Hiv Oral Manifestation

Oral Manifestations of
HIV
Presentation by
Dr.A.Kameswara Rao
P.G.Student
Dept. of Oral pathology & Microbiology
GITAM Dental College & Hospital
Contents :
Introduction
Demographics
Classification of Oral
Manifestations
Individual diseases
Conclusion
Introduction
Acquired immunodeficiency syndrome (AIDS) is an infectious disease caused by the
HIV, and is characterized by profound immunosuppression that leads to opportunistic
infections, secondary neoplasm and neurologic manifestations.
Oral manifestations of HIV infection are important in the AIDS epidemic and some of
them could be used to assess the status of immunosuppression and determine the
prognosis of the disease.
Early diagnosis and appropriate treatment of oral lesions have great influence on
patients general health and can reduce the mortality rate of the disease.
Courtesy : Ashish S. Bodhade. Oral manifestations of HIV infection and their correlation with CD4 count. Journal of Oral Science2011;53(2):203-211,
Introduction
Oral lesions may:
(1) Indicate HIV infection in previously undiagnosed cases
(2) Predict HIV disease progression
(3) Represent early clinical features of clinical AIDS (for example, oral Kaposis
sarcoma)
(4) Form traditional entry or exit determinants for antiretroviral therapy
(5) Be determinants of anti-opportunistic infection therapy
(6) Be used in disease staging and classification
(7) Act as markers of other more subtle mucosal immunodeficiency states often missed
on clinical examination
(8) Lead patients to seek treatment because of pain/discomfort or aesthetic reasons
(9) Individually correlate with CD4 levels in severely immunosuppressed patients
(10) Correlate with CD4 levels when grouped together
(11) Act as cofactors affecting the rate of HIV disease progression.
Courtesy : Iain L C Chapple, John Hamburger. The significance of oral health in HIV disease. Sex Transm Inf 2000;76:236243.
Demographics
Since the beginning of the epidemic, almost 78 million people have been infected with
the HIV virus and about 39 million people have died of HIV.
Globally, 35.0 million [33.237.2 million] people were living with HIV at the end of
2013.
An estimated 0.8% of adults aged 1549 years worldwide are living with HIV, although
the burden of the epidemic continues to vary considerably between countries and
regions.
The National AIDS Control Organization (NACO) estimated that 1.8-2.9 million HIVpositive individuals were living with HIV/ AIDS in India in 2007.
Courtesy : WHO Global Health Observatory Data, NACO HIV Data
Classification
There are two main classification systems of oral lesions associated with HIV infection.
Based on the etiology of the oral lesions.
According to this system, orofacial lesions are classified as bacterial, viral, or fungal
infections or as neoplastic lesions or other conditions.
Courtesy : Nicoleta Vaseliu. Oral Manifestations of HIV Infection .
Oral Manifestations of Acquired Immunodeficiency Syndrome (AIDS)

Infections :
More Common
Less Common
Fungal
Candidiasis
HIV-related gingivitis
Bacterial
HIV-associated periodontitis
NUG
Viral
HSV
VZV
EBV
HPV
CMV
Aspergillosis
Histoplasmosis
Cryptococcosis
Geotrichosis
Mycobacteriumavium
Klebsiella pneumoniae
Enterobacter
Escherichia coli
Salmonella enteritidis
Cat-scratch disease
Sinusitis
Exacerbation of periapical
inflammatory disease
Submandibular cellulitis
Courtesy : Neville. Oral and Maxillofacial pathology.2 nd edition.pp237-240
Oral Manifestations of Acquired Immunodeficiency Syndrome (AIDS)

More Common
Less Common
Neoplasms :
Kaposis sarcoma
Non-Hodgkin's lymphoma
Squamous cell carcinoma
Lymphadenopathy
Cervical
Neurologic
Trigeminal neuropathy
Facial palsy
Miscellaneous
Aphthous ulcerations
Necrotizing stomatitis
Toxic epidermolysis
Delayed wound healing
Thrombocytopenia
Xerostomia or sicca like syndrome
Hyperpigmentation
Granuloma annulare
Exfoliative cheilitis
lichenoid reactions
Classification
The second, more widely used, systemrecommended by the EC Clearinghouse on Oral
Problems Related to HIV Infection and WHO Collaborating Centre on Oral
Manifestations of the Human Immunodeficiency Virusclassifies orofacial lesions into
three groups according to the degree of their association with HIV infection.
Courtesy : Classification and diagnostic criteria for oral lesions in HIV infection. JOPM 1993;22(7): 289-
Group 1
Lesions strongly associated with HIV infection
Candidiasis
Erythematous
Pseudomembranous
Hairy leukoplakia
Kaposis sarcoma
Non-Hodgkins lymphoma
Periodontal disease
Linear gingival erythema
Necrotizing (ulcerative) periodontitis
Necrotizing (ulcerative) gingivitis
Group 2
Lesions less commonly associated with HIV infection
Bacterial infections
Mycobacterium aviumintracellulare
Mycobacterium tuberculosis
Viral infections
Herpes Simplex virus
Human papillomavirus (wart-like
lesions)
Condyloma acuminatum
Focal epithelial hyperplasia
Verruca vulgaris
Varicella zoster virus
Herpes zoster
Varicella
Melanotic hyperpigmentation
Necrotizing (ulcerative) stomatitis
Salivary gland disease
Dry mouth due to decreased salivary
flow rate
Unilateral or bilateral swelling of the
major salivary glands
Thrombocytopenic purpura
Ulceration NOS (not otherwise specified)
Group 3
Lesions seen in HIV infection
Bacterial infections
Actinomyces Israel
Escherichia coli
Klebsiella pneumoniae
Cat-scratch disease
Viral infections
Cytomegalovirus
Molluscum contagiosum
Fungal infection other than candidiasis
Cryptococcus neoformans
Geotrichum candidum
Histoplasma capsulatum
mucormycosis/ zygomycosis
Aspergillus flavus
Drug reactions (ulcerative,

erythema multiforme, lichenoid,
toxic epidermolysis.)
Epithelioid (bacillary) angiomatosis
Neurologic disturbances
Facial palsy
Trigeminal neuralgia
Classification
Reduction of circulating CD4 count is the main criteria for assessing the
immunosuppression status in HIV-positive patients.
The normal number of circulating CD4 cells ranges from 600 to 1600 cells/mm, but the
initial signs of immunosuppression occur when CD4 count is lower than 500 cells/mm3.
Courtesy : Mithra N. Hegde et al. Oral lesions and immunosuppression in HIV patients. Biodiscovery 2012 ;
Classification
WHO immunological classification on the basis of CD4 count
Group 1
>500/ml
Group2 Mild
350-499/ml
Group 3 Advanced
200-349/ml
Group 4 Severe
<200/ml
Courtesy : Mithra N. Hegde et al. Oral lesions and immunosuppression in HIV patients. Biodiscovery 2012 ;
Candidiasis
The most common intra oral manifestation of HIV infection.
Based on clinical appearance, oral candidiasis can appear as
erythematous or atrophic candidiasis,
pseudomembranous candidiasis,
hyperplastic or chronic candidiasis, and
angular cheilitis.
Courtesy : Jha R et al:. Oral Manifestations of HIV-AIDS: A Diagnostic and Management Dilemma. Journal of Research in Medical and Dental Science 2014:2(1):96-
Pseudomembranous Candidiasis
The pseudomembranous form of candidiasis is characterized by the presence of
multifocal smooth white papular lesions that can usually be rubbed away, leaving a red
surface, and surface pseudohyphae can be readily detected.
Courtesy : Louis de Repentigny et al. Immunopathogenesis of Oropharyngeal Candidiasis in Human Immunodeficiency Virus Infection. CLINICAL
Pseudomembranous Candidiasis
Hyphae are numerous and extend into the spinous cell layer in pseudomembranous
candidiasis, accompanied by parakeratosis, acanthosis, and spongiosis of the infected
superficial epithelium . An abundant mononuclear cell response is observed in the
submucosa
Erythematous Candidiasis
The erythematous form presents as diffuse and multiple foci of macular erythema
involving the palate, oropharynx, buccal mucosa, and dorsal tongue, but hyphae are
frequently absent, while blastoconidia may be found on an atrophic epithelial surface.
Erythematous Candidiasis
Characterized by abundant neutrophilic micro abcesses in the parakeratin layer of the
epithelium, while microabcesses are rarely found in pseudomembranous candidiasis. An
abundant mononuclear cell response is observed in the submucosa
Chronic Hyperplastic Candidiasis

- severe immune suppression /long standing disease.
white non removable plaque which may be stained by food.
can occur on any mucosal surface.
Angular Chelitis
Radiating fissures from labial commissure, sometimes covered with a pseudomembrane.
Hyper keratosis may be seen peripheral to the fissures.
opening of mouth becomes restricted and painful.
MICROBIOLOGY REVIEWS 2004,:17(4)729759
Candidal species
The majority of patients are infected with C. albicans,
Other species are
Candida tropicalis,
Candida parapsilosis,
Candida guillermondii,
Candida glabrata, (Sole cause of recurrent candidiasis)
Candida dubliniensis.
Depletion of CD4+ cells below a critical threshold of 200 cells/mm3 most often triggers
the onset of candidiasis
Pathogeneis
The ability of C. albicans to infect such diverse host niches is supported by a wide range
of virulence factors and fitness attributes.
A number of attributes, including the morphological
transition between yeast and hyphal forms,
the expression of adhesins and invasins on the cell surface,
thigmotropism, the formation of biofilms,
phenotypic switching and
the secretion of hydrolytic enzymes are considered virulence factors.
Rapid adaptation to fluctuations in environmental pH, metabolic flexibility, powerful
nutrient acquisition systems are other attributes.
Courtesy : Franois L. Mayer. Candida albicans pathogenicity mechanisms. Virulence 2013:4(2)119128.
Polymorphisms
C. albicans is a polymorphic fungus that can grow either
as ovoid-shaped budding yeast,
as elongated ellipsoid cells with constrictions at the septa (pseudohyphae) or
as parallel-walled true hyphae.
Further morphologies include
white and opaque cells, formed during switching, and
chlamydospores, which are thick-walled spore-like structures
Transition
The transition between yeast and hyphal growth forms is
termed dimorphism.
The hyphal form is more invasive than the yeast form.
Smaller yeast form is believed to represent the form
primarily involved in dissemination
Factors influencing transition
Yeast
Hyphae
Low pH (<6)
high pH (> 7)
starvation,
the presence of serum or N-acetylglucosamine,
physiological temperature and CO2
In healthy individuals
Salivary flow protects the oral cavity by dislodging yeasts and bacteria, which are then
removed by swallowing and this process may be facilitated by binding of C. albicans to
salivary mucins or to a nonmucin proteoglycan.
In HIV Patients
In patients with advanced HIV infection, the salivary flow rate is reduced by 40%.
The incidence of oral candidiasis is also enhanced in patients with acidic saliva , and a
low pH increases the adherence of C. albicans to epithelial surfaces.
Glucose supplementation of saliva augments the growth rate and the resulting acidic pH
provides the required environment for activity of Candida secretory aspartyl proteinases,
(Saps) which enhance virulence by degrading mucins, which play an important role in
lubrication of epithelial surfaces and host defense.
Adhesions
C. albicans has a specialized set of proteins (adhesins) which mediate adherence to other
C. albicans cells to other microorganisms, to abiotic surfaces and to host cells.
Agglutinin-like sequence (ALS) proteins
Hypha-associated glycosyl phosphatidyl inositol-linked protein
cell-surface associated proteases
integrin-like surface protein
Invasion
Induced endocytosis
Active penetration
Expresses specialized proteins on the cell surface

(invasins) that mediate binding to host ligands
(such as E-cadherin on epithelial cells and Ncadherin on endothelial cells, thereby triggering
engulfment of the fungal cell into the host cell.
Secreted aspartic proteases

Lipases
Phospholipases,
(detaches epithelial cell desmosomes)
Even non viable fungi can enter the cell
Only viable fungi can enter
Non Immunological Defense

Several salivary anticandidal proteins, including lysozyme, lactoferrin, the histatins,
calprotectin, and antileukoprotease, inhibit the growth of C. albicans and its attachment
to the oral epithelium.
In HIV
Lysozyme
Hydrolysis of N-glycosidic
linkages in the microbial cell
wall and injury to the
cytoplasmic membrane
Levels are increased and so the

activity of lysozyme is doubtful
Lactoferrin
damage to the fungal cell wall

and activation of intracellular
autolytic enzymes
Levels may be normal,

decreased or increased because
of source is from
submandibular gland not
parotid
Non Immunological Defense

In HIV
Histatins
disrupt cell membranes
decreased concentrations of
histatins causes increased
tendency to oral candidiasis
Calprotectin
inhibits the growth by

depriving the fungus of zinc
concentrations of calprotectin
are deficient in HIV-infected
patients
Antileukoprotease
Unknown
Decreased
Biofilm Formation
Catheters, dentures (abiotic) and mucosal cell surfaces (biotic) are the most common
substrates.
Biofilms form in a sequential process including adherence of yeast cells to the substrate,
proliferation of these yeast cells, formation of hyphal cells in the upper part of the
biofilm, accumulation of extracellular matrix material and, finally, dispersion of yeast
cells from the biofilm complex
Hydrolases
Following adhesion to host cell surfaces and hyphal growth, hyphae secrete hydrolases
to facilitate active penetration into the cells.
They are : proteases, phospholipases and lipases.
Immunological Defence
glucan and chitin, mannan contents of cell wall are recognised by the Toll Like
Receptors.
TLR-2 and TLR-4 represent the main TLRs involved in the signalling cascades
Treatment
Treatment is much more difficult in patients with AIDS.
Nystatin often is ineffective.
Topical clotrimazole is associated with an improved response.
In spite of this success, topical therapy is associated with a high recurrence rate .
The systemic azoles (fluconazole, ketoconazole, itraconazole) produce longer diseasefree intervals but itraconazole and ketoconazole require gastric acidity for adequate
absorption, and all three agents are associated with a number of drug interactions.
In addition, widespread use of systemic azoles has led to an increased prevalence of
drug- resistant candidiasis.
Oral Hairy Leukoplakia

Oral hairy leukoplakia (OHL) was first discovered by Greenspan in 1984 and was
described as asymptomatic, white, nonscrapable, vertically corrugated hyperkeratotic
hair-like projections that appear on the lateral border of the tongue.
Caused by the EpsteinBarr Virus (EBV), the lesion is said to be an early indicator of an
immune deficiency status rather than being a marker for HIV infection.
Courtesy : Ajay Reginald and B. Sivapathasundharam.. Oral hairy leukoplakia: An exfoliative cytology study. Contemp Clin Dent. 2010 Jan-Mar; 1(1): 1013.
.
Cytology
Cowdry A inclusion bodies: an
eosinophilic and central intranuclear
inclusion body surrounded by a clear
space
Ground glass nuclei: an eosinophilic

or basophilic inclusion body
homogenizing the whole surface and
exhibiting peripheral margination of
chromatin
Courtesy : Ajay Reginald and B. Sivapathasundharam.. Oral hairy leukoplakia: An exfoliative cytology study. Contemp Clin Dent. 2010 Jan-Mar; 1(1): 1013.
.
Histopathology
OHL is characterized by acanthosis of the surface epithelium and irregular
hyperkeratosis.
Ballooning of epithelial cells is noted within the superficial stratum spinosum.
Peripheral beading of the chromatin in superficial epithelial cells is characteristic of
the lesion results from the multiplication of EBV
Courtesy : Joanne Leger Prasad. Oral hairy leukoplakia in patients without HIV: presentation of 2 new cases. Oral Surgery, Oral Medicine, Oral Pathology and Oral
Radiology. 2014,;118,(5): e151e160
Treatment
Treatment of OHL usually is not needed, although slight discomfort or aesthetic concerns
may necessitate therapy.
Acyclovir produces rapid resolution but recurrence is expected with a discontinuation
of therapy.
Topical treatment with retinoids or podophyllum resin has resulted in temporary
remissions.
In addition, HIV therapy with zidovudine appears to affect EBV and result in significant
regression .
Kaposis Sarcoma(KS)
First described by the Hungarian dermatologist Moritz Kaposi in 1872, KS is a
multifocal neoplasm of vascular endothelial cell origin.
KS is traditionally separated into four different types:
Classic: which primarily affects elderly men of Mediterranean and eastern
European origin;
Endemic: which is common in parts of Africa; (lymphadenopathic)
Epidemic or AIDS-associated; and
Transplantation-associated.
Courtesy : Kishore Shetty. Management of oral Kaposis sarcoma lesions on HIV-positive patient using highly active antiretroviral therapy: Case report and
a review of the literature. Oral Oncology Extra October 2005 ;41(9) :226229.
Classic`
Endemic
affects older males

of Italian, Slavic, or Jewish
ancestry
endemic to
young African children
often associated with altered

immune states as well
as lymphoreticular and
other malignancies
presents as a localized
or generalized
enlargement of lymph
node chains, including
the cervical nodes.
Cutaneous multifocal bluered nodules develop on the

lower extremities and slowly
increase in size and numbers,
Oral involvement in
this form of the disease is
quite unusual,
Transplantation
HIV Associated
seen in 1% to 4% of renal
transplant recipients
often as an early sign of

the disease. young adults
Average Age :39 yrs
follows a fulminating
course with visceral
involvement and minimal
skin or mucous
membrane
involvement.
Sarcomatous involvement
occurs on the skin as well
as in internal organs
cutaneous locations,
especially along
lines of cleavage and on the
tip of the nose.
Salivary glands are

effected
oral mucosal lesions are

rare
strong predilection
for palatal, gingival, and
lingual mucosa
Courtesy : Gnepp. Diagnostic Surgical pathology of Head and Neck 2 nd edition;238-239.
Clinical features
Early oral mucosal Kaposi sarcoma is flat
and slightly blue, red, or purple that do
not blanch on pressure.
With time, the lesion becomes more
deeply discolored, and surface papules
and soft nodules develop, usually
remaining less than 2 cm in size.
Clinical features
If the lesion overlies bone, it may invade and/ or
necrose the bone, and occasional lesions are so
hemorrhagic or so painful.
Individual lesions may coalesce, and occasional
patients never develop the nodular variant.
Cervical lymph node and salivary gland enlargement
may also be seen.
Etiology
In 1994 HHV-8/KSHV was first detected in KS specimens.
KSHV is now considered the causative agent of AIDS-associated, classic, endemic, and
iatrogenic KS.
Courtesy : Badari Rao. Kaposis sarcoma: Insights into its understanding. International Journal of Contemporary Dental and Medical Reviews (2014), Article ID
031114, 4 Pages
Pathogenesis
The pathogenesis of AIDS-associated KS is multifactorial and involves KSHV, altered
expression and response to cytokines and stimulation of KS growth by HIV transactivation protein (tat).
KSHV is a necessary but solely not a sufficient cause of KS.
It encodes protein homologs of interleukin-6, chemokines of the macrophage
inflammatory protein family, cell cycle regulators of the cyclin family, and anti-apoptotic
genes of the bcl-2 family.
The HIV tat protein can promote the growth of spindle cells of endothelial origin but
only in the presence of inflammatory cytokines
031114, 4 Pages
Pathogenesis
circulatingKSprogenitorcellsandcellslatentlyinfectedwithKSHVseeksitesofpre
existinginflammationlikeperiodontaldiseasesites
ExposuretoinflammatorycytokinesIFNresultsindifferentiationoflatentlyinfected
cellsintoKSlikespindlecellsandinducesKSHVreactivation
reactivationofKSHVleadstoexpressionofpathogenicgenessuchasviralIL6thatin
turnactivatevascularendothelialgrowthfactorandinduceangiogenesis;
thecreationofinflammatoryangiogenicenvironmentincreasestheavailabilityof
infectablecells,i.e.endothelialandKSspindlecells
cellsbecomeresponsivetoHIVtatproteinwhichaugmentstheinflammatoryangiogenic
statebytheincreasingbasicfibroblastgrowthfactor,IFN,andVEGF
031114, 4 Pages
Histological features
Has a similar histopathologic appearance in all its clinical

subtypes.
The early lesion (patch stage) is characterized by a
proliferation of small veins and capillaries around one or
more dilated vessels.
A pronounced mononuclear inflammatory cell infiltrate,
including mast cells, is often noted, as are scattered
erythrocytes and hemosiderin deposits.
There may be an inconspicuous perivascular
proliferation of spindle cells, but cellular atypia is
minimal.
More advanced lesions are nodular and show increased
numbers of small capillaries or dilated vascular channels
interspersed with proliferating sheets of sarcomatous or
atypical spindle cells, often with large numbers of
extravasated erythrocytes and abundant hemosiderin
deposition.
Slit like vascular channels without a visible endothelial lining
are typically interspersed within the spindle cells.
Lesion cells have somewhat enlarged, hyperchromatic nuclei
with mild to moderate pleomorphism
Treatment
KS responds to radiation or systemic chemotherapy (singly or in combination), such as

vinblastine, vincristine. etoposide, bleomycin, Adriamycin, actinomycin D, doxorubicin, or
alpha-interferon.
Oral lesions frequently are a cause of major morbidity, as a result of pain, bleeding, and
functional interferences.
Intralesional injection of oral lesions with vinblastine is effective and may be repeated if
required .
Intralesional injection of a sclerosing agent, sodium tetradeeyl sulfate, has been effective
for problematic intraoral lesions less than 2.5 cm in diameter.
Problematic lesions also may be removed by surgical excision, cryotherapy, laser ablation.
Non Hodgkins Lymphoma

High-grade NHL was first reported in 1984.
The relative risk of NHL among HIV-infected patients is 150-250-fold higher than in the
general population.
Incidence of NHL accounts for 2%3% of newly diagnosed AIDS cases and occurs
when CD4+ count is less than 100cells/ml.
HIV-associated lymphomas include (1) high-grade B-cell lymphomas: Burkitt
lymphoma, diffuse large B-cell lymphoma with centroblastic features and with
immunoblastic features and (2) unusual lymphomas, primary effusion lymphoma and
plasmablastic lymphoma of the oral cavity.
Courtesy : Dattatray G. Saple et al. Lymphoma in HIV patients: Varied presentations. Indian J Med Paediatr Oncol. 2010;31(1)3942.
WHO Classification of lymphoid malignancies associated with HIV infection

Lymphomas also occurring in immunocompetent patients
Burkitt and Burkitt-like lymphomas
Diffuse large B-cell lymphomas
Centroblastic
Immunoblastic (including primary CNS lymphoma)
Extranodal MALT lymphoma
Peripheral T-cell lymphoma
Classical Hodgkin lymphoma
Lymphoma occurring more specifically in HIV-positive patients
Primary effusion lymphoma
Plasmablastic lymphoma of the oral cavity
Lymphoma occurring in other immunodeficiency states
Polymorphic B-cell lymphoma (PTLD-like)
Courtesy : Prakash Vishnu and David M. Aboulafia.. AIDS-Related Non-Hodgkin's Lymphoma in the Era of Highly Active Antiretroviral Therapy. Advances in
Hematology
Pathogenesis
DefectiveTCellSurveillance
longtermstimulationandproliferation
ofBlymphocytes
immunestimulationbyHIVandreactivationofpreviousEBVinfection
IntheabsenceofEBVinfectionHIVinducestheproductionofinflammatorycytokines
thatcauseBcellstimulation,proliferation,andactivation
celllinesderivedfromAIDSrelatedNHLhavebeenfoundtoexpresscytokines
includinginterleukin6,interleukin10,andtumournecrosisfactor
Courtesy : Tom Powles, Gail Matthews, Mark Bower. AIDS related systemic non-Hodgkins lymphoma. Sex Transm Inf 2000;76:335341.
Burkitt Lymphoma
Burkitts Lymphoma (BL) is a highly aggressive form of NonHodgkins lymphoma
which was first described in 1958 by Dennis Burkitt in Africa.
EBV infection and chromosomal translocation resulted in dysregulation of c-MYC
oncogene are the etiological factors.
Courtesy : Soujanya Pinisetti. HIV Associated Intraoral Burkitts Lymphoma: A Case Report. J Clin Diagn Res. 2013 Dec; 7(12): 30883089.
Classification
Endemic
Sporadic
Endemic to young African

children
occurs worldwide, with no specific

geographic or climatic association.
Involves jaw bones, kidneys,

GIT, ovaries and breast
involves abdomen and ileocecal

areas.
Immunodeficiency Associated
often as an early sign of
the disease. young adults
Average Age :39 yrs
accounts for 12% of lymphomas in accounts for 30-40% of Nonadults and for 40% of lymphomas in Hodgkins lymphomas
children
Clinical features:
HIV patients with Burkitts lymphoma are usually younger as compared to patients with
diffuse large B cell lymphomas and they have CD4 counts greater than 200 cells/l.
Manifests as a soft tissue mass with or without ulceration, tissue necrosis and it occurs
commonly on gingiva, palate and alveolar mucosa, with rapid growth and destruction .
The earliest clinical sign of Burkitts lymphoma of jaws is mobility and exfoliation of
the teeth
Pathogenesis
HIV infection causes polyclonal activation of B cells in an uncontrolled manner.
The genetic instability of EBV positive, aberrantly regulated B cells leads to a risk of cmyc rearrangement and then, to lymphoma.
C-myc rearrangement is a crucial event in lymphoma genesis
Histology
Classic
characterized by a mass of diffuse,
neoplastic, noncleaved uniform,
medium sized B- lymphocytes with
round nuclei and multiple nucleoli of
with numerous mitotic figures admixed
with numerous tangible body
macrophages with apoptotic debris,
giving a picture of starry sky.
Plasmacytoid
Shows a typical starry sky appearance
with an infiltrate of neoplastic lymphoid
cells . Under higher magnification, these
medium-sized neoplastic lymphoid cells
were characterized by abundant basophilic
cytoplasm and an eccentric nucleus,
suggestive of plasmacytoid differentiation
accounts for 12% of lymphomas in adults
and for 40% of lymphomas in children
oral mucosal lesions are rare
Atypical
Diffuse infiltrate of atypical lymphoid
cells with abundant apoptotic debris and
scattered tingible body macrophages.
Large B Cell Lymphoma

Diffuse large B-cell lymphoma (DLBCL) is the most common of the aggressive NHLs in
the United States.
80% of the cases are composed of cells resembling germinal center centroblasts.
The immunoblastic type (10% of the cases) has more than 90% immunoblasts.
Other morphologic variants include the T-CellRich/Histiocyte-Rich variant which has a
prominent background of reactive T cells and histiocytes.
Courtesy : Jonathan W. Friedberg . Diffuse Large B-Cell Lymphoma. Hematol Oncol Clin North Am. 2008 Oct; 22(5): 941ix.
Linear Gingival Erythema

This unusual pattern of gingivitis appears with a
distinctive linear band of erythema that involves the free
gingival margin and extends 2 to 3 mm apically .
The alveolar mucosa and gingiva may demonstrate
punctate or diffuse erythema.
This form of gingivitis does not respond to improved
plaque control and often exhibits a greater degree of
erythema than would be expected for the amount of
plaque in the area.
Linear Gingival Erythema

It is of questionable etiology and pathogenesis while not
all the cases show distinct fiery red band along the
gingival margin.
However c.albicans can be isolated in more than 50% of
cases.
Courtesy : elegraki, Arista. Paediatric AIDS--related linear gingival erythema: a form of erythematous candidiasis? J Oral Pathol M.ed 1999
Necrotising ulcerative gingivitis

Refers to ulceration and necrosis of one or more inter
dental papillae with no loss of periodontal attachment.
Patients with NUG have interproximal gingival necrosis,
bleeding, pain , and halitosis.
Necrotising ulcerative gingivitis

NUG the immunosuppression may be induced by stress or
poor diet.
Smoking in subjects with poor oral hygiene also
contributes
to both.
ANUG is a fusospirochaetal infection involving Treponema
vincentii and Fusobacterium nucleatum.
Courtesy : Iain L C Chapple, John Hamburger. The significance of oral health in HIV disease. Sex Transm Inf 2000;76:236243.
Necrotising ulcerative peridontitis

Characterized by gingival ulceration and necrosis
associated with rapidly progressing loss of periodontal
attachment.
Although severe cases can affect all teeth, multiple isolated
defects often are seen and contrast with the diffuse pattern
associated with typical chronic periodontitis.
Edema, severe pain, and spontaneous hemorrhage
are common.
Deep pocketing usually is not seen because extensive
gingival necrosis typically coincides with loss of the
adjacent alveolar
bone
Necrotising Stomatitis
In patients with gingival necrosis, the process occasionally
extends away from the alveolar ridges , more than 10 mm
beyond the gingival margin and creates massive areas of
tissue destruction termed necrotizing stomatitis.
The process clinically resembles noma and may involve
predominantly soft tissue or extend into the under lying
bone, resulting in extensive sequestration.
Treatment
The treatment of NUG and NUP revolves around debridement, anti microbial therapy,
immediate follow up care, and long-term maintenance.
The initial removal of necrotic tissue is necessary combined with povidine iodine
irrigation.
The use of systemic antibiotics usually is not necessary, but metronidazole has been
administered to patients with extensive involvement that is associated with severe acute
pain.
All patients should use chlorhexidine mouth rinses initially and for long- term
maintenance.
Monthly recalls are necessary until the process stabilizes; evaluations then are performed
every 3 months.
Aphthous Ulcers
Lesions that are similar clinically to aphthous ulcerations
occur with increased frequency in patients infected with
HIV.
All three forms (minor, major, and herpetiform) are seen.
As immunosuppression becomes more profound, major
aphthous ulcerations demonstrate an increased prevalence.
HPV Infection
HPV is responsible for several facial and oral lesions in
immunocompetent patients.
Most frequent of which are the verruca vulgaris
(common wart) and oral squamous papilloma.
An increased prevalence of HPV-related lesions is noted in
HIV- infected patients, and most are located in the
anogenital areas.
HIV-infected patients often demonstrate more unusual
variants such as HPV- 7 (associated with butcher 's warts)
or HPV-32 (often noted in Heck's disease)
Papilloma
Focal epithelial hyperplasia
Most common of benign epithelial tumors of the oral cavity
Benign hyperplastic lesion of the oral cavity that is caused by HPV

infection
Exophytic proliferations arranged in a finger-like

configuration, giving a cauliflower-like clinical appearance.
Majority are pedunculated, some are sessile.
circumscribed, sessile, soft, and elevated nodules of the oral

mucosa . Although beginning as separate nodules, the lesions often
become confluent and cover large areas of the oral mucosa of the
lips and buccal surfaces as well as the tongue
Squamous papillomas are small exophytic lesions with a

central fibrovascular core covered by stratified,
parakeratinized
epithelium
Acanthosis and elongation and anastomosing of the rete ridges, do

not form fibrovascular cores as seen in papillomas.
Courtesy :Barnes. Surgical pathology of head and neck.211-215.
Verruca vulgaris
Condyloma acuminatum
warty exophytic lesion that resembles verrucae in other sites,

including the skin. It is caused by the HPV
oral wart, moist wart, caused by HPV and appears one to three
months after exposure
Young adults and children are most often affected. It

is thought that autoinoculation of virus.
Verruca have an entirely exophytic growth pattern. Common
sites include the lips, palate, alveolar ridge, and gingiva
appear as soft verrucous nodules or multiple adjacent papillary

clusters that tend to coalesce into soft, pink cauliflower-like
masses, although isolated lesions may occur
Reveals long vascular cores coated in thick layers of

epithelial
cells that form pointed projections. Rete ridges often seem to
radiate outward from a central point. Koilocytes are often
noted
Pronounced spinous layer hyperplasia and cellular ballooning, and

mitoses are seen extending into the spinous layer. The base of the
rete ridges are often bulbous. The lesions show parakeratosis,
acanthosis, and papillomatosis. the base is sessile, and there is
parakeratin crypt formation
Courtesy :Barnes. Surgical pathology of head and neck.211-215.
Molluscum contagtosum 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.
In immuno competent individuals, the lesions are selflimiting and typically involve the genital region or trunk.
5% to 10% of HIV-infected patients are affected and the
facial skin commonly is involved
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.
Small fungal organisms are visible within the cytoplasm
of histiocytes and multinucleated giant cells.
These phagocytic cells may be present in sheets or in
organized granulomas
Herpes Simplex
Early in the course of HIV disease, HSV infections are
usually self-limited.
Grouped lesions appear, ulcerate, and heal, usually in less
than 2 weeks.
Presence of mucocutaneous HSV infection for longer than 1
month is suggestive of advanced HIV infection.
Tender, often painful, ulcerative lesions of the lip are the
hallmark of HSV in HIV-infected patients.
Courtesy : Jordan W. Tappero et al Cutaneous Infections In Hiv-infected Patients. Clinical Microbiology Reviews.1995;8(3):440450.
The virus exerts its main effects on the epithelial cells.
Infected epithelial cells exhibit acantholysis, nuclear clearing,
and nuclear enlargement, which has been termed ballooning
degeneration.
The acantholytic epithelial cells are termed Tzanck cells.
Nucleolar fragmentation occurs with a condensation of
chromatin around the periphery of the nucleus.
Multinucleated, infected epithelial cells are formed when
fusion occurs between adjacent cells
Courtesy : Neville. Oral and Maxillofacial pathology.2 nd edition.pp 217-219.
Herpes Zoster
HIV-infected persons may develop primary varicella (chicken
pox) when exposed to VZV for the first time .
In addition, serum antibodies to VZV do not appear to prevent
varicella in HIV-infected persons, and varicella can recur.
Varicella infections typically follow a benign course, with
resolution of scattered vesicular lesions in the absence of
therapy.
Onset of disease occurring with average CD4 lymphocyte
counts of 315 cells per mm3.
Herpes Zoster
Among HIV-infected children, HZ may develop rapidly
following primary VZV infection
HZ in asymptomatic HIV-infected patients typically pursues a
benign course, with resolution of vesiculobullous lesions over
2 to 3 weeks, often without specific antiviral chemotherapy.
However, severe painful ulcerations followed by postherpetic
neuralgia upon healing are not uncommon.
In addition, recurrent HZ occurs in up to 22% of HIV-infected
Patients.
Herpes Zoster
In addition to the vesiculobullous lesions commonly seen
with disseminated VZV, patients with advanced HIV infection
may develop unusual lesional patterns associated with
acyclovir
resistance: ecthymatous, crusted, punched out ulcerations or
true verrucous lesions, which may be seen alone or in
association with the vesicular, ecthymatous lesions.
Cytomegalo virus
CMV-related oral ulcerations, although infrequent, are a
recognized complication of HIV infection.
The diagnosis of oral CMV is based upon the presence of large
intranuclear and smaller cytoplasmic CMV inclusions in the
endothelial cells at the base of the ulcerations.
These infections usually manifest in stage IV of the infection
when there is advanced immunosupression with a CD4 count
below 50.
Courtesy : Smrati Bajpai and A. R. Pazare. Oral manifestations of HIV. Contemp Clin Dent. 2010;1(1)15.
Tuberculosis
Tuberculosis is a chronic infectious disease caused by Mycobacterium tuberculosis.
Worldwide, more than 1 billion people are infected, with 8 million new cases and 3 million
deaths per year.
The HIV epidemic, increased immigration from countries with endemic tuberculosis,
transmission of tuberculosis in crowded or unsanitary environments, and a decline of the
health care infrastructure are the main causes for transmission.
Most infections are the result of direct person-to- person spread through airborne
droplets from a patient with active disease.
Courtesy : Neville. Oral and Maxillofacial pathology.2 nd edition.pp173-175.
Tuberculosis
Primary
Secondary
Occurs in previously unexposed

people
active disease usually develops later

in life from a reactivation of
organisms in a previously infected
person . This reactivation is typically
associated with compromised host
defenses and is called secondary
tuberculosis
Almost always involves the lungs.

The organism initially elicits a
nonspecific, chronic
inflammatory reaction.
Secondary tuberculosis often is

associated with old age. povert y. and
crowded living conditions. AIDS
represents one of the strongest risk
factors for progression from infection
to disease.
Disseminated
Diffuse dissemination through the
vascular system may occur and has
been termed miliary tuberculosis.
Clinical Features
Primary tuberculosis is usually asymptomatic. Occasionally, fever and pleural effusion
may occur.
Classically, the lesions of secondary tuberculosis are located in the apex of the lungs but
may spread to many different sites by expectorated infected material or through the
lymphatic or vascular channels.
Patients have a low-grade fever, malaise, anorexia,weight loss, and night sweats.
With pulmonary progression a productive cough develops often with hemoptysis or chest
pain.
Clinical Features
Head and neck involvement is not rare.
The most common extrapulmonary sites in the head and neck are the cervical lymph nodes
followed by the larynx and middle ear.
Much less common sites include the nasal cavity, nasopharynx, oral cavity, parotid gland,
esophagus, and spine.
Oral manifestations
Oral lesions of tuberculosis arc uncommon, with most cases appearing as a chronic
painless ulcer.
Less frequent presentations include nodular, granular, or (rarely) firm leukoplakic areas.
Most of the lesions represent secondary infection from the initial pulmonary lesions.
It is unclear whether these develop from hematogenous spread or from exposure to
infected sputum.
Oral manifestations
Primary oral tuberculosis without pulmonary
involvement is rare.
When present, primary oral tuberculosis usually involves
the gingiva, mucobuccal fold and areas of inflammation
adjacent to teeth or in extraction sites.
Secondary oral lesions are mostly present on the tongue,
palate and lip.
Granulomas, which are circumscribed collections
of epithelioid histiocytes, lymphocytes, and
multinucleated
giant cells, often with central caseous necrosis are seen.
In a person with tuberculosis, one of these granulomas is
called a tubercle, Special stains , such as the ZiehlNeelsen or other acid-fast stains, are required to
demonstrate the mycobacteria
Histoloplasmosis
Histoplasmosis. the most common endemic respirator y fungal infection produced by
Histoplasma capsulatum .
In healthy patients. the infection typically is subclinical and selflimiting, but clinically
evident infections do occur in immuno compromised individuals.
Although a number of deep fungal infections are possible in patients with AIDS,
histoplasmosis is the most common , with disseminated disease noted in approximately
5% of AIDS patients residing in areas where the fungus is endemic
Clinical features
The signs and symptoms associated with dissemination are
nonspecific 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.
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.
Cryptococcosis
Cryptococcosis is a relatively uncommon fungal disease caused by the yeast
Cryptococcus neoformans.
This organism normally causes no problem in immunocompetent people, but it can be
devastating to the immunocompromised patient.
It is the most common life threatening fungal infection in HIV patients.
The disease has a worldwide distribution because of its association with the pigeon.
Grows as a yeast both in the soil and in infected tissue.
The organism usually produces a prominent mucopolysaccharide capsule.
Clinical features
Primary cryptococcal infection of the lungs is often asymptomatic;
However, a mild flulike illness may develop.
Patients complain of productive cough, chest pain, fever and
malaise.
Dissemination of the infection is common in immuno compromised
patients, and the most frequent site of involvement is the meninges,
followed by skin, bone and the prostate gland.
The lesions appear as erythematous papules or pustules that may
ulcerate discharging a pus like material rich in cryptococcal
organisms Courtesy : Neville. Oral and Maxillofacial pathology.2 nd edition.pp237-240
Mucormycosis
Zygomycosis is an opportunistic, frequently fulminant, fungal infection that is caused by
class Zygomycetes, including Absidia, Mucor, Rhizomucor, and Rhizopus.
Zygomycosis may involve any one of several areas of the body, but the rhinocerebral
form is most relevant to the oral health care provider.
Clinical features
Patients may experience nasal obstruction, bloody nasal discharge, facial pain or
headache, facial swelling or cellulitis, and visual disturbances with concurrent proptosis.
Symptoms related to cranial nerve involvement (e.g., facial paralysis) are often present .
With progression of disease into the cranial vault, blindness, lethargy, and seizures may
develop, followed by death .
Oral manifestations
If the maxillary sinus is involved, the initial presentation
may be seen as intraoral swelling of the maxillary alveolar
process, the palate, or both.
If the condition remains untreated, palatal ulceration may
evolve, with the surface of the ulcer typically appearing
black and necrotic.
Massive tissue destruction may result if the condition is
not treated.
Shows extensive necrosis with numerous large,
branching, non septate hyphae at the periphery.
The hyphae tend to branch at 90-degree angles.
The extensive tissue destruction and necrosis is due to
the preference of the fungi for invasion into small blood
vessels.
This disrupts normal blood flow to the tissue, resulting
in infarction and necrosis.
Salivary gland disease

HIV-associated salivary gland disease also can arise anytime
during infection.
Clinically obvious salivary gland disease is noted in
approximately 5% of HIV- infected patients, with a greater
prevalence noted in children.
The main clinical sign is salivary gland enlargement,
particularly affecting the parotid.
Bilateral involvement is seen in about 60% of the patients with
glandular changes and often is associated with cervical
lymphadenopathy.
Diffuse Infiltrative lymphoctosis Syndrome

DILS is a disorder in patients with HIV-1, characterized by
salivary and lacrimal glandular swelling and sicca symptoms of
varying intensity, frequently accompanied by persistent
circulating and visceral CD8-positive lymphocytic infiltration.
The reported prevalence varies between 0.85 3%.
Patients with DILS generally present in an early HIV stage, have
higher CD4+ cell counts (commonly above 200/l).
Most of the patients have CD8+ lymphocytosis (counts > 835/l)
and some CD8+ hyper lymphocytosis (counts > 1500/l).
Courtesy : Levay. Diffuse Infiltrative Lymphocytosis Syndrome. SA Fam Pract 2008;50(2):42-44
Clinical Features
Their characteristics include a persistent circulating CD8 lymphocytosis, diffuse CD8
lymphocytic tissue infiltration with a generalized lymphadenopathy, and parotid gland
enlargement.
CD8 lymphocytosis observed in DILS most commonly involves the salivary glands,
lungs, liver, kidney, gastrointestinal tract, muscle and peripheral nerve system.
Sjogrens syndrome
DILS
CD4 cells predominate
CD4 cells are diminished, CD8 cells predominate
serum antibodies associated with an autoimmune

disease are seen
antibodies are not seen
Courtesy : Louis Mandel, David Kim, and Claribel. Parotid gland swelling in HIV diffuse infiltrative CD8 lymphocytosis syndrome.OOO1998;565-569.
Hyperpigmentation
Hyperpigmentation 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.
Several medication s taken by AIDS patients (e.g.,
ketoconazole,
clofazimine, pyrimethamine, zidovudine) may cause the
increased melanin pigmentation.
Hyperpigmentation
Adrenocortical destruction has been reported from several of the infections associated
with AIDS, resulting in an Addisonian pattern of pigmentation .
Finally, pigmentation with no apparent cause has arisen in HIV-infected patients, and
some investigators have theorized that this may be a direct result of the HIV infection.
Thrombocytopenia
Thrombocytopenia has been reported in nearly 10% of patients with HIV infection and
may occur at any time during the course of the disease.
Some reports show that megakaryocytes have CD4 molecules and may be an additional
target for the HIV virus.
Cutaneous lesions are present in most cases, but oral lesions do occur with petechiae,
ecchymosis, or spontaneous gingival hemorrhage.
References
Neville. Oral and Maxillofacial pathology.2nd edition.pp237-240.
Ashish S. Bodhade. Oral manifestations of HIV infection and their correlation with
CD4 count. Journal of Oral Science2011;53(2):203-211.
Iain L C Chapple, John Hamburger. The significance of oral health in HIV disease.
Sex Transm Inf 2000;76:236243.
WHO Global Health Observatory Data, NACO HIV Data.
Classification and diagnostic criteria for oral lesions in HIV infection. JOPM
1993;22(7): 289-291.
Mithra N. Hegde et al. Oral lesions and immunosuppression in HIV patients.
Biodiscovery 2012 ;(4)3:1-6.
Nicoleta Vaseliu. Oral Manifestations of HIV Infection .
References
Jha R et al.Oral Manifestations of HIV-AIDS: A Diagnostic and Management

Dilemma. Journal of Research in Medical and Dental Science 2014:2(1):96-102.
Louis de Repentigny et al. Immunopathogenesis of Oropharyngeal Candidiasis in
Human Immunodeficiency Virus Infection. CLINICAL MICROBIOLOGY
REVIEWS 2004,:17(4)729759.
Franois L. Mayer. Candida albicans pathogenicity mechanisms. Virulence
2013:4(2)119128.
Ajay Reginald and B. Sivapathasundharam.. Oral hairy leukoplakia: An exfoliative
cytology study. Contemp Clin Dent. 2010 Jan-Mar; 1(1): 1013.
Joanne Leger Prasad. Oral hairy leukoplakia in patients without HIV: presentation of 2
new cases. Oral Surgery, Oral Medicine, Oral Pathology and Oral Radiology.
2014,;118,(5): e151e160.
Badari Rao. Kaposis sarcoma: Insights into its understanding. International Journal
of Contemporary Dental and Medical Reviews (2014), Article ID 031114, 4 Pages.
References
Gnepp. Diagnostic Surgical pathology of Head and Neck 2nd edition;238-239.
Soujanya Pinisetti. HIV Associated Intraoral Burkitts Lymphoma: A Case Report. J
Clin Diagn Res. 2013 Dec; 7(12): 30883089.
Tom Powles, Gail Matthews, Mark Bower. AIDS related systemic non-Hodgkins
lymphoma. Sex Transm Inf 2000;76:335341.
Louis Mandel, David Kim, and Claribel. Parotid gland swelling in HIV diffuse
infiltrative CD8 lymphocytosis syndrome.OOO1998;565-569.
Thank You

Hiv Oral Manifestation

Încărcat de

Informații document

Titlu original

Drepturi de autor

Formate disponibile

Partajați acest document

Partajați sau inserați document

Opțiuni de partajare

Vi se pare util acest document?

Este necorespunzător acest conținut?

Drepturi de autor:

Formate disponibile

Hiv Oral Manifestation

Încărcat de

Drepturi de autor:

Formate disponibile

Oral Manifestations of

Courtesy : Nicoleta Vaseliu. Oral Manifestations of HIV Infection .

Oral Manifestations of Acquired Immunodeficiency Syndrome (AIDS)

Courtesy : Neville. Oral and Maxillofacial pathology.2 nd edition.pp237-240

Oral Manifestations of Acquired Immunodeficiency Syndrome (AIDS)

Courtesy : Neville. Oral and Maxillofacial pathology.2 nd edition.pp237-240

Drug reactions (ulcerative,

Chronic Hyperplastic Candidiasis

Courtesy : Franois L. Mayer. Candida albicans pathogenicity mechanisms. Virulence 2013:4(2)119128.

Courtesy : Franois L. Mayer. Candida albicans pathogenicity mechanisms. Virulence 2013:4(2)119128.

Expresses specialized proteins on the cell surface

Secreted aspartic proteases

Even non viable fungi can enter the cell

Only viable fungi can enter

Courtesy : Franois L. Mayer. Candida albicans pathogenicity mechanisms. Virulence 2013:4(2)119128.

Non Immunological Defense

Levels are increased and so the

damage to the fungal cell wall

Levels may be normal,

Non Immunological Defense

disrupt cell membranes

inhibits the growth by

Courtesy : Franois L. Mayer. Candida albicans pathogenicity mechanisms. Virulence 2013:4(2)119128.

Courtesy : Franois L. Mayer. Candida albicans pathogenicity mechanisms. Virulence 2013:4(2)119128.

Oral Hairy Leukoplakia

Ground glass nuclei: an eosinophilic

Courtesy : Neville. Oral and Maxillofacial pathology.2 nd edition.pp237-240

affects older males

often associated with altered

Cutaneous multifocal bluered nodules develop on the

often as an early sign of

Salivary glands are

oral mucosal lesions are

Courtesy : Gnepp. Diagnostic Surgical pathology of Head and Neck 2 nd edition;238-239.

Courtesy : Gnepp. Diagnostic Surgical pathology of Head and Neck 2 nd edition;238-239.

Courtesy : Gnepp. Diagnostic Surgical pathology of Head and Neck 2 nd edition;238-239.

Has a similar histopathologic appearance in all its clinical

KS responds to radiation or systemic chemotherapy (singly or in combination), such as

Non Hodgkins Lymphoma

WHO Classification of lymphoid malignancies associated with HIV infection

Endemic to young African

occurs worldwide, with no specific

Involves jaw bones, kidneys,

involves abdomen and ileocecal

Large B Cell Lymphoma

Linear Gingival Erythema

Linear Gingival Erythema

Necrotising ulcerative gingivitis

Courtesy : Neville. Oral and Maxillofacial pathology.2 nd edition.pp237-240

Necrotising ulcerative gingivitis

Necrotising ulcerative peridontitis

Courtesy : Neville. Oral and Maxillofacial pathology.2 nd edition.pp237-240

Courtesy : Neville. Oral and Maxillofacial pathology.2 nd edition.pp237-240

Focal epithelial hyperplasia

Most common of benign epithelial tumors of the oral cavity

Benign hyperplastic lesion of the oral cavity that is caused by HPV

Exophytic proliferations arranged in a finger-like

circumscribed, sessile, soft, and elevated nodules of the oral

Squamous papillomas are small exophytic lesions with a

Acanthosis and elongation and anastomosing of the rete ridges, do

Courtesy :Barnes. Surgical pathology of head and neck.211-215.

warty exophytic lesion that resembles verrucae in other sites,

Young adults and children are most often affected. It