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HIV/AIDS

Alma Mutiarani Widi Marsha F. Lily Sutanto Sabila Madeina Amaliyatus Silmi
1406528301 1506668795 1506736285 1506728472 1406528314

Pasien pria usia 28 tahun dikonsul dari Gedung A RSCM. Pasien dikonsulkan
ke bagian penyakit mulut dengan diagnosis kerja toxoplasma ensefalitis,
HIV positif belum diberi ART, gangguan oklusi, dan sariawan. Pada
pemeriksaan, pasien mengeluhkan mulut tidak bisa dibuka lebar. Pada
pemeriksaan intraoral, ditemukan ada ulkus pada mukosa bukal regio 47,
berbentuk ireguler, dalam, dan terasa nyeri. Pasien ada riwayat kejang
sebelum masuk rawat inap rumah sakit. Pasien tidak ada riwayat transfusi
darah, tato, bukan pengguna narkoba suntik, namun ada riwayat
promiskuitas.
What is HIV?

The human immunodeficiency virus (HIV) infects cells of the


immune system, destroying or impairing their function.
Infection with the virus results in progressive deterioration
of the immune system, leading to "immune deficiency."
(WHO)

HIV is a virus spread through certain body fluids that


attacks the body’s immune system, specifically the CD4
cells (CDC)
What is AIDS?

Acquired immunodeficiency syndrome (AIDS) is a term


which applies to the most advanced stages of HIV
infection. It is defined by the occurrence of any of more than
20 opportunistic infections or HIV-related cancers. (WHO)

AIDS is the most severe phase of HIV infection. People with


AIDS have such badly damaged immune systems that they
get an increasing number of severe illnesses, called
opportunistic illnesses. (CDC)
Classification
Staging of HIV infection is important for selecting patients for
treatment and assessing prognosis, and for epidemiological studies. The
Centers for Disease Control/World Health Organization classification
takes both clinical and laboratory findings into account.
Epidemiology
People living with HIV/AIDS

36.9 million
people living with HIV/AIDS
worldwide in 2017

Mortality
940 000
people died of HIV-related
illnesses worldwide in 2017

Prevention

129
low- and middle-income
countries reported a total of
150 million people tested in
2014
Epidemiology

Laporan Perkembangan HIV-AIDS Tahun 2017. Kementrian Kesehatan Republik Indonesia.


Epidemiology

Laporan Perkembangan HIV-AIDS Tahun 2017. Kementrian Kesehatan Republik Indonesia.


Epidemiology

Laporan Perkembangan HIV-AIDS Tahun 2017. Kementrian Kesehatan Republik Indonesia.


Who Is at Risk for HIV?

Gay and Blacks/African Transgender


Bisexual men Americans and Women
Hispanics/Latinos

Injection Drug Blood recipients


Users
Etiology

‐ AIDS is caused by HIV, a


nontransforming retrovirus of the
lentivirus family.
‐ There are two HIV subtypes
HIV-1 and HIV-2, mainly HIV-1.
‐ HIV-1 and HIV-2 differ in
antigens and nucleic acids, but
are transmitted similarly, have
similar biological properties, and
both are capable of causing
disease.
Pathogenesis

‐ HIV contains several so-called ‘core’ proteins and is


surrounded by an envelope containing ‘coat’ proteins,
one of which, recognizes the host cell CD4 receptor.
‐ HIV then binds to, and later damages, host cells bearing
the T4 or CD4 receptor via the gp120 protein.
‐ CD4 cells are mainly helper-inducer T lymphocytes,
monocytes and macrophages, Langerhans cells, brain
glial cells and some colonic cells.
Pathogenesis

‐ Brain tissue, in particular the cells of monocyte–


macrophage lineage, can become infected with HIV.
‐ Neurological damage may also be mediated by the
production by HIV-infected macrophages of factors that
affect neuronal cell function or neural transmitters.
‐ After primary infection with HIV, acute viraemia results in
widespread dissemination of HIV and, in one third, in a
clinical seroconversion illness resembling glandular fever
Pathogenesis

‐ The virus is trapped in follicular dendritic cells in lymphoid


tissue germinal centres and there is expansion of a subset
of CD8 cells that are precursors of HIV-specific cytotoxic T
cells.
‐ Pro-inflammatory cytokines including interleukin-6 (IL-6),
tumour necrosis factor, gamma-interferon and IL-10 are
also overexpressed and may represent an unsuccessful
attempt at protective response. Dendritic cells are involved
in the initiation and propagation of HIV infection in CD4
cells.
Pathogenesis

‐ Antibodies to HIV develop and appear in the serum


within 6 weeks to 6 months from infection
(seroconversion) but, within this window, the patient may
be seronegative (though HIV may be detected by the
polymerase chain reaction; PCR).
‐ After infection of CD4+ cells, there is usually a long
asymptomatic period, but as HIV damages CD4 cells in
the immune and nervous systems the risk of
development of severe immunodeficiency, and symptoms
of disease, rises with time.
Pathogenesis

‐ HIV damage to CD4+


lymphocytes leads to a
lymphopenia over about 6 months
to 10 years, a fall in the ratio of
helper (CD4+) to suppressor
(CD8+) lymphocytes, a profound
defect in cell-mediated immune
reactivity, and HIV disease, which
manifests with infections.
Transmission and Risk Factors

HIV is transmitted mainly by body fluids, mostly by:


 sexual intercourse – saliva, semen and blood may
contain HIV
 contaminated blood, blood products and donated
organs
 contaminated needles – intravenous drug users and
needlestick injuries in health care workers
 vertical transmission (mother to child) – in utero,
during childbirth and via breast milk.
Transmission and Risk Factors

‐ The virus is transmitted mainly by intimate sexual contact


and can infect anyone who practises risky behaviours such
as having sexual contact with an infected person or
someone whose HIV status is unknown without using a
condom.
‐ Sexual transmission of HIV is more likely during HIV
seroconversion or in advanced AIDS.
‐ Saliva and breast milk may contain HIV, but transmission
via the orogenital route is uncommon. However, saliva
transmission may result from human bites
Transmission and Risk Factors

‐ Persons infected with HIV, especially those who


abuse drugs intravenously or/and who are sexually
promiscuous, may also be co-infected with other
agents.
‐ Transmission by needlestick injury is an occasional
risk for health care workers.
Transmission and Risk Factors

‐ Transmission of HIV can also occur via infected


blood or blood products, including plasma, or
tissues, such as in transplantation, but, in
developed countries, screening of blood and plasma
for HIV antibody, and heat-treatment of clotting
factor concentrates has substantially reduced the
risk.
Transmission and Risk Factors

‐ Children can contract HIV intrapartum or via breast


milk; approximately one-quarter of all untreated
pregnant women infected with HIV pass the
infection to their babies, and the figure rises to one-
third if the infant is breast-fed.
‐ Antiretroviral drugs reduce this transmission.
Transmission and Risk Factors

‐ HIV is not spread through casual contact, such as


the sharing of food utensils, towels and bedding,
swimming pools, spas, telephones or lavatory seats.
‐ PREVENTION of HIV/AIDS:
‐ the use of condoms,
‐ the cessation of needle-sharing
‐ screening blood and tissue before transfer to a
recipient
‐ the use of antiretroviral drugs for children born
to HIV infected mothers.
Diagnosis
means ‘through knowledge’ and entails acquisition of data
about the patient and their complaint using the senses
Diagnosis is made by examination, which comprises the:

03 Laboratory
examination

History
(anamnesis)
01 02
Physical
examination -
clinical features

History (Anamnesis)

The history should be carefully taken to elicit


possible exposures to human
immunodeficiency virus (HIV). The risk factors
mentioned above must be considered.
• Fever

Physical Examination Acute HIV


Infection



Malaise
Lymphadenopathy
Myalgia
- Clinical Features (A)

Infection with HIV may be staged • Asymptomatic  often for years


according to its clinical features Continuing • Viraemia
HIV Infection • Generalized lymphadenopathy
(A)

• Infections
• Neoplasms
HIV • Neuropsychiatric disease
Disease (B) • General deterioration

• Serious infections
AIDS (C) • Neoplasms


Laboratory Examination
ELISAs, Rapid Tests, Semi-
quantitative Antibody Assays,
Immunologic Western Blot Assays, Immune
System Deterioration as a
Consequence of HIV Infection.

HIV Culture, HIV NAATs, HIV


Laboratory Examination Virologic DNA Assays, HIV RNA Assays,
p24 Antigen Assays.

Blood-tests CD4 Count


Laboratory Examination
ELISA
Western Blot Assays
Enzyme-Linked Immunosorbent Assay,
detect the presence of HIV
antibodies in the blood or oral fluid; Detect antibodies for HIV in the
positive result on ELISA must be blood; typically is used to confirm a
confirmed by a second test to reactive ELISA test result as being
receive a definitive diagnosis of HIV truly positive.
infection.

p24 Antigen Assays

The viral protein p24 exists either


bound to antip24 antibody or
unbound (free) in the bloodstream of
HIV infected individuals.
Laboratory Examination – CD4 Count

A laboratory test that measures the number of CD4 T lymphocytes


(CD4 cells-white blood cells that fight infection) in a sample of blood. In people
with HIV, the CD4 count is the most important laboratory indicator of immune
function and the strongest predictor of HIV progression. The CD4 count is also
used to monitor a person’s response to antiretroviral therapy (ART).
Oral Manifestations of HIV &
Pharmacotherapy
1993 EC-Clearinghouse
Classification of Oral
Lesions Associated
with HIV (HIV-OL)
Oral Candidiasis (OC)

‐ Most common HIV-OL especially in HIV-infected patients


without access to HAART (highly active antiretroviral
therapy) or those who started their therapy late.
‐ Strongly associated with a low CD4 count.
‐ Pathogens: Candida albicans, other Candida species (C.
krusei, C. glabrata, C. dublinensis).
‐ Three forms commonly present:
‐ Erythematous candidiasis
‐ Pseudomembranous candidiasis
‐ Angular cheilitis
Erythematous candidiasis

‐ Red, flat, atrophic lesion on the


dorsal surface of the tongue or
on the hard or soft palates.
‐ Tends to be symptomatic 
oral burning (eating salty or
spicy foods or drinking acidic
beverages).
‐ More prevalent among HIV
patients than in general
population.
Pseudomembranous candidiasis

‐ Painless creamy white plaque-like lesions


on the tongue, palate, buccal mucosa, or
oropharynx.
‐ Frequently asymptomatic.
Angular cheilitis
• Can occur with or without erythematous or
pseudomembranous candidiasis.
• Painful erythema, fissuring or erosion of the
corners of the mouth covered with fine scale.
Therapy of Oral Candidiasis

Systemic Treatment Local Treatment

‐ Preferred therapy: Fluconazole 100 mg ‐ Preferred therapy (or) :


PO QD for 7-14 days ‐ Clotrimazole troches 10 mg PO
‐ Alternative therapy (or) : 5 times daily
‐ Itraconazole oral solution 200 mg ‐ Miconazole mucoadhesive
PO QD for 7-14 days buccal tablet 50 mg QD for 5d
‐ Posaconazole oral solution 400 ‐ Alternative therapy (and) :
mg PO BID once, then 400 mg
daily ‐ Nystatin suspension 4-6 ml
QID or 1-2 flavored pastilles 4-
‐ Fluconazole-refractory OC (or) : 5 times daily
‐ Itraconazole oral solution ≥ 200 ‐ Clorhexidine 0.12% oral rinses
mg PO QD
‐ Posaconazole 400 mg BID
‐ Voriconazole 200 mg BID
Oral Hairy Leukoplakia

‐ Reliable indicator of low CD4 count.


‐ Benign epithelial hyperplasia on the
lateral borders of the tongue.
‐ More prevalent in males.
‐ Caused by latent Epstein-Barr virus
(EBV) reactivation.
‐ Appears as white, corrugated
lesion on the lateral borders of the
tongue that can not be wiped
away.
‐ Might be unilateral or bilateral.
Therapy of Oral Hairy Leukoplakia

Systemic Treatment Local Treatment

‐ Note: Scarcity of evidence ‐ Possible efficacy of (or):


for OHL treatment, lesions ‐ podophyllin resin 25%
recur when treatment is application
discontinued. ‐ podophyllin resin 25%
‐ Acyclovir or other systemic and acyclovir 5%
antiviral treatments: cream
valacyclovir, ganciclovir,
foscarnet, famciclovir, and ‐ surgery and topical
valganciclovir. tretinoin (retinoic acid,
vitamin A)
Non-Hodgkin’s Lymphoma (NHL)

‐ EBV drives a range of malignancies of


the lymphatic system, associated with
B-cell non-Hodgkin’s lymphomas.
‐ NHLs are 60 times more common in
HIV-infected patients, compared to
general population.
‐ 25% of all extranodal NHLs are located
in oral cavity.
‐ Oral NHL clinically presents as growth
and ulceration.
‐ Commonly affects gingival, palatal, and
alveolar mucosa; may mimic dental
infections.
Therapy of Non-Hodgkin’s Lymphoma

Systemic Treatment Local Treatment

‐ Acyclovir inhibits viral DNA ‐ None


synthesis in lytic infection,
but not latent infection.
‐ Complex cytokine or
cytotoxic therapies
oncological treatment.
‐ Prognosis is poor, with mean
survival time of less than 1
year, despite treatment with
multidrug chemotherapy.
Kaposi’s Sarcoma (KS)
‐ Most frequent HIV-associated oral malignancy.
‐ Caused by human herpes virus-8 (HHV-8)
that is also called Kaposi sarcoma-associated virus.
‐ HHV-8 infection drives endothelial cells to a form of
neoplastic hyperproliferation.
‐ Early KS lesions commonly present in mouth,
especially palate and gingiva.
‐ Color of lesions may vary from purple or red to brown,
or yellow-brown.
‐ KS lesions can grow to a very considerable size,
sometimes may ulcerate.
‐ Lesions of greater size  greater risk of
complications: haemorrhage, secondary infection,
destruction of bone and periodontium, serious
aesthetic and functional problem.
Therapy of Kaposi’s Sarcoma

Systemic Treatment Local Treatment

‐ Mild-to-moderate KS: ‐ Intralesional vinblastine


initiation or optimization and sodium tetradecyl
of antiretroviral therapy sulfate 3%
(ART) ‐ Radiation therapy (600-
‐ Advanced KS: 2,000 cGy), laser therapy
chemotherapy + ART
Periodontal Diseases Associated with HIV

Linear gingival Nectorizing


erythema or ulcerative
marginal disease
gingivitis

Necrotising
stomatitis
Linear Gingival Erythema (LGE)

‐ Distinct fiery red band along the


margin of the gingiva.
‐ Most frequently found in anterior
teeth, sometimes with bleeding
and discomfort.
‐ Aetiology seems to involve an
invasion by Candida species of
the gingival tissue.
‐ Manifests in
immunocompromised patients
with CD4+ T lymphocyte counts
<200 cells/mm+
Therapy of Linear Gingival Erythema

Systemic Treatment Local Treatment

‐ If Candida is identified: ‐ Improved oral hygiene


antifungal drugs (same ‐ Clorhexidine 0.12% oral
as oral candidiasis rinses
treatment)
‐ Periodontal debridement
Necrotizing Ulcerative Disease (NUD)
‐ Necrotizing ulcerative disease can
sometimes progress to necrotizing
stomatitis.
‐ NUD is usually followed by fever, malaise,
halitosis, and lympthadenopathia.
‐ NUD is more common among
immunocompromised patients, especially if
they have psychological/motivational
problems, poor nutrition, and use tobacco
or other drugs.
‐ NUD sometimes might develop as a
symptom of immune reconstitution disease
after initiation of HAART.
Necrotizing Ulcerative Disease (NUD)
‐ Sub-classified as necrotizing ulcerative gingivitis (NUG)
and necrotizing ulcerative periodontitis (NUP).
‐ NUG characteristics:
‐ rapid onset
‐ acute painful inflammation of gingiva with rapid
destruction of soft tissues.
‐ NUP:
‐ Bleeding
‐ extremely sharp pain
‐ ulcerated gingival papillae
‐ rapid and extensive soft tissue necrosis
‐ advanced loss of periodontal attachment,
frequently leading to bone exposure, and crater-
shaped defects, sequestration of a significant
piece of alveolar bone.
‐ Microorganisms associated with NUP: Porphyrmonas
gingivalis, Tannerella forsythia, Dialister pneumosintes,
Aggregatibacter actinomicetemcomitans.
Therapy of Necrotizing Ulcerative Disease

Systemic Treatment Local Treatment

‐ Metronidazole (250 mg ‐ Clorhexidine 0.12% oral


orally 4 times daily for 10
days)
rinses
‐ Or other systemic antibiotics: ‐ Periodontal debridement
tetracycline, clindamycin,
amoxicillin, and amoxicillin-
clavulanate potassium
‐ Adequate pain management
Bacterial Infections

‐ Extra-pulmonary tuberculosis (TB)


becomes more common and affects
many internal body sights as
immunosuppresion of HIV infected
patient progresses.
‐ Mycobacteria occasionally caused
painless, irregular oral lesions usually
covered by a gray-yellowish exudate.
‐ Surrounding tissues are inflamed and
indurated.
‐ Affected areas: dorsum of the tongue,
lip, buccal mucosa, and palate.
Bacterial Infections
There is a link between TB and oral candidiasis  TB diagnosis must
be sought when a patient presents with oral candidiasis.

Therapy of Bacterial Infections (TB)


Systemic Treatment Local Treatment

‐ Management is systemic in the ‐ None


hands of a specialist physician.
Melanotic Pigmentation
‐ Can be found in patients with long HIV
history.
‐ Etiology
 increased release of α melanocyte-
stimulating hormone caused by
deregulation of cytokines in HIV disease
 use of melanocyte-stimulating drug :
antiretrovirals, antifungals
‐ Treatment  surgery, cryosurgery,
electrosurgery, or different types of laser
surgery
Salivary Gland Disease
‐ HIV assoclated salivary gland disease also can arise anytime during
infection
‐ 5% of HIV infected patients,with a greater prevalence in children
‐ Clinical sign is salivary gland enlargement, particularly affecting
parotid. 60%  Bilateral
‐ Treatment
 Systemic : Adequate ART
 Local : Repeated aspiration, drinking more water, chewing
sugar free gum
Trombocytopaenic Purpura
‐ The most common autoimmune
phenomenon in AIDS
‐ Can be an early sign
‐ Oral purple patches which may be
mistaken for Kaposi's sarcoma, petechiae
or blood blisters  haemostasis test and
if necessary, biopsy
‐ Blood test (Platelet counts below
50,000/mm3)
‐ Treatment  Plasmapheresis, fresh
plasma, ART even with stable numbers of
CD4 cells
Aphthous Ulceration
• Occur with increased frequency in patients
infected with HIV
• All three forms (minor, major, and
herpetiform) are seen: however, major
aphthous ulcerations an increased
prevalence (Diameter >10mm)
• Location  most common (lips, palate)
dorsum tongue
• Duration  more than 2 weeks
• Treatment
 Systemic : Thalidomide (200 mg/d for
4-6 weeks)
 Local : Chlorhexidine 0.12% oral rinses
Herpes Simplex Infection
• Usually HSV-1, occasionally HSV-2
• It might manifest as herpes labialis or primary
herpetic gingivostomatitis
• Clinical feature  diffuse mucosal ulcerations
• In HIV-infected patients, the lesions are more
widespread, occur in an atypical pattern, and
may persist for months
• Location  often on tongue,
lips, hard palate and gums
• Treatment  Valacyclovir 1 g, or Famciclovir
500 mg, or Acyclovir 400 mg for 5 to 10 days
Herpes Zoster Infection
• Recurrent VZV infection is common in
HIV-infection infected patients, but the
course is more severe.
• Clinical features
Oral : Unilateral, severe, pain and /or
paresthesia occurs
Extraoral : Rash is ipsilateral in the
dermatome, passing through macular,
papular, vesicular and pustular stages
before crusting and healing
• Treatment  Valacyclovir 1g, or
Famciclovir 500 mg, or Acyclovir 800 mg 5
times daily for 7-10 days
Condyloma Acuminatum

‐ Clinical features  painless,


cauliflower shaped, pink. As
imunosuppresion progresesses,
multiple or big lesions might develop
‐ Location  tongue or fauces
‐ Treatment  involve surgery, laser
surgery, or cryotherapy
Management of HIV/AIDS
MEDICAL MANAGEMENT
‐ Treatment goals :
reduce HIV-
associated morbidity restore and preserve
and prolong the immunologic
duration and quality function
of survival

maximally and
durably suppress prevent HIV
plasma transmission
HIV viral load

J.W. Little, D.A. Falace. Dental Management of Medically Compromised Patient 8 th ed. 2012. US; Elsevier.
MEDICAL MANAGEMENT

‐ Antiretroviral therapy (ART)  achieve viral suppression and immune


reconstitution while at the same time preventing emergence of
resistance and limiting drug toxicity.
‐ Longterm goals are to delay disease progression, prolong life, and
improve quality of life.
‐ Treatment often is organized into three major areas:
(1)ART
(2)prophylaxis for opportunistic infections
(3)treatment of HIV-related complications
J.W. Little, D.A. Falace. Dental Management of Medically Compromised Patient 8 th ed. 2012. US; Elsevier.
ART and HAART

‐ The major goal of ART is to restore immune dysfunction by


inhibiting viral replication  viral load is below the detection limit
of the assay at 4 to 6 months.
‐ Experts recommend starting treatment in all patients with
symptoms ascribed to HIV infection.
‐ HAART is defined as the use of at least three active antiretroviral
medications.

J.W. Little, D.A. Falace. Dental Management of Medically Compromised Patient 8th ed. 2012. US; Elsevier.
ART and HAART

‐ ART :
 recommended when the CD4+ count < 350 cells/μL and in those
with plasma HIV RNA levels greater than 55,000 copies/Ml.
 strongly recommended for patients with CD4+ T cell counts
lower than 200 cells/μL and for those with AIDS.

‐ Treatment is generally initiated for asymptomatic patients who have


a rapid drop in CD4+ T cell count or high viral loads.

J.W. Little, D.A. Falace. Dental Management of Medically Compromised Patient 8 th ed. 2012. US; Elsevier.
ART and HAART
‐ The classification of antiretroviral agents :

Nucleoside reverse Non-nucleoside


Protease inhibitors transcriptase reverse
(PIs) inhibitors (NRTIs) transcriptase
inhibitors (NNRTIs)

Nucleotides Entry inhibitors

J.W. Little, D.A. Falace. Dental Management of Medically Compromised Patient 8 th ed. 2012. US; Elsevier.
Antiretroviral
Medication
DENTAL MANAGEMENT

‐ Dental treatment of the patient with HIV infection/AIDS involves


determining :
 the current CD4+ lymphocyte count
 the level of immunosuppression of the patient
 the level of viral load  may be related to susceptibility to
opportunistic infections and rate of progression of AIDS.
‐ Patients who have been exposed to the AIDS virus and are HIV-
seropositive but asymptomatic may receive all indicated dental
treatment  patients with a CD4+ cell count > 350/μL.
‐ Patients who are symptomatic for the early stages of AIDS (i.e., CD4+
cell count < 200/μL) have increased susceptibility to opportunistic
infection  prophylactic antibiotics

J.W. Little, D.A. Falace. Dental Management of Medically Compromised Patient 8th ed. 2012. US; Elsevier.
Antimicrobial
Prophylaxis

71
DENTAL MANAGEMENT

‐ Dentists should continuously monitor dental and oral health


for disease progression  if any oral manifestations of HIV
are present, the first priority is to relieve pain and treat
infections.
‐ In planning invasive dental procedures  white blood cell
count and platelet count.
‐ Medical consultation is necessary for symptomatic HIV-
infected patients before surgical procedures are performed.

J.W. Little, D.A. Falace. Dental Management of Medically Compromised Patient 8th ed. 2012. US; Elsevier.
DENTAL MANAGEMENT
TRANSMISSION OF HIV
‐ The risk of HIV transmission from infected patients to health care workers is very
low, reportedly about 3 of every 1000 cases (0.3%)  needlestick or other sharp
instrument transmitted blood from a patient to a health care worker.
‐ Transmission of HIV lower than HBV (26%) and HCV (10%).
‐ After a needlestick : wounds and skin sites exposed to blood or body fluids should
be washed and mucous membranes flushed with water.
‐ The rate of transmission of HIV can be reduced by postexposure prophylaxis (PEP)

J.W. Little, D.A. Falace. Dental Management of Medically Compromised Patient 8th ed. 2012. US; Elsevier.
Post-exposure Prophylaxis (PEP)
‐ PEP means taking antiretroviral medicines (ART) after being potentially
exposed to HIV to prevent becoming infected.
‐ PEP should be used only in emergency situations and should be initiated as
soon as possible after the exposure, ideally within an hour, following a careful
risk assessment.
‐ In a change to previous guidelines, PEP is now generally not recommended
after 72h post-exposure.
‐ Use PEP once or twice daily for 28 days.
‐ NOT a substitute for regular use of HIV prevention methods, such as pre-
exposure prophylaxis (PrEP), which means taking HIV medicines daily to lower
your chance of getting infected.

https://www.hiv.gov/hiv-basics/hiv 75
Post-exposure Prophylaxis (PEP)

‐ The recommended follow-up period after occupational exposure to


HIV has been shortened and is now a minimum of 12 weeks after
the HIV exposure or, if PEP has been taken, a minimum of 12 weeks
from when PEP was stopped.
‐ The PEP regimen for starter packs is:
 Truvada (245mg tenofovir and 200mg emtricitabine (FTC)) once
a day
 Kaletra (200mg lopinavir and 50mg ritonavir) twice a day

76
CONTROL INFECTION

‐ Avoiding exposure to blood and bodily fluids is the primary way to


prevent transmission of HIV in dental care settings.
‐ Standard precautions should be followed with all patients, whether
or not they have been diagnosed with HIV  wear barrier
precautions (e.g., gloves, masks, and protective eyewear) whenever
there is potential for contact with body fluids, non-intact skin, or
mucous membranes.
‐ Protective equipment must be removed after leaving work areas,
and remember that gloves are never to be reused.

https://www.ada.org/en/member-center/oral-health-topics/hiv
STANDARD PRECAUTION
GLOVES
‐ Wear gloves:
 If you have open or healing wounds, or skin infections.
 When in contact with saliva, mucous membranes, or blood.
 When in contact with blood-soiled items, body fluids or surfaces contaminated by them.
 When examining all oral lesions.
‐ Replace torn or punctured gloves immediately.
‐ Use new gloves for every patient.
GOWN
‐ Wear gowns when blood or body fluids are likely to soil clothing.
‐ Change gowns daily or when visibly soiled with blood or body fluids.
Wear masks, face/eye protection or chin-length plastic face shields (with safety glasses or goggles)
to protect your mouth and nose (oral and nasal mucosa) from the splatter of blood, saliva or gingival
fluid.

https://www.ccohs.ca/oshanswers/diseases/aids/dental.html
STANDARD PRECAUTION
‐ Use disposable materials. Dispose in plastic bags.
‐ Place needles and sharp instruments in puncture-resistant containers before disposal.
‐ Routinely sterilize instruments used in all dental procedures  store in sterile packs or
pouches.
‐ Sterilize after each use any other dental instruments that come in contact with oral
tissues such as amalgam condensers, plastic instruments of handpieces and burs. High-
level disinfect if sterilization is not possible.
‐ Cover equipment and surfaces that may become contaminated and are not easy to clean
with impervious-backed paper, tin foil or clear plastic wrap. Remove and replace the
covering for each patient.
‐ Thoroughly clean blood and saliva from supplies used in mouth (impression material, bite
registration). Clean and disinfect.

https://www.ccohs.ca/oshanswers/diseases/aids/dental.html
References

‐ Scully C. Medical Problems in Dentistry. 6th ed. Elsevier; 2010.


‐ Little JW, Falace D, Miller CS, Rhodus NL. Dental Management of the Medically Compromised
Patient Missouri: Elsevier; 2013.
‐ Laporan Perkembangan HIV-AIDS Tahun 2017. Kementrian Kesehatan Republik Indonesia.
http://siha.depkes.go.id/portal/files_upload/Laporan_HIV_AIDS_TW_4_Tahun_2017__1_.pdf
‐ https://www.who.int/gho/hiv/
‐ Aškinytė D, Matulionytė R, Rimkevičius A. Oral manifestations of HIV disease: A review.
Stomatologija [Internet]. 2015;17(1):21–8. Available from:
http://www.ncbi.nlm.nih.gov/pubmed/26183854
‐ Laskaris G. Pocket atlas of oral diseases, 2nd ed. Stuttgart: Thieme; 2006.
‐ Cawson , Odell. Essentials of Oral Pathology and Oral Medicine. 7th ed. 2003
‐ Scully C. Oral Medicine and Pathology at a Glance. 2010
‐ Neville. Oral and Maxillofacial Pathology. 2nd ed. 2002

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