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ORAL MANIFESTATIONS OF HIV

BY

DR IDAEWOR OPEYEMI EMMANUEL

OUTLINE
Introduction/History. Classification of oral meanifestations

of HIV. Clinical features. Differential diagnosis. Diagnosis. Treatment. Prognostic Significance.

INTRODUCTION : History The pandemic, acquired immunodeficiency syndrome (AIDS) was

first reported in 1981.By 1992 , 11 million people were said to be affected. Already more than 30 million people have died of AIDS; 34 million people around the world are living with HIV. The impact of HIV is more severe in Africa ,esp sub-saharan Africa. South Africa has more people living with HIV than any other country in Africa. The infection is lifelong and once acquired , can be transmitted to others. 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 the number and function of CD4+ T-cells. Clinical symptoms appear as the virus destroys blood cells important for maintaining immunity. Progressive destruction of immune function allows the development of opportunistic infections and neoplasms leading to AIDS.

Oral lesions are frequent and varied and are among the first

symptoms of the infection . The presence of pseudomembranous oral candidiasis and hairy leukoplakia indicates a strong likelihood that the infection 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 physical examination. Early recognition , diagnosis , and treatment of HIVassociated oral lesions may reduce morbidity. Effect of HAART on oral manifestations include: significant reduction in oral hairy leukoplakia, necrotizing ulcerative periodontitis ; no significant reduction in candidiasis, oral ulcers , 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 not been documented.

CLASSIFICATION OF ORAL LESIONS ASSOCIATED WITH HIV.


Strongly associated with HIV (Group 1) ,pseudomembranous , erythematous , hyperplastic candidiasis.
Hairy leukoplakia
Linear gingival erythema Necrotizing ulcerative gingivitis Necrotizing ulcerative

Less commonly associated with HIV (Group 2)


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

Candidiasis angular cheilitis

periodontitis
Kaposis sarcoma Non-Hodgkins lymphoma

Group 3. Lesions possibly associated with HIV

infection. Bacterial infections (excluding gingivitis/periodontitis): Actinomyces israeli Enterobacter cloacae Escherichia coli Klebsiella pneumoniae Mycobacterium avium intracellulare Cat-scratch disease Drug reaction (ulcerative , erythema multiformes , lichenoid reaction).

exacerbation of atypical periodontitis Fungal infections other than candidiasis : Aspergillus flavus Geotrichum candidum Mucoraceae Neurologic disturbances : Facial palsy Osteomyelitis Sinusitis Submandibular cellulitis Squamous cell carcinoma Toxic epidermolysis Neutropenic Ulceration.

FUNGAL LESIONS Oral Candidiasis :

Introduction Most commonly associated with Candida albicans. Other species such as C. glabrata and C. tropicalis are frequently part of the normal oral flora. NB: Candida glabrata is intrinsicaly azole-resistant (fluconazole). Fluconazole is the most widely used systemic agent for moderate and severe disease. Itraconazole, Voriconazole, posaconazole (oral suspension) are reserved for cases of fluconazole resistance. Factors associated with azole-resistant disease include prior exposure to azoles , low CD4+ cell count , and presence of non-albican species. Most persons with HIV infection carry a single strain of Candida during clinically apparent candidiasis and when candidiasis is quiescent.

-Factors which predisposes patients to develop candidiasis include : infancy , old age, antibiotic therapy, steroid and other immunosuppressive drugs, xerostomia, anemia, endocrine disorders and primary and acquired immunodeficiency. - Reports describe oral candidiasis during the acute stages of HIV. - occurs with falling CD4+T-cell count in middle and late stages of HIV disease. - The 3 common presentations of oral candidiasis are angular cheilitis, erythematous candidiasis and pseudomembranous candidiasis.

Angular cheilitis
Presents as erythema or fissuring either

unilaterally or bilaterally at the corners of the mouth . 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 topical antifungal cream applied directly to the affected areas 4 times a day for 2-week treatment period.

Erythematous Candidiasis May be the most underdiagnosed and misdiagnosed oral

manifestation of HIV disease. The condition presents as a red , flat , subtle lesion on the dorsal surface of the tongue or on the hard or soft palates May present as a kissing lesion if a lesion is present on the 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 or spicy food or drinking acidic beverages. Clinical diagnosis is based on appearance , as well as on the 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.

Pseudomembranous Candidiasis (oral thrush) Appears as creamy, white ,curd-like removable plaques on the oral mucosa are caused by overgrowth of fungal hyphae mixed with desquamated epithelium and inflammatory cells Occurs on the buccal mucosa, tongue, and other oral mucosal surfaces. It may involve any part of the pharynx. The plaques can be wiped away ,typically leaving a red or bleeding underlying surface. The most common organism involved is Candida albicans species. For both pseudomembranous and erythematous candidiasis lesion, diagnosis is based on appearance.

Hyperplastic Candidiasis. Unusual in persons with HIV infection. Lesions appear white and hyperplastic. The white areas are due to hyperkeratosis, and , unlike the plaques of pseudomembranous candidiasis, cannot be removed by scraping. Lesion may be confused with hairy leukoplakia. Diagnosis of hyperplastic candidiasis is made from histologic appearance of hyperkeratosis and the presence of hyphae . Periodic acid-Schiff (PAS) stain is often used to demonstate hyphae.

Differential diagnosis
Erythematous candidiasis should be

differentiated from other red lesions , such as Kaposi s sarcoma or erythroplakia. Inflamatory responses often associated with Candida infection may be absent in immunocompromised patients The creamy white plaques of pseudomembranous candidiasis are removable while the white lesions of hairy leukoplakia are non-removable.

Diagnosis Candidiasis is diagnosed by its clinical appearance and by detection of organisms on smears. Specimen collection : smears are taken by gently drawing a wooden tongue depressor across the lesion. The

specimen is then transferred into a drop of KOH on a glass slide and protected by a cover slip. The smear is examined under the microscope and Candida is detected by finding hyphae and blastospores they are rarely seen in healthy individuals in carrier state Culture media: cultures are grown on specific media, such as Sabourauds agar culture is useful for establishing Candida species but not diagnosis. Treatment Maybe treated either topically or systemically; treatment should be maintained for at least 2 weeks to reduce organism colony-forming units to levels low enough to prevent recurrence.

Topical treatment Preferred because they limit systemic absorption but the effectiveness depends on patients compliance. Topical medication requires the patient to hold the medication in the mouth for 20 to 30 minutes. If the patient uses sweetening formulation, consider the concurrent treatment daily fluoride rinse (fluorigard) for 1 min once a day and then expectorated. Topical medications include clotrimazole (oral troche , 10mg tablet) Nystatin preparation include suspension, a vaginal tablet , and oral pastille (200,000 units) dissolved slowly in the mouth. Amphotericin B (0.1mg/ml). 5 to 10 ml of oral solution is used as a rinse and then expectorated 3 to 4 times daily.

Systemic treatment Effective agents include: Ketoconazole (Nizoral) , 200mg tablet taken with food once daily. Careful

monitoring of liver function is necessary for long-term use. Fluconazole (Diflucan) is a triazole antifungal agent effective in treating candidiasis (100mg tablet taken once daily for 2 weeks) Itraconazole (100mg capsule) may also be used (200mg daily orally for 14 days). 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 are potent CYP450 inducers ) phenytoin, cyclosporin A, terfenadine, digoxin, coumarin-like medications , and oral hypoglycemic medications.

Prognostic factors both erythematous and pseudomembranous oral candidiasis are

associated with increased risk for the subsequent development of opportunistic infections and correlates with falling CD4+T-cell counts.

Histoplasmosis may initially present in the oral cavity. These lesion appears as ulcerations that can

affect any mucosal surface. Diagnosis requires biopsy.


Cryptococcus Neoformans.
it may cause an ulcerated mass in the hard

palate.

VIRAL LESIONS Herpes simplex Herpes simplex virus (HSV)-1 infection is widespread and oral lesions are common. Most orofacial herpetic lesions are due to HSV type 1 ;a

small percentage may be caused by HSV2 secondary to anogenital contact. Herpes simplex causes both primary and secondary or recurrent disease in the oral cavity. Primary herpetic gingivostomatitis commonly occurs in children and young adults and maybe followed by recurrences. Following the primary episode , the virus migrates through some unknown mechanism , along the periaxon sheath of the trigeminal nerve to the trigeminal ganglion where it becomes latent. .

No major histocompatibilty (MHC) antigen are expressed ; so there is no T-cell response during latency. Reactivation of virus may follow exposure to sunlight(fever blisters ) , exposure to cold (cold sore) , trauma , stress , or immunosuppression , causing a secondary or recurrent infection Recurrent oral herpes occurs at any age extraorally or intraorally.

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 form crust. Recurrent intraoral herpes appears as clusters of painful small vesicles that rupture and ulcerate and usually heal within 1 week to 10 days.

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

Treatment No treatment will permanently eradicate herpes

simplex infections , but acyclovir may shorten the 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 for lesions on the lips. Foscarnet or phosphonoformate is used to combat acyclovir-resistant strains.

Prognostic Significance
There is no know association between

recurrent intraoral herpes and more rapid progression of HIV disease. However , there is clinical impression that recurrent herpes simplex infection may be more common in patients with symptomatic HIV disease.

Herpes Zoster. Primary varizella zoster virus infection in seronagative


individuals are known as varizella or chickenpox The reactivation of varizella zoster virus (VZV) causes herpes 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 vesicles appear on the facial skin , lips , and oral mucosa. Skin and oral lesions are frequently unilateral and follow the distribution of the maxillary and/or mandibular branches of the trigeminal nerve.

The skin lesions form crusts and the oral lesions coalesce to form large ulcers.
The ulcers frequently affect the gingiva , so

tooth 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 is considerably higher than that recommended for the treatment of herpes simplex.

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 mucous membranes of persons with HIV disease. Anal warts have recently been reported among homosexual men. Because , the HPV types found in oral lesions in HIV-infected persons are different from the HPV type associated with anogenital warts , the term condylomata acuminata is not appropriate for oral HPV lesions. Lesion may appear as solitary or multiple nodules.

They may be sessile or pedunculated and appear as multiple , smooth-surfaced raised masses resembling focal epithelial hyperplasia or as multiple , small papilliferous or cauliflower-like projections. 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 in HIV-infected persons than in the general population.

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 repeat procedures may be necessary.

Cytomegalovirus Oral ulcers caused by cytomegalovirus (CMV) have been reported. This can appear on any mucosal surface. It may be confused with aphthous ulcers, necrotizing ulcerative periodontitis and lymphoma. Unlike aphthous ulcer, which usually have any erythematous margin, CMV ulcers appear necrotic with a white halo. Diagnosis of CMV ulcer is made from a biopsy.Immunohistochemistry may also be helpful.

CMV ulcer in the oral cavity usually occur in individuals with disseminated CMV disease.
Diagnosis of CMV-infected oral ulcers should be

followed by examination for the systemic disease. CMV ulcers resolves when ganciclovir is used to treat CMV disease.

Oral Hairy Leukoplakia and Epstein-Barr Virus Presents as a non-movable, corrugated or hairy white 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 with asymptomatic HIV infection. It becomes more common as the CD4+ T-cells count falls. HL is in group 4 , category C2 of the original Center for 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 like recipients of bone marrow, cardiac , and renal transplants.

Hairy Leukoplakia and Progression of HIV Disease. Diagnosis of HL is an indication of both HIV infection

and immunodefiency. It is an indication for a work-up to evaluate and treat HIV. HL correlates with a statistical risk for more rapid progression of HIV disease. Progression to CDC-defined AIDS is more rapid in those HIV-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 hairy

leukoplakia lesion (with Epstein-Barr virus). Intraepithelial Langerhanss cells are reduced or absent in HL lesions which correlates with the presence of viral antigens.

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 markedly resembling hairs; occasionally , some areas may be smooth or flat. Lesion occurs most commonly on the lateral margins of the tongue and may spread to cover the entire dorsal surface HL can spread onto the ventral surface of the tongue and buccal mucosa (flat in appearance).Rarely , they occur on the soft palate. HL usually does not cause symptoms.

Differential diagnosis and Definitive diagnosis Candida albicans may be found in association with HL

lesions , 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 sponge nevus, dysplasia, and squamous cell CA. HL should be diagnosed by biopsy for definitive diagnosis. The typical microscopic appearance of HL include acanthosis, 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 EBV using in-situ hybridization performed on biopsy specimen.

Treatment HL is usually asymptomatic and does not require treatment. Usually resolves with onset of Highly Active

Antiretroviral 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, and aerosolized pentamidine.

BACTERIAL LESIONS Periodontal Disease Is a fairly common problem in both asymptomatic and 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.

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 as petechiae- 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 a characteristic cratered appearance.

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 soft tissue. Typically, these losses occur simultaneously with no formation 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 necrotic bone may appear along the gingival margin. The bone may eventually sequestrate. Patients with NUP and necrotizing stomatitis frequently complain of extreme pain and spontaneous bleeding, fetid odor, deep jaw pain.

Treatment Clinicians should refer patients to a periodontist or dentist for management. The ff protocol has achieved reasonable success :

plaque removal, local debridement (removal of necrotic tissues), irrigation with Betadine 10% solution (povidone-iodine), scaling and root planing, and maintenance with chlorhexidine gluconate mouth rinse ,0.12% (Peridex-R) once or twice daily. In case of NUP , metronidazole (one 250mg tablet four times daily), amoxillin/clavunate (Augmentin) (one 250mg tablet three times daily) , or clindamycin (one 300mg tablet three times daily) should be added to the treatment regimen. Therapeutic strategies and frequent recall appointments can produce effective local treatment of NUP and LGE.

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 from a specially stained (acid-fast) biopsy specimen ( blood or sputum) which will be Mycobacterium avium-intracellulare.
Bacillary Angiomatosis It is not a common manifestation of HIV. a vascular proliferative disease caused by Bartonella

henselae. 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 Kaposi Sarcoma May occur intraorally , either alone or in association

with skin and disseminated lesions. May be the first manifestion of late-stage HIV disease (AIDS). Occurs most commonly in men ; it has been observed in women. It appears as red , blue or purplish lesion. It may be flat or raised , solitary or multiple. The most common oral site is the hard palate; lesion may also occur in any other part of the hard palate including 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 become infected good oral hygiene is essential to minimize these complications.

Differential Diagnosis 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 a biopsy of oral KS; however, aspiration of a lesion prior to biopsy may be useful to rule out a hemangioma. Small , flat lesions in early stages have a different histologic appearance from larger , nodular and advanced 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 the mouth. KS maybe an indicator of progression to severe immunosuppression.

Treatment Determined on the basis of number , size, and location of the oral

KS lesions. The choice of therapy depends on the effect of treatment on the adjacent mucosa, pain associated with treatment, interference with eating and speaking, and the patients preference. Thorough dental prophylaxis ( S&P) should be performed before initiating therapy for KS lesions involving the gingiva in order to improve 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 carbon dioxide laser) or with localized intralesional chemotherapy (0.1 to 0.2mg per ml solution of vinblastine) useful for treating lesions particularly on the palate or gingiva. Radiation therapy may be indicated for large , multiple lesions. Side effects include xerostomia and mucositis.

LYMPHOMA Diffuse, undifferentiated non-Hodgkins lymphoma (NHL) is a

frequent HIV-associated malignancy. Most are of B-cell origin and Ebstein-Barr virus occurs in cells from several cases. Lymphoma can occur anywhere in the oral cavity; there may be soft tissue involvement with or without involvement of underlying bone. The lesion may present as firm, painless swelling that may be ulcerated. Some oral lesions may appear as shallow ulcerations. Oral NHL may appear as solitary lesions with no evidence of disseminated disease. Oral NHL may be confused with major aphthous ulcer and rarely as pericoronitis associated with an erupting third molar. Diagnosis of NHL must be made by histologic examination of biopsy specimen. The patient must be referred for further evaluation for disseminated disease and its subsequent treatment.

OTHER ORAL LESIONS ASSOCIATED WITH HIV DISEASE 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 stress and unidentified infectious agents. In HIV-infected patients, the ulcers are well circumscribed with erythematous margins , OR, lesions are characterized by a halo of inflammation 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 14 day period observed in immunocompetent individuals. The ulcers of the minor RAU type appear as solitary lesions of about 0.5 to 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 by vesicles. Healing occurs in 1-2 weeks in immunocomptent individuals. The major RAU type appears as extremely large (2 to 4cm )necrotic ulcers.

The major RAUs are very painful and may persist for several weeks. This type

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 as lymphoma, or opportunistic infection , such as histoplasmosis. The ulcers usually occur on nonkeratinized mucosa this differentiates them from those caused by herpes simplex.

Treatment Topical corticosteroids for RAU: The RAU type ulcers usually respond well to topical 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 Orabase applied 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 then expectorated 2 to 3 times daily is helpful for multiple ulcers and for those where topical ointments are hard to apply.

Systemic corticosteroids for severe major RAU or refractory RAU : For HIV-infected persons with oral and gastrointestinal aphthous-like ulcers, systemic steroid therapy (prednisone 40 to 60mg/day for 7 to 10 days , then taper) has been reported helpful.biopsy prior to treatment should be considered. Consult primary care physician 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 times daily. 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: gag reflex 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.

Idiopathic Thrombocytopenic Purpura oral lesion may be the first manifestation of this

condition. Petchiae , ecchymoses, and hematoma can occur anywhere 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 other vascular lesions and KS. Because of potential bleeding risk, the clinician should obtain blood and platelet counts before performing other diagnostic procedures.

Salivary Gland Disease and Xerostomia Salivary gland disease associated with HIV infection (HIV

SGD) can present as xerostomia with or without (unilateral or bilateral) salivary gland enlargement. Xerostomia is a major contributing factor in dental decay in HIV- infected individuals due to changes in quantity and quality of saliva, including diminished antimicrobial properties ( of saliva). Salivary gland enlargement in children and adults with HIV infection usually involve the parotid gland. The enlarged salivary glands are soft but not fluctuant. In some cases, enlarged salivary glands may be due to lympho-epithelial cysts. Labial salivary gland biopsy reveals histologic features similar to those in Sjogrens syndrome. In HIV-SGD, however , the lymphocytic infiltrate is predominantly CD8+ cells, unlike that in Sjogrens syndrome, which is predominantly CD4 +cells

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 gland secretion , 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 stimulants

such as sugarless gum, sugarless hard lozenges or sugarless candies 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 primary care physician before prescribing.

Neutropenic Ulceration are very painful ulcerations that can appear on both keratinized and non-keratinized tissues. They are associated with absolute granulocyte counts of less than 800/microlitre. They are being found with increasing frequency in the HIV-infected population. Large , unusual-looking , or fulminant ulcers in the oral cavity that cannot be otherwise explained should prompt suspicion of these condition. Patient should receive granulocyte colonystimulating factor treatment prior to systemic or topical steroid treatment , depending on the size and location of the lesion.

REFERENCES David A Reznik, DDS. Oral manifestations of

HIV.Perspective Oral manifestations, volume 13 , Issue 5, December 2005/January 2006 , Deborah Greenspan, DSC, BDS, University of Carlifornia San 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. (May 2012 publication). Joseph A. Regezi, James J. Sciubba , Richard C.K Jordan. Pathogenesis of herpes simplex infections. Pathogenesis of Varizella zoster infection. Clinical features of aphthous ulcers. Oral pathology text(clinical pathologic correlations). 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 oral medicine;seventh edition, 2002. 24:313.

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