Herpetic Gingivostomatitis

Article Author:
Minira Aslanova
Article Editor:
Patrick Zito
Updated:
10/27/2018 12:31:37 PM
PubMed Link:
Herpetic Gingivostomatitis

Introduction

Herpetic gingivostomatitis is a condition that most often results from initial gingiva (gums) and oral mucosa infection with herpes simplex virus type 1 (HSV-1). While herpetic gingivostomatitis is the most common cause of gingivostomatitis in children before the age of 5, it can also occur in adults.[1] The condition is characterized by a prodrome of fever followed by an eruption of painful, ulcerative lesions of the gingiva and mucosa, and often, yellow, perioral, vesicular lesions. HSV-1 is usually spread from direct contact or via droplets of oral secretions or lesions from an asymptomatic or symptomatic individual. Once a patient is infected with the herpes simplex virus, the infection can recur in the form of herpes labialis with intermittent re-activation occurring throughout life.[2]

Etiology

Two, double-stranded DNA viruses of the Herpesviridae family, HSV-1 and HSV-2, are known to cause primary and recurrent herpetic gingivostomatitis. HSV-1 is mostly responsible for oral, ocular, and facial infections, while HSV-2 results primarily in herpetic lesions of the genital and cutaneous lower body. While most cases of herpetic gingivostomatitis are associated with HSV-1 infection, cases have been reported, mostly in older patients, of HSV-2 isolation. Oral infection with HSV-2 is probably transmitted through orogenital contact and has also been observed in HIV-positive patients and those on immunosuppressive therapy.[3]

Epidemiology

Primary herpetic gingivostomatitis typically occurs in children younger than the age of 5, but can also occur in adolescents and adults. It is estimated that almost 90% of the world’s population is seropositive for HSV-1 by age 35, and half of the individuals carrying the virus will experience reactivation in the form of herpes labialis. Herpetic gingivostomatitis is equally distributed amongst gender and race groups and is not found to have a particular seasonal or geographic distribution.[4],[5]

Pathophysiology

The pathogenesis of herpetic gingivostomatitis involves replication of the herpes simplex virus, cell lysis, and eventual destruction of mucosal tissue. Exposure to HSV-1 at abraded surfaces allows the virus to enter and rapidly replicate in epidermal and dermal cells. This results in the clinical manifestation of perioral blisters, erosions of the lips and mucosa, and eventual hemorrhagic crusting. Sufficient viral inoculation and replication allow the virus to enter sensory and autonomic ganglia, where it travels intra-axonally to the ganglionic nerve bodies. HSV-1 most commonly infects the trigeminal ganglia, where the virus remains latent until reactivation most commonly in the form of herpes labialis.[2]

Histopathology

Histological appearance of a mucosal herpetic infection includes degeneration of stratified squamous epithelium cells, acantholysis, and formation of an inflammatory infiltrate around the capillaries of the dermis. The characteristic intranuclear inclusion bodies known as Cowdry type A are found on light microscopy showing arrays of viral capsids and electron dense glycoproteins.[6] Cowdry type A bodies are eosinophilic inclusion bodies that are also found in varicella-zoster, making the histologic lesions of herpetic gingivostomatitis and varicella indistinguishable. Direct immunohistochemistry using fluorescent antibodies can be used to further distinguish between the herpes virus and the varicella virus.[7]

History and Physical

The initial sign of herpetic gingivostomatitis is inflammation of the oral and perioral mucosa, followed by rapidly spreading ulcerative and vesicular lesions on the gingiva, palate, buccal, and labial mucosa. The ulcerative lesions eventually rupture and become flat, yellow lesions with a red, pseudomembrane ranging from 2 to 5 mm in size. The ulcers are described as painful, quick to bleed, and typically heal without scarring in 2 to 3 weeks. Associated symptoms of herpetic gingivostomatitis include a prodrome of fever, anorexia, irritability, and lymphadenitis primarily in the cervical and submandibular region.[8]

Evaluation

The diagnosis of herpetic gingivostomatitis is usually clinical, based on the appearance of perioral and oral ulcers. However, if additional testing is required, herpetic gingivostomatitis can be confirmed diagnostically using a direct immunofluorescent examination of ulcer scrapings or blister fluid. Another test that can be used but is not entirely diagnostically reliable is the Tzanck smear. The Tzanck smear will confirm the presence of a virus in active lesions but fails to distinguish between HSV-1, HSV-2, and varicella-zoster virus.[9]

Treatment / Management

The most important component in the management of herpetic gingivostomatitis is hydration. Adequate hydration is often achieved with pain control; thus, analgesics such as oral acetaminophen and oral rinses are encouraged to make the patient more comfortable and promote fluid intake. It is important to note that patients who are unable to drink to maintain proper hydration should be hospitalized. Other indications for hospitalization include immunocompromised children, patients who develop eczema herpeticum, and HSV spread that results in encephalitis or pneumonitis.[10]

Immunocompetent patients with significant pain or refusal to drink can be administered oral acyclovir if they present within 96 hours of disease onset.[11] Studies show that administration of oral acyclovir within 96 hours of disease onset can result in reduced viral shedding, early resolution of lesions, and improvement in eating difficulties.[7] Immunocompromised patients with herpetic gingivostomatitis can benefit from intravenous (IV) acyclovir to shorten the duration of symptoms and lesions. In patients with acyclovir-resistant herpetic gingivostomatitis, foscarnet 80 to 120 mg per kg per day is the recommended drug.[12]

Barrier lip creams such as petroleum jelly have been suggested to prevent adhesions in patients with active herpetic gingivostomatitis.

Differential Diagnosis

Without perioral and oral lesions, the diagnosis of herpetic gingivostomatitis can often be overlooked. In the pediatric population, the child’s decreased appetite can be attributed to changes in diet or teething.[9] Despite the largely based clinical diagnosis of herpetic gingivostomatitis, it is important first to rule out other diseases that present similarly, keeping in mind the age group and past medical history of the patient. Some of the differential diagnoses to keep in mind when considering herpetic gingivostomatitis include:

  • Aphthous ulcers: Characterized by gray membranes and peripheral erythema, aphthae are small oral ulcers that, unlike the lesions of herpetic gingivostomatitis, are rarely found fixed on the mouth[13]
  • Herpangina: The Coxsackie-A virus causes herpangina. Typical presentation includes small blisters (unlike the large ulcers found in herpetic gingivostomatitis) with gray-fibrous membrane and peripheral erythema limited to the soft palate and high fever.
  • Infectious mononucleosis: Unlike herpetic gingivostomatitis, infectious mononucleosis presents with fever and lymphadenopathy. On physical exam, infectious mononucleosis is characterized by oral petechiae with occasional gingivostomatitis and ulceration.
  • Behcet syndrome: An inflammatory disorder characterized by recurrent aphthous ulcers and several systemic complications including genital lesions, arthritis, uveitis, and gastrointestinal manifestations mimicking irritable bowel syndrome.
  • Varicella: Characterized by vesicular lesions on the scalp and trunk, and small ulcers found in the posterior oral cavity.[7]

Complications

Complications of herpetic gingivostomatitis may include:[14]

  1. Dehydration
  2. Herpes labialis
  3. HSV encephalitis
  4. Herpetic whitlow
  5. Herpetic keratitis
  6. Eczema herpetic[15]