Oral frictional hyperkeratosis (morsicatio buccarum): an entity to be considered in the differential diagnosis of white oral mucosal lesions.

A 55-year-old man presented with desquamating lesions on his bilateral buccal mucosa intermittently for approximately 3 years. The alteration in texture within his mouth created an uncomfortable sensation and, at times, the lesions spontaneously peeled away requiring him to spit repeatedly. The patient denied any history of trauma, cheek biting, or use of tobacco products. On initial examination, the patient was asymptomatic and the oral mucosa had no abnormal findings, but on repeat examination when symptoms were present, the patient had shaggy white plaques on the bilateral buccal mucosa limited to the line of dental occlusion (Figure 1). The plaques could be easily peeled away from the underlying skin with a cotton swab without any pain, leaving behind normal underlying mucosa. A review of the prior biopsy of the affected mucosa revealed an irregularly hyperplastic epithelium with foci of ballooned epithelial cells within the upper layer, parakeratosis, and bacterial overgrowth (Figure 2). Microscopic examination of fragments of mucosa peeled away from the affected area revealed fragments ofparakeratotic cornified material colonized by numerous bacteria (Figure 3). Results from periodic acid-Schiffstain revealed no fungal elements. The diagnosis of oral frictional hyperkeratosis was established based on the clinical and microscopic findings. It was concluded that the hyperkeratosis was likely caused by bite trauma or grinding of the teeth while the patient was asleep. Triamcinolone 0.1% ointment in Orabase and tretinoin 0.05% gel were ineffective. The patient found that rinsing with hydrogen peroxide solution was most helpful in reducing the lesions. A bite guard was recommended by an oral and maxillofacial surgeon, but the patient has yet to use it.

Cutaneous Co-infected Cytomegalovirus and Herpes Simplex Virus Perigenital Ulcers in Human Immunodeficiency Virus Patients.

There is uncertainty regarding the pathogenic nature of cytomegalovirus in cutaneous lesions co-infected with herpes simplex virus. It is widely believed that herpes simplex virus is the main pathogenic factor in such lesions and that cytomegalovirus plays little if any role. There are, however, isolated case reports that describe cytomegalovirus as an important driving pathogen in such lesions. The authors present two human immunodeficiency virus patients who have cytomegalovirus and herpes simplex virus co-infected perigenital ulcers, one of whom improved on valacyclovir, while the other, who was already on valacyclovir for chronic herpes simplex virus suppression, showed no improvement with a single dose of cidofovir. He only showed rapid improvement when treated with valganciclovir. The latter patient underscores the viewpoint that at least in some cases, cytomegalovirus may be an important driving force behind the formation of such lesions. The authors therefore recommend that clinicians be aware of the possible pathogenic role of cytomegalovirus in these ulcers, and, in nonhealing ulcers, use anti-cytomegalovirus agents to prevent the onset of systemic disease. These results warrant further study of the pathogenesis of cytomegalovirus in co-infected herpes simplex virus ulcers.