Journal of Orthodontics, Vol. 40, 2013, 77–80
CLINICAL SECTION
Necrotizing ulcerative gingivitis and the orthodontic patient: A case series Indiya Sangani, Eileen Watt and David Cross Glasgow University, Glasgow, UK
Necrotizing ulcerative gingivitis (NUG) can be a painful periodontal disease that can lead to loss of the interdental papillae. It is usually accompanied by systemic signs of fever, malaise and cervical and submandibular lymphadenopathy. It is caused by the profileration of anaerobic bacteria and has been linked to smoking and immunosuppression. This case series reports the occurrence of NUG in orthodontic patients and demonstrates that there is a varying scale of severity of the condition. Orthodontists should be aware of the clinical signs of NUG to ensure early detection and treatment of their patients in order to prevent irreversible loss of the interdental papillae and reduce the likelihood of recurrence. A treatment regime is suggested. Key words: Necrotizing ulcerative gingivitis, orthodontics, treatment Received 9 May 2012; accepted 14 October 2012
Introduction The orthodontic patient is at risk of developing demineralization and gingival disease if oral hygiene is not rigorous.1 Orthodontists must advise their patients on maintaining excellent oral hygiene before and during treatment so that damage to the dentition and periodontium is kept to a minimum.2 Necrotizing ulcerative gingivitis (NUG) is a painful periodontal disease characterized by red, ulcerated gingivae, halitosis and punched out interdental papillae.3 It is usually accompanied by systemic signs of fever, malaise and both cervical and submandibular lymphadenopathy. Patients can also be susceptible to recurrence of the disease.3,4 NUG generally affects females and males equally in Western countries, presenting most commonly in the 18– 30 year old patient.5 There are no reports of the prevalence of NUG in orthodontic patients in the literature published to date. Epidemiological studies of oral disease carried out in 1950s–1960s reveal a 5% disease incidence of NUG in school children and young adults.5,6 However, recent crosssectional studies of 1200 Turkish school children and an American study of 10 030 individuals aged between 2 and 17 years failed to reveal any cases.7,8 These investigations show that NUG can occur in orthodontic patients but that they may not necessarily present with the classical signs and symptoms. We suggest that there is a scale of severity of this disease, which the clinician must be made aware of, as the most minor form of NUG may be mistaken for marginal gingivitis or even overlooked. As NUG can lead to irreversible destruction Address for correspondence: Dr David Cross, Glasgow University, Glasgow, Lanarkshire, UK. Email:
[email protected] # 2013 British Orthodontic Society
of the gingivae it is important that it is detected early. The prevalence of the disease in the orthodontic patient is unknown but may be expected to be higher than in the general population due to the increased risk factors for plaque accumulation during treatment.9,10
Case report 1 A 15-year-old non-smoking female with a clear medical history presented 18 months into orthodontic treatment with submandibular lymphadenopathy and malaise, pain from the gingivae, halitosis and generalized loss of interdental papillae affecting the upper and lower anterior teeth in particular. This case showed all the typical features of NUG (Figure 1). Treatment involved oral hygiene instruction, debridement of areas affected, and a prescription of metronidazole 200 mg, three times daily for 3 days with a chlorhexidine mouthwash to be used twice a day for 7 days. The NUG resolved at the follow-up appointment two weeks later. At the patients next routine adjustment visit it was noted that the lower labial segment teeth were affected again with a milder form of NUG and that there was an absence of systemic symptoms. Local debridement and chlorhexidine were used and the patient’s gingival condition improved markedly (Figure 1)
Case report 2 An 18-year-old non-smoking female presented after 34 months of orthodontic treatment with clinical signs of
DOI 10.1179/1465313312Y.0000000037
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Figure 1
Clinical Section
(a) NUG in a 15-year-old patient. (b) Milder form of NUG without systemic symptoms seen in the same patient
NUG localized to the lower labial segment (Figure 2). There was no systemic involvement. She had a clear medical history. Treatment involved a conservative approach with local debridement and a prescription of chlorhexidine mouthwash to be used twice a day for 7 days. This regime was successful in treating the NUG.
Case report 3 An 18-year-old male smoker with unremarkable medical history presented after 17 months of orthodontic treatment with complete loss of interdental papillae and some minor sloughing affecting the interdental papillae between the lower central incisors (Figure 3). The patient had no recollection of any previous episode of NUG and no records of acute symptoms were made by the clinician. Treatment of marginal gingivitis was
Figure 2
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NUG localized to the lower labial segment
conservative and involved debridement and chlorhexidine mouthwash for one week.
Case report 4 An 18-year-old female occasional smoker with no relevant medical history attended for a routine orthodontic visit 9 months into orthodontic treatment. She had the classical signs of NUG, including marked gingivitis, ulcerated gingivae, halitosis and loss of interdental papillae of affected teeth (Figure 4). These were accompanied by the systemic signs of submandibular lymphadenopathy, but no pain or malaise. The treatment was local debridement (Figure 4), oral hygiene instruction, chlorhexidine mouthwash and a prescription of metronidazole. At review one week later her gingival condition had improved but gingivitis remained and she is currently undergoing but further OHI and scaling.
Figure 3 Loss of interdental papillae and some minor sloughing affecting the interdental papillae between the lower central incisors
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Clinical Section
NUG and orthodontics
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Figure 4 (a) Classic NUG. (b) Appearance after local debridement
Discussion NUG is caused by the proliferation of anaerobic bacteria and involves Fusobacterium nucleatum, Treponema denticola, Treponema macrodentium, Prevotella intermedia and Porphyromonas gingivalis.11 Disease results when these bacteria proliferate, imbalancing the normal oral flora. Oral hygiene and emotional stress have been shown to be predisposing factors. Smoking can be a risk factor associated with the disease; a study in 1983 of a 100 adult cases of NUG found that 98 out of the 100 patients were smokers.12 It is interesting to note that two of the cases presented had a history of smoking. Pre-existing medical conditions compromising the immune system, such as AIDS and glandular fever can also predispose the patient to NUG.3 Diagnosis of NUG is made clinically and it is usually treated in two stages; first controlling the acute presentation and then by preventing recurrence. Treatment involves careful debridement of slough and plaque debris in the affected areas (Figures 4b).3 Patients should be advised an antibacterial mouthwash to be used three times daily for 1–2 weeks, and prescribed a short course of metronidazole 200 mg to be taken three times daily for three days if there are systemic signs.3,5 Once the acute phase has remitted, meticulous oral hygiene should be implemented along with supra and sub gingival scaling in order to reduce the likelihood of recurrence.3,5 NUG is diagnosed from a set of clinical signs and symptoms, which often involve systemic features in the acute presentation. The patients presented in this case series suggest that there may be a mild form of NUG as only one of these patients presented with all the classical features of acute infection, indeed most presented without pain. These clinical findings are in agreement
with Campbell et al. who also noted the varying scale of severity of the disease in a case series of four patients.13 Table 1 illustrates the classical features of NUG compared to the mild form described in some of our cases. It is also important to note that not all of our patients were smokers as usually this is one of the major risk factors associated with NUG.
Conclusion
N
The prevalence of NUG in the orthodontic patient is unknown but orthodontic patients may be at higher risk of developing NUG than other patients due to the plaque retentive element of most orthodontic treatment.
Table 1 Clinical presentation of classical NUG and mild NUG with suggested treatment regime.
Necrotizing ulcerative gingivitis
Necrotizing ulcerative gingivitis
Classical signs
Mild signs
Pain Halitosis Bleeding Loss of papillae Ulceration Lymphadenitis Malaise
No pain Halitosis may not be present Bleeding Loss of papillae Ulceration No lymphadenitis No malaise
Treatment Local debridement Chlorhexidine mouthwash Metronidazole tds 200 mg 3 days Review 1 week
Local debridement Chlorhexidine mouthwash Review 1–2 week
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N
N N N
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Clinical Section
The orthodontist should be aware of the varying clinical signs of NUG in both classical and mild forms, so that treatment may be started as soon as possible to prevent the irreversible destruction of the interdental papillae. Simple treatment using local debridement and prescription of 0.2% chlorhexidine mouthwash can be used effectively in cases with no systemic involvement. Metronidazole 200 mg tds for 3 days should be prescribed if there is systemic involvement in addition to those measures recommended for simple treatment. Patients should be reviewed 1–2 weeks following treatment of NUG and require careful monitoring is recommended to ensure recurrence is detected early.
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5. Eley BM, Soory M, Manson JD. Chapter 25: acute necrotising ulcerative gingivitis. In Eley BM, Soory M, Manson JD (eds.). Periodontics, 6th Edn. Edinburgh/New York: Saunders/Elsevier, 2010, 376–79. 6. Falker WA Jr, Martin SA, Vincent JW, et al. A clinical and demographic and microbiologic study of ANUG patients in an urban dental school. J Clin Periodontol 1987; 14: 307–14. 7. Parlak AH, Koybasi S, Yavuz T, et al. Prevalence of oral lesions in 13–16 year old students in Duzce, Turkey. Oral Dis 2006; 12: 553–58. 8. Shulman JD. Prevalence of oral mucosal lesions in children and youths in the USA. Int J Paediatr Dent 2005; 15: 89–97. 9. Davies TM, Shaw WC, Worthington HV, Addy M, Dummer P, Kingdon A. The effect of orthodontic treatment on plaque and gingivitis. Am J Orthod Dentofacial Orthop 1991; 99: 155–61. 10. Atack NE, Sandy JR, Addy M. Periodontal and microbiological changes associated with the placement of orthodontic appliances. A review. J Periodontol 1996; 67: 78–85. 11. Loesche WJ, Syed SA, Laughton BE, et al. The bacteriology of acute necrotising ulcerative gingivitis. J Periodontol 1982; 53: 223–30. 12. Kowolik MJ, Nisbet T. Smoking and acute ulcerative gingivitis. Br Dent J 1983; 154: 241–42. 13. Campbell CSM, Bradshaw M, Deas DE. Necrotising ulcerative gingivitis: a discussion of four dissimilar presentations. Tex Dent J 2011; 128: 1041–51.
