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A Collection of Conditions Affecting the Mouth

Torus Palatinus
Ahmed Tarig Ahmed, MD

This painless, hard mass was noted on the palate of a 73-year-old woman with hypertension during a routine follow-up visit. The mass had been present for more than 30 years.

Torus palatinus is a benign developmental exostosis of the palate. The prevalence in the United States is approximately 20%, and it is more common in women.1 The cause is unknown; it is believed to be multifactorial.2,3

Most affected patients are asymptomatic, and only reassurance is needed. Ulcers can develop from repeated trauma, however. Surgery is required if a torus palatinus becomes too large and interferes with the fabrication of dentures or other prosthesis.4

References:

  1. Kolas S, Halperin V, Jefferis K, Huddleston S, Robinson HB. The occurrence of torus palatinus and torus mandibularis in 2,478 dental patients. Oral Surg Oral Med Oral Pathol. 1953;6(9):1134-1141.
  2. Haugen LK. Palatine and mandibular tori: a morphologic study in the current Norwegian population. Acta Odontol Scand. 1992;50(2):65-77.
  3. Reichart PA, Neuhaus F, Sookasem M. Prevalence of torus palatinus and torus mandibularis in Germans and Thai. Community Dent Oral Epidemiol. 1988;16(1):61-64.
  4. Woo JK. Torus palatinus. Am J Phys Anthropol. 1950;8(1):81-111.

 

Geographic Tongue
Robert P. Blereau, MD

The smooth areas in the typical “mapping” of geographic tongue, shown here, represent flattened or denuded filiform papillae. The cause of this common condition of the mouth is unknown.

The case of this 5-year-old girl is unusual because the geographic mapping—which in most cases appears only on the dorsum of the tongue—extends to the ventral surface of the girl’s tongue.

According to the patient’s mother, the child’s tongue had always had this appearance. The only reported symptom was an occasional burning sensation when the girl ate ketchup.

Geographic tongue usually is asymptomatic, but sour or salty foods may cause burning or pain. This can be relieved with application of a triamcinolone, 0.1%, dental paste.

 

Oral Lichen Planus
Taina A. Trevino, MD, Hillary F. Cohen, and Jason Rubin, MD

For 5 days, a 19-year-old young adult had nasal congestion, dry and itchy eyes, edematous lips, nausea, and sore throat. His medical history was significant for meningitis in infancy, herpes simplex virus (HSV) gingivostomatitis, and a tooth extraction 2 weeks earlier. He was in college and lived with his mother. He was taking no medications other than nonsteroidal anti-inflammatory drugs (NSAIDs) for pain. He smoked cigarettes and marijuana and was sexually active.

On physical examination, his temperature was 38.1°C, and his heart rate and blood pressure were stable. A vesicular lesion was noted in the right superior palpebral conjunctiva; the sclerae were mildly injected. The lips were dry, cracked, and slightly edematous; there was mild pharyngeal erythema, and vesicular lesions were visible on the gums, soft palate, and posterior oropharynx.

The patient was admitted to the inpatient unit, and intravenous acyclovir was started. Over the next few days, the oral lesions began to ulcerate and spread and were extremely painful. He was unable to eat or speak. He was given patient-controlled analgesia with morphine and parenteral nutrition.

A biopsy of one of the oral lesions revealed vascular mural C3 deposition. Oral lichen planus was diagnosed. Serologies were negative for HSV, Epstein-Barr virus, cytomegalovirus, and HIV. Results of all other tests were normal.

Although lichen planus classically manifests as a cutaneous rash of purple, polygonal, pruritic papules and plaques (known as the 5 P’s), the disease can affect the scalp, nails, genitalia, eyes, oral cavity, and even the esophagus. Oral lichen planus typically presents as 1 of 3 major clinical forms: reticular, atrophic, or erosive. This patient had erosive lichen planus, the most severe form of the disease, which exhibits denuding and sloughing of the mucocutaneous surface, represented either by erythematous bullae and ulcers or by a desquamative gingivitis.1 The lesions are found most commonly on the buccal mucosa; however, the tongue and labial mucosa may be involved.

Lichen planus is uncommon in children and adolescents, which may explain why it is frequently misdiagnosed as candida infection, HSV infection, and recurrent aphthous stomatitis in this population.1 Confirmation of a clinical diagnosis of lichen planus with mucosal biopsy for histologic examination and direct immunofluorescence usually is necessary. Direct immunofluorescence may show immunoglobulin M and complement deposition in a subepidermal distribution, as well as fibrin and fibrinogen deposited in a linear pattern at the basement membrane.2

Our patient had many of the risk factors associated with lichen planus, including smoking, alcohol consumption, oral trauma (eg, tooth extraction), and NSAID use. Other triggers include citrus and spicy foods, stress, and systemic illness.

The mainstay of treatment is corticosteroids, which alleviate symptoms and alter disease progression. Topical corticosteroids have been shown to be as effective as systemic corticosteroids in decreasing symptoms and improving remission rates and are accompanied by fewer adverse effects.3 Educating patients on how to reduce exposure to offending agents is paramount to decrease the risk of an exacerbation.

This patient was treated with intravenous and topical corticosteroids. A dramatic improvement was seen within 2 days. Before discharge, the treatment regimen was switched to oral corticosteroids. Outpatient dermatologic and dental follow-up visits were scheduled. Dermatologic follow-up is recommended indefinitely, because the risk of malignant transformation in patients with oral lichen planus is reported as being increased compared with that in the general population. In patients with erosive lichen planus, the risk of squamous cell carcinoma may be from 0.4% to 5%.1

References:

  1. Eisen D. The clinical features, malignant potential, and systemic associations of oral lichen planus: a study of 723 patients. J Am Acad Dermatol. 2002;46(2):207-214.
  2. Sugerman PB, Savage NW. Oral lichen planus: causes, diagnosis and management. Aust Dent J. 2002;47(4):290-297.
  3. Carbone M, Goss E, Carrozzo M, et al. Systemic and topical corticosteroid treatment of oral lichen planus: a comparative study with long-term follow-up. J Oral Pathol Med. 2003;32(6):323-329.

 

Acute Lymphoblastic Lymphoma
Kenneth S. Brooks, PA-C

One of the red flags of tonsillitis is asymmetry.1 This 27-year-old US Army soldier presented with his right tonsil markedly enlarged compared with the left one. The posterior cervical chain of lymph nodes also was swollen.

Results of a complete blood count essentially were normal. Chest and abdominal computed tomography scans were unremarkable, except for 1 or 2 reactive mediastinal lymph nodes.

The patient was referred to an otolaryngologist, and he underwent a tonsillectomy. Subsequent pathology studies confirmed the diagnosis of acute lymphoblastic lymphoma with bone marrow involvement, and the patient began a regimen of cancer chemotherapy.

Reference:

  1. Beaty MM, Funk GF, Karnell LH, et al. Risk factors for malignancy in adult tonsils. Head Neck. 1998;20(5):399-403.

 

Focal Epithelial Hyperplasia
Stamatia Alexiou, MD, Gary Griffin, MD, Brett Laggan, DDS, and James J. Burns, MD, MPH

A 10-year-old African American boy presented with lumps in the mouth that had been present for the past 2 years. The lesions had increased in size and number. They generally were asymptomatic but would become painful and bleed when the child accidentally bit them.

The boy had been born vaginally to an HIV-negative mother who had no history of genital warts. Family history was negative for condylomata. 

He denied any sexual abuse, and the findings of social services’ investigation were negative. Review of systems was negative for cough, stridor, or hoarse voice.

On physical examination, approximately 30 to 40 pink, soft papulonodules of 0.2 to 0.5 cm with a verrucous surface were noted on the tongue, buccal mucosae, and labial mucosae. The lesions were nontender except where they had been traumatized by biting. The child had a 2-mm wart on his hand, but no other lesions were present. Physical examination findings were otherwise normal.

The results of a complete blood cell count were normal, as were immunoglobulin levels. HIV test results were negative.

The patient received a diagnosis of Heck disease.

First described in 1965, focal epithelial hyperplasia, also known as Heck disease, is a rare, benign condition caused primarily by human papillomavirus (HPV) types 13 or 32, although other HPV types (eg, HPV-11) have been isolated.1,2 Poor hygiene, malnutrition, and AIDS may be contributing factors.3 Focal epithelial hyperplasia affects the oral mucosa, gingiva, tongue, and lips and is characterized by multiple, small, circumscribed, clustered papules or raised plaques. Rarely, genital and anal mucosa may be affected. The lesions usually are painless.

Focal epithelial hyperplasia is seen more commonly among the Eskimos and Native American population and is relatively rare in the white, Asian, and African American populations. The disease primarily affects children and young adults.

Diagnosis. The diagnosis can be made clinically and confirmed by histologic findings and detection of HPV. In this patient, a biopsy confirmed the presence of HPV, which the pathologist suspected to be a low-virulence HPV type, which are present in most cases. HPV typing, which is costly, usually is performed in cases with cytologic atypia or histologic features suggestive of a highly virulent type. Histologically, the condition is characterized by parakeratosis, epithelial hyperplasia, focal acanthosis, fusion, and thickening and elongation of rete ridges.

Management. Treatment usually is for aesthetic purposes and includes surgical excision, cryotherapy, carbon-dioxide laser ablation,4 topical interferon,4 and imiquimod.5 

Cimetidine has been found to have immunomodulating properties, with increased cell-mediated immune response through activation of natural killer cells, inhibition of suppressor T-cells, and increased production of cytokines and interferon.6 Use of cimetidine in the therapy of warts in children is supported by uncontrolled studies and several case series, which report remission rates up to 81%.7

Complications. Laryngeal papillomatosis can cause changes in the larynx and respiratory tract. This benign neoplastic disease is most commonly caused by HPV-6 and HPV-11.8 It is unclear whether patients with focal epithelial hyperplasia should be monitored by a pulmonologist, especially when HPV-11 is isolated from the oral mucosa.

Outcome of the case. This patient underwent local surgical excision with a scalpel and laser on 2 occasions 3 weeks apart. Given the increasing size and number of the oral lesions, cimetidine was added to augment the treatment regimen before surgery. Postoperatively, he was given topical and oral analgesia for pain, with generally good results.

After a thorough literature search, we decided to refer him to a pulmonologist. Bronchoscopy revealed several subglottic papules. No high-risk HPV types were identified. However, this did not exclude HPV-13 and HPV-32, the types commonly responsible for focal epithelial hyperplasia. Findings from a chest computed tomography scan to rule out pulmonary involvement were normal.

Several weeks later, the patient was referred to an otolaryngologist, who noted complete resolution of all papules. At the child’s most recent follow-up, he had no visible recurrence and no pain. He returned to school for the new academic year and was doing well.

References:

  1. Bassioukas K, Danielides V, Georgiou I, Photos E, Zagorianakou P, Skevas A. Oral focal epithelial hyperplasia. Eur J Dermatol. 2000;10(5):395-397.
  2. Padayachee A, van Wyk CW. Human papillomavirus (HPV) DNA in focal epithelial hyperplasia by in situ hybridization. J Oral Pathol Med. 1991;20(5): 210-214.
  3. Hashemipour MA, Shoryabi A, Adhami S, Honarmand HM. Extensive focal epithelial hyperplasia. Arch Iran Med. 2010;13(1):48-52.
  4. Akyol A, Anadolu R, Anadolu Y, Ekmekci P, Gürgey E, Akay N. Multifocal papillomavirus epithelial hyperplasia: successful treatment with CO2 laser therapy combined with interferon alpha-2b. Int J Dermatol. 2003;42(9):733-735.
  5. Yasar S, Mansur AT, Serdar ZA, Goktay F, Aslan C. Treatment of focal epithelial hyperplasia with topical imiquimod: report of three cases. Pediatr Dermatol. 2009;26(4):465-468.
  6. Mitsuishi T, Iida K, Kawana S. Cimetidine treatment for viral warts enhances IL-2 and IFN-γ expression but not IL-18 expression in lesional skin. Eur J Dermatol. 2003;13(5):445-448.
  7. Orlow S, Paller A. Cimetidine therapy for multiple viral warts in children. J Am Acad Dermatol. 1993;28(5 pt 1):794-796.
  8. Zawadzka-Głos L, Jakubowska A, Chmielik M, Bielicka A, Brzewski M. Lower airway papillomatosis in children. Int J Pediatr Otorhinolaryngol. 2003;67(10):1117-1121.