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636 MOSCA & ROSE HATHORN
of chimpanzees native to west equatorial Africa [4]. This simian virus may
have spread to humans through exposure to infected blood while hunting
chimpanzees, or through the consumption of infected chimpanzee ‘‘bush-
meat.’’ Each virus type has viral subtypes, known as clades, that have
been isolated in distinct geographical regions. Intracellular infection in hu-
man cells requires cell surface receptors and coreceptors, which exhibit ge-
netic polymorphisms that provide specificity and modulate the virus’s
ability to infect cells. In North America, clade B is the predominate viral
subtype. Researchers at Johns Hopkins showed that HIV disease may prog-
ress more rapidly with certain viral clades. For example, increased virulence
is associated with clade D in Africa [5].
HIV infects tissue-bound Langerhans or follicular dendritic cells, which
process virus as nonself antigen to activate circulating CD4þ T lympho-
cytes, also called helper T cells because they serve to coordinate HIV-specific
immune response. Cells with intracellular pathogens must express viral pro-
teins in association with specific receptors at the cell surface for infection to
be recognized by the cytotoxic immune cells or to stimulate antibody pro-
duction. Activated CD4þ T lymphocytes transport HIV to lymphoid or-
gans, such as the gut-associated lymphoid tissue, where virus replication is
accelerated through normal antigen amplification mechanisms. HIV-specific
CD8þ T lymphocytes differentiate to destroy activated CD4þ T lympho-
cytes infected with the virus, which in turn stimulates production of more
CD4þ T lymphocytes. In 1995, Shaw and colleagues [6] demonstrated
that viral loads are sustained by a delicate balance between T-cell–mediated
virus replication (production) and T-cell–mediated viral destruction (clear-
ance). Once this cycle of HIV infection is established, the immune system
cannot eliminate virus completely, causing a progressive T-lymphocyte de-
pletion, destruction of the architecture of the lymphoid organs, and inability
to mount a cell-mediated immune response to any infection. HIV-positive
individuals have increased susceptibility to opportunistic infections that
are challenging to treat and may lead to death.
HIV’s genome contains three structural and six regulatory genes that en-
code at least 15 viral proteins associated with its pathogenicity and viral rep-
lication. A cell envelope glycoprotein, GP160, is the principal viral antigen
and has a GP120 external segment and GP41 transmembrane segment
(Fig. 1). Viral proteins have become important targets for the development
of antiretroviral drug therapies. In the mid-1990s, researchers found that
some infected cells have beta-chemokine receptors, CCR5 and CXCR4,
that participate in binding and entry of HIV into host cells, and ligands
for these receptors could inhibit attachment [7]. HIV strains that use
CCR5 as coreceptors are called R5 viruses and those that use CXCR4 are
called X4 viruses. Clade-A HIV uses only CCR5 while clade D uses
CXCR4 and may be more virulent. R5 viruses cannot infect cells with
CXCR4 receptors and X4 viruses cannot infect cells with CCR5 receptors.
Studies of genetic polymorphisms led to the discovery that individuals
HIV-POSITIVE PATIENTS 637
Fig. 1. Organization of the HIV-1 virion. (Courtesy of the Office of Communications and Pub-
lic Liaison, National Institute of Allergy and Infectious Diseases, National Institutes of Health,
Bethesda, MD.)
homozygous for a deletion of 32 base pairs in the CCR5 gene could not be
infected in vitro with R5 viruses [8]. These individuals comprise about 1% of
white populations and are extremely resistant to HIV, even with repeated
viral exposures.
HIV/AIDS epidemiology
The World Health Organization estimates that over 50 million people
have been infected with HIV worldwide, with more than 25 million infec-
tions reported in Africa. Southeast Asia, Latin America, and Eastern Eu-
rope account for about 10 million cases, and an estimated 1.2 million
people have HIV infection in North America. Western and Central Europe
combined have fewer than 750,000 reported cases of HIV infection. An es-
timated 40,000 cases of HIV infection occur in the United States each year.
In the United States, 33 states using confidential, name-based reporting,
provide HIV/AIDS prevalence data to the Centers for Disease Control, and
all 50 states report AIDS. In the past 2 decades, the number of reported
AIDS cases has fallen due primarily to improvements in antiretroviral treat-
ment regimens, and increased use of medical care through regional, state,
and local programs funded by the federal Ryan White Comprehensive
AIDS Resources Emergency Act. Trends demonstrate a decrease in AIDS
among white males who have sex with males, but an increase in AIDS
among non-Hispanic blacks. From 2001 through 2004 in the United States,
157,252 cases of HIV infection were reported to the Centers for Disease
Control. Non-Hispanic black males had the largest percentage of HIV infec-
tions in every transmission category, and, among females, non-Hispanic
blacks had the most cases (69%) [13]. Non-Hispanic blacks account for
up to 12% of the United States population, yet they accounted for half of
all AIDS cases diagnosed in 2004. In 2004, the rate of AIDS diagnoses
for non-Hispanic black women was 23 times the rate for white women;
the rate of AIDS diagnoses for non-Hispanic black men was 8 times the
rate for white men.
Dental treatment
Oral health and medical care providers should collaborate in the manage-
ment of patients with HIV disease. The immunological deficit in cell-medi-
ated immunity leads to oral conditions that provide a ‘‘window’’ to the onset
of acute HIV infection. By examining oral conditions, care providers can
measure adherence and effectiveness of antiretroviral treatment regimens,
and detect changes in quality of life. The most effective professional rela-
tionships in HIV patient care are personal, caring, and ‘‘relationship-
centered.’’ To enhance patient-care relationships, the health care profes-
sional may find that the best opportunities to confer with patients are at
any of the three milestones along the course of a person’s experience with
HIV infection. These milestones are the initial diagnosis, the onset of clinical
symptoms, and the initiation of antiretroviral treatment regimens. A de-
tailed health history should be taken using a nonjudgmental approach.
This must include specific nonjudgmental questioning about sexual activity
and illicit drug use. Box 1 details health history findings that indicate the
need for voluntary HIV testing.
642
Table 1
Antiretroviral drug therapies for HIV infection
Common
HIV-POSITIVE PATIENTS
a
Used with pediatric HIV infection.
643
644 MOSCA & ROSE HATHORN
Many HIV-positive patients who receive medical care do not receive den-
tal care primarily because of the burden of medical costs and a lack of dental
insurance requiring additional out-of-pocket expense. A study of 635 HIV-
positive patients at the University of Alabama School of Medicine showed
that medical expenditures for HAART were relatively constant at approxi-
mately $10,500 per patient per year no matter the CD4þ cell count [16]. The
HIV Cost and Services Use Study provides a national perspective on self-
reported measures for HIV-infected persons. The study used nationally rep-
resentative sample of 2466 HIV-positive subjects and a weighted design to
control for nonresponse, making the sample representative of a broader
population of 219,700 [17,18]. Total out-of-pocket health expenditures for
this population were $20.5 million. Those working full-time or part-time
spent $207 on dental treatment compared with $108 spent by those not
working. Cost of care was highest for people with CD4 counts !50 cells/mL
($172) compared with higher CD4 counts. Thirty-four percent (72,700) felt
their overall oral health was ‘‘fair to poor,’’ and 18% (22,000) had not re-
vealed their HIV status to their dental provider.
Xerostomia or dry mouth may occur in up to 40% of HIV-positive pa-
tients in association with side effects from antiretroviral and antidepressant
medications, tobacco use, and proliferation of CD8þ T lymphocytes in sal-
ivary gland tissue. Xerostomia may significantly increase the risk for dental
caries and acute gingivitis in HIV-positive patients. Patients should receive
counseling about these risks and instructions to use artificial saliva products
as needed.
Bartonellosis
Bartonella is a gram-negative bacterial infection that causes cat scratch
disease and an oral condition called bacillary angiomatosis, which may
clinically resemble Kaposi’s sarcoma lesions in mucosa. Regional
HIV-POSITIVE PATIENTS 645
Table 2
Treatment recommendations for oral conditions associated with HIV
Oral conditions Treatment options
Angular cheilitis Ketoconazole 2% cream
Dispense 30 g; apply to area 4/d for 2 wk.
Erythematous candidiasis Clotrimazole troches 10 mg
Dispense 70. Dissolve in mouth 5/d for 2 wk.
Nystatin oral suspension 500,000 U
Swish 1 teaspoon in mouth for 5 min,
4/d for 2 wk.
Pseudomembranous candidiasis Fluconazole 100 mg
Dispense 15 tabs, 2 tabs on first day,
then 1 tab/d for rest of period.
Diflucan 200 mg
Dispense 5 tabs, take 1 tab/d.
Oral hairy leukoplakia Acyclovir 4 g/d
For temporary relief. Treatment
usually not required.
Oral warts Cryotherapy or surgical excision
Imiquimod 5% cream
For lesion on lips. Dispense 3 g, apply
1/d at bedtime, 3d per wk.
Apthous ulcerations Orabase cream
Place with a cotton swab over ulcer 3/d.
Ulcerations from Herpes simplex virus Acyclovir 400 mg
Dispense 30 tabs, 1 tab 3/d for 10 d.
Linear gingival erythema 0.12% chlorhexidine rinse
With oral hygiene instruction and dental cleaning.
Necrotizing ulcerative periodontitis Augmentin 875 mg
Dispense 14 tabs, 1 tab 2/d for 7 d.
Rigorous debridement along with 0.12%
chlorhexidine rinse.
Kaposi’s sarcoma Incisional biopsy
With follow-up with patient’s primary physician.
Possible radiation or chemotherapy as treatments.
Candidiasis (mucocutaneous)
Oropharyngeal candida (OPC), as with esophageal and vulvovaginal can-
didiasis, is caused by yeast, chiefly Candida albicans, and less frequently
by Candida glabata, Candida tropicalis, and Candida kruseii. Fungi are nor-
mal inhabitants of the gastrointestinal tract and colonization of oral mucosa
is common. Diagnosis is made by clinical appearance, and the
646 MOSCA & ROSE HATHORN
pseudomembranous variant, also known as thrush (Fig. 2), is the most com-
mon presentation, especially in HIV-positive children. The pseudomembra-
nous variant appears as a cottage-cheese–like or curd-like exophytic
material on the epithelial tissue on all locations in the oral cavity, and it
can be easily wiped off. Histological examination is generally not necessary,
but specimen samples can be used to confirm diagnosis. Typically, scraping
with a blade or cytology brush collects material, which can be gently
smeared on a glass slide and viewed microscopically after placing one or
two drops of 10% potassium hydroxide solution. Fungal organisms have
characteristic pseudohyphae and budding characteristic of reproduction.
The erythematous or atrophic variant appears as flat or macular with red
color, and is sometimes accompanied by pain (Fig. 3). It may occur simul-
taneously with or independent of the pseudomembranous variant. Angular
cheilitis is a fungal infection of the labial commissures that characteristically
appears as erythema or depigmentation with tissue fissures or ‘‘cracking’’
(Fig. 4).
Mild episodes can be treated with topical antifungal medications, while
moderate-to-severe conditions will typically require systemic therapy. Nys-
tatin is a topical azole antifungal drug with minimal side effects, but sweet-
ening agents in its suspension may be cariogenic. Clotrimazole is another
azole that is available as a spray, solution, and troche for oral usage. It
has few side effects but is poorly absorbed in the gastrointestinal tract and
must dissolve slowly in the mouth to be effective. Clotrimazole may be
less cariogenic than nystatin. Fluconazole was the first triazole drug avail-
able as tablet or suspension, and it demonstrates good gastrointestinal ab-
sorption with minimal dependence on gastric acidity or food intake.
Itraconazole, available as a capsule or oral suspension, is a triazole drug
that demonstrates better absorption after food intake. Voriconazole has
the most significant drug interactions with some antiretroviral drugs and
should be considered for use if resistance to fluconazole occurs [19]. The
most commonly reported side effects for the triazole drug class are head-
ache, dyspepsia, diarrhea, nausea, vomiting, hepatitis, and skin rash.
Condyloma acuminatum
Condyloma acuminatum is an asymptomatic mucocutaneous infection of
the skin or mucosa of the oral cavity or anogenital region caused by human
papilloma virus (HPV), which can be transmitted sexually (Fig. 5). More
than 100 HPV types have been identified. HPV is a DNA virus type and
is epitheliotropic, which means it contains epithelia growth factor and
may induce distinct squamous cell proliferations. Some high-risk HPV geno-
types have been associated with premalignant and malignant lesions, and
HPV types 6 and 11 are most commonly associated with condylomata.
Cryptococcosis
Cryptococcus neoformans is a fungal infection that most commonly man-
ifests as a meningoencephalitis. Symptoms include headache, nausea, irrita-
bility, and diminished cognitive function, and physical findings include
cranial nerve palsies, hyperreflexia, and papilledema. Rarely, intraoral ulcer-
ations may occur in mucosal tissues with dissemination of cryptococcosis
[20]. Treatment of crytococcal meningoencephalitis requires multiple drug
therapies using amphotericin B, flucytosine, and fluconazole.
Cryptosporidosis
Cryptosporidium is a spore-forming protozoa infection that causes severe
watery diarrhea and epigastric pain. The most common site of infection is
the small intestine, and infection may be transmitted person-to-person or
by drinking contaminated water. Precautions to prevent disease include
proper hand washing and disinfectant cleaning or disposal of contaminated
materials. Treatment includes replacement of lost fluid volume and the use
of the antibiotic combination of trimethoprim and sulfamethoxazole or
ciprofloxan.
HIV-POSITIVE PATIENTS 649
Hairy leukoplakia
Hairy leukoplakia is caused by infection of epithelia cells with Epstein–
Barr virus, and presents clinically as white, ragged, and corrugated or irreg-
ular lesions involving the later and dorso-lateral tongue. Lesions may be
unilateral or bilateral. Diagnosis can be confirmed by tissue biopsy. Histio-
logically, hairy leukoplakia exhibits hyperparakeratosis, often with hair-like
projections, epithelia hyperplasia, vacuolated epithelial cells (koilocyte-like),
and little or no inflammatory infiltrate in the underlying connective tissue
(Fig. 6). Hairy leukoplakia generally does not require treatment unless cos-
metically objectionable. Treatment options include the use of zidovidine,
podophyllin, and interferon. Regardless of treatment, lesions may spontane-
ously resolve and recur.
Histoplasmosis
Histoplasma capsulatum is a fungus comprised of hyphae with characteris-
tic macroconidia or sexual spores. Histoplasma is found in soil and transmis-
sion is exogenous, but person-to-person transmission does not occur. Defense
against infection requires a healthy-cell–mediated response to stimulate mac-
rophages that engulf fungus and halt progression of disease. Histoplasmosis
may infect lungs, bone, and the central nervous system, and clinical findings
include fever, weight loss, skin or mucosal lesions, and respiratory symptoms,
such as cough and shortness of breath. Dissemination of histoplasmosis to the
oral mucosa may occur primarily on the gingival, tongue, palate, and buccal
mucosa. Gingival lesions will appear as diffuse granulomatous inflammation
with progressive alveolar bone erosion and loosening of teeth. Management of
histoplasmosis includes obtaining blood cultures for fungal sepsis and treat-
ment with liposomal amphotericin B or itraconazole.
Kaposi’s sarcoma
Kaposi’s sarcoma is the most prevalent AIDS-associated intraoral malig-
nancy. Kaposi’s sarcoma occurs more commonly in homosexual and
bisexual males and is rarely seen in HIV-positive women and children. Ka-
posi’s sarcoma is an angioproliferative disease which may develop from hu-
man herpesvirus 8 (HHV-8) infection of mesenchymal progenitor cells.
Defined as a hyperplastic reactive inflammatory disease, Kaposi’s sarcoma
is characterized by mucosal lesions that begin as macular patches with red
or bluish-purple color, which may become darker and exophytic with ulcer-
ations as lesions advance (Figs. 7 and 8). Kaposi’s sarcoma may resemble
bacillary epithelial angiomatosis. Male homosexuals have the highest risk
of contracting Kaposi’s sarcoma. The hard palate is the most common
oral site, followed by the maxillary gingival. Small intraoral lesions may
be treated using intralesional injections of vinblastine sulfate or sclerosing
solution sodium tetradecyl sulfate. Local anesthesia should be infiltrated be-
fore injections to minimize pain associated with intralesional chemotherapy.
Lymphoma
Lymphoma is malignant neoplasm of lymphoid cells. The risk for AIDS-
related lymphomas increases with a CD4þ T-cell counts of !100 cells/mL.
Lymphomas are primarily non-Hodgkin’s, B-cell (humoral) malignancies,
Mycobacterium tuberculosis
Approximately one third of AIDS-related deaths worldwide are due to
tuberculosis (TB), and in Africa one third of people infected with TB are in-
fected with HIV. This pattern is most likely due to increased reactivation of
latent TB infections as well as higher primary rates of TB. All patients with
TB should be tested for HIV. Pulmonary TB is the most common clinical
manifestation. However extrapulmonary disease affecting the liver, spleen,
or kidney may occur in HIV-positive patients with CD4þ T cells !100
cells/mm3 [21]. Tuberculin skin testing with purified protein derivative
(delayed-type hypersensitivity response) is used to identify latent TB.
Some patients may have a problem complying with the requirement to
return so that skin induration can be checked. Tests read after a delay of 72
hours or more and found to be negative should be repeated. Active TB in
HIV-positive patients increases HIV viral RNA levels, which decrease after
treatment of TB is initiated. Treatment includes 6 months of treatment with
isoniazid, rifampin, pyrazinamide, and ethambutol. Side effects of therapy
include liver function abnormalities, rash, and peripheral neuropathy.
Pneumocystosis
Due to the efficacy of antiretroviral agents and use of prophylactic regi-
mens, pneumocystis carinii pneumonia (PCP) now occurs less frequently
than it did during the first decade of the AIDS epidemic. The occurrence
of PCP is more likely due to lack of medication compliance, poor access
to medical care, or lack of awareness of HIV infection, though drug resis-
tance is also possible. Clinical symptoms include fever, nonproductive
cough, and shortness of breath. Chest radiographs reveal characteristic
diffuse infiltrative pulmonary infiltrates, and diagnosis is confirmed by
bronchoalveolar lavage and induced sputum examination. Trimethoprim–
sulfamethoxazole remains the drug of choice in treatment, and prophylactic
use of one single-strength tablet per day is still considered the standard of
care for patients with CD4þ T-lymphocyte counts of !200/ml or who pres-
ent with oropharyngeal candidiasis or other AIDS-defining infection.
Toxoplasmosis
Toxoplasma gondii, a protozoal infection in the general population, rep-
licates intracellularly in the host tissues, yet produces no or few clinical
HIV-POSITIVE PATIENTS 653
Vesicular-ulcerative conditions
Aphthous ulceration
Aphthous ulceration is the most commonly reported type of ulcers in
HIV-positive patients and its etiology remains undetermined (Fig. 10). Ul-
cers appear clinically as painful, round-to-oval, yellow or white, and are sur-
rounded by a halo of erythema. HIV-positive patients usually experience
increased frequency and severity of typical minor aphthous ulcers. Aph-
thous ulcers are usually treated with topical or systemic corticosteroids.
Thalidomide is also used, but pregnant women must be excluded because
of thalidomide’s teratogenic effects.
Herpes simplex
Herpes simplex virus (HSV) is a double-stranded DNA capsule enclosed
in a lipid envelope that is characteristically able to induce latency with peri-
odic reactivation of infection. HSV-1 is associated primarily with orolabial
lesions and HSV-2 with genital lesions. HIV infection on oral mucosa pres-
ents as an erythematous pruritus that develops into painful vesicles and
ulcerates over a brief period, accompanied by painful regional lymphade-
nopathy. In contrast to the yellow or white pseudomembrane in aphthous
ulcerations, HSV ulcers typically have a red center surrounded by a yellow
or white border. Orolabial HSV infections may occur on all oral mucosa
and can be more prolonged and severe than with HIV-negative individuals.
CD4þ T-lymphocyte counts have greater risk than nonsmokers for develop-
ing candidiasis and hairy leukoplakia. Prior or current use of alcohol and
other drugs may increase complications, especially if hepatomegaly occurs
with viral co-infection or drug therapy. Patients should also receive safe-
sex counseling regarding oral sexual behaviors. For example, patients
should be told that Epstein–Barr virus may be transmitted by oral sex.
Dental treatment sequencing should be approached as a component of
medical care. Patients with low CD4þ T-lymphocyte counts (ie, !200
cell/mL) are predisposed to HIV-associated oral infections that require spe-
cific treatment. The dentist’s first priorities are to relieve pain and treat the
infection. Next, the dentist should implement prevention regimens to pre-
vent concomitant disease. The third task is to restore function so that pa-
tients can eat and maintain their nutrition. Enhanced preventive care
compromising bimonthly prophylaxis and chlorhexidine mouth rinses to
prevent gingivitis may improve the patient’s psychological health, but there
is no evidence that this will reduce the occurrence of AIDS-related opportu-
nistic infections. Lastly, the dentist must provide esthetic procedures to im-
prove self-esteem and enhance psychological health. It is both safe and
desirable to assure that regular comprehensive dental care is available to
HIV-positive patients. In the United States, Title I, II, III and IV of the fed-
eral Ryan White Comprehensive AIDS Resources Emergency Act supports
oral health services for HIV-positive persons. Additionally, Section F of the
act provides the Dental Reimbursement Program, which retrospectively
compensates unreimbursed dental schools, dental hygiene programs, and
postdoctoral dental training programs for providing dental care to people
with HIV.
Table 3
Web resources for dental care providers
Website Name Description
http://www.hivdent.org HIV Dent Developed by Dr. David Resnick at
Grady Health Systems in Atlanta,
Georgia. Provides basic information
about clinical care and about
manifestations of HIV.
http://www.iasusa.org International Provides treatment guidelines and
AIDS Society publishes Topics in HIV Medicine.
http://www.hivguidelines.org New York State Provides treatment guidelines and
Department of best practices.
Health AIDS
Institute
http://www.ucsf.edu/hivcntr/ National HIV/AIDS Developed by the University of
Clinicians’ California at San Francisco.
Consultation Center Provides treatment guidelines and
best practices.
http://www.critpath.org/daac/ Dental Alliance for Dental treatment site that contains
AIDS/HIV Care links to other information sites.
656 MOSCA & ROSE HATHORN
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