Trench Mouth

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A 37-year-old male patient presented with severe pain and bleeding of gingiva with inability to eat spicy food for 6 days. The patient was systemically healthy, but a heavy smoker for 3 years (15 cigarettes per day) and also under heavy stress due to family problems. He also complained of “metallic” taste and “pasty” saliva. Intraoral examination revealed necrotizing lesions of maxillary and mandibular gingiva, with the surface covered by white pseudomembrane slough (Figure, black arrows). Bilateral submandibular lymph nodes were tender on palpation, and there was increased body temperature of 103°F. Panoramic radiograph showed no loss of alveolar bone. Blood analysis was normal and the HIV serostatus was negative. The diagnosis arrived at was Trench mouth, or Vincent's gingivostomatitis – after taking into consideration the clinical features and eliminating a similar condition called primary herpetic gingivostomatitis caused by herpes simplex virus-1 – seen predominantly in children with vesicle formation of the gingiva. The patient was advised to stop the smoking habit. Treatment consisted of removal of the pseudomembrane and the necrotic part of gingiva under local anesthesia, with the patient advised to take adequate rest and proper diet. He was prescribed amoxicillin 500 mg and paracetamol 325 mg every 6 hours for 5 days, and local application of metronidazole gel 3 times a day for 5 days. For maintenance of oral hygiene, the patient was advised to rinse his oral cavity with 3% hydrogen peroxide and sterile warm saline (1:1) 4 times a day, along with 0.12% chlorhexidine mouthrinse for 7 days. One-year follow-up revealed completely healed gingiva with no recurrence of the lesion. Vincent's gingivostomatitis is also called trench mouth, because its incidence increased during World War I in military personnel who fought in trenches dug in the ground. The causative organisms implicated in trench mouth are Prevotella intermedia, Fusobacterium nucleatum, and Porphyromonas gingivalis, which are normal commensals of the oral cavity; however, when the local resistance of the gingiva becomes impaired due to certain predisposing factors, these organisms become pathogenic.1Enwonwu C.O. Falkler W.A. Idigbe E.O. Oro-facial gangrene (noma/cancrum oris): pathogenetic mechanisms.Crit Rev Oral Biol Med. 2000; 11: 159-171Crossref PubMed Scopus (99) Google Scholar, 2Enwonwu C.O. Epidemiological and biochemical studies of necrotizing ulcerative gingivitis and noma (cancrum oris) in Nigerian children.Arch Oral Biol. 1972; 17: 1357-1371Abstract Full Text PDF PubMed Scopus (95) Google Scholar The main predisposing factors are stress and smoking, which leads to altered cytokine response that affects the recruitment of macrophages and fibroblasts, causing impaired host immune response to periodontal bacteria.3Deinzer R. Kottmann W. Forster P. et al.After-effects of stress on crevicular interleukin-1 beta.J Clin Periodontol. 2000; 27: 74-77Crossref PubMed Scopus (25) Google Scholar Reduction in tissue inhibitor of matrix metalloproteinase (known as TIMP1) levels due to smoking also leads to impaired tissue turnover.4Knuutinen A. Kokkonen N. Risteli J. et al.Smoking affects collagen synthesis and extracellular matrix turnover in human skin.Br J Dermatol. 2002; 146: 588-594Crossref PubMed Scopus (131) Google Scholar The mainstay of treating this condition is proper diagnosis, stress control, and stoppage of any habit, along with adequate diet and nutrition.