Oral Manifestations of HIV Infection - PDF - PDF

Document Sample
Oral Manifestations of HIV Infection - PDF - PDF Powered By Docstoc
					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. 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. 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.

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. 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 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 • 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.

Classification of Orofacial Lesions Associated with HIV
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.
188 188

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 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.

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.

Table 1. Orofacial lesions associated with HIV/AIDS in adults
Lesions strongly associated with HIV infection • Candidiasis – Erythematous – Pseudomembranous • Hairy leukoplakia • Kaposi’s sarcoma Lesions less commonly associated with HIV infection • Non­Hodgkin’s lymphoma • Periodontal disease – Linear gingival erythema – Necrotizing (ulcerative) gingivitis – Necrotizing (ulcerative) periodontitis • Viral infections – Herpes simplex virus – Human papillomavirus (wart­like lesions) – Condyloma acuminatum – Focal epithelial hyperplasia – Verruca vulgaris – Varicella zoster virus – Herpes zoster – Varicella

1 2

• Bacterial infections – Mycobacterium avium­intracellulare – Mycobacterium tuberculosis • Melanotic hyperpigmentation • Necrotizing (ulcerative) stomatitis • Salivary gland disease – Dry mouth due to decreased salivary flow rate – Unilateral or bilateral swelling of the major salivary glands • Thrombocytopenic purpura • Ulceration NOS (not otherwise specified) Lesions seen in HIV infection • Bacterial infections – Actinomyces Israel – Escherichia coli – Klebsiella pneumoniae • Cat­scratch disease • Drug reactions (ulcerative, erythema multiforme, lichenoid, toxic epidermolysis • Epithelioid (bacillary) angiomatosis • Neurologic disturbances – Facial palsy – Trigeminal neuralgia
189

3

• Fungal infection other than candidiasis – Cryptococcus neoformans – Geotrichum candidum – Histoplasma capsulatum – Mucoraceae (mucormycosis/ zygomycosis) – Aspergillus flavus • Recurrent aphthous stomatitis • Viral infections – Cytomegalovirus – Molluscum contagiosum

HIV Curriculum for the Health Professional

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).

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.

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

Table 2. Orofacial lesions associated with pediatric HIV infection
Lesions commonly associated with pediatric HIV infection • Oral candidiasis – Pseudomembranous – Erythematous – Angular cheilitis • Herpes simplex virus infection • Linear gingival erythema • Bacterial infections of oral tissues • Periodontal diseases – Necrotizing ulcerative gingivitis – Necrotizing ulcerative periodontitis – Necrotizing stomatitis • Xerostomia • Seborrheic dermatitis • Neoplasms – Kaposi’s sarcoma and non­Hodgkin’s lymphoma • Oral hairy leukoplakia • Tuberculosis­related ulcers • Parotid enlargement (swelling of the major salivary glands) • Recurrent aphthous ulcers – Minor – Major – Herpetiform

1 2 3

Lesions less commonly associated with pediatric HIV infection • Viral infections – Cytomegalovirus – Human papillomavirus – Molluscum contagiosum – Varicella zoster virus – Herpes zoster – Varicella

Lesions strongly associated with HIV infection but rare in children

190

Oral Manifestations of HIV Infection

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.

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.

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

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

Figure 6. Recurrent minor Aphthous Ulcers in an HIV-infected adult
191

HIV Curriculum for the Health Professional
Table 3. Therapeutic options for the most common HIV-associated oral manifestations23,34,35,36,37
Oral Lesion Oral Candidiasis (Erythematous, Pseudomembranous, and Hyperplastic) Treatment for Adults Topical • Nystatin (Mycostatin) • Oral gel: apply gel q8h or q6h, for 10­14 days • Cream: Apply q12h, for 10­14 days Systemic • Nystatin (Mycostatin) 400,000­600,000 U q6h, for 14 days • Ketoconazole (Nizoral) 200­400 mg PO q.d. • Fluconazole (Diflucan) 50­100 mg PO q.d. • Itraconazole (Sporanox) (Capsules or solution) 200 mg PO qd for 7 days • Amphotericin B10 mg IVq6h, for 10 days Treatment for Children Topical • Nystatin suspension 200,000­ 400,000 U/day divided in 4­6 doses, for 14 days • Clotrimazole troches 10 mg q8h or q6h, for 4 weeks • Gentian violet 1% aqueous solution painted in the affected areas q8h antifungal agents are administered Systemic • Ketoconazole 3.5­6.6 mg/kg/day in a single dose • Fluconazole 6 mg/kg on day 1, then 3 mg/kg qd, up to 2 weeks • Itraconazole 100 mg PO, daily for children older than 3 years Comments • Different forms of oral candidiasis may occur simultaneously. • Hyperplastic candidiasis requires systemic treatment. • Ketoconazole may interact with Lopinavir­Ritonavir (Kaletra) at doses >200 mg/day. • Topical fluoride should be used if for long periods to counteract high sugar content of some antifungal medications. • Amphotericin B may be used in azole­resistant infections. • Amphotericin B may also be available as a topical preparation. • Dentures should be removed when medication is applied.

Prophylaxis • Clotrimazole 10 mg PO q8h or q12h for long period Prophylaxis • Nystatin 100,000­400,000 U PO • Fluconazole 100 mg q12h for long period PO qwk, for long period • Fluconazole 3­6 mg/kg PO daily or weekly for long period Angular Cheilitis Topical • Nystatin­triamcinolone (Mycolog II) ointment applied on the affected areas after meals and at bedtime • Clotrimazole 1% (Mycelex) cream • Miconazole 2% cream applied q12h on the affected areas, for 1­2 weeks Systemic • Acyclovir (Zovirax) 800 mg PO q4h, for 10 days • Foscarnet 24­40 mg/kg PO q8h, for resistant herpetic lesions Topical • Lesions tend to heal slowly • Nystatin­triamcinolone (Mycolog II) because of the repeated opening ointment applied on the affected of the mouth. areas after meals and at bedtime • Clotrimazole 1% (Mycelex) cream • Miconazole 2% cream applied q12h on the affected areas, for 1­2 weeks

Herpes Simplex Virus (HSV) Infection

Systemic • Acyclovir 10 mg/kg PO q4h or q6h • Acyclovir 10 mg/kg IV q8h • Foscarnet 24­40 mg/kg PO q8h, for resistant herpetic lesions

Linear Gingival Erythema (LGE)

Local • Scaling and root planing • 0.12% Chlorhexidine gluconate (Periogard, Peridex) 0.5 oz q12h rinse, for 30 sec. and spit

Local • Scaling and root planing • 0.12% Chlorhexidine gluconate (Periogard, Peridex) 0.5 oz q12h rinse, for 30 sec. and spit

• Ganciclovir, Valacyclovir and Famciclovir are probably effective. • Foscarnet is the drug of choice for Acyclovir­resistant cases. • Patients taking Acyclovir should be instructed to drink plenty of fluids. • Topical antiviral medications may be used for labial and perioral herpetic lesions. • Prophylaxis is recommended: brushing, flossing, and use of mouth rinses. • Antifungal agents may be useful in the treatment of LGE. Continued on next page

192

Oral Manifestations of HIV Infection
Table 3. Therapeutic options for the most common HIV-associated oral manifestations23,34,35,36,37 (continued)
Oral Lesion Linear Gingival Erythema (LGE) Treatment for Adults Local • Scaling and root planing • 0.12% Chlorhexidine gluconate (Periogard, Peridex) 0.5 oz q12h rinse, for 30 sec. and spit Topical • Chewing or sucking sugarless candy • Frequent sips of water • Commercial artificial saliva substitutes • Topical fluoride products Systemic • Pilocarpine (Salagen) 5 mg PO q8h before meals; it may increase to 7.5 mg PO q8h Parotid Enlargement (of major salivary glands) Systemic • Non­steroidal anti­inflammatories • Analgesics • Antibiotics • Steroids Systemic • Non­steroidal anti­inflammatories • Analgesics • Antibiotics • Steroids Local • Podophyllin resin 25% 1­2 applica­ tions on the affected areas, at 1 week apart • Retinoic acid (Tretinoin) • Surgical excision • Surgical removal of the parotid gland may be necessary for esthetic reasons. Treatment for Children Local • Scaling and root planing • 0.12% Chlorhexidine gluconate (Periogard, Peridex) 0.5 oz q12h rinse, for 30 sec. and spit Topical • Chewing or sucking sugarless candy • Frequent sips of water • Commercial artificial saliva substitutes • Topical fluoride products Comments • Prophylaxis is recommended: brushing, flossing, and use of mouth rinses. • Antifungal agents may be useful in the treatment of LGE. • Good oral hygiene measures and diet control (control of sugar and sugary foods) are recommended to prevent dental caries. • Mouth rinses with high alcohol content should be avoided due to drying effect.

Xerostomia

Oral Hairy Local Leukoplakia (OHL) • Podophyllin resin 25% 1­2 applications on the affected areas, at 1 week apart • Retinoic acid (Tretinoin) • 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 Local • Debridement of affected areas • Irrigation with povidon­ Necrotizing iodine (10% Betadine) Ulcerative • 0.12% chlorhexidine Periodontitis (NUP), gluconate (Peridex, Periogard) mouth rinse Necrotizing q12h Stomatitis (NS) Necrotizing Ulcerative Gingivitis (NUG),

• Recurrence often occurs after the treatment is discontinued. • OHL is rare in children. Symptomatic and extensive lesions may require topical treatment. • OHL has been shown to disappear in patients receiving zidovudine (AZT).

Local • Debridement of affected areas • Irrigation with povidon­iodine (10% Betadine) • 0.12% chlorhexidine gluconate (Peridex, Periogard) mouth rinse q12h

• Prolonged use of chlorhexidine may cause staining of teeth, tongue, and restorations; taste alteration; and mucosal desquamation and irritation. • Metronidazole should not be given to patients taking didanosine (ddI) or zalcitabine (ddC), because it may potentiate peripheral neuropathy.

Continued on next page
193

HIV Curriculum for the Health Professional
Table 3. Therapeutic options for the most common HIV-associated oral manifestations23,34,35,36,37 (concluded)
Oral Lesion Necrotizing Ulcerative Gingivitis (NUG), Treatment for Adults Treatment for Children Comments Systemic • Metronidazole (Flagyl) 250 mg PO q8h or 500 mg q12h, for 7­10 days Necrotizing • Clindamycin (Cleocin) Ulcerative 150 mg PO q6h or Periodontitis (NUP), 300 mg PO q8h, for 7 days • Amoxicillin clavulanate Necrotizing (Augmentin) 250 mg PO Stomatitis (NS) q12h, for 7 days Oral Ulcers (Recurrent Aphthous Ulcers) Topical • Triamcinolone in Carboxymethylcellulose 0.1% paste • Betamethasone phosphate: – 0.5 mg tablet dissolved in 10 ml mouthwash and rinse q4h – spray on ulcer (1 spray = 100 μg) up to 800 μg • Fluocinonide (Lidex) 0.05% ointment applied on ulcer q4h • Dexamethasone elixir (0.5 mg/5ml) rinse and expectorate 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 • Podophyllin resin 25% applications q6h for long period • Surgical excision • Laser ablation • 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.

Systemic (See chart on previous page) • Metronidazole (Flagyl) 15­35 mg/kg PO q8h, for 7­10 days • Clindamycin (Cleocin) 20­30 mg/kg PO q6h, for 7 days • Amoxicillin clavulanate (Augmentin) 40 mg/kg PO q8h, for 7 days

Topical • Triamcinolone in Carboxymethyl­ cellulose 0.1% paste applied in a thin layer q6h daily • Betamethasone phosphate: – 0.5 mg tablet dissolved in 10 ml mouthwash and rinse q4h – spray on ulcer (1 spray = 100 μg) up to 800 μg • Fluocinonide (Lidex) 0.05% ointment q4h • Dexamethasone elixir (0.5 mg/5ml) rinse and expectorate Systemic • Prednisone 2 mg/kg q6h, for 5­7 days with gradual tapering

• Major aphthous ulcers usually require systemic steroids. • Aphthous ulcers may be exacebated by stress. • Iron, vitamin B12, and folate deficiencies should be ruled out. • Dexamethasone elixir should be used for multiple ulcers or ulcers not accessible for topical applica­ tion. • Thalidomide is indicated only when recurrences are severe and frequent. • The treatment with Thalidomide should be monitored thoroughly due to its teratogenicity. Birth control measures are required.

Topical • Podophyllin resin 25% applications q6h for long period • Surgical excision • Laser ablation • Cryotherapy

• The recurrence rate is high. • Concurrent therapeutic approaches should be considered.

194

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. 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).

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.

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).

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

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).
195

HIV Curriculum for the Health Professional

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.

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. 2. Winfert M, Grimes RM, Lynch DP. Oral manifestations of HIV infection. Ann. Intern. Med. 1996;125:485­496. 3. Kamiru HN, Naidoo S. Oral HIV lesions and oral health behaviour of HIV positive patients attending Queen Elizabeth II Hospital, Maseru, Lesotho. SADJ 2002;57:479­482. 4. Patton LL, Phelan JA, Ramos­Gomez FJ, et al. Prevalence and classification of HIV­associated oral lesions. Oral Dis. 2002;8(Suppl 2):98­109. 5. Chapple ILC, Rout PJ, Basu MK. Gingival Kaposi’s sarcoma: the first indication of HIV infection. Dent. Update 1992;19:296­301. 6. Klein RS, Harris CA, Small CB, et al. Oral candidiasis in high­risk patients as the initial manifestations of the acquired immunodeficiency syndrome. N. Engl. J. Med. 1984;311:354­358. 7. Centers for Disease Control and Prevention. 1993 revised classification system for HIV infection and expanded surveillance case definition for AIDS among adolescents and adults. MMWR Recomm. Rep. 1993;41(RR­17):1­19. 8. Ramos­Gomez FJ, Petru A, Hilton JF. Oral manifestations and dental status in paediatric HIV infection. Int. J. Paediatr. Dent. 2000;10:3­11. 9. Magalhaes GM, Bueno DF, Serra E. Oral manifestations of HIV positive children. J. Clin. Pediatr. Dent. 2001;25:103­106. 10. Nicolatou O, Theodoridou M, Mostrou G. Oral lesions in children with perinatally acquired immunodeficiency virus infection. J. Oral Pathol. Med. 1999;28:49­53. 11. Begg MD, Lamster IB, Panageas KS. A prospective study of oral lesions and their predictive value for progression of HIV disease. Oral Dis. 1997;3:176­ 183. 12. Chapple ILC, Hamburger J. The significance of oral health in HIV disease. Sex Transm. Inf. 2000;76:236­ 243. 13. Katz MH, Mastrucci T, Leggott PJ, et al. Prognostic significance of oral lesions in children with perinatally acquired human immunodeficiency virus infection. Am. J. Dis. Child. 1993;147:45­48.

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.
196

Oral Manifestations of HIV Infection
14. Barasch A, Safford MM, Catalanotto FA, et al. Oral soft tissue manifestations in HIV­positive vs. HIV­ negative children from an inner city population: a two­year observational study. Pediatr. Dent. 2000;22:215­220. 15. Schmidt­Westhausen AM, Priepke F, Bergmann FJ, et al. Decline in the rate of oral opportunistic infections following introduction of highly active antiretroviral therapy. J. Oral Pathol. Med. 2000;29:336­341. 16. Darbyshire J. Therapeutic interventions in HIV infection—a critical review. Trop. Med. Int. Health 2000;5:A26­A31. 17. Scully C, Diz Dios P. Orofacial effects of antiretroviral therapies. Oral Dis. 2001;7:205­210. 18. Royce RA, Luckman RS, Fusaro RE, et al. The natural history of HIV­1 infection: staging classifications of disease. AIDS 1991;5:355­364. 19. EC Clearinghouse on Oral Problems Related to HIV Infection and WHO Collaborating Centre on Oral Manifestations of the Human Immunodeficiency Virus. An update of the classification and diagnostic criteria of oral lesions in HIV infection. J. Oral Pathol. Med. 1991;20:97­100. 20. EC Clearinghouse on Oral Problems Related to HIV Infection and WHO Collaborating Centre on Oral Manifestations of the Human Immunodeficiency Virus. Classification and diagnostic criteria for oral lesions in HIV infection. J. Oral Pathol. Med. 1993;22:289­291. 21. Ramos­Gomez FJ, Flaitz CM, Catapano P, et al.; Collaborative Workgroup on Oral Manifestations of Pediatric HIV Infection, Oral AIDS Center, University of California, San Francisco, San Francisco, California. Classification, diagnostic criteria, and treatment recommendations for orofacial manifestations in HIV­infected pediatric patients. J. Clin. Pediatr. Dent. 1999;23:85­96. 22. Kline MW. Oral manifestations of pediatric human immunodeficiency HIV infection: a review of the literature. Pediatrics 1996;97:380­388. 23. Kline MW. Cutaneous and oral manifestations of pediatric HIV infection. In Pizzo PA & Wilfert CM (Eds.): Pediatric AIDS: The Challenge of HIV Infection in Infants, Children, and Adolescents. 3rd ed. Baltimore: Williams & Wilkins, 1998. 24. Flaitz CM, Hicks MJ. Oral manifestations in pediatric HIV infection. In: Shearer WT & Hanson CI (Eds.): Medical Management of AIDS in Children. Philadelphia: Saunders, 2003. 25. Schiodt M, Pindborg JJ. AIDS and the oral cavity: epidemiology and oral manifestations of HIV infection: a review. Int. J. Oral Maxillofac. Surg. 1987;16:1­14. 26. Ramos­Gomez FJ, Hilton JF, Canchola AJ, et al. Risk factors for HIV­related orofacial soft­ tissue manifestations in children. J. Pediatr. Dent. 1996;18:121­126. 27. Walling DM. Oral hairy leukoplakia: an Epstein­Barr virus­associated disease of patients with HIV. Res. Initiat. Treat Action 2000;6:10­15. 28. Lifson AR, Hilton JF, Westenhouse JL, et al. Time from seroconversion to oral candidiasis or hairy leukoplakia among homosexual and bisexual men enrolled in three prospective cohorts. AIDS 1994;8:73­79. 29. Berthold P. Noma: a forgotten disease. Dent. Clin. N. Am. 2003;47:559­574. 30. Enwonwu CO, Falkler WA, Idigbe EO, et al. Noma (cancrum oris): questions and answers. Oral Dis. 1999;5:144­149. 31. Schiodt M. Less common oral lesions associated with HIV infection: prevalence and classification. Oral Dis. 1997;3:S208­S213. 32. Clark PC, Flaitz CM, Nichols CM, et al. Oral human papillomavirus infection in HIV: clinicopathologic correlations. J. Dent. Res. 1998;77:250A. 33. Brothell DJ, Jutai DK, Hawkins RJ. An update of mechanical oral hygiene practices: evidence­based recommendations for disease prevention. J. Can. Dent. Assoc. 1998;46:295­306. 34. Gage TW, Picket FA. Mosby’s Dental Drug Reference. 6th ed. St. Louis: Mosby, 2003. 35. Naidoo S, Chikte U. HIV/AIDS—the evolving pandemic and its impact on oral health in sub­ Saharan Africa. SADJ 1999;54:661­630.

197


				
DOCUMENT INFO