HIV IN PEDIATRIC DENTISTRY

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CONTENTS:
Introduction
Definition
Types of HIV
History
Epidemiology
Structure of HIV
Pathogenesis of HIV
Transmission of HIV
Process of disease progrssion
Stages of hiv infection
Clinical manifestations
Oral manifestations
Diagnosis
Control of the disease ; prevention & treatment
Dental mnagement for HIV infected patients
Precautions to be followed in dental practice against HIV exposure
Future prospects
Conclusion
References 2
 INTRODUCTION

 Infection with HIV results in profound immunosuppression , rendering the host

susceptible to the development of various opportunistic infections and
neoplasm.

 Compared with adults , the progression of HIV infection is more rapid and
severe in infants and children due to ongoing development of different organ
systems and an immature immune system that is less resistant to infection.

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 The oral cavity is particularly susceptible to infection since it harbors
numerous microorganisms that thrive in conditions of
immunosuppression and cause characteristic fungal, viral, bacterial, and
neoplastic lesions.

 Oral lesions are frequently among the first symptoms in HIV infected
children.

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 Early detection of HIV-related oral lesions can be
used to diagnose HIV infection, elucidate
progression of the disease, predict immune status,
and provide timely therapeutic intervention.

• HIV is the infectious stage of the condition,

AIDS is the disease phase.

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 WHAT IS AIDS ?

 Acquired means one can get infected with it.

 Immune Deficiency means breakdown or

inability of certain components of the immune

system to function, thus making a person

susceptible to certain diseases that they would

not ordinarily develop.

 Syndrome means a group of health problems

that make up a disease.

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 WHAT IS HIV?

H – Human – This particular virus can only infect human beings.

I – Immunodeficiency – HIV weakens the immune system by destroying
important cells that fight disease and infection.
V – Virus – A virus can only reproduce itself by taking over a cell in the
body of its host.
Human Immunodeficiency Virus is a lot like other Viruses, but the
difference is that, immune system can clear most viruses out of the body,
but can not get rid of HIV.

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HIV is an RNA based virus that causes AIDS
1. Attacks the Immune System

2. Destroys the body’s defenses against diseases

3. Body becomes vulnerable to infections & cancers that don’t normally

develop in healthy people.

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 DEFINITION
 AIDS was originally defined by CDC as “the presence of a reliably
diagnosed disease that is at least moderately indicative of an
underlying defect in cell mediated immunity.”
The current surveillance of definition categorizes HIV infected
person on the basis of clinical condition associated with HIV
infection & CD4 + T lymphocyte counts.
or
AIDS is a clinical entity characterized by profound loss of immune
function associated with a depletion of CD4+T lymphocyte.

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 TYPES OF HIV

HIV type 1
most common
Most pathogenic strain of the virus.
Has subtypes M, N, O and P (M is most predominant)

HIV type 2
Mainly in West Africa
 Less easily transmitted
 Longer period from initial infection
 Onset of illness is delayed 10
 HISTORY

•AIDS was first reported on June 5 1981, when the U.S. Centers for
Disease Control and Prevention recorded a cluster of Pneumocystis carinii
pneumonia in five homosexual men in Los Angeles.

•In India, the 1st description of AIDS came in Chennai where 6 women out
of 125 who were screened were HIV positive in high risk group of
prostitutes.

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 EPIDIMEOLOGY

•Perinatal transmission accounts for most HIV infections among

children.
•Pediatric AIDS contribute to 2% of all HIV infected case in developed
countries as compared with 15-20% in developing countries.
• In US, approximately 7,000 infants, 1,000–2,000 of whom are HIV
infected, are born to HIV infected women each year.
• In US, HIV is currently the seventh leading cause of death in children
1–4 years of age and the fourth among women 25–44 years of age.

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 STRUCTURE OF HIV

HIV is a retrovirus.
Spherical, 80-100nm diameter
Central core made up of proteins, 2
identical copies of single stranded RNA
associated with enzyme reverse
transcriptase.
Surrounded by a bilayered lipid
membrane studded with 2 viral
glycoproteins gp120 and gp41.

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 Both the ends of viral RNA have identical regions that contain
regulation & expression genes of HIV. The remainder genome has 3
major section :-
 Gag region –encode for protein of the internal structure of the virus.
 Pol region –encode for viral enzyme. Ex: Reverse transcriptase,
protease, integrase etc
 Env region – encode for viral envelop protein.

 The classical structural scheme of the genome is “5LTR-gag-pol-env-

3LTR”.
 LTR (long terminal repeat) represent the two end parts of the viral
genome that are connected to the cellular DNA of the host cell after
integration. 14
 PATHOGENESIS OF HIV DISEASE
Interaction of gp120 of HIV to CD4+ molecule of T cell

Internalization of virion

Uncoating of virion

Proviral DNA unintegrated, integrated

Activated CD4+ T cell Inactive CD4+ T cell

Budding of virus particles, syncitia formation

Latent phase
Cytopathic phase

Quantitative depletion qualitative failure of CD4+ T

Of CD4+ T cell cells to respond to antigens
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 TRANSMISSION OF HIV
3 modes of transmission of HIV:
1. Sexual contact: accounts for more than
75% of infections world wide.
2. Parenteral transmission
3. Perinatal transmission: Mother to the
new born infant. It can occur in 3 ways:
a. Transplacentally during pregnancy
b. During delivery
c. Postnatally during breast feeding.

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HIV Transmission requires
1. Infected body fluid
AND
2. Entry into the body
Four Fluids, if infected, can transmit HIV
a. Blood
b. Semen
c. Vaginal Secretions
d. Breast Milk

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What happens when HIV enters the human body?
1. WINDOW PERIOD
 Time from initial infection with HIV to time antibodies are detectable
(usually 3-8 weeks)
 Period varies between individuals & depends on the test used
 95% of people develop antibodies within 3-4 months
 HIV antibody tests may give negative results in an infected person
during this period

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2. SEROCONVERSION
 The change from non-detectable antibody test
(Negative test) to detectable antibody levels
(Positive test) is referred to as seroconversion
 Seroconversion marks end of the window
period
 Presents with non specific symptoms e.g.
fever, flu, headache, general weakness, poor
appetite, etc
 Symptoms short lived; patient improves in 2-
4 weeks

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3. STAGES OF DISEASE DEVELOPMENT
Stage 1: acute viral infection (1 to 3 weeks):
No symptoms or any of the following mononucleosis like
symptoms:
Fever, malaise, headache, myalgia, arthralgia,
lymphadenopathy, hepatosplenomegaly,
meningitis, rashes, encephalitis.
Stage 1 ends with the production of high
titers of anti- HIV antibodies at 2 to 3 months
post infection.
Anti HIV antibodies are usually detectable
by ELISA by 3 to 4 weeks.
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Stage II- completely asymptomatic:

Clinically silent.
Lasts for 6 or more years in 65-85%of the cases.
Production of large amounts of anti- HIV antibody.
HIV is detectable in blood, semen and cervical secretions.
Continuous and gradual decline of CD4+ T cells.

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Stage III- overt disease:
Severity is directly related to the decline of CD4+ T cells, which cause
diminished function by B cells,
T cells, macrophages and NK cells and leads to
opportunistic infections and spontaneous neoplasms.
Multiple symptoms & conditions
TB of the lungs
Diarrhoea for more than a month
Oral thrush
>10% unintended weight loss
Persistent fevers (unexplained) for more than a
month
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Stage IV

Multiple symptoms and conditions e.g.

Cancers like Kaposi’s sarcoma
Oesophageal candidiasis
Pneumonia
Cryptococcal meningitis
TB outside the lungs

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 STAGES OF HIV INFECTION
The 2008 revised HIV case definition was used to classify HIV infection
among adults and adolescents and among children:

HIV infection, stage 1: No AIDS-defining condition and either CD4 count

of >500 cells/μL or CD4 percentage of total lymphocytes of >29.

HIV infection, stage 2: No AIDS-defining condition and either CD4 count

of 200–499 cells/μL or CD4 percentage of total lymphocytes of 14–28.

HIV infection, stage 3 (AIDS): Documentation of an AIDS-defining

condition or either a CD4 count of <200 cells/μL or CD4 percentage of total
lymphocytes of <14.

HIV infection, stage unknown: No reported information on AIDS-defining

conditions and no information available on CD4 count or percentage.

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CLINICAL MANIFESTATIONS
• Generalized lymphadenopathy, fever, weight
loss, and chronic diarrhea
• Marked suppression of immune function
resulting in opportunistic infections such as:
pneumocystis carinii pneumonia, cytomegalovirus
(CMV) infections, tuberculosis, and
cryptococcosis
• Neoplasms (usually non-Hodgkin’s lymphoma)

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BEHAVIORAL
• Apathy
• Depression
• Anorexia
• Fatigue

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CLASSIFICATION OF ORAL LESIONS OF PEDIATRIC
HIV INFECTION: (Flaitz &Hicks, 2003; Fonseca et al., 2000).

1. Oral lesions commonly associated with paediatric HIV

infection
 Candidiasis-
•Pseudomembranous
•Erythematous
•Angular cheilitis
Herpes simplex viral infection
Linear gingival erythema
 Major salivary gland enlargement
 Recurrent aphthous ulcers-
Minor, major, and herpetiform 28
2. Oral lesions less commonly associated with paediatric HIV
infection
Bacterial infections
 Periodontal diseases
• Necrotizing ulcerative gingivitis (NUG)
• Necrotizing ulcerative periodontitis (NUP)
• Necrotizing stomatitis (NS)
 Viral infections (cytomegalovirus, human papilloma virus, varicella
zoster virus, molluscum contagiosum)
 Xerostomia

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3. Oral lesions strongly associated with HIV infection but rare in
children
•Kaposi’s sarcoma
•Non-Hodgkin’s lymphoma
•Oral hairy leukoplakia
•Tuberculosis-related ulcers

4. Oral conditions with increased severity in pediatric HIV infection

•Gingivitis and periodontitis (increased gingival and plaque indices)
• Over-retained primary teeth
• Delayed eruption of primary and permanent teeth
• Primary dentition caries

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These lesions have also been grouped according to their aetiology
as:

•Neoplastic conditions
• Bacterial infections
• Fungal infections
• Viral infections
• Autoimmune disorders
• Neurological disturbances
• Other conditions.

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Oral Manifestations in HIV/AIDSInfected Children Charles Mugisha
Rwenyonyia et al European Journal of Dentistry July 2011 - Vol.5

Objectives: To assess factors influencing the distribution of oral

manifestations in HIV/AIDS-infected children attending the Paediatric
Infectious Disease Clinic in Mulago Hospital, Kampala. Methods: This was a
cross-sectional study comprising 237 children aged 1 to 12 years. The
parents/guardians were interviewed to obtain demographic information, oral
hygiene practices, dietary habits and health seeking behaviours as well as any
medications taken. The children were clinically examined for oral lesions
based on World Health Organization criteria with modifications.

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Cervical lymphadenopathy, oral candidiasis and gingivitis were the most
common soft tissue oral lesions: 60.8%, 28.3% and 19.0%, respectively.
Except for dental caries, the overall frequency distribution of soft tissue
oral lesions was significantly lower in children on highly active
antiretroviral therapy (HAART) as compared to their counterparts not on
HAART. The prevalence of dental caries in deciduous and permanent
dentitions was 42.2% and 11.0%, respectively. Tooth brushing and previous
visits to the dentist were indirectly and significantly associated with dental
caries. About 5.9% (n=14) of the children had <200 CD4 T-lymphocyte
cells per µl of blood.
Conclusions: The majority of the children had one or more oral lesions,
particularly in the group not on HAART. Some of the lesions were
associated with discomfort during oral functions. 33
ORAL CANDIDIASIS
The most common HIV-related oral lesion.
Manifestation of oral candidiasis can be a
marker for progression of disease in infected
children.
The first clinically observable manifestation
of HIV infection
A predisposing factor is xerostomia, which is
a common side effect of some antiretroviral drugs.
Affects upto 72% of HIV infected children.
clinical manifestations: pseudomembranous, erythematous, hyperplastic,
angular chelitis, median rhomboid glossitis; the most common one being the
pseudomembranous type.
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PSEUDOMEMBRANOUS CANDIDIASIS
This presents as non-adherent multifocal, creamy
white to yellow papules or plaques
overlying the oral mucosa.
 Removal of this material often leaves an
erythematous mucosal surface, which
occasionally bleeds.
 It typically occurs on the buccal mucosa,
mucobuccal folds, dorsolateral tongue and the
oropharynx.

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ERYTHEMATOUS CANDIDIASIS
This varies from diffuse to patchy redness
throughout the oral mucosa.
Commonly located on the palate and the dorsum of
the tongue.
Median Rhomboid Glossitis is a specific type of
erythematous candidiasis that presents as red, smooth,
depapillated, persistent oral patch in the middle of the
dorsum of the tongue.
Tenderness or a burning sensation may be
experienced.

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ANGULAR CHELITIS

Appears as erythema or fissures at the

commissures of the lips.
They are typically bilateral, and multiple red
papules may be found when the adjacent perioral
skin is involved.
Frequently accompanies intra-oral candidiasis.
 In patients with deeply pigmented skin,
depigmentation may occur at the site of angular
cheilitis.

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TREATMENT:
In infants and small children, candidial lesions can be treated by swabbing with
nystatin
TOPICAL AND SYSTEMIC ANTIFUNGAL MEDICATIONS FOR
PEDIATRIC POPULATIONS WITH ORAL CANDIDIASIS

AGENT DOSAGE
Topical
Oral nystatin suspension 2 to 5 mL, 4 to 6 times/day
Clotrimazole troches 10-mg tablet, 3 to 5 times/day

Systemic
Fluconazole 3 to 5 mg/kg once daily
Itraconazole 100 mg/day orally for children >3 years of age
Ketoconazole 5 to 10 mg/kg/day

5 to 7 days of therapy is often sufficient to clear symptoms of oral candidiasis.

Antifungal therapy should be continued 1 to 2 weeks after clinical resolution of
the lesions.
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HERPES SIMPLEX VIRUS INFECTION
This is the most common viral muco-cutaneous disease affecting HIV-
positive children.
The majority of oral lesions are caused by herpes simplex virus type1
(HSV-1).
 Prevalence ranges from 2% - 24% in Paediatric HIV studies.
 HIV positive children who have two or more herpetic infection episodes
within 1year are classified as having moderately symptomatic HIV disease.
(Caldwell et al., 1994).

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There is widespread mucosal erythema, vesicles and painful coalescing
ulcers.
The gingiva, palate, dorsum of tongue, lip and
the peri-oral skin are the commonest sites.
Excessive drooling of saliva and pharyngitis
often accompanies this infection.

TREATMENT
Acyclovir 200 – 400mg tabs 6 hourly for 10-14 days
Foscarnet 24 – 40mg/kg 8 hourly (very severe cases only) for 14-21days.

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LINEAR GINGIVAL ERYTHEMA:
Most common form of HIV associated
periodontal disease in HIV infected
children.
Most commonly associated with the upper and
lower anterior gingival tissues.
Appears as an erythematous linear band on the
marginal/ attached gingiva.
Bleeding is seen after gentle probing.
Treament: appropriate antifungal therapy.

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PAROTID SWELLING
Occur in 20- 47% of HIV infected children.
In patients with severe immune suppression.
Usually asymptomatic, bilateral and
spontaneously resolves and recurs.
Sialadenitis may be seen.
Parotitis may present as diffuse facial swelling
which is sometimes tender, xerostomia, cervical
lymphadenopathy and enlarged palatine tonsils.
Treatment: clindamycin, in a dosage of 8-25mg/kg/day.
A therapeutic alternative antibiotic is penicillin,
considering the gastrointestinal effects of clindamycin.
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RECURRENT APHTHOUS ULCERS
16% of the children with HIV.
In HIV disease all 3 forms of recurrent
aphthous ulcers are seen.
Aphthous ulcers in HIV-infected children
can present serious problems, such as pain and
impaired ability to eat.
 Diagnosis is based on characteristic clinical
appearance of deep, painful, round-to-oval, yellow-
white ulcers surrounded by a halo of erythema.
Most aphthous ulcers in children with HIV resolve
spontaneously.
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TREATMENT:
Topical steroid such as fluocinomide, clobetasol propionate and
dexamethasone elixir is the first choice. In severe cases, a short course of
prednisolone is indicated.
Antifungal agents to prevent oropharyngeal candidiasis are added when
steroids are used.

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HIV ASSOCIATED PERIODONTAL DISEASES
HIV infected children from developing countries
appear to be more susceptible to necrotising periodontal diseases.
A declining immune system with CD4 + cell counts below 200
cells/mm is associated with necrotising ulcerative periodontitis
and necrotising stomatitis.

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NECROTIZING ULCERATIVE GINGIVITIS:

Predisposing factors: stress,

immune suppression, malnutrition
and pre existing gingivitis.
Punched out, ulcerated papilla
with bleeding and pain,
lymphadenopathy, fetid odour and fever.

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NECROTISING ULCERATIVE PERIODONTITIS (NUP)
NUP has been reported in 0-4% of children.
It presents as severe soft tissue necrosis along with destruction of the
periodontal attachment and bone over a short period of time.
Spontaneous gingival bleeding or bleeding when brushing and severe,
deep, aching pain in the alveolar bone.
The alveolar bone may be exposed in the most severe cases.
Severe gingival recession resulting from rapid bone loss and soft
tissue necrosis.
Premature exfoliation of primary teeth.

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NECROTISING STOMATITIS:
This presents as an acute and painful
ulceronecrotic lesion on the oral mucosa.
The lesion starts from the oral mucosa and may
extend to alveolar bone and contiguous soft
tissues. The underlying bone may be exposed.

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TREATMENT
Topical :
Gentle debridement of affected areas to minimize bleeding and pain
Irrigation with 10%Betadine povidone -iodine or 1:4 hydrogen
peroxide to aid debridement.

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Systemic Treatment
Metronidazole (Flagyl) 125 mg tablets 8hourly for 7days
 Amoxicillin (Amoxil) 250 mg 8 hourly for 7 days
If the patient is allergic to penicillin: Erythromycin enteric coated 250mg
tablet 8 hourly for 7 days
The patient should be re-evaluated after one week of treatment and the
medication should be repeated if response is not satisfactory.
Supportive therapy: Multivitamins

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HERPES ZOSTER
The Center for Disease Control and Prevention has classified an HIV-
infected child with herpes zoster involving at least 2 distinctive episodes or
more than one dermatome as being moderately symptomatic.
Results from a reactivation of latent varicella zoster virus.
Prodromal symptoms -Fevers, complaints of sensitive teeth, headache,
paresthesia . A well-delineated unilateral maculo-papular rash that becomes
ulcerated follows.
Involvement of the second and third branches of the trigeminal nerve
produces oral lesions on oral mucosa that extend to the midline.
Most cases heal without complications in children except for facial skin
scarring.
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XEROSTOMIA
Has been observed in pediatric patients and
can cause increased incidence of dental caries,
candidiasis.
Clinical features include dry mouth, mucosa
that is desiccated and is at higher risk for
opportunistic infections such as
candidiasis and increased caries, severely
reduced salivary flow rates which results in a
high fluid consumption, eating of watery, loose
foods, and complaints of dry mouth.

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KAPOSI’S SARCOMA:
Kaposi’s sarcoma and other neoplasms are
rarely found in children with HIV.
The incidence of HIV associated cancers
in symptomatic children is less than 2%.
Presents as a flat, nodular or ulcerated
mass.
Palate, gingiva and tongue are most
commonly involved sites.

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ORAL HAIRY LEUKOPLAKIA
This is an opportunistic infection caused by the
Epstein-Barr virus (EBV) and is a marker for
increasing immunodeficiency.
It is a common oral manifestation of HIV infection
in adults but rare in children infected with HIV.
It presents as white non-removable lesions with
corrugated surface appearing bilaterally on the lateral
border of the tongue.

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DENTAL CARIES:
HIV-infected children are at greater risk for
dental caries than children without HIV infection.
Prevalence of dental caries is particularly high
in children below 5 years of age.
Rampant caries among these children is
attributed to bottle feeding with sugary drinks,
poor oral hygiene, use of sugary syrup medicines
(ziduvudine, nystatin).
Extrinsic factors such as diet, socioeconomic
status, lack of caregiver knowledge may be
additional risk factors.
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TREATMENT:
The long term use of Ziduvudine, nystatin may lead to increased incidence
of caries because of their high dextrose or sucrose content. Topical fluoride
should thus be prescribed.
Restoration of carious teeth and continuous caries prevention is important,
as it has been shown microscopically that deep dental caries may act as a
reservoir for Candida species in HIV infected individuals.

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Oral lesions and dental caries status in perinatally HIV-infected children
in Northern Thailand S. Pongsiriwet et al International Journal of Paediatric
Dentistry Volume 13, Issue 3 pages 180–185, May 2003.

Objective. To describe the prevalence of oral lesions and dental caries status
in perinatally HIV-infected children.
Forty children with perinatal HIV infection, from early infancy to 12 years of
age, were included in the study. These children were examined for oral
lesions and dental caries. A number of children receiving antifungal and
antiretroviral (ART) therapy were recorded.

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Results. The dft and dfs scores were  5·0 and 10 respectively. A total of 57·5% of
the children had one or more oral lesions. Oral candidiasis and hairy leukoplakia
were the most common oral lesions. Only 12·5% of children had received ART. A
total of 22·5% of the children had a history of receiving antifungal therapy.
Conclusions. Oral lesions and dental caries were relatively high in this study.
Consequently, treatment and prevention for oral lesions and dental caries are
inevitably required for children with HIV infection in Northern Thailand.
Furthermore, ART should be made available for all HIV-infected children to
decrease the prevalence of HIV-associated oral lesions.

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 DIAGNOSIS

CLINICAL LABORATORY
FINDINGS

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 CLINICAL DIAGNOSIS
As per WHO, AIDS is defined as the existence of at least 2 major signs
associated with at least 1 minor sign, in the absence of known secondary
causes of immunosuppression.

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Major signs include:
•Weight loss of > 10% of body weight.
•Chronic diarrhea of > 1 month duration.
•Prolonged fever for > 1 month.
Minor signs are:
•Recurrent oropharyngeal candidiasis
•Persistent generalised lymphadenopathy
•Persistent cough > 1 month
•Generalised pruritic dermatitis
•Recurrent herpes zoster
•Progressive disseminated herpes simplex infection.

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Expanded WHO case definition for AIDS surveillance: -
HIV antibody test positive
One or more of the following condition present.
1.Weight loss >10% of body weight or cachexia with diarrhea or fever or
both, intermittent or constant for at least 1 month.
2.Cryptococcal meningitis
3.Tuberculosis
4.Kaposi sarcoma
5.Neurological impairment
6.Candidiasis of Oesophagus
7.Recurrent episodes of Pneumonia
8.Invasive cervical cancer 62
 LABORATORY DIAGNOSIS
1. Specific tests:
i. Antigen detection: ELISA
ii. Virus isolation: isolated from CD4 lymphocytes of peripheral blood,
bone marrow and serum. Important test for diagnosis in window
period when antibodies are absent in serum of patient.
iii. Detection of viral nucleic acid: polymerase chain reaction (PCR).
iv. Antibody detection: most commonly employed technique. IgM
antibodies appear 1st usually in about 3-4 weeks after infection
followed by IgG antibodies.

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v. Serological tests: There are 2 types of serological tests:
screening and supplemental
SCREENING TESTS:
a. ELISA
•Used to determine the presence of antibodies to HIV in
the blood.
• Highly sensitive and specific test.
b. Rapid tests:
• Tests take less than 30 minutes.
• Does not require expensive equipment.
c. Simple tests: 1 to 2 hrs.

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SUPPLEMENTAL TESTS:
a. Western blot test:
• HIV proteins are separated by polyacrylamide gel electrophoresis.
• The separated proteins are blotted on to strips of nitrocellulose paper.
• These strips are reacted with test sera.
• Antibodies to HIV proteins, combine with different fragments of HIV.
• The position of the colour band on the strip indicates the fragment of
antigen with which antibodies have reacted.
b. Indirect immunofluorescence test

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2. Non- specific tests:
I. Total and differential leucocyte count: leucopenia and lymphocyte
count less than 400/μl
II. T- lymphocyte subset assays

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DIAGNOSIS IN CHILDREN

 Children < 18 months

 Polymerase chain reaction (PCR)
 Blood sample culture test
 P24 antigen test
 Children >18 months
 ELISA
 WESTERN BLOT Assay
 Indirect immunofluorescent assay

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Test for < 12 month of age child

 HIV DNA PCR

1. Preferred virological assay in developed countries
2. Almost 40% of infected newborns have +ve test in first two days of
life.
3. >90% testing +ve by 2 week of age
 PLASMA HIV RNA ASSAY
1. It detect viral replication
2. More sensitive than HIV DNA PCR

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HIV CULTURE
 Similar sensitivity to HIV DNA PCR
 The major disadvantage of this is technically more complex &
expensive.
 Results are often not available for 2-4 weeks as compared to 2-
3days with PCR.
P24 ANTIGEN ASSAY
 It is cheaper, highly sensitive & easy to perform.
 It is not recommended in infant < 1 month of age.

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CONTROL OF AIDS/HIV

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1. PREVENTION:
a. Education: Health education
•Avoiding indiscriminate sex
•Use of condoms
•Avoid sharing razors and tooth brushes
•Comprehensive sex education programmes in school.
•Public awareness campaigns for HIV.
•Educational material and guideline for prevention should be made wide
available.
•All mass media channels should be involved in educating the people on
AIDS, its nature of transmission & prevention.
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b. Prevention of blood borne HIV transmission:
People with high risk should be urged to refrain from donating
blood, body organs, sperm or other tissues.
All blood should be screened before transfusion
Transmission of infection to haemophiliacs can be reduced by
introducing heat treatment of factor viii & ix.
c. Strict sterilization practice in hospitals and clinics
d. Disposable needles and syringes should be used
e. Universal precautions by health care workers.

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Prevention is described as being at three
levels:
PRIMARY

SECONDARY

TERTIARY

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Primary
●
Primary HIV prevention refers to activity
focused on preventing uninfected people
becoming infected.

Secondary HIV prevention aimed at enabling people with

●

Secondary HIV to stay well (e.g. testing to allow people to know their
status; welfare rights advice; lifestyle behaviour ; anti–
discriminatory lobbying).

Tertiary
Tertiary HIV prevention aims to minimise the effects of ill–
●

health experienced by someone who is symptomatic with

HIV disease (e.g. the prophylactic use of drugs and
complementary therapies ) 74
TWO APPROACHES TO DISEASE PREVENTION
RISK AVOIDANCE:
•Avoiding sex with multiple partners
•Abstaining from drug use or use of other skin piercing
instruments.
•Safe And Appropriate Use Of Injections
•Reducing Unnecessary Transfusions

RISK REDUCTION:
•Use of condoms.
•Short-course Monotherapy with Zidovudine ,Nevirapine To
Mothers And Babies
•Elective Caesarean Delivery
•Breastmilk Replacement

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ABC APPROACH

Abstinence
Avoid exposure Mutual faithfulness

A  

Be faithful
Reduce exposure (Partner reduction)

B
Block exposure Condom use
effectively

C
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 2. ANTIRETROVIRAL TREATMENT

To suppress HIV replication.

Halts progression of HIV disease
Allows partial reconstitution of the immune system.

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There are 4 different classes of anti retroviral medications available :

1. Nucleoside Reverse Transcriptase Inhibitors.(NRTIs):

• Interupts reverse transcriptase.
• Ex. Zidovudine(AZT), Lamivudine (3TC), Stavudine (d4T)

2. Non nucleoside Reverse Transcriptase Inhibitors (NNRTIs):

• Blocks the action of reverse transcriptase by binding to the active site
of the enzyme.
• Ex. Efavirenz (EFV), nevirapine. (NVP)

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3. Protease inhibitors:
• Block HIV replication by preventing the proper clipping of
proteins .
• Ex. Nelfinavir (NFV), Ritonavir (RTV), Indinavir (IDV).

4. Fusion inhibitors:
• Rarely used
• Expensive
• Must be administered intravenously.
• Used in patients with high level resistance to many of other
antiretrovirals.

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 HAART Regimen: (Highly Active Anti Retroviral Therapy):

Consists of 2 NRTIs combined with an NNRTI or a PI.

REGIMEN ADVANTAGES DISADVANTAGES

AZT+ 3TC+EFV •Simple •Contraindicated in pregnant

•Less potential for skin and liver women .
toxicity. •CNS side effects.
•Well tolerated •Anemia

AZT+3TC+NVP •Less potential for CNS side •Higher potential for skin, liver
effects. toxicity
•Not contraindicated in •anemia
pregnancy

(AZT- Ziduvudine, 3TC- Lamivudine, EFV- efivirenz, NVP- Nevirapine ) 80

d4T+3TC+EFV •Simple •Contraindicated in
•Unlikely to induce anemia pregnant women
•Less potential for skin and •CNS side effects
liver toxicity

d4T+3TC+NVP •Simple •Liver, skin toxicity.

•Unlikely to induce anemia •Less potent.
•Less potential for CNS side
effects
•Can be given for pregnant
women.

(d4T- Stavudine, 3TC- Lamivudine, EFV- Efivirenz, NVP- Nevirapine)

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OTHER MEDICATIONS:

Antimicrobials for the treatment of or prophylaxis against opportunistic

infections.
Agents used for the control of symptoms associated with HIV or
HAART.
•Anti nausea medications: metoclopromide
•Anti diorrheal: Imodium
•Anorexia : Megestrol acetate
•Peripheral neuropathy: Amytriptyline.

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3. POST EXPOSURE PROPHYLACTIC TREATMENT:

•It refers to anti retroviral drug therapy within hrs following

accidental exposure to virus.
•Following needle stick injury, the part should be thoroughly washed
with soap & water.
•The injured finger should not be put in the mouth.
• Open wounds should be irrigated with saline.
•Antiseptic agent can be applied but caustic agents should be
avoided.

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 Following treatment is recommended by the US center for disease control
and prevention for health care workers accidentally exposed to HIV: -
Zidovudine( 200mg three times daily) +Lamivudine (150 mg twice
daily) for 4 weeks

If “ source individual have advance aids : Nelfinavir(750 mg 3 times

daily) +zidovudine +lamivudine

If “ source” individual failed on zidovudine +lamivudine therapy then

stavudine +didanosine

 For needle stick: ZDV+3TC 1 month, but in high risk (high viral RNA
copies) a combination of ZDV+3TC+Indinavir 84
4. PREVENTION OF INFECTION TO
BABY BY HIV POSITIVE MOTHER
a)zidovudine( 300mg three times daily) –to
pregnant mothers from 10-12th week of
pregnancy or immediately after diagnosis.
b)During labour- zidovudine I.V
c)New born -Syrup zidovudine( three times
daily for 6 weeks)
d)Single dose of Neverpin (200 mg) at the
time of labour.

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5. PRIMARY HEALTH CARE:
 Because of its wide range of implication, AIDS touches all
aspects of primary health care including mother & child
health, Family planning & education.
 It is important that AIDS control programmes should not be
developed in isolation.
 Integration in to country’s primary health care system is
essential.

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DENTAL MANAGEMENT FOR HIV INFECTED
PATIENTS:

1. Treatment planning:
 Alleviation of pain
 Restoration of function
 Prevention of further disease
 Consideration of esthetics.
 Short appointments
 Avoid multiple appointments as much as possible.
 Consideration must be given to addressing the patient’s immediate needs.

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2. ANTIBIOTIC COVERAGE:
NEUTROPENIA
CD4+ cell counts <200
Patients with valvular defects.

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3. BLEEDING DISORDERS, ANEMIA:
Conservative tooth by tooth approach should be taken.
If extensive surgical treatment is needed, consult with the patient’s
physician.

4. LOCAL ANESTHETICS:
No contraindication for use of LA.
For patients with bleeding disorders, deep nerve block injections should
be avoided.

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5. PREVENTIVE TREATMENT:
Establishing and maintaining good oral health to ensure that the patient is
free of pain and infection, sustain proper nutrition.
Routine dental prophylaxis, fluoride treatment, sealants and patient
education.
Proper home care techniques like daily brushing and flossing, fluoride
rinses.
Asymptomatic patients should be seen for routine cleanings and evaluation
every 6 months.

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Oral soft tissue lesions are common throughout the course. Therefore, a
thorough soft tissue examination should be performed at each recall
appointment.
Patient counseling should include the importance of meticulous oral
hygiene, diet modification, the use of at home fluoride treatment and
sugarless sialogogues.
Smoking, caffeine, alcohol including alcohol containing mouth rinses and
sugar sweetened and acidic drinks should be avoided.

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MANAGEMENT OF DENTAL EMERGENCIES
DENTAL PAIN:
•Administration of analgesics and antibiotics if infection is present.
•Before institution of any emergency procedure, body temperature and
blood pressure of the patient should be checked.
•If the patient is running a fever, consultation with the physician is
necessary.

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PULPITIS:
•Vital signs and cardiovascular history are taken followed by LA to control
pain.
•With pain under control, x rays and final clinical evaluation of restorability
of the tooth is achieved.
• If the tooth is not restorable, extraction should be performed.
•If extraction is not advised, drainage has to be established.
•Exposed pulp can be left open temporarily.
•Irreversible pulpitis and necrotic pulp are treated by pulpectomy.
•Pulpectomy should be followed by irrigation, instrumentation and filling
the canal with CaOH paste.

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IMPORTANCE OF ORAL HEALTH CARE FOR HIV INFECTED
PATIENTS:

Oral manifestations are common in people with HIV infection.

Oral lesions may be an early indicator of a decline of immune function.
Controlling a focal infection within the oral cavity may eliminate adverse
consequences such as systemic infections.
Poorly functioning dentition can adversely affect the quality of life.

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PRECAUTIONS TO BE FOLLOWED IN DENTAL
PRACTICE AGAINST HIV EXPOSURE:
•All patients should be treated as if they are infectious.
•Double gloves, surgical masks, protective eye wear or chin length plastic
face shields.
•Sterilize hand pieces after use with each patient. Instruments used for
HIV positive patients should be sterilized separately.
•Use disposable materials. Dispose in plastic bags. Place needles and sharp
instruments in puncture-resistant containers before disposal. Check with
local municipality for disposal of contaminated waste.
•Store sterilized instruments in sterile packs or pouches.

95
•Sterilize after each use other dental instruments that come in contact with
oral tissues such as amalgam condensers, plastic instruments of handpieces
and burs.
•Cover with impervious-backed paper, tin foil or clear plastic wrap
equipment and surfaces that may become contaminated and are not easy to
clean. Remove and replace for each patient.
•Thoroughly clean blood and saliva from supplies used in mouth
(impression material, bite registration). Clean and disinfect.

96
NOTE:
HIV is rarely transmitted by oral secretions.
Hypotonic disruption may be a major mechanism by which saliva kills
infected mononuclear leukocytes and prevents their attachment to
mucosal epithelial cells and production of infectious HIV, thereby
preventing transmission.

(Arch Intern Med. 1999 Feb 8;159(3):303-10.

Why is HIV rarely transmitted by oral secretions? Saliva can disrupt orally shed,
infected leukocytes. Baron S, Poast J, Cloyd MW.)

97
 FUTURE PROSPECTS
HIV Vaccine-
Several vaccine are under study keeping in mind the objective for the control
of AIDS.
1. Preventive vaccine
2. Therapeutic vaccine
3. Perinatal vaccine
Type of vaccines-
4. Whole virus vaccine –live attenuated & inactivated
5. Subunit virus vaccine-envelop protein & core protein
6. Live virus vector of HIV gene with vaccinia virus recombinants &
adeno virus recombinants
7. Anti idiotype HIV vaccine. 98
T-cell responses induced in normal volunteers immunized with a DNA-
based vaccine containing HIV-1 env and rev MacGregor etal  November 8, 2012
An effective HIV-1 vaccine will likely need to induce strong cell-mediated
immunity in humans. Therefore, the ability of a DNA HIV-1 vaccine to induce a
T-cell response in HIV-1 seronegative humans was examined.
Design: Individuals were enrolled in a phase I clinical trial of safety and immune
responses to an env/rev-containing plasmid at doses of 100, 300 or 1000 μg.
Peripheral blood mononuclear cells (PBMC) samples were analyzed by standard
lymphocyte proliferation, cytotoxic T lymphocyte (CTL) and ELISPOT
techniques.
It was observed that HIV-1 DNA plasmid vaccines induce CD4 T-helper cell
responses in humans. Furthermore, this report demonstrates the high level of
immunogenicity of rev and its importance as a component of a prophylactic
99
vaccine for HIV-1
GENE THERAPY

 This therapy requires the introduction of anti HIV gene into the cells to
prevent or inhibit HIV 1 viral gene expression of function & consequently
to limit HIV replication & AIDS pathogenesis.
 Gene also down regulate HIV in contrast to conventional drug thearpy.

100
 CONCLUSION
Oral cavity is the mirror of general health.
Oral manifestations are common and prevalent in paediatric HIV infection
and have been found to be the earliest indicators of HIV infection.
Early intervention in HIV disease is crucial for each individual according
to his/her risk and seroconversion status.
The use of oral lesions as predictors of disease progression could be of
immense importance.

101
Primary oral health care for HIV infected children should include a
careful oral examination at regular intervals to ensure early detection and
intervention for pseudomembranous candidiasis and other infections and
to prevent more deterioration of the immune system and further
opportunistic infections.
Preventive oral health care can improve a child's overall health.
Though these measures cannot stop HIV disease progression, in the
absence of medications, improved diagnosis of the oral manifestations
can enhance case management, ensure better oral health outcomes,
reduce morbidity and improve quality of life of HIV-infected children.

102
 REFERENCES
HIV AIDS IN Dental practice hanbook for dental practitioners. S R Prabhu.
Textbook of microbiology for dental students by Prof. C P Baveja
Textbook of clinical medicine for dental students by S N Chug.
Textbook of oral medicine by Anil Govindrao Ghom- 2nd edition.
Why is HIV rarely transmitted by oral secretions? Saliva can disrupt orally shed,
infected leukocytes. Baron S, Poast J, Cloyd MW. Arch Intern Med. 1999 Feb
8;159(3):303-10.
Infection control knowledge and practices related to HIV among Nigerian dentists
Omolara Gbonjubola Uti et al
J Infect Dev Ctries 2009; 3(8):604-610.
Centers for Disease Control and Prevention. HIV Surveillance Report, 2013; vol.
25.
Management of HIV/AIDS Patients in Dental Practice Continuing Education
Course. Charles John Palenik, Susan L. Zunt; Revised November 7, 2007. 103
Recommendations of the U.S. Public Health Service Task Force on the Use of
Zidovudine to Reduce Perinatal Transmission of Human Immunodeficiency Virus;
August 5, 1994 / Vol. 43.
Dental Standards of Care Committee. Oral Health Care for People With HIV
Infection: HIV Clinical Guidelines for the Primary Care Practitioner. New York State
Department of Health AIDS Institute; December 2001.
Oral Health Fact Sheet for Dental Professionals Children with Human
Immunodeficiency Virus (HIV).
Oral Manifestations of Paediatric HIV Infection Omolola Orenuga, Mutiat Obileye,
Christiana Sowole and Gbemisola Agbelusi. 14, November, 2011
Oral Manifestations in HIV/AIDSInfected Children . Charles Mugisha Rwenyonyi
et al.; European Journal of Dentistry July 2011 - Vol.5.
Orofacial and systemic manifestations in 212 paediatric HIV patients from
Chennai, south India. Kannan Ranganathan et al; international journal of pediatric
dentistry. 2010; 20 104
THANK YOU………..
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