Herpetic gingivostomatitis

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Gingivostomatitis
Herpesgingiva.JPG
Classification and external resources
Specialtyinfectiology, oral medicine
ICD-10A69.1, B00.2,
ICD-9-CM054.2, 523.10
MedlinePlus001052

Gingivostomatitis (also known as primary herpetic gingivostomatitis or orolabial herpes) is a combination of gingivitis and stomatitis, or an inflammation of the oral mucosa and gingiva.[1] Herpetic gingivostomatitis is often the initial presentation during the first ("primary") herpes simplex infection. It is of greater severity than herpes labialis (cold sores) which is often the subsequent presentations. Primary herpetic gingivostomatitis is the most common viral infection of the mouth.[2]

Primary herpetic gingivostomatitis (PHGS) represents the clinically apparent pattern of primary herpes simplex virus (HSV) infection, since the vast majority of other primary infections are symptomless. PHGS is caused predominantly by HSV-1 and affects mainly children. Prodromal symptoms, such as fever, anorexia, irritability, malaise and headache, may occur in advance of disease. The disease presents as numerous pin-head vesicles, which rupture rapidly to form painful irregular ulcerations covered by yellow–grey membranes. Sub-mandibular lymphadenitis, halitosis and refusal to drink are usual concomitant findings.[3]

Pathophysiology[edit]

Herpetic gingivostomatitis originates from a primary infection of HSV-1. The series of events that take place during this infection include replication of the herpes simplex virus, cell lysis and finally, destruction of the mucosal tissue.[4]

HSV-1 can very easily enter and replicate within epidermal and dermal cells through skin or mucosal surfaces which have abrasions.[4] This results in numerous small vesicles or blisters of up to 1-2mm on the oral mucosa, erosions on the lips, eventual hemorrhagic crusting and even ulceration, covered by a yellowish-grey pseudomembrane, surrounded by an erythematous halo.[5][6]

As the virus continues to replicate and incolulate in great amounts, it can enter autonomic or sensory ganglia, where it travels within axons to reach ganglionic nerve bodies. HSV-1 most commonly infects the trigeminal ganglia, where it remains latent. If reactivated, it presents as herpes labialis, also known as cold sores.[4]

Histopathology[edit]

The histological appearance of a herpetic infection on the mucosa includes degeneration of stratified squamous epithelial cells, the loss of intercellular connections and inflammatory infiltrate around the capillaries of the dermis layer.[4] An intact herpetic vesicle presents as an intraepithelial blister histologically. This vesicle is caused by rupture and distension of the virally epithelial cells by intracellular oedema and coalescence of disrupted cells.

Rupturing of the infected cells cause a great number of viral particles to be released, rendering them the ability to affect adjacent epithelial cells and even the sensory axons of the trigeminal nerve. Histologically, these infected cells have a eosinophilic cytoplasm and large, pale vesicular nuclei, appearing swollen under the microscope. The cytoplasms of the infected cells fuse, collectively forming giant cells with many nuclei. The balloon cells and multi-nucleated giant cells can often be identified in smears taken from an intact vesicle or from one which has been recently ruptured.[6]

The lamina propria shows a variable inflammatory infiltrate, the density of which depends on the stage and severity of the disease, and inflammatory cells also extend into the epithelium.[6]

Cowdry type A bodies are intranuclear inclusion bodies visible under light microscopy. They show electron dense glycoproteins and viral capsids.[7] Both Cowdry type A bodies can both be found in varicella zoster and herpetic gingivostomatitis, making it impossible to distinguish between both eosinophilic bodies. One way to distinguish between the herpes virus (and hence herpetic gingivostomatitis) and varicella virus is by direct immunohistochemistry using fluorescent antibodies.[8]

Aetiology and Causes[edit]

Herpetic gingivostomatitis is an infection caused by the Herpes Simplex Virus (HSV).  The HSV is a double-stranded DNA virus categorised into two types; HSV-1 and HSV-2.  HSV-1 is predominantly responsible for oral, facial and ocular infections whereas HSV-2 is responsible for most genital and cutaneous lower herpetic lesions.  Both HSV-1, and HSV-2 can be the cause of herpetic gingivostomatitis,[8] although HSV-1 is the source of infection in around 90% of cases.[9]

Herpetic gingivostomatitis infections can present as acute or recurrent.  Acute infection refers to the first invasion of the virus, and recurrent is when reactivation of the latent virus occurs.[10]  Acute herpetic gingivostomatitis primarily occurs in children, particularly of those under the age of six years old.[11]

On external surfaces the virus is short lived, however it is extremely contagious.  Most people acquire the virus via direct contact, it can enter the body by disrupting the integrity of skin, mucous membranes or enter via infected secretions such as saliva.  The virus replicates once it has penetrated the epithelial cell, then it travels to the corresponding nerve ganglion (i.e. trigeminal ganglion) via sensory nerves endings.  At the nerve ganglion the virus enters a latent phase and remains dormant until it is reactivated.  Reactivation can be spontaneous or stimulated by a number of factors such as: reinfection by direct effect of stimuli, immunosuppression, ultraviolet light, febrile illnesses and stress.[8][9]

Risk factors[edit]

  1. Age:
    • Primary herpetic gingivostomatitis is common in children from 6 months to 5 years old.  This virus is also common in young adults aged around 20-25.[8]
  2. Immune System:
  3. Environment:
    • As this virus is very contagious it has the potential to spread quickly in enclosed environments e.g. nurseries and orphanages.[8]
  4. Epidemiology:
    • Those living in developing countries are at a higher risk of HSV-1 infection. It has been reported that around a 1/3rd of children living in developing countries are HSV-1 positive by 5 years old and 70-80% of the population are infected by the age of adolescence.  In developed countries only 20% of children are infected at the age of 5 and there is no significant increase in disease prevalence until 20–40 years old where the percentage of infected individuals ranges from 40-60% [12]
  5. Socio-economic Status:
  6. Race:
    • Studies have demonstrated that in the USA 35% of African Americans by the age of 5 have presented with the disease whereas only 18% of White Americans are affected.[12]

Symptoms[edit]

Herpes lesions on the gingiva.[13]

The symptoms can be mild or severe and may include:

  • Not able to chew or swallow
  • Sores on the inside of the cheeks or gums
  • Fever
  • General discomfort, uneasiness, or ill feeling
  • Very sore mouth with no desire to eat
  • Halitosis (bad breath)

Diagnosis[edit]

Differential Diagnosis[edit]

Gingivostomatitis symptoms in infants may wrongly be dismissed as teething. "Coincidentally, primary tooth eruption begins at about the time that infants are losing maternal antibody protection against the herpes virus. Also, reports on teething difficulties have recorded symptoms which are remarkably consistent with primary oral herpetic infection such as fever, irritability, sleeplessness, and difficulty with eating."[14] "Younger infants with higher residual levels of antibodies would experience milder infections and these would be more likely to go unrecognized or be dismissed as teething difficulty."[15]

Gingivostomatitis must also be differentiated from herpangina, another disease that also commonly causes ulcers in the oral cavity of children, but is caused by the Coxsackie A virus rather than a herpes virus.[16] In herpangina, ulcers are usually isolated to the soft palate and anterior pillar of the mouth.[16] In herpetic gingivostomatitis, lesions can be found in these locations, but they are almost always accompanied by ulcerations on the gums, lips, tongue or buccal mucosa and/or by hyperemia, hypertrophy or hemorrhage of the gums.[16]

Treatment[edit]

Treatment includes fluid intake, good oral hygiene and gentle debridement of the mouth, as well as oral acyclovir. In healthy individuals the lesions heal spontaneously in 7–14 days without scarring.

See also[edit]

References[edit]

  1. ^ "Gingivostomatitis" at Dorland's Medical Dictionary
  2. ^ "Oral Complications of Cancer and Its Management". By Andrew Davies, Joel Epstein. Oxford University Press, 2010. p195
  3. ^ "Herpes simplex virus infection, with particular reference to the progression and complications of primary herpetic gingivostomatitis", A. Kolokotronis, S. Doumas, Clinical Microbiology and Infection, Volume 12, Issue 3, pages 202–211, March 2006. http://onlinelibrary.wiley.com/doi/10.1111/j.1469-0691.2005.01336.x/full
  4. ^ a b c d Aslanova, Minira; Zito, Patrick M. (27 October 2018). "Herpetic Gingivostomatitis". National Center for Biotechnology Information.
  5. ^ Arduino, Paolo G.; Porter, Stephen R. (2008-02-01). "Herpes Simplex Virus Type 1 infection: overview on relevant clinico-pathological features*". Journal of Oral Pathology & Medicine. 37 (2): 107–121. doi:10.1111/j.1600-0714.2007.00586.x. ISSN 1600-0714.
  6. ^ a b c V., Soames, J. (2005). Oral pathology. Southam, J. C. (4th ed.). Oxford: Oxford University Press. ISBN 9780198527947. OCLC 57006193.
  7. ^ Leinweber, Bernd; Kerl, Helmut; Cerroni, Lorenzo (2006-01-01). "Histopathologic Features of Cutaneous Herpes Virus Infections (herpes Simplex, Herpes Varicella/zoster): A Broad Spectrum of Presentations With Common Pseudolymphomatous Aspects". The American Journal of Surgical Pathology. 30 (1): 50–58. doi:10.1097/01.pas.0000176427.99004.d7. ISSN 0147-5185.
  8. ^ a b c d e f Nasser, Fedorowicz,Khoshnevisan, Tabarestani, Mona, Zbys, Mohammad, Maryam Shahiri (8 October 2008). "Acyclovir for treating primary herpetic gingivostomatitis". Cochrane Libary.
  9. ^ a b M. Kaye, Kenneth. "Herpes Simplex Virus (HSV) Infections". MSD Manuals. Retrieved 27 November 2018.
  10. ^ L Wiler, Jennifer (September 2006). "Diagnosis: Recurrent Herpes Gingivostomatitis". Emergency Medicine News. 28: 34.
  11. ^ D Goldman, Ran (May 2016). "Acyclovir for herpetic gingivostomatitis in children". Acyclovir for herpetic gingivostomatitis in children.
  12. ^ a b "Herpes Simplex Virus" (PDF). Retrieved 27 November 2018.
  13. ^ Dorfman, J. The Center for Special Dentistry.
  14. ^ "Herpetic gingivostomatitis and teething difficulty in infants". David L. King, William Steinhauer, Franklin Garcfa-Godoy, Cassandra J. Elkins. PEDIATRIC DENTISTRY MARCH/APRIL, 1992 VOLUME 14, NUMBER 2. p83
  15. ^ "Herpetic gingivostomatitis and teething difficulty in infants". David L. King, William Steinhauer, Franklin Garcfa-Godoy, Cassandra J. Elkins. PEDIATRIC DENTISTRY MARCH/APRIL, 1992 VOLUME 14, NUMBER 2. p84
  16. ^ a b c PARROTT, RH; WOLF, SI; NUDELMAN, J; NAIDEN, E; HUEBNER, RJ; RICE, EC; McCULLOUGH, NB (August 1954). "Clinical and laboratory differentiation between herpangina and infectious (herpetic) gingivostomatitis". Pediatrics. 14 (2): 122–9. PMID 13185685.

External links[edit]