Hiv infection /certified fixed orthodontic courses by Indian dental academy

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HIV Infection

Contents
• Introduction
• Epediomology
• Clinical Features
• Oral Manifestations
• Mode of transmission
• Pathogenesis
• Anti retroviral drugs
• HIV Vaccine

• Anti retroviral drugs and oral diseases
• Anti retroviral drugs and oral side effects
• Orthodontic Care
• Infection control
• Post exposure prophylaxis
• Preventive Measures to reduce transmission.
• Conclusion
• References

Introduction
• AIDS was first recognized in the United States
in the summer of 1981, when the U.S. Centers
for Disease Control and Prevention (CDC)
reported the unexplained occurrence of
Pneumocystis carinii pneumonia in five
previously healthy homosexual men in Los
Angeles and of Kaposi's sarcoma in 26
previously healthy homosexual men in New
York and Los Angeles.

• Within months, the disease became recognized
in male and female injection drug users (IDUs)
and soon thereafter in recipients of blood
transfusions and in hemophiliacs.
• As the epidemiologic pattern of the disease
unfolded, it became clear that a microbe
transmissible by sexual (homosexual and
heterosexual) contact and blood or blood
products was the most likely etiologic agent of
the epidemic.

• In 1983, human immunodeficiency virus
(HIV) was isolated from a patient with
lymphadenopathy, and by 1984 it was
demonstrated clearly to be the causative agent
of AIDS.
• In 1985, a sensitive enzyme-linked
immunosorbent assay (ELISA) was developed,
which led to an appreciation of the scope and
evolution of the HIV epidemic at first in the
United States and other developed nations and
ultimately among developing nations
throughout the world

Epidemiology
Global estimates for adults and children by
the end of 2004
• 40 million people are living with HIV infection
• 4.9 million people have new HIV infection
• 3 million people have lost their lives
• 90% live in developing countries
• India – 2nd to South Africa

40 million Adults and children estimated to be living
with HIV/AIDS December 2004
Western
Europe
570 000
North Africa
& Middle
East
550 000
Sub-Saharan
Africa
29.4
million
Eastern
Europe
& Central Asia
1.2
million
South
& South-East
Asia
6 million
Australia
& New
Zealand
15 000
North
America
980 000
Caribbean
440 000
Latin
America
1.5
million
East Asia &
Pacific
1.2 million

In India
• First case recognized– in Chennai in 1986
• 5 million Men are affected
• 1.9 Million – Women
• 5,50,000 – Children
• M:F – 1.7 : 1
• 37% - are under age of 30

Clinical Features of HIV Infection
Four stages-
1. Primary infection
2. Asymptomatic infection
3. Mildly Symptomatic disease
4. Acquired immunodeficiency syndrome

Primary infection
• Symptomatic in 70-80% cases
• Occurs 2-6 weeks after exposure
• Plasma HIV-RNA levels > 1 million copies/ml
• CD4 count – 300-400 cells/cumm
• Symptomatic recovery occurs after 1-2 weeks

Clinical Features include-
• Fever with rash,
• Pharyngitis with cervical lymphadenopathy
• Headache
• Myalgia/arthralgia
Asymptomatic infection
• Infected individual remains well with no
evidence of disease except the presence of
generalized lymphadenopathy
• Lasts for 7-10 yearswww.indiandentalacademy.com

Mildly Symptomatic disease
• Indicates some impairment of cellular immune
system.
Clinical features-
• Oral hairy leukoplakia
• Oropharyngeal candidiasis
• Chronic Weight loss
• Diarrhea
• Herpes zoster infection
• Fever and night sweatswww.indiandentalacademy.com

Acquired immunodeficiency syndrome
Characterized by development of specified
opportunistic infections and neoplasms
Clinical features-
• Dementia
• Cryptococcal meningitis
• Cerebral toxoplasmosis
• Cerebral lymphoma
• CMV Retinitis

• Oesophageal candidiasis
• Pulmonary TB
• Diarrhoea
• Kaposi Sarcoma
• Non-Hodgkin Lymphoma

Oral Manifestation- Adults

Oral Manifestation- Pediatric Patient

Group 1-Oral Lesions Strongly
Associated with AIDS (AIDS Defining
Oral Diseases)

Candidosis
Prevelance- 55 to 69 %
Clinical features- White or
yellow plaques that can be
wiped off to reveal an
erythematous surface that
may bleed.
Definitive diagnosis-An
effective response to
antifungal agents.
•Smears or cultures for the
presence of candida
albicans or other species
Pseudomembraneous

Erythematous
Prevalence- 25- 50%
Clinical features- Red patches,
most commonly found on
the palate and dorsal surface
of the tongue.
• White spots and plaques
may also be seen, although
erythema predominates.
Defenitive diagnosis- the
detection of candida
albicans by smear and/or
culture, and response to
antifungal therapy, may help
to establish the diagnosis.

Angular Chelitis
Prevelence- 13-26%
Clinical features
• Inflammation/irritation
• Cracking and fissuring
• Pain upon opening the
mouth
• Reduced vertical dimension
Definitive diagnosis:
• An effective response to
antifungal agents.
• smears or cultures for the
presence of candida albicans
are essential for diagnosis.

Hairy Leukoplakia- Epstein Barr Virus

Prevelence-25-38%
Clinical features -Bilateral
whitish/grey lesions on
lateral margins of the
tongue.
• Non scrapable, and typically
may have vertical
corrugations.
• May extend to the dorsal
and ventral surface.
• Defenitive diagnosos-
Biopsy with demonstration of
Epstein Barr virus,
• Lack of response to
antifungals.

Kaposi’s Sarcoma

Prevelence 20-50%
Clinical features- Caused by HHV 8
• One or more erythematous, slightly bluish or
violaceous macules or swellings,with or
without ulceration.
• Most common on the palate or gingiva and
the dorsum of the tongue
• Defenitive diagnosis-Biopsy.

Non-Hodgkin’s Lymphoma
Clinical features -Firm,
rubbery, pink, reddish or
purple
swelling, with or without
ulceration.
• Predilection for the gingival
palatal mucosa.
Defenitive diagnosis- Biopsy
• Appropriate
immunocytochemical or
molecular biological
investigations

Periodontal Diseases
Linear Gingival
Erythema
Prevelence - 47%
Clinical features-Distinct
fiery red band along the
margin of the gingiva,
disproportionate to the
amount of plaque seen.
• No pockets, ulceration or
attachment
loss.
Defenitive diagnosis- None,
• But does not respond well
to oral hygiene measures.
• Microbiology not yet
established.

• Necrotizing Gingivitis Necrotizing Periodontitis

Clinical features- Soft tissue loss as a result of
ulceration or necrosis.
• Destruction may cross the mucogingival junction.
• Exposure, destruction, or sequestration of bone
• teeth may loosen, and pain may be experienced.
Definitive criteria:
• None.

Group 2-Oral Lesions Associated
with AIDS (AIDS Associated Oral
Diseases)

Herpes Simplex Virus

• Prevelence 1.7 to 27%
Clinical features- Vesicles that coalesce into
bullae and break
• Some report a tingling sensation
• Occur on fixed and keratinized tissue
• Painful
• May have systemic manifestations

Human Papilloma Virus
Prevelence 9 to 18 %
Clinical features- Condyloma
acuminatum begin as a smooth-
surface papule
• Rough fingerlike projections
• Occur mainly on keratinized
mucosa
• Tend to reccur
• May interfere with eating and
swallowing and may bleed
• Not painful
• Transmissible

HERPES ZOSTER INFECTION
Prevelence 17%
• Indicator of severe HIV infection, but seems to be unlikely.
• Preceded by vesicles – rupture – ulceration .
• Ulcers – multiple shallow, small with erythematous base, distributed
unilaterally along a division of 5th cranial nerve.
• Pain, tenderness.
Definitive criteria:
• Histologic staining for multinucleated giant cells with intranuclear
inclusions
• Direct immunofluorescence
• cytology smears taken from the lesions

Salivary Gland Enlargement
• Prevalence - 3-10%
• Arises as a consequence of
reactive/ inflammatory
conditions, infections and
neoplasm
• Most frequently is due to
diffuse infiltration of CD8
lymphocytes.

Psychological Impact

Mode of Transmission
Sexual transmission- HIV infection is
predominantly a sexually transmitted disease
world wide.
• In US 42% new infections are among
homosexuals and 33% are among
heterosexuals.
• Male to female transmission is 8 times more
efficient than female to male.

• Blood and blood products- 90 to 100%
individuals who receive HIV contaminated
whole blood transfusion, packed red blood
cells, platelets, leukocytes, and plasma,
• In contrast, hyperimmune gamma globulin,
hepatitis B immune globulin, plasma derived
hepatitis B vaccine and Rh immune globulin
are not associated with transmission of HIV
infection. The procedure involved in
processing these products either inactivates or
remove the virus.

Occupational Transmission of HIV
• There is a small, but definite, occupational risk of HIV
transmission to health care workers and laboratory
personnel and others, particularly when sharp objects
are used.
• An estimated 600,000 to 800,000 health care workers
are stuck with needles or other sharp medical
instruments in the United States each year.
• Large, multi-institutional studies have indicated that the
risk of HIV transmission following skin puncture from
a needle or a sharp object that was contaminated with
blood from a person with documented HIV infection is
–0.3% and after a mucous membrane exposure it is
0.09%.

HIV transmission after non-intact skin exposure has
been documented, but the average risk for
transmission by this route has not been precisely
determined; however, it is estimated to be less
than the risk for mucous membrane exposure.
An increased risk for HIV infection following
percutaneous exposures to HIV-infected blood is
associated with
1. Exposures involving a relatively large quantity
of blood, as in the case of a device visibly
contaminated with the patient's blood,
2. A procedure that involves a needle placed
directly in a vein or artery, or a deep injury.www.indiandentalacademy.com

Factors that might be associated with
mucocutaneous transmission of HIV include
1. Exposure to an unusually large volume of
blood,
2. Prolonged contact, and
3. Blood from patients with advanced-stage
disease, probably owing to the higher titer of
HIV in the blood
4. Presence of more virulent strains of virus.

Maternal – Fetal/Natal Transmission
• The relative proportions of mother-to-child
transmissions were
1. 23 to 30% before birth,
2. 50 to 65% during birth, and
3. 12 to 20% via breast-feeding.
Risk of transmission increases with the increase
in the number of plasma HIV RNA count.

Transmission by other body fluids
• Although HIV can be isolated typically in low
titers from saliva of a small proportion of infected
individuals, there is no convincing evidence that
saliva can transmit HIV infection, either through
kissing or through other exposures, such is
occupationally to health care workers.
• Saliva contains endogenous antiviral factors
1. HIV -specific immunaglobulins of IgA, IgG, and
IgM isotypes
2. Large glycoproteins such as mucins and
thrambospondin 1 which sequester HIV into
aggregates far clearance by the hast

3. A number of soluble salivary factors inhibit HIV
to various degrees in vitro, probably by targeting
host cell receptors rather than the virus itself.
Perhaps the best studied of these, secretary
leukocyte protease inhibitor (SLPI), blocks HIV
infection in several cell culture systems, and it is
found in saliva at levels that approximate those
required far inhibition of HIV in vitro.
4. Sub-mandibular saliva reduces HIV infectivity
by stripping gp120 from the surface of the virus
and that saliva-mediated disruption and lyses of
HIV infected cells occurs because of the
hypotonicity of oral secretions.

• Transmission of HIV by human bite can occur
but is a rare event.
• Although virus can be identified, if not
isolated, from virtually any any fluid, there is
no evidence that HIV transmission can occur
as a result of exposure to tears, sweat, and
urine.

Classification Of Retroviruses

Morphology of HIV Virus

Role of CD4 Cells in Immunity

Co-receptor For HIV Virus And Cell
Membrane Fusion
• HIV virus infect CD4 T
lymphocyte which has a co-
receptor – CCR5
• And Macrophage/Monocyte
which have co-receptor –
CXCR4

Life cycle of the virus

Life Cycle of the HIV Virus and
Mechanism of Anti retroviral Therapy

Investigations
Antibody Based
• Sreening Test- ELISA 99.5% sensivity.
• Confirmatory Test- Western Blot; high
specificity.
Virus based tests
• Viral culture
• Polymerized chain reaction(RNA, DNA PCR)
• P24 antigen detection

Salivary tests

Serologic Test For HIV Diagnosis

Western Blot Test

Medical Management of HIV infection
Aims
• Reduce the viral load (<50 copies/ml)
• Improve the CD4 count (above200cells/cumm)
• Improve the quality of life without
unacceptable drug related side effects
• Reduce transmission

Nucleoside reverse
transcriptase inhibitors
(N R T I s )
Zidovudine, Stavudine
Lamivudine, Didanosine
Abacavir Emitricitabine
Zalcitabine.
Non-nucleoside reverse
transcriptase inhibitors
(NN R T I s)
Delavirdine , Nevirapine,
Efavirenz.
Protease inhibitors (P I s) Indinavir, Ritonavir,
Saquinavir, Tipranavir,
Nelfinavir, Lopinavir,
Atazanavir, Fosamprenavir,,
Amprenavir,.
Antiretroviral drugs

NRTI’s

NNRTI’s

Protease’s Inhibitor

• Treatment with a combination of drugs is termed
Highly Active Antiretroviral Therapy (HAART).
• Z DV, Abacavir, and Tenofovir
• Lopinavir / ritonavir and Efavirenz

• A number of clinical trials ranging from several
small phase I trials and fewer intermediate-sized
phase II trials to determine safety and
immunogenicity have taken place and are under
way.
• The single completed phase III trial of a
recombinant gpl20 protein failed to show
protection despite evidence of HIV -specific
antibodies and CD4 + T cells in phase II. These
results suggest the potential importance of CD8+
T cell immunity in host defense against HIV -1.
HIV Vaccines

• The furthest advanced among the current phase
II trials in-volves a combination approach
using a live canarypox vector expressing one
or multiple HIV epitopes given together with
gpl20 or using the gpl20 as a boost.
• This approach has resulted in neutralizing
anti-bodies in virtually all recipients and HIV -
specific cytolytic T cells in -30% of
individuals at any given time during the course
of the trial.

HART and Oral Diseases
• Since the introduction of specific anti-HIV-
therapies there have been striking changes in
the frequency and character of the oral
complications of HIV disease.
• Anti-retroviral drugs significantly lessen HIV
viral load, increase CD4+ T-cell count and
lessen the frequency and severity of
opportunistic diseases. It would thus be
expected that HAART will reduce most HIV
related oral diseases

• 30% decrease in the frequency of HIV-related
oral manifestations was described in Spanish
patients receiving HAART.
• HAART decreased the prevalence of Oral
hairy leukoplakia (25.8 down to 11.4%) and
necrotizing periodontal disease (4.8 down to
1.7%), whilst increased salivary gland disease
(1.8–5%)

HAART And Oral Side Effects
• A range of oral diseases can arise as a
consequence of HAART. These adverse orofacial
side effects are usually not very troublesome
• The oral side effects of some NRTIs are related to
the bone marrow suppression, and they can
manifest as neutropenic mouth ulcers. Erythema
multiforme and toxic epidermal necrolysis have
also been described, as well as lichenoid
reactions, particularly related to zidovudine. This
drug can also give rise to mucocutaneous
hyperpigmentation by an, as yet, unknown
mechanism www.indiandentalacademy.com

Melanotic Hyperpigmentation

• Adverse effects seem to be less common with
NNRTIs; however, erythema multiforme has
been described in association with NNRTIs,
particularly Nevirapine
• Protease inhibitor-related oral side effects
include taste abnormalities, affecting about
10–20% of patients, and oral and perioral
paraesthesia. Ritonavir in particular can give
rise to circumoral paraesthesia in over 25% of
patients

HAART And Vertical Transmission
• Treatment with Zidovudine alone of an HIV
infected pregnent women from the beginning
of 2nd trimester through the delivery and of the
infant for 6 weeks following birth can reduce
the risk from 22% to < 5%
• Rate of vertical transmission can be < 1%
with combined retroviral therapy.

Orthodontic Treatment
• Overall, the provision of orthodontic treatment for
HIV – infected individuals in asymptotic stage is
same to that of non- infectious patients.
1) Treatment Planning- should be based on the
condition of the patient
eg Mental condition of the patient
Financial condition
2) Antibiotic prophylaxis
Neutropenia

3) Before inititing the procedure-
antibacterial mouthrinses
- in patients with the history of increased
bleeding tendencies placement of separators
and bands should be avoided.

Infection control
1)Barrier techniques – Gloving, Hand washing, wearing masks,
protective eye wears, Gowns, Disposable caps etc.
2)Sterilization
- Cleaning of instrumentsusing ultrasonic cleaner
- Heat sterilization – Autoclave, Dry heat
3)Disinfection – Ethyl alcohol, isopropyl alcohol
Phenols
Sodium Hypochloride
Gluteraldehyde

Post Exposure Prophylaxis
• First aid should be given immediately after the
injury.
• Punture wounds & other cutaneous injuries –
rinsed thoroughly with water or saline and then
washed with soap and water
• Mucosal exposures involving mouth should be flushed
vigorously with water
• Eyes – irrigated with water , saline or sterile eye
irrigants

• Combination therapy is now recommended for
occupational post-exposure prophylaxis (PEP)
• Recommended PEP is Zidovudine ,
Lamivudine and Indinavir for 28 days.
• Post exposure follow up HIV testing- 6 weeks,
3 months, and 6 months

Preventive measures for HIV
transmission
• Comprehensive sex education
programmes in schools
• Public awareness campaigns for HIV
• Easily accessible/discreet testing
centres
• Safe sex practices
• Effective treatment of HIV-infected
persons www.indiandentalacademy.com

• Routine screening of donated blood,
• Education/training (universal
precautions, needle stick avoidance)
• Counselling about planning/risks of
pregnancy if HIV-seropositive
• Measures to reduce vertical transmission
• Post exposure prophylaxis

Conclusion
• All the dental care providers should remain
alert to the oral conditions that may represent a
manifestation of HIV infection
• The dental profession has an essential role to
play in identifying the oral manifestations of
HIV disease and AIDS, and in management of
oral conditions that are associated with
immunodeficiency.

Reference
1. Kasper- Harrision’s Principles of internal
Medicine 16th ed McGraw Hill Publication.
1059-1139.
2. Greenberg- Burket’s Oral Medicine,
Diagnosis & Treatment . 10th ed Elsever
Publication 538-556.
3. Neville- Oral and Maxillofacial pathology –
2nd ed, W.B. Saunder’s Company. 235-249

4. S Rajendra- Shafer’s textbook of oral pathology-
5th Ed Elsevier Publication 488-497.
5. Mosca NG .HIV-positive patients: dental
management considerations. Dent Clin North
Am. 2006 Oct;50(4):635-57
6. Hodgson TA- Oral lesions of HIV disease and
HAART in industrialized countries. Adv Dent
Res. 2006 Apr 1;19(1):57-62.
7. Patton-HIV disease.Dent Clin North Am. 2003
Jul;47(3):467-92.

8. Barr CE- Practical considerations in the treatment
of the HIV-infected patient. Dent Clin North Am.
1994 Jul;38(3):403-23.
9. Frezzini C- Current trends of HIV disease of the
mouth. J Oral Pathol Med. 2005 Oct;34(9):513-
31.
10. Hodgson TA Oral lesions of HIV disease and
HAART in industrialized countries. Adv Dent
Res. 2006 Apr 1;19(1):57-62.
11. Petersen PE -Policy for prevention of oral
manifestations in HIV/AIDS: the approach of the
WHO Global Oral Health Program. Adv Dent
Res. 2006 Apr 1;19(1):17-20

12. Owotade FJ - Clinical experience with
parotid gland enlargement in HIV infection: a
report of five cases in Nigeria. J Contemp Dent
Pract. 2005 Feb 15;6(1):136-45.
13. Ceballos-Salobreña AThe effect of
antiretroviral therapy on the prevalence of
HIV-associated oral candidiasis in a Spanish
cohort. Oral Surg Oral Med Oral Pathol Oral
Radiol Endod. 2004 Mar;97(3):345-50.
14. Patton LL -Prevalence and classification of
HIV-associated oral lesions. Oral Dis. 2002;8
Suppl 2:98-109.

15. Valiathan Ashima, KL Pai, Sunil Sachdeva &
Snehalata Oberoi: Aids in Dentistry. Journal of
International College of Dentist1997; 41: 15-
20.

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