The document provides an overview of HIV/AIDS, including its history, virology, transmission, stages of infection, oral manifestations, and diagnosis. It traces the origins of HIV from chimpanzees in central Africa in the early 20th century. It describes how HIV attacks and destroys CD4 cells, progressively weakening the immune system over many years until the body is vulnerable to opportunistic infections and cancers associated with AIDS. Common oral signs of HIV infection include oral candidiasis, hairy leukoplakia, and Kaposi's sarcoma.

1. 1

2. 2

3. 3

4.  Introduction
 History
 Definition
 Virology
 Sign & Symptoms
 Mode of transmission Mode of transmission
 Clinical stages
 Oral manifestation
 Diagnosis
 Treatment
 Myths
 Prevention
 Conclusion
 References
4

5.  A – Acquired – not inherited
 I - Immune - attacks the immune system I - Immune - attacks the immune system
 D – Deficiency – lack of
 S – Syndrome – a group of symptoms or illnesses that
occur as a result of HIV infection
5

6. H – Human – isolated from the human species
I – Immunodeficiency-lacking the ability to fight diseasesI – Immunodeficiency-lacking the ability to fight diseases
V –Virus – disease causing agent
6

7.  For many people, living with AIDS or HIV
also means living with considerable
uncertainty.
 The complexity of HIV infection means The complexity of HIV infection means
that you cannot be sure whether or when
you may become ill or indeed with what.
 The long but unpredictable length of time
between initial infection and first illness
poses many and yet unanswered questions
about HIV.
7

8.  It is caused by human immunodeficiency
virus (hiv) & is characterized by
immunosuppressive, which leads to spectrum
of clinical manifestations that includeof clinical manifestations that include
opportunistic infections , secondary
neoplasm & neurologic manifestation.
8

9. 9

10.  The story begins sometime close to 1921, somewhere
between the Cameroon and the Congo River in the former
Belgian Congo.
 It involves chimps and monkeys, hunters and butchers, “free It involves chimps and monkeys, hunters and butchers, “free
women” and prostitutes, syringes and plasma-sellers, evil
colonial lawmakers and decent colonial doctors with the best
of intentions.
 And a virus that, against all odds, appears to have made it
from one ape in the central African jungle to one Haitian
bureaucrat leaving Zaire for home and then to a few dozen
men in California gay bars before it was even noticed —
about 60 years after its journey began.
10

11.  Working slowly forward from 1900, Dr. Pepin explains how
Belgian and French colonial policies led to an incredibly
unlikely event: a fragile virus infecting a small minority of
chimpanzees slipped into the blood of a handful of hunters,
one of whom must have sent it down a chain of “amplifiers”one of whom must have sent it down a chain of “amplifiers”
— disease eradication campaigns, red-light districts, a Haitian
plasma center and gay sex tourism.
Without those amplifiers, the virus would not be what it now
is: a grim pilgrim atop a mountain of 62 million victims, living
and dead.
11

12.  HIV/AIDS –THE EARLY DAYS…………
HOWTHE NIGHTMARE BEGAN?
“In June of 1981 we saw a young gay man with the most
devastating immune deficiency we had ever seen. We said,
“we don’t know what this is, but we hope we don’t ever
see another case like it again”.
- Dr. Samuel Broder, USA
12

13.  GRID – Gay Related Immune Deficiency
 Gay compromise syndrome – Lancet
 Gay cancer
 Community acquired immune dysfunction
 Hella’s disease
13

14. How, when and where did the virus first
come from ?
 What type of virus is HIV?
 Did HIV come from an Simian Immune Deficiency
Virus?
14

15.  1.The hunter theory
15

16. 2.The oral polio vaccine theory
3.The contaminated needle theory
4.The colonialism theory
5.The conspiracy theory
16

17. When did the virus first appear in humans?
 1959 – Plasma sample from an adult male of
Democratic Republic of Congo.
 1969 –Tissue sample of an American teenager who
died in St. Louis.
 1976 –Tissue sample from a Norwegians sailor.
17

18.  When did the HIV-2 virus get passed to humans?
 Where exactly did the epidemic first develop?
18

19.  According toWHO :
One or more opportunistic infections listed inOne or more opportunistic infections listed in
clinical features that are at least moderately
indicative of underlining cellular immune deficiency.
19

20.  Human immunodeficiency virus
 Class - Retroviruses
 Family – Lentivirinae ( lenti= slow acting) Family – Lentivirinae ( lenti= slow acting)
Types of HIV:
 Based on geographical distribution, biological &
molecular
 Characteristics & extent of transmissibility:
HIV 1
HIV 2
20

21.  Types of HIV 1:
Based on DNA sequencing:
Group M (major, world wide distribution) Group M (major, world wide distribution)
 Group O (outlier, restricted toWest Africa)
 Group N ( rare, highly divergent)
HIV 2:
 Restricted toWest Africa.
21

22.  The virus causing AIDS was independently
identified by a team of French scientists led by
Dr. Luc Montagnier at French Pasteur Institute in Paris
and American scientists lead by Dr. Robert C. Gallo of
National Cancer Institute in 1983.National Cancer Institute in 1983.
 Lymphadenopathy AssociatedVirus – French
 HumanT Lymphocytotropic Virus III – Americans
 In 1986 theWHO International Committee on
Nomenclature ofViruses named the virus as Human
ImmunodeficiencyVirus.
22

23. 23

24.  Immune System
 Central Nervous System
24

25.  Immunology: cells and tissues involved in
recognizing and attacking foreign substances
in the body e.g. bacteria, viruses, fungi and
parasites.
 Immunity: the condition of being immune.
Immunity can be innate or the result of a
previous exposure.
 Antigen: any substance capable of triggering
an immune response.
25

26.  Of the white blood cell pool, lymphocytes
primarily drive the immune system.
 Lymphocytes (2 major types which protect
host):
 Lymphocytes (2 major types which protect
host):
• formed in bone marrow and
produce antibodies after
exposure to an antigen.
(1) B cells
• processed in the thymus
(two subtypes)(2) T cells:
26

27. Subtype 1: Regulator cells also known as
helper or CD4 cells (“generals” in army of
immune system which recognize “invaders”
and summon armies of cells to mount a direct
attack)attack)
Subtype 2: Fighter or effector cells also
known as cytotoxic or CD8 cells (bind
directly to antigen and kill it)
27

28.  2 types of CD4 cells:
(1) Memory cells: those programmed to
recognize a specific antigen after it has been
previously seen.previously seen.
(2) Naïve cells: non-specific responders.
 CD4 cells replicate 100 million times a day.
CD4 CELLS ARETHE TARGET CELLS OF HIV.
28

29. 29

30.  Short, flu-like illness - occurs one to six weeks after
infection.
 No symptoms at all.
Infected person can infect other people. Infected person can infect other people.
30

31.  Lasts for an average of ten years .
 This stage is free from symptoms.
 There may be swollen glands.
 The level of HIV in the blood drops to very low
levels.
 HIV antibodies are detectable in the blood.
31

32.  The symptoms are mild.
 The immune system deteriorates .
 Emergence of opportunistic infections and cancers.
32
6 month ~ Years ~ Years ~ Years ~ Years
Virus
Antibody

33.  The immune system weakens.
 The illnesses become more severe leading to The illnesses become more severe leading to
an AIDS diagnosis.
33

34.  This is the period of time after becoming infected
when an HIV test is negative.
 90 % of cases test positive within three months of
exposure.exposure.
 10 % of cases test positive within three to six
months of exposure.
34

35. HIVVirus T - Cell HIV Infected
T-Cell
New HIV Virus
PATHOPHYSIOLOGYOF HIVVIRUS
35

36. 1. Adsorption
2. Penetration
3. Uncoating
4. Biosynthesis4. Biosynthesis
36

37. 37

38.  Stage I: HIV infection is asymptomatic and not
categorized as AIDS.
 Stage II: Includes minor mucocutaneous
manifestations and recurrent upper respiratory tract
infections.infections.
 Stage III: Includes unexplained chronic diarrhea for
longer than a month, severe bacterial infections and
pulmonary tuberculosis.
 Stage IV: Includes toxoplasmosis of the brain,
candidiasis of the esophagus, trachea, bronchi or
lungs and Kaposi's sarcoma; these diseases are
indicators of AIDS.
38

39.  The Centers for Disease Control (CDC) has a disease
classification system based on immune function and
clinical status.
 Each patient is classified with a number which is Each patient is classified with a number which is
reflective of CD4 count, and a letter reflective of
clinical status.
 This provides prognostic information for providers
where a patient fits along the continuum of illness
and as to what conditions, if any, he or she may be
at risk.
39

40. 40

41.  For clinical & research studies, persons
exhibiting complex clinical problems &
immunological or hematological
abnormalities on the lab test, have beenabnormalities on the lab test, have been
classified as havingAIDS related complex .
 These are the following symptoms seen
41

42.  Minor signs:
 Repeated common infections (pneumonitis,
otitis,pharyngitis )
 Gen. Lymphadenopathy
Oropharyngeal candidiasis
 Gen. Lymphadenopathy
 Oropharyngeal candidiasis
 Persistent cough for > 1 month
 Disseminated maculo-papular rashes
42

43.  Chronic diarrhea for
> 1 month
Major signs:
 Loss of body
weight orweight or
failure to
thrive
43

44.  Prolonged fever for > 1 month
44

45. Lab findings :
 Decreased no. of T helper cell.
 Decreased ratio ofT helper cells toT
suppressor cells.
45
suppressor cells.
 Anemia or leukopenia or thrombocytopenia
or lymphopenia.
 Increased serum globulin level.

46.  Primary HIV Infection
 Mononucleosis - like illness in about 50% of patients
▪ Symptoms - fever, fatigue, lymph nodes swelling, rash, or
meningitismeningitis
▪ ELISA for HIV antibodies may be briefly (2-6 weeks)
negative, but high levels of viremia (> 10 6 copies / ml)
 Higher levels of viremia predict:
▪ severe symptoms during primary infection
▪ rapid progression to AIDS
▪ high infectivity for sexual partners
46

47.  Early immune defficiency
 Not always asymptomatic - patients may be
vigorously healthy or have mild fatigue orvigorously healthy or have mild fatigue or
low grade fevers (eg, occasional night
sweats), but no illnesses indicating
immunosuppression
 CD4 counts may range from normal (>500)
to very low (<50)
47

48.  Intermediate immune deficiency
- viral replication is very high
- CD4 cell turnover is rapid
- subtle signs and symptoms indicating
compromise of immune system begin to
- subtle signs and symptoms indicating
compromise of immune system begin to
appear
- enlarged lymph node at least 1cm in two or
more non contiguous extra inguinal sites,
that persists for at least 3 months.
- CD4 cell count 200 – 500/cu mm
48

49.  Advance immune defficiency
 Virus which proliferates throughout the
body overcomes the immune system.
Minor opportunistic infections develop Minor opportunistic infections develop
like oral candidiasis, herpes zoster.
 Generalised lymphadenopathy and
splenomegaly
 pts progress to AIDS in few months
 CD4 cell count < 200/cu mm
49

50.  In the end stage, disease represents the
irreversible break down of immune defense
mechanism.
prey Patient becomes preyto progressive
opportunistic infections and malignancies.
50

51.  “Fortunately for the human race, HIV does not
spread through water, food or air. If it did, our
species might be threatened with extinction”.
 1. Blood and blood derived products (>90%)
51

52.  Sexual intercourse (>70%)
 Vertical transmission (15% - 40%)
52

53.  Injection drug use transmission ( 0.5% - 1%)
 Transmission of HIV to health care workers
 Percutaneous exposure – 0.3%
 Exposure of mucous membrane in the eye, nose
or mouth – 0.1%
53

54.  Percutaneous injuries to dentists are caused
by
 Burs-(37%), syringe needles (30%), sharp
instruments (21%),instruments (21%),
 orthodontic wires (6%), suture needles (3%),
scalpel
 blades (1%), and other objects (2%). In recent
years,
 however, needlestick injuries have dropped
dramatically.
54

55. 55

56. 56

57.  Approximately 70 to 80 percent of people with
HIV/AIDS will experience an oral manifestation.
 Treating routine problems as soon as possible Treating routine problems as soon as possible
can prevent more serious infections.
 Almost all of the infections we see, appear in
people who are not infected with HIV/AIDS, but
they appear more frequently and with more
severity in people who are infected .
57

58. • LIPS AND GUMS
• CHEEKS
TONGUE• TONGUE
• FLOOR OF THE MOUTH
• ROOF OF THE MOUTH
• LYMPH NODES
58

59.  FUNGAL
 VIRAL
 BACTERIAL
ULCERATIVE ULCERATIVE
 NEOPLASTIC
59

60.  WHO Classification:
Based on the strength of association of the oral
lesions with HIV infection:
 Group I : Lesions strongly associated with
HIV infection.
 Group II: Lesions less commonly associated with
HIV infection.
 Group III : Lesions possibly associated with HIV
infection.
60

61. Group I : Lesions Strongly Associated With HIV
Infection
 Candidiasis :
ErythematousErythematous
Hyperplastic
Thrush
 Hairy leukoplakia (EBV)
 HIV gingivitis
 Necrotising ulcerative gingivitis
 HIV periodontitis
 Kaposi sarcoma
 Non-Hodgkin’s lymphoma
61

62. Group II : Lesions Less Commonly Associated With
HIV Infection
 Atypical ulceration
 ITP
Salivary gland disease
 ITP
 Salivary gland disease
Xerostomia
Swelling of major salivary gland
 Viral infections
CMV
HSV
HPV
 Varicella zoster virus
Herpes zoster
62

63. Group III : Lesions Possibly Associated With
HIV Infection
Bacterial infections Bacterial infections
 Fungal infections
 Catscratch disease
 Sinusitis
 Melanotic hyperpigmentation
63

64. 64

65.  Inflammation/irritation
 Cracking and fissuring
 Pain upon opening the mouth
 Susceptible to infection Susceptible to infection
TREATMENT
• Antifungal medication
• Correct vertical dimension
65

66. 66
It is superficial infection of upper layer of oral mucous membrane & results in formation of
patchy white plaque or flecks on mucosal membrane.

67.  Multiple white to yellow soft plaques
 Plaques easily removed by gauze
 Areas may bleed and burn
 Taste alterations Taste alterations
 Xerostomia
TREATMENT
• Antifungal medication
67

68. 68

69.  Spotty appearance
 May look like pizza burn
 Mistaken for trauma, infections, radiation,
xerostomiaxerostomia
 Pain is less severe than pseudomembranous
candidiasis
TREATMENT
• Antifungal medications
69

70. 70

71.  Asymptomatic
 Predictive of disease progression
 Affects the lateral border and ventral tongue,
and buccal vestibuleand buccal vestibule
 Can result from epithelial hyperplasia,
secondary to a reactivation of latent EBV
 TREATMENT
• Usually none
• Occasionally antivirals
71

72. 72
It is a DNA nucleus which can remain latent in host neural cell ,therefore invading host
immune response.

73.  Vesicles that coalesce into bullae and break
 Some report a tingling sensation
 Occur on fixed and keratinized tissue
 Painful Painful
 May have systemic manifestations
TREATMENT
• Antivirals
73

74. 74

75.  Some begin as a smooth-surface papule
 Rough fingerlike projections
 Occur mainly on keratinized mucosa
 Tend to reoccur Tend to reoccur
 May interfere with eating and swallowing
and may bleed
 Not painful
 Transmissible
TREATMENT
• Excision
75

76. 76

77.  Most common oral bacterial infection among
HIV infected persons
 Contributing factors include poor diet, poor
oral hygiene, and lack of salivaoral hygiene, and lack of saliva
 Mainly due to overgrowth of normal flora
 TREATMENT
• Deep scaling and root planning
• Good home care
• Antimicrobial rinses
77

78. 78

79.  Inflammation
 Spontaneous bleeding
 Not always painful
 May occur without the presence of plaque May occur without the presence of plaque
 Microbiologic profile of gingival fluids is
same as for Periodontal Disease
 Early manifestation of HIV
 TREATMENT
• Periodontal scaling
• Peridex
79

80. 80

81.  Crater type sore on mucous membrane
 Pus formation
 Painful
 Interference with speech and swallowing Interference with speech and swallowing
 Stress, Acidic Foods, Trauma
 CMV (Cytomegalovirus) are clinical identical
TREATMENT
Topical steroids mixed with Orabase
81

82. 82

83.  It is very aggressive ,causing extensive tissue
ulceration.
 Necrosis with exposure of alveolar bone,sevre loss
of attachment & formation of interproximal craters.of attachment & formation of interproximal craters.
 NUP is acute & painful,involving bone
sequestration,without deep pockets
Treatment
 Broad spectrum antibiotic
 Scaling,root planing,oral hygine.
 Surgery if necessary.
83

84. 84

85.  Lesions begin flat and painless and can
progress to painful papules and nodules
 It is mainly seen in men with AIDS
 Recent studies indicate that it may be caused Recent studies indicate that it may be caused
by a sexually transmitted herpes virus-HHV 8
TREATMENT
• Radiation therapy
• Chemotherapy
• Immuno-modulator drugs
85

86. 86

87.  Second most common malignancy in AIDS
 Tumors present intraorally as soft tissue masses
 Grows faster and spreads outside the lymph
system in those with AIDSsystem in those with AIDS
TREATMENT
• Radiation therapy
• Chemotherapy
• Immuno-modulator drugs
87

88.  HIV spreads by closed mouth kissing
 HIV spreads by caring for the HIV+ve, sharing
clothes,
 toilets, clothes, eating together, coughing & toilets, clothes, eating together, coughing &
sneezing,
 shaking hands.
88

89.  HIV spreads by mosquito or insect bite
 HIV is a gay disease
 Medicine kills people and not AIDS
 There is a vaccine for AIDS There is a vaccine for AIDS
 AIDS affect adults and not children
89

90.  The principles of infection control remain
constant, whether HIV, HBV, HCV or other
infectious agents are the cause for concern.
 The components of Universal Precautions
include:
The components of Universal Precautions
include:
1. Personal protective equipment, e.g., wearing
gloves, gowns, eye protection and other
protective gear;
90

91. 2. Hand washing,
3. Decontamination, e.g., appropriate cleaning
methods to decontaminate surfaces objects,
etc.; andetc.; and
4. Waste disposal, e.g., liquid or non-liquid form,
double bagging and labeling.
91

92.  SUCTION BOTTLE- 30ml of 2 % gluteraldehyde
& 60ml of 2% hypochloride .They should be
emptyed ,rinsed then autoclaved.
92

93.  Occurs due to rotary instrument used in dental practice.
 Prompt removal of such spill as early as possible is
important.
 The area should be covered with sodium hypochloride 1% &
left for 30 seconds.left for 30 seconds.
 Person undertaking removal of spatter should wear gloves
& other protective gear & mop & send for incineration.
 Visible organic material- cleaned with absorbent material
 Nonporous surface should be cleaned & decontaminated
with registered hospital disinfectant effective against
HBV,HIV.
 Blood spill on carpeting & cloth furnishings are difficult to
manage-therefore avoided.
93

94. 94

95. Safe Sex Safe Blood Safe Razor
Safe Needle Safe Motherhood
95

96.  CDC recommends that all members of dental
team,who are exposed to blood, should be
vaccinated against hepatitis B .
96

97.  Decontamination of the wound- exposed
area should be decontaminated (soap &
water to percutaneous injury sites)
Counseling for health care workers Counseling for health care workers
 Lab testing
97

98.  Basic two drug regimen
 Zidovudine 300 mg/bid for four weeks
Lamivudine 150 mg/bid for four weeks Lamivudine 150 mg/bid for four weeks
 Expanded three drug regimen
 Zidovudine + lamivudine +indinavir
500mg/tid
98

99. 1. Virus based tests
2. Anti HIV antibody tests
3. Immunological tests and Surrogate
MarkersMarkers
4. Salivary tests
99

100. 100

101.  Confidentiality
 Informing other health care professionals
 Informing spouse or other sexual partner
 Consent for HIV testing
101

102.  No name is used
 Unique identifying number
 Results issued only to test recipient
102
23659874515
Anonymous

103.  Person’s name is recorded along with HIV
results
 Name and positive results are reported to the
State Department and the Centers for DiseaseState Department and the Centers for Disease
Control and Prevention
 Results issued only to test recipient.
103

104. a) Viral culture-
Directly detects virus & is highly specific.
Positive during window period &
terminal phase , when ELISA may beterminal phase , when ELISA may be
negative .
It takes 2-4 weeks for result to be out.
With availability of PCR , it is not done
routinely.
104

105. 2Types- i) For DNA of provirus present in
infected host cell.
ii) For HIV RNA from plasma.
Highly specific & sensitive for early diagnosis in
newborn.
Results available in 24- 48 hrs.
Limitations – cost & sophisticated lab
equipment.
105

106.  Positive during window period & late
phase of infection. But negative during
low viral load. Therefore it is not for
routine diagnosis.routine diagnosis.
 Used in blood banks where p24 antigen,
with ELISA, can shorten window period
of diagnosis.
106

107.  ELISA – 99% sensitive and specific
- negative during window
period and last phase
- cheaper than PCR & Culture- cheaper than PCR & Culture
- cannot be used in new borns
upto 18 months
107

108.  Western blot analysis -
- more specific than ELISA
- detects specific antibodies and shows
them as separate bands on gelsthem as separate bands on gels
- negative during window
period and last phase.
- cannot be used in new borns
upto 18 months
108

109.  Decrease in CD4 Cell +T-CELL –DESEASE
PROGRESSION.PROGRESSION.
109

110.  Saliva & GCF are used.
 HIV IgG antibody is designed specifically-oral
testing.
It is specific & sensitive. It is specific & sensitive.
110

111.  There is currently no vaccine or cure for HIV
or AIDS.
 Drugs
 Psychological counseling Psychological counseling
 Patients education
 Other measures – symptomatic treatment
111

112.  Fusion inhibitors-Similar to viral gp41 & inhibits viral entry
into host cell.
 Nucleoside reverse transcriptase inhibitor(NRTIs)-They
become incorporated into growing DNA chain , terminate
elongation & decrease/prevent HIV REPLICATION in
infected cell.infected cell.
 Non-Nucleoside reverse transcriptase inhibitor(NNRTIs) –
bind near catalytic site of reverse transcriptase & inhibit
crucial step in reverse transcription of RNA genome into
double stranded retroviral DNA.
 Protease inhibitor(PIs)- blocks the cleavage of viral
protein during asssembly & maturation, a process
essential for newly formed virus to become infecious.
112

113.  CLASSIFICATION
1. Inhibitors of viral attachment
E.g.. rs CD4
2. Reverse transcriptase inhibitors
- Nucleoside analogue reverse transcriptase inhibitors (NRTIs)- Nucleoside analogue reverse transcriptase inhibitors (NRTIs)
E.g.. Zidovudine(AZT), Didanosine, Stavudine,Lamivudine(3TC)
- Non nucleoside analogue RT inhibitors (NNRTIs)
E.g.. Nevirapine, Delavirdine, Effirvarez
3. Protease inhibitors (PI)
E.g.. Saquinavir, Ritonavir, Indinavir, Nelfinavir
4. Integrase inhibitors
Phase I trial not complete as yet
5. Agents that block virus assembly and budding
E.g.. Interferon
113

114.  Highly Active Anti RetroviralTherapy (HAART)
 Internationally recommended three drug Internationally recommended three drug
combination therapy. It is the combination of
 2 NRTI + 1 PI
 2 NRTI + 1 NNRTI
 1 NRTI + 1 NNRTI + 1 PI
 2 NRTI + Hydroxyurea
114

115.  Combine 1 choice from column A & 1 from
Column B
Column A Column B Column A Column B
 Indinavir Zidovudine + Didanosine
 Nelfinavir Stavudine + Didanosine
 Ritonavir Zidovudine + Zalcitabine
 Squinavir Stavudine + Lamivudine
115

116.  NRTIs – eg: zidovudine
anemia ,neutropenia,peripheral neuropathy.
 NNRTIs – eg: EFAVIRENZ
Fever, rise in liver enzyme, neuropsychiatricFever, rise in liver enzyme, neuropsychiatric
symptoms.
 PI s – eg: indinavir
GI intolerance, urinary calculi, rash, dizziness.
116

117.  Various forms of alternative medicine have
been used to treat symptoms or alter the
course of the disease.
Acupuncture has been used to alleviate some Acupuncture has been used to alleviate some
symptoms, such peripheral neuropathy, but
cannot cure the HIV infection
117

118.  VitaminA supplementation in children
probably has some benefits.
 Daily doses of selenium can suppress HIV
viral burden with an associated improvementviral burden with an associated improvement
of the CD4 count. Selenium can be used as an
adjunct therapy to standard antiviral
treatments, but cannot itself reduce
mortality and morbidity.
118

119.  Current studies indicate that that alternative
medicine therapies have little effect on the
mortality or morbidity of the disease, but
may improve the quality of life of individualsmay improve the quality of life of individuals
afflicted withAIDS.
 The psychological benefits of these therapies
are the most important use.
119

120.  Active or passive vaccines with the capability
of immunizing healthy individuals or stopping
further spread of HIV remain in the research
stages and are not yet ready for use.stages and are not yet ready for use.
 But the clock is running quickly: only an
effective vaccine will be financially feasible
world wide and promise the capability to
reduce the developingAIDS pandemic in the
world .
120

121.  To date the most promising are genetic
vaccines, eg. Directly injected plasmid bound
DNA of certain HIV genes, which elicit a
potent host immune responsepotent host immune response
121

122. PEGNANCYAND PEP
 After 36 weeks of gestation Zidovudine 300
mg/bid
Short course perinatal prophylaxis
 Nevirapine- single dose at the onset of labour
and to the newborn within 48 hours.
 Zidovudine IV at the onset of labour and the
neonate treated for 6 weeks.
122

123.  Should be done at the time of exposure, at 6
weeks following exposure & at 12 weeksweeks following exposure & at 12 weeks
following exposure.
123

124.  Helps patients to understand & cope with HIV
test results.
 Provides patient with further information.
Helps patient to make short & long term Helps patient to make short & long term
future plans to improve quality of life.
124

125.  “To care is a duty; to prevent is a
responsibility. Prevention and care are the
twin engines that should drive our effort for
the containment of AIDS”.the containment of AIDS”.
Prof.V. Ramalingaswami
125

126.  AIDS - difficult to get, impossible to cure, easy to
prevent.
 The best form of protection from AIDS is
PREVENTIONPREVENTION
126

127. 127

128. 1. TEXTBOOK OF MICROBIOLOGY: 17TH EDITION: C K J PANIKER.
2. BURKET’S ORAL MEDICINE. DIAGNOSIS ANDTREATMENT10TH
EDITION: GREENBERG AND GLICK.
3. PARK’STEXTBOOK OF PREVENTIVE AND SOCIAL MEDICINE:
18TH EDITION:K PARK
3. PARK’STEXTBOOK OF PREVENTIVE AND SOCIAL MEDICINE:
18TH EDITION:K PARK
4. TEXTBOOK OF ORAL &MAXILLOFACIAL SURGERY ,SECOND
EDITION :NEELIMA ANIL MALIK.
5. HIV & AIDS IN DENTAL PRACTICE,FIRST EDITION :ANIL KHOLI
6. SHAFER’STEXTBOOK OF ORAL PATHOLOGY,5TH EDITION : R
RAJENDRAN
128