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Herpetic Gingivostomatitis

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Minira Aslanova Rimsha Ali

Beth Israel Medical Center UPMC
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Last Update: September 29, 2020. Introduction

Etiology
Introduction Go to:
Epidemiology
Herpetic gingivostomatitis is a manifestation of herpes simplex virus type 1 (HSV-1) and is characterized by high-
Pathophysiology
grade fever and painful oral lesions. While herpetic gingivostomatitis most commonly occurs in children from ages 6
months to 5 years, it may also occur in adults.[1] HSV-1 is usually spread from direct contact or via droplets of oral Histopathology

secretions or lesions from an asymptomatic or symptomatic individual. Once a patient is infected with the herpes History and Physical
simplex virus, the infection can recur in the form of herpes labialis (cold sores) with intermittent re-activation Evaluation
occurring throughout life.[2]
Treatment / Management

Etiology Go to: Differential Diagnosis

The causative agent is Herpes simplex virus type 1 (HSV-1), which belongs to the alphaherpesvirus group. The virus Complications

is enveloped and has a linear double-stranded DNA genome. HSV-1 is mostly responsible for oral, ocular, and facial Deterrence and Patient Education
infections as it has a tropism for oral epithelium. While most cases of herpetic gingivostomatitis are associated with
Enhancing Healthcare Team Outcomes
HSV-1 infection, some adult cases have been reported where HSV-2 was isolated from the oral lesions. Oral infection
Continuing Education / Review Questions
with HSV-2 is probably transmitted through orogenital contact and has also been observed in HIV-positive patients
and patients undergoing immunosuppressive therapy.[3] References

Epidemiology Go to:
Related information
Primary herpetic gingivostomatitis typically occurs in children younger than the age of 5 years, but can also occur in
PMC
adolescents and adults. HSV-1 is usually acquired in childhood by coming into contact with the oral secretions. It is
PubMed
estimated that almost 90% of the world’s population is seropositive for HSV-1 by 35 years of age, 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
Similar articles in PubMed
distribution.[4][5]
Acute herpetic gingivostomatitis associated with herpes simplex
virus 2: report of a case. [J Int Oral Health. 2014]
Pathophysiology Go to:
Nongenital herpes simplex virus.
Both HSV-1 and HSV-2 have three major biological properties that play an important role in disease pathogenesis. [Am Fam Physician. 2010]

These include neurovirulence, latency, and reactivation. Neurovirulence is the ability to invade and replicate in the Primary herpes simplex virus type 1 gingivostomatitis in pediatric
nervous system, and latency is the ability to maintain the latent infection in the nerve cell. Reactivation is the ability personnel. [Infection. 1997]
to replicate and cause the disease process again, once induced by specific stimuli. HSV-1 causes herpes Review Herpes simplex virus infection, with particular reference
gingivostomatitis and eventually herpes labialis using the same biological properties. The pathogenesis of herpes to the progression and complications of [Clin
primary
Microbiol
herpetic
Infect. 2006]
gingivostomatitis involves the replication of the herpes simplex virus, cell lysis, and eventual destruction of mucosal Review Herpes Simplex Virus Type 1 infection: overview on
tissue. Exposure to HSV-1 of the abraded surfaces allows the virus to enter and rapidly replicate in epidermal and relevant clinico-pathological features. [J Oral Pathol Med. 2008]
dermal cells. This results in the clinical manifestation of perioral blisters, erosions of the lips and mucosa, and See reviews...
eventual hemorrhagic crusting. Sufficient viral inoculation and replication allow the virus to enter sensory and
See all...
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]
Recent Activity
Histopathology Go to: Turn Off Clear

Herpetic Gingivostomatitis - StatPearls

Histological appearance of a mucosal herpetic infection includes degeneration of stratified squamous epithelial cells,
acantholysis, and formation of an inflammatory infiltrate around the capillaries of the dermis. The characteristic
Milk-Alkali Syndrome - StatPearls
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
Hyperammonemia - StatPearls
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
Tools and Strategies for Quality Improvement and Patient
the varicella virus.[7]
Safety - Patient Safety...

History and Physical Go to: Emotional Intelligence in Internal Medicine Residents:

Educational Implications ...
Primary herpes gingivostomatitis usually occurs in children who have not been previously exposed to the virus. It
See more...
may be asymptomatic in some cases, but most cases develop a prodrome of fever, anorexia, irritability, and the
development of painful oral lesions. Associated symptoms include malaise, lethargy, and cervical or submandibular
lymphadenopathy.[8]

The initial sign of herpetic gingivostomatitis is hyperemia of the oral and perioral mucosa, followed by rapidly
spreading vesicular lesions on the gingiva, palate, buccal, and labial mucosa. The lesions may ulcerate and then
eventually rupture. On physical examination, they may appear as flat, yellowish in color, and approximately 2 to 5
mm in size. The ulcers are quick to bleed and typically heal without scarring in 2 to 3 weeks.

Recurrent herpes lesions commonly develop in one-third of the patients who have experienced primary herpetic
gingivostomatitis. The patient’s symptoms include burning and itching, followed by the formation of vesicular lesions
in a localized area. The lesions mostly develop on keratinized skin such as the vermillion border of the lips, perioral
skin, or the hard palate. The lesions may develop when the patient is under physical or emotional stress or systemic
illness. Other triggers include sunlight exposure and trauma. The lesions occur in the same area during every episode
of recurrence, and systemic manifestations such as malaise and lymphadenopathy are mild.[9]

Evaluation Go to:

The diagnosis of herpetic gingivostomatitis is usually clinical, based on the patient’s history and physical
examination. The appearance of the oral vesicular and ulcerative lesions is sufficient for the diagnosis. However, if
additional testing is required, herpetic gingivostomatitis can be confirmed using a direct immunofluorescent
examination of ulcer scrapings or blister fluid. Another test that can be used but is not entirely reliable for diagnosis is
the Tzanck smear, which shows the cytologic changes induced by the herpes virus. The Tzanck smear will confirm the
presence of a virus in the active lesions but fails to distinguish between HSV-1, HSV-2, and varicella-zoster virus.[10]
The gold standard for diagnosis is the isolation of the virus in tissue culture. Antibody testing can help demonstrate
seroconversion but does not yield a diagnosis.

Treatment / Management Go to:

Herpes gingivostomatitis is generally a mild and self-limited condition, and supportive care is generally adequate.
Barrier lip creams such as petroleum jelly have been suggested to prevent adhesions in patients with active herpetic
gingivostomatitis. 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.[11]

Several studies suggest the usage of acyclovir cream or oral suspension in a rinse and swallow technique.[7]
Immunocompetent patients with significant pain or refusal to drink can be administered oral acyclovir if they present
within the first 72 hours of disease onset.[12]

Differential Diagnosis Go to:

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. Table 1 explains the
differences in causation and clinical presentation of several childhood disorders that may be confused with herpes
gingivostomatitis. Some of the differential diagnoses to keep in mind when considering herpetic gingivostomatitis
include:

Herpes zoster

Primary chickenpox

Behcet disease

Herpetiform aphthae

Erythema multiforme

Acute necrotizing gingivostomatitis

Reactive arthritis

Cytomegalovirus ulceration

Traumatic ulcers

Burns, chemical and thermal

Factitial injuries

Vesiculobullous disease

Complications Go to:

Complications of herpetic gingivostomatitis may include:[13]

1. Dehydration

2. Herpes labialis

3. HSV encephalitis

4. Herpetic whitlow

5. Herpetic keratitis

6. Eczema herpeticum[14]

Deterrence and Patient Education Go to:

The patients and their families should be informed that the disease is generally mild and self-limited. They should be
told about the appropriate management strategy that includes supportive care with pain control, adequate hydration,
and a healthy diet. The patients should be managed at home but should be monitored closely for the development of
any complications, such as difficulty in eating or drinking, or worsening of lesions. The patients and their families
(especially in the case of young children) should be in regular contact with the primary treating physician. The patient
should also be educated about the recurrence of the oral lesions (herpes labialis or cold sores) that may develop in
one-third of the patients who develop primary herpetic gingivostomatitis.

Enhancing Healthcare Team Outcomes Go to:

Herpes gingivostomatitis is a viral infection characterized by high-grade fever and painful oral lesions, occurring most
commonly in children from ages 6 months to 5 years. Out-patient management is sufficient in most situations, but
hospital admission may be warranted if the patient develops complications. The disease is best managed by an
interprofessional team that includes a primary care provider, an internist, a pediatrician, a nurse practitioner, an
emergency department physician, an infectious disease specialist, and a pharmacist. Coordination by different health
care experts is necessary to improve patient outcomes and enhance patient care.

Continuing Education / Review Questions Go to:

Access free multiple choice questions on this topic.

Earn continuing education credits (CME/CE) on this topic.

Comment on this article.

Figure

Differential diagnosis of pediatric oral lesions. Contributed by Rimsha Ali,

MD

References Go to:

1. Tovaru S, Parlatescu I, Tovaru M, Cionca L. Primary herpetic gingivostomatitis in children and adults.
Quintessence Int. 2009 Feb;40(2):119-24. [PubMed]
2. Arduino PG, Porter SR. Herpes Simplex Virus Type 1 infection: overview on relevant clinico-pathological
features. J Oral Pathol Med. 2008 Feb;37(2):107-21. [PubMed]
3. George AK, Anil S. Acute herpetic gingivostomatitis associated with herpes simplex virus 2: report of a case. J Int
Oral Health. 2014 Jun;6(3):99-102. [PMC free article] [PubMed]
4. Taieb A, Body S, Astar I, du Pasquier P, Maleville J. Clinical epidemiology of symptomatic primary herpetic
infection in children. A study of 50 cases. Acta Paediatr Scand. 1987 Jan;76(1):128-32. [PubMed]
5. Cataldo F, Violante M, Maltese I, Traverso G, Paternostro D. [Herpetic gingivostomatitis in children: the clinico-
epidemiological aspects and findings with acyclovir treatment. A report of the cases of 162 patients]. Pediatr Med
Chir. 1993 Mar-Apr;15(2):193-5. [PubMed]
6. Leinweber B, Kerl H, Cerroni L. Histopathologic features of cutaneous herpes virus infections (herpes simplex,
herpes varicella/zoster): a broad spectrum of presentations with common pseudolymphomatous aspects. Am J
Surg Pathol. 2006 Jan;30(1):50-8. [PubMed]
7. Mohan RP, Verma S, Singh U, Agarwal N. Acute primary herpetic gingivostomatitis. BMJ Case Rep. 2013 Jul
08;2013 [PMC free article] [PubMed]
8. Yarom N, Buchner A, Dayan D. Herpes simplex virus infection: part I--Biology, clinical presentation and latency.
Refuat Hapeh Vehashinayim (1993). 2005 Jan;22(1):7-15, 84. [PubMed]
9. Leung AKC, Barankin B. Herpes Labialis: An Update. Recent Pat Inflamm Allergy Drug Discov. 2017;11(2):107-
113. [PubMed]
10. Mortazavi H, Safi Y, Baharvand M, Rahmani S. Diagnostic Features of Common Oral Ulcerative Lesions: An
Updated Decision Tree. Int J Dent. 2016;2016:7278925. [PMC free article] [PubMed]
11. Faden H. Management of primary herpetic gingivostomatitis in young children. Pediatr Emerg Care. 2006
Apr;22(4):268-9. [PubMed]
12. Amir J, Harel L, Smetana Z, Varsano I. Treatment of herpes simplex gingivostomatitis with aciclovir in children:
a randomised double blind placebo controlled study. BMJ. 1997 Jun 21;314(7097):1800-3. [PMC free article]
[PubMed]
13. Amir J, Harel L, Smetana Z, Varsano I. The natural history of primary herpes simplex type 1 gingivostomatitis in
children. Pediatr Dermatol. 1999 Jul-Aug;16(4):259-63. [PubMed]
14. Tamay Z, Ozcekert D, Onel M, Agacfidan A, Guler N. A child presenting with primary gingivostomatitis and
eczema herpeticum. Minerva Pediatr. 2016 Feb;68(1):72-3. [PubMed]

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