Candidiasis is a fungal infection caused by the organism Candida albicans. Candidiasis is the most common oral fungal infection in humans and is present intraorally in 30%-50% of people without clinical manifestation. Candida albicans is found in almost 60% of dentate patients older than age 60 years. There are several types of candidiasis. The three main factors that contribute to these different types of infection are the patient’s immune status, status of oral mucosa, and the strain of C. albicans. Pseudomembranous candidiasis (thrush) is characterized by removable white plaques, a burning sensation, and a foul taste. Plaques commonly occur on the buccal mucosa, tongue, and palate. Erythematous candidiasis presents as red macular lesions that evoke a burning sensation. These lesions occur on the posterior hard palate, buccal mucosa, and the dorsum of the tongue.13
Central papillary atrophy, otherwise known as median rhomboid glossitis, exhibits red, atrophic mucosal areas that are typically asymptomatic and located on the midline posterior dorsal surface of the tongue. Chronic multifocal candidiasis also presents as a red lesion but often with removable white plaques and may present either with a burning sensation or without symptoms. This infection can typically be seen on the posterior palate, posterior dorsal tongue, and the angles of the mouth. Angular chelitis occurs at the angles of the mouth and often causes a raw, irritated feeling that creates a red, fissured appearance.13
Denture stomatitis, also referred to as chronic atrophic candidiasis or denture sore mouth, presents as a red, asymptomatic lesion confined to the palate in denture-bearing areas. Hyperplasic candidiasis, also known as candidal leukoplakia, is characterized by irremovable white plaques that are mostly asymptomatic and occur on the anterior buccal mucosa. Mucocutaneous candidiasis presents on the tongue, palate, and buccal mucosa, with both white plaques as well as reddish areas. The white plaques may or may not be removable. The diagnosis of candidiasis is usually made based on the clinical signs combined with cytologic studies, although culture studies may not be possible in an office setting. A culture can be obtained by rubbing a cotton swab over the lesion and placing the specimen on Sabouraud agar medium.13
A number of antifungal medications can be used to treat candidiasis. Nystatin must be used multiple times on a daily basis as either a suspension or a lozenge. This medication can also be combined with triamcinolone acetonide cream or ointment and applied topically to the angular chelitis form of candidiasis. Similar to Nystatin, clotrimazole must also be taken several times a day to be effective. Clotrimazole may also be applied topically to treat angular chelitis. Ketoconazole may be taken in a single daily dose, but it is hepatotoxic and is associated with drug interactions with macrolide antibiotics, possibly causing cardiac arrhythmias. Ketoconazole is not recommended as the first line of defense for routine candidiasis.13
Most recently approved are the triazole class of antifungals, which include fluconazole and itraconazole. Both drugs have similar efficacy to clotrimazole and may have significant drug interactions with a number of medications. These agents may be taken once a day.13
Iodoquinol has antifungal properties and may be effective in the treatment of angular chelitis when combined with a cream or corticosteroid. If treatment does not resolve with antifungal therapy, a biopsy may be warranted to determine if another underlying condition is responsible. If infection recurs, the patient may be immunosuppressed. A thorough workup should be performed.13
Acute necrotizing ulcerative gingivitis
Acute necrotizing ulcerative gingivitis (ANUG) is characterized by punched-out lesions of the interdental papillae and sometimes accompanied by a gingival edema. ANUG is associated with local pain, spontaneous bleeding, or—in response to minimal trauma—alterations in taste and a foul breath. Such systemic signs of infections as fever and malaise may be present.13
ANUG is caused by acute infection of the gingiva with such organisms as Prevotella intermedia, alpha-hemolytic streptococci, Actinomyces species, or any of a number of different oral spirochetes. ANUG may result in accelerated destruction of affected tissues as well as local or systemic spread of infection. This infection is most often seen in smokers and correlates highly with the amount of tobacco used per day. ANUG may also occur in immunocompromised patients during chemotherapy. Treatment includes antibiotics, nonsteroidal anti-inflammatory drugs, gingival curettage, and topical anesthetics for pain relief. Saline rinses as well as oral rinses with 3% hydrogen peroxide are also used as part of a treatment plan.13
The generic term oral nevus includes malformations of the skin and mucosa that may be congenital or developmental. Acquired melanocytic nevus is the most common type and results from proliferation of cells from the neural crest or nevus cells. Nevus cells have the ability to produce melanin. Most acquired melanocytic nevi develop before age 35 years.
The pigmented nevi are uncommon in the oral cavity compared with their occurrence on the skin. The most common locations for oral nevi are the hard palate and gingiva, followed by the buccal mucosa. Acquired melanocytic nevi evolve through characteristic clinical stages, which correlate with specific histologic features. Specific types include junctional, compound, and intramucosal nevi. In the oral cavity, the intramucosal type is most common. Nevus cells may proliferate over many years to produce an elevated, soft papule with a smooth surface known as a compound nevus.5
Congenital melanocytic nevi may be present in 1% of U.S. newborns, with 15% of these lesions noted in the head and neck area.5 Clinically, the junctional nevus is the earliest presentation in nevus evolution and appears as a well-demarcated, brown or black macule which is usually <5 mm in diameter. The junctional nevus may persist or may enlarge as nevus cells continue to proliferate. Compound nevi can be seen intraorally as well, such as in the floor of the mouth and hard palate regions. The intramucosal nevus may be raised in the oral cavity but they usually do not have a papillomatous surface and frequently appear macular.
Treatment is usually for cosmetic reasons. However, 3%-15% of large congenital nevi may undergo malignant transformation into melanoma.5 Large lesions should be excised when possible through conservative excision. A rare condition of patients with multiple large nevi results in central nervous system melanotic neoplasms, meningeal melanosis, or melanoma.5 All patients with multiple large nevi that are not excised should have careful, regular follow-up examinations. A biopsy is indicated for benign mucosal lesions that recur and a repeat biopsy is necessary for any lesion that spreads or changes in clinical appearance.
Oral infections with herpes simplex virus (HSV) may occur in infancy. The condition is usually asymptomatic and is not associated with significant morbidity. The initial infection may be painful with an acute outbreak of oral vesicles that coalesce in erythematous ulcerations. The vermillion of the lips and perioral region may also be affected. Other findings include lymphadenopathy, fever, chills, anorexia, and irritability. The virus lingers, usually in the trigeminal ganglion, and may reactivate during times of stress or depressed immunity. During reactivation, the virus may cause lesions of the labial mucosa. Known triggers for the activation of the latent virus particles include ultraviolet light, fatigue, stress, and menstruation.14 Lesions may affect 15%-45% of the U.S. population. The appearance is usually localized clusters of small vesicles along the vermillion of the lip and adjacent skin. The course of the infection includes vesicular appearance, rupture, ulceration, and crusting of the lesions within 24 to 48 hours. Healing occurs spontaneously in seven to 10 days.
Treatment includes oral antiviral agents acyclovir (Zovirax) or valacyclovir (Valtrex), which may reduce the course of infection when initiated at the onset or prodrome of the infection. Topical penciclovir cream (Denavir) 1% may also reduce the healing time and is palliative throughout the course of the infection. Only a slight reduction in the course of the infection occurs with these agents. Recurrent herpetic infections should not be treated with corticosteroids.
Careful history-taking and complete oral examination allows recognition and diagnosis of oral pathology. Many conditions, such as RAS, may reflect a nutritional deficiency. Systemic conditions (e.g., autoimmune disorders) may manifest first in the oral cavity. Such factors as poor oral hygiene, tobacco and alcohol use, or poorly fitting denture prosthesis may contribute to the presence of the oral lesion. The clinician who is aware of common entities, contributing factors, and treatment modalities will be best equipped to recognize and treat the lesions of the oral cavity. n
Dr. Weiss is an oral & maxillofacial surgery resident; Dr. Nelson is an oral & maxillofacial surgery fellow; and Dr. Dym is Chairman, Department of Dentistry and Oral & Maxillofacial Surgery, all at The Brooklyn Hospital Center in Brooklyn, N.Y. The authors have no relationships to disclose relating to the content of this article.
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