A description of HIV Virus, AIDS and its role in the causation of Periodontal disease has been described

1. Good Morning

3. Contents
• History and Introduction.
• HIV.
• Pathogenesis of HIV Infection.
• Oral Manifestations.
• Periodontal Management of HIV Infected
Patient.
• Laboratory Investigations of HIV.
• Conclusion.

4. 1981 Newyork and Los Angeles
Two Rare Diseases
Kaposi’s Sarcoma, Seen Only in Old People
Young Homosexual Males
Pneumocystitis Carinii Pneumonia
Treatment : Pentamidine Antifungal Agent ( Regular Doses)
Doses after Doses Were Required, Still Could Not Cure the
Disease, remissions were common
Signs of An Impending
Disaster, An Catastrophe

5. 1983, Luc Montagnier
Pasteur Institute, Paris
Retrovirus -------- Lymphadenopathy associated virus ( LAV )
1984 Robert Gallo
NCI National Cancer Institute, USA Quest for cancer causing
viruses
Retrovirus --------AIDS patients
Human T Cell lymphotrophic virus - III
1986 International Committee on virus nomenclature
Generic Name; Human Immunodeficiency Virus ( HIV )

7. Under Reporting
Under Diagnosis
Delayed Reporting
Delayed Diagnosis
14000 new infections
5 Per minute,
7000 per day
After the Turn of Horrifying Pictures, It Was the Turn of Numbers
20 Million Have Already Died
60 Million Are on Their Way

8. By 2005 between 2.4 million and 3.3 million
individuals were estimated to have lost their
lives worldwide as the result of HIV.
The increase in numbers of patients living with AIDS
in the United States and other developed countries
has resulted in part from prolonged survival.

9. AIDS or Accquired Immuno Deficiency Syndrome
• Caused by HIV or Human Immunodeficiency virus
• HIV belongs to the Lenti virus
• Subclass of the Retroviridae family
• “ Lenti ” in Greek means “Slow”
All the viruses in Lenti virus family have long incubation period
• Retro Virus --- A Back Ward Step in Biological Information
Occurs During Viral Replication Due to One of Its Key Enzyme
Reverse Transcriptase

10. HIV ( Human Immunodeficiency Virus )
• HIV 1 ( most common, seen throughout the world )
• HIV 2 ( confined to West Africa and Western & Southern India )
Retrovirus family
Lenti virus subclass
• Human immunodeficiency virus
• Simian Immunodeficiency Virus,
• Visna Virus of Sheep
• Bovine Immunodeficiency Virus

11. Genomic Differences in Two Strains
• HIV 1 Has 10 Subtypes
• A,B C,D,E,F,G,H,I,J (Group M or Major ) C - Common in India
• HIV 2 Is Less Virulent Than HIV 1
Origin or Evolution of HIV
• From Africa, a Jump of Virus From One Species to Another i e,
• HIV-1 Chimpanzees,
• HIV -2 Sooty Mangabey Monkeys

12. HIV Is a Spherical Virus Which Has a Cone - Shaped Core Surrounded
by an Lipid Envelope From the Host Cell Membrane
1) Core,
2) Matrix,
3) Envelope
STRUCTURE

13. Reverse
transcriptase
Core Protein
Matrix Protein
Lipid Bilayer
Surface
Glycoprotein
gp120
Trans membrane
pedicle gp41

14. • Major Capsid Protein p24
• Two Copies of Genomic RNA
• Three Viral Enzymes 1) Protease,
2) Reverse Transcriptase,3) Integrase,

15. Envelope contains
• knoblike spikes on the surface (gp120 )
• Anchoring transmembrane pedicle ( gp41)
• gp120 leads to binding of the virus to the CD4 receptor on
T- lymphocyte
• gp41 leads to cell fusion

16. HIV Has 9 Genes :
1) Three Structural Genes ;( specific to HIV )
2 ) Six Regulatory Genes Or Non Structural Genes
(Common to all Retro viruses )
Genomic
structure

17. Structural genes : 1) gag 2) env 3) pol
Non structural genes or regulatory genes
1) tat 2) rev
3) vif 4) nef
5) vpu (HIV -1 ) 6) vpx ( HIV -2)
gag genes --------p24, p17, p7 or p9
pol genes --------Reverse transcriptase, Integrase,
Protease
env genes--------- gp 120, gp40

19. CD - 4 is a cell surface receptor molecule for HIV expressed mainly
on T- lymphocytes also seen on macrophages, brain microglial
cells,langerhans dendritic cells
For binding & fusion to take place coreceptors are also essential.
CCR5 Macrophages
CXCR( fusin ) T-lymphocytes
CD 4: Cluster of Differentiation

20. CD4 or Helper T cells act as regulators of immune response
Produce
• Cytokines
• Chemotactic factors
• Hematopoietic growth factors
So loss of this master cell causes a dampening effect on the entire
immune system
Once T- lymphocytes are affected there is secondary dysregulation of
B- lymphocytes.
So both Humoral and Cell mediated immunity are affected

21. 1. Binding
HIV binds to the CXCR4 receptor on the target cell.
The process of HIV entry begins with binding of the
viral envelope glycoprotein gp 120 to the CD4 cell
surface.

22. 2. Infection
Once attached to the cell surface the virus fuses with
the cell membrane infecting the healthy cell.

23. 1) Initial step in the infection is
the binding of gp120( envelope
glycoprotein) to CD4 molecules
2) Binding leads to
conformational changes that
results in formation of a new
recognition site on gp120 for the
coreceptor CCR5 or CXCR4

24. Conformational changes in gp41 result in insertion of a fusion
peptide at the tip of gp41 . So there is fusion of the virus into the
cell membrane of the target cells

25. Reverse Transcriptase acts here
T- Lymphocyte Becomes a Production House of Fresh HIV
Integrase

26. 1986 Walter Reed Classification System
1986 Center for Disease Control
1993 Center for Disease Control Combined These Two Earlier
Systems
CD4 Counts
( Normal CD4 Counts Are 600 to 1500 Cells / C Mm of Blood )
( Normal CD8 Counts Are 300 to 1000 Cells / C Mm of Blood )
CD4 Counts Are Higher in Children,
Less in Morning and Increases in Evening

27. Center for disease control classification according to CD4 counts
CD4 counts
• < 200 cell /c mm
• 200 - 499 / c mm
• >500 / cmm
Walter Reed classification
• Asymptomatic or PGL or Acute HIV
• Symptomatic Infection
• AIDS Indicator Condition

28. A3, B3, C3, C1, C2 are AIDS
If CD 4 count is less than 200 /c mm without any
symptoms- its AIDS
Rest are HIV infected
CD4 Cell
categories
Asympto
matic or
PGL
Symptoma
tic
AIDS
Indicator
Conditions
>500 /c
mm
A1 B1 C1
200-
499/cmm
A2 B2 C2
< 200
/cmm
A3 B3 C3
1993 CDC CLASSIFICATION

29. High concentration of HIV has been noted in
• blood,
• semen,
• CSF
Low concentration is noted in
• tears,
• breast milk
• and saliva
Transmission: Sexual contact
Exposure to blood & blood products
IV drug abuse
Vertical transmission ( Mother to infant )

30. Viral
load
3mnths 6 mnths 12 yrs
Primary Asymptomatic period Terminal AIDS
105 or 106

31. Rate of Progression :
Time taken to convert from primary HIV infection to AIDS
Depends upon
• Age
• Way the virus was acquired,
• Treatment that is being given
• Socio- economic status
On an average 12 yrs .
Slow progressors
Rapid progressors

32. Classification of Oral lesions in AIDS & HIV Infection
Bacterial Infections
• Linear Gingival Erythema
• Necrotizing Ulcerative Periodontitis
• Necrotizing ulcerative gingivitis
Fungal Infections
• Candidiasis
• Pseudomembranous
• Hyperplastic
• Erythematous
• Angular cheilitis

33. Viral Infections
• Epstein-Barr Virus (Oral Hairy leukoplakia)
• Herpes Simplex Virus
• Varicella-Zoster Virus
• Cytomegalovirus infections
Neoplasms
Kaposi’s sarcoma
Hodgkin's lymphoma
Oral pigmentations

34. Periodontal management of HIV infected patients
1) Health Status
Is it AIDS or HIV Infection ?
• Delayed wound healing,
• Increased post operative infections are a concern if patient is
having AIDS ( A3, B3, C3, C1, C2)
• If its HIV infection with near normal CD4 counts, low viral
bioload patient can be treated in normal way
2 ) Goals of Therapy :
a) Control of HIV associated mucosal lesions
b )Treatment of choice : Conservative , Nonsurgical
periodontal therapy.

35. Supportive Periodontal therapy :
Frequent recalls of 2 to 3 months
Antibiotics should be given only after consultation with the
physician.
Infection Control measures :
Universal precautions according to CDC
Rules of OSHA.( Occupational safety and health administration )
Infection can transmit from
• Patient to Patient
• Dentist to Patient
• Patient to Dentist
However all these rare

36. Transmission From Dentist to Patient
•Dentist in Florida Dr.David Acer ( Gay )
•1990 Weeks Before His Death Informed All His Patients of His
Health Status ( Terminal AIDS ) .
•All Dental Treatment in His Clinic Were Done Acc to Universal
Precautions (CDC) & OSHA Rules
• By 1991 , 23yr old young girl a patient of Dr Acer …...
• Soon 4 more patients filed similar complaints
• Proper history, Phylogeny and autopsy samples of Dr Acer.
• Estate of Dentist Compensation
• Only Recorded Case of Dentist to Patient Transmisssion

37. Candidiasis
Candida is a fungus normally found in the oral cavity
Types: ( seen in 90 % of AIDS patients )
1) Pseudomembranous candidiasis
2) Erythematous candidiasis
3) Angular Chelitis
4) Hyperplastic candidiasis

38. Oral Thrush( Pseudomembranous ) :
Presents as painless or slightly sensitive white lesions that
can be readily scraped & separated from the surface of the
oral mucosa. Most common on hard and soft palate

39. Hyperplastic Candidiasis
Least common form
Can be seen on the tongue and buccal mucosa
More resistant to removal than the other types

40. Erythematous Candidiasis :
Can be a component of the pseudomembranous type, appearing as
red patches on the buccal or palatal mucosa or it may be associated
with depapillation of the tongue

41. Angular cheilitis
• The commissures of the lips appear
erythematous with surface crusting and
fissuring.
Severe angular cheilitis. A, Before treatment. B, After treatment
with systemic fluconazole.

42. Treatment :
Early oral lesions are responsive to topical antifungal therapy
Amphoterecin B
Itraconazole
Nystatin
Oral topical antifungal agents ------ large amounts of sucrose
Long term doses will be cariogenic
Vaginal agents which have no sucrose is given, but are less
efficacious. (sucrose free topical agents have been developed )
Resistant cases need systemic treatment :
Ketoconazole 200mg
Fluconazole 100 mg
Itraconazole

43. Kaposi’s Sarcoma : 1872.
Rare , multifocal , vascular neoplasm. M to F is 20 : 1
New strain of Herpes virus ( HHV -8 ), KS- herpes virus
Decreasing immuno-competence, resulting in activation of the latent
HHV-8.
Malignant tumor ( localized & slowly growing lesion )
In HIV infected, its very aggressive
Painless, reddish purple macules
which slowly become nodular.

44. Intraoral Kaposi's sarcoma. A, Multiple painless, nonelevated palatal lesions.
B, Palatal Kaposi's lesion that interfered with function and required treatment.
C, Gingival lesion that created an esthetic concern for the patient

45. Microscopically :
Endothelial cell proliferation with formation of atypical vascular
channels
Extravascular hemorrhage with hemosiderin deposition
Spindle cell proliferation in association with atypical vessels.
Mononuclear inflammatory infiltrate having mainly plasma cells

46. Kaposi’s sarcoma : Renal transplant patients, lupus erythematosus
Immunosuppresants & HIV -ve
But in an HIV + ve individual presence of Kaposi’s Sarcoma converts
the diagnosis into AIDS.
Treatment : Antiretoviral drugs
• LASER excision
• Radiation therapy
• Interferon 
• Chemotherapeutic agent
• Intralesional injection of Vinblastine
Nichols 1993
Every 15 days ; success seen in 70%

47. Bacillary(epitheloid) angiomatosis
• Infectious vascular proliferative disease with clinical
and histologic features similar to Kaposi's sarcoma.
• Caused by rickettsia-like organisms (eg.,
Bartonellacea, rochalimaea quintana)
• Gingival BA manifests as red, purple or blue
edematous soft tissue lesions that may cause
destruction of periodontal ligament and bone.
• Treatment by using erythromycin or doxycycline.

48. Bacillary angiomatosis mimicking Kaposi's sarcoma.

49. Oral Hairy Leukoplakia
• Seen on lateral border of the tongue
• Can be unilateral or bilateral
• Appear as faint white vertical streaks or thickened & furrowed
areas exhibiting a shaggy keratotic surface.
• Causative is Epstein Bar Virus (EBV)

50. Oral hairy leukoplakia on left lateral border of tongue.
A, Clinical view. B, Biopsy of oral hairy leukoplakia. Note the
ballooned epithelial cells near the surface of the epithelium.

51. Histologically :
• Thickened parakeratin
• Surface corrugations & balloon cells
in the upper spinous layers.
• Balloon cells resembling koilocytes
• These koilocytes contain the EBV
• There is lack of inflammation in the
lamina propria.
Treatment :
Little advantage in treating hairy leukoplakia
LASER or Conventional Surgery
Topical Retinoids or Acyclovir

52. Pindborg & Schidt 1987
HIV associated gingivitis HIV- G
HIV associated periodontitis HIV- P
HIV- G Linear Gingival Erythema
HIV- P Necrotizing Ulcerative Periodontitis
Linear Gingival Erythema :
• Erythematous gingival band, dark or fiery red in color, that often
extends into attached gingiva. Plaque is minimal
• Does not respond to treatment
• Localized or generalized

53. LGE : Can serve as a precursor for NUP
Microflora of both are the same
Treatment : Meticulous oral hygiene
Scale & polish affected areas & perform subgingival
irrigation with Chlorhexidine
If they persist retreat or diagnosis changes to
candidiasis (systemic flucocanozle)

54. Necrotizing Ulcerative Periodontitis (NUP)
AIDS patients with advanced immune suppression,
CD4+ cell counts < 100 cell per mm3.
NUP ----- few teeth or in severe cases it may affect all teeth.
Intense pain ( severe bone pain, as if the teeth were hitting the bone.)
Marked necrosis of soft tissue with rapid periodontal ligament and bone
destruction.
Spontaneous gingival bleeding .

55. Therapeutic Protocols for NUP Includes:
•Gentle debridement of affected areas to minimize bleeding and pain.
• Irrigation with 10% Betadine (povidone-iodine) to aid debridement.
•If possible root planning and scaling under LA again with 10%
Betadine as irrigant.
•Instruct patient to maintain a methodical and careful oral hygiene
regimen.
Systemic Treatment
Rx: Metronidazole (Flagyl) 250 mg tablets 4 tab / day for 1 week

56. If the patient presents with severe pain, necrosis and fever, then
other antibiotics need to be prescribed
• Rx: Amoxicillin 500 mg Tablets ( QID )
• Rx: Clindamycin 300 mg capsules (QID )
If the patient is allergic to either of the above, then prescribe:
Rx: Erythromycin enteric coated 500 mg Tablets

57. Necrotizing Ulcerative Stomatitis
• NUS may be severely
destructive and acutely painful
• It may affect oral soft tissue and
underlying bone.
• It may occur separately or as an
extension of NUP.
• Appears identical to noma.
• Treatment may include
metronidazole and an
antimicrobial mouthrinse like
chlorhexidine gluconate.
Necrotizing ulcerative
stomatitis (NUS) in left
mandibular molar area.

58. Lab Investigations of HIV :
• ELISA or Enzyme linked Immunosorbent Assay
• Rapid HIV tests
• Western Blot tests
• Polymerase Chain Reaction (PCR)
• Oral HIV tests
Screening tests :
• ELISA or Enzyme linked Immunosorbent Assay
• Rapid HIV tests
• Oral HIV tests
Confirmatory tests :
Western Blot & PCR

59. ELISA :
• Detects antibodies to HIV
• Especially the antibodies to p24 antigen
• Time is required for development of antibodies, till then false
negative reaction may occur.
• False positive reactions may develop in leprosy, pregnancy
• So a very good screening test.
• But if pt turns positive , should be confirmed with other
confirmatory tests.

60. Rapid HIV Test :
Disadvantage of ELISA :
Two weeks for results
• 30 to 40 % did not return to check the results.
• Most of them were positive
• Pregnant patient’s treatment could be started if they were positive.
A rapid test for detecting antibodies to HIV U.S. in 1996.
Usually in 20 -30 minutes,
The U.S. Food and Drug Administration currently has licensed only
one rapid HIV test called the Single Use Diagnostic System for HIV-1
(SUDS™). Several others are in development.

61. The rapid HIV test is an ELISA test.
• Normal ELISA is analyzed in large batches along with other
individual tests.
• Rapid test is analyzed alone.
• Higher cost
• Fast result, which reduces the number of people who never return to
find out their results.
However, if the rapid test is positive, Western blot has to be done for
confirmation.
TRIDOT
• PAT ( Particle Agglutination Test )

62. HIV-1
HIV-2
Control
Antigens are coated over an
membrane, blood if contains anti
HIV antibodies will show color
changes

63. Polymerase chain reaction (PCR) is a new blood test that looks
for HIV genetic information.
It has very limited availability. It is expensive and labor intensive.
Advantage is that the test can detect the virus even in someone
who is newly infected.
The FDA has indicated that the development and
implementation of tests for HIV genetic material such as PCR is
warranted.

64. Oral HIV test
The inside of the mouth is gently scraped and the saliva is tested
for the presence of HIV antibodies. The result is as accurate as the
blood tests because the saliva is tested using an EIA test and then a
Western blot test if necessary.

65. Drugs :Nuclease Reverse transcriptase inhibitors;
1) Zidovudine ( Azidothymidine ) 2) Didanosine
3) Zalcitabine 4) Stavudine
5) Lamivudine
Non nucleoside reverse transcriptase inhibitors
1) Nevirapine 2) Delaviridne 3) Efavirenz
Protease Inhibitors :
1) Saquinavir 2) Ritonavir
3) Indinavir 4) Nelfinavir
5) Amprenavir 6) Lopinavir
HAART ( Highly Active Anti Retoviral Therapy)

66. Drugs in the treatment
of HIV

67. periodontal maintenance recall visits should be conducted at
short intervals (2 to 3 months) and any progressive
periodontal disease treated vigorously.
The primary goals of dental therapy should be the restoration and
maintenance of oral health, comfort, and function.
Acute periodontal and dental infections should be managed, and
the patient should receive detailed instructions in performance
of effective oral hygiene procedures.

68. Prevention
• Education, counseling, and behavior modification are the
cornerstones of an HIV prevention strategy.
• Widespread voluntary testing, together with counseling of
infected individuals, is recommended.
• The practice of "safer sex"
• Breast feeding is absolutely contraindicated when a mother is
HIV positive.
• Clotting factor concentrates are heat-treated, essentially
eliminating the risk to hemophiliacs who require these
products

69. Red Ribbon Foundation
EDUCATE TO PREVENT - RESEARCH TO CURE
The Red Ribbon Foundation was founded in 1993 in
memory of Singer/songwriter Paul Jabara, who conceived of
and distributed the first Red Ribbon,
and who died of AIDS.

70. • The Red Ribbon is the
international symbol for HIV and
AIDS awareness.
• Worn to demonstrate care and
concern about HIV and AIDS
issues.
• The Red Ribbon offers a symbol
of hope and support for those
living with HIV and AIDS
• Reminder that AIDS continue to
grow around the world and is not
going away anytime soon.

71. • Vaccines :
• Revolving around p24 which mutates, envelope
proteins which again mutate.
• Strains A to J in Group M & Group O
• Phase I and/or phase II trials
• - Naked DNA vaccines
• - Modified vaccinia Ankara (MVA)
• - Salmonella
• - Venezuela equine encephalitis (VEE) virus
• Live attenuated HIV vaccines  not yet tried.

72. Conclusion :
“There is nothing in this world the species by name homo
sapiens will not conquer.”
So like every other disease, AIDS will also be conquered.
Thank You.

73. Thank You.
Have a nice day