effects of hiv and aids on periodontium

1. HUMAN IMMUNODEFICIENCY VIRUS
(HIV) and the periodontium
Dr. D.Navya, MDS

2. INTRODUCTION
• Virus that causes AIDS.
• Formerly known as HTLV-III and
lymphadenopathy-associated virus.
• A retrovirus that primarily infects vital
components of the human immune system such
as CD4+ T cells, macrophages and dendritic
cells.
• It also directly and indirectly destroys CD4+ T
cells.

3. Mode of transmission
1. Un protected sex
2. Sharing of needles
3. Unsafe Blood
4. Improperly sterilized hospital tools
5. Parent to child

4. SALIVA AND HIV TRANSMISSION:
There is only a very slight evidence that HIV may be
transmitted by saliva, for the following reasons.
• Only a small amount of HIV infected individuals
harbour the virus in whole saliva
(e.g. in one study HIV was detected in mixed saliva of
5% of infected individuals and only in one of 15 parotid
saliva samples).

5. • In any case HIV virions cannot exist in cell free State in
saliva, and estimates are that there is less than one
infectious particle of HIV per milliliter of mixed saliva
• Saliva contains IgA group antibodies to HIV proteins
(p24, gp120, gp160) which may neutralize the infectivity
of the virus.

6. • Other HIV inhibitory factors in saliva include high
molecular weight mucins thought to entrap the virus,
proline rich proteins, and a serine protease inhibitor
termed salivary leucocyte protease inhibitor (SLPI).
• The latter possibly blocks cell surface receptors needed
for entry of HIV into the cells.
• The virus looses its infectivity when exposed to mixed
saliva for 30 minutes

7. PATHOGENESIS
• Direct Cell Killing:
• Antigenic Diversity:
• Receptor Signalling:

8. Direct Cell Killing:
• This was the first mechanism suggested, based on the
behaviour of certain laboratory isolates of HIV.
• Subsequent experiments suggested that there is not
sufficient virus present in AIDS patients to account for all
the damage seen.
• Although killing of CD4+ cells may contribute to the
overall pattern of pathogenesis seen in AIDS.
e.g. disturbances in cell biochemistry
may also affect the regulation of the immune system:

9. Antigenic diversity
• This theory holds that the continual generation of new
antigenic variants eventually overcomes the immune
system, leading to its collapse.
There is no doubt that new antigenic variants of HIV
constantly arise during the long course of AIDS
• It has not been completely established how this might
lead to the collapse of the immune system, but it is
envisaged that there might be an effect, with each new
variant contributing to the slight but irreversible decline
in immune function.

10. Receptor signalling
• There have been several reports that HIV
binding to CD4 induces an intracellular
signal which may have a detrimental effect
on cells.
• However, there is a second component to the
HIV receptor which is required for cell entry:
chemokine receptors such as CXCR4 &
CCR5.
• Although HIV-mediated signal transduction
is not required for fusion & entry, at least
some HIV isolates induce a signal when the
envelope protein binds to CCR5.

11. CDC SURVILLANCE CASE CLASSIFICATION
AIDS PATIENTS HAVE BEEN GROUPED as follows
according to the CDC classification 1993
Category A
Includes patients with acute symptoms or asymptomatic
diseases ,along with individuals with persistent
generalized lymphadenopathy ,with or without malaise
,fatigue, or low grade fever

12. Category B;
patients have symptomatic conditions such as
oropharyngeal or vulvo vaginal candidiasis,
herpes zoster ,oral hairy leukoplakia,idiopathic
thrombocytopenia or constitutional symptoms of
fever , diarrhea, and weight loss

13. Category C;
patients are those with outright AIDS ,as
manifested or identified through CD4 T
lymphocyte levels or <200cells /mm3

14. Cell count Disease
400 Most patients have no signs
of immunosupression
301 to 400 Bacterial skin infection
Staphylococcus
201 to 300 Herpes zoster
Candidiasis
Tinea pedia
Oral hairy leukoplakia

15. 101 to 200 Pneumocystis carnii
Histoplasmosis
Coccidiomycosis
Cryptococcal
Toxoplasmosis
Herpes simplex
Cryptosporidiosis
Kaposi sarcoma
0 to 100 Wasting syndrome
Cytomegalovirus
Lymphoma
Mycobacterium avium
complex

16. STAGE OF
ILLNESS
Acute
retroviral
Syndrome
Window
Period
HIV
positive
asympt
omatic
phase
HIV positive
symptomatic
phase
AIDS
Symptoms
Fever, skin
rash
Nil Nil
Prolonged fever,
recurrent common
infections, TB,
diarrhoea,
Generalized
lymphadenopathy
AIDS defining
illness,
Opportunistic
infections, wasting
syndrome,
dementia positive
HIV test:
ELISA/WB
Onset
Within 2 -4
weeks of
infection
From time of
getting HIV
infected
6-12 weeks
after HIV
infection
About 2-5 years after HIV
infection
5-10 years after
getting HIV infection
Diagnosis
PCR Antigen
test
PCR or P 24
antigen test
3 ELISA or 1
WB & 1
ELISA
2 ELISA and 2 major
symptoms
2 ELISA and AIDS
defining illness
Transmission
of disease
YES YES YES YES YES

17. DIAGNOSIS
• It is possible to diagnose HIV infection by isolating the
virus itself from a blood sample or by demonstrating the
presence of HIV antigen in the blood.
• ENZYME-LINKED IMMUNOSORBENT ASSAY (ELISA)
• WESTERN BLOT (IMMUNOBLOT)
• POLYMERASE CHAIN REACTION (PCR)

18. GENERAL MANIFESTATIONS OF AIDS:
• Clinical findings in Acute HIV syndrome include,
GENERAL:
• Fever,
• Pharyngitis
• lymphadenopathy
• Headache / Retroorbital pain
• Arthralgias / Myalgias
• Lethargy /Malais
• Nausea, Vomiting, Diarrhoea.
• Anorexia / Weight loss,

19. NEUROLOGIC:
• Meningitis,
• Encephalitis,
• Peripheral neuropathy
DERMATOLOGIC :
• Erythematous maculopapular rash
• Mucocutaneous ulceration.

20. Severe
weight loss
Persistent
headache
High fever
White
patches on
tongue
Heavy night
sweats
Loss of
appetite
Memory loss
Chronic
Diarrhea
Fatigue &
muscle
weakness
Swelling
Lymph
Nodes
Symptoms of HIV infection

21. ORAL MANIFESTATIONS OF HIV INFECTION:
• In 1993, European Commission (EC) clearing house on
oral problems related to HIV Infection and WHO
collaborating center on Oral Manifestations of
Immuno-deficiency virus released following
classifications.

22. Group 1: lesions strongly associated with HIV infection.
1. Candidiasis
2. Hairy Leukoplakia
3. Kaposi’s sarcoma
4. Non- Hodgkin’s lymphoma
5. periodontal diseases
-Linear gingival erythema,
-Necrotising ulcerative gingivitis,
-Necrotising ulcerative periodontitis

23. Group 2: Lesions less commonly associated with
HIV infection
1 .Bacterial infections
-Mycobacterium avium-intercellulare
-Mycobacterium tuberculosis.
2. Melanotic hyperpigmentation
3. Necrotising ulcerative stomatitis

24. Group 3: Lesions seen in Hiv infection
1.Bacterial infections
-Actinomyces israelli
-Escherichia coli
-Klebsiella pneumoniae
-Cat-scratch disease
2. Drug reactions (ulcerative, erythema
multiformae, lichenoid reaction, toxic
epidermolysis)
3. Epitheloid (bacillary) angiomatosis

25. Fungal infections other than candidiasis
-Cryptococcus neoformans
-Geotrictum candidum
-Histoplasma neoformans
-Miscoraceae (zygomycosis)
-Aspergillus flavus

26. 5. Neurological disturbances
-Facial palsy
-Trigeminal neuralgia
6. Recurrent apthous
stomatitis(RAS)
-Viral infections
-CMV
-Molluscum Contagiosum.

27. Oral candidiasis
Etiology: candida albicans
4 clinical patterns are seen,
1.Pseudomembranous,
2.Erythema,
3.Hyperplastic
4.Angular cheilitis:

28. PSEUDOMEMBRANOUS
• Presents as painless or slightly sensitive
• Yellowish-white curd like lesions that can be readily
scraped and separated from the surface of the oral
mucosa.
• -Mostly seen on hard,soft palate, buccal and labial
mucosa but can occur anywhere in the oral cavity

29. ERYTHEMATOUS

31. Angular chelitis

32. Diagnosis:
• Diagnosed by its clinical appearance
• PAS staining for candidal hyphae
• Culturing organism on sabouraud’s agar
• When oral candidiasis appears in patients with no
apparent predisposing causes, the clinician should be
alerted to the possibility of HIV infection.

33. Treatment:
Topical drugs
• Clotrimazole 10 mg tablets 3 to 5 tab for 7 to14 days
• Nystatin oral suspension
1,00,000u/ml administer 240ml rinse with 1tsp(5ml)
• Clotrimozole ointment 15 gm tube apply to affected area
• Itraconazole oral suspension 100 to 200 mg once daily
for 7 to 28 days
Systemic drugs:
• ketaconazole, 200mg tabs take 2 tabs immediately,
then 1 or 2 tabs daily with food for 5 to 14 days.

34. Etiology: Epstein Barr Virus (EBV)
Clinical Features:
• It appears bilaterally on lateral borders of the tongue as
painless,faint white vertical streaks.
(or)
• Thickend & furrowed areas with shaggy keratotic
surface with vertical striations imparting corrugated
appearance.
• Microscopically-lesion shows a hyperparakeratotic
surface with projections that often resembles hairs.
HAIRY LEUKOPLAKIA:

36. Histological features:
• Epithelial hyperplasia with acanthosis & hyperkeratosis
• Varying numbers of lightly stained,swollen,balloon cells
in upper prickle cell layer are seen.
• Dense aggregates of nuclear chromatin material
marginated along the nuclear membrane known
as nuclear beading is seen.

37. Treatment:
• Use of antiviral agents such as acyclovir or valacyclovir
are often responsive.
• Lesions can be successfully removed with laser of
conventional surgery.
• HAART has resulted in a greatly diminished incidence of
OHL.

38. • It is a multifocal neoplasm of vascular endothelial origin.
Etiology: Human Herpes virus-8 is involved.
Clinical features:
• Commonly palate, gingival, tongue & oropharynx are
affected.
• Red to purple macular nodular or raised & ulcerated
lesions appear.
• Colour darkens as the lesion ages.
Kaposi sarcoma

42. Treatment:
• The advent of HAART has resulted in a marked reduction
in the incidence of kaposi sarcoma
• Treatment can also be through antiretroviral agents
• Laser excision, radiation therapy, and intralesional
injection with vinblastine.

43. Non hodgkins lymphoma
Etiology: Epstein-Barr virus.
Clinical features:
• Lesions present as a large, painful ulcerated
mass on the palate or gingival tissues.
Treatment:
• Combination of chemotherapy & radiation

45. Periodontal diseases
Etiology:
In HIV-positive patients, the predisposing factors
include
• Age, smoking, viral load
Microorganisms such as
• Fusobacterium nucleatum
• Prevotella intermedia
• Actinobacillus actinomycetemcomitens.

46. Clinical features:
Periodontal lesions include
1. Linear gingival erythema (LGE) –
It is a non- plaque induced gingivitis which
is erythematous.
2. Necrotising Ulcerative Periodontitis.
3. Necrotising Stomatis.
4.Chronic periodontitis.

47. Linear gingival erythema
• It is a distinct fiery red band along the margin of gingiva
• The amount of erythema is disproportionately intense for
the amount of plaque
• There is no ulceration present and according to
EC – WHO criteria there is no evidence of pocketing or
attachment loss
• Charecerstic feature of this lesion is it doesnot respond
well to improved oral hygiene

49. TREATMENT
• Prominent feature is it does not respond to the plaque
control.
• Conventional therapy plus rinsing with 0.12%
chlorhexidine gluconate twice daily has shown significant
improvement after treatment in HIV uninfected patients
• However HIV associated free gingival erythema did not
respond to removal of plaque by intense scaling and root
planing and improved plaque control alone or
supplimented with povidine – iodine

50. Necrotizing ulcerative periodontitis
• Necrosis and ulceration of the coronal portion of
interdental papillae and gingiva margin.
• Painful bright red marginal gingiva that bleeds easily.
• Deep interdental osseous craters typical periodontal
lesions of NUP.
• Advanced lesions lead to severe bone loss, tooth mobility
and ultimately tooth loss.
• The periodontal attachment and bone loss is extremly
rapid.

52. Necrotizing ulcerative gingivitis
• NUG is characterized by sudden onset of symptoms
• Lesions are punched out, crater like depressions at the crest
of interdental papillae, extending to the marginal gingiva and
rarely to the attached gingiva and oral mucosa.
• The surface of gingival craters is covered by a gray,
pseudomembranous slough demarcated from the remainder of
gingival mucosa by a pronounced linear erythema.

54. TREATMENT
• Basic treatment may consists of cleaning and
debridement of affected areas with a cotton pellet soaked
in peroxide after application of a topical anaesthetic.
• An antimicrobial oral rinse such as chlorhexidine
gluconate 0.12% given.
• Systemic antibiotics such as metronidazole or amoxicillin
given for patients with moderate to severe tissue
destruction.

55. HERPES SIMPLEX VIRUS
INFECTION:
 Clinically seen as vesicles on lip and adjacent
facial skin which rapidly break down to produce
shallow ulcers.
 Lesions on gingival, referred as Acute Herpetic
Gingivostomatitis are seen.
 Lesions can be treated using acyclovir.

57. Aphthous ulcers
• In HIV-infected patients, these ulcers are large and more
extensive usually measure more than 2cm in diameter
with regular borders.
• It is characterised by development of painful,
recurring solitary or multiple ulcerations of oral
mucosa.
• The apthous ulcer begins as a single or multiple
superficial erosions covered by a grey membrane .
• It has a well circumscribed margin surrounded by an
erythematous halo.

59. Chronic periodontitis
• It has been defined as an infectious disease resulting in
inflammation of the supporting tissues of the teeth,
progressive attachment and bone loss.
Clinical findings
• supragingival and subgingival accumulation
• gingival inflammation
• pocket formation
• loss of periodontal attachment
• loss of alveolar bone
• occasional suppuration.
• Gingival recession and early attachment loss are more
common in HIV groups.

60. Treatment
• Treatment decisions should be based on the overall
Health
Status of the patient
Degree of potential involvement
 With proper home care and appropriate periodontal
treatment and maintainance, HIV positive individuals
can anticipate reasonably good periodontal health
throughout the course of their disease.

61. Treatment
• The Food and Drug Administration (FDA) has approved a
number of drugs for treating HIV infection.
• The first group of drugs used to treat HIV infection,
called nucleoside reverse transcriptase (RT) inhibitors,
interrupts an early stage of the virus making copies of
itself.

62. IF MOTHER IS HIV POSITIVE
MOTHER
• First 14 to 34 weeks Azathioprine has to be taken
• Later HAART is prescribed
INFANT
• Baby should take an antiretroviral drug called
ZIDOVIDINE syrup for 6 weeks after birth.
• After 6 weeks TRIMETHOPRIM OR SULPHAMETHEZOLE
(SEPTRA) for 6 weeks.

63. HIV VACCINES
There are three types of vaccines:
Preventive: to protect against those people who are not
already HIV positive
Therapeutic: to stimulate the immune system in HIV
positive individuals and prevent progression to AIDS.
Prenatal: to prevent spread to the fetus in a pregnant
woman.

64. Highly Active Antiretrovial Therapy (HAART)
Fusion Inhibitor
Nucleoside Analogs/ Nuceloside Reverse
Transcriptase Inhibitors
Non Nucleotide Reverse Transcriptase Inhibitors
Protease Inhibitors

65. Nucleoside
Analogs/
Nuceloside
Reverse
Transcripta
se
Inhibitors
Nucelotide
Reverse
Transcripta
se
Inhibitors
Protease
inhibitors
Non-
Nuceloside
Reverse
Transcripta
se
Inhibitors
Zidovudine
Didanosine
Stavudine
Lamivudine
Adefovir
Tenofovir
Saquinavir
Ritonavir
Indinavir
Nelfinavir
Nevirapine
Delaviradine
Efavirenz

66. The class of drugs, called nucleoside analogs, include
• Zidovidine – 500mg / day in 2 to 4 divided doses
• Didanosine – 200 mg twice daily
• stavudine - 400mg twice daily
• Lamivudine – 150 mg once daily for HIV

67. • The drugs called protease inhibitors, interrupt the virus
from making copies of itself at a later step in its life cycle.
They include
• Ritonavir – 600 mg twice daily
• Indinavir – 800 mg thrice daily
• Nelfinavir – 750 mg thrice daily

68. Conclusion