Oral Herpes Simplex : Primary Form and Rrecurrent Form

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The herpes simplex virus is a DNA virus, there are two types: herpes simplex type I (HSV I) and type II (HSV II); the first (HSV I) has a tropism for orofacial tissues and causes clinical manifestations charged to the oral mucosa, pharynx, eye, and skin of the face and trunk above the diaphragm, is transmitted through saliva and contact with active lesions; HSV II has instead tropism for the genital mucosa and to the skin below the diaphragm and is transmitted through sexual intercourse. The HSV II can also be seen at the level of the oral cavity as a result of gold-genital sex (is responsible for about 10% of oral herpes infections), rarer is the reverse, namely that the HSV Infected mucous membranes genitals. Both viruses have the characteristic of remaining in a state of latency in the nervous tissue and more specifically in the cells of the sensory trigeminal ganglia (HSV I) and lumbosacral (HSV II), being able to be reactivated after precipitating factors such as exposure to solar radiation , intense cold, stress, fever, trauma, hormonal changes (menstruation) and systemic pathological conditions in which is to be affected immunity (especially cell-mediated). The reactivation follows the appearance of clinical symptoms recurring.


So we have said that the oral lesions are caused mainly by HSV I on which the infection has been used increasingly as evidenced by the high rate at which there is the presence of circulating antibodies in the general population (about 90 % of cases ) . In the course of primary infection in most infected subjects the disease remains subclinical and can be demonstrated contact with the virus only through blood tests that show the presence of anti – HSV antibodies . In symptomatic forms ( approximately 10 % of cases ) after a period of incubation varying from a few days to two weeks , manifests a vesicular – ulcerative eruption localized to the oral tissues and perioral level known as primary herpetic gingivostomatitis .


Herpetic gingivostomatitis PRIMARY usually affects children with a peak incidence between 2 and 4 years, after incubation of a few days there is a prodromal phase that lasts 1-2 days with fever, headache and general malaise, followed by eruptive phase in which the primary lesion through a period followed by a papular erythematous initial phase and then a vesicular phase, the rupture of the vesicle leaves ulceration (ulcerative phase) surrounded by an erythematous and edematous mucosa. Over a period of 3-5 days longer follow eruptive cycles for which it is possible to appreciate an oral clinical examination the whole range of possible lesions and mucosal ie erythematous, papules, vesicles and ulcers. The vesicular rash may appear on the skin, vermilion border of the lip or oral mucosa. At the level of intra-oral lesions can affect any home mucosa and this differentiates them from injury of recurrent forms that are primarily localized in the mucosal areas where the epithelium is more keratinized: gums and hard palate.

It ‘cervical lymphadenopathy in addition to general symptoms such as fever, arthralgia, malaise and fatigue. Healing happens in a couple of weeks. Following the resolution of primary herpetic gingivostomatitis the virus migrates through largely unknown mechanisms, along the nerve sheaths of the trigeminal nerve to the semilunar ganglion of Gasser where he remained in a state of latency. Reactivation of the virus can be determined by exposure to sunlight or at low temperatures (the so-called “fever lip”), trauma, stress, hormonal changes, or were immunocompromised. The reactivated virus were to reverse the nerve fibers of the trigeminal nerve to reach the epithelial surface where viral replication takes place, resulting in a vesiculobullous eruption localized erosive without systemic involvement (ie lacking the general symptoms of infection present in symptomatic primary form) probably thanks to previous sensitization of the immune system occurred following the first contact with the virus. When even the secondary injury will be healed the virus will return to the level of ganglion Gasser and will not be able to highlight the epithelial layer



And ‘ the manifestation of the reactivation of the virus . Rarely is a sign of a re-infection by viruses of external origin . Relapse occurs up to 40 % of infected individuals ( ie the subjects that have come in contact once with the virus ) , and in those who have experienced primary herpetic gingivostomatitis and in those in which the first contact with the virus does not caused clinically detectable disease. The secondary forms are generally preceded by a prodromal phase characterized by tingling , burning and pain at the site where the lesions appear . It follows the eruptive phase with the appearance of numerous vesicles of small size usually grouped in clusters that breaking leave ulcerations that tend to merge with each other , the lesions heal in a few weeks without scarring .


Most of the lesions is manifested at the level of the vermilion border of the lip and the skin perilabiale , this form of herpetic infection is called Herpes Labialis , at skin level to the ulcerative phase follows a crusty phase , rarely these lesions go on to secondary bacterial infection . In intraoral recurrent forms are affected gums and hard palate that is, the oral mucosa areas where the epithelium is more keratinized . Relapses can occur with a frequency varying from one episode per month up to one episode a year tending to decrease in frequency with increasing age .


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