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Dental Professionals and HIV- Part 1
A Peer-Reviewed Publication
Written by Richard H. Nagelberg, DDS
Abstract
Educational Objectives
Author Profile
With the introduction of highly active antiretroviral therapy (HAART) for HIV, AIDS
is now manageable and patients are living lives relatively free of many of the oral
conditions that characterized the disease prior to and during previous treatment
regimens. Although the incidence of oral diseases has improved, many patients
with HIV and emerging AIDS may still develop one or more oral conditions that
dental professionals need to be aware of when examining the patient with AIDS.
Effective office infection control procedures to prevent spread of the disease are as
important today as they were 30 years ago when AIDS was first confronted. This
educational course is divided into two parts. The first part reviews current science
related to the immune events associated with the oral route of transmission of
the virus, new information on the pathogenesis of the disease, concepts related
to the oral cavity as a viral reservoir for HIV and oral pathology that is associated
with AIDS. The second part deals with the practical clinical considerations that
need to be addressed when treating the AIDS patient.
At the conclusion of this educational
activity participants will be able to:
1. Discuss the pathogenesis of HIV
disease and the oral cavity as a
viral reservoir for HIV.
2. Discuss the oral conditions which
may predict HIV disease.
3. Discuss oral diseases and conditions which can occur with HIV
and AIDS.
4. Discuss treatment strategies for
HIV related oral candidiasis.
Dr. Richard Nagelberg has been practicing general dentistry in suburban
Philadelphia for 32 years. He has international practice experience, having
provided dental services in Thailand, Cambodia, and Canada. He is co-founder
of PerioFrogz.com, an information services company, and an advisory board
member, speaker, key opinion leader and clinical consultant for several dental
companies and organizations. Richard has a monthly column in Dental Economics magazine, “GP Perio-The Oral-Systemic Connection”. He is a recipient of Dentistry Today’s Top Clinicians in CE, 2009-2015. A respected member of the dental
community, Richard lectures internationally on a variety of topics centered on
understanding the impact dental professionals have beyond the oral cavity. Dr.
Nagelberg can be reached at [email protected].
Author Disclosure
Dr. Nagelberg is Editorial Director, Dental Education, PennWell Publishing.
Go Green, Go Online to take your course
Publication date: June 2015
Expiration date: May 2018
Supplement to PennWell Publications
PennWell designates this activity for 3 continuing educational credits.
Dental Board of California: Provider 4527, course registration number CA# 03-4527-15003
“This course meets the Dental Board of California’s requirements for 3 units of continuing education.”
The PennWell Corporation is designated as an Approved PACE Program Provider by the
Academy of General Dentistry. The formal continuing dental education programs of this
program provider are accepted by the AGD for Fellowship, Mastership and membership
maintenance credit. Approval does not imply acceptance by a state or provincial board of
dentistry or AGD endorsement. The current term of approval extends from (11/1/2011) to
(10/31/2015) Provider ID# 320452.
1506DE_69 69
This educational activity was developed by PennWell’s Dental Group with no commercial support.
This course was written for dentists, dental hygienists and assistants, from novice to skilled.
Educational Methods: This course is a self-instructional journal and web activity.
Provider Disclosure: PennWell does not have a leadership position or a commercial interest in any products or services
discussed or shared in this educational activity nor with the commercial supporter. No manufacturer or third party has had
any input into the development of course content.
Requirements for Successful Completion: To obtain 3 CE credits for this educational activity you must pay the required
fee, review the material, complete the course evaluation and obtain a score of at least 70%.
CE Planner Disclosure: Heather Hodges, CE Coordinator does not have a leadership or commercial interest with products
or services discussed in this educational activity. Heather can be reached at [email protected]
Educational Disclaimer: Completing a single continuing education course does not provide enough information to result
in the participant being an expert in the field related to the course topic. It is a combination of many educational courses
and clinical experience that allows the participant to develop skills and expertise.
Image Authenticity Statement: The images in this educational activity have not been altered.
Scientific Integrity Statement: Information shared in this CE course is developed from clinical research and represents
the most current information available from evidence based dentistry.
Known Benefits and Limitations of the Data: The information presented in this educational activity is derived from the
data and information contained in reference section. The research data is extensive and provides direct benefit to the patient
and improvements in oral health.
Registration: The cost of this CE course is $59.00 for 3 CE credits.
Cancellation/Refund Policy: Any participant who is not 100% satisfied with this course can request a full refund by
contacting PennWell in writing.
6/8/15 1:25 PM
Educational Objectives
At the conclusion of this educational activity participants will
be able to:
1. Discuss the pathogenesis of HIV disease and the oral cavity
as a viral reservoir for HIV.
2. Discuss the oral conditions which may predict HIV
disease.
3. Discuss oral diseases and conditions which can occur with
HIV and AIDS.
4. Discuss treatment strategies for HIV related oral candidiasis.
Abstract
With the introduction of highly active antiretroviral therapy
(HAART) for HIV, AIDS is now manageable and patients are
living lives relatively free of many of the oral conditions that
characterized the disease prior to and during previous treatment
regimens. Although the incidence of oral diseases has improved,
many patients with HIV and emerging AIDS may still develop
one or more oral conditions that dental professionals need to be
aware of when examining the patient with AIDS. Effective office infection control procedures to prevent spread of the disease
are as important today as they were 30 years ago when AIDS
was first confronted. This educational course is divided into
two parts. The first part reviews current science related to the
immune events associated with the oral route of transmission of
the virus, new information on the pathogenesis of the disease,
concepts related to the oral cavity as a viral reservoir for HIV and
oral pathology that is associated with AIDS. The second part
deals with the practical clinical considerations that need to be
addressed when treating the AIDS patient.
The Science of HIV
Immunodeficiency is the end result of HIV infection. The
pathogenesis of the disease and how HIV causes immune
dysfunction is not completely understood. Even though there
appears to be an initial stimulation of the immune system by
the virus, the subsequent immune response is not sufficient to
completely eliminate it. Infection chronicity results in exhaustion of the immune system; but the molecular mechanisms
underlying this process remain unclear. A complete review
of what is known of the cellular events associated with HIV
infection is beyond the scope of this course. For the clinician
interested in additional in-depth study, a thorough description
of the pathophysiology of AIDS is presented by T Morgensen
and colleagues in an article in Retrovirology, 20101.
One interesting detail presented in the Morgensen et al article is that massive depletion of CD4+ memory T cells occurs
in mucosal tissue during infection with HIV. They note that
ultimately 60% of cells in the mucosa disappear. In addition to
damage to the adaptive immune system there is also dysregulation of the innate immune defense system that is composed of
associated eosinophils, monocytes, macrophages, natural killer
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cells, toll-like receptors, the complement system, and numerous proteins produced by epithelial cells.
The oral mucosal epithelium and proteins expressed by this
tissue are an important component of innate immune defense
and protect from the incursion of infectious microorganisms
into the mucosal tissue. In a study analyzing proteins expressed
by HIV infected HAART subjects and healthy controls, 61
proteins were found to be differentially expressed between
those subjects infected and those not infected.2 Involved proteins were either down-regulated or up-regulated. The downregulated proteins were those associated with maintenance of
protein folding, pro-inflammatory and anti-inflammatory responses, and redox homeostasis (chemical reactions involving
change in the oxidation state of organics and detoxification).
Up-regulated proteins included many that have been found
to be involved in the maintenance of cellular integrity. The
authors of this study conclude that “the toxic side effects of
HAART and/or HIV chronicity silence expression of multiple
proteins that in healthy subjects function to provide robust innate immune responses and combat cellular stress”. The above
functional cellular changes are thought to contribute in part
to the development of chronic oral disease (e.g. periodontitis,
candidiasis, salivary gland disease, oral warts, aphthous ulcers
associated with viral, bacterial and fungal organisms) in the
HIV infected subject and also those on HAART therapy.3,4,5,6
HAART has made AIDS a chronic disease. The life expectancy of HIV patients has increased dramatically and many
HIV related oral complications have decreased. However several oral diseases and the HIV virus itself continue to endure,
even with HAART treatment. HIV remains dormant in T
cells, macrophages, and dendritic cells and can later re-emerge
to cause latent infection. The occurrence of oral pathology
resulting from HIV infection is suggested as a reason for the
recrudescence of the virus. Support for this idea comes from
studies that suggest pro-inflammatory cytokines/chemokines,
and other mediators produced by immune and non-immune
cells inhibit or stimulate HIV reemergence.7
These findings have given rise to the question: are oral infections a potential risk factor for the reactivation of the HIV virus
and do they have an effect on the success or failure of HAART
treatment?8 As Gonzalez, Ebersole, and Huang hypothesize in
their review article published in Oral Disease, 2009, the research
that has been done defining molecular mechanisms involved
in reactivation and reveals association between infection and
latent emergence of HIV9 coupled with the clinical evidence
that supports a correlation between HIV viral load and oral
infectious diseases such as periodontal disease, hairy leukoplakia, and candidiasis.10,11,12 This suggests that there may
be more than a hypothetical connection between non HIV
opportunistic infection and HIV latency and reactivation.
While more research is needed to carefully assess the potential association and the precise nature of any connection
between viral reactivation and oral disease, the studies cited
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by Gonzalez, et al, underscore the importance of identifying
oral disease in the HIV patient and the need for appropriate
treatment.
A 2015 study has indicated that gingival crevicular fluid
(GCF) may be a better diagnostic medium for detection of
HIV than saliva. In this study the authors were examining
GCF for the detection of anti-HIV antibodies in HIVinfected individuals. The author's results were as follows:
"When compared with serum, the sensitivity, specificity,
and positive and negative predictive values of GCF were
100% respectively." 58
Oral Pathology and HIV
It has been estimated that 40-50 percent of HIV positive
patients will develop oral disease.13 A 2015 study of HIV
infected patients concluded; "The most common oral presentations were severe periodontitis, pseudomembranous
candidiasis and xerostomia.59 In patients with AIDS the
incidence can approach 80 percent. In a study by R Kumar,
et al,14 61.65 percent of 326 children ages 1-14 with HIV had
oral lesions. Of those, approximately 21 percent were diagnosed with oral candidiasis (OC), 17 percent with angular
cheilitis, 8 percent with acute necrotizing ulcerative gingivitis
(ANUG), 8 percent with necrotizing ulcerative periodontitis
(NUP), 6 percent with linear gingival erythema, and 3 percent with aphthous ulcers. Clinical evidence suggests that the
prevalence of oral disease varies depending on gender, age,
location and level of public health awareness. Other conditions that can present orally that are reported in association
with HIV include herpes simplex virus (HSV-1) as well as
herpes zoster and Epstein-Barr virus, oral hairy leukoplakia,
HPV subtypes 16 and 18, Kaposi’s sarcoma non-Hodgkin’s
lymphoma, tuberculosis and salivary gland disease.15
With the exception of oral candidiasis, which is the most
common infection seen in HIV patients throughout the world,
locality may be important in terms of the prevalence of some
of the oral diseases that can develop in the HIV patient. For
example, HIV patients in Africa and Latin America frequently
develop Kaposi’s sarcoma and those from Thailand, histoplasmosis and penicilliosis when the disease is advanced.16 Understanding regional differences is reported to be an important
factor in determining the World Health Organization’s (WHO)
classification of HIV-associated oral lesions.17
Before discussing each oral lesion, it is important to note
their significance with respect to HIV infection. First, a
number of lesions, including oral candidiasis, hairy leukoplakia, Kaposi’s sarcoma, linear gingival erythema, necrotizing
ulcerative gingivitis, necrotizing ulcerative periodontitis and
non-Hodgkin's lymphoma lesions are said to be strong indicators of the presence of HIV infection. Further, oral candidiasis
and hairy leukoplakia are considered sentinel lesions. Certain
oral lesions help to predict the progression of HIV disease to
AIDS. For example, the development of pseudo membranous
candidiasis, as defined by clinical presentation in addition to
serology, has been used in this manner. The prevalence of oral
lesions parallels the decline of CD4+ cells and an increasing
viral load and the chronicity associated with certain oral lesions
is indicative of potential HAART treatment failure.
Lesions
Oral Hairy Leukoplakia
Oral hairy leukoplakia (OHL) is an asymptomatic condition.
The mucosal tissue on the lateral border of the tongue becomes
whitened and the filiform papillae project from the surface like
thick hairs. The lateral surface may also appear corrugated.
The Epstein-Barr virus has been shown to be associated with
mucosal change but it is unclear if it is directly involved with
the etiology of OHL. Treatment is not typically necessary unless the problem becomes cosmetic. Interventions with limited
supportive evidence include topical application of podophyllum resin solution 25%18, and prescription of systemic oral
acyclovir.19 Ablation of the lesions with cryotherapy has also
been suggested as a treatment option.20
Candidiasis
Pseudomembranous candidiasis (candidosis) occurs more
frequently than any other oral mucosal disease associated with
HIV and AIDS. A number of yeast species have been identified as causing candidiasis but candida albicans is the one most
commonly found in patients with HIV infection.21 Other fungal
infections associated with the candida organism include erythematous candidosis, angular cheilitis, and hyperplastic candidosis.22,23 HAART treatment of HIV and AIDS has reduced
the prevalence of some oral lesions but this may not be, as a
general rule, the case with oral candidiasis.24,25 The frequency
of oral candidiasis has been found to correlate with falling
CDV+T lymphocyte counts and an elevation of the HIV
viral load.26 For example, in one study, patients with CD4+
lymphocyte counts below 200 x 10(6)/l and CD4+ percentages below 14% showed a significantly higher frequency of OC
(57.9% and 48.0%, respectively (Campo J, J Oral Pathol Med).27
Oral candidiasis has also been associated with the emergence of
AIDS, particularly in children.28
Oral pseudomembranous candidiasis is characterized by
whitened milk curd like structures that easily wipe off, leaving
a raw erythematous and often bleeding mucosal base. In the
erythematous form of the infection, the dorsum of the tongue
is eroded and there is corresponding erythema of the palate.
Edema and erythema of the mucosa contacting an oral appliance characterizes denture stomatitis caused by candida.
Antifungal medications found to be useful in treating oral
candidiasis include nystatin (Mycostatin®), the imidazoles such
as clotrimazole and ketoconazole, and triazole agents such as
fluconazole.29,30 The following describes dosage considerations
for a number of the useful antifungal medications. Topical
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preparations are typically taken for 10-14 days but may have to
be prescribed longer in the HIV patient. The patient’s attending physician should be consulted to eliminate potential treatment duplication errors, particularly if long term prescription
is necessary.
Nystatin oral suspension 500,000 units/tsp (brand names
Mycostatin®, Nilstat®, Nystex®); Dispense 240 mls; Sig: 1 tsp
tid; rinse for two minutes and swallow.
Ketoconazole cream 2% (brand name Nizoral®); dispense 15
gm tube; Sig: apply to the affected area once daily at bedtime.
Clotrimazole vaginal cream 1% (OTC – brand names
Gyne-Lotrimin®, Mycelex-G®); Dispense one tube; Sig: apply to the denture or partial and the involved oral mucosa four
times a day.
Clotrimazole troches 10 mg (brand name Mycelex®);
Dispense 70 troches; Sig: dissolve one troche in the mouth 5
times a day. Do not chew.
Nystatin Pastilles – 200,000u (brand name Mycostatin®
pastilles); Dispense 70 pastilles; Sig: dissolve one pastille in the
mouth 5 times a day. Do not chew.
Miconazole nitrate vaginal cream 2% (OTC – brand
name Monistat®); Dispense one tube; Sig: apply to the denture
and to the involved oral mucosa four times a day.
In patients with removable prostheses, dental treatment
should include not only prescription of medication but also
instruction on the disinfection of appliances. Denture soaking
solutions coupled with application of an antifungal powder or
cream to the contacting surface of the appliance normally helps
to prevent reinfection. As an example, an appliance can be
soaked overnight in a one percent chlorhexidine/hypochlorite
solution. In the morning this is followed by the application of
miconazole denture lacquer prior to insertion. The extent to
which this regimen helps patients with HIV is unclear as there
is little supportive research evidence, but empirical evidence
suggests that it may be helpful in reducing oral yeast counts.
Nystatin ointments and powders can be used to ‘treat’ appliances per the following instructions:
Nystatin ointment; dispense 15 gm tube; Sig: apply a thin
coat to the denture and affected area after each meal.
Nystatin topical powder; dispense 15 gm tube; Sig: apply to dentures/prostheses after each meal and after cleaning the appliance.
In the patient with dry mouth and candidiasis, a chewing
gum or candy with xylitol is recommended to stimulate daytime salivary flow. Products that improve night (sleep) dryness
such as Xylimelts® (OraHealth, Inc.) help to stimulate flow and
alter the perception of dryness.
Antifungal medication has been associated with allergy and
GI problems. Nystatin suspension also contains sugar so if the
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patient has teeth, good oral hygiene is important to prevent
decay; particularly if treatment is extended over a prolonged
period of time. A suspension of nystatin can also be used as a
disinfectant for a patient’s acrylic prostheses (see above).
It should be appreciated that ketoconazole absorption is
reduced when antacid medication is taken concurrently. The
oral use of vaginal creams (miconazole nitrate vaginal cream
or clotrimazole vaginal cream) to treat oral candidiasis remains
controversial. However sugar content (in contrast to clotrimazole troches) is minimal in these formulations which may be
advantageous in cases involving the need for long-term application. In addition, antifungal troches may not be well tolerated in
the patient with dry mouth. Pregnant or breast feeding patients
should consult with their physician prior to use of any of these
antifungal medications. All of the troches described above provide good contact of drug with the mucosa over time.
In the HIV patient with compromised immune function,
prescription of systemic antifungal agents such as ketoconazole
(Nizoral®), fluconazole (Diflucan®), itraconazole (Sporanox®)
and amphotericin B (Fungizone®) should be left to the attending physician. Keep in mind that problems with resistance to
the azoles such as fluconazole and cross-resistance between
some of the antifungal agents is potentially problematic in the
HIV patient with advanced disease.30,31,32 Another factor which
warrants consideration is counseling the HIV patient with oral
lesions to stop smoking and maintain good oral hygiene.
Kaposi’s Sarcoma
Kaposi’s sarcoma (KS) has four clinical-epidemiological variants, all of which can occur in the mouth. Human herpes virus
8 seems to be involved in lesion development, although other
factors (e.g. immune impairment, angiogenic mediators, and
genetic predisposition) also appear to be important in the etiology of the condition.33 Oral HIV-KS presents in a variety of
forms, most typically solitary or multifocal macular, papular,
or nodular purple-brownish or reddish blue exophytic lesions.
Secondary overlying candidiasis may produce a whitened surface on some of the lesions. The lesions of oral HIV-KS may be
located in any area of the mouth or the oropharyngeal region but
the palate and gingiva are most frequently involved. (Figure 1)
Figure 1. Kaposi's Sarcoma Provided by Dolphine Oda, University of Washington
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This is not a condition that is treated via dental intervention.
In terms of medical intervention, it is reported that HAART
plus chemotherapy is more effective than HAART alone in
treating Kaposi’s sarcoma.33
Figure 2. Necrotizing ulcerative periodontitis. Courtesy of Dr. Valli Meeks
Diseases of the Gingiva and Periodontium
HIV associated immunosuppression increases susceptibility to
gingival and periodontal disease.34 Gingival inflammation (gingivitis) in the HIV patient is termed linear gingival erythema.
HIV-associated periodontitis is termed necrotizing ulcerative
periodontitis or necrotizing gingivostomatitis. Both conditions are
caused by opportunistic aerobic and anaerobic bacteria. Porphyromonas gingivalis, Treponema denticola, and Tannerella forsythia are three of several anaerobic organisms considered important
in the causation of HIV related periodontal diseases. The evidence
suggests that opportunistic infection in HIV periodontal disease
and disease progression is related to CD4+ T cell counts. There is
also evidence that highly-active antiretroviral therapy (HAART)
alters subgingival biofilm in patients with periodontal disease.
However, different HAART drug combinations (e.g. proteaseinhibitor-based or non-nucleoside reverse transcriptase inhibitor)
appear to alter pathologic bacteria differentially and this may be
an important factor involved in disease etiology and intervention.35
Linear Gingival Erythema
This condition, characterized by bright red gingiva bordering the
teeth that is configured in a linear band up to 4 mm wide, is seen in
HIV infection. Unlike other gingival conditions involving inflammation and erythema, the tissue does not typically bleed when
probed or brushed. Histological evaluation of tissue in patients
with this condition has yielded yeast cells and hyphae identified as
Candida dubliniensis, a relatively newly identified yeast varietal
apparently only associated with HIV, which suggests that the
condition may be a unique form of erythematous candidiasis.36,37
Management includes instruction in good oral hygiene. In
addition, the condition may be susceptible to antifungal medication. However resistance to fluconazole (one of the antifungal
drugs used as intervention for this disease) may be problematic as
resistance has occurred in vitro following exposure to the drug.38
Highly active antiretroviral therapy (HAART) of HIV appears,
generally, to reduce periodontal diseases and may help in management of linear gingival erythema.39
Necrotizing Gingivostomatitis (i.e. Necrotizing
Gingivitis, Necrotizing Periodontitis, or
Necrotizing Stomatitis)
Necrotizing gingivostomatitis is a rare condition associated with
HIV infection. It can result in limited pathology (e.g. necrosis of
the tip of one or more papillae), more generalized tissue destruction (e.g. necrosis of entire papilla or several papillae and the
attached gingiva), or significant tissue destruction (e.g. not only
mucosal necrosis but exposure of bone). It is a painful condition
that may also include loosening of the involved teeth (Figures 2, 3).
Figure 3. Necrotizing Ulcerative Gingivitis. Courtesy of Dr. Valli Meeks
Dental treatment of necrotizing gingivostomatitis is aimed at
reducing tissue morbidity.40 Intervention should include scaling
and root planning combined with antimicrobial and antibiotic
medication. Appropriate antibiotics, depending on the type of bacteria involved in the infection, include metronidazole, tetracycline,
clindamycin, amoxicillin, or amoxicillin-clavulanate potassium. It
should be appreciated that use of antibiotic can increase the risk of
candidiasis so co-treatment with antifungals may be necessary.41
One antibiotic regimen42 that is reported to have clinical support
includes prescription of 250mg metronidazole taken 3 times a
day for 5 to 7 days combined with 250mg amoxicillin-clavulanate
potassium also taken 3 times a day for 5-7 days. It has also been
suggested that chlorhexidine 15cc used as a rinse twice a day and
intrasulcular lavage with povidone-iodine may also be helpful in
controlling necrotizing ulcerative periodontitis, (NUP).
Instruction in home care is also important, although in one
study comparing HIV positive with seronegative patients, oral
hygiene was found to be better in the HIV patients than in the
non-HIV patients, with this clinical factor having no apparent
effect on disease status.43
Aphthous Ulcers
Recurrent aphthous ulceration (RAU) can also occur in the
HIV positive patient.44 Lesions may be single or multiple and
tend to be deep, painful, and persistent. Increased severity of
the condition is thought to be related to a reversed CD4:CD8 T
cell ratios, lower CD4 cell counts, and an inverse relationship
between these cells and activated gamma delta lymphocytes.45
Dental management is limited primarily to the application of
topical medications. Drug approaches are largely empiric and,
per a Cochrane Database Systematic Review published in 2012,
have not been supported by appropriate randomized controlled
trials. The authors of the above study conclude that “there is
a need for well designed studies to evaluate the efficacy and
safety of topical agents”.46,47 Nonetheless, topical medications
represent the standard of care and include corticosteroids, antibiotics, and antifungal medications which have shown to be
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helpful in reducing symptoms and lesion duration in non-HIV
patients with aphthous ulcers. Vitamin B12 and folate deficiencies have not been found to increase the risk of RAU in HIV
patients. Laser ablative therapy might also be considered in
some patients as it has been shown, based on at least one case
study, to help reduce lesion severity and induce remission.48
Viral Infection
Viral infections occurring in HIV patients are the same that occur in non-HIV individuals; but some oral viral conditions such
as Herpes zoster and Herpes labialis are reported to occur more
frequently in HIV infected patients and secondary effects can
be more damaging (e.g. jaw necrosis following herpes zoster).49
Other herpes viruses associated with oral pathology in the
HIV patient include HPV-16, HPV-18, HPV-33, and HPV-35
(these viruses cause verruciform conditions such as condylomata
and papilloma). A 2015 study of oral human papillomavirus
infection in HIV-positive and HIV-negative dental patients
had the following conclusions: "The observed risk factor associations with oral HPV in HIV-negative patients are consistent
with sexual transmission and local immunity, whereas in HIVpositive patients, oral HPV detection is strongly associated with
low CD4+ T-cell counts." HIV patients can also experience
other herpes viruses including; HHV-4 (Epstein-Barr or HBV
which causes oral hairy leukoplakia), HHV-8 (associated with
and probably causative with respect to Kaposi’s sarcoma), and
HHV-1 (which causes primary and recurrent ulceration). In
immunocompromised patients herpetic lesions present in an
atypical manner. For example, oral pathology can appear as
white nodules, non-vesicular ulcerations, fissures, and masses.
As occurs with aphthous ulceration, ulcerative lesions may be
severe and painful.50 (Figure 4)
Figure 4. HPV in HIV-infected Individual
74
HIV-Salivary Gland Disease (HIV-SGD)
Patients with HIV may develop a condition termed HIV
Salivary Gland Disease (HIV-SGD). Subjective complaints
include dry mouth or xerostomia that is not associated with
medication, xerogenic agents or other diseases known to
decrease salivation. The condition involves either unilateral
or bilateral painful diffuse soft tissue swelling of the major
glands. HIV-SGD can also affect the minor glands and clinically appears similar to sialadenitis. The underlying histology
of the condition in the major salivary glands includes lymphatic infiltrates and hyperplastic lymph nodes. Change in
salivary constituents result from the disease. These include
lower secretory sodium, calcium chloride, cystatin, lysozyme,
and anti-oxidant capacity; with all thought to impact the development of oral disease in the patient with HIV.54 As with
other oral pathologies, the presence of HIV-SGD is considered an important indicator of HIV disease.17 There appears
to be an increase in HIV-SGD as HIV progresses,55 even with
HAART. And the type of HAART used to treat HIV (nonPI or PI (protease inhibitor) based) may differentially affect
salivary gland abnormality. In one study of 668 HIV positive
women, it was found that PI-based HAART therapy was a
significant risk factor for gland enlargement and reduction in
flow.56 It is suggested that this latter occurrence may represent
a phenomena associated with the restoration of the immune
system, termed reconstitution.57
Supportive salivary therapy includes prescription or recommendation of salivary stimulants, oral moisturizing products,
and instructions regarding fluid intake and oral hygiene.
Conclusion
This first section of a two part series on Dentistry and HIV has
explored immune system dysregulation, cellular protein regulation and HAART, HIV reactivation and its possible relationship to oral disease. Estimates are that 40-50 percent of patients
infected with HIV will develop oral pathology and this rises to
80 plus percent in patients with AIDS. HAART may reduce
the incidence of some oral conditions, but appears to have less
of an impact on other diseases that a dental professional might
encounter in the HIV patient. Knowing what oral diseases or
infections are predictive of potential HIV infection, which
diseases/infections occur during AIDS, and when and how to
manage HIV related problems is an important component in
the overall dental management of the HIV patient.
Oral Cancer
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with HPV-16 infection and HIV there is a high risk (14.6
times greater than controls) of developing oral cancer.52,53 If
an HIV patient is suspected of having oral cancer, he/she
should be referred for biopsy.
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34.
357:1411–1412.
Greenspan D, Gange SJ, Phelan JA, Navazesh M, Alves ME, et al. Incidence
of oral lesions in HIV-1-infected women: reduction with HAART. J Dent
Res. 2004; 83:145–150.
Oguariri RM, Brann TW, Imamichi T. Hydroxyurea and interleukin-6
synergistically reactivate HIV-1 replication in a latently infected promonocytic
cell line via SP1/SP3 transcription factors. J Biol Chem. 2007; 282:3594–3604.
Gonzalez OA, Ebersole JL, Huang CB. Oral infectious diseases: a potential
risk factor for HIV virus recrudescence? Oral Dis. 2009 July; 15(5): 313–327.
(http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4131204/.
Stevens M, De Clercq E, Balzarini J. The regulation of HIV-1 transcription:
molecular targets for chemotherapeutic intervention. Med Res Rev. 2006;
26:595–625.
Alpagot T, Duzgunes N, Wolff LF, Lee A. Risk factors for periodontitis in
HIV patients. J Periodontal Res. 2004; 39:149–157.
Alpagot T, et al. Longitudinal evaluation of prostaglandin E2 (PGE2) and
periodontal status in HIV + patients. Arch Oral Biol. 2007; 52:1102–1108.
Ramirez-Amador V, et al. Synchronous kinetics of CD4+ lymphocytes and
viral load before the onset of oral candidosis and hairy leukoplakia in a cohort
of Mexican HIV-infected patients. AIDS Res Hum Retroviruses. 2005;
21:981–990.
Lacovou E, et al. Diagnosis and treatment of HIV-associated manifestions in
otolaryngology. Infect Dis Rep. 2012; 4(1):e9 http://www.ncbi.nlm.nih.gov/
pmc/articles/PMC3892662/; accessed 10/18/14.
Kumar RK, et al. Associated oral lesions in human immunodeficiency virus
infected children of age 1 to 14 years in anti-retroviral therapy centers in Tamil
Nadu. Contemp Clin Dent. 2013. 4(4):467-471.
Johnson NW. The mouth in HIV/AIDS: markers of disease status and
management challenges for the dental profession. Aust Dent J. 2010 Jun; 55
Suppl 1:85-102.
Ranganathan K, Hemalatha R. Oral lesions in HIV infection in developing
countries: an overview. Adv Dent Res. 2006 Apr 1; 19(1):63-8.
Patton LL, et al. Prevalence and classification of HIV-associated oral lesions.
Oral Dis. 2002; 8 Suppl 2:98-109.
Gowdey G, Lee RK, Carpenter WM. Treatment of HIV-related hairy
leukoplakia with podophyllum resin 25% solution. Oral Surg Oral Med Oral
Pathol Oral Radiol Endod. Jan 1995;79(1):64-7.
Resnick L, Herbst JS, Ablashi DV, eet al. Regression of oral hairy leukoplakia
after orally administered acyclovir therapy. JAMA. Jan 15 1988; 259(3):384-8.
Goh BT, Lau RK. Treatment of AIDS-associated oral hairy leukoplakia with
cryotherapy. Int J STD AIDS. Jan-Feb 1994; 5(1):60-2.
Anwar K, Malik A, Subhan K. Profile of candidiasis in HIV infected patients.
Iran J Microbiol. Dec 2012; 4(4): 204–209.
Bendick C, Scheifele C, Reichart PA. Oral manifestations in 101 Cambodians
with HIV and AIDS. J Oral Pathol Med. 2002; 31:1–4.
Chidzonga MM. HIV/AIDS orofacial lesions in 156 Zimbabwean patients at
referral oral and maxillofacial surgical clinics. Oral Dis. 2003; 9:317–22.
Patton LL, McKaig R, Strauss R, Rogers D, Eron JJ., Jr Changing prevalence
of oral manifestations of human immuno-deficiency virus in the era of
protease inhibitor therapy. Oral Surg Oral Med Oral Pathol Oral Radiol
Endod. 2000; 89:299–304.
Leao JC, et al. Oral Complications of HIV Disease. Clinics (Sao Paulo). May
2009; 64(5): 459–470.
Butt FM, Vaghela VP, Chindia ML. Correlation of CD4 counts and CD4/
CD8 ratio with HIV-infection associated oral manifestations. East Afr Med J.
2007; 84:383–8.
Campo J Oral candidiasis as a clinical marker related to viral load, CD4
lymphocyte count and CD4 lymphocyte percentage in HIV-infected
patients. 2002, Jan; 31(1):5-10.
Ramos-Gomez FJ, Flaitz C, Catapano P, Murray P, Milnes AR, Dorenbaum
A. Classification, diagnostic criteria, and treatment recommendations for
orofacial manifestations in HIV-infected pediatric patients. Collaborative
Workgroup on Oral Manifestations of Pediatric HIV Infection. J Clin Pediatr
Dent. 1999; 23:85–96.
Drugs and medications – Nilstat oral. Available at http://www.webmd.
com/drugs/mono-8206-NYSTATIN+SUSPENSION+-+ORAL.asp
x?drugid=52772&drugname=Nilstat+Oral)(Myostatin pastilles, drugs
and treatment. Available at: http://www.revolutionhealth.com/drugstreatments/mycostatin-pastilles#how_take.
Multiple authors. Clinician’s Guide to Treatment of Common Oral
Conditions. The American Academy of Oral Medicine; Spring, 1997.
http://www.webmd.com/drugs/mono-8206-NYSTATIN+SUSPENSION
+-+ORAL. aspx?drugid=52772&drugname=Nilstat+Oral; Title: drugs and
medications – Nilstat oral; accessed 010/20/14.
http://www.revolutionhealth.com/drugs-treatments/mycostatinpastilles#how_take; Title: myostatin pastilles, drugs and treatmen; assessed
10/20/14.
Razia A, et al. Oral HIV-Associated Kaposi Sarcoma: A Clinical Study from
the Ga-Rankuwa Area, South Africa. AIDS res treat, 2012; http://www.ncbi.
nlm.nih.gov/pmc/articles/PMC3447356.
John CN, Stephen LX, Joyce Africa CW. Is human immunodeficiency
virus (HIV) stage an independent risk factor for altering the periodontal
status of HIV-positive patients? A South African study. BMC Oral Health.
2013 Dec 3;13:69.
35. John CN, et al. BANA-Positive Plaque Samples Are Associated with
Oral Hygiene Practices and Not CD4+ T Cell Counts HIVPositive
Patients Int J Dent. 2012; 2012: 157641. Published online Nov 1, 2012.
doi: 10.1155/2012/157641 http://www.ncbi.nlm.nih.gov/pmc/articles/
PMC3509373.
36. Velegraki A, et al. Paediatric AIDS--related linear gingival erythema: a form of
erythematous candidiasis? J Oral Pathol Med. 1999 Apr; 28(4):178-82.
37. Schorling SRThe role of Candida dubliniensis in oral candidiasis in human
immunodeficiency virus-infected individuals. Crit Rev Microbiol. 2000;
26(1):59-68.
38. Moran GP, et al. Antifungal drug susceptibilities of oral Candida dubliniensis
isolates from human immunodeficiency virus (HIV)-infected and non-HIVinfected subjects and generation of stable fluconazole-resistant derivatives in
vitro. Antimicrob Agents Chemother. 1997 Mar; 41(3):617-23.
39. Kroidl A, et al. Prevalence of oral lesions and periodontal diseases in HIVinfected patients on antiretroviral therapy. Eur J Med Res. 2005 Oct 18;
10(10):448-5.
40. Ryder MI. Periodontal management of HIV-infected patients. Periodontol
2000. 2000 Jun; 23:85-93.
41. Gowdey G, Alijanian A. Necrotizing ulcerative periodontitis in an HIV
patient. J Calif Dent Assoc. 1995 Jan;23(1):57-9.
42. http://www.hivguidelines.org/clinical-guidelines/hiv-and-oral-health/
clinical-manifestations-and-management-of-hiv-related-periodontaldisease.
43. Horning GM, Cohen ME. Necrotizing ulcerative gingivitis, periodontitis,
and stomatitis: clinical staging and predisposing factors. J Periodontol. 1995
Nov;66(11):990-8.
44. Patton LLOral lesions associated with human immunodeficiency virus
disease. Dent Clin North Am. 2013 Oct;57(4):673-98.
45. MacPhail LA, Greenspan JS. Oral ulceration in HIV infection: investigation
and pathogenesis. Oral Dis. 1997 May;3 Suppl 1:S190-3.
46. Kuteyi T, Okwundu CI. Topical treatments for HIV-related oral ulcers.
Cochrane Database Syst Rev. 2012 Jan 18; 1:CD007975.
47. MacPhail LA, Greenspan JS. Oral ulceration in HIV infection: investigation
and pathogenesis. Oral Dis. 1997 May; 3 Suppl 1:S190-3.
48. Caputo BV, et al. Laser Therapy of Recurrent Aphthous Ulcer in Patient with
HIV Infection. Case Rep Med. 2012; 2012:695642.
49. http://manbironline.com/std/hiv_Opportunistic_Infections.html; assessed
10/27/14,; Title: HIV ~ Opportunistic Infections in AIDS.
50. Viral Infections of the Mouth Author: Sara C Gordon. http://emedicine.
medscape.com/article/1079920-overview#aw2aab6b3.
51. Grulich AE, van Leeuwen MT, Falster MO, Vajdic CM. Incidence of cancers
in people with HIV/AIDS compared with immunosuppressed transplant
recipients: a meta-analysis. Lancet. 2007; 370:59–67.
52. Stier, E. Human Papillomavirus Related Diseases in HIV-infected individuals.
Curr Opin Oncol. Sep 2008; 20(5): 541–546.
53. Risk factors for oral HPV infection among a high prevalence population of
HIV-positive and at-risk HIV-negative adults. Authors: Daniel C. Beachler,
Kathleen M. Weber, and Gypsyamber D’Souza; http://www.ncbi.nlm.nih.
gov/pmc/articles/PMC3280125/.
54. Lin AL, Johnson DA, Stephan KT, Yeh CK. (2003). Alteration in salivary
function in early HIV infection. J Dent Res 82:719-724.
55. Patton LL, McKaig R, Strauss R, Rogers D, Eron J. (2000). Changing
prevalence of oral manifestations of human immuno-deficiency virus in the
era of protease inhibitor therapy. Oral Surg Oral Med Oral Pathol Oral Radiol
Endod 89:299-304.
56. Navazesh M, et al. Effect of HAART on Salivary Gland Function in the
Women’s Interagency HIV Study (WIHS) Oral Dis. Jan 2009; 15(1): 52–60.
57. Jeffers L, Webster-Cyriaque. Viruses and Salivary Gland Disease (SGD);
Lessons from HIV SGD. Adv Dent Res. 2011; 23(1):79-83.
58. Atram P, et al. Gingival crevicular fluid: As a diagnostic marker in HIV
positive patients. J Int Soc Prev Community Dent. 2015 Jan-Feb;5(1):24-30.
doi: 10.4103/2231-0762.151969.
59. Pakfetrat A, et al. Oral manifestations of human immunodeficiency virusinfected patients. Iran J Otorhinolaryngol. 2015 Jan;27(78):43-54.
60. Muller K, et al. Oral Human Papillomavirus Infection and Oral Lesions in
HIV-Positive and HIV-Negative Dental Patients. J Infect Dis. 2015 Feb 13.
pii: jiv080. [Epub ahead of print]
Author Profile
Dr. Richard Nagelberg has been practicing general dentistry in suburban Philadelphia for 32 years. He has
international practice experience, having provided dental services in Thailand, Cambodia, and Canada. He is cofounder of PerioFrogz.com, an information services company, and an advisory board member, speaker, key opinion
leader and clinical consultant for several dental companies and organizations. Richard has a monthly column in
Dental Economics magazine, “GP Perio-The Oral-Systemic Connection”. He is a recipient of Dentistry Today’s
Top Clinicians in CE, 2009-2015. A respected member of the dental community, Richard lectures internationally
on a variety of topics centered on understanding the impact dental professionals have beyond the oral cavity. Dr.
Nagelberg can be reached at [email protected].
Author Disclosure
Dr. Nagelberg is Editorial Director, Dental Education, PennWell Publishing.
DENTALECONOMICS.COM | 06.2015
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Online Completion
Use this page to review the questions and answers. Return to www.ineedce.com and sign in. If you have not previously purchased the program select it from the “Online Courses” listing and complete the online
purchase. Once purchased the exam will be added to your Archives page where a Take Exam link will be provided. Click on the “Take Exam” link, complete all the program questions and submit your answers. An
immediate grade report will be provided and upon receiving a passing grade your “Verification Form” will be provided immediately for viewing and/or printing. Verification Forms can be viewed and/or printed anytime
in the future by returning to the site, sign in and return to your Archives Page.
Questions
1. The end result of HIV infection is:
a.
b.
c.
d.
Immunodeficiency
Robust immune function
Increase in the CD4/CD8 ratio
All of the above
2. During HIV infection which of the following events occur?
a. There is massive depletion of CD4+ memory T cells
in the mucosal tissue
b. There is dysregulation of innate immune defenses
c. The oral mucosal epithelium differentially expresses
proteins with up-regulation of some and downregulation of others
d. All of the above
3. In a study of HIV infection and HAART,
down regulated proteins were the ones
associated with:
a.
b.
c.
d.
Maintenance of protein folding
Anti and pro-inflammatory responses
All of the above
None of the above
4. HIV remains dormant in which type of
cells?
a.
b.
c.
d.
T cells
Macrophages
Dendritic cells
All of the above
5. In patients with recrudescent HIV, which of
the following factors has been suggested as
the cause?
a. Additional exposure to HIV via new inoculation.
b. The occurrence of oral pathology and associated
pro-inflammatory mediators
c. HAART drugs
d. Lack of good oral hygiene
6. Which of the following statements is
accurate?
a. It is estimated that from 40-50 percent of HIV
positive patients will develop oral disease.
b. In patients with AIDS the incidence of oral pathology
approaches 60 percent.
c. Both a and b
d. Neither a or b
7. R Kumar, et al, found that 61.65 percent
of 326 children age 1-14 with HIV had
oral lesions. Which oral disease was most
prevalent?
a.
b.
c.
d.
Angular cheilitis
Necrotizing ulcerative gingivitis
Oral candidiasis
Linear gingival erythema
8. In HIV patients the presence of oral disease
has been found to be related to other factors
besides the virus including:
a.
b.
c.
d.
Gender
Location
Level of public health awareness
All of the above
9. Which of the following oral conditions
is considered a sentinel lesion indicating
possible HIV infection?
a.
b.
c.
d.
Non-Hodgkin's lymphoma
Hairy leukoplakia
Linear gingival erythema
Kaposi's sarcoma
10. Which of the following oral condition(s)
are considered to be strong indicators of the
presence of HIV infection?
a.
b.
c.
d.
1506DE_76 76
Necrotizing ulcerative gingivitis
Necrotizing ulcerative periodontitis
Oral candidiasis
All of the above
11. Oral hairy leukoplakia occurs with HIV
infection. Which of the following statements
accurately describes the condition?
a. It is asymptomatic
b. The filiform papillae on the lateral surface of the
tongue project from the surface like thick hairs
c. Both a and b
d. Neither a or b
12. Limited evidence provides support for
which of the following treatments for oral
hairy leukoplakia?
a.
b.
c.
d.
Ablation with cryotherapy
Topical application of podophyllum resin solution
Prescription of systemic oral acyclovir
All of the above
13. Which type of oral fungal infection occurs
most frequently in HIV patients?
a.
b.
c.
d.
Pseudomembranous candidiasis
Erythematous candidosis
Angular cheilitis
Hyperplastic candidosis
14. The yeast species that has been most
identified as causing oral disease in the HIV
patient is:
a.
b.
c.
d.
Candida dubliniensis
Candida albicans
Both a and b
Neither a or b
15. Which of the following statements is
accurate?
a. The frequency of oral candidiasis correlates with
falling CD4+ lymphocyte counts
b. Oral candidiasis has been associated with emergence
of AIDS in children
c. Both a and b
d. Neither a or b
16. Antifungal medications found to be useful
in treating oral candidiasis include:
a.
b.
c.
d.
Nystatin
Clotrimazole
Triazole agents
All of the above
17. In the HIV patient with candidiasis which
of the following should also be included with
overall care?
a. Instruction in good oral hygiene
b. Recommendation for gum or candy if there is
daytime dry mouth
c. Prescription of miconazole nitrate vaginal cream if
caries is a comorbid disease
d. All of the above
18. Oral lesions in patients with oral HIV-KS
are most frequently found on the:
a.
b.
c.
d.
Palate
Tongue
Buccal mucosa
Floor of the mouth
19. Patients with HIV can develop gingival
inflammation. This condition is termed:
a.
b.
c.
d.
Gingivitis
Linear gingival erythema
Desquamative gingivitis
Erythematous gingivitis
20. HIV infection can lead to a rare but serious
periodontal condition. The term that is
currently used to describe this condition is:
a.
b.
c.
d.
Necrotizing gingivitis
Necrotizing periodontitis
Necrotizing gingivostomatitis
All of the above
21. The treatment of HIV related periodontal
disease includes antibiotic coverage. Which
one of the following strategies appears to
have clinical support?
a. Prescription of 250mg metronidazole taken 3 times a
day for 5-7 days
b. Prescription of 250mg metronidazole taken 3 times
a day for 5 -7 days coupled with 250mg amoxicillin
clavulanate potassium taken 3 times a day for 5-7 days.
c. Prescription of 500mg metronidazole taken 3 times a
day for 5-7 days
d. Prescription of 500mg metronidazole taken 3 times
a day for 5-7 days coupled with 500mg amoxicillin
clavulanate potassium taken 3 times a day for 5-7 days
22. The full extent of necrotizing gingivitis in
HIV patients may include:
a. Necrosis of the tip of one or more papilla
b. Necrosis of entire papilla or several papillae and the
attached gingiva
c. Necrosis of the mucosa and exposure of bone
d. All of the above
23. In HIV patients with recurrent aphthous
ulceration (RAU) lesions are often:
a.
b.
c.
d.
Deep, painful, and persistent
Shallow and non-painful
Both a and b
Neither a or b
24. In regards to the treatment of HIV related
aphthous ulceration, which of the following
statements is accurate?
a. Drug interventions are largely empiric and lack well
designed efficacy studies
b. Thalidomide can be prescribed by certified dentists
for treatment of significant disease
c. Both a and b
d. Neither a or b
25. Which of the following statements most
accurately reflects current science with
respect to the management of HIV related
aphthous ulceration?
a. Vitamin B12 and folate deficiencies have been found
to increase the risk of RAU in HIV patients
b. Vitamin B12 and folate deficiencies have not been
found to increase the risk of RAU in HIV patients
c. Vitamin C reduces the risk of RAU in HIV patients
d. Vitamin D reduces the risk of RAU in HIV patients
26. Viral infections occurring in HIV patients
include:
a.
b.
c.
d.
Herpes zoster
Herpes labialis
HPV-16
All of the above
27. Viral infection in the HIV patient from
HPV-16 causes:
a.
b.
c.
d.
Verruciform conditions
Oral hairy leukoplakia
Kaposi’s sarcoma
All of the above
28. In the HIV immunocompromised patient,
viral induced pathology may include:
a.
b.
c.
d.
White cheese-like superficial mucosal tissue swelling
Non-vesicular mucosal ulcerations
Both a and b
Neither a or b
29. Some studies suggest that in patients with
HPV-16 infection and HIV there is:
a.
b.
c.
d.
A low risk of developing oral cancer
A high risk of developing oral cancer
HPV-16 has not been associated with cancer risk
A greater risk of contracting other viral infections
30. Patients with HIV can develop salivary
gland disease (HIV-SGD). Which of the
following statements is accurate with respect
to this condition?
a. The condition can involve major and minor glands
b. The underlying histology of the condition involves
lymphatic infiltrates as well as hyperplastic lymph nodes
c. Salivary gland involvement changes salivary constituents
d. All of the above
6/8/15 1:25 PM
ANSWER SHEET
Dental Professionals and HIV- Part 1
Name:
Title:
Address:
E-mail:
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Requirements for successful completion of the course and to obtain dental continuing education credits: 1) Read the entire course. 2) Complete all information
above. 3) Complete answer sheets in either pen or pencil. 4) Mark only one answer for each question. 5) A score of 70% on this test will earn you 3 CE credits. 6)
Complete the Course Evaluation below. 7) Make check payable to PennWell Corp. For Questions Call 216.398.7822
If not taking online, mail completed answer sheet to
Academy of Dental Therapeutics and Stomatology,
Educational Objectives
A Division of PennWell Corp.
1. Identify the latest information on the pathogenesis of HIV disease and concepts related to the oral cavity
as a viral reservoir for HIV.
P.O. Box 116, Chesterland, OH 44026
or fax to: (440) 845-3447
2. Identify which oral conditions may be predictive of HIV disease.
3. Identify oral diseases that can occur with HIV and AIDS.
For IMMEDIATE results,
go to www.ineedce.com to take tests online.
Answer sheets can be faxed with credit card payment to
(440) 845-3447, (216) 398-7922, or (216) 255-6619.
4. Implement treatment strategies for HIV related oral candidiasis.
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