Viral Induced oral lesions

Department of Oral Medicine and Periodontology Faculty of Dentistry University of the Western Cape
Lecture Notes 2011

Infections and the oral cavity

Oral cavity is the site of both local and systemic disease Includes infections by bacteria, fungi and viruses Localized or generalised effect Viral infection mostly affects children, older adults and the immunocompromised

Types of lesions that can be induced by viruses

I. II. III. IV.

VesiculoVesiculo-Bullous and erosive lesions VerrucalVerrucal-Papillary lesions SiteSite-specific lesions Salivary gland lesions

Viral induced Vesiculo-bullous and Vesiculoerosive lesions

Clinical Definitions

Vesicle: Elevated blisters of clear fluid less than 1cm in diameter Bullae: Elevated blisters of clear fluid more than 1cm in diameter Erosion: Moist red lesions caused by rupture of vesicles or bullae

Viruses that cause vesiculo-bullous vesiculolesions

Several exist, the most common include; Herpesviruses Enteroviruses Measles

Herpes viruses

DNA type virus Each affected individual remains a reservoir of infection for life recurrence is possible 80 known herpes viruses 8 cause human infection, most of which have oral manifestations; 1. Herpes simplex virus 1 (HHV1) 2. Herpes simplex virus 2 (HHV2) 3. Varicella-Zoster virus (HHV3) Varicella4. Epstein-Bar virus (HHV4) Epstein5. Cytomegalovirus (HHV5) 6. HHV6 7. HHV7 8. Kaposi-sarcoma associated herpes virus (HHV8) Kaposi-

HHV1 and HHV2

HSVHSV-1 Spread predominantly through infected saliva or contact with active peri-oral perilesions. Adapted best to oral, facial and ocular areas. Pharynx, intra-oral sites, intralips, eyes and skin above the waist often involved. HSVHSV-2 Transmitted predominantly through sexual contact. Adapted best to genital areas. Typically involves genitalia and skin below the waist. Clinical lesions produced by both types are identical. The antibodies directed against one cross-react against the other. cross-

Pathogenesis of HHV1
Primary infection
Typically occurs at young age (often asymptomatic). Virus then taken up by sensory nerves and transported to the associated sensory or, less frequently autonomic ganglia. With oral HSV-1 the trigeminal HSVganglion is colonized with virus remaining at this site in a latent state. Virus uses axons of sensory neurons to travel back and forth to peripheral skin or mucosa.

Incubation period - usually 3-9 days 3Developing countries; 50% of population exposed by 5 yrs of age 95% by 15 yrs Universal by 30 yrs Privileged groups; low childhood exposure followed by second peak during college years

Clinical features of HHV1 infection

HSVHSV-1 exposure at early age (children) gingivostomatitis HSVHSV-1 initial exposure later in life (adults) primary herpetic

pharyngotonsillitis

In addition to clinically evident infections, HSV has been implicated in a number of non-infectious processes. More than non50% of cases of erythema multiforme are preceded by a symptomatic recurrence of HSV, 3-10 days earlier. Some attacks 3of EM are chronic enough to warrant antiviral prophylaxis.

Clinical features of Primary herpetic gingivostomatitis (Primary infection-Children) infection

Most common pattern of symptomatic primary HSV infection (90% + HSV-1) HSVMost cases arise between 6 mnths and 5 yrs (peak prevalence between 2 and 3 yrs). Rare before 6 mnths because of maternal anti- HSV-antibodies anti- HSVOnset abrupt, often accompanied by anterior cervical lymphadenopathy, chills, fever, general malaise and sore mouth lesions. Vary from mild to severely debilitating Affected mucosa develops numerous pinhead vesicles, which rapidly collapse to form numerous small, red lesions. They enlarge slightly and develop central areas of ulceration covered by yellow fibrin. Adjacent ulcerations may coalesce to form larger, shallow irregular ulcerations Both, lining and attached oral mucosa can be affected Number of lesions, highly variable Most cases gingiva enlarged, painful and extremely erythematous

PHGS continued

Affected gingiva often exhibits punched-out punchederosions along the midfacial free gingival margins Vermillion border of lips may be involved Satellite vesicles of peri-oral periskin are fairly common SelfSelf-inoculation of fingers, eyes and genital areas can occur Mild cases usually resolve within 5-7 days; severe 5cases may extend to two weeks

PHGS continued

Clinical features of pharyngotonsillitis (Primary infection-Adults) infection

Not all cases exhibit clinical features some symptomatic cases exhibit pharyngotonsillitis. Sore throat, fever, malaise and headaches are initial symptoms Numerous small vesicles on tonsils and posterior pharynx Rapid rupture of vesicles leading to numerous shallow ulcers, which can coalesce. Diffuse, grayish-yellow grayishexudate may form over the ulcers Most HSV-1 but increasing proportions of HSV-2 HSVHSVClinical presentation closely resembles pharyngitis secondary to streptococci or infectious mononucleosis

Secondary/ recurrent HSV-1 infection HSVOccurs with reactivation of the virus. Symptomatic recurrences are fairly common and affect the epithelium supplied by the sensory ganglion. Conditions such as old age, ultraviolet light, emotional stress, pregnancy, allergy, trauma, respiratory illness, menstruation, systemic diseases or malignancy have been associated with reactivation.

Clinical features of secondary herpes infection

Most common site of recurrence for HSVHSV-1 is the vermillion border and adjacent skin of lips herpes labialis (cold sore or fever blister) Prodromal signs and symptoms (pain, burning, itching, tingling, localized warmth, erythema of involved epithelium) arise 6-24hrs before the 6lesions develop Multiple small, erythematous papules develop and form clusters of fluidfluidfilled vesicles. Rupture and crust within 2 days. Release of virus-filled virusfluid may result in the spreading of the lesions on lips previously cracked from sun. Recurrences are less common on skin of nose, chin or cheek

Recurrences can also affect oral mucosa. In immunoimmunocompetent patients, involvement is limited almost always to keratinized mucosa that bond to bone (attached gingiva and hard palate) Symptoms are less intense. 113mm vesicles; rapidly collapse and form a cluster of erythematous macules. Healing takes place in 7-10 7days (refer to lectures on HIV/AIDS regarding recurrent herpes in immunocompromised patients)

Other examples of herpes labialis

Extraoral recurrent herpes

Intraoral recurrent herpes

Intraoral recurrent herpes

Intraoral recurrent herpes

Diagnosis of HHV1 infections

With a thorough knowledge of clinical presentation the clinician can make a strong presumptive diagnosis of HSV infection. On the occasion where it could be confused with another disease, then laboratory confirmation is desirable: viral isolation from tissue culture inoculated with fluid of intact vesicle clinical tests for HSV antigens or nucleic acids in specimens of active lesions 4serologic tests for HSV antibodies are positive 4-8 days after initial exposure two most commonly used diagnostic procedures are the cytology smear and tissue biopsy, with cytologic study being biopsy, least invasive and most cost effective. Although VZV produces similar changes, but these two infections can usually be differentiated on clinical basis

Treatment and Prognosis

Primary Herpetic Gingivostomatitis
Treated best symptomatically. If diagnosed early, antiviral medications can symptomatically. have significant impact. Patient needs to be instructed to restrict contact with active lesions to prevent spread to other sites and people. Young children need to take enough fluids to prevent dehydration. Soft bland diet. Acyclovir. When Acyclovir. When administered in a rinse and swallow technique (Acyclovir suspension) during first 3 symptomatic days, significant acceleration is seen in a clinical resolution. Once therapy is initiated, development of new lesions ceases. Associated eating and drinking difficulties, pain, healing time, duration of fever and viral shedding are shortened dramatically. Antiviral medication in capsule or tablet form take time to exert a significant effect. Aciclovir/valaciclovir (100(100-200mg Acyclovir 5 times a day) NonNon-steroidal anti-inflammatory medications, such as ibuprofen, also help to antimedications, alleviate discomfort Local antiseptics (0.2% CHX mouthrinse)

Herpes labialis.
Acyclovir remains an effective option. Minimizes recurrences if administered prophylactically. Pain associated with intra-oral secondary herpes usually is not intraintense and most patients do not require treatment. Chlorhexidine may anti-viral effects and appears to function antisynergistically with acyclovir. ImmunoImmuno-compromised patients with HSV infections often require intravenous anti-viral medications to control the problem. antiFurthermore, severely immuno-compromised individuals, such as immunobone marrow transplant patients and those with AIDS , often need prophylactic doses of oral acyclovir. Resistance of viruses to medication may develop.

HHV3

Also known as Varicella-Zoster Virus (VZV) and Varicellais similar to HSV in many respects. The cause of Chickenpox (Varicella) via primary infection and Shingles (Zoster) via recurrence Spread through air droplets or direct contact with active lesions.

Pathogenesis and Clinical features of HHV3 infection (Primary infection-Chickenpox) infection

Chickenpox represents the primary infection with VZV; latency follows, and recurrence is possible as Shingles/Herpes Zoster, often after many decades. Most cases of chickenpox arise between ages of 5 and 9 Incubation period 14 to 21 days (average 15 days) Followed by fever, malaise, pharyngitis, cervical lymphadenopathy and rhinitis (less common in older children and adults) Followed by a characteristic rash that begins on face and trunk, followed by involvement of extremities.

Clinical features of HHV3 (Primary infection) continued

Each skin lesion undergoes stages of erythema>papules>vesicle>hardened crust. Centrally located vesicle is surrounded by a zone of erythema (dewdrop on a rose petal) and often occurs in crops. Lesions typically continue to erupt for 4 days. Affected persons are contagious from 2 days before rash until all the lesions crust. Severity of skin involvement is variable. Complications may include secondary skin infections, encephalitis, cerebellar ataxia, pneumonia, Reye syndrome and more. Infection during pregnancy can produce congenital or neonatal chickenpox and early in pregnancy can result in spontaneous abortion or congenital effects. Immunocompromised patients the infection can be severe

Oral lesions associated with Primary HHV3 infection

Common and may precede the skin lesions. Lesions indistinguishable from HSV1 Lesions begin as 3-4mm white opaque vesicles 3that rupture to form 1-3mm ulcerations. 1Palate and buccal mucosa involved most frequently. Gingival lesions resemble those of primary HSV but are relatively painless and no associated gingivitis.

Diagnosis
Clinical Can usually be made from a history of exposure to VZV within the last 3 weeks and presence of typical rash. Confirmation Obtained through the demonstration of viral cytopathological effects present within the epithelial cells harvested from vesicular fluid. Cytologic alterations are virtually identical to those described for HSV. Antibody titre Serum samples taken to demonstrate significant increase in antibody titers. Rapid diagnosis Rapid diagnosis from fluorescein-conjugated VZV monoclonal antibodies can fluoresceinbe performed.

Treatment and Prognosis

Primarily symptomatic-similar to HSV1 infection symptomaticWarm baths with soap or baking soda + calamine lotion and systemic diphenhydramine used to relieve pruritis Antipyretics other than aspirin to reduce fever Antiviral medication not recommended in immunoimmunocompetent children with uncomplicated chickenpox In immunocompromised patients varicella-zoster varicellaimmunolobulin (VZIG) can be given to modify the clinical manifestations of the infection Vaccine is effective and is given routinely between 121218 mnths

Pathogenesis and Clinical features of HHV3 recurrence (Shingles/Herpes Zoster)

After initial infection with VZV (chickenpox), the virus is transported up the sensory nerves and establishes latency in the dorsal spinal ganglia Clinical evident herpes zoster occurs after reactivation of the virus, with the involvement of the distribution of the affected sensory nerve Occurs during the lifetime of 10-20% of individuals and prevalence of attack 10increases with age Immunosuppression, treatment with cytotoxic drugs, radiation, presence of malignancies, old age, alcohol abuse and dental manipulations are predisposing factors for reactivation

Clinical features of HHV3 recurrence (Shingles/Herpes Zoster) continued

3 phases prodromal, acute and chronic Prodromal phase During initial viral replication, active ganglionitis develops with resultant neuronal necrosis and severe neuralgia. This inflammatory reaction is responsible for the prodromal symptoms of intense pain that precedes the rash in more than 90% of cases. May be accompanied by fever, malaise and headache normally present 1 to 4 days before development of cutaneous or mucosal lesions. Pain may also be present as sensitive teeth, otitis media, migraine headaches; depending on the dermatome affected. (10% may have no prodromal pain). Virus travels down nerve and pain intensifies. Pain has been described as burning, tingling, itching, prickly. Pain develops in the area of the epithelium innervated by the affected sensory nerve (dermatome). Usually one dermatome affected, but involvement of two or more can occur

Acute phase:
Begins as the involved skin develops clusters of vesicles set on an erythematous base. Within 3-4 days vesicles become pustular and ulcerate, with crusts 3developing after 7-10 days. Lesions tend to follow path of affected nerve and 7terminate at midline. Rash resolves within 2-3 weeks in otherwise healthy 2individuals. On healing, scarring with hypopigmentation or hyperpigmentation is not unusual. Oral lesions occur with trigeminal nerve involvement and may be present on movable or attached mucosa. Lesions often extend to the midline and frequently are present in conjunction with involvement of the skin overlying the affected quadrant. Like varicella, individual lesions present as 1-4mm white 1opaque vesicles which rupture to form shallow ulcerations. Ocular involvement is not unusual. This may lead to significant morbidity, including permanent blindness. Facial paralysis has been seen in association with herpes zoster of the face or external auditory canal. canal.

Chronic phase: phase:

Many patients do not progress to the chronic phase This occurs when the neuralgia associated pain persists longer than 3 months after the initial presentation of the acute rash. This is termed post-herpetic neuralgia (in up to 15% of patients postand in at least 50% of patients older than 60 yrs) Pain described as burning, throbbing, aching, itching or stabbing, often with flares caused by light stroking of the area. Most neuralgias resolve within 1 year. Rare cases last for a long time.

Diagnosis:

Often made from clinical presentation Atypical cases viral culture (takes at least 24hrs) Cytologic smear shows cytopathological effects as seen in varicella and HSV Rapid diagnosis: use of direct staining of cytologic smears with fluorescent monoclonal antibodies for VZV

Treatment and prognosis:

Fever: antipyretics that do not contain aspirin Antipruritics like diphenhydramine to decrease itching Skin lesions kept dry and clean to prevent secondary infection Antibiotics to treat such secondary infections Systemic steroids Early therapy with anti-viral medications such as acyclovir, antivalacyclovir, famcyclovir, accelerate healing of cutaneous and mucosal lesions, reduce duration of acute pain and decrease duration of post herpetic neuralgia. (most effective if initiated within 72hrs after development of the first vesicle). vesicle). Once skin lesions have healed, neuralgia may become the worst aspect of the disease and often is most difficult to resolve successfully.

HHV4

HHV4 also known as Epstein-Barr Virus (EBV) EpsteinLike other HHVs, EBV remains in the host for life. Associated with a number of extra-oral intra-oral extraintralesions

Clinical features of HHV4 infection (Children)

Usually become infected through contaminated saliva on fingers, toys or other objects Exposure usually occurs by age 3 Usually asymptomatic. Children younger than 4yrs with symptoms most have, fever, lymphadenopathy, pharyngitis, rhinitis or cough and hepatosplenomegaly Children older than 4 yrs affected similarly, but lower prevalence of hepatosplenomegaly, rhinitis and cough

Clinical features of HHV4 infection (Adults)

Most symptomatic HHV4 infections arise in young adults. Spread is through direct salivary transfer, such as shared straws or kissing Young adults fever, lymphadenopathy, pharyngitis and tonsillitis (Infectious mononucleosis/Classic glandular fever) Adults older than 40 fever and pharyngitis are predominant (less than 30% demonstrate lymphadenopathy) Other possible significant complications include splenic rupture, thrombocytopenia, auto-immune hemolytic autoanemia and neurological problems with seizures

Infectious mononucleosis/Classic glandular fever

Syndrome of fever, malaise and lymphanopathy Commonly caused by EBV but may be caused by other infections 2 types exist Febrile type high fever with rubelliform rashes and sometimes jaundice Angiose type (Has oral features) sore throat, petechiae at the junction of the hard and soft palate, whitish exudate on the tonsils, tonsils, pharyngeal oedema, occasional mucosal or gingival ulceration Rare enlargement of parotid lymphoid tissue that may lead to facial nerve palsy Sometimes IM may be associated with cervical lymph node enlargement and splenomegaly

Diagnosis of Infectious mononucleosis

Suggested by clinical presentation and should be confirmed through laboratory procedures:

WBC count increased; differential count shows lymphocytosis Atypical lymphocytes usually present in peripheral blood Classic serologic finding in EBV is the presence of the PaulPaulBunnell heterophil antibody (rapid test for these antibodies is available and inexpensive). Children younger than 4 yrs frequently have negative results. If Paul-Bunnell is negative :- indirect immunofluorescent Paul:testing to detect EBV-specific antibodies EBV-

Treatment and prognosis:

No specific treatment Most cases of infective mononucleosis resolve within 4-6 weeks NonNon-aspirin containing antipyretics and NSAIDs can be used to minimize most common symptoms Patients with significant enlargement of spleen should avoid contact sport to prevent rare possibility of splenic rupture NB treatment of pharyngitis and tonsillitis with ampicillin and penicillin should be avoided because use of these drugs in IM has been associated with higher than normal prevalence of allergic skin rashes Many suggest corticosteroids but leads to immunosuppression and the immune-system is important for fighting infection. immuneCorticosteroid use produces a shortened duration of fever and shrinkage of enlarged lymphoid tissues but its usage should be restricted to life-threatening cases life-

Other conditions caused by HHV4

Chronic EBV disease; persistent infection, 25-40yrs, malaise, disease; 25fatigue, fever, resemble multiple sclerosis, negative PaulPaulBunnell test Duncans disease; rare, severe mononulceosis, immunoblastic disease; sarcoma or lymphoma Burkitts lymphoma predominantly in Africa, children < 12 yrs age, massive swellings affecting mandible, pain, paraesthesia, bone destruction, chemotherapy effective Oral hairy leukoplakia predominantly HIV infected individuals

Viral Induced oral lesions 2

Department of Oral Medicine and Periodontology Faculty of Dentistry University of the Western Cape
Lecture Notes 2011

HHV5

Also known as Cytomegalovirus Similar to other HHV (ie. after initial infection, latency and reactivation is possible under favourable conditions). CMV can reside in salivary gland cells, endothelium, macrophages and lymphocytes. Most disease is found in neonates or in immunosuppressed adults Infants contracted through placenta, during delivery or breast feeding Adolescence predominantly from sexual activity Also has been from blood transfusion and organ transplantation

Clinical features of HHV5 infection

90% are asymptomatic Neonatal infection infant ill within a few days. Hepatosplenomegaly, thrombocytopenia (with petechial hemorrhages) and encephalitis leading to severe mental and motor retardation. Acute adult infection clinical pattern similar to that of infectious mononucleosis. Fever, malaise, myalgia, abnormal liver function tests and atypical peripheral lymphocytes. Third of patients demonstrate pharyngitis and lymphadenopathy Rare immunocompetent patients may show signs of an acute sialadenitis that of all major and minor salivary glands. Presents as xerostomia, pain and enlargement of parotid and submandibular glands

Diagnosis and Treatment options

Combination of the clinical features and other examinations Biopsy : Recommended for chronic ulcerations that are not responsive to conservative therapy. Specific verification by electron microscopy, viral antigens by immunohistochemistry, viral culture and rising antibody titers Most CMV infections resolve spontaneously. Therapy is often required in the immuno-suppressed immunopatient. patient. Ganciclovir is the drug of choice

The Enteroviruses

Encompasses the poliovirus, coxsackievirus A and B, echovirus and groups. Unlike HHV all lack the ability to cause latent infection!!!! Most are asymptomatic and subclinical. subclinical. When symptomatic they are associated with rashes. Infections may arise at any age, but most occur in infants and young children.

Pathogenesis and Clinical features of The Enterovirus Infections

Transmitted via fecal-oral route. During the acute phase of infection, fecalthe virus can also be transmitted through saliva or respiratory droplets. Only Herpangina, Hand-Foot-andMouth Disease and Acute Hand-Foot-and Lymphonodular Pharyngitis are discussed. All 3 are related closely discussed. and should not be considered as entirely separate infections. A1Herpangina usually produced by coxsackie A1-6, 8, 10 or 22. Certain other coxsackie As, Bs, echo- or enterovirusses may also echopresent the infection. Hand-foot-andHand-foot-and-mouth disease usually caused by coxsackie A16, but again some of the other groups may cause the disease.

Herpangina

So called because it resembles the lesions of HHV Most cases are mild or sub-clinical. subBegins with an acute onset of sore throat, dysphagia and fever, occasionally accompanied by cough, rhinorhea, anorexia, vomiting, diarrhea, myalgia and headache Small number of oral lesions, usually two to six, develop in the posterior area of the mouth, usually behind the hard-soft palate hardjunction in the area of the tonsillar pillars Affected areas begin as red macules, which form fragile vesicles that rapidly ulcerate. (average 2-4mm in diameter) 2Unlike HHV they DO NOT CLUSTER Systemic symptoms resolve within a few days Ulcerations usually take 7-10 days to heal 7Treatment: Mostly symptomatic, Analgesics, Antihistamines and Fluid intake

Hand-foot-andHand-foot-and-mouth disease
Most well known enterovirus infections Like herpangina, the skin rash and oral lesions typically associated with flu-like flusymptoms (sore throat, dysphagia, fever). Occasionally accompanied by cough, rhinorrhea, anorexia etc. Name describes location of lesions Oral lesions and those on hands almost always are present; involvement of other skin sites is more variable Oral lesions arise without prodromal symptoms and precede the development of cutaneous lesions sore throat and mild fever present Cutaneous lesions range from few to dozens and primarily affect the borders of the palms and soles and ventral surfaces and sides of fingers and toes. (rarely other sites) Cutaneous lesions begin as erythematous macules, that develop central vesicles and heal without crusting.

Oral lesions resemble those of herpangina but may be more numerous and are not confined to the posterior areas of the mouth. (numbers range from 1-30). 1Most common on buccal mucosa, labial mucosa and tongue, but any area of oral mucosa may be involved. Keratinized tissue such as hard palate and gingiva NOT typically involved Individual vesicular lesions rapidly ulcerate and are typically 2-7mm in diameter. Most resolve within 1 2week.

Acute Lymphonodular Pharyngitis

Characterized by sore throat, fever, and mild headache,which may last from 4-14 days 4Low numbers of yellow to dark pink nodules develop on the soft palate or tonsillar pillars. Nodules represent hyperplastic lymphoid aggregates and resolve within 10 days without vesiculation or ulceration

Diagnosis and Management

Diagnosis: Diagnosis from clinical presentation

Atypical presentation laboratory confirmation. Viral isolations from culture can be performed and analysis of stool specimens is best technique in patients with only mucosal lesions. Culture of cutaneous lesions is best for diagnosis of hand-foot-and-mouth disease hand-foot-and-

Management: In most instances, the infection is self-limiting and without selfsignificant complications. Directed at symptomatic relief. relief.

Measles (Rubeola)
Aetiology and Pathogenesis

Highly contagious viral infection caused by a member of the paramyxovirus family of viruses (measles virus) (measles virus) RNA virus related structurally and biologically to orthomyxovirus family, which cause mumps and influenza (flu) Virus spread by airborne droplets through respiratory tract Not related to German measles (Rubella) caused by virus of togavirus family, but may share some clinical features

Clinical features

Predominantly a disease of children, often seasonally Incubation period of 7-10 days 7prodromal symptoms of fever, malaise, coryza (nose cold), conjunctivitis, photophobia and cough develop. In 1-2 days, pathognomonic, small, erythematous 1macules with white necrotic centers appear in the buccal mucosa called Kopliks spots These spots usually precede the characteristic, maculopapular skin rash of measles (head and neck, followed by trunk and extremities) Complications : encephalitis and thrombocytopenic purpura. purpura. Secondary infection may develop as otitis media or pneumonia

Diagnosis and Treatment

Diagnosis
Clinical signs and symptoms Also laboratory confirmation can be made through virus culture or serological tests for antibodies to measles Presently measles is part of a vaccination program

Treatment
Supportive therapy of bed rest, fluids, adequate diet analgesics

VerrucalVerrucal-Papillary lesions
Oral squamous papilloma / Oral verruca vulgaris  Condyloma acuminatum  Focal Epithelial Hyperplasia


Site specific white lesion



Hairy Leukoplakia

Systemic virus affecting salivary glands



Mumps

Viral induced Verrucal-Papillary Verrucallesions

Oral Squamous Papilloma / Oral Verruca Vulgaris

Oral squamous papilloma is a generic term that includes papillary and verrucal growths composed of benign epithelium and minor amounts of supporting connective tissue It is the most common papillary lesion of oral mucosa (including vermilion)

Pathogenesis
Aetiology

Human Papilloma Virus. A DNA virus (Papovavirus group) Some oral squamous papillomas have been shown to be associated with the same human papilloma virus (HPV) subtype that causes cutaneous warts (subtypes 2, 6, 11) Other oral papillomas have been associated with different HPV subtypes Actual synthesis or replication of HPV occurs within the nuclei of epithelial cells as a result of stimulation of cellular DNA synthesis

Clinical features
Oral squamous papillomas may be found on the vermilion portion of the lips and any intraoral mucosal site, with predilection for the hard and soft palates and the uvula (latter three sites are most common) Lesions generally measure less than 1cm and appear as exophytic granular to cauliflower-like surface alterations cauliflowerUsually solitary in their presentation, although on occasion, multiple lesions may be noted. Lesions are generally asymptomatic

Diagnosis and Management

Differential diagnosis When solitary: verruciform xanthoma, warty dyskeratoma and acuminatum Verruciform xanthoma: distinct predilection for gingiva and alveolar ridge Warty dyskeratoma (Dariers disease): generally multiple Condyloma: usually larger with broader base Treatment and prognosis Infectivity of HPV is of low order Route of transmission is unknown for oral lesions, although direct contact would be favoured Surgical removal is treatment of choice excision or laser ablation. Recurrence is rare

Condyloma acuminatum

Infectious lesion characteristically located in the anogenital region but may involve the oral mucosa Common warm, moist squamous epithelial surface Increasing frequency within AIDS group of patients Aetiologically related to HPV subtypes 6 and 11 Early condyloma acuminatum formation group of multiple pink nodules that grow and ultimately coalesce

Result is a soft, pedunculated to sessile, exophytic papillary growth that may be keratinized or non-keratinized nonAt times may be rather extensive, but are generally self-limiting selfTreatment is generally simple surgical excision, including cryotherapy and laser ablation. Recurrences are common

Focal Epithelial Hyperplasia

Identified as a distinct entity in 1965 Early studies described lesions in American Indians and Eskimos Recent studies have identified other populations and ethnic groups including South Africans, Mexicans and Central Americans A rare disorder

Aetiology and Clinical Features

Aetiology and Pathogenesis

Definitive cause unknown Theories range from local low-grade irritation to vitamin lowdeficiencies Recently convincing evidence indicated that HPV subtype 13 plays an important aetiologic role, with suggestions that genetic factors are involved Characterized by the presence of multiple nodular soft tissue masses distributed over the oral mucosal surfaces, especially buccal mucosa, labial mucosa and tongue Lesions may appear as discrete papules or as clusters of papules, often similar in colour to the surrounding mucosa

Clinical features

If found in areas of occlusal trauma, they may appear whitish Lesions are asymptomatic and are often discovered incidentally. Initially described in children, this condition is now known to affect a wide age range with equal gender distribution

Diagnosis and Treatment

Differential diagnosis

Would include verruca vulgaris and muliple squamous papillomas Lesions of Dariers disease Oral manifestation of Crohns disease Pyostomatitis vegetans

Treatment

No particular treatment indicated, especially with widespread involvement Surgical removal may be used if few lesions are present Spontaneous regression has been noted in many cases

Viral induced-Site specific white inducedlesions

Hairy Leukoplakia
Aetiology and pathogenesis

Unusual white lesion along the lateral margins of the tongue Evidence that this form of leukoplakia represents an opportunistic infection related to the presence of the EpsteinEpsteinBarr virus (a herpes virus) This lesion has been associated with the subsequent or concomitant development of the clinical and laboratory features of AIDS in up to 80% of cases Have also been found in other patients (non AIDS) who are immunosuppressed

Clinical features

Clinical appearance can be quite variable, with unilateral and bilateral presentations Irregular surface contour that is often folded or corrugated is characteristic Other lesions may be smooth or macular Vast majority have been located along the lateral margins of the tongue Less commonly, lesions have extended onto the dorsal surface of the tongue and rarely onto the buccal mucosa, floor of the mouth, or palate In general, no associated symptoms, although a suprainfection with Candida albicans might appear

Differential diagnosis and Management

Differential diagnosis

Idiopathic leukoplakia Leukoplakia associated with tobacco use Lichen planus Chronic hyperplastic candidiasis

Treatment and prognosis

Critical for this diagnosis to be confirmed after its clinical identification No specific treatment for hairy leukoplakia HIV+ patients: probability of AIDS developing in in individuals with hairy leukoplakia is nearly 50% at 16 months and up to 80% by 30 months

Systemic Virus affecting Salivary Glands

Mumps
An infectious, acute viral sialadenitis primarily affecting the parotid glands Most common of all salivary gland diseases with a year-round yearendemic pattern (seasonal peaks noted = late winter / spring)

Aetiology

Paramyxovirus 2-3 week incubation period precedes clinical symptoms Transmission by direct contact with salivary droplets

Clinical features

Patients develop fever, malaise, headache and chills in addition to pre-auricular pain preSalivary glands, usually parotid, demonstrate 70% of bilateral infection Swelling of glands reaches maximum proportion within 2-3 2days Dimunition of swelling noted approximately 10 days after onset of symptoms M=F (especially children and young adults)

Possible complications

Adults may develop orchitis or oophoritis which can occasionally result in sterility Mumps is a systemic infection and may involve glandular and other tissues in the body including liver, pancreas, kidneys and nervous system Severe local pain often noted; especially on jaw movement Stensens duct may become partially occluded as the gland swells, with sharp pain secondary to stimulation of secretory mechanism by food or drink

Differential diagnosis and Treatment

Differential diagnosis

Bacterial infections: Acute bacterial infection usually presents as suppurative parotitis with tenderness, redness of skin overlying glands and pus suppuration from ductal opening Salivary calculi may produce swelling Salivary glands may be enlarged in sarcoidosis, lymphoma, Sjgrens syndrome

Treatment and prognosis

Symptomatic therapy and bed rest with analgesics Complete recovery is generally the rule Uncommon: nerve deafness and bilateral testicular atrophy Prophylactic vaccine available

The end
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