this ppt describes about oral manifestations of HiV. classification of orofacial lesions associated with hiv are discussed in details

2.  Acquired immunodeficiency is caused by human
immunodeficiency virus (HIV) & is characterized by
immunosuppression, which leads to a spectrum of
clinical manifestations like oppurtunistic infections,
secondary neoplasms & neurologic manifestations.
 HIV-1  AIDs in central Africa & rest of world
 HIV-2  AIDs in India & west Africa

4. HIV is an RNA retrovirus
Virus envelop & has an Numerous
external spikes formed by
glycoproteins-120 & glycoprotein-41,
Inner core with 2 component
proteins P18,P24
 Enzyme reverse transcriptase
capable of retrograde transcription
of viral RNA to viral DNA

5.  HIV infection initially may be asymptomatic or an acute
response may be seen.
 develops within I to 6 weeks after exposure in 50% to 70% of
infected patients.
 The symptoms bear some resemblance to those of infectious
mononucleosis (e.g.. generalized lymphadenopathy. Sore throat ,
fever, maculo-papular rash, headache, myalgia, arthralgia,
diarrhea, photophobia, peripheral neuropathies).
 Oral changes may include mucosal erythema and focal
ulcerations.

6.  In some patients (before development of overt AIDS).
there is a period of chronic fever. weight loss. diarrhea.
oral candidiasis, herpes zoster, and /or oral hairy
leukoplakia. This has been termed AIDS- related
complex (ARC).
 Eventually, the immune function ceases, resulting in
advanced HIV infection.
 Characterized by a CD4 cell count of <50 cells/mm3,
overwhelming oppurtunistic infections & death.

8.  Most common intra oral manifestation of HIV infection
and often is the presenting sign that leads to the initial
diagnosis.
 Approximately one third of HlV- Infected individuals and
more than 90% of patients with AIDS develop oral
candidiasis at some time during their disease course.
 The following four clinical patterns are seen;
• Pseudo-membranous
• Erythematous
• Angular cheilitis

9.  Erythematous candidiasis presents as a red, flat,
atrophic lesion on the dorsal surface of the tongue or on
the hard or soft palates.
 The condition tends to be symptomatic, with patients
complaining of oral burning, most frequently while
eating salty or spicy foods or drinking acidic beverages.
 Erythematous candidiasis
form is more prevalent
among HIV patiens than in
general population

10.  Pseudomembranous candidiasis presents as painless
creamy white plaque-like lesions on the tongue,
palate, buccal mucosa, or oropharynx and is
frequently asymptomatic.
 The plaques can be wiped away, typically leaving a red
or bleeding underlying surface.

11.  Angular cheilitis can occur with or without
erytematous or pseudomembranous candidiasis.
 It presents as painful erythema, fissuring or erosion of
the corners of the mouth covered with fine scale

13.  Periodontal diseases are a group of diseases that affect
periodontal tissues.
 Periodontal disease associated with HIV are classified:
Linear gingival erythema or marginal gingivitis,
Necrotizing ulcerative disease,
Necrotising stomatitis

14.  Distinct fiery red band along the
margin of the gingiva, most
frequently found in anterior
teeth, accompanied in some
cases by bleeding and
discomfort.
 The aetiology of this oral disease
seems to involve an invasion by
Candida species of the gingival
tissue .
 It manifests in
imunocompromised patients
with CD4+ T lymphocyte counts
<200 cells/mm3

15.  Necrotising ulcerative
disease (NUD)
1. necrotising ulcerative
gingivitis (NUG)
2. necrotising ulcerative
periodontitis (NUP).
 NUG is characterized by
rapid onset and acute
painful inflammation of
gingiva with rapid
destruction of soft tissues.

16.  Necrotising ulcerative periodontitis NUP is escorted by
bleeding,
extremely sharp pain,
ulcerated gingival papillae,
rapid and extensive soft tissue necrosis and
advanced loss of periodontal attachment,
frequently leading to bone exposure, and crater shaped
defects, sequestration of a significant piece of alveolar
bone

17.  In patients with gingival necrosis, the process occasionally
extends away from the alveolar ridges and creates massive areas
of tissue destruction termed necrotizing stomatitis.
 May involve predominantly
soft tissue or extend into the
underlying bone, resulting in
extensive sequestration
 Although this process initially
was thought to be an extension
of NUP, necrotizing stomatitis
has arisen on the oral mucosa
separate from the gingiva
(not overlying bone),

18.  most common EBV-related lesion in
patients with AIDS.
 Has a somewhat distinctive (but not diagnostic) pattern of
hyperkeratosis and epithelial hyperplasia that is characterized by white
mucosal lesions that do not rub off .
 Most cases of OHL occur on the lateral border of the tongue and range
in appearance from faint white vertical streaks to thickened and
furrowed areas of leukoplakia, exhibiting a shaggy keratotic surface.
 The lesions may become extensive and cover the entire dorsal and
lateral surfaces of the tongue.
 Rarely, involvement also has been observed on the buccal mucosa, Soft
palate, pharynx, or esophagus.

19.  Histopathologically, OHL exhibits thickened parakeratin, which
demonstrates surface corrugations or thin projections.
 The epithelium is hyperplastic and contains a patchy band of
lightly stained "ba lloon cells" in the upper spinous layer .
 Close examination of the superficial epithelium reveals scattered
cells with nuclear clearing and a characteristic pattern of
peripheral margination of chromatin termed nuclear beading.
 The nuclear alterations are created by extensive EBV replication
that displaces the chromatin to the nuclear margin.
 Dysplasia is not noted.
 Heavy candidal infestation of the parakeratin layer is typical, and
the normal inflammatory reaction to the fungus usually is
absent.

21.  KS is a multi focal neoplasm of vascular
endothelial cell origin.
 most cases have been seen in association with AIDS.
 Human herpes virus type 8(HHV-8) is noted within the
tumor and thought to be involved in the neoplasm's
development.
 KS begins with single or, more frequently multiple lesions
of the skin or oral mucosa .
 The trunk, arms, head, and neck are the most commonly
involved anatomic sites

22.  Oral lesions are seen in approximately 50% of affected patients
and are the initial site of involvement in 20% to 25%.
 Although any mucosal site may be involved, the hard palate,
gingiva, and tongue are affected most frequently.
 When present on the palate or gingiva , the neoplasm can invade
bone and create tooth mobility.
 The lesions begin as flat, brown or reddish purple zones of
discoloration that do not blanch with pressure.
 With time, the involved areas may develop in to plaques or
nodules.
 Pain, bleeding , and necrosis may become a problem and
necessitate therapy

24.  Definitive diagnosis requires biopsy.
 Treatment ranges from localized injections of chemo
therapeutic agents, such as vinblastine sulfate, to
surgical removal.
 Oral hygiene must be stressed.
 Systemic chemotherapy may be the treatment of
choice for patients with extraoral and intraoral
Kaposi’s sarcoma.

25.  Lymphoma in patients with AIDS is typically exhibited in
extranodal locations, with the CNS being the most
common site.
 Oral lesions may occur and most often present as a soft
tissue enlargement of the palate, gingiva, tongue, tonsils or
maxillary sinus.
 Intraosseous involvement also has been documented, and
it may resemble diffuse progressive periodontitis with loss
of periodontal attachment and loosening of teeth.
 In these cases, widening of the periodontal ligament and
loss of lamina dura frequently are noted and represent
clues to the diagnosis.

26.  The treatment usually is
combination
chemotherapy, and
radiation is reserved for
local control of the
disease.
 These malignancies are
aggressive, and survival
usually is measured in
months from the date of
discovery

27.  Herpes simplex virus (HSV)-1 infection is widespread and oral
lesions are common.
 start as a small crop of vesicles that rupture to produce small,
painful ulcerations that may coalesce.
 Lesions usually erupt on lips and
keratinized tissues, including the
hard palate and gums
 Herpetic ulcerations are often self
limiting, although the use of an
antiviral medication such as
acyclovir is sometimes necessary
to control the outbreak.

28.  Contact with the varicella-zoster virus (VZV) may result in
varicella (chicken pox) as a primary infection and herpes
zoster (shingles) as a reactivated infection.
 Herpes zoster infection of the oropharyrngeal regions
results from reactivation of latent VZV, harbored in the
trigeminal nerve, in response to immune deterioration.
 Multiple dermatomes might be involved or herpetic lesions
might get secondarily infected.
 The lesions are usually associated with severe postherpetic
neuralgia

29.  An increased prevalence of HPV-related lesions is
noted in HIV- infected patients, and most are located
in the anogenital areas.
 Oral involvement also may be seen.
 Although usual types of HPV may be present in
intraoral lesions, HIV-infected patients often
demonstrate more unusual variants such as HPV- 7 or
HPV-32

30.  The oral lesions usually
are multiple and may be
located on any mucosal
surface.
 The labial mucosa,
tongue, buccal mucosa,
and gingiva are frequent
sites.
 The lesions may exhibit a
cluster of white, spikelike
projections, pink
cauliflower- like growths,
or slightly elevated
sessile papules

31.  Histopathologically, the
lesions may be sessile or
papillary and covered by
acanthotic or
hyperplastic stratified
squamous epithelium.
 The affected epithelium
often demonstrates
vacuolization of
numerous epithelial cells
(koilocytosis) and
occasionally may exhibit
mild variation in nuclear
size

32.  Immunohistochemistry or DNA in situ hybridization
often is used to confirm the presence and type of HPV
with in histopathologic specimens.
 Dysplasia has been noted within HPV-related lesions
in patients with AIDS and mandates close observation
of affected patients for development of squamous cell
carcinoma.
 The treatment of choice is surgical removal; however,
recurrences are common, especially in patients with
significant immune deficiency.

33.  Hyper-pigmentation of the skin, nails, and mucosa has
been reported in HIV-infected patients.
 The changes are similar microscopically to focal melanosis
with increased melanin pigmentation observed in the basal
cell layer of the affected epithelium.
 Reasons for intra-oral pigmentation include:
 Increased release of α melanocyte-stimulating hormone
caused by deregulation of cytokines in HIV disease;
 Use of melanocyte-stimulating drugs; antiretrovirals,
antifungals and
 Addison's disease

34.  Clinically results in gland enlargement and diminished
flow of secretions.
 The enlargement typically involves the tail of the parotid
gland or, less commonly, the submandibular gland,
 May present uni- or bilaterally with periods of increased or
decreased size.
 Patients suffer from reduced salivary flow and mouth
dryness.
 Histologically, there may be lymphoepithelial infiltration
and benign cyst formation

35.  Reported in nearly 10% of patients with HIV infection and
may occur at any time during the course of the disease.
 Characterized by reduced production of platelets due to
drugs, malnutrition, immunologic alterations, microbial
invasion or due to course of HIV disease.
 Cutaneous lesions are present in most cases, but oral
lesions do occur with petechiae, ecchymosis, or
spontaneous gingival hemorrhage.
 Platelet transfusion or corticosteroid therapy

36.  Histoplasmosis is the most common, with disseminated
disease noted in approximately 5% of AIDS patients
residing in areas where the fungus is endemic.
 signs and symptoms associated with dissemination are non
specific and include fever, weight loss, splenomegaly, and
pulmonary infiltrates.
 Oral lesions are not uncommon and usually are caused by
blood borne organisms or spread from pulmonary
involvement.

37.  the most common oral
presentation of
histoplasmosis is a
chronic, indurated
mucosal ulceration with
a raised border.
 The oral lesions may be
singular or multiple and
any area of the oral
mucosa may be Involved.

38.  Microscopically, the small
fungal organisms are
visible within the
cytoplasm of histiocytes
and multinucleated giant
cell s.
 These phagocytic cells may
be present in sheets or in
organized granulomas
The therapy of choice for disseminated histoplasmosis has been
intravenous amphotericin B. but itraconazole has been shown to be
effective with fewer adverse reactions and better patient compliance.
Ketoconazole is another alternative.

39.  Molluscum contagiosum is
an infection of the skin
caused by a poxvirus.
 The lesions are small, waxy,
dome-shaped papules that
often demonstrate a central
depressed crater.
 Approximately 5% to 10%
of HIV-infected patients
are affected and the facial
skin commonly is involved

40.  Histopathologically, the surface
epithelium forms several
hyperplastic downgrowths.
 This involuting epithelium
contains numerous large,
intracytoplasmic inclusions
known as molluscum bodies.
 In the center of the lesion, the
keratin layer often disintegrates
and releases the adjacent
molluscum bodies, hence the
central crater.
Local therapy (e.g.. curettage. cryosurgery , cautery) usually is
painful and often disappointing because of frequent
recurrences.

41.  Lesions that are similar clinically
to apthous ulcerations occur
with increased frequency in
patients infected with HIV.
 All three forms (minor, major,
and herpetiform) are seen
 however, almost two third s of
the patients have the usually
uncommon herpetiform and
major variants
Treatment with potent topical or intralesional corticosteroids has
been successful in a number of patients.
Not all lesions respond. and recurrences are common.

42.  SCC of the oral cavity,
pharynx, and larynx has been
reported in HIV-infected
patients.
 These neoplasms are
associated with the same
cancer risk factors as the
general population but tend
to occur at a younger age.
 Surgical resection, radiation
therapy or combined
radiation and chemotherapy

43.  Initial regimens consist of two nucleoside reverse
transcriptase inhibitors and one or two protease inhibitors,
 Alternatively. two nucleoside reverse transcriptase
inhibitors and a nonnucleoside reverse transcriptase
inhibitor can be used
 Although no cure exists, survival times are increasing as a
result of earlier diagnosis and improved therapy.
 THE BEST DEFENSE AGAINST THE DISEASE IS
PREVENTION OF THE INITIAL INFECTION.