The Journal of the American Dental Association
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J Am Dent Assoc, Vol 139, No 2, 159-161.
© 2008 American Dental Association

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CLINICAL PRACTICE

Indurated tongue lesion



Satish K.S. Kumar, BDS, MDSc, Amen Dhyllon, BDS and Parish P. Sedghizadeh, DDS, MS


   THE CHALLENGE
 TOP
 THE CHALLENGE
 THE DIAGNOSIS
 DIFFERENTIAL DIAGNOSIS
 CONCLUSION
 REFERENCES
 
A 58-year-old woman visited the emergency department at the University of Southern California (USC) School of Dentistry, Los Angeles, with a chief complaint of a sore and swollen tongue. The emergency department clinician referred her immediately to the Orofacial Pain and Oral Medicine Center, USC School of Dentistry, for further evaluation and treatment.

The patient reported having first noticed the lesion on her tongue 10 days earlier. The lesion increased in size during the next few days. She could not recall having experienced any trauma to her tongue before the onset of the lesion and denied any history of similar lesions. She had been taking over-the-counter acetaminophen for pain and cephalexin, an oral antibiotic that her physician prescribed, neither of which improved the lesion. Her medical history was unremarkable, and she was not taking any medications other than those for the tongue lesion. The patient reported having allergies to penicillin and codeine. She denied any current or previous tobacco use in any form, and she reported drinking alcohol occasionally.

One of us (S.K.S.K.) performed an extraoral examination, which revealed no abnormalities or lymphadenopathy. The intraoral examination revealed an exophytic, erythematous swelling on the right dorsal surface of the anterior tongue. The lesion had an ovoid central ulceration measuring about 1 centimeter in diameter, which was covered by a yellow-white fibrinouslike membrane. On palpation, the lesion was indurated (Figure 1Go).


Figure 1
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Figure 1. A large indurated lesion on the dorsal surface of the anterior tongue. The clinician (S.K.S.K.) performed an incisional biopsy during the patient’s initial visit.

 
To reach a definitive diagnosis, the clinician (S.K.S.K.) performed an incisional biopsy while the patient was under local anesthesia. The lesion began to regress spontaneously within one week after the incisional biopsy (Figure 2Go). Within three weeks, it was almost completely healed (Figure 3Go). The histologic examination ruled out a malignancy.


Figure 2
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Figure 2. A fibrinous exudate covering of the lesion sloughed off within one week after the incisional biopsy, leaving a raw superficial ulcerated base.

 

Figure 3
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Figure 3. The clinician (S.K.S.K). observed almost complete spontaneous healing of the ulcer within three weeks after the patient’s initial visit.

 
Can you make the diagnosis?

  1. syphilis
  2. major aphthous ulcer
  3. traumatic ulcerative granuloma with stromal eosinophilia
  4. deep fungal infection
  5. neutropenic ulcer


   THE DIAGNOSIS
 TOP
 THE CHALLENGE
 THE DIAGNOSIS
 DIFFERENTIAL DIAGNOSIS
 CONCLUSION
 REFERENCES
 
C. traumatic ulcerative granuloma with stromal eosinophilia Traumatic ulcerative granuloma with stromal eosinophilia (TUGSE) presents as an indurated, ulcerative, nontender lesion of the oral mucosa, most commonly seen on the tongue. TUGSE also has been referred to as a traumatic granuloma, an eosinophilic ulcer, a traumatic eosinophilic granuloma and an ulcerative eosinophilic granuloma. A similar ulceration appears in infants, usually on the ventral surface of the anterior tongue secondary to trauma from newly erupted primary teeth, especially the mandibular incisors. The ulceration in infants is referred to as Riga-Fede disease.1

TUGSE presents as a single lesion or multiple lesions; the lesion size ranges from 0.3 to 5.0 cm, with a median size of 2.0 cm.2,3 Although trauma has been identified in about 50 percent of cases, the exact etiology is not clearly understood, and many cases have been reported in patients without any history of trauma.1 In addition, the presence of multiple ulcers excludes trauma as the only predisposing factor.2 This condition has a slight predilection for men, with male-to-female ratios ranging from 1.6:1 to 5.2:1.1,4 Lesions can develop in any age group, but the mean age at onset is 58 years.1

The tongue is the most commonly affected intraoral site, followed by the lip, palate and gin-giva.4 These ulcers usually are self-limiting in nature without any recurrence unless a known source of trauma (for example, an adjacent broken tooth) continues to irritate the tissue.5 Histopathologic findings reveal ulcerated oral stratified squamous mucosa with chronic inflammatory cells, including eosinophils and histiocytes, within the connective tissue and base of the ulcer. Typically, no cellular atypia or significant mitotic activity is present, and no evidence of infection or a foreign body is seen in patients with TUGSE.6 Some studies have reported the presence of CD30 antigens, claiming that TUGSE is a simulator of CD30+ lymphoproliferative disorders.7,8

These lesions usually heal spontaneously within two to nine weeks.6 An incisional biopsy for definitive diagnosis begins the healing process and is the recommended form of treatment.5 Investigators have reported various treatment modalities, including 0.1 percent triamcinolone acetonide wash,7 oral antibiotics,7 steroids (topical and systemic),5 electrocoagulation,9 liquid nitrogen and irradiation. However, in most cases, clinicians should avoid aggressive therapy because the lesion heals spontaneously within weeks.6,10


   DIFFERENTIAL DIAGNOSIS
 TOP
 THE CHALLENGE
 THE DIAGNOSIS
 DIFFERENTIAL DIAGNOSIS
 CONCLUSION
 REFERENCES
 
The presentation of indurated ulcers on the tongue with elevated borders mimics the clinical presentation of malignancies, such as oral cancer (squamous cell carcinoma), lymphoma, salivary gland tumors and metastatic tumors. Clinicians should consider traumatic ulcerations, proliferative reactive processes other than TUGSE (such as atypical histiocytic granuloma and proliferative myositis) and certain infections (such as primary syphilis, histoplasmosis and blastomycosis) in the differential diagnosis. The histologic differential diagnosis may include many lesions that exhibit significant numbers and infiltration of eosinophils within connective tissue, such as Langerhans cell disease, Kimura disease, angio-lymphoid hyperplasia with eosinophilia, certain types of lymphomas, allergic reactions and parasitic diseases.5 We strongly recommend a clinico-pathologic correlation to establish an accurate diagnosis.


   CONCLUSION
 TOP
 THE CHALLENGE
 THE DIAGNOSIS
 DIFFERENTIAL DIAGNOSIS
 CONCLUSION
 REFERENCES
 
Although TUGSE resembles malignant lesions such as oral squamous cell carcinoma, a history of a recent onset and short duration of the lesion, a possible source of trauma and spontaneous regression of the lesion after an incisional biopsy should reveal the benign nature of this lesion. Clinicians should avoid invasive treatment until a definitive diagnosis has been established with an incisional biopsy, which begins the healing process of this benign lesion.


   FOOTNOTES
 

Dr. Kumar is an assistant professor of clinical dentistry, Orofacial Pain and Oral Medicine Center, University of Southern California School of Dentistry, 925 W. 34th St., Room 130, Los Angeles, Calif. 90089-0641, e-mail "satish.kumar{at}usc.edu". Address reprint requests to Dr. Kumar.


Dr. Dhyllon is a final-year dental student, Advanced Standing Program for International Dentists, University of Southern California School of Dentistry, Los Angeles.


Dr. Sedghizadeh is an assistant clinical professor, Division of Diagnostic Sciences and Center for Craniofacial Molecular Biology, University of Southern California School of Dentistry, Los Angeles.


Diagnostic Challenge is published in collaboration with the American Academy of Oral and Maxillofacial Pathology and the American Academy of Oral Medicine.


   REFERENCES
 TOP
 THE CHALLENGE
 THE DIAGNOSIS
 DIFFERENTIAL DIAGNOSIS
 CONCLUSION
 REFERENCES
 

  1. Elzay RP. Traumatic ulcerative granuloma with stromal eosinophilia (Riga-Fede’s disease and traumatic eosinophilic granuloma). Oral Surg Oral Med Oral Pathol 1983;55(5):497–506.[Medline]

  2. Burgess GH, Mehregan AH, Drinnan AJ. Eosinophilic ulcer of the tongue. Arch Dermatol 1977;113(5):644–5.[Abstract/Free Full Text]

  3. Doyle JL, Geary W, Baden E. Eosinophilic ulcer. J Oral Maxillofac Surg 1989;47(4):349–52.[Medline]

  4. Sklavounou A, Laskaris G. Eosinophilic ulcer of the oral mucosa. Oral Surg Oral Med Oral Pathol 1984;58(4):431–6.[Medline]

  5. Gopalakrishman R, Miloro M, Allen CM. Indurated ulceration of the tongue. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1996;82(2):119–21.[Medline]

  6. Gerber ME, Myer CM 3rd. Eosinophilic ulcer of the tongue. Otolaryngol Head Neck Surg 1997;117(6):715–6.[Medline]

  7. Segura S, Romero D, Mascaro JM Jr, Colomo L, Ferrando J, Estrach T. Eosinophilic ulcer of the oral mucosa: another histological simulator of CD30+ lymphoproliferative disorders. Br J Dermatol 2006;155(2):460–3.[Medline]

  8. Ficarra G, Prignano F, Romagnoli P. Traumatic eosinophilic granuloma of the oral mucosa: a CD30+(Ki-l) lymphoproliferative disorder? Oral Oncol 1997;33(5):375–9.[Medline]

  9. Lombardi T, Kuffer R, Samson J. Eosinophilic ulceration of the oral mucosa: a case report. Int J Oral Maxillofac Surg 1993;22(6): 366–7.[Medline]

  10. Lourenco SV, Silva MA, Nico MM. An ulcer on the lip. Clin Exp Dermatol 2005;30(2):199–200.[Medline]





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