gingivitis, trench mouth, acute ulcerative gingivitis or necrotizing gingivitis is a rare rapidly destructive infectious disease of the gum tissue (the tissues that surround and support your teeth) that occurs in people with poor oral hygiene, impaired immune system (immunocompromised patients), malnutrition, poor living conditions and intense psychological stress (mental stress) affecting less than 1% of the general population ¹, ², ³. Other risk factors have been reported as predisposing factors of necrotizing ulcerative gingivitis include tobacco smoking, preexisting gingivitis, and trauma  ⁴, ⁵, ⁶. Acute necrotizing ulcerative gingivitis (ANUG) is characterized by the sudden onset of inflammation, pain, and the presence of “punched-out” crater-like lesions (ulcers) of the interdental gum tissue ³.

Acute necrotising ulcerative gingivitis (ANUG) is more common in young adults with human immunodeficiency virus (HIV) infection, but reports of necrotizing ulcerative gingivitis in young children with malnutrition are not uncommon ⁷, ³. In the United States, ANUG is limited primarily to Whites ⁸. Due to the increasing number of patients with an immunocompromised condition, especially HIV-infected patients, Rowland ⁵ reported that necrotizing ulcerative gingivitis may be the first sign of HIV infection.

Acute necrotizing ulcerative gingivitis (ANUG) is commonly due to an opportunistic bacterial infection and is predominantly associated with fusiform and spirochete bacteria ². One study identified spirochetes and a majority of Gram-negative bacteria, including Bacteroides intermedius and Fusobacterium spp. as the most common causes ⁹, ¹⁰. Another study described the bacteria associated with ANUG to include Treponema spp., Selenomonas spp., Fusobacterium spp., and Prevotella intermedia ¹. Acute necrotizing ulcerative gingivitis (ANUG) is closely associated with spirochetes and gram-negative bacteria, which can be identified on gram stain (if performed) ³.

Acute necrotizing ulcerative gingivitis (ANUG) is largely based on a detailed history and physical exam; therefore, physical examination is critical. Acute necrotizing ulcerative gingivitis (ANUG) diagnosis is based on 3 essential findings: sore gums (usually of rapid onset), bleeding gums and the most diagnostic characteristic, ulceration and necrosis of the interdental gum tissue ⁵, ³, ⁴, ⁶. Systemic symptoms such as lymphadenopathy (enlarged lymph nodes) and malaise can also be found on physical exam, as well as a fetid odor of the breath and pseudomembrane formation on the gums ².

However it was found in an old data that 14% of cases of acute necrotizing ulcerative gingivitis (ANUG) had no pain and another 40% suffered only mild pain ¹¹. Fetid breath or “fetor ex ore” and pseudomembrane formation may be secondary diagnostic features ⁵, ³, ⁴, ⁶, ¹². Moreover, lymphadenopathy is an infrequent finding ¹. The presence of lymphadenopathy is probably related to the severity of the disease since it is usually observed in advanced cases  ⁵.

The diagnosis of ANUG is associated with poor oral hygiene and weakening of the host immune system, particularly in the setting of HIV infection ¹. Nutritional deficiencies, poor living conditions, as well as the context of psychological stress, have commonly been observed as predisposing factors ¹, ³.

The treatment of acute necrotizing ulcerative gingivitis (ANUG) is based on combining mechanical removal of tartar with local and/or systemic antibiotics, treating malnutrition and improving oral hygiene ¹³, ³. Metronidazole (250 mg 3 times a day) is a common first drug choice due to its activity against anaerobes ¹⁴, ¹⁵, ². Other systemic antibiotics have also been suggested with “acceptable” results and are considered on a case-by-case basis include penicillin, tetracyclines, clindamycin, amoxicillin, or amoxicillin with clavulanate ¹⁴, ². Oral penicillin, for example, was demonstrated in one study to show significant clinical improvement in three to six days ¹⁰. Although oral antibiotics have been shown to be beneficial, topical antimicrobials are not recommended because of the large numbers of bacteria present within the tissues, where the local drug will not be able to achieve adequate concentrations ¹⁴, ². Importantly, the addition of antifungal agents is indicated in immunosuppressed patients who undergo antibiotic therapy ¹⁵, ¹.

You may be asked to visit a dentist to have your teeth professionally cleaned and to have the plaque removed, once your gums feel less tender. You may need to get numb for the cleaning. You may need frequent dental cleaning and examinations until the disorder is cleared.

To prevent acute necrotizing ulcerative gingivitis (ANUG) from coming back, your dentist may give you instructions on how to:

• Maintain good general health, including proper nutrition and exercise
• Maintain good oral hygiene
• Reduce stress
• Stop smoking

Adequate treatment usually prevent the progression of the disease and ulcer healing is expected in a few days. However, without treatment acute necrotizing ulcerative gingivitis (ANUG) can lead to further deterioration in some cases to ulcerative necrotizing stomatitis, necrotizing ulcerative periodontitis (NUP) and, finally, to gangrenous stomatitis also called Noma which is a rapidly progressing severe gangrenous disease of the mouth and the face which is commonly fatal ³, ¹⁴, ¹⁶, ¹⁷, ¹⁸, ¹³.

Figure 1. Acute necrotising ulcerative gingivitis

[Surce ¹⁹ ]

Acute necrotizing ulcerative gingivitis causes

Acute necrotizing ulcerative gingivitis (ANUG) is a rare rapidly destructive infectious disease of the gum tissue that occurs in people with poor oral hygiene, impaired immune system (immunocompromised patients), malnutrition, poor living conditions and intense psychological stress (mental stress) ⁷, ⁵. Other risk factors have been reported as predisposing factors of necrotizing ulcerative gingivitis include tobacco smoking, preexisting gingivitis, and trauma  ⁴, ⁵, ⁶.

ANUG has been documented by historians since the 4th century BCE. Acute necrotizing ulcerative gingivitis (ANUG) from the ancient world were among fighting troops, necrotizing ulcerative gingivitis was classically seen among military personnel during World War 1 and in the modern world it is still common among soldiers, presumably due to multiple risk factors including poor oral hygiene, intense psychological stress and malnutrition ⁷, ³. Prospective clinical studies have found a disrupted ability to cope with psychological stress, immunosuppression, and tobacco use to be strongly associated epidemiologically with the development of ANUG ⁵.

Physiologic factors that play a main role in ANUG include psychological stress, poor diet, insufficient sleep, alcohol, tobacco, poor oral hygiene, preexisting gingivitis, and HIV infection ². These factors have been shown to impair the host immune response, which facilitates bacterial pathogenicity. Psychological stress reduces the gingival microcirculation and salivary flow and increases adrenocortical secretions, which can modify the function of polymorphonuclear leukocytes and lymphocytes ². This alters the immune response as well as the patient’s behavior and mood, resulting in insufficient oral hygiene, malnutrition, and increased tobacco consumption ¹. Similarly, poor diet results in increased histamine concentration and increased capillary permeability of the gingiva, which leads to decreased polymorphonuclear leukocyte chemotaxis ¹.

ANUG is commonly due to an opportunistic bacterial infection and is predominantly associated with fusiform and spirochete bacteria ². One study identified spirochetes and a majority of Gram-negative bacteria, including Bacteroides intermedius and Fusobacterium spp. as the most common causes ⁹, ¹⁰. Another study described the bacteria associated with ANUG to include Treponema spp., Selenomonas spp., Fusobacterium spp., and Prevotella intermedia ¹. Acute necrotizing ulcerative gingivitis (ANUG) is closely associated with spirochetes and gram-negative bacteria, which can be identified on gram stain (if performed) ³.

Acute necrotizing ulcerative gingivitis symptoms

Acute necrotizing ulcerative gingivitis (ANUG) is characterized by the sudden onset of inflammation, pain, and the presence of “punched-out” crater-like lesions (ulcers) of the interdental gum tissue ³.

Symptoms of acute necrotizing ulcerative gingivitis often begin suddenly. They include:

• Bad breath
• Crater-like ulcers between the teeth
• Fever
• Foul taste in the mouth
• Gums appear red and swollen
• Grayish film on the gums
• Painful gums
• Severe gum bleeding in response to any pressure or irritation

Acute necrotizing ulcerative gingivitis complications

Acute necrotizing ulcerative gingivitis may lead to devastating tissue damage in the form of necrotizing periodontitis, necrotizing stomatitis, and cancrum oris (noma), which is frequently fatal ³, ¹⁴, ¹⁶, ¹⁷, ¹⁸, ¹³.

Acute necrotizing ulcerative gingivitis diagnosis

Acute necrotizing ulcerative gingivitis (ANUG) is largely based on a detailed history and physical exam; therefore, physical examination is critical. Acute necrotizing ulcerative gingivitis (ANUG) diagnosis is based on 3 essential findings: sore gums (usually of rapid onset), bleeding gums and the most diagnostic characteristic, ulceration and necrosis of the interdental gum tissue ⁵, ³, ⁴, ⁶. Systemic signs and symptoms such as lymphadenopathy (enlarged lymph nodes), fever, and malaise can also be found on physical exam, as well as a fetid odor of the breath and pseudomembrane formation on the gums ².

However it was found in an old data that 14% of cases of acute necrotizing ulcerative gingivitis (ANUG) had no pain and another 40% suffered only mild pain ¹¹. Fetid breath or “fetor ex ore” and pseudomembrane formation may be secondary diagnostic features ⁵, ³, ⁴, ⁶, ¹². Moreover, lymphadenopathy is an infrequent finding ¹. The presence of lymphadenopathy is probably related to the severity of the disease since it is usually observed in advanced cases  ⁵.

The typically clinical appearance of necrotizing ulcerative gingivitis is related to its histopathological aspect. Four different layers have been described from the most superficial to the deepest layers of the lesion ¹:

1. The bacterial area with a superficial fibrous mesh composed of degenerated epithelial cells, leukocytes, cellular rests, and a wide variety of bacterial cells, including rods, fusiforms, and spirochetes
2. The neutrophil-rich zone composed of a high number of leukocytes, especially neutrophils, and numerous spirochetes of different sizes and other bacterial morphotypes located between the host cells
3. The necrotic zone, containing disintegrated cells, together with medium- and large-size spirochetes and fusiform bacteria
4. The spirochetal infiltration zone, where the tissue components are adequately preserved but are infiltrated with large- and medium-size spirochetes. Other bacterial morphotypes are not found.

The bacteria commonly associated with necrotizing ulcerative gingivitis and found in lesion layers includes Treponema spp., Selenomonas spp., Fusobacterium spp., and Prevotella intermedia. Other microorganisms have also been described, although these were defined as “variable” flora and were not present in all cases ²⁰. A gram stain of gingival tissue has been shown to be useful in supporting the diagnosis, but it is not required and is not always performed because this typical microbiological description can also be detected in healthy, gingivitis, or periodontitis sites ¹⁴, ¹², ¹⁰.

The diagnosis of ANUG is associated with poor oral hygiene and weakening of the host immune system, particularly in the setting of HIV infection ¹. Nutritional deficiencies, poor living conditions, as well as the context of psychological stress, have commonly been observed as predisposing factors ¹, ³.

Acute necrotizing ulcerative gingivitis differential diagnosis

Acute necrotizing ulcerative gingivitis diagnosis may be confused with other bacterial infections and also many viral infections. Considerations for a differential diagnosis should include bacterial infections like gonococcal or streptococcal gingivitis, acute herpetic gingivostomatitis, infectious mononucleosis, and also with some mucocutaneous conditions such as desquamative gingivitis, multiforme erythema, and pemphigus vulgaris ¹⁵, ¹². Clinicians should consider ANUG in HIV-infected individuals, even if CD4+ T-lymphocyte counts have remained stable.

Acute necrotizing ulcerative gingivitis treatment

Treatment of ANUG is determined on a case-by-case basis, often with a multi-factorial approach that is tailored to the extent of the infection and to what the individual can tolerate ⁹. Acute necrotizing ulcerative gingivitis treatment should be approached in successive stages, including treatment of the acute phase, treatment of any preexisting condition, treatment of disease complications, and transition to supportive or maintenance phase ¹.

Treatment of the acute phase aims to halt tissue destruction and to control the patient’s discomfort. This involves gentle, ultrasonic debridement of superficial gingival plaques and calculi along with localized oxygen therapy, directed at necrotic lesions ¹. The use of 0.12% chlorhexidine gluconate mouth rinse should be considered, a suggested regimen being twice a day for 30 days ²¹. Systemic antibiotics are considered in the acute phase in cases with poor response to debridement or those with symptoms of systemic involvement, including fever, malaise and vomiting ¹.

Metronidazole (250 mg 3 times a day) is a common first drug choice due to its activity against anaerobes ¹⁴, ¹⁵, ². Other systemic antibiotics have also been suggested with “acceptable” results and are considered on a case-by-case basis include penicillin, tetracyclines, clindamycin, amoxicillin, or amoxicillin with clavulanate ¹⁴, ². Oral penicillin, for example, was demonstrated in one study to show significant clinical improvement in three to six days ¹⁰. Although oral antibiotics have been shown to be beneficial, topical antimicrobials are not recommended because of the large numbers of bacteria present within the tissues, where the local drug will not be able to achieve adequate concentrations ¹⁴, ². Importantly, the addition of antifungal agents is indicated in immunosuppressed patients who undergo antibiotic therapy ¹⁵, ¹.

After the acute phase has been controlled, treatment of any preexisting condition, such as chronic gingivitis, should be started. This stage involves professional prophylaxis in the form of scaling and root planning and the establishment of maintenance of oral hygiene methods by the patient ²¹. Existing predisposing factors, including smoking, poor sleep hygiene, and stress, should be addressed ¹⁴, ¹⁵. Gingivectomy and/or gingivoplasty procedures can treat any superficial craters ¹; periodontal flap surgery, or even regenerative surgery, is more suitable options for deep craters or for necrotizing ulcerative periodontitis (NUP) ¹⁴, ¹⁵.

The main goal of the maintenance phase is to comply with oral hygiene practices and control any predisposing factors ¹⁴, ¹⁵. If proper maintenance is not carried out, relapses are likely to occur.

In summary, the treatment of ANUG consists of a multifactorial approach involving superficial debridement, oral hygiene instruction, utilization of antimicrobial mouthwash and oral antibiotics, and initiation of a comprehensive prophylaxis plan involving root planning and predisposing factor management ⁹.

Acute necrotizing ulcerative gingivitis prognosis

Adequate acute necrotizing ulcerative gingivitis treatment usually prevents the progression of the disease, and ulcer healing can be expected in a few days. Without treatment acute necrotizing ulcerative gingivitis (ANUG) can lead to further deterioration in some cases to ulcerative necrotizing stomatitis, necrotizing ulcerative periodontitis (NUP) and, finally, to gangrenous stomatitis also called Noma which is a rapidly progressing severe gangrenous disease of the mouth and the face which is commonly fatal ³, ¹⁴, ¹⁶, ¹⁷, ¹⁸, ¹³.

1. Malek R, Gharibi A, Khlil N, Kissa J. Necrotizing Ulcerative Gingivitis. Contemp Clin Dent. 2017 Jul-Sep;8(3):496-500. doi: 10.4103/ccd.ccd_1181_16[↩][↩][↩][↩][↩][↩][↩][↩][↩][↩][↩][↩][↩][↩][↩][↩][↩][↩]
2. Aaron SL, DeBlois KW. Acute Necrotizing Ulcerative Gingivitis. [Updated 2023 Jul 20]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK562243[↩][↩][↩][↩][↩][↩][↩][↩][↩][↩][↩][↩][↩]
3. Mizrahi Y. [NUG–necrotizing ulcerative gingivitis: a review]. Refuat Hapeh Vehashinayim (1993). 2014 Jul;31(3):41-7, 62. Hebrew.[↩][↩][↩][↩][↩][↩][↩][↩][↩][↩][↩][↩][↩][↩][↩][↩][↩]
4. Niklaus Lang, Soskolne WA, Gary Greenstein, David Cochran, Esmonde Corbet, Huan Xin Meng, et al. Consensus Report: Necrotizing Periodontal Diseases. Annals of Periodontology. 1999;4:78.[↩][↩][↩][↩][↩][↩]
5. Rowland RW. Necrotizing ulcerative gingivitis. Ann Periodontol. 1999 Dec;4(1):65-73; discussion 78. doi: 10.1902/annals.1999.4.1.65[↩][↩][↩][↩][↩][↩][↩][↩][↩][↩][↩]
6. Atout RN, Todescan S. Managing patients with necrotizing ulcerative gingivitis. J Can Dent Assoc. 2013;79:d46[↩][↩][↩][↩][↩][↩]
7. Hu J, Kent P, Lennon JM, Logan LK. Acute necrotising ulcerative gingivitis in an immunocompromised young adult. BMJ Case Rep 2015. 2015 pii: Bcr2015211092[↩][↩][↩]
8. Melnick SL, Roseman JM, Engel D, Cogen RB. Epidemiology of acute necrotizing ulcerative gingivitis. Epidemiol Rev. 1988;10:191-211. doi: 10.1093/oxfordjournals.epirev.a036022[↩]
9. Dufty J, Gkranias N, Donos N. Necrotising Ulcerative Gingivitis: A Literature Review. Oral Health Prev Dent. 2017;15(4):321-327. doi: 10.3290/j.ohpd.a38766[↩][↩][↩][↩]
10. Kaplan D. Acute necrotizing ulcerative tonsillitis and gingivitis (Vincent’s infections). Ann Emerg Med. 1981 Nov;10(11):593-5. doi: 10.1016/s0196-0644(81)80200-4[↩][↩][↩][↩][↩]
11. Barnes GP, Bowles WF 3rd, Carter HG. Acute necrotizing ulcerative gingivitis: a survey of 218 cases. J Periodontol. 1973 Jan;44(1):35-42. doi: 10.1902/jop.1973.44.1.35[↩][↩]
12. Folayan MO. The epidemiology, etiology, and pathophysiology of acute necrotizing ulcerative gingivitis associated with malnutrition. J Contemp Dent Pract. 2004 Aug 15;5(3):28-41.[↩][↩][↩][↩]
13. Jiménez LM, Duque FL, Baer PN, Jiménez SB. Necrotizing ulcerative periodontal diseases in children and young adults in Medellín, Colombia, 1965–2000. J Int Acad Periodontol. 2005 Apr;7(2):55-63.[↩][↩][↩][↩]
14. Herrera D, Alonso B, de Arriba L, Santa Cruz I, Serrano C, Sanz M. Acute periodontal lesions. Periodontol 2000. 2014 Jun;65(1):149-77. doi: 10.1111/prd.12022[↩][↩][↩][↩][↩][↩][↩][↩][↩][↩][↩][↩][↩]
15. Bermejo-Fenoll A, Sánchez-Pérez A. Necrotising periodontal diseases. Med Oral Patol Oral Cir Bucal. 2004;9 Suppl:114-9; 108-14. English, Spanish.[↩][↩][↩][↩][↩][↩][↩][↩]
16. Srour ML, Marck K, Baratti-Mayer D. Noma: Overview of a Neglected Disease and Human Rights Violation. Am J Trop Med Hyg. 2017 Feb 8;96(2):268-274. doi: 10.4269/ajtmh.16-0718[↩][↩][↩]
17. Mortazavi H, Safi Y, Baharvand M, Rahmani S. Diagnostic Features of Common Oral Ulcerative Lesions: An Updated Decision Tree. Int J Dent. 2016;2016:7278925. doi: 10.1155/2016/7278925[↩][↩][↩]
18. Horning GM, Cohen ME. Necrotizing ulcerative gingivitis, periodontitis, and stomatitis: clinical staging and predisposing factors. J Periodontol. 1995 Nov;66(11):990-8. doi: 10.1902/jop.1995.66.11.990[↩][↩][↩]
19. Loeb, M., Reid, M., Buchanan, W., & Bain, J. (2017). Necrotizing Ulcerative Gingivitis in the Setting of Vitamin B12 Deficiency: ACase Report. oral health and dental management, 2017, 1-6.[↩]
20. Loesche WJ, Syed SA, Laughon BE, Stoll J. The bacteriology of acute necrotizing ulcerative gingivitis. J Periodontol. 1982 Apr;53(4):223-30. doi: 10.1902/jop.1982.53.4.223[↩]
21. Martos J, Ahn Pinto KV, Feijó Miguelis TM, Cavalcanti MC, César Neto JB. Clinical treatment of necrotizing ulcerative gingivitis: a case report with 10-year follow-up. Gen Dent. 2019 May-Jun;67(3):62-65.[↩][↩]