Good Morning

AIDS AND PERIODONTIUM

GUIDED BY:Dr. M.B. Mishra
Dr. Devraj C. G.
Dr. Pratibha Anand Nayak
Dr. Setu Mathur
Dr. Ashish Yadav
Dr. Swati sharma

PRESENTED BY
Shrishtee Pal
Final year

CONTENTS
Introduction
Structure of HIV
Classification
Oral and periodontal
manifestation of HIV
infection
Gingival and periodontal
diseases
Dental treatment
complications
Periodontal treatment
protocol

AIDS
Acquired immunodeficiency syndrome
Caused by Human
Immunodeficiency virus
(HIV)
Characterized by
profound impairment of
immune system.

HISTORY AND ORIGIN

HIV originated in West-central

Africa during the late
nineteenth or early twentieth
century.
1st reported in the year 1981
(June 5)

STRUCTURE OF HIV
VIRUS

It is a retrovirus
with two copies of
single stranded
RNA enclosed by a
conical caspid
comprising the viral
protien p24.

The single-strand
RNA is tightly
bound to
thenucleocapsidp
roteins,p10
andenzymesthat
are indispensable
for the

A matrix composed of an
association of the viral
protien p17 surrounds the
caspid, ensuring the
integrity of the virion
particle.
The envolope is formed
when the caspid buds from
the host cell, taking some of
the host- cell membrane with
it. The envolope includes the
glycoprotiens gp120 and

GENOME OF HIV

HIV TROPISM

HIV tropism refers to the cell type

that the HIV infects and replicates
in. HIV tropism of a patients virus is
measured by the TROFILE ASSAY.

HIV can infect a variety

ofcellssuch asCD4+ helper Tcellsandmacrophagesthat express
theCD4molecule on their surface.
HIV-1 entry to macrophages and T
helper cells is mediated not only
through interaction of the virion
envelope glycoproteins (gp120) with

 Macrophage

(M-tropic) strains of HIV-1

use the beta-chemokine receptorCCR5for
entry and are thus able to replicate in
macrophages and CD4+ T-cells. These
strains are now called R5 viruses.
T-tropic isolates strains replicate in
primary CD4+ T-cells as well as in
macrophages and use the alphachemokine receptor,CXCR4, for entry.
These strains are now called X4 viruses.

REPLICATION
AND
TRANSCRIPTION

ASSEMBLY AND RELEASE

The Env polyprotein (gp160) goes
through theendoplasmic reticulum
and is transported to
theGolgicomplex where it is cleaved
byproteaseand processed into the
two HIV envelope glycoproteins gp41
and gp120. These are transported to
theplasma membrane of the host cell
where gp41 anchors the gp120 to the
membrane of the infected cell.
The Gag and Gag-Pol polyproteins
also associate with the inner surface
of the plasma membrane along with

During maturation, HIV proteases

cleave the polyproteins into
individual functional HIV proteins
and enzymes. The various structural
components then assemble to
produce a mature HIV virion. The
mature virus is then able to infect
another cell.

PATHOPHYSIOLOGY
HIV causes AIDS by depleting CD4+T helper
lymphocytes.
The mechanism of CD4+T cell depletion differs in
the acute and chronic phases.
During the acute phase, HIV-induced cell lysis and
killing of infected cells bycytotoxic Tcells which
accounts for CD4+T cell depletion,
althoughapoptosismay also be a factor.
During the chronic phase, the consequences of
generalized immune activation coupled with the
gradual loss of the ability of the immune system
to generate new T cells appear to account for the
slow decline in CD4+T cell numbers.

CELLS EFFECTED BY HIV:

Thevirus entering through which ever route,
acts primarily on the following cells:
Lymphoreticular system
CD4+T-Helper cells
Macrophages
Monocytes
B-lymphocytes
Certainendothelial cells
Central nervous system:
Microgliaof the nervous system
Astrocytes
Oligodendrocytes
Neurons indirectly by the action
ofcytokinesand thegp-120

Overview of Infection
The viral load is kept at
a steady state; half life
for infected cells is
roughly 1.5 days.
In addition to these lytic
cells, there are small
numbers of latent cells
that can persist for long
periods of time.
Diagnosis for AIDS
includes finding the HIV
virus in the patient,
<200 TH cells/mm3,

 Normal CD4 : CD8 is 1.5-2 and it get

reversed in AIDS.
B-cell dysregulation and altered
neutrophil function.
Increase risk of malignancy and
disseminated infections.
Increased risk of adverse drug reaction.
Epithelial cells of mucosa may become
infected.

Access of virus into blood stream.

Oral transmucosal viral transmission
after mild or severe traumatic injury
or puncture of mucous membranes.
Infection of circulatory host defense
cells.
HIV has been detected in most body
fluids.
High quantities only in blood,
semen, cerebrospinal fluid.

CLASSIFICATION
In developing countries, theWorld Health
Organizationstaging system for HIV
infection and disease, using clinical and
laboratory data, is used.

In developed countries, theCenters for

Disease Control (CDC) Classification System
is used.

WORLD HEALTH ORGANISATION

CLASSIFICATION :
Stage I :
and is not

HIV infection is asymptomatic

categorized as AIDS.

Stage II : Includes minor mucocutaneous

manifestations
and recurrent upper respiratory
tract infections.
Stage III : Includes unexplained chronic
diarrhea for
longer than a month, severe
bacterial infections
and pulmonary tuberculosis.

CDC surveillance case classification:

Category A

Category B

Category C

includes
patients with
acute
symptoms or
asymptomatic
disease,
along with
individual
with
persistent
generalized
lymphadenop
athy with or
without
malaise,
fatigue or low
grade fever.

patient have
symptomatic
condition,
such as
oropharyngea
l or
vulvovaginal
candidiasis,
herpes zoster,
oral hairy
leukoplakia,
idiopathic
thrombocytop
enia, or
constitutional
symptoms of
fever,
diarrhea, and
weight loss.

patients are
those with
outright AIDS,
as manifested
by life
threatening
conditions or
identified
through CD4
+T
lymphocytes
level < 200
cells/cubic
mm.

SHARING
NEEDLES WITH
INFECTED
PERSON

SEXUAL
TRANSMISSION

CAUSES
TRANSMISSION
FROM INFECTED
MOTHER TO
FETUS

INFECTION
FROM BLOOD
PRODUCTS

HIGH RISK POPULATION

Homosexual and bisexual
men
User of illegal injection
drugs
Persons with hemophilia or
other coagulation disorders
Recipient of blood
transfusion before 1985
Infants of HIV-infected
mother
Promiscuous heterosexuals
Individual who engage in

Estimated per act risk for acquisition of HIV by

exposure route (US only) :
Exposure route

Estimated chance of
infection

Sexual intercourse

90%

Blood transfusion

80%

Childbirth

25%

Needle- sharing injection drug 0.067%

use

MAIN SIGN AND SYMPTOMS

TESTING FOR HIV

Enzyme-linked immunosorbent
assay (ELISA).
Western blot.
Indirect fluorescent antibody
(IFA).
Polymerase Chain Reaction
(PCR).

MANAGEMENT
ANTI VIRAL THERAPY :
HAART

Abacavir- a
nucleoside analog
reverse
transcriptase
inhibitor

The
chemical
structure of
Abacavir

ORAL AND PERIODONTAL

MANIFESTAIONS OF HIV
INFECTION
Oral Candidiasis
Oral Hairy Leukoplakia
Kaposis Sarcoma and
Other Malignancies
Bacillary (epitheloid)
Angimatosis
Oral Hyperpigmentation
Atypical Ulcers

ORAL CANDIDIASIS
Most common oral lesion in
HIV disease
Candida- fungus (C.albicansmost common)
Diminished host resistancedebilitated patients or in
patients receiving
immunosuppressive therapy
4 clinical presentations:
pseudomembranous,
erthymatous, hyperplastic,
angular cheilitis

PSEUDOMEMBRANOUS CANDIDIASIS
(THRUSH)
Painless or slightly
sensitive, yellow-white
curd like lesion, can be
scraped and separated
from surface of oral
mucosa
Hard palate, soft palate,
buccal or labial mucosacommon.
ERYTHMATOUS CANDIDIASIS
Red patches on buccal or
palatal mucosa
Depapillation of the tongue

HYPERPLASTIC CANDIDIASIS
Least common form.
Buccal mucosa and tongue
More resistant to removal

ANGULAR CHELITIS
Commissures of lips
appear erythmatous with
surface crusting and
fissuring.

COMMON ANTIFUNGAL THERAPEUATIC

AGENTS FOR ORAL CANDIDIASIS
TOPICAL DRUGS
1. Clotrimazole tablets
2. Nystatin
3. Clotrimazole ointment
4. Miconazole 2% ointment
5. Itraconazole oral suspension
6. Fluconazole oral suspension
7. Amphotericin B oral suspension
SYSTEMIC DRUGS
8. Ketoconazole
9. Fluconazole
10.Itraconazole

ORAL HAIRY LEUKOPLAKIA

Exclusively on lateral border of
tongue
Sometimes on dorsum of tongue,
buccal mucosa, floor of mouth,
retromolar area, soft palate
Bilateral distribution
Asymptomatic, poorly demarcated
keratotic area
Vertical striations imparting
corrugated appearance or the
surface may be shaggy and appear
hairy when dried

 Treatment- antiviral drug, laser or

conventional surgery ,topical
application of podophyllin,
retinoids or intereferon.

KAPOSIS SARCOMA AND OTHER

MALIGNANCIES

Kaposis sarcoma
Non-Hodgkins
lymphoma
Oral squamous cell
carcinoma

KAPOSIS SARCOMA:
Most common oral
malignancy associated
with AIDS.
Palate and gingiva
Early lesion- painless,
reddish, purple macule
Later- nodule, papule
or nonelevated macule
Male: Female- 20:1
Human herpesvirus-8

 T/t- antiretroviral agents, laser

excision, cryotherapy, radiation
therapy, interlesional injection
with vinblastin, interferonalpha, sclerosing agents,
chemotherupatic drugs

BACILLARY (EPITHELIOID)
ANGIOMATOSIS
Infectious vascular
proliferative disease
Clinically and
histologically similar to
KS
Believed to be caused by
rickettsia-like organism
Red, purple, blue
edematous soft tissue
lesion
Cause destruction of pdl
and bone

 T/t- broad spectrum

antibiotics
conservative
periodontal therapy
excision of lesion

ORAL HYPERPIGMENTATION
Spot or striation on
buccal mucosa, palate,
gingiva, tongue
Prolonged use of
drugs- zidovudine,
ketoconazole,
clofazimine
Adrenocorticoid
insufficiency
prolonged use of
ketoconazole or by
pneumocystic carinii,

ATYPICAL
ULCERS
Multiple
etiologies-Neoplasms- lymphoma, KS,
squamous cell
carcinoma
- Bacterial- Klebsiella pneumoniae,
Enterobactor cloacae, E. coli
- Viral- Herpes simplex virus,
varicella-zoster virus, Epstein barr
virus, cytomegalovirus
-HIV-associated neutropenia
Atypical, large, nonspecific, painful
ulcers

HERPETIC LESION

Involve all mucosal

surface and extend to
the skin
Persist for months
T/t- topical or systemic
antiviral drug

RECURRENT APTHOUS STOMATITIS

Increased incidence
May involve oropharynx,
esophagus, or other
area of gastrointestinal
tract
T/t- topical or
intralesional
corticosteriods,
chlorhexidine or other
antimicrobial mouth
rinses, oral tetracycline
rinses, topical
amlexanox

GINGIVAL AND PERIODONTAL DISEASES

LINEAR GINGIVAL ERYTHEMA
A persistent, linear, easily
bleeding, erythematous
gingivitis
Localized or genralized
i.
may be limited to
marginal tissue
ii. May extent into attached
gingiva in a punctate or
diffuse erythema
iii. May extent into alveolar
mucosa

T/t- Affected site scaled

and polished, subgingival
irrigation with
chlorhexidine or 10%
povidine iodine
If associated with candida
infection-antifungal agents

NECROTIZING ULCERATIVE GINGIVITIS

Caused by fusiform bacillus
and borellia vincentii
Affected gingiva may be
exquisitely painful

 Basic treatment- cleaning and

debridement of affected area with
a cotton pellet soaked in peroxide
after application of local anesthetic
Escharotic oral rinses such as
hydrogen peroxide- rarely used
Seen daily or every other day for
1st week
After initial healing- scaling and
root planning
Chlorehexidine gluconate 0.12%
oral rinse
Systemic antibiotics- for moderate
to severe tissue destruction,
localized lymphadenopathy

NECROTIZING ULCERATIVE PERIODONTITIS

Extension of NUG in
which bone loss and
periodontal attachment
loss occur
Soft tissue necrosis,
rapid periodontal
destruction and
interproximal bone loss
Usually localized,
generalized when
marked reduction in
CD4 + cell depletion

 T/t- local debridement,

scaling and root planing, inoffice irrigation with
antimicrobial agent,
establish meticulous oral
hygiene
In severe cases- antibiotic
therapy with prophylactic
topical or systemic
antifungal agent

NECROTIZING ULCERATIVE STOMATITIS

Severely destructive
and acutely painful
Affect significant area
of soft tissue and
underlying bone.
Occur separately or
as an extension of
NUP
Often associated with
severe suppression of
CD4 immune cells

 T/t- antibiotic and

antimicrobial mouth rinse
If osseous necrosis- remove
affected bone to promote
healing

CHRONIC PERIODONTITIS
Gingival recession and early
attachment loss- more in HIV
groups.
HIV infected patients are
potential candidates for
conventional periodontal
treatment procedure to include
periodontal surgery and implant
placement.
Treatment decision should be
based on overall health status of
the patient, the degree of
periodontal involvement and the
motivation and ability of patient
to perform effective oral hygiene.

DENTAL TREATMENT COMPLICATIONS

ADVERSE DRUG EFFECT
Foscarnet, interferon, 2-3-dideoxycytidine
(DDC)- oral ulceration
Didanosine- erythma multiforme
Zidovudine, ganciclovir- leukoplakia
Drug induced mucositis, lichenoid drug
reaction
HAART drugs- mild conditions or kidney stones,
increased insulin resistance, gynecomastia,
toxic epidermal necrolysis, blood dyscarasias,
oral wart
Hepatitis and HIV co-infection- liver cirrhosis
Lipodystrophy
Perioral adverse effect- xerostomia, altered
taste sensation, perioral paresthesia,
exfoliative cheilitis.

PERIODONTAL TREATMENT PROTOCOL

Health status
Infection control measures
Goal of therapy
Maintenance therapy
Psychological factors

HEALTH STATUS
Health history, physical evaluation, and
consultation with patients physician.
Important information regarding patients
immune status
- CD4+ T4 lymphocyte level
- Current viral load
- Difference in current and previous CD4+ T4
cell and viral load count
- Duration of HIV infection
- History of drug abuse, sexually transmitted
diseases, multiple infections, other factors
- Medication
- Adverse side effects from medication

INFECTION CONTROL MEASURES

Based on guidance from
American Dental association
(ADA) and CDC
Universal precaution
Immunocompromised
patients are potentially at
risk of acquiring as well as
transmitting infection.
Double barrier technique.

GOAL OF THERAPY
Primary goal- restoration
and maintenance of oral
health, comfort and function
Acute periodontal and
dental infections should be
managed
Conservative, nonsurgical
periodontal therapy should
be treatment option

MAINTENANCE THERAPY
Patient should maintain
meticulous personal oral
hygiene
Periodontal maintenance
recall visits at short
intervals (2-3 months)
Progressive periodontal
disease treated vigorously.
Systemic antibiotic therapy
should be administered with
caution.

PYSCHOLOGICAL FACTORS
HIV infection of neuronal cells
may affect brain function and
lead to outright dementia.
Psychological factors are
numerous even in the
absence of neuronal lesions.
Maintenance of medical
confidentiality
Display concern and
understanding for patients
situation
Treatment should be provided

CONCLUSION
As the virus spreads the
immune system gets
weakened. Thus how the
immunity is compromised
and gets more prone to
oppurtunistic infections.
AIDS also effects the
periodontium n leads to
gingival and periodontal
destruction.

Thank you

Know Aids - No Aidsroad sign inSpiti

Valley,Himachel Pradesh, India, 2010