HIV/AIDS
Oral lesions
• EC clearinghouse on oral problems related to HIV
infection & the WHO collaborating center
classification (1995)
• Presumptive criteria : relate to the initial clinical
appearance of the lesion.
• Definitive criteria : they are the result of special
investigations for absolute diagnosis.
• These two added give the diagnostic criteria of the
oral manifestation of HIV infection.
Classification of Oral Conditions by Degree of
Immune Suppression (ODHIS)
< 500 CD4+ count
Erythematous candidiasis
Oral Hairy Leukoplakia
Hyposalivation
Linear gingival
erythema (LGE)
Human papilloma
virus (HPV)
< 200 CD4+ count
Hyperplastic candidiasis
Major aphthous ulcers
Chronic HSV
Necrotizing ulcerative
periodontitis (NUP)
Histoplasmosis
ORAL CANDIDIASIS
• Most common intraoral
opportunistic fungal infection in
HIV infection.
• 4 clinical presentations:
Pseudomembranous candidiasis :
• White to yellowish white plaques
which can be easily scraped off,
exposing red areas.
• Usually extensive involving more
than 1 site.
• May involve oropharynx &
oesophagus.
• Erythematous candidiasis:
• Red lesions commonly
located on the dorsum of
the tongue, palate &
buccal mucosa.
• Tongue lesions are also
c/as central papillary
atrophy.
Hyperplastic candidiasis :
• White plaques which
cannot be removed by
scrapping.
• Diagnosis is through
biopsy & response to
anti fungal treatment
• Angular cheilitis
• Erythema/
fissuring/scaling of
angles of the mouth.
• It can be due to :
• candida albicans &
staphylococcus
aureus
• staphylococcus
aureus alone.
• candida albicans
alone.
Significance of oral candidiasis in HIV infection
1. It may be the 1st of the earliest observable clinical feature of
HIV infection.
2. Lesions of oral candidiasis are highly prevalent in HIV infected
& other clinical populations & have a variety of clinical
appearances so thoughtful diagnosis is required.
3. Oral candidiasis in HIV infection patients is painful & chronic &
may become resistant to available drugs so initial treatment
should be followed by regular clinical recalls.
Diagnosis
• - clinical appearance.
• - biopsy : PAS staining for candidal hyphae.
• - culture on sabouraud’s agar.
Treatment
• Topical antifungal agents : nystatin or clotrimazole.
• Systemic antifungal agents : flucanozole or itraconazole.
Periodontal lesions
• 3 patterns of PD diseases are strongly associated with HIV
infection.
• Linear gingival erythema
• Necrotizing ulcerative gingivitis
• Necrotizing ulcerative periodontitis
Linear gingival erythema
• Distinctive linear band of
erythema that involves the
free gingival margin &
extends 2-3mm apically.
• Gingiva & alveolar mucosa
may show punctate or diffuse
erythema.
• Does not respond to
improved plaque control.
• Exhibits greater degree of
erythema expected for the
amount of plaque.
Treatment:
• In many instances, it resolves after professional plaque
removal, improved oral hygiene & use of CHx
• Cases resistant to initial therapy respond to systemic
antifungal medications – flucanozole/ ketoconazole.
Necrotizing ulcerative gingivitis ( NUG)
• Ulceration & necrosis of one
or more interdental papillae
with no loss of PD
attachment.
• Interproximal gingival
necrosis, bleeding, pain &
halitosis.
Necrotizing ulcerative periodontitis (NUP)
• Gingival ulceration & necrosis
associated with rapidly
progressing loss of PD
attachment.
• Edema, severe pain &
spontaneous hemorrhage are
common.
• Loss of more than 6mm of
attachment within a 6month
period is not unusual.
• Treatment
• Does not respond to conventional PD therapy.
• Rx of NUG & NUP involves debridement, antimicrobial
therapy, immediate follow up care & long term
maintenance.
• After initial debridement, removal of additional
diseased tissue within 24 hrs.
• 7-10 days follow up for 2-3 appointments, then monthly
recalls, then 3monthly recalls.
Necrotizing stomatitis (NS)
• Massive areas of tissue destruction.
• Involve predominantly soft tissue or extend into the
underlying bone.
• Areas of ulceration & necrosis may show infection with one or
more agents, such as CMV, EBV, HSV.
Herpes simplex virus (HSV)
• Same % in HIV infected patients as in immunocompetent
population i.e 10-15%
• More wide spread, shows an atypical pattern & may persist
for months.
Prevalence increases once the CD4+ count drops below 50.
Persistence of active sites of HSV infection for more than 1month in
a patient with HIV is one accepted definition of AIDS.
Varicella zoster virus (VZV)
• Common in HIV infected
patients.
• More severe with increased
morbidity & mortality.
• Patients are younger than
40 yrs.
• Initially, HZV is confined to a
dermatome but persists
longer than usual.
Ebstein - Barr virus (EBV)
• The most common EBV
associated lesion in AIDS
patient is oral hairy
leukoplakia (OHL).
• Hyperkeratosis & epithelial
hyperplasia characterized by
white mucosal lesions that
do not rub off.
• Faint white vertical streaks to thickened & furrowed areas of
leukoplakia.
• Lesions may become extensive.
• Most commonly seen on lateral border of tongue.
• Histology:
• Thickened parakeratin showing
surface corrugations or thin
projections.
• Epithelium contains a patchy
band of lightly stained “baloon
cells” in the upper spinous
layer.
• Superficial epithelium reveals
scattered cells with nuclear
chromatin & a characteristic
peripheral margination of
chromatin c/as nuclear
beading.
• Created by extensive EBV replication that displaces the
chromatin to the nuclear margin.
• Heavy candidal infestation of parakeratin.
• Normal inflammatory reaction to fungus is absent.
• Diagnosis:
• Clinical features are sufficient for presumptive
diagnosis.
• Definitive diagnosis – demo. Of EBV by in situ
hybridization, PCR, IHC, southern blotting or EM.
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Treatment:
Not needed.
Acyclovir or desiclovir.
Topical Rx with retinoids or podophyllum resin.
Kaposi’s sarcoma (KS)
• Multifocal neoplasm of vascular endothelial cell origin.
• HHV8 is considered to be involved in the tumor
development.
• Begins with single or multiple lesions of the skin or oral
mucosa.
• Most commonly seen on the trunk, arms, head & neck.
• Oral lesions (50%) common on hard palate, gingiva &
tongue.
• Can invade bone & create tooth mobility.
• Lesions begin as flat, brown or reddish purple zones of
discoloration that do not blanch on pressure.
• May develop into plaques or nodules.
• Pain, necrosis & bleeding +/-.
• It’s a progressive malignancy that may disseminate
widely to LN or other organs.
• Diagnosis:
• Presumptive : clinical presentation.
• Definitive : biopsy.
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Treatment :
Usually palliative.
Radiation or systemic chemotherapy.
Oral lesions – intralesional injection of vinblastine,
sclerosing agent.
• Surgical excision, cryotherapy, laser ablation or
electrosurgery.
Aphthous ulceration
• Increased frequency.
• All 3 forms are seen but 2/3rd of the patients usually
have uncommon herpetiform & major variant.
• Increased prevalence as the immunosuppression
becomes profound.
• Biopsy should be considered if the lesion is atypical or
does not respond to therapy.
• Another causes might be revealed like HSV, CMV, deep
fungal infection or neoplasia.
Treatment:
• Potent topical or intralesional CS.
• Recurrences are common.
• Secondary candidiasis may be a complication.
• Systemic CS are avoided.
• Thalidomide for lesions unresponsive to topical CS but
used only for a short term as it enhances the production
of HIV.
Thrombocytopenia
• 10% of HIV infected patients.
• May occur at any time during the
course of the disease.
• Megakaryocytes have CD4
molecules & may be an additional
target for the HIV virus.
• Cutaneous lesions are more
common.
• Oral lesions : petechiae,
ecchymosis or spontaneous
gingival hemorrhage.
HIV associated salivary gland disease.
• 5% of HIV infected patients.
• More common in children.
• Salivary gland enlargement, particularly parotid.
• Bilateral involvement in 60% patients.
• Often associated with cervical lymphadenopathy.
• Xerostomia.
• Diffuse infiltrative lymphocytosis syndrome ( DILS):
• CD8 lymphocytosis & lymphadenopathy along with salivary
gland enlargement.
• Glandular involvement arises from CD8 lymphocytic
infiltration.
• Often followed by lymphoepithelial cyst formation in the
parotid.
Treatment:
• Oral prednisolone or antiretroviral therapy.
• Parotidectomy or radiation therapy.
• Increased risk for B cell lymphoma so monitoring by FNAC is
prudent.
Hyperpigmentation
• Skin, nails & mucosa.
• Similar microscopically to focal melanosis.
• Increased melanin pigmentation seen in basal cell layer of
the affected epithelium.
• Thought to be caused by the medications taken by AIDS
patient like ketoconazole, clofazimine, pyrimethamine,
zidovudine.
• Adrenocortical destruction is seen in AIDS patients.
Lymphoma
• 2nd most common malignancy seen in HIV infected
patients.
• 3% of HIV infected patients.
• Prevalence – 60 times more than seen in normal
population.
• Most common is non hodgkin’s B cell lymphoma.
• May arise from a combination of EBV, antigenic
stimulation & immune dysfuntion.
• Typically exhibited in extranodal
sites, most common in CNS.
• Oral lesions seen as soft tissue
enlargement of the palate or
gingiva.
• Intraosseous involvement
resemble diffuse progressive
periodontitis.
• Widening of PDL & loss of lamina
dura.
Treatment:
• Combined chemotherapy & radiation.
• In aggressive malignancies, survival usually in
months.
• Major cause of morbidity & mortality in HIV
infected patients.
Oral squamous cell carcinoma
• Oral cavity, pharynx & larynx.
• Same clinical presentation & anatomic distribution.
• Associated with same risk factors.
• Younger age.
• Same Rx protocol followed.