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HIV Curriculum for the Health Professional Oral Manifestations of HIV Infection Nicoleta Vaseliu, DDS, MS,
HIV Curriculum for the Health Professional
Oral Manifestations of HIV Infection
Nicoleta Vaseliu, DDS, MS, OMFS
Harrison Kamiru, BDS, MS, DrPH
Mark Kabue, BDS, MS, MPH, DrPH
Objectives
1. Discuss the importance of oral and dental care
for patients with human immunodeficiency virus
(HIV) infection.
2. Review the classification of orofacial lesions
associated with HIV infection in adults and
children.
3. Describe the clinical presentation and
management of the most common oral
manifestations of HIV infection.
In developed countries, HIV disease progression is
monitored by two key laboratory markers: CD4 + lympho­
cyte count and HIV viral load. Unfortunately, these tests
are not readily available in many developing countries.
There, other important clinical findings guide clinicians
in the evaluation and treatment of HIV disease. Because
the oral cavity is easily accessible to clinical examination,
orofacial lesions associated with HIV infection may be
used as clinical markers of HIV disease progression.
Key Points
1. Oral health care is an important part of HIV
primary care.
2. Oral manifestations are common clinical findings
in children and adults with HIV infection.
The advent of highly active antiretroviral therapy
(HAART) in 1996 greatly reduced the mortality and
morbidity of HIV­infected patients who have access to
treatment. The incidence rates of many opportunistic
infections associated with HIV disease have decreased,
including that of HIV­associated orofacial lesions.
3. Early diagnosis and management of oral mani­
festations is important to prevent complications
and improve quality of life.
Importance of Oral Manifesta­
tions of HIV Infection
Since human immunodeficiency virus (HIV) infection
Evaluation of oral health status is an important part
of routine health care. A thorough oral examination is
important at every stage in the management of HIV
disease. It is also desirable to encourage collaboration
among general medical practitioners, infectious­
disease doctors, general and pediatric dentists, and oral
pathologists to provide the best care possible for HIV­
infected patients.
was first described in 1981, a variety of oral conditions
associated with HIV disease have been documented.
Studies have shown that 70%­90% of HIV­infected
individuals will develop at least one oral manifestation
during the course of the disease. A review of the dental
literature shows that HIV­associated orofacial lesions
have been considered
Classification of Orofacial Lesions
Associated with HIV
• clinical indicators of HIV infection in otherwise
healthy, undiagnosed individuals;
• early clinical features of HIV infection;
• clinical markers for the classification and staging of
HIV disease; and
• predictors of HIV disease progression.
There are two main classification systems of oral lesions
associated with HIV infection. The first is based on the
etiology of the oral lesions. According to this system,
orofacial lesions are classified as bacterial, viral, or fungal
infections or as neoplastic lesions or other conditions.
The second, more widely used, system—recommended
by the EC Clearinghouse on Oral Problems Related to
HIV Infection and WHO Collaborating Centre on Oral
Manifestations of the Human Immunodeficiency Virus—
classifies orofacial lesions into three groups according
to the degree of their association with HIV infection.
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Oral Manifestations of HIV Infection

Tables 1 and 2 show this classification of orofacial lesions associated with HIV/AIDS in adults and children, respectively.

Clinical Presentation and Management

Oral Candidiasis

Oral candidiasis is the most common orofacial manifes­ tation of HIV infection. Its prevalence may depend on study population, diagnostic criteria, study design, and availability of antiretroviral therapy. Reported prevalence rates have varied widely, to as high as 72% in children and 94% in adults. Oral candidiasis is also a significant predictor of HIV disease progression in both adults and children. The median time of survival from its clinical diagnosis to death is 3.4 years among HIV­infected children. The main etiologic factor of oral candidiasis is the fungus Candida albicans, although other species of Candida may be involved.

Clinical appearance. Oral candidiasis is often observed

in one of the following four clinical forms: erythematous (atrophic) candidiasis, pseudomembranous candidiasis, hyperplastic candidiasis, and angular cheilitis.

1. Erythematous (atrophic) candidiasis appears clinically as multiple small or large patches, most often localized on the tongue and/or palate (Figure 1).

2. Pseudomembranous candidiasis (oral thrush) is characterized by the presence of multiple superficial, creamy white plaques that can be easily wiped off, revealing an erythematous base (Figure 2). They are usually located on the buccal mucosa, oropharynx, and/or dorsal face of the tongue.

3. Hyperplastic candidiasis lesions appear white and hyperplastic and cannot be removed by scraping. This form of oral candidiasis is rare in HIV­ infected individuals.

Table 1. Orofacial lesions associated with HIV/AIDS in adults

Lesions strongly associated with HIV infection

 
 
•

Candidiasis

•

Non­Hodgkin’s lymphoma

1

– Erythematous

•

Periodontal disease

– Pseudomembranous

– Linear gingival erythema

•

Hairy leukoplakia

– Necrotizing (ulcerative) gingivitis

 
•

Kaposi’s sarcoma

– Necrotizing (ulcerative) periodontitis

Lesions less commonly associated with HIV infection

 
 
•

Bacterial infections

•

Viral infections

 

– Mycobacterium avium­intracellulare

– Herpes simplex virus

– Mycobacterium tuberculosis

– Human papillomavirus (wart­like lesions)

2

•

Melanotic hyperpigmentation

– Condyloma acuminatum

•

Necrotizing (ulcerative) stomatitis

– Focal epithelial hyperplasia

•

Salivary gland disease

– Verruca vulgaris

 

– Dry mouth due to decreased salivary flow rate

– Varicella zoster virus

– Unilateral or bilateral swelling of the major salivary glands

– Herpes zoster

– Varicella

 
•

Thrombocytopenic purpura

 
•

Ulceration NOS (not otherwise specified)

Lesions seen in HIV infection

 
 
•

Bacterial infections

•

Fungal infection other than candidiasis

 

– Actinomyces Israel

– Cryptococcus neoformans

– Escherichia coli

– Geotrichum candidum

– Klebsiella pneumoniae

– Histoplasma capsulatum

3

•

Cat­scratch disease

– Mucoraceae (mucormycosis/ zygomycosis)

•

Drug reactions (ulcerative, erythema multiforme, lichenoid, toxic epidermolysis

– Aspergillus flavus

 
•

Recurrent aphthous stomatitis

 
•

Epithelioid (bacillary) angiomatosis

•

Viral infections

•

Neurologic disturbances

– Cytomegalovirus

 

– Facial palsy

– Molluscum contagiosum

– Trigeminal neuralgia

 

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HIV Curriculum for the Health Professional

HIV Curriculum for the Health Professional Figure 1. Erythematous candidiasis in an HIV-infected child 4. Angular

Figure 1. Erythematous candidiasis in an HIV-infected child

4. Angular cheilitis is characterized by the presence of erythematous fissures at the corners of the mouth. It is usually accompanied by another form of intraoral candidiasis.

Treatment. Treatment with topical and systemic antifungal agents is recommended (Table 3).

Oral Hairy Leukoplakia

Oral hairy leukoplakia (OHL) is more common among HIV­infected adults than among HIV­infected children. The reported prevalence of OHL in adults is about 20%­ 25%, increasing as the CD4 + lymphocyte count decreases, whereas in children the prevalence is about 2%­3%. The

whereas in children the prevalence is about 2%­3%. The Figure 2. Pseudomembranous candidiasis in an HIV-infected

Figure 2. Pseudomembranous candidiasis in an HIV-infected child

presence of OHL is a sign of severe immunosuppression. OHL is a significant predictor of HIV disease progression in adults. Although its etiology is not clear, OHL seems to be caused by Epstein­Barr virus infection.

Clinical appearance. OHL presents as white, thick patches that do not wipe away and that may exhibit vertical corrugations with a hairlike appearance (Figure 3). The lesions usually start on the lateral margins of the tongue and sometimes inside the cheeks and lower lip. They may be unilateral or bilateral, and they are asymptomatic. OHL is often associated with oral candidiasis.

Table 2. Orofacial lesions associated with pediatric HIV infection

Lesions commonly associated with pediatric HIV infection

 
 
•

Oral candidiasis

•

Parotid enlargement (swelling of the major salivary glands)

1

– Pseudomembranous

•

Recurrent aphthous ulcers

– Erythematous

– Minor

– Angular cheilitis

– Major

 
•

Herpes simplex virus infection

– Herpetiform

•

Linear gingival erythema

 

Lesions less commonly associated with pediatric HIV infection

 
 
•

Bacterial infections of oral tissues

•

Viral infections

•

Periodontal diseases

– Cytomegalovirus

2

– Necrotizing ulcerative gingivitis

– Human papillomavirus

– Necrotizing ulcerative periodontitis

– Molluscum contagiosum

– Necrotizing stomatitis

– Varicella zoster virus

 
•

Xerostomia

– Herpes zoster

•

Seborrheic dermatitis

– Varicella

Lesions strongly associated with HIV infection but rare in children

 

3

•

Neoplasms

 

Kaposi’s sarcoma and non­Hodgkin’s lymphoma

•

Oral hairy leukoplakia

 
•

Tuberculosis­related ulcers

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Oral Manifestations of HIV Infection

Oral Manifestations of HIV Infection Figure 3. Oral Hairy Leukoplakia in an HIV-infected adult Treatment. OHL

Figure 3. Oral Hairy Leukoplakia in an HIV-infected adult

Treatment. OHL usually does not require any treatment, but in severe cases systemic antivirals are recommended (Table 3). When OHL is associated with oral candidiasis, therapeutic management of oral candidiasis is required.

HIV-Associated Periodontal Disease

Periodontal (gum) disease is common among HIV­ infected patients. It is characterized by bleeding gums, bad breath, pain/discomfort, mobile teeth, and some­ times sores. Its reported prevalence ranges widely, between 0% and 50%. Left untreated, HIV­associated periodontal disease may progress to life­threatening infections, such as Ludwig’s angina and noma (cancrum oris).

Clinical appearance. Four forms of HIV­associated periodontal disease have been described: linear gingival erythema, necrotizing ulcerative gingivitis

(NUG), necrotizing ulcerative periodontitis (NUP), and necrotizing stomatitis.

1. Linear gingival erythema is characterized by the presence of a 2­ to 3­mm red band along the marginal gingiva, associated with diffuse

red band along the marginal gingiva, associated with diffuse Figure 4. Linear Gingival Erythema in an

Figure 4. Linear Gingival Erythema in an HIV-infected adult

erythema on the attached gingiva and oral mucosa (Figure 4). The degree of erythema is disproportionately intense compared with the amount of plaque present on the teeth.

2. NUG is more common in adults than in children. It is characterized by the presence of ulceration, sloughing, and necrosis of one or more interdental papillae, accompanied by pain, bleeding, and fetid halitosis.

3. NUP is characterized by the extensive and rapid loss of soft tissue and teeth.

4. Necrotizing stomatitis is thought to be a con­ sequence of severe, untreated NUP. It is charac­ terized by acute and painful ulceronecrotic lesions on the oral mucosa that expose underlying alveolar bone.

Treatment. Management and control of HIV­associated periodontal disease begin with good daily oral hygiene. In addition to brushing, flossing and use of mouthwash solutions are effective ways to prevent and control periodontal disease. Table 3 presents various therapeutic options.

disease. Table 3 presents various therapeutic options. Figure 5. Recurrent Herpes Simplex in an HIV-infected child

Figure 5. Recurrent Herpes Simplex in an HIV-infected child

Figure 5. Recurrent Herpes Simplex in an HIV-infected child Figure 6. Recurrent minor Aphthous Ulcers in

Figure 6. Recurrent minor Aphthous Ulcers in an HIV-infected adult

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Table 3. Therapeutic options for the most common HIV-associated oral manifestations 23,34,35,36,37

Oral Lesion

Treatment for Adults

Treatment for Children

Comments

Oral Candidiasis (Erythematous, Pseudomembranous, and Hyperplastic)

Topical

Topical

•

Different forms of oral candidiasis may occur simultaneously.

•

Nystatin (Mycostatin)

•

Nystatin suspension 200,000­

•

Oral gel: apply gel q8h or q6h, for 10­14 days

400,000 U/day divided in 4­6 doses, for 14 days

•

Hyperplastic candidiasis requires systemic treatment.

•

Cream: Apply q12h, for 10­14 days

•

Clotrimazole troches 10 mg q8h or q6h, for 4 weeks

•

Ketoconazole may interact with Lopinavir­Ritonavir (Kaletra) at doses >200 mg/day.

   
•

Gentian violet 1% aqueous solution painted in the affected areas q8h

Systemic

•

Topical fluoride should be used if for long periods to counteract high sugar content of some antifungal medications.

•

Nystatin (Mycostatin) 400,000­600,000 U q6h, for 14 days

antifungal agents are administered

Systemic

•

Ketoconazole (Nizoral) 200­400 mg PO q.d.

•

Ketoconazole 3.5­6.6 mg/kg/day in a single dose

•

Amphotericin B may be used in azole­resistant infections.

•

Fluconazole (Diflucan) 50­100 mg PO q.d.

•

Fluconazole 6 mg/kg on day 1, then 3 mg/kg qd, up to 2 weeks

•

Amphotericin B may also be available as a topical preparation.

•

Itraconazole (Sporanox) (Capsules or solution)

•

Itraconazole 100 mg PO, daily for children older than 3 years

•

Dentures should be removed when medication is applied.

200

mg PO qd for 7 days

   
•

Amphotericin B10 mg IVq6h, for 10 days

Prophylaxis

•

Clotrimazole 10 mg PO q8h or q12h for long period

Prophylaxis

•

Nystatin 100,000­400,000 U PO

•

Fluconazole 100 mg PO qwk, for long period

q12h for long period

•

Fluconazole 3­6 mg/kg PO daily or weekly for long period

Angular

Topical

Topical

•

Lesions tend to heal slowly because of the repeated opening of the mouth.

Cheilitis

•

Nystatin­triamcinolone (Mycolog II) ointment applied on the affected areas after meals and at bedtime

•

Nystatin­triamcinolone (Mycolog II) ointment applied on the affected areas after meals and at bedtime

•

Clotrimazole 1% (Mycelex) cream

 
•

Miconazole 2% cream applied q12h

•

Clotrimazole 1% (Mycelex) cream

on the affected areas, for 1­2 weeks

•

Miconazole 2% cream applied q12h on the affected areas, for 1­2 weeks

 

Herpes Simplex

Systemic

Systemic

•

Ganciclovir, Valacyclovir and Famciclovir are probably effective.

Virus (HSV)

•

Acyclovir (Zovirax)

•

Acyclovir 10 mg/kg PO q4h or q6h

Infection

800

mg PO q4h,

•

Acyclovir 10 mg/kg IV q8h

•

Foscarnet is the drug of choice for Acyclovir­resistant cases.

for 10 days

•

Foscarnet 24­40 mg/kg PO q8h, for

•

Foscarnet 24­40 mg/kg PO q8h, for resistant herpetic lesions

resistant herpetic lesions

•

Patients taking Acyclovir should be instructed to drink plenty of fluids.

   
•

Topical antiviral medications may be used for labial and perioral herpetic lesions.

Linear Gingival

Local

   

Local

•

Prophylaxis is recommended:

Erythema

•

Scaling and root planing

•

Scaling and root planing

brushing, flossing, and use of mouth rinses.

(LGE)

•

0.12% Chlorhexidine gluconate (Periogard, Peridex) 0.5 oz q12h rinse, for 30 sec. and spit

•

0.12% Chlorhexidine gluconate (Periogard, Peridex) 0.5 oz q12h rinse, for 30 sec. and spit

•

Antifungal agents may be useful in the treatment of LGE.

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Oral Manifestations of HIV Infection

Table 3. Therapeutic options for the most common HIV-associated oral manifestations 23,34,35,36,37 (continued)

Oral Lesion

Treatment for Adults

Treatment for Children

Comments

Linear Gingival

Local

Local

•

Prophylaxis is recommended:

Erythema

•

Scaling and root planing

•

Scaling and root planing

brushing, flossing, and use of mouth rinses.

(LGE)

•

0.12% Chlorhexidine gluconate (Periogard, Peridex) 0.5 oz q12h rinse, for 30 sec. and spit

•

0.12% Chlorhexidine gluconate (Periogard, Peridex) 0.5 oz q12h rinse, for 30 sec. and spit

•

Antifungal agents may be useful in the treatment of LGE.

Xerostomia

Topical

Topical

•

Good oral hygiene measures and diet control (control of sugar and sugary foods) are recommended to prevent dental caries.

•

Chewing or sucking sugarless candy

•

Chewing or sucking sugarless candy

•

Frequent sips of water

•

Frequent sips of water

•

Commercial artificial saliva

•

Commercial artificial saliva substitutes

substitutes

•

Mouth rinses with high alcohol content should be avoided due to drying effect.

•

Topical fluoride products

•

Topical fluoride products

 

Systemic

 
•

Pilocarpine (Salagen)

5

mg PO q8h before

meals; it may increase to 7.5 mg PO q8h

Parotid

Systemic

Systemic

•

Surgical removal of the parotid gland may be necessary for esthetic reasons.

Enlargement (of

•

Non­steroidal

•

Non­steroidal anti­inflammatories

major salivary

anti­inflammatories

•

Analgesics

glands)

•

Analgesics

•

Antibiotics

 
•

Antibiotics

•

Steroids

•

Steroids

 

Oral Hairy Leukoplakia (OHL)

Local

Local

•

Recurrence often occurs after the treatment is discontinued.

•

Podophyllin resin 25% 1­2 applications

•

Podophyllin resin 25% 1­2 applica­ tions on the affected areas, at 1 week apart

 
•

OHL is rare in children. Symptomatic and extensive lesions may require topical treatment.

on the affected areas, at

1

week apart

•

Retinoic acid (Tretinoin)

•

Retinoic acid (Tretinoin)

•

Surgical excision

•

OHL has been shown to disappear in patients receiving zidovudine (AZT).

•

Surgical excision

 

Systemic

•

Acyclovir (Zovirax) 800 mg PO q4h or q6h, for 14 days

 
•

Famciclovir 500 mg PO q8h, for 5­10 days

•

Valacyclovir 1000 mg PO q8h, for 5­10 days

Necrotizing

Local

Local

•

Prolonged use of chlorhexidine may cause staining of teeth, tongue, and restorations; taste alteration; and mucosal desquamation and irritation.

Ulcerative

•

Debridement of affected areas

•

Debridement of affected areas

Gingivitis (NUG),

•

Irrigation with povidon­iodine

•

Irrigation with povidon­ iodine (10% Betadine)

(10% Betadine)

Necrotizing Ulcerative Periodontitis (NUP),

•

0.12% chlorhexidine gluconate

•

0.12% chlorhexidine gluconate (Peridex, Periogard) mouth rinse

(Peridex, Periogard) mouth rinse

•

Metronidazole should not be given to patients taking didanosine (ddI) or zalcitabine (ddC), because it may potentiate peripheral neuropathy.

q12h

Necrotizing

q12h

 

Stomatitis (NS)

 

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HIV Curriculum for the Health Professional

Table 3. Therapeutic options for the most common HIV-associated oral manifestations 23,34,35,36,37 (concluded)

Oral Lesion

Treatment for Adults

Treatment for Children

Comments

Necrotizing

Systemic

Systemic

(See chart on previous page)

Ulcerative

•

Metronidazole (Flagyl)

•

Metronidazole (Flagyl) 15­35 mg/kg

Gingivitis (NUG),

250

mg PO q8h or

PO q8h, for 7­10 days

500

mg q12h, for 7­10 days

•

Clindamycin (Cleocin) 20­30 mg/kg

Necrotizing Ulcerative Periodontitis (NUP),

•

Clindamycin (Cleocin)

PO q6h, for 7 days

150

mg PO q6h or

•

Amoxicillin clavulanate (Augmentin)

300

mg PO q8h, for 7 days

40 mg/kg PO q8h, for 7 days

 
•

Amoxicillin clavulanate (Augmentin) 250 mg PO q12h, for 7 days

 

Necrotizing

Stomatitis (NS)

Oral Ulcers

Topical

Topical

•

Major aphthous ulcers usually require systemic steroids.

(Recurrent

•

Triamcinolone in Carboxymethylcellulose 0.1% paste

•

Triamcinolone in Carboxymethyl­ cellulose 0.1% paste applied in a thin layer q6h daily

Aphthous Ulcers)

•

Aphthous ulcers may be exacebated by stress.

•

Betamethasone phosphate:

•

Betamethasone phosphate:

•

Iron, vitamin B12, and folate deficiencies should be ruled out.

– 0.5 mg tablet dissolved in 10 ml

– 0.5 mg tablet dissolved in 10 ml mouthwash and rinse q4h

mouthwash and rinse q4h

•

Dexamethasone elixir should be

– spray on ulcer (1 spray = 100 μg) up to 800 μg

used for multiple ulcers or ulcers not accessible for topical applica­ tion.

– spray on ulcer (1 spray = 100 μg) up to 800 μg

•

Fluocinonide (Lidex) 0.05% ointment q4h

•

Thalidomide is indicated only when recurrences are severe and frequent.

•

Fluocinonide (Lidex) 0.05% ointment applied on ulcer q4h

•

Dexamethasone elixir (0.5 mg/5ml) rinse and expectorate

 
•

The treatment with Thalidomide should be monitored thoroughly due to its teratogenicity. Birth control measures are required.

•

Dexamethasone elixir (0.5 mg/5ml) rinse and expectorate

Systemic

•

Prednisone 2 mg/kg q6h, for 5­7 days with gradual tapering

Systemic

   
•

Prednisone starting at 30­40 mg PO daily with taper over 1 month for severe disease resistant to topical agents

•

Thalidomide 200 mg PO daily

Oral Warts

Topical

Topical

•

The recurrence rate is high.

•

Podophyllin resin 25% applications q6h for long period

•

Podophyllin resin 25% applications q6h for long period

•

Concurrent therapeutic approaches should be considered.

•

Surgical excision

 
•

Surgical excision

•

Laser ablation

•

Laser ablation

•

Cryotherapy

•

Cryotherapy

 

Systemic

•

Cimetidine (Tagamet)

600

mg PO q6h, for long

period (months)

•

Interferon alfa–n3 SC/IM 3,000,000 U (1 ml) qwk, for several weeks

Abbreviations used in Table 3: PO = per os (by mouth); IV = intravenous; qd = every day; qwk = every week; q2h = every two hours; q4h = every four hours; q6h = every six hours; q8h = every 8 hours; q12h = every 12 hours.

190

Oral Manifestations of HIV Infection

Noma, also known as cancrum oris, is a gangrenous condition that affects primarily children. Noma has been reported mainly in developing countries in West Africa, but cases have also been described in other parts of the world. It is a multifactorial disease. The most important risk factors are poverty, chronic malnutrition, poor oral hygiene, and severe immunosuppression. Though considered a preventable disease, noma has a case fatality rate of 70%­90% if left untreated.

Herpes Simplex Virus Infection

Herpes simplex virus (HSV) infection may be either primary (herpetic gingivostomatitis) or secondary (herpes labialis). The prevalence of oral HSV infection varies between 10% and 35% in HIV­infected adults and children. The presence of HSV infection for more than 1 month constitutes an AIDS­defining condition.

Clinical appearance. HSV infection appears as a crop of vesicles usually localized on the keratinized mucosa (hard palate, gingiva) and/or vermillion borders of the lips and perioral skin (Figure 5). The vesicles rupture and form irregular painful ulcers. They may interfere with mastication and swallowing, resulting in decreased oral intake and dehydration.

Treatment. Systemic therapy with antiviral agents is recommended (Table 3). The treatment is more effective if it is instituted in the prodromal stage of infection.

Recurrent Aphthous Ulcers

Recurrent aphthous ulcers (RAUs) occur in about 1%­7% of HIV­infected patients. They are painful ulcers on the nonkeratinized oral mucosa, such as labial and buccal mucosa, soft palate, and ventral aspect of the tongue. Severe recurrent aphthous lesions usually occur when the CD4 + lymphocyte count is less than 100 cells/μL. This result may be suggestive of HIV disease progression. The etiology of RAUs is not well known.

Clinical appearance. RAUs may present as minor, major, or herpetiform aphthae. Minor aphthous ulcers are ulcers less than 5 mm in diameter covered by pseudomembrane and surrounded by an erythematous halo. They usually heal spontaneously without scarring (Figure 6). Major aphthous ulcers resemble minor aphthous ulcers, but they are fewer and larger in diameter (1­3 cm), are more painful, and may persist longer. Their presence interferes with mastication, swallowing, and speaking. Healing occurs over 2­6 weeks. Scarring is common. Herpetiform

aphthous ulcers occur as a crop of many small lesions (1­2 mm) disseminated on the soft palate, tonsils, tongue, and/or buccal mucosa.

Treatment. The first line of management of RAUs is pain control and prevention of superinfection. Depending on the severity of the ulcers, topical and/or systemic steroid agents are recommended (Table 3).

Parotid Enlargement and Xerostomia

Parotid enlargement is commonly associated with HIV infection in children (10%­30%) and less commonly in adults. It occurs in the late course of HIV infection and is associated with a slower rate of HIV disease progression. The median time from its diagnosis to death has been reported to be 5.4 years among HIV­infected children. Lymphocytic infiltration of the salivary glands may be an etiologic factor.

Clinical appearance. Parotid enlargement occurs as unilateral or bilateral swelling of the parotid glands. It is usually asymptomatic and may be accompanied by decreased salivary flow (xerostomia or dry mouth). Problems with dry mouth in HIV­infected patients are often caused by medications that interfere with salivary secretion, such as antihistamines, antianxiety medications, antidepressants, and some antiretroviral drugs (didanosine and zalcitabine).

Treatment. Treatment is required only in severe cases and may consist of systemic analgesics, anti­ inflammatories, antibiotics, and/or steroids (Table 3).

Human Papillomavirus Infection (Oral Warts)

The incidence of oral warts due to human papillomavirus infection has increased dramatically since the era of HAART. The lesions are more prevalent in adults (1%­4% of cases) than in children.

Clinical appearance. Oral warts may appear cauliflower­ like, spiked, or raised with a flat surface. They are asymptomatic. The most common location is the labial and buccal mucosa. The most common clinical presentation is multifocal flat lesions resembling focal epithelial hyperplasia (Heck’s disease).

Treatment. Treatment may be required for patients with multiple lesions. Topical and systemic agents and various surgical approaches are available (Table 3).

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General Management Considerations

To prevent the need for expensive dental services, it is imperative to treat the oral manifestations of HIV infection at all levels of care. Personal oral hygiene practices, such as tooth brushing and use of interdental cleaning aids, are the most effective ways of maintaining good oral health.

At the primary level of oral care, prevention of oral diseases takes priority. Prevention involves improving oral hygiene awareness through health education at the individual and community levels. Oral health education messages should be made visible in all community forums. Home­based care providers should undergo training in basic oral hygiene practices so that they can impart these to patients under their care. Use of simple materials such as warm salty mouth rinse or commercial mouthwash (chlorhexidine) can improve basic oral hygiene cost­effectively. Patients whose manual dexterity is intact should be taught appropriate brushing techniques. Other adjuvant oral hygiene methods, such as flossing and use of interdental toothbrushes, will depend on the availability and affordability of supplies.

The secondary level of oral care involves visits to clinical care facilities. Depending on local resources, the health cadre available at this level may range from nursing staff at a health center to primary care physicians. In some countries, health centers may have no oral health personnel or may offer only relief of pain with analgesics and extractions. Health care workers at this level should be trained to recognize suspicious lesions that may be oral manifestations of HIV infection, and they should know when and where to refer patients to a higher level of oral care.

At the tertiary level of oral care, a dentist should be available to make definitive diagnoses of oral lesions and provide professional oral services such as prophylaxis, restorations, biopsies, and the prescription of appropriate medication.

Acknowledgment

We thank Professor Sudeshi Naidoo, Department of Community Dentistry, Faculty of Dentistry and WHO Collaborating Centre, University of the Western Cape, South Africa, for providing the pictures of oral lesions used in this chapter.

References

1.

Arendorf TM, Bredekamp B, Cloete CAC, et al. Oral manifestations of HIV infection in 600 South African patients. J. Oral Pathol. Med. 1998;27:176­179.

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