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International Journal of Surgery Case Reports logoLink to International Journal of Surgery Case Reports
. 2023 Jul 1;109:108460. doi: 10.1016/j.ijscr.2023.108460

Traumatic ulcer of the tongue mimicking a malignant lesion: Case report

Hajar Ouaabbou 1,, Soukayna Bahbah 1, Saliha Chbicheb 1
PMCID: PMC10372728  PMID: 37473621

Abstract

Introduction and importance

The most prevalent oral ulcers are those caused by trauma, and their etiopathogenesis has been frequently obvious. Yet, oral ulcers can be misdiagnosed and managed incorrectly.

Case presentation

A 25-year-old patient presented to our service with a painful lesion on the right lateral border of the tongue that had evolved for one week. A possible traumatic factor was identified. The ulcer completely recovered once the trauma's cause was removed. An accurate diagnosis was achieved by combining a precise physical examination with clinical follow-up.

Clinical discussion

Single oral ulcers have various clinical presentations that can be confusing. Some of them may mimic oral squamous cell carcinoma (OSCC), especially when accompanied by any induration. Determining the cause of oral ulceration requires a careful medical history and a clinical examination with inspection and palpation, which may be combined with other accessory investigations if necessary.

Conclusion

This clinical case reinforces the importance of investigating local causes before moving on to systemic ones. We present differential diagnosis and management algorithm of single oral ulcers.

Keywords: Single oral ulcer, Traumatic oral ulcer, Oral squamous cell carcinoma, Differential diagnosis, Management, Case report

Highlights

  • A single oral ulcer has various clinical presentations and may mimic malignant lesions, especially when accompanied by any induration.

  • It is important to look for local oral ulcer causes first before moving on to systemic ones.

  • Traumatic oral ulcers should heal within 2 weeks of the removal of the injury's factor. This period can be longer, especially in immunologically compromised patients.

  • A non-healing oral ulcer must have a histopathological investigation.

1. Introduction and importance

Oral ulcers are frequent lesions resulting from many underlying etiologic factors. Traumatic ulcers are most common on the buccal mucosa (28.5 %), tongue (16.6 %), and lower lips (8.3 %) [1]. They may result from physical, chemical, or thermal injuries. Teeth can alter the soft tissues of the mouth due to improper positioning, sharp or jagged edges due to tooth decay or fractures, or defective restorations [2].

The diagnosis of a single and isolated oral ulcer can be confusing. Oral ulcers may present in various forms and have multiple etiologies [3]. Ulcers may form as a result of local or systemic causes. An oral ulcer is most often benign, yet the elimination of oral squamous cell carcinoma (OSCC) must be an absolute priority in this context, even if the clinical presentation appears reassuring [2]. We present a patient with an ulcer affecting the tongue whose clinical features refer to malignization. This case has been reported in line with the SCARE 2020 criteria [4].

2. Case presentation

A generally healthy 25-year-old man without vices presented to our oral surgery department with a painful lingual lesion that had appeared a week earlier. The patient complained of severe pain that was made worse by food and tooth contact, as well as eating difficulties.

On palpation of the right submandibular area, a tender, firm, and mobile adenopathy was noted. No lymph nodes were palpable in the other region of the neck.

Intraoral examination revealed a coated tongue with a large and solitary lingual mass. The lesion was 20 mm × 20 mm in diameter, rubbery in consistency but not indurated on palpation, with an infiltrated and exophytic base, elevated borders, and the center covered with fibrinous exudate (Fig. 1). The lesion was on the right lateral border of the tongue, adjacent to the right mandibular second molar.

Fig. 1.

Fig. 1

Large tongue ulcer with raised margins, an exophytic base, and a fibrinous exudate-covered center.

The 47 was significantly decayed, fractured, and presented a sharp lingual edge on palpation. The patient reported episodes of pain and swelling in relation to the tooth (Fig. 2a). The radiography showed a profound coronary radioluscence invaded the pulp chamber of the tooth, with periapical radioluscence around the root apex (Fig. 2b). The vestibular decayed area has reached down to the bone level. There was not enough sound tooth tissue to allow for a restoration of any kind. Consequently, 47 was unrestorable and tooth removal was indicated.

Fig. 2.

Fig. 2

A) Buccal view of the causal tooth 47, showing the sharp lingual edge. B) Panoramic X-ray C) extraction of 47.

Based on the history and clinical appearance, the differential diagnosis was lingual traumatic ulcer and malignant lesion of the tongue. Extraction of the 47 fractured was planned in order to follow the evolution of the lesion and eliminate any traumatic cause (Fig. 2c).

The patient was instructed to eat preferably soft foods, avoid hot and spicy foods, and insist on oral hygiene and tongue scraping. Antiseptic mouthwash and topical gel based on hyaluronic acid were prescribed and applied four times a day for about a week. Three days later, the ulcer had diminished in size and had become erythematous (Fig. 3). Two weeks later, the lesion showed significant regression. The lesion healed completely after 1 month (Fig. 4).

Fig. 3.

Fig. 3

Slight resolution of the ulcer 3 days after extraction of the 47.

Fig. 4.

Fig. 4

Ulcer completely healed after 1 month.

Eventually, the accurate diagnosis was a traumatic ulcer on the tongue.

3. Discussion

Oral ulcers are a simple lesion characterized by a loss of substance, affecting the epithelium and underlying connective tissue. Their ulcerated nature differentiates them from other lesions, which correlates to a deep histological involvement of the oral mucosa [5].

The most important characteristic of an ulcer is its evolution. Usually, an ulcer occurs in three phases: extension, transition, and healing or repair [6]. Acute ulcers often last less than two weeks and are painful, which motivates the patient to consult. The ulcer may develop into chronicity if the etiologic factor persists. It becomes chronic, reactive, and exophytic [7]. A persistent ulcer can be a sign of squamous cell carcinoma, particularly when associated with any induration [8].

Determining the cause of an oral ulcer requires a careful medical history and a clinical examination with inspection and palpation, which may be combined with other accessory investigations if necessary. Traumatic ulcers are not always easy to diagnose, especially when there is no history of trauma. Self-induced injuries caused by a parafunctional habit are uncommon and challenging to identify. In such circumstances, the traumatic origin of oral lesions may be underestimated and improperly handled [3].

In our case, the patient reported no recent history of trauma. However, with a meticulous clinical examination, we were able to detect the sharp edge of the tooth adjacent to the ulcer, which was the cause of the lesion. The ulcer completely recovered once the trauma's cause was removed. This paper reinforces the importance of looking for local oral ulcer causes first before moving on to systemic ones.

Given the variety of their causes and clinical presentations, the diagnosis of traumatic lesions may be relatively challenging. Differential diagnosis of a single oral ulcer includes many entities (Table 1):

  • Traumatic ulcer is usually painful. It presents as an erythematous lesion with elevated margins and a removable yellowish-white necrotic pseudomembrane and heals when the irritant factor is eliminated [7].

  • Eosinophilic ulcer, or traumatic ulcerative granuloma with stromal eosinophilia (TUGSE), is a benign, reactive, and self-limiting lesion with an unclear pathogenesis. Clinically, the lesion manifests as an isolated ulcer with elevated and indurated margins in addition to a white or yellowish base. It can be either asymptomatic or associated with mild to severe pain, and in most cases, it affects the tongue [9].

  • Necrotizing sialometaplasia is a rare benign condition of the salivary glands. It appears on the hard palate following chronic irritation, ischemia, and necrosis of the tissue salivary glands to the palate. It manifests as a deep and fully necrotic ulceration [10].

  • Single aphthae: We differentiate between small common aphthae (3 to 6 mm) and giant aphthae (1 to 2 cm). An aphthous ulcer is a round or oval ulceration with a fibrinous base and an erythematous periphery. Sometimes, it loses its peripheral red halo during the healing process and is frequently mistaken for a traumatic ulcer. Aphthae causes are multiple (stress, food, immunodeficiency, vitamin B12 deficiency, etc.). Depending on the size, healing takes between 10 and 15 days. Giant aphthae may take much longer [11].

  • Malignant ulcerations are notorious in the oral cavity for their ability to mimic benign ulcerative lesions [2]. Oral squamous cell carcinoma (OSCC) accounts for 80.05 % of all oral cancer cases [12]. Most often, carcinomas have an ulcero-vegetative aspect. The induration increases with the progression of the lesion and indicates infiltration of the underlying planes [6]. Chronic mechanical irritation has repeatedly been reported to be a possible risk factor for oral cancer. The lesions can result from dental or prosthetic factors, usually in relation to functional factors, involving mainly the tongue edges and oral mucosa. However, the current literature shows little evidence to support an association between chronic mechanical trauma and oral carcinogenesis [13].

    Rarely, other malignancies may manifest in the oral cavity as deep ulceration, such as non-Hodgkin's lymphoma and centro-facial malignant granuloma. Metastasis of primary tumors can also appear as ulcers in the oral cavity [5].

  • Infections may also cause oral ulceration even without general symptoms, especially viral infections such as those due to Epstein-Barr virus, Herpes simplex virus (HSV), Cytomegalovirus (CMV), or Human immunodeficiency virus (HIV) [14]. Other less likely differential diagnoses include deep mycotic or fungal infections (candidiasis, histoplasmosis) and mycobacterial infections (syphilis, tuberculosis) [11,15,16].

  • Ulceration can be the manifestation of certain systemic diseases: Crohn's disease, Horton's disease, granulomatosis with polyangiitis, agranulocytosis, etc. Drug reactions can also manifest as an oral ulcer. The medical history guides the diagnosis. The drug's cessation allows healing [6].

Table 1.

Differential diagnosis of solitary oral ulcers.

Single ulcer Etiopathogenesis Clinical presentation
Regional/general signs Histopathology
Size Form Margins Periphery Base Palpation
Traumatic ulcer Trauma Variable Variable Regular elevated keratinized No red halo Fibrinous or necrotic Flexible No Stratified squamous epithelium hyperplastic or not, hyperkeratosis, or not, hyperkeratosis or not, basement membrane consisting of granulomatous infiltrate tissue
Common aphthae Stress, food, immunodeficiency, vitamin deficiency <1 cm Round/oval Regular Red halo fibrinous, necrotic Soft No Non-specific: Inflammatory cells, predominately T-cells, with high local levels of TNF-α
Giant APHTHAE ≥1 cm Irregular Elevated
Eosinophilic ulcer Unknown chronic irritation 1 cm to 2 cm Irregular, Self-limiting, Elevated indurated Red halo Deep yellow fibrinous Indurated No Granulomatous inflammatory infiltration predominately of eosinophils and histiocytes, extending into deep underlying tissue,
Oral squamous cell carcinoma Risk factors: tobacco, alcohol, HPV 16 Variable Variable irregular + Elevated everted shredded Variable Variable Indurated beyond the lesion Satellite adenopathy Proliferation of epithelial tumor cells invading the chorion in the form of lobules and/or spans. (severe dysplasia, carcinoma-in-situ, or frankly invasive carcinoma)
HIV-seropositive ulcer Human immunodeficiency virus (HIV) Variable Linear Elevated Red halo Digging and deep Rubbery No Extensive necrosis, leukocytoclasia, vasculitis with luminal fibrin clots and an intense inflammatory cellular infiltrate predominated by CD68+ atypical large cells, normal-sized and crescent-shaped nuclei macrophages, interspersed by CD8+ T lymphocytes.
Tuberculous ulcer Mycobacterium tuberculosis (MTB) ≥1 cm Irregular Elevated No red halo Yellow-gray Rubbery Satellite adenopathy pulmonary symptoms +/− Chronic granulomatous infiltrate (Langhans giant cells and lymphocytes), with acid-fast rods on Ziehl-Neelsen stain
Syphilitic ulceration Treponema pallidum (TP) ≥1 cm Self-limiting Regular elevated everted Red halo Fibrinous/greyish-white Indurated Satellite adenopathy Non-specific Epithelial changes and inflammatory infiltrations with mainly plasma cells and inflammatory cells
Histoplasmosis ulcer Histoplasma capsulatum (HC) ≥1 cm Round/Oval Elevated Whitish halo Digging and deep Indurated Weight loss, fever, dysphagia, adenopathy Characteristic: intense histiocytic inflammatory infiltrate associated with rounded fungal structures
Necrotizing sialometaplasia Smoker, alcoholic, bulimic. 1 cm to 5 cm Oval or elongated Irregular undermined Indurated Red halo Deep, fully necrotic No tender No Lobular necrosis and squamous metaplasia of ducts and acini, immunohistochemistry identify residual myoepithelial cells, as demonstrated by calponin

Spontaneous healing of ulcers is stimulated by saliva, secretory immunoglobulin A (sIgA), and growth factors [17]. The use of a short course of topical corticosteroids (2–6 days) will be especially indicated in oral mucosal diseases that have a natural tendency towards spontaneous resolution once we have removed the causative source [18]. The efficacy of hyaluronic acid (HA) on oral ulcers is rarely reported. Recently, the importance of HA has increased because of its role in the growth, development, and repair of tissues [19]. Herbal ingredients (Jatropha multifida) can also be used as alternative medicines [17]. CO₂ laser therapy accelerates the healing and relieves the pain of ulcers in the oral mucosa [20]. The pain, inflammation, and bleeding from the ulcers may often lead to inadequate oral hygiene, resulting in poor plaque control and exacerbation of erosive disease [8] (Fig. 5).

Fig. 5.

Fig. 5

Management algorithm of single oral ulcers.

Oral ulcers with a possible traumatic etiology are not biopsied. Traumatic ulcers should heal within 2 weeks of the removal of the injury's factor. This period can be longer, especially in immunologically compromised patients. A suspicious lesion or non-healing ulcer must have a histopathological investigation [11]. In small ulcers (<5 mm in diameter), an excisional biopsy is recommended, whereas in larger ulcers (>5 mm in diameter), an incisional biopsy is preferred. The specimen must include part of the ulcer and the perilesional tissue, including the unaffected surrounding epithelium. The center of the ulcer alone usually does not show diagnostic features. Scalpel or punch biopsies are preferred; other techniques (lasers, electrical scalpels) are not recommended [7].

4. Conclusion

The clinical presentation of traumatic lesions varies significantly. Mechanical trauma must be retained when faced with dental, prosthetic, and functional factors susceptible to causing an oral ulcer. A biopsy is indicated for suspicious lesions and ulcers that do not respond to treatment as expected after removal of the possible causal factor.

Patient perspective

Patient was satisfied with the result.

Patient consent

Written informed consent was obtained from the patient for publication of this case report and accompanying images. A copy of the written consent is available for review by the Editor-in-Chief of this journal on request.

Provenance and peer review

Not commissioned, externally peer-reviewed.

Funding

N/A.

Ethic approval

N/A. Case reports are exempted from ethical approval in our institution (Faculty of Dentistry, Mohammed V University in Rabat, Morocco).

Author contribution

Hajar Ouaabbou designed the concept, analyzed and interpreted the findings, wrote and reviewed the final paper under the supervision of Soukayna Bahbah and Saliha Chbicheb. All authors read and approved the final manuscript.

Guarantor

Hajar Ouaabbou.

Research registration number

N/A.

Declaration of competing interest

None.

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