5.3 Viral infections

5.3.1 Diseases caused by the „herpes simplex virus“

Herpes simplex virus is so common in the population that we can speak of an almost 100% rate of infection in the population. The primary infection usually occurs between the ages of 1 and 5 years. Two types of the virus are known – Type 1 (HSV-1) and Type 2 (HSV-2). The virus is transmitted through a direct contact with an infected person; Type 1 is usually transmitted via oral whereas Type 2 via genital secretions, the final distribution of the areas afflicted by both types of viruses however is more or less the same. Following an infection with either HSV-1 or HSV-2 (whether manifesting clinically or not), the production of specific neutralizing and complement fixing antibodies begins within 1 week. Even so, the virus latently survives in the ganglia of sensory nerves and may cause recurrences in the skin and mucous membranes via the retrograde intra-axonal transport.

Primary herpetic gingivostomatitis


Herpetic stomatitis is the most common clinical manifestation of primary infection caused by HSV (particularly Type 1), particularly in children at the age of 1-5 years. The next wave occurs usually in adolescence and adulthood up to the age of 35 years. It is transmitted by direct contact or by airborne infectious droplets; the incubation period is approximately 7 days.

Clinical picture: The disease begins with the prodromal stage with non-characteristic flu-like general symptoms (fever, headache, cervical pain, backache, loss of appetite and fatigue). Within 2-3 days, those symptoms disappear and a generalized intraoral disease will develop, characterized with the typical eruption of multiple tiny intraepithelial blisters on the erythematous oral mucosa. Predilection sites include the gingiva (which becomes diffusely red and oedematous), the tongue dorsum and the mucosa of the hard palate. Changes in the palatal gingiva behind the upper incisors are very typical, major inflammatory hyperplasia of interdental papillae can be found.

Changes in the palatal mucosa in the region of molars can be observed in children with deciduous teeth. Blisters quickly merge and break to form very painful erosions and ulcerations. The tongue has heavy whitish coating – sometimes with a diagnostically valuable herpetic blisters or erosions on the tip and along the sides of the tongue. Hypersalivation is common as well as the indistinct mouth odour (foetor ex ore). The perioral affliction of the vermilion and facial skin is not a rule. Food intake, swallowing and sometimes pronunciation are impaired. Submandibular and superficial cervical lymph nodes are painful and swollen. The disease will usually disappear spontaneously in 7-10 days; erosions will heal completely (ad integrum). As an after-effect of the reduced oral hygiene during the outbreak (i.e. poorer oral hygiene due to the intense pain), plaque-induced gingivitis may persist. There are usually no early complications; patients with atopic eczema however may experience dissemination of the infection, with a clinical picture of eczema herpeticatum Kaposi. Generalization of the complaints or neurological complications (meningoencephalitis) may pose a danger in immunodeficient individuals. The disease is recurrent in approx. 30% of patients, it however usually takes a form of herpes labialis (cold sores) or recurrent herpetic stomatitis.

Th.: The therapy is symptomatic – a diet of suitable consistency (pulpy, non-irritating) is recommended along with the sufficient intake of liquids. Before a meal, a mucosal anaesthetic can be applied, the oral cavity can be washed using herbal infusions, a 0.25 % solution of ZnSO4 with virostatic and antiseptic effects (Zn2+ ions inhibit viral DNA-polymerase through a not yet been fully elucidated mechanism) or 0.12 % aqueous solution of chlorhexidine. Antiseptics can only be used at prescribed concentrations and for a required period of time (otherwise, there is a risk of developing an undesirable dysmicrobia in the oral cavity). The frequency of washing varies (2-10× daily). The use of virostatics is usually not necessary, they are needed only in patients who are generally seriously ill. No surgical procedures can be performed in the mouth during the manifestation of the disease.

Dif. dg.: The following symptoms are very important for diagnosis: an acute diffuse gingivitis, usually with fibrin deposits and typical localization on the palatal gingiva behind the upper incisors; intense whitish coating of the tongue with tiny erosions along the sides and on the tip of the tongue; swelling of lymph nodes; and alteration of the general condition in the prodromal stage (which represents a difference from ulcerative gingivostomatitis). It is necessary to differentiate this disease from the first attack of erythema multiforme in the form of the Stevens-Johnson syndrome (which always affects the vermilion zone with symptoms including bleeding crevices and haemorrhagic crusts with the nasal apertures, conjunctivae, genitals and skin being also affected; general symptoms are however less expressed). Rarely, acute gingivostomatitis can occur during infectious mononucleosis (which however usually shows as a part of the general picture including pseudomembranous angina, hepatomegaly, typical changes in the blood count, and serological evidence of EBV). Enteroviral stomatitis does not affect the gingiva.

Pustulosis varioliformis (eczema herpeticum, Kaposi varicelliform eruption)

This serious form of primary infection caused by HSV can occur in atopic individuals (usually in infants) suffering with a generalized eruption of vesicles turning into pustules and subsequently in erosions or crusts. This is usually associated with the alteration of the general condition and accompanied by fever, fatigue or even affliction of internal organs (meningoencephalitis, pneumonia). Oral symptoms occur in 10-15% of patients who develop painful erosions in the mouth that are more severe than those associated with herpetic stomatitis.

Th.: General application of virostatic agents – acyclovir, symptomatic therapy, or gamma-globulin. Antibiotics can be administered for prophylaxis.

Profylakticky lze podat ATB.

Dif. dg.: It is necessary to differentiate this disease from EEM that typically occurs at a different age and is usually associated with polymorphic cutaneous manifestations.

Recurrent herpetic stomatitis (intraoral herpes, stomatitis herpetica recidivans)


This collective term describes recurrent diseases of the oral mucosa after the formation of specific protective mechanisms – it is not a primary infection. It develops as a result of reactivation of a latent HSV infection; this form is a less common clinical manifestation than herpes simplex (labialis). The causes of reactivation are not usually established.

Local prodromal symptoms (burning, pain) may or may not precede the eruption of blisters; headache may occur in some cases. The disease usually affects the keratinized sections of the oral mucosa (gingiva, hard palate, tongue dorsum). The blisters are usually not detected since their roof peels off quickly and they turn into erosions that are very painful and tend to merge. The lips can also be affected. The surrounding mucosa is erythematous and swollen; regional lymph nodes are usually not affected. Spontaneous healing takes 5-10 days, complications usually only occur in predisposed individuals (oncological or immunodeficient patients) in whom a caudal propagation of the mucosal disease (pain during swallowing!), process dissemination and generalization are possible. The skin and mucous membranes of the genitals can also be affected. The frequency of recurrences varies.

Th.: The treatment is, just like in herpetic gingivostomatitis, local and symptomatic. In immunodeficient patients, acyclovir can be used. For prophylaxis of the recurrences, immunomodulators can be administered (transfer-factor, gamma-globulins – only after an immunological examination!).

Dif. dg.: Compared to the herpetic gingivostomatitis, the alteration of the general condition and a two-stage course of the disease are missing. Distinguishing this disease from the herpetiform type of recurrent aphthae can be difficult; those however do not have the tendency to combine and never affect the keratinized region of the oral mucosa (!). When suspecting an autoaggressive disease from the group of pemphigus/pemphigoid diseases, a biopsy and immunofluorescent examination are necessary..

Labial herpes simplex (herpes simplex labialis, herpes labialis)


This is the most common clinical form of activation of the latent HSV-infection in the orofacial region due to the virus persisting in the trigeminal ganglion (the Gasserian ganglion). It repeatedly affects the lips with a very variable frequency of recurrences. Many external and internal factors may be involved in the reactivation of the latent infection, such as UV-B radiation, trauma, fatigue, mental and/or physical stress, other viral infections or menstruation.

Clinical picture: In the majority of patients, the eruption of labial herpes is preceded by a short-lasting paresthesia at the site of the later manifestation of the disease. Shortly, an eruption of blister(s) appears in the vermilion zone of (usually) one lip. The erupted intraepithelial blisters merge and dry out to form tiny crusts, or break to form erosions. The affected part of the lip is red, oedematous and painful. Painful crevices can be formed in the region of mouth corners, causing difficulty while opening the mouth. The general alteration of the condition is absent. The affliction tends to heal spontaneously. Secondary impetiginization through the autoinoculation of streptococcal or staphylococcal infection of the herpetic manifestation may occur, particularly in children.

The condition may deteriorate if the affected site is traumatized during dental examination.

Th.: Therapy should be initiated as soon as possible, ideally as soon as the prodromal stage! Local application of virostatics such as acyclovir (acyclic nukleosid inhibitor of viral DNA polymerasis) is possible. The application can be associated with mild local irritation manifesting as erythema and paresthesis.

Dif. dg.: Differentiation from other lip-affecting diseases is usually not difficult. Recurrent aphthae do not affect the vermilion zone, pyodermia (folliculitis, furuncle) primarily affects the cutaneous part of the lip and their course and clinical picture are not interchangeable with HSV affliction.

5.3.2 Diseases of the „Varicella zoster virus“ group

Varicella (chicken pox)

Varicella is a very contagious disease caused by varicella-zoster virus (VZV) that also causes shingles. It affects predominantly children, with almost 100% manifestation in sensitive individuals, and is transmitted via the air-borne route or through direct contact. The clinical progression of the disease is usually mild (it can be more serious in adults), with symptoms including fever, eruption of blister exanthemas on the skin or enanthema on mucous membranes. The incubation period is 3 weeks. Since the eruption comes in waves, the picture is typically polymorphic; symptoms on mucous membranes usually precede the eruption of skin manifestations (morphoea) and usually prevail on the palate (hard and soft), lips and gingiva.

Dif. dg.: The presence of the blisters in the scalp is important for confirming the diagnosis. Intra intraoral efflorescences must be distinguished from all erosions-causing diseases. Especially in children, the disease is often of epidemic character – it is necessary to observe the epidemiological situation.

Th.: Therapy is only symptomatic.

Herpes zoster (shingles)


Herpes zoster virus is identical with varicella virus. Varicella is the primary infection, the virus (VZV) then persists in the spinal ganglions, maintaining the capability of reactivation. When spread via blood, it may induce a disease on the oral mucosa that closely resembles varicella, including the diseases of the skin of the head and body. The manifestations of herpes zoster at this stage are however less common on the head and neck and more common in the areas sensitively innervated by spinal nerves.

A secondary attack of the cerebrospinal ganglia of cephalic peripheral nerves is the starting point for a neurodermal viral disease. The disease manifests itself when the organism is weakened; symptoms include facial neuralgias with sensation disorders. Warning! The manifestation of zoster infection can be a paraneoplastic syndrome and may indicate the presence of malignancy!

In persons over 50 years of age, vaccination against the VZV reduces (by means of blocking the viral activation) the risk of both shingles and of post-herpetic neuralgias.

Herpes zoster of the trigeminal nerve (herpes zoster n. trigemini, zoster facialis)

This disease is caused by the reactivation of endogenous viral infection of varicella-zoster virus (VZV) persisting in the trigeminal ganglion (the Gasserian ganglion); the mucosa of the oral cavity can be affected if zoster symptoms are present in the cephalic region sensitively innervated with the 2nd or 3rd branch of the trigeminal nerve. Zoster facialis occurs in approx. 10-20 % of herpes zoster cases.

Clinical picture: Mild prodromes (fatigue, loss of appetite) are followed by neuralgic pain in the region of the affected nerve. In most patients, the oral mucosa is affected together with skin regions of the respective dermatome.

If the 2nd branch (maxillary nerve, n. maxillaris) is involved, herpetic efflorescences on the facial skin in the facial/cheek region (including the upper lip and the nasal wing) and in the temporal region occur. In the mouth, the vestibular mucosa (buccal, labial mucosa in the region of the upper lip and upper alveolus) and the hard palatine mucosa (the region of palatine nerves, nn. palati) are predominantly affected.

An affliction of the 3rd branch (the mandibular nerve, n. mandibularis) results in the eruption of blisters on the facial skin in the mental region including the lower lip, perimandibular and preauricular regions. The intraoral manifestations occur on the mucosa of the frontal two thirds of the tongue (along the lingual nerve, n. lingualis), the floor of the mouth, the lower lip and the alveolar process. Again, pain of various degrees of severity (or sensation disorders – hypersthesia, paresthesia) occurs before the eruption of blisters. The skin shows dark red, maculopapular exanthema (enanthema on the mucosa), followed by the eruption of blisters that are covered with crusts when on skin or turning into erosions when on the mucosa. The affliction is usually unilateral and does not overreach the central line! After healing that usually takes 2-3 weeks, postherpetic pain refractory to therapy may persist.

Th.: Systemic application of virostatic drugs (acyclovir in sufficient doses!) Adjunctive painkiller therapy with local symptomatic treatment.

Dif. dg.: Herpetic stomatitis – frequent recurrences, mucosal manifestations do not reflect the innervation of individual areas of the oral cavity and cross the central line. The pain is usually less severe. Sometimes, it may be difficult to distinguish it from acute pain of odontogenic origin or from the essential trigeminal neuralgia; personal history, complex examination of the oral cavity including X-ray, neurological and ENT examinations help in differentiation).

Herpes zoster n. facialis (zoster oticus)

It occurs due to the reactivation of latent VZV infection persisting in the geniculate ganglion (ggl. geniculi) of the intermediate nerve (n. intermedius). Clinical symptoms are very variable, affecting skin and mucosal regions of the head, which are sensitively innervated by the facial nerve. An affliction combining this disease with other cephalic nerves at the same time is called Ramsay-Hunt syndrome.

Zoster oticus occurs relatively rarely. Sometimes, it is preceded by prodromal symptoms such as otalgia with propagation into the regions of the neck, shoulder or chest, disorders of sensation in the area of the auricle and the external auditory canal. Intraoral symptoms are usually more extensive than skin symptoms, being localized in the frontal two thirds of the tongue (via chorda tympani) and on the soft palate. Mucosal symptoms (blisters or erosions) are very painful and make a food intake, swallowing and speech difficult.

The condition is often accompanied by facial plegia that causes additional problems such as motor disorders of mimic muscles and lagophthalmos. Symptoms disappear spontaneously in 14-28 days; the affliction of the facial nerve with motor disorders of facial muscles however often persists.

Th.: Same as the treatment of herpes zoster of the trigeminal nerve.

5.3.3 Epstein-Barr virus and cytomegaloviruses group diseases

Infectious mononucleosis (monocytic angina, Pfeiffer’s disease)


The usual cause is EBV (the Epstein-Barr virus). It is most prevalent in younger people (teenagers). The infection is transmitted by saliva and is possible both from an infected individuals or from clinically healthy carriers. After the incubation period, the disease initially manifests through unspecific general symptoms (fever, loss of appetite, tiredness), followed rarely by an acute ulcerative gingivostomatitis (although some forms are clinically indistinguishable from the herpetic form) that can be accompanied by quickly disappearing petechiae on the soft palate (Holzer’s sign) or by temporary facial oedemas (Bass/Hoagland sign). Subsequently, pseudomembranous angina develops, with coatings that may spread from tonsils into the surroundings. In some cases, only acute pharyngitis develops, accompanied by painful swallowing, oedema of the pharynx and larynx, and inspiratory stridor. Submandibular and painless cervical lymphadenopathy is always present. Some individuals also show enlarged lymph nodes in other parts of the body and/or hepatosplenomegalia. Neurological complications such as meningitis, meningoencephalitis, polyradiculoneuritis or organ-specific complications (hepatopathy, pancreatitis, nephritis) can also occur. The disease usually lasts relatively long and in some patients, it tends to chronicity.

Dg.: Blood count examination shows lymphocytosis with atypical lymphoid cells; the high count of monocytes (up to 50%) is typical as well as the positive Paul-Bunnel test and laboratory signs of hepatopathy. Virological examination is performed to detect antibodies against viral antigens VCA, EBNA; analysis of IgG and IgM antibodies against CMV-infection is sometimes also necessary.

Th.: The systemic therapy falls within the scope of specialists in infectious diseases; bed rest along with liver diet and intake of hepatoprotective products are of utmost importance. Only gradual return to normal activities is recommended. If an acute gingivostomatitis develops, local symptomatic therapy (anaesthetics, antiseptic mouthwashes) is recommended.

Dif. dg.: Streptococcal tonsillitis (angina lacunaris, lacunar tonsillitis) regresses after 2-3 days of ATB treatment and the enlarged tonsils are painful. Herpetic gingivostomatitis has a typical two stage course of disease (the systemic complaints regress with onset of intraoral problems) and the pseudomembranous angina is absent. Herpangina is not accompanied by lymphadenopathy, the problems are usually less serious. Especially in children, it is necessary to differentiate with developing acute hemoblastosis with signs of acute pharyngitis or tonsillitis accompanied by the significant general alteration of the patient’s condition (blood count!).

„Hairy“ leukoplakia


This manifestation of EBV infection is characterized by changes on the oral mucosa, most commonly on the tongue. It appears as fuzzy-looking white patches with an evenly arranged, folded mucous surface on the tongue’s edges in the frontal two thirds of the tongue (pars oralis linguae). Leukoplakia can also manifest on the tongue’s dorsum and apex. Sometimes, it can also occur on the labial, buccal or palatine mucosa where it however does not have the typical appearance (the folding of the mucous epithelium typical of the tongue is absent). The finding is usually permanent; it however may sometimes regress spontaneously or after therapy.

In HIV-positive patients, the occurrence of hairy leukoplakia indicates a poor prognosis and progression of HIV infection into the AIDS phase. In 80 % of HIV patients, this progression occurs within 30 months after the development of hairy leukoplakia.

Histopathology: Hyperkeratosis, acanthosis and ballooning degeneration of the epithelial cells of the mucosa with pycnotic nuclei in the stratum spinosum are observed. Pseudohyphae of Candida yeasts often grow into the superficial layers of the keratinized mucous epithelium. Eosinophilic inclusions (classified using PCR as the Epstein-Barr virus) can be seen in the epithelial cells.

Th.: Systemic virostatic treatment (acyclovir) is prescribed; where yeasts are found, antimycotic therapy should be also administered. Nowadays, however, the prevailing opinion is that it is not necessary to treat hairy leukoplakia unless the condition is causing the patient local subjective problems.

Dif. dg.: When developing on the sides of the tongue, it is necessary to distinguish it from relatively common changes caused by chronic trauma of the tongue (frictional keratosis), which usually bears signs of teeth impressions or changes caused by biting (the same can be true of buccal or labial mucosa). The tongue can be sensitive or even painful. The usual „smoker’s“ leukoplakia can affect any part of the oral mucosa. Histopathologically, eosinophilic inclusions typical of hairy leukoplakia are absent. Lingua geographica in the stage of „healing“ of the epithelium can also resemble „hairy“ leukoplakia. Clinically, however, the picture quickly changes, typically within several days. The acute or pseudomembranous forms of oral candidosis can also resemble this condition; in candidosis, however, the symptoms are also present on other parts of the oral mucosa and the vicinity of the white lesions is notably erythematous. Patients usually complain about burning sensation and pain.

Cytomegalovirus disease

The disease is caused by CMV; usually, it results from reactivation of a latent (endogenous) infection due to deficiency/failure of the immune system. It is therefore not a primary infection.

Clinical picture: Isolated or multiple defects sensitive to touch appear on erythematous mucosa – erosions to ulcerations of various diameters, usually only vaguely circumscribed. The most common site is the soft palate (including the uvula), followed by hard palate, gingiva, vestibular and lingual mucosa. They persist for several weeks and mostly, they heal spontaneously (albeit scars may sometimes remain). The disease can recur or be more extensive, affecting even the esophagus or more distal segments of the GIT.

Dg.: As neither the morphological picture nor localization are specific, the clinical diagnosis must be verified by histopathological examination (the presence of infected epithelium with „owl’s eye“ inclusions). Virological examination (a direct proof of viral DNA is preferred to that of specific antibodies).

Th.: Application of antiviral therapeutics is possible, it is however usually not necessary due to the high tendency to spontaneous healing. Local symptomatic treatment focused on relieving the complaints and supporting healing of the mucosal defects is recommended.

Dif. dg.: For therapeutic reasons, it is important to distinguish this disease from other mucosal defects such as erosions or ulcerations using targeted tests and examinations (histopathological, virological, bacteriological, mycological, etc.).

5.3.4 Enterovirus infections



This disease is caused by the Coxsackie A, Coxsackie B or ECHO virus. It usually affects children or young people, forming a kind of small seasonal (summer) epidemics disappearing within two weeks. The transmission of infection is possible both by a direct contact or via air-borne droplets. It usually presents as acute stomatitis with pharyngitis, usually with vague clinical problems (sore throat, headache, vomiting, diarrhoea, fever). In the oral cavity, small blisters or erosions are formed (usually well circumscribed, rarely merging) on the mucosa of the soft palate, tonsils and pharyngeal mucosa. Subjectively, the biggest discomfort is typically associated with swallowing.

Th.: Symptomatic local therapy focusing on reducing the subjective complaints – non irritating food, sufficient hydration, antiseptic mouthwashes).

Dif. dg.: Hand, foot and mouth disease has skin symptoms in addition to the mucosal. Herpetic gingivostomatitis usually has a more serious course, the affected areas are bigger, affecting the gingiva and hard palate. In herpes zoster, the affliction is strictly unilateral (besides the skin and mucosal symptoms, pain and sometimes neurological symptoms that may also occur are different) and it predominantly affects a different age category. Eruptions of petechiae on the soft palate in young individuals with tonsillitis that subsequently quickly disappear may indicate infectious mononucleosis.

Vesicular stomatitis with exanthema on hands and feet (hand, foot and mouth disease)


This disease is caused by enteroviruses, usually by Coxsackie A, Coxsackie B or ECHO-virus. Its etiopathogenesis and clinical manifestation are similar to those of herpangina, from which it differs by the presence of maculopapular and vesicular exanthema affecting the hands and feet (sometimes also skin of other parts of the body). The disease can affect any part of the oral mucosa and pharynx, except for the gingiva.

Th. and Dif. dg: It is identical with that treatment of herpangina.

5.3.5 Measles (morbilli)

This disease is caused by a virus of the paramyxoviruses group and affects predominantly children under 6 years of age.

Clinical picture: A gradually increasing body temperature is accompanied by catarrhal symptoms (coryza, dry cough, conjunctivitis). The temperature recedes after 2 days, only to return again, which is accompanied by an aggravation of the other symptoms and appearance of a maculopapular exanthema, the patches of which have a tendency to merge, typically progressing from the forehead, the region behind the ears and neck to the face, body and limbs.

In the oral cavity, enanthema develops, usually manifesting sooner than the exanthema. The buccal mucosa in the region of molars shows red round patches with small necroses known as Koplik's spots. Erythematic patches can also occur on the palate and labial mucosa.

Th.: Prevention – vaccination – is the key; if the disease still manifests, symptomatic therapy is administered.

5.3.6 Infections caused by the human papillomavirus (HPV)


Human papillomavirus is a DNA virus of the Papillomaviridae family. At present, more than 130 types of HPV are known. From the perspective of oncogenic potential, low-risk and high-risk types are being distinguished:

Low-risk HPVs (2, 4, 6, 11, 13 and 32) are the agents behind benign cutaneous and mucosal (oral, genital) acanthomas: verruca vulgaris on the skin, mucosal viral papilloma (common warts) on the oral mucosa, condylomata accuminata in the genital region as well as on the oral mucosa, or a rare focal epithelial hyperplasia – so-called Heckʼs disease.

The term high-risk HPV covers in particular types 16, 18, 31, 33 and 35 that may lead to the development of squamous cells carcinoma, which (in the region of the head and neck) means almost exclusively oropharyngeal region. Approximately 90 % of HPV-positive oropharyngeal carcinomas is associated with the subtype 16. The prevalence of these tumours has grown recently. HPV-related oropharyngeal carcinomas possess, compared to those associated with smoking or other risk factors, different epidemiological, clinical and molecular characteristics and are characterized by a better prognosis and response to the therapy (Gurín et al., 2019).

HPV is considered to be an opportunistic infection more common among the patients with sexually transmitted diseases and in immunocompromised persons. The papillomavirus infects the basal epithelial cells (both of the skin and mucosa); it does not enter the bloodstream but leads to the production of antibodies (which is typically utilized for vaccination against HPV). The transmission of HPV occurs through both the direct and indirect routes (often by sexual intercourse, microinjuries of the skin or mucosa can act as gateways). The virus is relatively resilient and in a moist environment, it can remain infectious for up to several months. The incubation period is long, the infection is symptoms-free in 80-90% of cases (and disappears spontaneously) while in 10 20 % of infected persons, clinical manifestations can be observed.

Clinical picture: If benign lesions appear on the oral mucosa (manifestations on the soft palate are more common due to the transition from squamous to columnar epithelium), they usually form tiny (below 5 mm) painless, often whitish solitary (or multiple) structures of papillomatous appearance that can be both pedunculated or sessile. Usually, young individuals between 25-30 years of age develop such lesions. Tumours in the oral cavity can manifest as whitish or erythematous spots, non healing ulcerations; in later stages, they can bleed. In the initial stages, the tumours of the oropharynx have no specific symptoms. They often mimic the symptoms of a chronic inflammation in the region such as sore throat or scraping in the neck, sensation of a foreign body, dysphagia, pain while swallowing (odynophagia), ear pain or rhinolalia. The progression of the tumour leads to accentuating the symptoms. The decomposition of the cancerous tissue is associated by bad breath (foetor ex ore), functional defects of the structures infiltrated by the tumorous process can also appear. Disease of the chewing muscles would manifest as a reduced motility of the lower jaw, infiltration of the muscles of the tongue, or as a reduced mobility manifesting as speech difficulties. If a nerve bundle is affected by an ingrowing tumour, we can observe a failure of its function (e.g. infiltration of the inferior alveolar nerve will cause a sensitivity defect on the skin in the lower lip region – Vincentʼs symptom). In general, we can observe that the patient loses weight. In some cases, the patient only comes when cervical resistance appears, which signifies the metastatic progression of the tumour into the cervical lymph nodes.

Dg: The diagnosis is based on results of the histopathological examination. When keratinocytes are infected by HPVs, the presence of koilocytes is a characteristic concomitant symptom. The overexpression of p16 protein, the surrogate marker of the presence of the high risk HPV 16, is used for immunohistological assessment of HPV-positive oropharyngeal squamous cell carcinoma. A direct diagnosis based on the proof of particles of the HPV virus or of HPV DNA in the affected cells is also possible.

Th.: Benign lesions can be removed surgically (full excision), laser removal can be also used (especially where multiple eruptions are concerned; correct diagnosis prior to the laser removal is a must); where HPV or oropharyngeal carcinoma is concerned, a complex oncological treatment is necessary.

Dif. dg.: HPV papillomas must be differentiated from non-viral mucosal papillomas, fibropapillomas and fibromas on the one hand and squamous cell carcinoma on the other.

5.3.7 Manifestations of the primary HIV infection in the oral cavity

Following an infection by human immunodeficiency virus (HIV), 50-80 % of patients develop signs of acute HIV infection. These symptoms are however vague (fever, myalgia and athralgia, fatigue, skin exanthema, lymphadenopathy – so-called mononucleosis-like syndrome). Acute pharyngitis is often present in the oral cavity at this stage as well as the eruption of superficial painful erosions on the hard palate that resemble aphthae (minor aphthae) but occur at unusual locations (recurrent aphthae never develop on the keratinized mucosa of the hard palate!). Erosions heal spontaneously within a week as well as the other symptoms of acute infection.

After the primary infection, a latency period follows (duration of this period is highly individual) during which the patient feels healthy and the CD4+ T-lymphocytes and macrophages that represent targets for the virus show normal values in the blood count. Later, however, when there is a notable drop in CD4 lymphocytes and the immunity breakdown, the patient ceases to be immune against infections and tumorous growth (see the chapter 6.1.4).