sign in sign up
<<
Home , Betamethasone phosphate, Hairy leukoplakia, Linear gingival erythema, Noma (disease), Oral candidiasis, Salivary gland disease

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

184 184 Oral Manifestations of HIV Infection

Tables 1 and 2 show this classification of orofacial Clinical appearance. Oral is often observed lesions associated with HIV/AIDS in adults and children, in one of the following four clinical forms: erythematous respectively. (atrophic) candidiasis, pseudomembranous candidiasis, hyperplastic candidiasis, and angular . Clinical Presentation and 1. Erythematous (atrophic) candidiasis appears Management clinically as multiple small or large patches, most often localized on the and/or (Figure 1). Oral candidiasis is the most common orofacial manifes­ 2. Pseudomembranous candidiasis (oral thrush) tation of HIV infection. Its prevalence may depend on is characterized by the presence of multiple study population, diagnostic criteria, study design, and superficial, creamy white plaques that can be availability of antiretroviral therapy. Reported prevalence easily wiped off, revealing an erythematous base rates have varied widely, to as high as 72% in children (Figure 2). They are usually located on the buccal and 94% in adults. Oral candidiasis is also a significant mucosa, oropharynx, and/or dorsal face of the predictor of HIV disease progression in both adults and tongue. children. The median time of survival from its clinical 3. Hyperplastic candidiasis lesions appear white and diagnosis to death is 3.4 years among HIV-infected hyperplastic and cannot be removed by scraping. children. The main etiologic factor of oral candidiasis is This form of oral candidiasis is rare in HIV- the albicans, although other species of infected individuals. Candida may be involved.

Table 1. Orofacial lesions associated with HIV/AIDS in adults Lesions strongly associated with HIV infection • Candidiasis • Non-Hodgkin’s – Erythematous • – Pseudomembranous – Linear gingival 1 • Hairy – Necrotizing (ulcerative) • Kaposi’s sarcoma – Necrotizing (ulcerative) periodontitis Lesions less commonly associated with HIV infection • Bacterial infections • Viral infections – Mycobacterium avium-intracellulare – virus – Mycobacterium tuberculosis – Human papillomavirus (-like lesions) • Melanotic hyperpigmentation – Condyloma acuminatum • Necrotizing (ulcerative) – Focal epithelial 2 • disease – Verruca vulgaris – Dry due to decreased salivary flow rate – Varicella zoster virus – Unilateral or bilateral swelling of the major – Herpes zoster salivary glands – Varicella • • Ulceration NOS (not otherwise specified) Lesions seen in HIV infection • Bacterial infections • Fungal infection other than candidiasis – Actinomyces Israel – – Escherichia coli – – Klebsiella pneumoniae – • Cat-scratch disease – Mucoraceae (/ ) • Drug reactions (ulcerative, , – flavus 3 lichenoid, toxic epidermolysis • Recurrent • Epithelioid (bacillary) angiomatosis • Viral infections • Neurologic disturbances – Cytomegalovirus – Facial palsy – – Trigeminal neuralgia

185 HIV Curriculum for the Health Professional

Figure 1. Erythematous candidiasis in an HIV-infected child Figure 2. Pseudomembranous candidiasis in an HIV-infected child

4. is characterized by the presence presence of OHL is a sign of severe . of erythematous fissures at the corners of the OHL is a significant predictor of HIV disease progression mouth. It is usually accompanied by another form in adults. Although its etiology is not clear, OHL seems to of intraoral candidiasis. be caused by Epstein-Barr virus infection.

Treatment. Treatment with topical and systemic Clinical appearance. OHL presents as white, thick agents is recommended (Table 3). patches that do not wipe away and that may exhibit vertical corrugations with a hairlike appearance (Figure Oral 3). The lesions usually start on the lateral margins Oral hairy leukoplakia (OHL) is more common among of the tongue and sometimes inside the cheeks and HIV-infected adults than among HIV-infected children. lower . They may be unilateral or bilateral, and they The reported prevalence of OHL in adults is about 20%- are asymptomatic. OHL is often associated with oral 25%, increasing as the CD4+ lymphocyte count decreases, candidiasis. 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 • Parotid enlargement (swelling of the major salivary glands) – Pseudomembranous • Recurrent aphthous ulcers – Erythematous – Minor 1 – Angular cheilitis – Major • Herpes simplex virus infection – Herpetiform • Lesions less commonly associated with pediatric HIV infection • Bacterial infections of oral tissues • Viral infections • Periodontal – Cytomegalovirus – Necrotizing ulcerative gingivitis – Human papillomavirus – Necrotizing ulcerative periodontitis – Molluscum contagiosum 2 – Necrotizing stomatitis – Varicella zoster virus • – Herpes zoster • Seborrheic dermatitis – Varicella Lesions strongly associated with HIV infection but rare in children • Neoplasms – Kaposi’s sarcoma and non-Hodgkin’s lymphoma 3 • Oral hairy leukoplakia • Tuberculosis-related ulcers

186 Oral Manifestations of HIV Infection

Figure 3. Oral Hairy Leukoplakia in an HIV-infected adult Figure 4. Linear Gingival Erythema in an HIV-infected adult

Treatment. OHL usually does not require any treatment, erythema on the attached gingiva and oral but in severe cases systemic antivirals are recommended mucosa (Figure 4). The degree of erythema is (Table 3). When OHL is associated with oral candidiasis, disproportionately intense compared with the therapeutic management of oral candidiasis is required. amount of plaque present on the teeth. 2. NUG is more common in adults than in HIV-Associated Periodontal Disease children. It is characterized by the presence of Periodontal (gum) disease is common among HIV- ulceration, sloughing, and necrosis of one or infected patients. It is characterized by bleeding , more interdental papillae, accompanied by pain, bad breath, pain/discomfort, mobile teeth, and some­ bleeding, and fetid halitosis. times sores. Its reported prevalence ranges widely, 3. NUP is characterized by the extensive and rapid between 0% and 50%. Left untreated, HIV-associated loss of soft tissue and teeth. periodontal disease may progress to life-threatening 4. Necrotizing stomatitis is thought to be a con­ infections, such as Ludwig’s angina and (cancrum sequence of severe, untreated NUP. It is charac­ oris). terized by acute and painful ulceronecrotic lesions on the that expose underlying Clinical appearance. Four forms of HIV-associated alveolar bone. periodontal disease have been described: linear gingival erythema, necrotizing ulcerative gingivitis Treatment. Management and control of HIV-associated (NUG), necrotizing ulcerative periodontitis (NUP), and periodontal disease begin with good daily . necrotizing stomatitis. In addition to brushing, flossing and use of 1. Linear gingival erythema is characterized by solutions are effective ways to prevent and control the presence of a 2- to 3-mm red band along periodontal disease. Table 3 presents various therapeutic the marginal gingiva, associated with diffuse options.

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

187 HIV Curriculum for the Health Professional

Table 3. Therapeutic options for the most common HIV-associated oral manifestations23,34,35,36,37 Oral Treatment for Adults Treatment for Children Comments Oral Topical Topical • Different forms of oral candidiasis Candidiasis • (Mycostatin) • Nystatin suspension 200,000­ may occur simultaneously. (Erythematous, • Oral gel: apply gel q8h 400,000 U/day divided in 4-6 doses, • Hyperplastic candidiasis requires Pseudomembranous, or q6h, for 10-14 days for 14 days systemic treatment. and Hyperplastic) • Cream: Apply q12h, for • troches 10 mg q8h or • may interact with 10-14 days q6h, for 4 weeks Lopinavir-Ritonavir (Kaletra) at • Gentian violet 1% aqueous solution doses >200 mg/day. Systemic painted in the affected areas q8h • Topical fluoride should be used if • Nystatin (Mycostatin) antifungal agents are administered for long periods to counteract high 400,000-600,000 U q6h, sugar content of some antifungal for 14 days Systemic medications. • Ketoconazole (Nizoral) • Ketoconazole 3.5-6.6 mg/kg/day in • may be used in 200-400 mg PO q.d. a single dose azole-resistant infections. • Fluconazole (Diflucan) • Fluconazole 6 mg/kg on day 1, then • Amphotericin B may also be 50-100 mg PO q.d. 3 mg/kg qd, up to 2 weeks available as a topical preparation. • Itraconazole (Sporanox) • Itraconazole 100 mg PO, daily for • should be removed when (Capsules or solution) children older than 3 years medication is applied. 200 mg PO qd for 7 days • Amphotericin B10 mg Prophylaxis IVq6h, for 10 days • Clotrimazole 10 mg PO q8h or q12h for long period Prophylaxis • Nystatin 100,000-400,000 U PO • Fluconazole 100 mg q12h for long period PO qwk, for long period • Fluconazole 3-6 mg/kg PO daily or weekly for long period Angular Topical Topical • Lesions tend to heal slowly Cheilitis • Nystatin- • Nystatin-triamcinolone (Mycolog II) because of the repeated opening (Mycolog II) ointment ointment applied on the affected of the mouth. applied on the affected areas after meals and at bedtime areas after meals and • Clotrimazole 1% (Mycelex) cream at bedtime • 2% cream applied q12h • Clotrimazole 1% on the affected areas, for 1-2 weeks (Mycelex) cream • Miconazole 2% cream applied q12h on the affected areas, for 1-2 weeks Herpes Simplex Systemic Systemic • Ganciclovir, Valacyclovir and Virus (HSV) • Acyclovir (Zovirax) • Acyclovir 10 mg/kg PO q4h or q6h Famciclovir are probably effective. Infection 800 mg PO q4h, • Acyclovir 10 mg/kg IV q8h • Foscarnet is the drug of choice for for 10 days • Foscarnet 24-40 mg/kg PO q8h, for Acyclovir-resistant cases. • Foscarnet 24-40 mg/kg resistant herpetic lesions • Patients taking Acyclovir should PO q8h, for resistant be instructed to drink plenty of herpetic lesions 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 brushing, flossing, and use of (LGE) • 0.12% • 0.12% Chlorhexidine gluconate mouth rinses. gluconate (Periogard, (Periogard, Peridex) 0.5 oz q12h • Antifungal agents may be useful in Peridex) 0.5 oz q12h rinse, for 30 sec. and spit the treatment of LGE. rinse, for 30 sec. and spit

Continued on next page

188 Oral Manifestations of HIV Infection

Table 3. Therapeutic options for the most common HIV-associated oral manifestations23,34,35,36,37 (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 (LGE) • 0.12% Chlorhexidine • 0.12% Chlorhexidine gluconate mouth rinses. gluconate (Periogard, (Periogard, Peridex) 0.5 oz q12h • Antifungal agents may be useful in Peridex) 0.5 oz q12h rinse, for 30 sec. and spit the treatment of LGE. rinse, for 30 sec. and spit Xerostomia Topical Topical • Good oral hygiene measures and • Chewing or sucking • Chewing or sucking sugarless candy diet control (control of sugar and sugarless candy • Frequent sips of water sugary foods) are recommended • Frequent sips of water • Commercial artificial to prevent dental caries. • Commercial artificial substitutes • Mouth rinses with high alcohol saliva substitutes • Topical fluoride products content should be avoided due to • Topical fluoride products drying effect.

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 Enlargement (of • Non-steroidal • Non-steroidal anti-inflammatories gland may be necessary for major salivary anti-inflammatories • Analgesics esthetic reasons. glands) • Analgesics • Antibiotics • Antibiotics • • Steroids Oral Hairy Local Local • Recurrence often occurs after the Leukoplakia (OHL) • Podophyllin resin • Podophyllin resin 25% 1-2 applica­ treatment is discontinued. 25% 1-2 applications tions on the affected areas, at • OHL is rare in children. on the affected areas, at 1 week apart Symptomatic and extensive lesions 1 week apart • Retinoic acid (Tretinoin) may require topical treatment. • Retinoic acid (Tretinoin) • Surgical excision • OHL has been shown to disappear • Surgical excision in patients receiving (AZT). Systemic • Acyclovir (Zovirax) 800 mg PO q4h or q6h, for 14 days • Famciclovir 500 mg PO q8h, for 5-10 days • Valacyclovir 1000 mg PO q8h, for 5-10 days Necrotizing Local Local • Prolonged use of chlorhexidine Ulcerative • of • Debridement of affected areas may cause staining of teeth, Gingivitis (NUG), affected areas • Irrigation with povidon-iodine tongue, and restorations; taste • Irrigation with povidon­ (10% Betadine) alteration; and mucosal Necrotizing iodine (10% Betadine) • 0.12% chlorhexidine gluconate desquamation and irritation. Ulcerative • 0.12% chlorhexidine (Peridex, Periogard) mouth rinse • Metronidazole should not be Periodontitis (NUP), gluconate (Peridex, q12h given to patients taking Periogard) mouth rinse didanosine (ddI) or zalcitabine Necrotizing q12h (ddC), because it may potentiate Stomatitis (NS) peripheral neuropathy.

Continued on next page

189 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 Treatment for Adults Treatment for Children Comments Necrotizing Systemic Systemic (See chart on previous page) Ulcerative • Metronidazole (Flagyl) • Metronidazole (Flagyl) 15-35 mg/kg Gingivitis (NUG), 250 mg PO q8h or PO q8h, for 7-10 days 500 mg q12h, for 7-10 days • Clindamycin (Cleocin) 20-30 mg/kg Necrotizing • Clindamycin (Cleocin) PO q6h, for 7 days Ulcerative 150 mg PO q6h or • Amoxicillin clavulanate (Augmentin) Periodontitis (NUP), 300 mg PO q8h, for 7 days 40 mg/kg PO q8h, for 7 days • Amoxicillin clavulanate Necrotizing (Augmentin) 250 mg PO Stomatitis (NS) q12h, for 7 days Oral Ulcers Topical Topical • Major aphthous ulcers usually (Recurrent • Triamcinolone in • Triamcinolone in Carboxymethyl­ require systemic steroids. Aphthous Ulcers) Carboxymethylcellulose cellulose 0.1% paste applied in a • Aphthous ulcers may be exacebated 0.1% paste thin layer q6h daily by stress. • • Betamethasone phosphate: • Iron, , and phosphate: – 0.5 mg tablet dissolved in 10 ml deficiencies should be ruled out. – 0.5 mg tablet dissolved mouthwash and rinse q4h • elixir should be in 10 ml mouthwash – spray on ulcer (1 spray = 100 μg) used for multiple ulcers or ulcers and rinse q4h up to 800 μg not accessible for topical applica- – spray on ulcer (1 spray • (Lidex) 0.05% tion. = 100 μg) up to 800 μg ointment q4h • Thalidomide is indicated only • Fluocinonide (Lidex) • Dexamethasone elixir (0.5 mg/5ml) when recurrences are severe 0.05% ointment applied rinse and expectorate and frequent. on ulcer q4h • The treatment with Thalidomide • Dexamethasone elixir Systemic should be monitored thoroughly (0.5 mg/5ml) rinse and • 2 mg/kg q6h, for 5-7 due to its teratogenicity. Birth expectorate days with gradual tapering control measures are required.

Systemic • Prednisone starting at 30-40 mg PO daily with taper over 1 month for severe disease resistant to topical agents • Thalidomide 200 mg PO daily Oral Topical Topical • The recurrence rate is high. • Podophyllin resin 25% • Podophyllin resin 25% applications • Concurrent therapeutic approaches applications q6h for q6h for long period should be considered. long period • 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 aphthous ulcers occur as a crop of many small lesions (1-2 condition that affects primarily children. Noma has been mm) disseminated on the , tonsils, tongue, reported mainly in developing countries in West , and/or buccal mucosa. but cases have also been described in other parts of the world. It is a multifactorial disease. The most important Treatment. The first line of management of RAUs is pain risk factors are poverty, chronic , poor control and prevention of superinfection. Depending on oral hygiene, and severe immunosuppression. Though the severity of the ulcers, topical and/or systemic considered a preventable disease, noma has a case fatality agents are recommended (Table 3). rate of 70%-90% if left untreated. Parotid Enlargement and Xerostomia Herpes Simplex Virus Infection Parotid enlargement is commonly associated with HIV Herpes simplex virus (HSV) infection may be either infection in children (10%-30%) and less commonly in primary (herpetic gingivostomatitis) or secondary adults. It occurs in the late course of HIV infection and is (). The prevalence of oral HSV infection associated with a slower rate of HIV disease progression. varies between 10% and 35% in HIV-infected adults and The median time from its diagnosis to death has been children. The presence of HSV infection for more than 1 reported to be 5.4 years among HIV-infected children. month constitutes an AIDS-defining condition. Lymphocytic infiltration of the salivary glands may be an etiologic factor. Clinical appearance. HSV infection appears as a crop of vesicles usually localized on the keratinized mucosa Clinical appearance. Parotid enlargement occurs as (hard palate, gingiva) and/or vermillion borders of the unilateral or bilateral swelling of the parotid glands. and perioral skin (Figure 5). The vesicles rupture and It is usually asymptomatic and may be accompanied form irregular painful ulcers. They may interfere with by decreased salivary flow (xerostomia or dry mouth). mastication and swallowing, resulting in decreased oral Problems with dry mouth in HIV-infected patients intake and dehydration. are often caused by medications that interfere with salivary secretion, such as antihistamines, antianxiety Treatment. Systemic therapy with antiviral agents is medications, antidepressants, and some antiretroviral recommended (Table 3). The treatment is more effective drugs (didanosine and zalcitabine). if it is instituted in the prodromal stage of infection. Treatment. Treatment is required only in severe Recurrent Aphthous Ulcers cases and may consist of systemic analgesics, anti- Recurrent aphthous ulcers (RAUs) occur in about 1%-7% inflammatories, antibiotics, and/or steroids Table( 3). of HIV-infected patients. They are painful ulcers on the nonkeratinized oral mucosa, such as labial and buccal Human Papillomavirus Infection (Oral Warts) mucosa, soft palate, and ventral aspect of the tongue. The incidence of oral warts due to human papillomavirus Severe recurrent aphthous lesions usually occur when infection has increased dramatically since the era of the CD4+ lymphocyte count is less than 100 cells/µL. This HAART. The lesions are more prevalent in adults (1%-4% result may be suggestive of HIV disease progression. The of cases) than in children. etiology of RAUs is not well known. Clinical appearance. Oral warts may appear cauliflower- Clinical appearance. RAUs may present as minor, major, like, spiked, or raised with a flat surface. They are or herpetiform aphthae. Minor aphthous ulcers are ulcers asymptomatic. The most common location is the less than 5 mm in diameter covered by pseudomembrane labial and buccal mucosa. The most common clinical and surrounded by an erythematous halo. They usually presentation is multifocal flat lesions resembling focal heal spontaneously without scarring (Figure 6). Major epithelial hyperplasia (Heck’s disease). aphthous ulcers resemble minor aphthous ulcers, but they are fewer and larger in diameter (1-3 cm), are more Treatment. Treatment may be required for patients with painful, and may persist longer. Their presence interferes multiple lesions. Topical and systemic agents and various with mastication, swallowing, and speaking. Healing surgical approaches are available (Table 3). occurs over 2-6 weeks. Scarring is common. Herpetiform

191 HIV Curriculum for the Health Professional

General Management References Considerations 1. Arendorf TM, Bredekamp B, Cloete CAC, et al. Oral To prevent the need for expensive dental services, it manifestations of HIV infection in 600 South African is imperative to treat the oral manifestations of HIV patients. J. Oral Pathol. Med. 1998;27:176-179. infection at all levels of care. Personal oral hygiene 2. Winfert M, Grimes RM, Lynch DP. Oral practices, such as tooth brushing and use of interdental manifestations of HIV infection. Ann. Intern. Med. cleaning aids, are the most effective ways of maintaining 1996;125:485-496. good oral health. 3. Kamiru HN, Naidoo S. Oral HIV lesions and oral health behaviour of HIV positive patients attending At the primary level of oral care, prevention of oral Queen Elizabeth II Hospital, Maseru, Lesotho. SADJ diseases takes priority. Prevention involves improving 2002;57:479-482. oral hygiene awareness through health education at the 4. Patton LL, Phelan JA, Ramos-Gomez FJ, et al. individual and community levels. Oral health education Prevalence and classification of HIV-associated oral messages should be made visible in all community lesions. Oral Dis. 2002;8(Suppl 2):98-109. forums. Home-based care providers should undergo 5. Chapple ILC, Rout PJ, Basu MK. Gingival Kaposi’s training in basic oral hygiene practices so that they sarcoma: the first indication of HIV infection.Dent. can impart these to patients under their care. Use of Update 1992;19:296-301. simple materials such as warm salty mouth rinse or 6. Klein RS, Harris CA, Small CB, et al. Oral candidiasis commercial mouthwash (chlorhexidine) can improve in high-risk patients as the initial manifestations of basic oral hygiene cost-effectively. Patients whose manual the acquired immunodeficiency syndrome.N. Engl. J. dexterity is intact should be taught appropriate brushing Med. 1984;311:354-358. techniques. Other adjuvant oral hygiene methods, such as 7. Centers for Disease Control and Prevention. 1993 flossing and use of interdental , will depend revised classification system for HIV infection and on the availability and affordability of supplies. expanded surveillance case definition for AIDS among adolescents and adults. MMWR Recomm. Rep. The secondary level of oral care involves visits to clinical 1993;41(RR-17):1-19. care facilities. Depending on local resources, the health 8. Ramos-Gomez FJ, Petru A, Hilton JF. Oral cadre available at this level may range from nursing manifestations and dental status in paediatric HIV staff at a health center to primary care physicians. In infection. Int. J. Paediatr. Dent. 2000;10:3-11. some countries, health centers may have no oral health 9. Magalhaes GM, Bueno DF, Serra E. Oral personnel or may offer only relief of pain with analgesics manifestations of HIV positive children. J. Clin. and extractions. Health care workers at this level should Pediatr. Dent. 2001;25:103-106. be trained to recognize suspicious lesions that may be 10. Nicolatou O, Theodoridou M, Mostrou G. Oral oral manifestations of HIV infection, and they should lesions in children with perinatally acquired know when and where to refer patients to a higher level immunodeficiency virus infection.J. Oral Pathol. of oral care. Med. 1999;28:49-53. 11. Begg MD, Lamster IB, Panageas KS. A prospective At the tertiary level of oral care, a dentist should be study of oral lesions and their predictive value for available to make definitive diagnoses of oral lesions and progression of HIV disease. Oral Dis. 1997;3:176- provide professional oral services such as prophylaxis, 183. restorations, , and the prescription of appropriate 12. Chapple ILC, Hamburger J. The significance of oral medication. health in HIV disease. Sex Transm. Inf. 2000;76:236- 243. Acknowledgment 13. Katz MH, Mastrucci T, Leggott PJ, et al. Prognostic significance of oral lesions in children with We thank Professor Sudeshi Naidoo, Department of perinatally acquired human immunodeficiency virus Community , Faculty of Dentistry and WHO infection. Am. J. Dis. Child. 1993;147:45-48. Collaborating Centre, University of the Western Cape, South Africa, for providing the pictures of oral lesions used in this chapter.

192 Oral Manifestations of HIV Infection

14. Barasch A, Safford MM, Catalanotto FA, et al. Oral 24. Flaitz CM, Hicks MJ. Oral manifestations in soft tissue manifestations in HIV-positive vs. HIV- pediatric HIV infection. In: Shearer WT & Hanson negative children from an inner city population: CI (Eds.): Medical Management of AIDS in Children. a two-year observational study. Pediatr. Dent. Philadelphia: Saunders, 2003. 2000;22:215-220. 25. Schiodt M, Pindborg JJ. AIDS and the oral cavity: 15. Schmidt-Westhausen AM, Priepke F, Bergmann FJ, et epidemiology and oral manifestations of HIV al. Decline in the rate of oral opportunistic infections infection: a review. Int. J. Oral Maxillofac. Surg. following introduction of highly active antiretroviral 1987;16:1-14. therapy. J. Oral Pathol. Med. 2000;29:336-341. 26. Ramos-Gomez FJ, Hilton JF, Canchola AJ, et 16. Darbyshire J. Therapeutic interventions in HIV al. Risk factors for HIV-related orofacial soft- infection—a critical review. Trop. Med. Int. Health tissue manifestations in children. J. Pediatr. Dent. 2000;5:A26-A31. 1996;18:121-126. 17. Scully C, Diz Dios P. Orofacial effects of antiretroviral 27. Walling DM. Oral hairy leukoplakia: an Epstein-Barr therapies. Oral Dis. 2001;7:205-210. virus-associated disease of patients with HIV. Res. 18. Royce RA, Luckman RS, Fusaro RE, et al. The natural Initiat. Treat Action 2000;6:10-15. history of HIV-1 infection: staging classifications of 28. Lifson AR, Hilton JF, Westenhouse JL, et al. Time disease. AIDS 1991;5:355-364. from seroconversion to oral candidiasis or hairy 19. EC Clearinghouse on Oral Problems Related to HIV leukoplakia among homosexual and bisexual Infection and WHO Collaborating Centre on Oral men enrolled in three prospective cohorts. AIDS Manifestations of the Human Immunodeficiency 1994;8:73-79. Virus. An update of the classification and diagnostic 29. Berthold P. Noma: a forgotten disease. Dent. Clin. N. criteria of oral lesions in HIV infection. J. Oral Pathol. Am. 2003;47:559-574. Med. 1991;20:97-100. 30. Enwonwu CO, Falkler WA, Idigbe EO, et al. Noma 20. EC Clearinghouse on Oral Problems Related to HIV (cancrum oris): questions and answers. Oral Dis. Infection and WHO Collaborating Centre on Oral 1999;5:144-149. Manifestations of the Human Immunodeficiency 31. Schiodt M. Less common oral lesions associated with Virus. Classification and diagnostic criteria for HIV infection: prevalence and classification.Oral Dis. oral lesions in HIV infection. J. Oral Pathol. Med. 1997;3:S208-S213. 1993;22:289-291. 32. Clark PC, Flaitz CM, Nichols CM, et al. Oral human 21. Ramos-Gomez FJ, Flaitz CM, Catapano P, et al.; papillomavirus infection in HIV: clinicopathologic Collaborative Workgroup on Oral Manifestations correlations. J. Dent. Res. 1998;77:250A. of Pediatric HIV Infection, Oral AIDS Center, 33. Brothell DJ, Jutai DK, Hawkins RJ. An update of University of California, San Francisco, San mechanical oral hygiene practices: evidence-based Francisco, California. Classification, diagnostic recommendations for disease prevention. J. Can. criteria, and treatment recommendations for Dent. Assoc. 1998;46:295-306. orofacial manifestations in HIV-infected pediatric 34. Gage TW, Picket FA. Mosby’s Dental Drug Reference. patients. J. Clin. Pediatr. Dent. 1999;23:85-96. 6th ed. St. Louis: Mosby, 2003. 22. Kline MW. Oral manifestations of pediatric human 35. Naidoo S, Chikte U. HIV/AIDS—the evolving immunodeficiency HIV infection: a review of the and its impact on oral health in sub- literature. Pediatrics 1996;97:380-388. Saharan Africa. SADJ 1999;54:661-630. 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.

193