HIV and AIDS /prosthodontic courses

HIV and AIDS
INDIAN DENTAL ACADEMY
Leader in continuing Dental Education
www.indiandentalacademy.com

CONTENTS
INTRODUCTION
HISTORICAL REVIEW
MECHANISM AND PATHOPHYSIOLOGY
CD4 ANTIGEN
INCIDENCE RATE
PART
I

Is HIV and AIDS the
same thing?

Virus is infectious particle with a single type of nucleic acid
RNA(ribonucleic acid) or DNA(deoxyribonucleic acid)
contained in a protein envelope called caspid and sometimes
covered by external envelope.
HUMAN IMMUNODEFICIENCY VIRUS
The virus that causes Acquired immunodeficiency
syndrome(AIDS) is called as HIV. There are two main types of
HIV, HIV-1 which is responsible for the pandemic and HIV-2
which results in less severe diseases.
HIV is a retrovirus having nucleic acid in the form of RNA and
during replication the RNA may be changed in DNA, utilizing
the enzyme reverse transcriptase which enables the host
integration in DNA.

HIV belongs to family lentivirus typically showing chronic
diseases with a long period of clinical latency, persistent viral
replication, and involvement of central nervous system.

Human Immunodeficiency
VirusesClassification
 Retroviridae (family)
 Lentivirus(Genus)
Characteristics
 100 nm in diameter
 Genome of two single strands of RNA
 Nine genes
Reverse Transcriptase
 RNA dependent DNA Polymerase
 Transcribe RNA into DNA

HIV
“Human Immunodeficiency Syndrome”
A specific type of virus (a retrovirus)
HIV invades the helper T cells to replicate itself.
No Cure

AIDS
 Acquired Immunodeficiency Syndrome
 HIV is the virus that causes AIDS
 Disease limits the body’s ability to fight infection
A person with AIDS has a very weak immune system
No Cure

AIDS = Acquired Immune
Deficiency Syndrome
 Acquired - because it's a condition one must acquire
or get infected with, not something transmitted
through the genes
 Immune - because it affects the body's immune
system, the part of the body which usually works to
fight off germs such as bacteria and viruses
 Deficiency - because it makes the immune system
deficient
 Syndrome - because someone with AIDS may
experience a wide range of different diseases and
opportunistic infections

HISTORICAL PROSPECTIVE OF AIDS
 Recognition of pneumocystis carinii pnemonia [pcp] and Kaposi ‘s
sarcoma in young healthy men in NYC and LOS ANGELES in
1981 was found.
 Case definition by CDC(centre for the disease control) isolation of
lymphadenopathy associated virus by PASTEUR INSTITUTE [Luc
MONTAGNIER].It included “limited number of specific
opportunistic diseases diagnosed by reliable methods in patients
with no other known causes of immunodeficiency.”
 ISLOATION of human T-lymphotropic virus, type III,[HTLV-III]
BY NCI/NIH [ROBERT GALLO]
 Recommendation of immunodeficiency virus HIV by a
international sub community on virus taxonomy

In 1983,Osleske J, et al reported the first case of unexplained
immunodeficiency syndrome (AIDS) in less than 11/2
years later
when acquired immunodeficiency syndrome(AIDS)was first
recognized in adults.
In 1986 first case of AIDS was reported in BOMBAY stated by
WHO and NACO(National AIDS control organization) ,India
1997.
In 1987,CDC modified the case definition of AIDS as a
disease ,at least moderately predictive of a defect in the cell
mediated immunity occurring in a person with no cause for
diminished resistance to that disease. Kaposi’s sarcoma and
pneumocystis carcinii pneumoniae were the most recognized
clinical manifestations of immunodeficiency syndrome.

The Human Immune Deficiency Viruswww.indiandentalacademy.com

 In 1996 it is stated that genome of HIV contains 3 structural
proteins and(gag, pol and env) and non structural and non
regulatory genes specific for the virus(-tat,rev,nef,vif and
vpr).Apart from this HIV 1contains VPU andHIV2 contains VPX.
Product of this genes acts as antigens and person serum acts as
antibodies to it.
Product of gag and pol gene are processed by viral protease, and
product of env gene is processed by cellular protease.Merle A
Sande and paul A volberding stated that these product of gag and
pol genes form the core of the mature HIV viron,whereas the
products of env genes are principle of exterior coat proteins.
Which are synthesized by gp-160 precursor that is cleaved by a
cellular protease in golgi apparatus to yield gp-120 and gp-41.

Gag Genes expressed as a precursor protein p55.which is cleaved
into 4 protiens,p17,p7,p9 and p24,which constitute the core and
shell of virus.p24 can be detected in the serum during the early
stage infection till the appearance of p24 antibody and the decline
of p24 antibody from the serum indicates the progression of
illness.
Pol Genes are translated from the same transcript as the gag
precursor they further get cleaved to produce several critical
viral enzymes including
reversetranscriptase,integrase,ribonuclease and aspartyl
protease.According to Anantnarayan it is expressed as precursor
protein which is cleaved into protein p31,p51. and p66.
Env Genes determine the synthesis of envelops glycoprotein
gp160 which is cleaved into two envelope gp-120 that forms the
surface spikes and gp-41 which is transmembrane anchoring
protein.

The spike gp-120 glycoprotein is the major envelope antigen and
the antibodies to gp120 are first to appear after the infection.
Non structural and Regulatory genes:
1.tat(Transactivation)gene: specifies the transactivating factor that
in collaboration with a cellular protein enhances expression of the
viral genes by increasing production of active messengers.
2.rev(Regulatory of virus)gene enhancing the expression of
structural proteins.
3.nef(Negative factor)gene: down regulating viral replication.
4.vif(viral infectivity factor):The gene influencing infectivity of viral
particles.
5.vpu(in HIV-1) & vpx(in HIV-2)gene enhances the maturation
and codes for small viral proteins of unknown function and helps in
distinguishing between HIV-1 and HIV-2.

The Viral Caspid: the viral caspid situated at the centre viral
particle is made of p24protein and p7 protein and
enzymes(reverse transcriptase and integrase)
MATRIX: the matrix is made of p17 proteins that forms the
internal lining of the viral particle.Viral protease is also found in
the matrix.
ENVELOPE: Derived from the fragments of the cytoplasmic
membrane of the host cell and acts as the outer cover of the
virus.This is further covered by gp120 external envelope
glycoprotein and gp41 transmembrane protein.

Origin of Human Immunodeficiency
Viruses
Existed As monkey virus in central Africa
HIV-1
Chimpanzee
Pan troglodytes
HIV -2
Sooty Mangabey
 Cerocebus atys
Transition from monkeys to humans around 1930

HUMAN RETROVIRIDAE[RETROVIRUSES]
Deltaretrovirus
Human T- lymphotropic virus, type I [HTLV-I]
Human T- lymphotrophic virus, type II[HTLV-II]
Lentivirus
Human immunodeficiency Virus type I[HIV-1]
 Group M
 Subtypes A-K
 Group O
 Group N
Human Immunodeficiency virus type II
 Subtype A-E
 Sumavirus
 Syncytial and foamy viruses of human.

VIRUS STABILITY
HIV, is inactivated by…
Heat in the autoclave or hot air oven
Glutraldehyde 2%
Hypochloride[10,000ppm];1 in 10 dilution of domestic
bleach
Disinfectants like alcohols.
The chemicals inactivate 105
units of viruses within few
minutes. But it is important to remember that disinfectants
are inactivated in the presence of organic material.

SURVIVAL OF VIRUS
 Virus may survive for up to 15 days at room temperature
 At 37 0
C virus can survive for 10-15 days
 Over 60 0
C virus is inactivated 100-fold each hour

GENOME OF HIV
Contains 6 regulatory genes
Contains 3 structural genes.

Mechanism of Pathogenecity Of HIV
 Envelop protein (gp120) of HIV binds with CD-
4 receptor on surface of-
T lymphocytes
Macrophages
Dendritic cells
Microglial cells
 Coreceptors for attachment of HIV
CCR5(T lymphocytes ,Macrophages ,Dendritic cells
,Microglial cells)
CXCR4(T –cells)

Normal mechanisms-pathogenic viruses-identified by macrophages-it
activate T lymphocytes-it get differentiated into effector cell like T
helper cell or T4 and T suppresor cell or T8-T4 cell secrete various
lymphokines which induce lymphocyte to differntiated into plasma
cell-it secrete specific antibodies against viral antigen-it destroy the
virus.
MECHANISM-HIV virus is lymphotropic virus-its primary target is
T4 cell-when the virus enters the blood stream,it integrates its gene
into DNA of some primary T4 lymphocyte-and this viral DNA then
becomes integrated into the host chromosomes-the chromosomal
integration is prerequisite for replication of retroviruses-viral genes
integrated into cells of own DNA,they can remain dormant for an
indefinite period-this is called as “Incubation period”-once viral
genes is activated,virus particles convert T4 lymphocytes into AIDS
virus-

When the number of T4 lymphocytes is Severly depleted,the immune
system collapses and variety of infections occur-at this stage patient
is said to have AIDS.

Pathophysiology AIDS Wasting
Oxidative Stress Micronutrient Deficiency
Malabsorption/
Dysphagia
Dietary Intake
Negative Energy
Balance
Intestinal Parasites
Protein Loss
Fat Loss
HIV
Opportunistic
InfectionImmune Function
Pro-inflammatory
Cytokines (TNF alpha)
Anorexia
Metabolic Rate
Endocrine Disorder
Skeletal Protein Breakdown
J AIDS 1988

HOW DOES HIV CAUSE
DISEASE?

Immune system ( Body’s
defense system)
2 main arms of the immune system.
Antibody-mediated immunity
Antibodies attack “free” organism in blood or lymph
Cell-mediated defense system
T-lymphocytes which attack and destroy infected cells

How does HIV cause disease
HIV attacks the body’s defense system
CD4 cells
Antibody production
T-cells that destroy
virus infected cells
HIV

Once HIV enters the body……..
Mucosal
tissue
Lymph glands
Few days
Blood spread
Blood
stream
Filtered in
lymph glands
Complete
body
defense
mechanism

Both CD4 cell Numbers and functi
affected !
T-cell infection leading to cell death
Large number of uninfected CD4 cells fuse with HIV infected cells. One
infected cell accounts for deaths of many uninfected cells
 CD4 cells do not function as well

AIDS
The result of infection with HIV is a inability of the body to
defend itself against other invaders leading to opportunistic
infections

CD4 Count in HIV infection
 The CD4 cell , also known as "T4" or "helper T cell“ is responsible for
signaling other parts of the immune system to respond to an infection.
 Normal counts range from 500 to 1500 cells per cubic millimeter of blood
 Initially in HIV infection there is a sharp drop in the CD4 count and then the
count levels off to around 500-600 cells/mm3
.
 CD4 count is a marker of likely disease progression. CD4 percentage tends
to decline as HIV disease progresses.
 CD4 counts can also be used to predict the risks for particular conditions
such as Pneumocystis carinii pneumonia, CMV disease or MAI disease.
 Treatment decisions are often based on Viral Load and CD4 count.

CD4 antigen is the main receptor for HIV entry:
HI V is an enveloped retrovirus that contains two copies of a
single stranded RNA(ssRNA) genome .Upon entry into a cell
the genome is reverse transcribed into complementary
DNA(cDNA) which is integrated into host cell
genome(provirus).
The basic gene stucture contains gag (core protien),pol(reverse
transcriptase,protease and integrase enzymes ), and
env(envelope protein)genes.
CD4 antigen is the main receptor for viral entry it is present on
CD4+ T lymphocytes,monocytes,dendritic cells (DCs) and
brain microglia.The envelope glycoprotein gp120 is also
capable of binding DC-SIGN.

HIV REPLICATION CYCLE:
1.BINDING:
The viral envelope glycoprotein gp120 binds to CD4 results in
conformational changes in gp120 that expose binding sites to
chemokine receptor,which serve as co-receptors for viral entry,these
chemokine receptor determines that HIV-1 variants can infect which
cell type.
Most primary isolates of HIV-1 uses CCR5 as coreceptor(R5)viruses.
2.PENETRATION:Interaction of gp120 with coreceptor releases
gp41,that enters in cell membrane and merges with it.Gp41 as
transmembrane part of the glycprotein gp160,is crucial for the
fusion of the viral and host cell membranes which creates a passage
to allow the viral nucleocaspid to enter the cell cytoplasm.

3.DECAPSIDATION:
Proteolytic enzymes of the cell cytoplasm digest the caspid of the
virus and facilitate the release of viral RNA and its enzymes.
4.REVERSE TRANSCRIPTION AND INTEGRATION.
Conversion of viral RNA into proviral DNA mediated by the viral
enzyme reverse transcriptase(RT),occurs in cytoplasm of the
target cell and is a crucial step in viral replication Cycle.
Viral reverse transcriptase facilitates the synthesis of DNA from
parent viral RNA.This proviral DNA (genome being of RNA
type)migrates to nucleus as viral integrase.
5.EXPRESSION OF INTEGRATED DNA:
Cellular RNA polymerase transcribes proviral DNA into viral
messenger RNA and genomic viral RNA.
.

6.VIRAL -ASSEMBLY- RELEASE- MATURATION:
Viral assembly takes place under the cell membrane in a region
modified by the binding to gp120 and gp41 cells on the
outside.Structural protiens gather around the two RNA
molecules which get covered by the cell membrane produce the
new immature viral particles.the new viruses can infect the other
cells.

Natural History of Untreated HIV
Infection

Above fig shows more severe infections are associated with
decreased CD4count.,this because the strong relationship
between CD4 count and risk of severe infection.AIDS can be
determine alone depending on the CD4 count if it is less than
200 cells /mm3

The Risk Involved
Sexual
- Heterosexual – 0.1% to 1%
- Homosexual – 0.3 % to 10 %
- Per sexual act risk is as follows –
- Heterosexual – 5/10,000 and homosexual – 50/10,000

INCIDENCE RATES OF HIV DISEASE
Overall,incidence rate of HIV in india is 0.7% of which
alarmingly high 16.6% is due to infected blood,uncleaned
syringes and other medical inefficiencies.In Maharashtra
incidence climbs upto 1.14% twice the national average.
GROUP 1992 1993 1994 1995 1996 1997 1998
PREGNANT
WOMEN
0.5 O.7 2.5 2.25 2.38 4.3 >2
BLOOD DONORS 1.5 2.1 1.7 1.7
INJECTING DRUG
USERS
26 31 31 33

HIV/AIDS Worldwide
• 38 million people live with
HIV/AIDS worldwide.
• Sub-Saharan Africa is home
to 70% of the people living
with HIV.
• 2.1 million children are infected
with HIV/AIDS in the world

Leading Causes of Death Among all over world
, 2002
Source: U.S. Centers for Disease Control and Prevention. National Vital Statistics Reports, Deaths:
Leading Causes for 2002. Public Health Service, 2003 (Vol. 53, No. 17)
Diabetes mellitusDiabetes mellitus
Cerebrovascular diseasesCerebrovascular diseases
SuicideSuicide
Nephritis, nephrosis & nephrotic syndromeNephritis, nephrosis & nephrotic syndrome
10
1
2
3
4
5
6
7
8
9
Deaths
0 500 1000 1500 2000 2500 3000 3500 4000 4500
AssaultAssault
Heart DiseaseHeart Disease
Unintentional injuryUnintentional injury
MalignantMalignant
neoplasmsneoplasms
HIV InfectionHIV Infection
CauseofDeath
Chronic liver diseaseChronic liver disease

Introduction
GlobalGlobal Sub-Saharan AfricaSub-Saharan Africa
People LivingPeople Living
With HIV/ AIDSWith HIV/ AIDS
(2005)(2005)
40.3 million40.3 million 25.8 million25.8 million
**57% women57% women
New HIV InfectionsNew HIV Infections
(2005)(2005)
4.9 million4.9 million
(14,000 people(14,000 people
infected everyday)infected everyday)
3.2 million3.2 million
(70%)(70%)
AIDS Related DeathsAIDS Related Deaths
(2005)(2005)
3.1 million3.1 million 2.4 million2.4 million

People Living With HIV in the U.S., by
Race/Ethnicity,
Black
White
Hispanic
Asian/PI
AI/AN
47%47%
34%34%
17%17%
1%1%
Source: Glynn et al. 2005 National HIV Prevention
Conference, Presentation T1-B1101.
Total:1,039,000 –
1,185,000 people
Asian/PI=Asian/Pacific Islander
AI/AN=American Indian/Alaska Native

HIV AIDS IN INDIA
India is a developing country with a wide base population
exceedings 112 millions susceptible for quick and high incidence
rate.The first case in India was reported in 1986.About two
decades the prevalance rates in adult population (15-49) age
group stands at 0.80 %.Comparatively India is a low prevalance
rate country that can get transfer into large absolute number of
HIV cases.
AS of 2002 the number of people living with HIV/AIDS was
4,580,000 and it was 5.206 millions with HIV and 11,608 with
AIDS reported in country upto 31 july 2005.It is estimated that
by 2010 HIV infected persons would be 20 to 25 million
people.with highest rate in Tamil nadu and Maharashtra.

The Global Scenario upto 2007,about 40.3 million people were
estimated to be living with HIV/AIDS including 2.3million
children,8million in age group of 15 to 24 years. INDIA ranks 2nd
in largest population of people suffering with HIV. After south
africa.
Indian scenario updated till 30 nov 2007 is total of 1,61,106 cases
of AIDS by the National AIDS Control Organization(NACO) till
30 NOV 2007.
Based on HIV prevalence rates in the adult population in the
states/union territories classified in groups.
Group I(High prevalance states)
Maharashtra,Tamil nadu,Karnataka,Andhra Pradesh, manipur,and
Nagaland where HIV infection had exceeded 5%in high risk
groups

GroupII (Moderate Prevalance states)
Gujarat,Goa,and UT of Pondicherry where the HIV prevalence has
reached 5% among high risk groups.
GroupIII(Highly Vulnerable states)
Assam,Bihar,Himachal pradesh,Kerala,Madhya pradesh,
Punjab,Rajasthan,UP, West bengal,
Chattisgarh,Jharkhand,Orrisa,uttarakhand,Delhi

The Statistics say…
Two Americans age 13-21 years are infected with HIV
every hour of every day (Youth and HIV/AIDS: An
American Agenda Report 1996)
10.3 million people aged 15-24 are living with HIV/AIDS
(Fact sheet on prevention HIV/AIDS among young
people by UNAIDS 1999)
900,000 North Americans are currently infected with
HIV, with 40,000 new infections yearly (Center for
Disease Control and Prevention, 2001)
Women aged 15-49 represent 43% of all new HIV
infections (The Joint United Nations Division on AIDS)

REFERENCES
 IMMUNOLOGY FIFTH EDITION :Richard A.Goldsby,
Thomas J.Kindt,Barbara A.Osborne.(pg no.329-442)
 MEDICAL MICROBIOLOGY 16th
EDITION: by David
Greenwood ,Richard C.B.Slack (pg 527-557)
 ANANTNARAYAN AND PANIKERS TEXTBOOK OF
MICROBIOLOGY 8th
EDITION (587-600)
 CLINICAL VIROLOGY MEMRD 3th EDITION by:Stevens
Specter,Richard Hodricke (pg513-554)
 ORAL AND MAXILLOFACIAL PATHOLOGY 3th
EDITION:by Brad W.Neville, Doughlas D. Damm(264-285).
 MEDICAL MICROBIOLOGYBY GREENWOOD SLACK
PEUTHERER 16TH
EDITION.Pg NO.392.

DENTAL MANAGEMENT OF PATIENT WITH HIV BY
MICHAEL GLICK.
ORAL MANIFESTATIONS OF HIV BY JOHN GREENSPAN
AND DEBORCH GREENSPAN.
AIDS AND ORAL HEALTH BY NS YADAV RUPAM SINHA.
ARTICLE FROM SCHOOL OF DENTISTRY By DR.JAIRAM
REDDY….. JOURNAL OF INTERNATIONAL ACADEMY
OF PERIODONTICS VOL 1-4 2007 Pg no.2-9 contro
HIV/AIDS related conditions with reference to periodontal
disease.

THANK YOU

PART II
CONTENTS
ROUTES OF INFECTION.
STAGING AND CLASSIFICATION.
LABORATORY DIAGNOSIS.

Routes of Spread
Sexual transmission – Bisexual , heterosexual
 Use of contaminated blood products –iv drug user,HIV contaminated
blood transfusion,blood clotting cooncentrate and organ transfusion
 Perinatal transfusion-in uterus
- during gestation period
-Post delivery
-During breast feeding
 other nosocominal routes .transmission from patient to
patient due to use of contaminated needle
Professional hazards-in health workers

Modes of HIV/AIDS Transmission

Through Bodily Fluids
Blood products
Semen
Vaginal fluids
Breast Milk

Through IV Drug Use
Sharing Needles
Without sterilization
Increases the chances of contracting HIV

Through Sex
Intercourse
Oral
Anal

Mother-to-Baby
Before Birth
During Birth
Postpartum
After the birth

What are the Chances of Mother –to-child
transmission(MTCT) of HIV
• If not receiving care ,women infected with HIV have a significantly
high chance of passing the virus to their infants during
,pregnancy,labour,delivery and or breast feeding.
• 20% to 30% before birth.
• 50% to 65% during birth
• 12% to 20% through breast feeding.
• In other words,for every 20 births of women with HIV,3 to 6
would be born infected,and another 2 to 4 would be infected if
bresatfed.

HIV patients may either walk in seeking treatmen or are referred
by medical practitioners,then patients status is generally revealed
in referral letter referring to physician.
1.patients may not know that they are HIV positive.
2.They know that they are HIV positive but they do not wish to
disclose their HIV status to the dental practitioner.
3.They know their HIV status and disclose it voluntarily to the
dental practitioner.
Considering the above possibilties it is important to consider every
patient should be consider potentially infectious.
HIV transmission is relatively small in work place (about 0.13%)
but proper control measures should be carried out properly.
On other hand transmission Hepatitis B is (about6-30%) in health
care settings.

DENTAL PRACTITIONERS
PRIMARY ROLE.
Their role includes:
1.Management of common dental problems.
2.Diagnosis of oral lesions associated with HIV infection and
appropriate treatment of them.
3.Communicating to the patients medical health provider
and providing proper treatment to any changes in systemic
health or any planned surgical procedures that may impact
patients health.

THE HIV DISEASE

Risk through Parental route
Pricks i.v drug abuse and cuts 03%-1%
Exposure to abraded mucosa 0.09%
Blood Transfusion 90%-95%

Phases of HIV and CDC Classification
Clinical Phase
 A-Early-acute Phase
 B-Middle,Chronic phase
 C-Final crisis

Phases of HIV and CDC Classification
• CDC Classification
 Group I –Acute infection
 Group II-Asymptomatic
 Group III – Persistant generalised Lymphadenopathy
 Group IV –
 Subgroup A – constitutional disease
 Subgroup B – Neurologic disease
 Subgroup C – Secondary infection
 Subgroup D – Secondary neoplasm
 Subgroup E – Other conditions

Interesting case statistics
• A longitudinal study carried out in U.S
• 55 health workers by 2002 investigated were
seroconverted……………………………..
• 19% - Lab workers
• 24% - Nurses
• 6% - Physicians
• 2% - Surgical technicians
• 1% - Dialysis technicians ,1% respiratory therapist,1health
aide and 1% the embalmer.

STAGING OF HIV INFECTION
STAGE CLINICAL MANIFESTATIONS CD4 CELL COUNT
ACUTE Mononucleosis like illness Normal
EARLY Asymptomatic or persistent
Generalized lymphadenopathy
Aseptic meningitis
Dermatologic manifestations
>400
MIDDLE Asymptomatic or persistent
Generalised lymphadeopathy
Hairy leukoplakia
Idiopathic thrmbocytopenia
200-400
LATE Opportunistic infections
Malignancy
Wasting
Dementia
<200

CDC Classification of HIV Infection
(1993 centre for disease control and prevention)
• Two categories and nine mutually exclusive stages.
• Clinical categories
 A-Early-acute Phase
 B-Middle,Chronic phase
 C-Final crisis
• CD-4 Cell Categories (Absolute number or %)
1. Category 1:>500 micro ltr or > 29% of total lymphocytes.
2. Category 2:200-499 micro ltr or 14-28% of total lymphocytes
3. Category 3:<200 micro ltr or < 14 % of total lymphocytes

HIV Infection Adults(Clinical category A)
• Following initial infection
Acute Retroviral Syndrome
• Infectious mononucleosis like or flu like illness
• 2 days to 4 weeks following infection
• Clinical manifestations –
- Fever,headache,lethargy,myalgias,photphobia,lymphadenop
athy,and a faint maculopapular rash.
• Resolution with in 30 days.
Asymptomatic
Persistent generalized lymphadenopathy.

HIV Infection Adults(Clinical category A)in
the adolscent less than 13 years
2 or more of the following
- Dermatitis
- Hepatomegaly
- Lymphadenopathy(>5mm at multiple sites)
- Spleenomegaly,parotidits
Recurrent or persistent sinusitis,otitis or upper respiratory
infection

HIV Infection Adults(Clinical category B)indicative
of cell mediated immunity
• Hepatitis
• HSV infection
• Recurrent(> episodes) stomatitis
• Multiple dermatomes or recurrent (> episodes) zoster infection
• Early onset (age-<1mo) bronchitis,pneumonitis or esophagitis.
• Leiomyosarcoma.
• Cervical carcinoma
• Lymphoid interstitial pneumonia
• Constitutional symptoms like fever(38.5*c )and diarrhoea
• Oral hairy leukoplakia
• Idiopathic thrombocytopenia
• Apulmonary lymphoid hyperplasia complex
• NephropTHY
• Nocardiosis
• Cong. Toxoplasmosis
• Disseminated Varicella

Late symptomatic-Category B
• Pulmonary or esophageal candidiasis
• Coccidiodomycosis
• Extrapulmonary cryptococosis
• Cryptosporidosis
• CMV infection
• Histoplasmosis
• Chronic mucocutaneous herpes simplex
• Encephalopathy
• Isosporiasis

HIV Infection Adults(Clinical category B)
• Invasive bacterial infection
• Persistent (>2 mo)oropharyngeal candidiasis (Patient age >6
mo)
• Cardiomyopathy
• Congenital CMV infection(onset before 1 mo of age)
• Chronic or recurrent diarrhoea
• Persistent(>1mo)fever
• Persistent(>1mo) hematologic disorders
• Anemia (< 8 mg/dl)
• Neutropenia (1X109
(< 1000/cumm)
• Thrombocytopenia (<100X109
(< 100,000/cumm)

Late symptomatic-Category B
• Kaposi Sarcoma
• Lymphoma
• MAC infection
• Mycobacterium kansasii infection
• PCP
• Recurrent Pneumonia
• Progressive multifocal encephalopathy
• Salmonellosis
• TB
• Toxoplasmosis

Full Blown AIDS(Clinical Category
C)
Disseminated CMV retinitis
Cryptococcal meningitis
Dementia,histoplasmosis
Disseminated CNS lymphoma
Progressive multifocal Leukoencephalopathy
Wasting syndrome.
Candidiasis of bronchi,trachea,or lung and esophageal candidiasis
Kaposo sarcoma,Burkitts lymphoma, and immunoblastic
lymphoma
Mycobacterium tuberculosis infection
Pneumocystis mutifocal encephalopathy

WHO CLINICAL STAGING FOR
HIV INFECTION AND DISEASE.
• CLINICAL STAGE 1:
• Asymptomatic
• Persistent generalised lymphadenopathy
• Performance scale 1:aysmptomatic and normal activity.
• CLINICAL STAGE 2:
• Weight loss>than 5%and<10%body weight
• Minor mucocutaneous symptoms(dermatitis,prurigo,fungal nail
infections,recurrent oral ulcerations,angular stomatitis.)
• Herpes zoster within the previous 5 years.
• Recurrent upper respiratory tract infection(bacterial sinusitis)
• Performance scale2:symtomatic,normal activity.

CLINICAL STAGE 3:
Weight loss>10%body weight
Unexplained chronic diarrhoea>1 month
Unexplained prolonged fever(intermittent or constant)>1month
Oral candidiasis
Oral hairy leukoplakia.
Pulmonary tuberculosis within the previous year.
Severe bacterial infections (i.e,pneumonia, pyomyositis)
Performance scale 3:bed ridden<50% of the day during the last
month.
CLINICAL STAGE 4:
HIV wasting syndrome(weight loss>10%body weight plus
unexplained chronic diarrhoea or chronic weakness and unexplained
Prolonged fever(>1month)www.indiandentalacademy.com

Pneumocystis carinii pneumonia.
Toxoplasmosis of the brain.
Cryptosporidiosis with diarrhoea for>1month
Extra pulmonary cryptococcosis.
CMV infection of an organ other than liver, spleen,or lymph nodes.
HSV infection , mucocutaneous>1month or visceral (any duration)
Progressive multifocal leukoencephalopathy.
Candidiasis of oesophagus,trachea,bronchi or lungs.
Extra pulmonary tuberculosis
Lymphoma
Kaposis”s sarcoma
Performance scale 4:bed ridden >50% of the day during last month

The greatest disease of mankind is not Acquired
Immunodeficiency syndrome but rather simply
the lack of affection and love among each
other…….

HAEMATOLOGY
Consumptive thrombocyotopenia is a common finding in
children with HIV infection and may be observed in 10% of
patients at initial diagnosis.
Anaemia occurs in as many as 80% of patients at some
time.Anaemia can have many etiologies in HIV infected
individuals and requires a workshop asdescribed in Medical
care.

Laborartory diagnosis of HIV
infection
 Standard algorithm consist of two test of the detection of
antibody HIV -1/2
 Screening
 .enzyme immunoassay[EIA]
 .enzyme linked immunosorbant assay[ELISA]
 .specialised Rapid Spot test
 Conformation
 .Western blot[WB]
 Polymerase chain reaction[PCR-RT PCR]

Western blot for HIV
There are different criteria for interpretation of HIV
Western blot result eg,CDC ,WHO,American red cross.
The most important antibodies are those against the
envolope glyocoproteins gp120 gp160 and gp41.
P24 antibody is usually present but may be absent in later
status of infection.

Laborartory diagnosis of HIV
infection[standard algorithm]
Specimen “initially reactive” by EIA/ELISA are retested in
duplicate
.one or both repeat test positive specimen are considered
repeatedly reactive for antibody
Specimen repeatedly reactive by EIA/ELISA then tested by
Western blot assay
Specimen reactive for both EIA/ELISA and WB are
considered positive for HIV infection

Quantification for viral load
The viral load can be quantified by using several HIV assays .
The number of virions in the peripheral blood is an
important indicator of diseases and of the effectiveness of
antiretro viral therapy [ART]
Assay of viral resistance
.viral resistance may be present

HIV INFECTIVITY
HIV infectivity of red blood cells components that were not
wasted before translucent decreases as storage time decreases
HIV contaminated red blood cells store for less than 8 days
are 96% infectious ,were as those stored for more than 3
weeks are 50% infectious

Chemical disinfectants for HIV
Sodium hypochloride-1gm/l concentrate is used to disinfect
infected blood bags[the bags are injected with the 30 ml of
sodium hypochloride left for 30 min] and then post
disinfecting the bags ,they were subsequently discarded by
incineration.

Transfusion transmission
 Lack of donor
 inadequte donor screening
 Lack of standard practices and
quality control
 Well trained and expert staff

Laboratory diagnosis

Testing Options for HIV

Anonymous Testing
No name is used
Unique identifying number
Results issued only to test recipient
23659874515
Anonymous

Confidential Testing
Person’s name is recorded along with HIV results
Name and positive results are reported to the State Department
and the Centers for Disease Control and Prevention
Results issued only to test recipient

Administration
Blood
Urine
Oral

Blood Detection Tests
Enzyme-Linked ImmunosorbentAssay/Enzyme
Immunoassay (ELISA/EIA)
Radio ImmunoprecipitationAssay/Indirect Fluorescent
AntibodyAssay (RIP/IFA)
Polymerase Chain Reaction (PCR)
Western Blot Confirmatory test

Urine Testing
Urine Western Blot
As sensitive as testing blood
Safe way to screen for HIV
Can cause false positives in certain people
at high risk for HIV

Oral Testing
Orasure
The only FDA approved HIV
antibody.
As accurate as blood testing
Draws blood-derived fluids from
the gum tissue.
NOT A SALIVA TEST!

Haematology
Pancyotopenia results from foliate deficeincy ,use of
pharamaceutical agents and infection with viruses such as
parvovirus b19
Neutropenia is observed in 10% pateints with early
asymptomatic infections and 50% of patients with AIDS
Blood smear may reveal large ovalocytes and
hypersegmented polymorpho nucleocytesin cases of foliate
deficeincy

Haematology
Cd4 plus lymphocyte count is a surrogate marker for disease
progerssion and should be monitored closely
The cd4 count should be obtained before therapy
Rapid disease in the count specvially in infants younger than
1 year is a poor prognostic sign and should start an alteration
of therapy

Once a patient likely said [“sometime I have this terrible
feeling that I am not dying from virus but from being
untouchable”]
HIV does not make patient dangerous to know so you can
shake their hands and give them a hug:heaven knows they
need it

EC- Clearing house classification of the oral
manifestations of HIV diseases in Adults
GROUP-1STONGLY ASSOCIATED WITH HIV INFECTION.
 Candidiasis;erythematous,ppseudomembraneous,angular
cheilitis.
 Hairy leukoplakia
 Kaposi’s sarcoma[KS]
 Non hodgkin’s lymphoma
 Periodontal diseases;linear gingival erythema,necrotizing
periodontitis

GROUP-2;LESS COMMONLY ASSOCIATED WITH HIV
INFECTION.
Bacterial infections;mycobacterium avium-intracellulare,
mycobacterium tuberculosis
Melanotic hyperpigmentation
Necrotizing ulcerative stomatitis
Salivary gland disease;dry mouth,unilateral or bilateral swelling
of major salivary glands
Thrombocytopenia purpura
Oral ulcerations(not otherwise specified)
Viral infections;herpes simplex,human papillomavirus,varicella-
zoster

GROUP-3; SEEN IN HIV INFECTIONS
 Bacterial infections;actinomyces israelil,Escherichia coli,Klebsiella
pneumonia
 Cat-scratch disease(Bartonella henselae)
 Epithelioid (bacillary)angiomatosis(Bartonella henselae)
 Drug reactions;ulcerative,erythema multiforme,lichenoid,toxic
epidermolysis
 Fungal infections other than candidiasis;cryptococcus
neoformans,Geotrichum candidum,Histoplasma
capsulatum,Mucoraceae(mucormycosis/zygomycosis),Aspergillus
flavus
 Neurologic disturbances;facial palsy, trigeminal neuralgia
 Recurrent apthous stomatitis
 viral infections;cytomegalovirus,molluscum contagiosum.

AIDS RELATED COMPLEX
It is a term used to describe patient with a HIV infection who have
only mild symptoms of illness such as swollen lymph glands.It was
introduced after discovery of the HIV,when the medical
community became aware of inherent difficulties in treating
patients suffering from advanced case of HIV which give rise to
term AIDS.In need to provide the patients emergency room
suferring from AIDS ,the word ARC was introduced.
Laboratory criteria to separate AIDS from ARC is a elevated or
hyperactive B-cell humoral immune responses compared to
depressed antibody activity in AIDS.And follicular or mixed
hyperplasia in ARC lymph glands leading to lymphocyte
degeneration leading to typical AIDS evolving succession of
histopathological lesions such as Kaposis sarcoma.

SIGN AND SYMPTOMS OF ARC
Swollen lymph glands
Enlarged lymph nodes
Fatique
Night sweats
Weight loss
Diarrhoea
Fever
An ARC requires any two or more symptoms and two or
more abnormal findings.It must be present for at least 3
months

LAB FINDINGS
Decreased number of T helper cells.
Decreased ratio of T helper cells to T suppresor cells.
Anemia or leukopenia or thrombocytopenia.
Increased serum globulin level.
Anergy is impaired or inability to react to skin antigens.

PART III
CONTENTS
ORAL MANIFESTATIONS
TREATMENT
COUNSELING

ORAL MANIFESTATIONS
And Oral and perioral lesions are common in HV infections and most oral
lesions accur in as early signs.
Scully C etal 1991 have documented oral disorders in HIV disease which were common or less common
in HIV patients.
More common Less common
A.INFECTIONS
FUNGAL 1.Candidiasis 1.Aspergillosis
2.Histoplasmosis
3.Cryptocoocus neoformans
4.Geotrichosis
BACTERIAL 1.HIV Gingivitis 1.Klebsiella
2.HIV periodontitis pneumonia
3.Necrotising gingivitis 2.Mycobacterium
4.Escheria coli avium
5.Salmonella enteritidis
6.Sinusitis
7.Exacerbation of apical infection
8.Submandibular cellulitis

More common Less common
VIRAL 1.HSV 1.HPV
2.VZV 2.CMV
3.EBV(Iincluding
hairy leukoplakia)
B.NEOPLASMS
1.Kaposis sarcoma 1.Non-hodgkins
lymphoma
2.squamous
cell ca.
C.NEUROLOGICAL DISTURBANCES
1.Paraesthesis
2.facial palsy
3.Hyperesthesia
4.Dysphagia
5.trigeminal neuralgia

D.MISCELLANEOUS
A. Recurrent apthous ulcer
B.Progressive necrotizing ulceration
C.toxic epidermolysis
D.Delayed wound healing
E.Thrombocytopenia
F.Xerostomia and sicca type syndrome
G.HIV embryopathy
H.Hyperpigmentation
I.Exfoliative chelitis
J.Lichenoid and other drug reactions

ORAL MANIFESTATIONS
CANDIDIASIS; commonly associated with candida albicans.It occurs
during the acute stage of HIV infection.bur it occurs most commonly
with the falling CD4+T cell count in middle and late stages of HIV
diseases.
Clinical features:site-hard palate and soft palate
Clinical appearances of oral candidiasis vary, most common include the
pseudomembraneous and erythematous candidasis ,which are
predicative of development of AIDS and angular cheilitis.
Symptoms:burning mouth problems in eating spicy, and changes in
taste.
Diagnosis:by clinical features,by detection of organsims by smears.

Oral candidiasis is often the first manifestations of HIV
disease.four forms of oral candidiasis have been identified:
1.Pseudomembranous candidiasis
Erythematous candidiasis (atropic)
Angular cheilitis
Hyperplastic candidiasis
Pseudomembranous candidiasis(Thrush)
Clinical features:Most common form of candidiasis in HIV
infected persons.
Lesions are characterised by yellow white,curd like loosely
adherent (wipable plaques),located anywhere in mouth.
Patient complains of taste disturbances and burning mouth.
According CDC it is associated with the increased risk for
subsequent development of opportunistic infections.www.indiandentalacademy.com

Erythematous candidiasis:
Clinical features:
Erythematous (atropic)macular patches on mucosal surfaces.
Dorsam of tongue shows depapillation and palatal mucosa is
affected.
Burning sensation and altered taste sensation.
Non specific clinical appearance so often get overlooked.
Angular cheilitis:
Characterised by fissures or linear ulcers at corner of mouth
unilaterally or bilaterally.
May be seen in association with oral candidiasis.
Hyperkeratosis often seen peripheral to fissures.
Restricted mouth opening and painful.

Hyperplastic candidiasis :
Also known as candidial leukoplakia,least common form of candidial
infections in HIV infected persons.
Characterised by white mucosal patches firmly adherent to the
underlying mucosa.
Hyperkeratosis is predominant feature responsible for white colour
patches.
It is more resistant to antifungal therapy.
Treatment:
 topical treatment:Nystatin (mycostatin)vaginl tablets 100,000U/tab
Nystatin oral suspension(100 000U/ml)used as mouth rinse with 1-5
ml suspension held in mouth for 5 min/4 times a day.
Systemic treatment:
Ketoconazole(Nizoral)200mg1 tab daily for 2 weekswww.indiandentalacademy.com

Fluconazole(diflucan)100mg per day for 2 weeks
Itraconazole(sporonax)200mg tabs daily with food
Drug interactions are commonly seen.Consult HIV specilalist.
For treatment of Angular cheilitis combination creams consisting
antifungal,antibacterial,with an anti inflammatory,anti pruritic
agents is used.for eg,Nystatin and triamcinalone acetonide topical
cream apply 3 times a day to be affected after food.
Clotrimazole cream:1% apply to the affected area 4 times after
food.
Once the acute phase of oral candidiasis has been bought under
control secondary prophylaxis may be considered.

Candidiasis on tongue
Extensive removable white plaques of
the left buccal mucosa
Recurrent herpes labialis

KAPOSIS SARCOMA: is also called as
angioreticuloendothelioma.Most common tumour associated with
AIDS. Higher incidence seen in homosexuals men with AIDS as
compared to hetrosexuals.
Kaposis sarcoma appear in various forms like.
Classic
African(cutaneous variant)
African lymphadenopathy variant)
Kaposis sarcoma associated with AIDS.
Classic type is a rare neoplasm and occurs in older man.appears as blue-black
macule in lower

extremities.whereas african Kaposis sarcoma and is an endemic disease and affects the
children of 10 years or younger patients.It appears as exophytic growth located in
legs and arms. Lymph node involvement is rare.Kaposis sarcoma is observed in
patients with kidney transplantation and those taking immunosupperssive drugs for
variety of diseases.
CLINICAL FEATURES:SITE:commonly seen in head and neck region.Tip of
nose is peculiar,it can involve lymph nodes,soft
tissues,extremities,GIT,lung liver,pancreas,spleen,and adrenal gland.
AGE:it occurs in children commonly in women.
APPEARANCE:it begins as multinucleated neoplastic process that manifests
as mutiple red or purple macules and in advanced stage a nodule occuring
on the skin or mucosal surface.

SIZE:size of it ranges from a few mm to cm or more in a diameter and
usually tender on palpation.
ORAL MANIFESTATIONS site:commonly on hard palate,lesion occurs
at any part of oral mucosa involving gingiva,soft palate,buccal
mucosa,and in the oropharnyx.
APPEARANCE:can appear as red;blue or purplish lesion.It may be flat
or raised solitary or multiple.Yellowish mucosa surrounds the lesion.,it
may get ulcerate and become infected.
T/T: includes surgical excision.
Radiation therapy indicated for large for and multiple lesions.
Intralesional injections of vincristine or vinblastin 0.02 mg/ml
Or sodium tetradecyl as a sclerosing agent are useful small lesions.
Before initiating treatment KS of gingiva a thorough oral prophylaxis.
Remissions are common.

Kaposis sarcoma:Multiple
macules seen on hands
HIV associated Kaposis sarcoma
Raised dark-red enlargement of
maxillary anterior facial gingiva .

PERSISTENT GENERALISED
LYMPHADENOPATHY
After seroversion,HIV disease often remains silent expect PGL.The
PGL consists of lypmhadenoapthy that has been present for longer
than 3 months and invlove two or more extra inguinal sites.the most
frequently involved sites are posterior, and anterior and cervical and
submandibular,occpital and axillary nodes.enlarement fluctuates
usually larger than 1cm and varies from 0.5 to 5.0cm.PGL does warn
of progression to AIDS.;almost one third of affected and untreated
patients will have diagnostic feature of AIDS within 5 years.

HIV associated
lymphoma:erythematous and
ulcerated soft tissue enlargement of
posterior maxillary

NON-HODGKINS LYMPHOMA:2nd
most common in malignancy
in HIV infected patients.This neoplasms occurs in approx 3% to 5% of
those with virus.NHL in patients with AIDS presents as high grade and
aggressive disease that frequently asssociated with widespread
involvement and short survival times.The majority NHLs are B-cell
lymphomas and include AIDS Burkitts lymphoma,anaplastic large cell
lypmphoma,immunoplasmacytoid lymphoma,primary effusion
,plasmablastic lymphoma.Neoplasms are associated with relationship
with EBV., Oral lesion are seen in approx 4% of patients with AIDS
related NHL and involve gingiva,palate,tongue,tonsil,or maxillary s

Sinus.Intraosseous involvement also has been documented and may
resemble diffuse progressive periodontitis with loss of periodontal
attachment and loosening of teeth ,where widening of periodontal
ligament and loss of lamina dura are noted.
LESS COMMONLY ASSOCIATED HIV INFECTIONS
MYCOBACTERIAL INFECTION:Best known is Mycobacterium
tuberculosis,while other include
M.avium,M.intercellulare,M.bovis,M.scrofulaceum,.Oral lesions are
uncommon and occur in less than 5% of individual wiith active
TB.Tongue is most commonly affected,but lesion can also be seen on
buccal mucosa,gingiva,floor of mouth,lips and palate.Affected areas
present as chronic ulcerations,granular leukoplakias or exophytic mass.

Hyperpigmentation of the skin,nails,and mucosa has been
reported in HIV infected pateints.Medications taken by the infected
patients{eg,ketoconazole,clofazimine,pyrimethamine,zidovudine}ma
y cause the increase in the melanin pigmentation.Adrenocortical
destruction has been reported,in AIDS resulting in the addisonian
pattern of pigmentation.
HERPES SIMPLEX VIRUS
Recurrent HSV infections occur in same percentage of HIV infected
patients as they do in it immunocometent population, but lesion are
more widespread,occur in atypical pattern and may persist for several
months.The prevalance of HSV lesions increases significantly once the
CD4 count drops below 50cells/mm3.It causes both primary(primary
herpetic gingivostomatitis)and recurrent or secondary
infection(herpes labialis)

Primary Herpetic Gingivostomatitis):
Oral involvement is uncommon in HIV infected patients.
C/f include; Diffuse gingival swelling and pain.
Multiple vesicles and erosions on attached gingiva and palatal
mucosa.
Fever, malaise,cerviacl lymphadenopathy and halitosis.
Primary herpetic pharyngitis is often present with diffuse erythema
of tongue, soft palate and posterior pharynx.
Recurrent Herpetic Infection:
Commonly involves the vermillion border of lips .In HIV intra oral
involvement of herpes and skin infection is commonly seen.
Intraoral lesion present as localised crop of vesicles on keratinizing
mucosa.
In HIV infected patients ulcers/erosions tends to persist if do notwww.indiandentalacademy.com

Resolve they fulfill the CDC criteria for AIDS.
TREATMENT:Acyclovir:200mg 1-2 cap 5 times a day for 10 days
Valaciclovir:500mg:per oral twice daily
Acyclovir:resistant herpes ulcerations sholud be consideredwhen
ulcers with confirm diagnosis of HSV infection do not respond to
acyclovir.
T/T with Foscarnet (40 mg/kg i.v every4 hrs fot 3 weeks)

VARICELLA –ZOSTER VIRUS
Recurrenr varicella zoster infection is fairly common in HIV infected
patients,but the course is more severe.Many of the patients are younger
than age 40,in contrast in contrast to cases in immunocompetent patients
that arise later in life.In early stage HIV related immunocompression
herpes zoster is confined to dermatome but persists longer than
usual..while in ful blown AIDS,herpes zoster usually begins in a classic
dermatomal distribution.
When the facial skin is involved the pateint experiences
itching,redness,veesicle formation and eventually ulceration and crusting
of ulcers with hyperpigmentation.
Lesions are unilateral in distribution following maxillary or mandibular
branches of trigeminal branches.
Prodormal symptoms with itching,burning,and tenderness are seen.
Intra oral lesions are painful they coalesce to form large ulcers.
Copmlication include of Post Herpetic neuralgia and systemic viral
dissemination.

Treatment:
Acyclovir 800mg five times daily for 10 days is recommended.
Foscarnet IV for refractory cases.
Symtomatic treatment for pain is needed.

Human papilloma virus showing warts
Treatment include Acyclovir 800mg five times daily is recommended.
HUMAN PAPILLOMA VIRUS INFECTIONS

Intraorally,involvement is severe and occasionally,leads to bone
sequestration and loss of teeth.In many instances tooth exfoliation may
be delayed a month or more after intial onet of Herpes zoster.
HUMAN PAPILLOMA VIRSUS
It is responsible for several facial and oral lesions in immunocompetent
patients,the the most frequent of which is verruca vulgaris(common
wart) and oral sqummous papilloma.An increased prevalance of HPV
related lesion is noted in HIV infections patients mostly seen in
anogenital areas.Although usual types of HPV may be present in intaoral
lesions.HIV infected patients often demonstrate more unusal variants
such as HPV-7(with butcher warts)or HPV-32(in multifocal epithelial
hyperplasia).
In HIV infected people,three types of HPV lesions are known to occur
in oral cavity.They are:
1.Oral warts.
2.Condyloma Acuminatum.
3.Focal Epithelial Hyperplasia.

ORAL WARTS:
Usaually small 1-3mm in diameter asymptomatic,nodular
,warty,cauliflower,like appearance.
May be solitary or multiple.
Affect non-keratinized mucosa
CONDYLOMA ACUMINATUM:
Generally a single lesion.
Nodular in appearance and often seen on floor of mouth,labial
mucosa and gingiva.
In HIV infected patients common seen in ano-genital lesions.
TREATMENT:include surgical removal followed by cauterization to
avoid recurrences,carbon dioxide laser surgery,topical application of
podophyllin resin and intra lesional injection of interferon.

ORAL HAIRY LEUKOPLAKIA
Vertical streaks of keratin along the lateral
border of tongue.

HAIRY LEUKOPLAKIA:presents as nonremovable,nonscrable
corrugated on “hairy”white lesion on lateral margins of tongue.
CLINICALLY occurs unilaterlly or bilaterally on the lateral border of the
tongue,also on the dorsum of the tongue,buccal mucosa,floor of
mouth,retromolar area,and soft palate
SURFACE appears to be corrugated,irregular,with prominent folds,or
projections resembling the hair
Clinical features are sufficient for presumptive diagnosis, for definitive
diagnosis demonstration of EBV within lesion is required can be
achievevd by in situ hybridisation,PCR,immunochemistry,sother
blotting, or electron microscopy.
T/T:As it is aymmptomatic clovin nature does not require any treatment,
but it responds to Acylovir.
Podophyllin and interferon are also used.
Recurrences are very common.

Sometimes white lesion satisfies the diagnosis of hairy leukolplakia,but
if EBV not present this is called as “pseudohairy”leukoplakia.
Also three atypical patterns of periodontal disease are associated
strongly with HIV .
1.Linear gingival erythema
2.Necrotizing ulcerative gingivitis
3.Nerotizing ulcerative periodontitis.

HIV associated necrotizing
ulcerative gingivitis.Multiple
punched out interdental papillae
of the mandibular gingiva.
HIV associated gingivitis:band of
erythema involving free gingival
margins

Necrotizing ulcerative
stomatitis wth atrophy and
necrosis of gingiva,The
interdental papilla is highly
hyperplastic and erythematous
lesion.
Necrotizing ulcerative
peridontitis with extensive
loss of periodontal support
without deeping of pockets.

OTHER MISCELLANEOS ORAL LESIONS.
1.Apthous Ulcers.
2.Xerostomia.
3.Linear Gingival Erythema.
4.Idiopathic Thrombocytopenia.
5.Lichenoid Reaction,Drug induced ulcers,and Pigmentation.
6.Oral and Facial Pain
7.Dental Caries.
8.Other dental infections.

LIKELY INCREASE RISK OF HIV TRANSMISSION
IN OCCUPATIONAL EXPOSURES.
PERCUTANEOUS INJURY
(eg.needlestick or broken skin)
MUCOCUTANEOUS INJURY
(eg.splash to eye or mouth)
1.Deep injury 1.Large volume of fluid.
2.Visibly bloody needle/device 2.Prolonged contact with fluid.
3.Source patient with end stage HIV.
4.High serum viral load in source patient
5.Healthcare worker not wearing gloves.
3.Source patient with end stage HIV.
4.High serum viral load in source patient.

Post exposure prophylaxis following an occupational exposure to
HIV: refers to the use of antiretroviral agents (ARVs)to reduce the
risk of transmission following a potentially infectious exposure.
Four week course of zidovudine(AZT) following an occupational
needlestick exposure to an HIV infected source reduce the risk of
HIV transmission by approx 80%.
Experimentally seen that percutaneous or mucosal exposure to
HIV,local replication of virus occur in tissue macrophages or
dentritic cells .And cytotoxic T-cells will soon start killing infected
target cells.If infection cannot contained at this stage,it is followed
within 2 to 3 days by replication of HIV in regional lymph nodes.
It is important to commence PEP within hours of percutaneous
injury.,inititation of PEP within 36 hours after a significanr exposure
may be considered with consultation with HIV clinician.

PEP REGIMEN
Basic regimens consist of two nucleoside reverse transcriptase
inhibitors(NRTIs) typically zidovudine plus lamivudine(3TC,
Epivir)
Expanded regimen consists of a basic regimen plus one or more
additional ARVs such as nelfinavir (NFV)or efavirenz(EFV).

TREATMENT AND PROGNOSIS
 Best defence against the disease is only the prevention to deisease.Antiretroviral therapy is effective but
is expensive and also associated with adverse reactions. Work is still preceeding toward the development
of safe and efective vaccine.
 ANTIRETROVIRAL THERAPY
1.Nucleoside reverse-transcriptase inhibitors
• Abacavir,didanosine,emtricitabine,lamivudine,stavudine,tenofovir,zalcitabine or
zidovudine
2.Nucleotide reverse transcriptase inhibitors
• Adefovir or tenofovir
3.Nonnucleoside reverse-transcriptase inhibitors
• Capravine,delaviridine,efavirenz,emivirine,or nevirapine
4.Protease inhibitors
• Amprenavir,,atazanavir,darunavir,fosamprenavir,indinavir, iopinavir/ritonavir,
5.Fusion inhibitors
• Enfuvirtide
6.Integrase inhibitors
• MK-0518(experimental)
7.CCR5 inhibitors
• Maraviroc (experimental),vicrivoc(experimental)

Drug CategoryDrug Category Mechanism of ActionMechanism of Action ExamplesExamples
Fusion InhibitorsFusion Inhibitors Blocks HIV entry into cellsBlocks HIV entry into cells Enfuvirtide (Fuzeon,Enfuvirtide (Fuzeon,
T-20)T-20)
Nucleoside analogNucleoside analog
reverse transcriptasereverse transcriptase
inhibitors (NARTI) orinhibitors (NARTI) or
nucleoside analogsnucleoside analogs
Inhibits HIV reverseInhibits HIV reverse
transcriptase, inhibits HIVtranscriptase, inhibits HIV
DNA synthesisDNA synthesis
abacavir (Ziagen, ABC)abacavir (Ziagen, ABC)
zidovudine (Retrovir, ZDV, AZT)zidovudine (Retrovir, ZDV, AZT)
didanosine (Videx, ddl)didanosine (Videx, ddl)
stavudine (Zerit, d4T)stavudine (Zerit, d4T)
lamivudine (Epivir, 3TC)lamivudine (Epivir, 3TC)
zalcitabine (HIVID, ddc)zalcitabine (HIVID, ddc)
tenofovir ( Viread, PMPA)tenofovir ( Viread, PMPA)
Protease inhibitorsProtease inhibitors
(PI)(PI)
Prevents cleavage andPrevents cleavage and
maturation of the HIVmaturation of the HIV
polypeptidespolypeptides
amprenavir ( Agenerase, AMP)amprenavir ( Agenerase, AMP)
indinavir (Crixivan, IDV)indinavir (Crixivan, IDV)
nelfinavir (Viracept, NFV)nelfinavir (Viracept, NFV)
ritonavir (Norvir, RTV)ritonavir (Norvir, RTV)
saquinavir (Invirase, Fortovase)saquinavir (Invirase, Fortovase)
lopinavir/ritonavir (Kaletra)lopinavir/ritonavir (Kaletra)
NonnucleosideNonnucleoside
inhibitors (NNRTIs)inhibitors (NNRTIs)
Binds directly with HIVBinds directly with HIV
efavirenz (Sustiva, EFV)efavirenz (Sustiva, EFV)
delavirdine (Rescriptor, DLV)delavirdine (Rescriptor, DLV)
nevirapine (Viramune, NVP)nevirapine (Viramune, NVP)

Antiviral Drug Therapy
Nucleoside/
Nucleotide
Analogues
Nonnucleosid
e Reverse
Transcriptase
Inhibitors
Protease
Inhibitors
Fusion
Inhibitors
Abacavir
Didanosine
Emtricitabine
Lamivudine
Stavudine
Tenofovir
Zalcitabine
Zidovudine
Delavirdine
Efavirenz
Nevirapine
Amprenavir
Atazanavir
Fosamprenavir
Indinavir
Lopinavir/Ritonavir
Nelfinavir
Ritonavir
Saquinavir
Enfuvirtide

Other medications
• Combivir (zidovudine/AZT,lamivudine)
• Trizivir (Ziagen/Retrovir/Epivir)
• Pharmacologic Treatment of Common Opportunistic
Infections and Malignancies in HIV Disease (Refer to Table
9-4, page 261 Lemone & Burke© 2004)

How HIV Drugs Work

Adverse Drug Effects
Mitochondrial
dysfunction
Metabolic
abnormalities
Hematologic
complications
Allergic
reactions
Lactic acidosis
Hepatic toxicity
Pancreatitis
Peripheral neuropathy
Lipodystrophy
Fat accumulation
Lipoatrophy
Hyperlipidemia/
? Premature CAD
Hyperglycemia
Insulin resistance/DM
Bone disorders:
oesteoporosis and
osteopenia
Bone marrow
suppression
Hypersensitivity
reactions
Skin rashes

Medication Side Effects
 Anorexia
 Sore/dry/painful mouth
 Swallowing difficulties
 Constipation/Diarrhea
 Nausea/Vomiting/Altered Taste
 Depression/Tiredness/Lethargy

Counseling

Pre-test Counseling
Transmission
Prevention
Risk Factors
Voluntary & Confidential
Reportability of Positive Test Results

Post-test Counseling
Clarifies test results
Need for additional testing
Promotion of safe behavior
Release of results

Opportunistic Infection
Treatment
Issued in an event where antiretroviral drugs are not
available

Four ways to protect yourself?
Abstinence
Monogamous Relationship
Protected Sex
Sterile needles

Abstinence
It is the only 100 % effective method of not acquiring
HIV/AIDS.
Refraining from sexual contact: oral, anal, or vaginal.
Refraining from intravenous drug use

Monogamous relationship
A mutually monogamous (only one sex partner)
relationship with a person who is not infected with HIV
HIV testing before intercourse is necessary to prove
your partner is not infected

Sterile Needles
If a needle/syringe is shared, it must be disinfected:
Fill the syringe with undiluted bleach and wait at least 30 seconds.
thoroughly rinse with water
Do this between each person’s use
Protected Sex
Use condoms as a protective measure,to prevent AIDS.

Needle Exchange Program
Non-profit
Organization, which
provides sterile needles
in exchange for
contaminated ones

Thank You!

HIV and AIDS /prosthodontic courses

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