Oral ManifestationS of HIV1 Main.pptx Last Save to Big Lappy.pptx EDITED.pptx11 (3)

7/28/2019 Oral ManifestationS of HIV1 Main.pptx Last Save to Big Lappy.pptx EDITED.pptx11 (3)

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BYDR IDAEWOR OPEYEMI EMMANUEL

ORAL MANIFESTATIONS OFHIV


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OUTLINE Introduction/History. Classification of oral meanifestations

of HIV. Clinical features. Differential diagnosis.

Diagnosis. Treatment. Prognostic Significance.


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INTRODUCTION :

History

The pandemic, acquired immunodeficiency syndrome (AIDS) wasfirst reported in 1981.By 1992 , 11 million people were said to be

affected. Already more than 30 million people have died of AIDS; 34million people around the world are living with HIV. The impact ofHIV is more severe in Africa ,esp sub-saharan Africa. South Africahas more people living with HIV than any other country in Africa.

The infection is lifelong and once acquired , can be transmitted toothers.

WHO classified 3 modes of transmission : sexual (horizontal) ,parenteral (innoculation of blood/blood products) , perinatal/vertical(from mother to fetus, before, during or after birth).

Haemophiliac patients and other transfusion patients are at risk.

The most serious consequence of HIV infection is the decline in thenumber and function of CD4+ T-cells.

Clinical symptoms appear as the virus destroys blood cells importantfor maintaining immunity.

Progressive destruction of immune function allows the developmentof opportunistic infections and neoplasms leading to AIDS.


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Oral lesions are frequent and varied and are among the firstsymptoms of the infection .

The presence of pseudomembranous oral candidiasis and

hairy leukoplakia indicates a strong likelihood that theinfection is progressing towards AIDS.

Early indicators of immunodeficiency occur in the oral cavity.

Careful history taking and detailed examination of the

patients oral cavity are important parts of the physicalexamination.

Early recognition , diagnosis , and treatment of HIV-associated oral lesions may reduce morbidity.

Effect of HAART on oral manifestations include: significant

reduction in oral hairy leukoplakia, necrotizing ulcerativeperiodontitis ; no significant reduction in candidiasis, oralulcers , Kaposis sarcoma.; increases salivary gland disease ,oral warts; and reduction of oral lesion from 47.6% to 37.5%

Transmission of HIV via aerosol in the dental office has notbeen documented.


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CLASSIFICATION OF ORAL

LESIONS ASSOCIATED WITH HIV.Strongly associated with HIV(Group 1)

Less commonly associatedwith HIV (Group 2)

Candidiasis angular cheilitis

,pseudomembranous ,

erythematous , hyperplastic

candidiasis.

Hairy leukoplakia

Linear gingival erythema

Necrotizing ulcerative gingivitis

Necrotizing ulcerative

periodontitis

Kaposis sarcoma

Non-Hodgkins lymphoma

Viral infections :

cytomgalovirus

herpes simplex virus human papillomavirus

verucca vulgaris

varicella zoster virus zoster ,varicella

Salivary gland disease xerostomia;salivary gland swelling

Thrombocytopenic purpura

Recurrent Aphthous ulcers

Melanotic hyperpigmentation

Cryptococcosis

Histoplasmosis


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Group 3. Lesions possibly associated with HIVinfection.

Bacterial infections (excludinggingivitis/periodontitis):

Actinomyces israeli

Enterobacter cloacae Escherichia coli

Klebsiella pneumoniae

Mycobacterium avium intracellulare Cat-scratch disease

Drug reaction (ulcerative , erythema

multiformes , lichenoid reaction).


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exacerbation of atypical periodontitis

Fungal infections other than candidiasis :

Aspergillus flavusGeotrichum candidum

Mucoraceae

Neurologic disturbances : Facial palsy

Osteomyelitis

Sinusitis

Submandibular cellulitis

Squamous cell carcinoma

Toxic epidermolysis

Neutropenic Ulceration.


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FUNGAL LESIONS

Oral Candidiasis :

Introduction

Most commonly associated with Candida albicans.

Other species such as C. glabrata and C. tropicalis arefrequently part of the normal oral flora. NB: Candidaglabrata is intrinsicaly azole-resistant (fluconazole).

Fluconazole is the most widely used systemic agent formoderate and severe disease.

Itraconazole, Voriconazole, posaconazole (oral suspension)are reserved for cases of fluconazole resistance.

Factors associated with azole-resistant disease include priorexposure to azoles , low CD4+ cell count , and presence ofnon-albican species.

Most persons with HIV infection carry a single strain ofCandida during clinically apparent candidiasis and when

candidiasis is quiescent.


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-Factors which predisposes patients to developcandidiasis include : infancy , old age, antibiotic

therapy, steroid and other immunosuppressivedrugs, xerostomia, anemia, endocrine disordersand primary and acquired immunodeficiency.

- Reports describe oral candidiasis during theacute stages of HIV.

- occurs with falling CD4+T-cell count in middleand late stages of HIV disease.

- The 3 common presentations of oral candidiasisare angular cheilitis, erythematous candidiasisand pseudomembranous candidiasis.


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Angular cheilitis

Presents as erythema or fissuring either

unilaterally or bilaterally at the corners of themouth .

It can occur with or without erythematous or

pseudomembranous candidiasis. It can persist for an extensive period of time if

left untreated.

Treatment involves the use of a topicalantifungal cream applied directly to the affectedareas 4 times a day for 2-week treatment period.


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Erythematous Candidiasis

May be the most underdiagnosed and misdiagnosed oralmanifestation of HIV disease.

The condition presents as a red , flat , subtle lesion on thedorsal surface of the tongue or on the hard or soft palates

May present as a kissing lesion if a lesion is present onthe tongue , the palate should be examined for a

matching lesion and vice versa. Lesion tend to be symptomatic; presenting complaints

include oral burning, most frequently while eating salty orspicy food or drinking acidic beverages.

Clinical diagnosis is based on appearance , as well as onthe patients medical history and virologic status.

The presence of fungal hyphae or, more likely,blastopores can be confirmed by performing a potassium

hydroxide (KOH) preparation.


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Pseudomembranous Candidiasis (oral thrush)

Appears as creamy, white ,curd-like removable

plaques on the oral mucosa are caused byovergrowth of fungal hyphae mixed withdesquamated epithelium and inflammatory cells

Occurs on the buccal mucosa, tongue, and other

oral mucosal surfaces. It may involve any part of thepharynx.

The plaques can be wiped away ,typically leaving ared or bleeding underlying surface.

The most common organism involved is Candidaalbicans species.

For both pseudomembranous and erythematouscandidiasis lesion, diagnosis is based on

appearance.


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Hyperplastic Candidiasis.

Unusual in persons with HIV infection.

Lesions appear white and hyperplastic. The white areas are due to hyperkeratosis,

and , unlike the plaques ofpseudomembranous candidiasis, cannot beremoved by scraping.

Lesion may be confused with hairyleukoplakia.

Diagnosis of hyperplastic candidiasis is madefrom histologic appearance of hyperkeratosisand the presence of hyphae .

Periodic acid-Schiff (PAS) stain is often used

to demonstate hyphae.


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Differential diagnosis

Erythematous candidiasis should be

differentiated from other red lesions , such asKaposi s sarcoma or erythroplakia.

Inflamatory responses often associated with

Candida infection may be absent inimmunocompromised patients

The creamy white plaques ofpseudomembranous candidiasis are removablewhile the white lesions of hairy leukoplakia arenon-removable.

Di i


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Diagnosis

Candidiasis is diagnosed by its clinical appearance andby detection of organisms on smears.

Specimen collection : smears are taken by gently drawinga wooden tongue depressor across the lesion. Thespecimen is then transferred into a drop of KOH on aglass slide and protected by a cover slip.

The smear is examined under the microscope and Candida

is detected by finding hyphae and blastospores theyare rarely seen in healthy individuals in carrier state

Culture media: cultures are grown on specific media,such as Sabourauds agar culture is useful forestablishing Candida species but not diagnosis.

Treatment

Maybe treated either topically or systemically;treatment should be maintained for at least 2 weeks toreduce organism colony-forming units to levels lowenough to prevent recurrence.


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Topical treatment

Preferred because they limit systemic absorption butthe effectiveness depends on patients compliance.

Topical medication requires the patient to hold themedication in the mouth for 20 to 30 minutes.

If the patient uses sweetening formulation, considerthe concurrent treatment daily fluoride rinse

(fluorigard) for 1 min once a day and thenexpectorated.

Topical medications include clotrimazole (oral troche, 10mg tablet)

Nystatin preparation include suspension, a vaginaltablet , and oral pastille (200,000 units) dissolvedslowly in the mouth.

Amphotericin B (0.1mg/ml). 5 to 10 ml of oral solutionis used as a rinse and then expectorated 3 to 4 times

daily.

Systemic treatment


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Systemic treatment

Effective agents include:

Ketoconazole (Nizoral) , 200mg tablet taken with food once daily. Carefulmonitoring of liver function is necessary for long-term use.

Fluconazole (Diflucan) is a triazole antifungal agent effective in treatingcandidiasis (100mg tablet taken once daily for 2 weeks)

Itraconazole (100mg capsule) may also be used (200mg daily orally for 14days).

Voriconazole (200mg tab): take I tablet twice daily for 2 weeks.

Fluconazole-resistant C. albicans has stronger attachment to tissues , more

difficult to wipe away than azole-susceptible candidiasis. Ketoconazole, fluconazole, and intraconazole may interact with other

medications including rifampicin, rifabutin, ritonavir, efavirenz (all arepotent CYP450 inducers ) phenytoin, cyclosporin A, terfenadine, digoxin,coumarin-like medications , and oral hypoglycemic medications.

Prognostic factors

both erythematous and pseudomembranous oral candidiasis areassociated with increased risk for the subsequent development ofopportunistic infections and correlates with falling CD4+T-cell counts.


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Histoplasmosis

may initially present in the oral cavity.

These lesion appears as ulcerations that canaffect any mucosal surface.

Diagnosis requires biopsy.

Cryptococcus Neoformans.

it may cause an ulcerated mass in the hard

palate.


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No major histocompatibilty (MHC) antigen are expressed ; sothere is no T-cell response during latency.

Reactivation of virus may follow exposure to sunlight(fever

blisters ) , exposure to cold (cold sore) , trauma , stress , orimmunosuppression , causing a secondary or recurrentinfection

Recurrent oral herpes occurs at any age extraorally orintraorally.

Clinical features of Herpes simplex

Herpes labialis occurs on the vermilion border of the lips.

the patient may reports a history of itching or pain , followed

by appearance of small vesicles which ruptures and formcrust.

Recurrent intraoral herpes appears as clusters of painfulsmall vesicles that rupture and ulcerate and usually healwithin 1 week to 10 days.


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The lesion usually occur on the keratinized or fixed mucosa ,such as the hard palate , and gingiva .

Lesion may arise on the dorsal surface of the tongue.

Differential daignosis of herpes simplex

Rising antibody titer from initial and convalescent sera confirm

primary herpetic gingivostomatitis. Examining smears of lesions (treated with Papanicolau stain)

for multinucleated giant cells confirms recurrent herpes.

It is possible to demonstrate herpes simplex type 1 or type 2 by

applying monoclonal antibodies to smears from the lesions. Recurrent aphthous ulcers always appear on nonkeratinized

mucosa.

Recurrent intraoral herpes may appear more frequently in HIV-

infected patients. The lesion may be painful and slow to heal.


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Treatment

No treatment will permanently eradicate herpes

simplex infections , but acyclovir may shortenthe healing time for individual episodes.

The optimum oral dosage of acyclovir is 1000 to

1600mg daily for 7 to 10 days. Topical acyclovir is not useful for treating

intraoral lesions and may not be effective forlesions on the lips.

Foscarnet or phosphonoformate is used tocombat acyclovir-resistant strains.


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Prognostic Significance

There is no know association between

recurrent intraoral herpes and more rapidprogression of HIV disease.

However , there is clinical impression that

recurrent herpes simplex infection may bemore common in patients with symptomaticHIV disease.


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Herpes Zoster.

Primary varizella zoster virus infection in seronagativeindividuals are known as varizella or chickenpox

The reactivation of varizella zoster virus (VZV) causesherpes zoster (shingles).

Reactivation occurs in malignancy ( lymphoma,leukemias), drug administration ,radiation or surgery

of the spinal cord , local trauma, and HIV infection. The disease occurs in the elderly and the

immunosuppressed.

Oral herpes zoster generally cause skin lesions.

Following a prodrome of pain , multiple vesiclesappear on the facial skin , lips , and oral mucosa.

Skin and oral lesions are frequently unilateral andfollow the distribution of the maxillary and/ormandibular branches of the trigeminal nerve.


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The skin lesions form crusts and the oral lesionscoalesce to form large ulcers.

The ulcers frequently affect the gingiva , sotooth pain may be an early complaint.

The appearance of the lesions and their

distribution are pathognomic. Acyclovir limits the duration of the lesion.

For herpes zoster , the standard oral dosage is

800mg five daily for 7 to 10 days which isconsiderably higher than that recommended forthe treatment of herpes simplex.


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Human Papillomavirus Lesions

Oral warts, papillomas, skin warts , and genital

warts are associated with the human papillomavirus(HPV).

Lesions are common on the skin and mucousmembranes of persons with HIV disease.

Anal warts have recently been reported amonghomosexual men.

Because , the HPV types found in oral lesions inHIV-infected persons are different from the HPV

type associated with anogenital warts , the termcondylomata acuminata is not appropriate for oralHPV lesions.

Lesion may appear as solitary or multiple nodules.


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They may be sessile or pedunculated and appear asmultiple , smooth-surfaced raised massesresembling focal epithelial hyperplasia or asmultiple , small papilliferous or cauliflower-likeprojections.

HPV types 7, 13, and 32 have been identified in

some of these oral warts. A biopsy is necessary for histologic studies.

Prognosis

There is no association between oral HPV lesions

and more rapid progression of HIV disease.However , oral warts are seen more commonly inHIV-infected persons than in the generalpopulation.


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Treatment

oral HPV lesions can be removed surgically using

local anethetic. Carbon dioxide laser surgery can remove

multiple flat warts.

However , relapses occur and several repeatprocedures may be necessary.


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Cytomegalovirus

Oral ulcers caused by cytomegalovirus (CMV)

have been reported. This can appear on anymucosal surface.

It may be confused with aphthous ulcers,necrotizing ulcerative periodontitis and

lymphoma. Unlike aphthous ulcer, which usually have any

erythematous margin, CMV ulcers appearnecrotic with a white halo.

Diagnosis of CMV ulcer is made from abiopsy.Immunohistochemistry may also behelpful.


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CMV ulcer in the oral cavity usually occur inindividuals with disseminated CMV disease.

Diagnosis of CMV-infected oral ulcers should befollowed by examination for the systemicdisease.

CMV ulcers resolves when ganciclovir is used totreat CMV disease.


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Oral Hairy Leukoplakia and Epstein-Barr Virus

Presents as a non-movable, corrugated or hairywhite lesion on the lateral margins of the tongue.

It occurs in all risk groups for HIV infections,although less commonly in children than in adults.

It occurs in about 20 % of persons withasymptomatic HIV infection.

It becomes more common as the CD4+ T-cells countfalls.

HL is in group 4 , category C2 of the original Centerfor Disease Control (CDC) definition of AIDS and in

B3 of the 1993 Criteria. No report describes HL in mucosal sites other than

the mouth.

HL occurs in non-HIV infected people likerecipients of bone marrow, cardiac , and renaltransplants.


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Hairy Leukoplakia and Progression of HIV Disease.

Diagnosis of HL is an indication of both HIV infectionand immunodefiency.

It is an indication for a work-up to evaluate and treatHIV.

HL correlates with a statistical risk for more rapidprogression of HIV disease.

Progression to CDC-defined AIDS is more rapid in thoseHIV-infected persons with HL than in those without HL ,even after adjustment for CD4+ T-cell count

Pathogenesis

There is deletion of the EBNA 2 gene in hairyleukoplakia lesion (with Epstein-Barr virus).

Intraepithelial Langerhanss cells are reduced or absentin HL lesions which correlates with the presence of viralantigens.


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Clinical Appearance and Manifestations.

HL lesions vary in size and appearance; it may be

unilateral or bilateral. The surface is irregular and may have prominent

folds or projections, sometimes markedlyresembling hairs; occasionally , some areas maybe smooth or flat.

Lesion occurs most commonly on the lateralmargins of the tongue and may spread to coverthe entire dorsal surface

HL can spread onto the ventral surface of the

tongue and buccal mucosa (flat inappearance).Rarely , they occur on the softpalate.

HL usually does not cause symptoms.


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Differential diagnosis and Definitive diagnosis

Candida albicans may be found in association with HLlesions , and hyphae may seen in specimen taken from

lesions and examined using potassium hydroxide. HL should be distinguished from other white lesions such

as lichen planus , idiopathic leukoplakia , white spongenevus, dysplasia, and squamous cell CA.

HL should be diagnosed by biopsy for definitivediagnosis.

The typical microscopic appearance of HL includeacanthosis, marked parakeratosis with formation of

ridges and keratin projections, areas of ballooning cells(which contains pyknotic nuclei or perinuclear haloes),and little or no inflammation in the connective tissue.

Definitve diagnosis of HL requires demonstration of EBVusing in-situ hybridization performed on biopsyspecimen.


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Treatment

HL is usually asymptomatic and does not requiretreatment.

Usually resolves with onset of Highly ActiveAntiretroviral Therapy (HAART ).

Clinicians should arrange evaluation of HIV disease

and appropriate treatment for patients with HL . Due to the anti-EBV activity of acyclovir, dose of

acyclovir(2.5 to 3mg per day for 2 to 3 weeks)usually eleminates HL: lesion usually recur with

cessation of treatment. Case reports describe HL disappearing during

treatment with ganciclovir , zidovudine, andaerosolized pentamidine.


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BACTERIAL LESIONS

Periodontal Disease

Is a fairly common problem in both asymptomaticand symptomatic HIV-infected patients.

Takes 2 forms :

necrotizing ulcerative periodontitis ( rapid and

severe)

linear gingiva erythema ( precursor of NUP).

Their presenting clinical features often differ from

those in non-HIV-infected persons.

LGE and NUP often occur in clean mouths - where

there is very little plaque or calculus to account for

the gingivitis.


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Linear Gingiva Erythema (red band gingivitis)

It presents as red band along the gingival margin.

It is seen most frequently in association with anterior

teeth but commonly extendly to the posterior teeth..

It can also present on attached and unattached gingiva aspetechiae- like patches.

it is basically a rapid destruction of soft tissue.

In LGE , the gingiva may be reddened and edematous.

Patients sometimes complain of spontaneous bleeding.

In acute onset ulcerative gingivitis , ulcers occur at the tip

of the interdental papilla and along the gingival margins;ulcers often elicit complaints of severe pain.

The ulcer heal, leaving the gingival papillae with acharacteristic cratered appearance.


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Necrotizing Ulcerative Periodontitis

Basically, rapid destruction of hard tissues occur here.

It is a marker of severe immune suppression.

may present as rapid loss of supporting bone and softtissue.

Typically, these losses occur simultaneously with noformation of gingival pockets.

Sometimes involving only isolated areas of the mouth. Teeth may loosen and eventually fall out.

Uninvolved sites can appear healthy.

Necrotizing stomatitis may develop, and area of necroticbone may appear along the gingival margin.

The bone may eventually sequestrate.

Patients with NUP and necrotizing stomatitis frequentlycomplain of extreme pain and spontaneous bleeding,fetid odor, deep jaw pain.


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Treatment

Clinicians should refer patients to a periodontist ordentist for management.

The ff protocol has achieved reasonable success :plaque removal, local debridement (removal ofnecrotic tissues), irrigation with Betadine 10%solution (povidone-iodine), scaling and root planing,and maintenance with chlorhexidine gluconatemouth rinse ,0.12% (Peridex-R) once or twice daily.

In case of NUP , metronidazole (one 250mg tabletfour times daily), amoxillin/clavunate (Augmentin)(one 250mg tablet three times daily) , or clindamycin

(one 300mg tablet three times daily) should beadded to the treatment regimen.

Therapeutic strategies and frequent recallappointments can produce effective local treatment

of NUP and LGE.


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MYCOBACTERIUM AVIUM-INTRACELLULARE

May present as palatal and gingival granulomatous masses,mycobacterial ulcers in the oral cavity.

An observation of acid-fast bacilli (AFB) will be made froma specially stained (acid-fast) biopsy specimen ( blood orsputum) which will be Mycobacterium avium-intracellulare.

Bacillary Angiomatosis It is not a common manifestation of HIV.

a vascular proliferative disease caused by Bartonellahenselae.

It responds to antimicrobial therapy.

It mimics Kaposis sarcoma clinically , and to some extent ,histologically.

It affects the skin more frequently than the oral cavity.

Biopsy is essential to exclude Kaposi s sarcoma.

NEOPLASTIC LESIONS


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Kaposi Sarcoma

May occur intraorally , either alone or in associationwith skin and disseminated lesions.

May be the first manifestion of late-stage HIV disease(AIDS).

Occurs most commonly in men ; it has been observedin women.

It appears as red , blue or purplish lesion. It may be flator raised , solitary or multiple.

The most common oral site is the hard palate; lesionmay also occur in any other part of the hard palateincluding the gingiva, soft palate , and buccal mucosa ,

and in the oropharynx. Occasionally , yellowish mucosa surround the KS

lesion.

Oral KS lesions may enlarge , ulcerate and becomeinfected good oral hygiene is essential to minimizethese complications.

Differential Diagnosis


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g KS must be distinguished from vascular lesions such as

hematomas, hemagiomas, other vascular tumors ,pyogenic granulomas , bacillary angiomatosis , and

pigmented lesions such as oral melanotic macules. Diagnosis is made from histologic examination.

There are usually no bleeding problems associated with abiopsy of oral KS; however, aspiration of a lesion prior tobiopsy may be useful to rule out a hemangioma.

Small , flat lesions in early stages have a differenthistologic appearance from larger , nodular andadvanced lesions.

Early lesions may be difficult to diagnose because they

resemble endothelial proliferation. KS may appear suddenly, within days of a normal oral

examination, in previously uninvolved areas of themouth.

KS maybe an indicator of progression to severe

immunosuppression.

Treatment


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Determined on the basis of number , size, and location of the oralKS lesions.

The choice of therapy depends on the effect of treatment on theadjacent mucosa, pain associated with treatment, interference witheating and speaking, and the patients preference.

Thorough dental prophylaxis ( S&P) should be performed beforeinitiating therapy for KS lesions involving the gingiva in order toimprove response to therapy.

Local application of sclerosing agents may reduce the size of the

lesion. Local treatment is appropriate for large KS lesions that interfere

with eating and talking.

Oral KS can be treated surgically ( under LA with a blade or carbondioxide laser) or with localized intralesional chemotherapy (0.1 to

0.2mg per ml solution of vinblastine) useful for treating lesionsparticularly on the palate or gingiva.

Radiation therapy may be indicated for large , multiple lesions. Sideeffects include xerostomia and mucositis.


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LYMPHOMA

Diffuse, undifferentiated non-Hodgkins lymphoma (NHL) is afrequent HIV-associated malignancy.

Most are of B-cell origin and Ebstein-Barr virus occurs in cells fromseveral cases.

Lymphoma can occur anywhere in the oral cavity; there may besoft tissue involvement with or without involvement of underlyingbone.

The lesion may present as firm, painless swelling that may beulcerated.

Some oral lesions may appear as shallow ulcerations.

Oral NHL may appear as solitary lesions with no evidence ofdisseminated disease.

Oral NHL may be confused with major aphthous ulcer and rarelyas pericoronitis associated with an erupting third molar.

Diagnosis of NHL must be made by histologic examination ofbiopsy specimen.

The patient must be referred for further evaluation fordisseminated disease and its subsequent treatment.

OTHER ORAL LESIONS ASSOCIATED WITH HIV DISEASE


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Oral Ulceration

They are recurrent aphthous ulcers (RAUs) and include minor RAUs ,major RAUs, and herpetiform RAUs

The cause of these ulcers are unknown. Proposed causes include stressand unidentified infectious agents.

In HIV-infected patients, the ulcers are well circumscribed witherythematous margins , OR, lesions are characterized by a halo ofinflammation and a yellow-gray pseudomembranous covering.

They are very painful , especially during consumption of salty , spicy ,or acidic foods and beverages , or hard , or rough foods.

In immunocompromised patients ulcers persist for longer than 7- to 14day period observed in immunocompetent individuals.

The ulcers of the minor RAU type appear as solitary lesions of about 0.5to 1.0 cm.

The herpetiform type appear as clusters of small ulcers (1 to 2mm)usually on the soft palate and oropharynx. Ulcers are not preceded byvesicles. Healing occurs in 1-2 weeks in immunocomptent individuals.

The major RAU type appears as extremely large (2 to 4cm )necroticulcers.

The major RAUs are very painful and may persist for several weeks. This typeheals with scar formation


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heals with scar formation.

Diagnosis

the ulcers may present a diagnostic problem.

Herpetiform RAUs may resemble the lesions of coxsackievirus infection.

The major RAUs may require biopsy to exclude malignancy, such aslymphoma, or opportunistic infection , such as histoplasmosis.

The ulcers usually occur on nonkeratinized mucosa this differentiates themfrom those caused by herpes simplex.

Treatment

Topical corticosteroids for RAU: The RAU type ulcers usually respond well totopical steroids such as

fluocinonides (0.05%) ointment mixed with equal parts Orabase applied 6

times daily or clobetasol (0.05%)ointment mixed with equal parts Orabaseapplied 3 times per day.

Triamcinolone, 0.1% in Orabase ( kenolog in Orabase) ; Amlexanox 5% paste : apply both to dried ulcer 2-4 times daily until healed.

Dexamethasone elixir (0.5mg/5ml) used as a mouth rinse and thenexpectorated 2 to 3 times daily is helpful for multiple ulcers and for thosewhere topical ointments are hard to apply.

Systemic corticosteroids for severe major RAU or refractory RAU : For HIV-infected


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Systemic corticosteroids for severe major RAU or refractory RAU : For HIV-infectedpersons with oral and gastrointestinal aphthous-like ulcers, systemic steroidtherapy (prednisone 40 to 60mg/day for 7 to 10 days , then taper) has been reportedhelpful.biopsy prior to treatment should be considered. Consult primary carephysician before prescribing.

Antibacterial agent for RAU: Chlorhexidine gluconate oral rinse 0.12%(Peridex) : rinse with 15ml for 30 second bid

and spit out the solution, for 1-2 weeks.

Tetracycline suspension : 125m/mL swish for 1-2 min and expectorate , bid.

Minocycline tablet , 100mg, I tab dissolved in water (suspension). Rinse 4-5 timesdaily.

Topical anaesthetic and coating agents for oral ulceration: Benzocaine in Orabase :apply a small amount with a cotton swab to the affected

area as needed for pain. Caution with allergy to esters or Novocain.

Viscous lidocaine 2% : swish with 5ml before meals and expectorate. Caution: gagreflex may be lost. Aspiration is possible.

Vitamin B complex , I tab 4 times daily.

Thalidomide (contraindicated in pregnancy): 200mg , 1-2 times daily for 3-8 weeks.

Zinc lozenges ; suck one lozenges 4- 6 times daily.

Vit C 500mg , 1 tablet 4 times daily.

Idi thi Th b t i P


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Idiopathic Thrombocytopenic Purpura

oral lesion may be the first manifestation of thiscondition.

Petchiae , ecchymoses, and hematoma can occuranywhere on the oral mucosa.

Spontaneous bleeding from the gingiva can

occur. Patient may report finding blood in his/her

mouth on waking.

The clinician must distinguish ITP from othervascular lesions and KS.

Because of potential bleeding risk, the clinicianshould obtain blood and platelet counts before

performing other diagnostic procedures.

Salivary Gland Disease and Xerostomia


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Salivary Gland Disease and Xerostomia

Salivary gland disease associated with HIV infection (HIV-SGD) can present as xerostomia with or without (unilateralor bilateral) salivary gland enlargement.

Xerostomia is a major contributing factor in dental decayin HIV- infected individuals due to changes in quantity andquality of saliva, including diminished antimicrobialproperties ( of saliva).

Salivary gland enlargement in children and adults withHIV infection usually involve the parotid gland.

The enlarged salivary glands are soft but not fluctuant.

In some cases, enlarged salivary glands may be due tolympho-epithelial cysts.

Labial salivary gland biopsy reveals histologic featuressimilar to those in Sjogrens syndrome.

In HIV-SGD, however , the lymphocytic infiltrate ispredominantly CD8+ cells, unlike that in Sjogrens

syndrome, which is predominantly CD4 +cells

Th ti l f HIV SGD i k


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The etiology of HIV-SGD is unknown.

Xerostomia is sometimes seen in individuals with HIV-SGD.

HIV-infected patients may also experience dry mouth in

association with medication that hinder salivary glandsecretion , such as didanosine(ddI) , antidepressants,antihistamines, and anti-anxiety drugs

Management

Removal of enlarged parotid glands is rarely recommended.

For individuals with xerostomia , the use of salivary stimulantssuch as sugarless gum, sugarless hard lozenges or sugarlesscandies may provide relief; acidic candies should be avoided as

they may lead to loss of tooth enamel. Lubricants : artificial salivary substitutes , Oral Balance

ointments

Systemic sialogogues : Pilocarpine (Salagen) consult primarycare physician before prescribing.


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Neutropenic Ulceration

are very painful ulcerations that can appear onboth keratinized and non-keratinized tissues.

They are associated with absolute granulocytecounts of less than 800/microlitre.

They are being found with increasing frequencyin the HIV-infected population.

Large , unusual-looking , or fulminant ulcers inthe oral cavity that cannot be otherwiseexplained should prompt suspicion of thesecondition.

Patient should receive granulocyte colony-stimulating factor treatment prior to systemic ortopical steroid treatment , depending on the sizeand location of the lesion.


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REFERENCES


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REFERENCES

David A Reznik, DDS. Oral manifestations ofHIV.Perspective Oral manifestations, volume 13 , Issue 5,December 2005/January 2006 ,

Deborah Greenspan, DSC, BDS, University of CarliforniaSan Francisco .Oral manifestations of HIV : HIV InSite,Knowledge Base Chapter , June 1998 ,.

Florida/Caribbean AIDS EDUCATION AND TRAINING

CENTRE (AETC). Oral manifestations of HIV/AIDS. (May2012 publication).

Joseph A. Regezi, James J. Sciubba , Richard C.K Jordan.Pathogenesis of herpes simplex infections. Pathogenesisof Varizella zoster infection. Clinical features of aphthous

ulcers. Oral pathology text(clinical pathologiccorrelations). Fourth edition, 2003; 1 :1-2;1 :7;2:40.

R.A. Cawson , E.W. Odell, S. Porter. Bacillary angiomatosis.Cawsons essentials of oral pathology and oralmedicine;seventh edition, 2002. 24:313.


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