Gingivostomatitis is the commonest clinical presentation of primary HSV-1 infection. Between 13% to 30% of children with primary herpes simplex viral infection present with gingivostomatitis . However, cold sores or herpes labialis may present afterwards.
Symptoms of herpetic gingivostomatitis appear within 7 days of contact with an infected individual, beginning with a clinical prodrome of fever, anorexia, malaise, insomnia, headache, and irritability. The carrier of the virus is often asymptomatic. The prodromal phase lasts about four days. The presence of oropharyngeal lesions make the prodrome more likely suggestive of herpes gingivostomatitis rather than teething which is the usual suspect of most parents with such prodromal symptoms.
The lesions appear initially as erythematous and edematous gingivae laden with small vesicles which eventually rupture. After the rupture of the cluster of vesicles, they turn yellow with a surrounding red halo. The ruptured vesicles then fuse to form large, painful oral and perioral ulcers. These lesions primarily appear in the oral mucosa, gingiva, tongue, and pharynx. In about 30% of cases, the lesions also occur in the lips and perioral areas .
These lesions are often accompanied by halitosis, anorexia, fever, arthralgia, headache, odynophagia, and submandibular/cervical lymphadenopathy . Odynophagia is usually expressed as refusal to drink which often leads to dehydration, the most frequent complication of herpetic gingivostomatitis.
Generally, symptoms may resolve spontaneously within a week, but some cases may take up to three weeks to achieve complete healing. After this infection has resolved, HSV moves to and remains latent in the trigeminal ganglion. Favorable conditions for reactivation such as cold, trauma, stress, immune compromise cause a reactivation and replication of the virus causing a recurrent stomatitis or herpes labialis.
The diagnosis of gingivostomatitis is largely clinical and is based on physical findings of the characteristic lesions. Laboratory investigations are often not necessary, however, they are indicated in cases where the infection is severe, lesions are not characteristics of HSV, or if the patient is pregnant or immune compromised.
A Tzanck test, which involves staining a superficial scraping taken from the base of a newly erupted vesicle , reveals multinucleated giant cells indicative of HSV or VZV infection. A Tzanck test is done with Wright-giemsa stain. A definitive diagnosis is made with polymerase chain reaction (PCR) tests, serological detection of the antigen, seroconversion of the appropriate serotype, and culture  . Culture of the discharge or smear from the base of a newly ruptured lesion is obtained.
Direct immunofluorescence assay of the oral and gingival smears or scrapings may also assist in the diagnosis of HSV gingivostomatitis.
In cases where the infection recurs frequently, doesn't respond to appropriate antiviral agents, or is recalcitrant to all forms of treatment, immunosuppression should be suspected and the underlying immune disease should be determined and co-managed.
Although, Gingivostomatitis is largely self-limited, antiviral medications may be necessary to expedite resolution of symptoms and reduce the severity of the infection . Oral acyclovir is the antiviral drug of choice for herpetic gingivostomatitis, however an appropriate dosing of the drug is unclear .
Supportive care is often employed along with antiviral therapy and is aimed at alleviating the symptoms and preventing the complications of the infection. An example of supportive care for herpectic gingivostimatitis is application of a lip barrier cream to prevent adhesion of the lips by fusion of adjacent ulcerated lesions.
Analgesics and antipyretics are also necessry in the management of gingivostmatitis. NSAIDs are indicated to relieve the pain and swelling associated with the lesions. Local anaesthetic solutions or mouthwashes containing xylocaine may be necessary for pain control in severe cases.
Gingivostomatitis is most commonly caused by HSV-1 and less commonly by certain bacteria species including streptococcus and actinomyces. Coxsackie virus is a less common viral cause of gingivostomatitis, which is transmitted via contact with objects contaminated with human feces. Poor oral hygiene is a key risk factor for gingivostomatis.
Gingivostomatitis constitutes about 1% of consultations in general practice. Although, prevalence of HSV-1 seropositivity varies with ethnicity, it may be observed in up to 85% of individuals in early adulthood. Between 20% to 40% of these seropositive individuals may have recurrent cold sores with a frequency ranging from 2 to 6 times every year.
An Amsterdam study noted that besides its variance with ethnicity, HSV-1 seropositivity was more prevalent among older patients and those of low socioeconomic status .
HSV-1 infection occurs worldwide, with humans are the only host of the organism. Transmission is therefore, by human-to-human contact with no intermediate host or vector involved.
HSV-1 as well as HSV-2 are members of the herpesviridae family and alphaherpesvirinae subfamily. It has a number of characteristic properties including : an ability to invade and multiply in the nervous system, ability to become latent in the neuronal ganglia proximal to the primary site of infection, and an ability to become reactivated in the presence favorable conditions.
In HSV infections primarily involving the orofacial region, the trigeminal ganglia is the commonest site of latency of the virus, while latency occurs in the sacral nerve root ganglia (S2 - S5) in genital herpes infection.
Reactivation of latent HSV with subsequent replication is often triggered by fever, trauma, menstruation, cold, psychological stress, and sunlight. Reactivation of the virus causes either an overt or an asymptomatic recurrent infection. However, reactivation is commoner and produces more significant morbidity in immunocompromised patients . Furthermore, in these patients, systemic spread of the infection is more likely. The tendency of HSV-1 infections to establish latency, regular reactivation, and viral shedding in asymptomatic patients is responsible for its endemicity .
HSV-1 is transmitted by contact with infected persons and the infection arises after the virus is introduced through breaks in the skin or into certain susceptible mucosal membranes including the mucosa of the cervix, conjunctiva, and oropharynx. Room temperature and drying are potent cause of inactivation of the virus, therefore, making transmission via formites and air almost impossible.
Good oral hygiene may reduce the risk of occurrence and recurrence of gingivostomatitis. Proper oral hygiene involves daily flossing, dental check-ups once every six months, toothbrushing twice daily, and ensuring mouth pieces such as dentures, or mouth instruments are kept clean before use.
To prevent transmission of the virus, one is advised to avoid touching or kissing the face of an individual infected with the virus. Also make-up tools and sharp objects belonging to an infected person should not be shared.
Proper hand washing is also critical in preventing herpes simplex gingivostomatitis. Hand washing is particularly necessary before and after eating and preparing meals, after changing the babies' diapers, and after using the toilet.
Gingivostomatitis which is also known as primary herpetic gingivostomatitis and orolabial herpes is the commonest presentation of primary HSV-1 infection in childhood. It presents with ulcerative lesions in the lips, gingivae, and oral mucosa.
Gingivostomatitis precedes herpetic labialis, which is commonly called cold sores, both of which are manifestations of primary HSV-1 infection. It is however more severe than cold sores. Primary hepetic gingivostomatitis is the commonest viral oral infection. The infection mainly affects children.
The infection usually manifests with an initial prodrome of low-grade fever, anorexia, malaise, nausea, vomiting, and irritability. These symptoms precede the appearance of erythematous and edematous gingivae laden with clusters of erythematous lesions which eventually rupture forming ulcerated lesions with yellow or gray base surrounded by red haloes. Other associated symptoms of gingivastomatitis include halitosis, painful swallowing with refusal to drink in children, and submandibular lymphadenopathy  . The symptoms usally resolve within approximately three weeks, however, they may persist in those who are immuncompromised.
A notable biological property of the HSV-1 virus is its ability to become latent in the proximal nerve ganglion for many years and become reactivated by certain factors such as trauma, fever, cold, stress, and menstrution, and immunosuppressive states.
Diagnosis of gingivostomatitis is often based on clinical grounds with physical examination of the characteristic oral lesions. However, in immunosupressed patients or pregnant women, and those who present with atypical lesions, further investigations including serology, scrapings of the oral lesions for microscopic analysis and culture, and polymerase chain reaction tests may be necessary.
Treatment of gingivostomatitis is often not necessary because the condition is self-limited, however, treatment with antiviral medications may be necessary especially in immunocompromised patients. However, supportive treatment including analgesics and antipyretics are generally indicated for symptomatic relief.
Maintaining a good oral hygiene is a key factor in reducing the risk of the infection.
Gingivostomatitis is a viral infection of the gums and the inner lining of the mouth. It is a very common infection and it is caused by a virus called human simplex virus type 1(HSV-1). It may occasionally be caused by a bacterial agent. Poor oral hygiene is a common risk factor for this infection.
Gingivostomatitis is most commonly caused by HSV-1 and occasionally by other agents including coxsackie virus, and bacteria. The coxsackie virus is spread by contact with objects contaminated with human feces.
HSV-1 has a tendency to stay latent inside nerve cells for many years without causing any symptoms before being reactivated to cause symptoms. Factors which trigger this reactivation of the virus includes fever, cold, trauma, sunlight, menstration and stress.
HSV-1 is the organism responsible for cold sores or fever blisters. Gingivostomatitis is most commonly seen in children.
Sign & Symptoms
This infection begins with a spectrum of symptoms including bad breath, fever, malaise, excessive crying, headache, loss of apetite, swollen and bleeding gums, difficult and painful swallowing, nausea, vomiting, and drooling in children. These symptoms precede the appearance of ulcers and rashes in the gum and inner part of the mouth, these rashes are red and eventually turn yellow with red haloes surrounding them when they burst. When these rashes Burt, they form ulcers or craters which may fuse to form larger ones.
These symptoms usually appear within a week of contact with an infected person and they usually disappear within three weeks of onset. However, the symptoms may persist and even become resistant to treatment in patients with weakened immune systems.
A diagnosis of gingivostomatitis can be made by the doctor after physical examination of the rashes and ulcers and noting the appearance of the gum. Further laboratory testing are not needed unless the patient is pregnant, the infecton is severe, the rashes do not look similar to what should be, or the patient has a weakened immunity.
Additional tests may include blood tests to check for the virus or antibodies to the virus, culture of the scrapings form the mouth lesions, or staining and microscopic viewing of the scrapings from the ulcers and rashes.
Although, gingivostomatitis usually resolve spontaneously within two to three weeks, medications may be necessary to alleviate the symptoms, prevent complications, and expedite recovery. Generally, an antiviral drug is prescribed, together with drugs which reduce the pain and fever. A mouthwash containing xylocaine, a local anesthetic, is also recommended to reduce the pain of the rashes and ulcers. Mouthwashes are available over-the-counter. Saltwater gargle is also recommended. The is done by adding half teaspoon of salt in 1 cup of water.
To prevent feeding difficulties, spicy, salty, and sour foods should be avoided as these may worsen the pain. Soft foods are also recommended to prevent trauma to the sores and persistence of symptoms.
Good oral hygiene is critical in preventing gingivostomatitis: Daily flossing, brushing of the teeth twice daily, and routine dental checks constitute good oral hygiene. Kissing an infected person or touching the sores with bare hands increase one's risk of gingivostomatitis.
Corey L. Herpes Simplex Virus. Mandell Gl, Bennett JE, Dolin R, eds. Principles and Practice of Infectious Diseases. 6th ed. Pennsylvania: Elsevier; 2005. Vol 2: 1762-80.
Kimberlin DW, Rouse DJ. Clinical practice. Genital herpes. N Engl J Med. 2004 May 6; 350(19):1970-7.
Mark KE, Wald A, Magaret AS, et al. Rapidly cleared episodes of herpes simplex virus reactivation in immunocompetent adults. J Infect Dis. 2008 Oct 15; 198(8):1141-9.