Description: Oral infection with herpesvirus occurs in three clinical forms. The most common type consists of recurrent small blisters on the lips commonly referred to as fever blisters or secondary herpes labial. The second type is a generalized oral infection called primary herpetic stomatitis. The third and least common form of oral herpes infection consists of small ulcers usually localized on palatal mucosa.

Herpes labialis is illustrated in (Fig. 16 and 17). This lesion is well known and unlikely to be a diagnostic problem. It tends to be a recurrent disease in teenagers and adults. Elapsed time between recurrences varies from person to person. Recurrences are thought to be triggered by exposure to sunlight, febrile diseases, physical and psychogenic trauma, and other irritants.

Generalized involvement of the oral mucous membrane is called primary herpetic stomatitis (Fig. 18 and 19). It is more commonly seen in children, but teenagers and adults are also affected. Patients initially have gingivitis with swollen and red marginal gingiva then small blisters appear throughout the mouth. The blisters break so quickly they are seldom seen by the dentist or physician. After they break, the lesions appear as small ulcers which resemble small aphthous lesions. This generalized infection is accompanied by fever, cervical lymphadenitis, and inability to eat or drink without considerable pain.

Patients who suffer localized intraoral herpes are few in number. For reasons yet to be explained, recurrent intraoral herpes infections tend to occur as small ulcers, mainly on the hard palate mucosa as shown in (Fig. 20).

Etiology: Herpesvirus hominis. Most oral lesions are caused by Type I virus but approximately 10% are thought to be caused by Type II.
Treatment: Acyclovir has shown promising results in the treatment of both first episode and recurrent genital lesions with expectations of the same for oral lesions. Acyclovir ointment (5%) applied 5 times daily to lip lesions shortens healing time by one day, and if applied early, increases the number of abortive lesions. Systemic acyclovir reduces both duration and symptoms of first episode genital lesions and markedly reduced the recurrences. No similar results have been reported with oral lesions. A number of treatments are of questionable value. These include topical ether, bioflavinoid-ascorbic acid complex and intramuscular adenosine. Lysine has been shown to be useless.

Prognosis: The outlook is good but lip lesions commonly reoccur. Once the virus has entered the body, it travels through nerve trunks to the nearest ganglion where it may lie dormant for the remainder of the patient's life. Future recurrences are thought to be brought about by the reawakening of the virus, which retraces its steps to cause new lesions in the same general area as the original point of entry. Thus, each recurrence is not a new and different infection from the outside but a recrudescence of the original infection. The ability of the virus to literally hide in deep ganglia makes total eradication almost impossible and will likely frustrate attempts at treatment for the foreseeable future.
Patients with widespread herpetic stomatitis should maintain liquids to prevent dehydration. A broad-spectrum antibiotic is commonly given to control secondary bacterial infection.
Clinicians should be aware that the herpesvirus may cause disseminated infection including encephalitis in which case the prognosis is extremely grave.

Differential diagnosis: Primary herpetic stomatitis may resemble oral lesions of erythema multiforme, but herpes can be diagnosed by exfoliative cytology. A characteristic multinucleated cell appears in the smear of herpes infections. Culture of the virus is possible if a viral laboratory is available. Lesions of herpangina and hand, foot, and mouth disease, both caused by Coxsackievirus, may clinically resemble oral herpes virus infections. .