answer sheet for lab 1

7/28/2019 Answer Sheet for Lab 1

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Dr. Tahani Abualteen

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Infections of the Oral Mucosa

LAB 1

Slide 5:1- Acute Herpetic Gingivostomatitis (primary infection of HSV)2- Herpes Simplex Virus type I (Most frequent cause of viral infections of the mouth)3- Transmitted by droplet spread orcontact with the lesion4-

5 days incubation period, then: 2 days of systemic Prodromal symptoms (acute onset ofmalaise, fever and lymphadenopathy)

the disease process may stop here (subclinical case) or it may continue to result in:

Multiple small vesicles (which can occur on any partof the oral mucosa andlips "keratinized& non-keratinized") with widespread gingival inflammation

Vesicles soon ulcerate Circumoral crustinglesions on the lips may occur when the exudates start to dry This infection is a self-limiting infection that usually takes 10-14 days to resolve

5- Majority of cases are subclinical6- Extraoral lesions may also be present, particularly in children (for example: vesicles may occur on

skin of chin as a result of drooling of saliva and on nail bedof fingers "herpetic whitlow" as a result

of sucking, and on eyes as a result of rubbing)

7- Following the primary infection, immunity to HSV develops but it does not fully protect againstrecurrent infections (but symptoms may be absent/minimal)

8- Shows an intraepithelial vesicle (within the thickness of epithelium NOT subepithelial) The vesicle results from degeneration and rupture of the virally infected epithelial cells A characteristic finding in herpetic infections (particularly herpes simplex and Varicella zoster) is

the ballooning degeneration which is acantholysis in the prickle cell layer due to viral

infection and which result in the formation of Tzanck cells which are large swollen infected

cells that have eosinophilic cytoplasm and large pale vesicular nuclei (nuclei with thin and

dispersed chromatin)

Enlarged, multinucleated epithelial cells may result from fusion of infected cells9- The virus gains access to the sensory axons of the trigeminal nerve and remains latent there (its

DNA transcription is blocked)

10- Supportive/symptomaticanalgesics to relieve pain Acyclovirin advanced cases

Slide 12:1- Recurrent herpes labialis (secondary infection of HSV)2- Herpes Simplex Virus type I (Most frequent cause of viral infections of the mouth)


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3- Reactivation of the virus which, following the primary infection, has remained latent in the

sensory ganglion of trigeminal nerve

Recurrence (viral reactivation) may be brought by a number of predisposing factors:o

Factors that may alter or suppress immunity (e.g. Menstruation, old age, stress, febrileillness "common cold", immunosuppressive drugs, AIDS )

o Factors that may damage the epithelial cells(e.g. mechanical trauma, UV light )4-

Systemic symptoms are usually absent in recurrent infections because of the immunity acquiredat the primary infection

Recurrent infections may result in asymptomatic shedding of HSV into the oral cavity or in localProdromal symptomsprior to vesicles eruption (e.g. tingling, itching, burning, or paresthesia)

After that patients develop clusters of vesicles and ulcers

Herpes labialis is usually unilateral Vesicles soon rupture and become crusted, and they usually heal within a week

5- If the patient recognizes the recurrent herpes labialis in the Prodromal stage (at the period of tinglingand burning sensation prior to vesicles eruption), then he may benefit from topical application of

alcohol, ice, or acyclovir as it is thought that these agents may lessen symptoms or they may shorten

the infection period

6- Recurrent intraoral lesions occur occasionally, almost always on the hard palate or gingiva(keratinized areas) and usually unilateral

7- This patient can transmit the virus to another one and cause primary infection if the recipient hasnever been exposed to the virus beforeThis recipient can't develop secondary infection immediately because secondary infection needs the

virus to be already latent there and then reactivated

8- Same as the previous case Slide 14:

1- Chickenpox (primary infection of VZV)2- Varicella zoster virus3- Transmitted by droplet spread orcontact with the lesion4-

The lesions of chicken pox may be found on the oral mucosa especially thesoft palate and mayprecede the characteristic skin rash

Lesions present as macules, papules, vesicles, or ulcerson skin and oral mucosa Systemic Prodromal symptoms may arise (acute onset of malaise, fever and lymphadenopathy) Skin lesions are pruritic & usually start in the trunk Oral lesions are usually asymptomatic

5- Following the primary infection, immunity to VZV develops but it does not fully protect againstrecurrent infections

6- Identical to HSV


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7- The virus gains access to the sensory axons of the trigeminal nerve and remains latent there (itsDNA transcription is blocked)

8- Supportive/symptomaticantihistamines, topical lotions

Acyclovir

in advanced cases Vaccine is available

Slide 18:1- Shingles or Zoster (secondary infection of VZV)2- Varicella zoster virus3-

Reactivation of the virus which, following the primary infection, has remained latent in thesensory ganglion of trigeminal nerve

Recurrence (viral reactivation) may be brought by a number of predisposing factors:o Decreased immune-competence:

Elderly patientsImmunosuppressive drugs

Multiple recurrence is rare (repeated attacks of Zoster are unusual since they require muchmore powerful predisposing factors compared to those needed for HSV recurrent infections)

4- Prodromal symptoms ofpain and paresthesia may arise forup to 2 weeks Characterized by unilateral vesicular eruptionsextending over one or more branches of

trigeminal nerve (lesions are restricted to one side and may end sharply at the midline) Shingles is an extremely painful condition Lesions usually run a course of about 14 days

5- Recurrent intraoral lesions occur occasionally, almost always on the hard palate or gingiva(keratinized areas) and usually unilateral

6- This patient can transmit the virus to another one and cause primary infection if the recipient hasnever been exposed to the virus before

This recipient can't develop secondary infection immediately because secondary infection needs the

virus to be already latent there and then reactivated

7- Same as the previous case8-

Trigeminal Nerve involvement: Ophthalmic division is most frequently involved Involvement of the maxillary or mandibulardivisions results in facial and dental pain Intra, extra oral lesions or both

9- Complications of shingles/zoster:

Post herpetic neuralgia (due to fibrosis around the nerves) so that pain will continue evenafter lesions subside


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Oral lesions almost always present, characterized by shallow painful ulcers, they may resembleHerpangina but can be larger

The disease may be distinguished by the presence of hand and foot lesions Self-limiting, usually lasts for7-10 days

Slide 24:1- Measles (Rubella)2- Paramyxovirus3-

Occurs predominantly in children Prodromal symptoms may resemble common cold Koplik spots on the oral mucosa which usually disappear as skin rash starts so they may be

overlooked or passed unnoticed

Skin rash (start on face, then go to trunk)

4- Otitis media, pneumonia, encephalitis, brain damage Noma may be a complication in malnourished patients

Slide 27:1- Necrosis and crater-like, punched out ulceration of interdental papilla and gingival margins2- Necrotizing Ulcerative Gingivitis (NUG) OR Acute Necrotizing Ulcerative Gingivitis (ANUG)

* *Endogenous, polymicrobial opportunistic infection

3-

Overgrowth of endogenous flora (fusospirochaetal complex)4-

Sudden onset ofnecrosis and crater-like, punched out ulceration of interdental papilla andgingival margins

Ulcerated areas are covered with a grey-green psuedomembrane which is demarcated from thesurrounding mucosa by a linear Erythema

** The psuedomembrane consists ofnecrotic tissue debris, inflammatory exudate and bacteria

Gingival bleeding Pain or soreness of the gums Halitosis (foul breath) Salivation Lymphadenopathy Persistent form is associated with AIDS

5- Predisposing factors: Immunosuppression Trauma Pre-existing chronic gingivitis Association with AIDS

Malnutrition and poverty

Smoking


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Stress, fatigue Poor oral hygiene

6- Clinical picture Demonstrating the fusospirochaetal complex in a gram-stained gingival smear

7- Chronic marginal gingivitis (but the punched-out necrotic papillae and the psuedomembraneguide the diagnosis)

8- Noma9-

Identify and eliminate the predisposing factor Gentle debridement of necrotic gingival tissue

Slide 29:1- Actinomycosis

** Endogenous, Polymicrobial, Chronic Suppurative (pus-forming) infection

2- Actinomyces species (Actinomyces israelli predominate)anaerobic gram positive bacteria3- Soft tissues of the submandibular region and neckare most commonly involved and Actinomyces

bacteria can gain access to this region through an infected root canal or lower third molar socket

4- Development offirm painless swelling which eventually softens and suppurates(accompanied

by the formation of pus which discharges through multiple sinuses)

These sinuses may release sulphur granules in the pus (yellowish granules composed of bacterialcolonies)

The multiple abscesses which eventually form tend to point on to the skin rather than themucosal surface and are accompanied by marked fibrosis of the surrounding tissues

5- Biopsy Demonstration of Actinomyces bacterial colonies in a culture

6- Granulomatous inflammationsurrounded by granulation tissue Transport of organisms by macrophages Central area of suppurative necrosis Characteristic featurebacterial colonies with radiating striae (rods) projecting into the

surrounding neutrophils

7- Long term high dose antibiotics (Penicillin or tetracycline) Slide 32:

1- Syphilis2- Treponema pallidum3- Primary syphilis:

Develops usually 2-3 week after the initial exposure to the bacteria


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Results in an ulcerreferred to as chancre which is characterized by: Shallow painless ulcer Indurated base Occurs at site of infection and is highly contagious

Usually occurs on genitaliabut in minority of patients may present on the oral mucosa(usually the lips & tongue)

Almost always associated with lymphadenopathy Heals spontaneously within 6 weeks Microscopically, the ulcer shows an ulcerated granulation tissue with dense mononuclear

infiltrate (composed mainly ofplasma cells)

4- Secondary syphilis: Develops usually about 6 weeks after the appearance of the primary chancre Characterized by:

Diffuse painless, maculopapular muco-cutaneous rash

30% have grayish mucosal necrosis which are called mucous patches Multiple mucosal patches may coalesce to produce lesions ofirregular outline called "snail-

track ulcers"

5- Tertiary syphilis (late-stage syphilis): Develops usually many years after the initial exposure to the bacteria Characterized by:

Gumma:- An area ofnecrosis associated with delayed type IV hypersensitivity reactions to

syphilitic antigens- Occurs especially on the hard palate leading to perforation into the nasal cavity- Histologically, Gumma consists of a central mass of Coagulative necrosis (no pus)

surrounded by granulation tissue infiltrated by macrophages and giant cells

Atrophic glossitis:- Atrophy and fibrosis of the tongue musculature due to endarteritis obliterans

(obliteration of arteries ends)

- This atrophy may be followed by Syphilitic leukoplakia Syphilitic leukoplakia:

- Hyperkeratosis- A premalignant lesion which may be followed by Sequamous cell carcinoma

Sequamous cell carcinoma6-

Infected mother will transmit the disease to her fetus since Treponema pallidum has the abilityto cross the placental barrier

Characterized by : Collapse of nasal bridge due to infection and destruction of the developing nasal bones

producing the saddle deformity of the bridge and thedished appearance of the face

Hutchinson triad (Blindness, deafness, dental anomalies)


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Dental anomalies related to congenital syphilis are caused by infection of the developingtooth germs of the permanent incisors and first molars and they include:

- Hutchinson incisors (also called notched teeth, screw-driver teeth): Incisors characterized by central notching of the incisal edge and a tapering

"screw-driver" appearance The maxillary central incisors are the most frequently involved

- Peg shaped laterals (conical and microdontic)- Moons or Mulberry molars:

Molars characterized by constricted atrophic cups with globular masses of hardtissue on their occlusal surface

The first permanent molars are the most frequently involved Slide 39:

1- Tuberculosis2- Mycobacterium tuberculosis3- Oral infection is not common, and oral lesions of tuberculosis may present as :

o Primary oral infectiono Secondary oral infection (associated with coughing-up of infected sputum from pulmonary

tuberculosis) and it is a more likely cause of oral lesions

4- Results in an ulcer referred to as "Classical TB ulcer" which is characterized by:

o Chronico Painlesso Induratedo Underminedo Covered with grayish-yellow slougho On the tongue

Other manifestations of Tuberculosis:o Gingival involvementgranulating gingival hyperplasiaso Tuberculouslymphadenitisgranulating cervical lymph nodes

5- Biopsy, to identify:o Granulomas with central necrosiso Acid Fast Bacilli

6- 2 antimicrobial agents: isoniazide and rifampicin for 4-8 months Slide 42:

1- Leprosy2- Mycobacterium leprae3- Two forms of infection exist:

o Tuberculoidlocalized infection (good immune response)o Lepromatouswidespread infection throughout the body (poor immune response)

4- Oral lesions occur almost exclusively in the Lepromatous type and they can be identified in 50% ofpatients


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4- Angular chelitis?5- Denture wearing and occlusal friction6- Lesions are seen most frequently on the buccal mucosa adjacent to the commissure of the lips7- Yes it can chronic multifocal oral candidosis8-

Non-homogenous leukoplakia (speckled/nodular)9- Biopsy (to confirm presence of hyphae and detect presence/degree of dysplasia)

10- Epithelium shows hyperkeratosis and prominent irregular acanthosis Candidal hyphae invade superficially into the Parakeratin layer, and NEVER penetrate

deeper into the prickle cell layer

Areas of atrophic epithelium may be present within the lesion and this is responsible for thespeckled erythematous appearance seen clinically

11-Yes it is a premalignant lesion for many reasons:

50% of lesions are associated with epithelial dysplasia

15% of lesionsprogress to true dysplasia Most of candidal Leukoplakias are non-homogenous Candida can generate carcinogens like nitrosamine

Slide 69:1- Chronic mucocutaneous candidosis (CMC) inherited or acquired condition, and may be

associated with endocrine disorders, or immunodeficiency

2- Oral mucosa is almost always involved3- Oral lesions resemble those seen in chronic hyperplastic candidosis BUT may involve any part of

the mucosa (not only the commissure area)

4- Yes it can Slide 82 & 83:

1- Hairy leukoplakia (secondary infection of EBV)2- EBV3-

Common in patients with late stage HIV infection, and its development may indicates theonset AIDS

Less common in non-HIV infected patients receiving immunosuppressive therapy (e.g. renaltransplant patients)

4- Presents as vertical white folds on lateral border of the tongue, with a raised, corrugated, or

hairy surface. However the lesions may also have a smooth flat surface

White folds can't be removed Occurs most frequently on the lateral borders of the tongue, bilaterally, but other areas of the

oral mucosa are affected

5- Candidal hyphae may be present but the candidosis is a secondary rather than a causal infectionbecause hairy leukoplakia has a rough surface that favors Candidal overgrowth


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6- NOT an idiopathic leukoplakia (since it has a recognizable cause and the term leukoplakia is used tosimply mean a white patch) & NOT a premalignant lesion

** Caused by opportunistic infection of the oral epithelium by EBV

7- Primary infection (eithersubclinically or as glandular fever) followed by latency in lymphocytesof oropharynx & salivary glands (Long term carrier state for EBV)

in immune-compromisedpatients followed by reactivation of the virus (continuous shedding of the virus from its latency

sites into saliva)leading to repeated re-infection of oral epithelial cells (especially those oflateralborder of the tongue)

** Infectious mononucleosis = primary infection of EBV

** Hairy leukoplakia = secondary infection of EBV (resulting from reactivation of the virus on

immune-suppression)

8- Minor trauma facilitates infection with virus (allows access of EBV from saliva to re-infectepithelial cells)

** Since lateral border of the tongue is frequently traumatized by biting/chewing (which damage

some of the cells), it is the most common site invaded by EBV upon secondary attacks

9- Marked reduction of langerhans cells10-Lateral border of the tongue11-

Acanthotic parakeratinized epithelium often with long finger-like surfaceprojections of Parakeratinproducing the hairy/corrugated appearance seen

clinically

Absence of inflammatory cells in epithelium and lamina propria Swollen or balloon cells with prominent cell boundaries in prickle cell layer below Parakeratin

Swollen cells contain EBV and have been described as "koilocyte-like cells,having smalldarkly staining nuclei and perinuclear vacuolization"

The term "koilocyte" should be confined to cells infected with HPV Slide 85:

1- Kaposis sarcoma2- Associated with infection by herpes virus referred to as HHV8 which appears to have a causal role3- Commonest tumor associated with AIDS (its prevelanact is now low, particular for patients on

HAART)

4- More common in males than in females Multifocal tumor (multiple lesions) involving skin & mucosal surfaces Presents first as reddish-purple patches (surface lesion) which then become nodular (soft tissue

enlargement)

Oral lesions may be the presenting feature and are seen most frequently on the palate Tip of the nose is the most frequent skin/facial site May be resistant to treatment (no curative treatment!) Recurrence BUT NO metastasis

5- Despite its name, it is not considered a true sarcoma (not a tumor arising from connective tissue) BUTit is a malignant neoplasm of endothelial cells (which are the cells lining blood vessels)


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6- Proliferating endothelial cells Cleft like vascular channels Extravasated RBC Inflammation Occasional atypical cells

Later stages more atypical cells Early stages difficult to differentiate it from other vascular lesions

7- Hemangioma & Pyogenic granuloma Slide 89:

1- HIV-Gingivitis (linear gingival Erythema)2- It may represent gingival hyperemia due to the release ofvasoactive cytokinesrather than gingival

inflammation3- Has been associated with Candida albicans


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answer sheet for lab 1

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