A 25-year-old male visited a general dentist for evaluation of multiple painful oral ulcerations.
Joen Iannucci Haring, DDS, MS
The patient first noted the ulcers several days earlier. He reported that, since the onset, the ulcers had increased in number. In addition, he stated that the ulcers were painful - both eating and drinking intensified the pain. When questioned about other signs and symptoms, the patient claimed an overall feeling of malaise, a low-grade fever, and swollen lymph nodes. The patient denied the presence of any skin lesions or the history of a previous episode.
A review of the patient`s medical history revealed no significant findings. At the time of the dental visit, the patient was taking ibuprofen to relieve the pain associated with the oral lesions. No other medications were reported.
Examination of the head and neck areas revealed several enlarged and tender submandibular lymph nodes. The patient`s blood pressure was within normal limits. No skin lesions were apparent in the head and neck region.
Oral examination revealed multiple small oral ulcerations scattered throughout the oral cavity. Both attached and unattached tissues were involved (see photo).
Based on the clinical information presented, which of the following is the most likely diagnosis?
* Hand, foot, and mouth disease
* Herpetiform aphthous ulcers
* Acute herpetic gingivostomatitis
* Erosive lichen planus
_ Acute herpetic gingivostomatitis
Acute herpetic gingivostomatitis is caused by the herpes simplex virus. The herpes simplex virus (HSV) is a DNA virus that belongs to the herpes family of viruses, Herpesviridae. The herpes family of viruses is unique in that, once an individual is infected, the virus remains within the host for life. Consequently, the individual infected with HSV remains a reservoir of infection and the virus is endemic worldwide.
The two types of the herpes simplex virus are HSV-1 and HSV-2. They both exhibit different epidemiological variations. HSV-1 is responsible for infections of the oral, facial, and ocular areas and is spread via saliva and oral lesions. HSV-2 is responsible for infections of the genitalia and is transmitted through sexual contact.
There are exceptions to these defined patterns. For example, HSV-1 can affect anatomic sites associated with HSV-2 and vice versa.
Oral herpetic infections resulting from HSV-1 present in one of two clinically evident patterns: primary infection and recurrent (secondary) infection. The initial infection of an individual without antibodies to HSV is termed the primary infection. This primary infection, by definition, occurs one time only, and any person without immunity to HSV is susceptible to such an infection.
HSV is an infectious disease. Contact with an infected person is necessary for exposure. Exposure to HSV-1 occurs when a person has direct contact with an active herpetic lesion (a "cold sore" or "fever blister," for example). Any activity that exposes a person to direct mucocutaneous contact with a herpetic lesion or exposes a person to saliva containing HSV-1 may result in the transfer of the virus. There is no documented evidence of HSV transmission from inanimate objects such as toilet seats, as well as swimming pools and hot tubs. Following exposure, the usual incubation period is three to nine days.
After incubation, the body responds in one of three possible ways:
- No infection occurs. The immune system eliminates the virus and no infection occurs. No antibodies to the virus are formed and no virus remains within the body.
- A subclinical infection occurs. The immune system fails as an infection develops. No signs or symptoms occur, and the patient is unaware of the infection.
Following infection, both antibodies to HSV-1 and the virus exist within the host. The individual becomes a lifelong carrier of the virus which lies dormant in sensory nerve ganglia until reactivated. Approximately 90 percent of primary HSV infections are subclinical. Consequently, most individuals do not know that infection has occurred.
- A clinical infection occurs. The immune system fails, and an infection known as acute herpetic gingivostomatitis develops.
Signs and symptoms occur, and the patient is aware of the infection. Following infection, both antibodies to HSV-1 and the virus exist within the host.
The individual becomes a lifelong carrier of the virus which lies dormant in sensory nerve ganglia until reactivated. Approximately 10 percent of primary HSV infections present as acute herpetic gingivostomatitis.
Acute herpetic gingivostomatitis is a primary HSV infection that, by definition, occurs one time only. "Acute" refers to a disease with a short and relatively severe course. "Herpetic" refers to the cause of this infection (HSV). "Gingivostomatitis" refers to inflammation of the oral tissues.
Although acute herpetic gingivostomatitis may occur in either children or adults, most cases arise between the ages of six months and five years. Clinical symptoms may vary from mild to severe and include an abrupt onset, fever, cervical lymphadenopathy, malaise, headache, and painful oral lesions.
Initially, oral lesions present as tiny vesicles that rapidly collapse to form small, shallow ulcerations. The ulcerations may coalesce to form larger, irregular-shaped ulcerations. Both movable and attached mucosa can be affected, as well as the vermilion of the lips. When the gingival tissues are involved, the gingiva appears swollen and erythematous. When the soft palate/tonsillar pillar area is involved, a sore throat is present.
The number of ulcerations present is variable. These lesions are painful and typically cause difficulties with eating and drinking. Dehydration may be a significant problem in young children. Resolution of mild cases of acute herpetic gingivostomatitis occurs in approximately one week, while more severe cases may last two weeks.
The diagnosis of acute herpetic gingivostomatitis is most often based on the clinical signs, symptoms, and patient history. Laboratory confirmation may be required in instances of a questionable diagnosis.
HSV isolation from tissue culture inoculated with the fluid from vesicular lesions is the preferred laboratory test. Cytologic smear techniques and tissue biopsy may also be used to establish a diagnosis. Serologic testing for antibodies to HSV is another method that can be used to diagnose acute herpetic gingivostomatitis. Such tests are positive four to eight days following exposure. In addition, serologic testing is useful in identifying previous subclinical (asymptomatic) HSV infections.
Most individuals with acute herpetic gingivostomatitis present at too late a stage for systemic antiviral medications, such as acyclovir (Zovirax), to exert a significant effect. The current FDA recommendation is that systemic acyclovir only be used to treat oral herpes in immunocompromised patients. Because there are no curative drugs for this disease, palliative and supportive measures are recommended instead.
Palliative measures include the use of a rinse to decrease mucosal discomfort and a nonsteroidal anti-inflammatory medication, such as ibuprofen, to alleviate fever and pain. Examples of topical rinses include 0.5 percent or 1 percent dyclonine hydrochloride (Dyclone) and diphenhydramine (Benadryl) elixir 12.5 mg/5 ml. mixed with Maalox.
Supportive measures include adequate fluid intake to prevent dehydration, as well as adequate nutrition and rest. It is important to note that topical steroids must be avoided as such medications tend to permit the spread of the virus.
The patient with acute herpetic gingivostomatitis should be instructed to restrict contact with active lesions in order to prevent the spread of the virus to others as well as to other body areas, especially the eyes and genitalia. Common sense should be used and patients should refrain from activities that may result in the spread of the virus.
Joen Iannucci Haring, DDS, MS, is an associate professor of clinical dentistry, Section of Primary Care, The Ohio State University College of Dentistry.