lia session 3 vesiculobulous diseases - viral
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t the end of the session student have to beable to explain the various virus infections oforal and perioral diseases
Learning objectives
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Diagram of the
oral tissues,
illustrating the
component
tissues and their
relativepositions.
1. Stratified squamous
epithelium.
2. Lamina propria
3. Loose connective
tissue
4. Mucous glands
5. Serous glands
(occasionally)
6. Sebaceous glands(Fordycs granuless)
7. Nerve
8. Bone
9. Cartilage
10. Skeletal muscle
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List as much as possible vesiculo-bulous
viral infections of the oral diseasesTimes 10 mnt.
Viral infection of the oral diseases
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Infection
Hard tissue J a w s
Dental pulpitis
Periapical abssess
Acute osteomyelits Chronic osteomyelitis
Osteitis
Oral tissue
Oral Mucosa Lips
Gingival
Palate mucosa
Tongue
Pharynx
Floor of the mouth
Sub mucous swelling
Gingival
Floor of mouth
Lips & buccal mucous
Tongue
Palate
Neck
Mucosal surface lesion Vesiculobulous diseases
Ulcerative condition White lesions
Red blue lesions
Pigmented lesions
Verrucal papillary lesion
Differential diagnosis approach
to jaw lesions
Cyst of the Oral Region
Odontogenic Tumors
Benign Non Odontogenic Tumor
Inflamatory Jaw Lesions
Malignant Non-odont Neoplasm
Metabolic and Genetic Jaw Diseases
Soft tissue
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Example 1
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odontogenicTeeth component
Pulpitis
Pericoronitis
Periapical absess
Periostitis
Subperiosteal absess
Sub mucous abscess
Cellulitis
Phlegmoon
Subcutan absess
Bacterial infection
Actinomycosis
NUG
Pericoronitis
Syphylis
Gonorhoue Sinusitis maxillaris
Tbc
Leprosi
Noma
Sinus cavernosus
thrombosis
Viral infection
Vesiculobulosa
Herpes simplex
Recurrent herpes
Varicellazoster virus
Hand foot mouth dis
Herpangina
Measeles
Mumps
Fungal infection
Candidiasis
Deepfungus infection Subcutaneus fungus inf.
Sporotricosis
Opportunistic Infection
Mucor mycosis
Aspergillosis
Infection
Non odontogenic
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Example 2
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Viral diseases
Herpes simplex
infection
Varicella infection
Hand foot mouth
disease
Herpangina
Measles
Vesiculo-bulous diseases
Condition related with
immunology defect.
Pemphigus vulgaris
Mucous membrane
pemphigoid
Bullous pemphigoid
Dermatitis
herpetiform
Linear Ig A disease
Heriditary diseases
Epidermolysis
bullosa
Example 3
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Viral diseases
Herpes simplex infection
Varicella infection
Hand foot mouth disease
Herpangina
Measles
Vesiculo-bulous diseases
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Virus groupDNA virus RNA virus
1 Poxvirus
Small pox
Molluscum contagi
Vaccina
1 Myxovirus Influensa
2Herpes
Virus
Herpes simplex
Herpes zoster/
varicellaCytomegallo
2Paramyxo
virus
Rabies
3Adeno
virus
Pharyngoconj.tiva
Epidemic keratocon
junctivitis
3 Rhabdovirus Rabies
4 Papo virus 4 ArbovirusEncephalitis
Yellow fever
5Parvo
virus5 Rheovirus ISPA
6 Picornavirus HFM
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Schematic representation of herpes simplex virus
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Schematic diagram of the productive (lytic) replication of herpes
simplex virus type 1 (HSV-1)
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HSV-1 is an obligate, intracellular parasite
Requires a healthy host mammalian cell to produce new
progeny viruses through a productive (lytic) replication
cycle
Following attachment of the virion to the host cell by
specific receptors (viral envelope glycoproteins gB and gC
and cell surface heparin sulfate),
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The nucleocapsid gains entry to the cell by fusion of the
envelope with the plasma membrane.
The nonenveloped nucleocapsid is transported via
cytoskeletal elements of the host cell to the nuclear pores
where the viral DNA is released into the nucleus.
A tegument protein of the parental virus rapidly inhibits host
protein synthesis to allow for efficient translation of virus-specific transcripts by host ribosomes.
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Primary infection: direct contact with H SV
HOSPESSeronegative
Primary disease
Primary Herpet ic
Gingivostomat i t is PHG
Herpet ic With low
Subclinical infection Secondary disease
Secon dary or Recurrent
Herpes Sim plex Infect ions
Herpes Labial is, Herpetic
Withlo w (l ips , palate,
gingiva, hand f inger)
HOST CARRIER
Seropositive
Virus
Reactivat ion
Sunlig ht, fever,
mechanicaltrauma, allergy,
worry resolut ion
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Pathogenesis of herpes simplex infections
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Vesiculo-bulous diseases
Group viral infections
1. Herpes simplex virus infection, HSV
o Is a vesicular eruption of the skin and mucosa
o Pathogenesis : (previous sl ide)
o 2 forms : primary
acute primary herpetic gingivostomatitis,
PHG
: secondary
secondary or recurrent herpes simplex
infection, herpes labialis, HSL
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A. Acute Primary Herpetic Ging ivostomati t is, PHG
The classical clinical presentation of PHG with markedly swollen
interdental papillae and bleeding areas.
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Prodromal period :
One single virus can not produce disease
To achieve a substantial number of viruses intracellularreplication take place
One week, during which the patient does not present
any symptom.
A. Acute Primary Herpetic Ging ivostomati t is, PHG
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Prodromal period :
The initial symptoms are a lack of sensation or a tingling
sensation in the affected areas which are usually
keratinized (masticatory) mucosa.
Vesicles, are the basic manifestations of the disease, follow
the initial sensation.
Bullae and ulcer forming: ..
A. Acute Primary Herpetic Ging ivostomati t is, PHG
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Bullae and ulcer forming :
These vesicles are intraepithelial in location, and they
eventually coalesce forming bullae which extend to the
dermis becoming subepithelial
Vesicles and bullae break, especially in intraoral locations,
mostly associated to mastication.
Upon opening the vesicles leave painful superficial ulcers.
A. Acute Primary Herpetic Ging ivostomati t is, PHG
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The ulcers are seen in any of the oral mucosas and theoropharynx.
Occasional crusting over these ulcers, especially on the
lip, is also seen in the late stage of the infection.
PHG is essentially an ulcerative gingivitis.
The gingiva is characterized by marked erythema,
especially of the interdental papillae.
There is increased body temperature, regional
lymphadenopathy and incapacity to eat properly due to the
painful lesions.
A. Acu te Primary Herpetic Gingivos tomati t is, PHG
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A. Acute Primary Herpetic Ging ivostomati t is, PHG
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The primary infection lasts up to two weeks and resolves
itself without leaving scars or sequelae.
The clinical manifestations are more severe in
immunocompromised patients especially those withadvanced AIDS, leukemia or transplant patients.
After the clinical and/or sub clinical infection subsides the
virus goes into latency by reaching the regional ganglion,
such as the Gasser ganglion, migrating through the nerve
axon. The affected patient then becomes a carrier.
A. Acute Primary Herpetic Ging ivostomati t is, PHG
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A. Acute Primary Herpetic Ging ivostomati t is, PHG
A severe case of PHG with a secondary superimposed infection. Note the
sero-purulent exudate. The photo shows several ulcers on the lower lip
mucosa of the same patient.
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B. Secondary Or Recu rrent Herpes Simplex Infect ion,
Herpes Simp lex Labial is, HSL
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Excitants such as: GI upsets, stress, menses, solar radiation,
extreme cold or other infections, will reactivate the virus in
around 40% of carriers.
This reactivation induces migration from the ganglion to theperipheral epithelial cells where the virus replicate.
This new viral load will produce recurrent lesions which are
generally less severe than the primary ones.
The recurrent lesions on the lips go through several clinical
stages which are: burning sensation, erythema of the
affected area, vesiculation, ulceration and crust formation.
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B. Secondary Or Recu rrent Herpes Simp lex Infect io n,
Herpes Simp lex Labial is, HSL
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B. Secondary Or Recurrent Herpes Simplex Infection, Herpes
Simplex Labialis, HSL
Recurrent herpes simplex, also known as recurrent herpes
labialis (cold sores)
As the name implies, develops on the lips, generally at thejunction of the vermilion and the skin.
It begins as a burning sensation which last several hours to
one day.
Erythema is the second stage which is followed by small
coalescing vesicles, which are short lived.
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B. Secondary Or Recurrent Herpes Simplex Infection, Herpes
Simplex Labialis, HSL
Eventually the ulcer becomes covered by a dark red-brown
crust.
As a rule these episodes last 10 to 14 days. Recur- rencesmay vary from 1 to several a year.
Secondary lesions also heal without scar formation.
The oral recurrent lesions generally occur in the lip'svermilion, but lesions may also develop in the attached
gingiva and/or hard palate.
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B. Secondary Or Recurrent Herpes Simplex Infection, HerpesSimplex Labialis, HSL
All these intraoral locations are covered by keratinizing
epithelium.
The gingival and palatal lesions resemble intraoral burns and
are quite painful.
As well as the primary lesions, the recurrent ones are also
highly contagious.
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RHS lesions which have been secondarily infected. Note pus inside of
the vesicles and also areas of ulceration on the vermilion.
Recu rrent Herpetic Infect ion, HS Labialis
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Differential Diagnosis
Erythema Multiformis EM
Recurrent Aphthous Stomatitis, R A U
Herpangina
NUG
HFM
Pemphigus
Pemphigoid
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Herpetic whitlow (HW)
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Another form of herpes simplex infection: a herpetic whitlow
(HW)
Generally acquired as a contagious disease.
HW mostly affects the fingers of dentists and dentalhygienist which had become in contact
Vesicles and bullae were present on the index finger which
accidentally injured herself while working on a patient with
PHG.
Herpetic Whit low (HW)
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2. Varicella-Zoster Virus Infection
Primary, varicella-zoster virus (VZV) infection in
seronegative patient is varicella or chickenpox
Secondary, or reactivated disease is known as herpes
zoster or shingles.
VZV is very similar to HSV: DNA core, protein capsid and
lipid envelop.
The ability of the virus to remain in sensory ganglia forindefinite periods after a primary infection is quite the
same.
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A cutaneous or mucosal vesiculoulcerative eruption
following reactivation of latent virus is also same typical.
Serious complications from chickenpox include bacterialinfections which can involve many sites of the body
including the skin, tissues
2. Varicella-Zoster Virus Infection
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Varicella - Zos ter V
Primary disease ( varicella, chickenpox)
Self-limiting
Common in children, vesicular eruption of trunk and head
and neck occures in crops
Systemic signs symptoms , fever, malaise
Symptomatic treatment
Secondary disease (herpes zoster, shingles)
Self limiting
Adults
Rash, vesicles, ulcers unilateral along dermatome
Post herpetic pain can be severe
Immunocompromised and lymphoma patients, at risk
Treated with acyclovir
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Varicel la (chickenpox)
Chickenpox which involve many sites of the body including the skin,
tissues and mucosa
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Varicella (chic kenpox )
Pathogenesis
Transmission through the inhalation of contaminated
droplets.
Rapidly spread among child to child Incubation in 2 weeks, virus proliferates within
macrophages
Viremia and dissemination to the skin and other organs
Systemic sign and symptom develop Reside in a latent undetectable form in sensory ganglia
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Clinical features
Chills, malaise and headache may accompany rash that
involves primarily the trunk and head and neck
Rashvesicular eruptionpustular and eventuallyulcerates
Crops of new lesion appear owing to repeated waves of
viremia
Self limiting and last several weeks.
Varicella (chickenpox)
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Clinical features
Oral mucous membranes my be involved in primary
disease and usually demonstrate multiple shalow ulcers
that are preceded by vesicles.
Healing on skin with scar formation
Complication including pneumonitis, encephalitis and
inflammation
Varicella (chic kenpox )
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Herpes- Zos ter
Prodromal symptom of pain or paresthesia develop
and persist for several days as the virus infects the
sensory nerve of a dermatome of trunk ,head and neck
A vesicular skin eruption that becomes pustular andeventually ulcerated follows.
Local cutaneous hyperpigmentation may also be noted
on occasion
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Herpes- Zos ter
Herpes zoster of around the neck
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Clinical features
Basically a condition of the older adult population and
of individuals who have compromised immune
responses.
Involvement of the the various branches of the
trigeminal nerve may result in unilateral oral, facial or
ocular lesions
Ramsay Hunt syndrome : facial paralysis, vesicles of
ipsilateral external ear, tinitus, deafness and vertigo.
Herpes- Zos ter
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Clinical features
Prodromal symptoms of pain or paresthesia, a well
delineated unilateral maculopapular rash appears
vesicular- pustular and then ulcerative.
Complication include secondary infection of ulcers
postherpetic neuralgia, motor paralysis and ocular
inflammation.
Herpes- Zos ter
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Herpes- Zos ter
Herpes zoster of the lingual
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Differential diagnosis
Clinically diagnosed by the history of exposure and by
the type and distribution of lesions.
The longer duration, greater intensity of prodromal
symptoms, unilateral distribution with abrupt ending atthe midline and post herpetic neuralgia are favor a
clinical diagnosis of herpes zoster.
Herpetic gingivostomatitis
Necrotizing ulcerative gingivitis
Varicella
Erythema multiforme
Herpes- Zos ter
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Hand -Foot and Mouth Disease
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Hand -Foot and Mouth Disease
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Clinical features
Affect children and younger than 5 years of age
Incubation: 1-2 weeks
Sign and symptom: mild to moderate in intensity and low
grade fever, malaise, lymhadenopathy and sore mouth
Oral vesicle quickly rupture to become ulcers covered by a
yellow fibrinous membrane surrounded erythematous halo.
Hand -Foot and Mouth Disease
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Clinical features
Oral lesion:
o A few (5-20) small vesicles that soon rupture, leaving
slightly painful, shallow ulcers surrounded by a red
halo
o Buccal mucosa, tongue and palate are most
frequently affected.
Skin
o Small vesicles with a narrow red halo lateral and
dorsal surfaces f the fingers and toes , palms
o soles and buttock are the sites of predilection
Hand -Foot and Mouth Disease
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Etiology and pathogenesis
Herpangina is an acute viral infection that is caused by
coxsackie type A virus (A1-6, A8, A10, A22)
Transmitted by contaminated saliva and occasionally
through contaminated feces
4. H e r p a n g I n a
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Clinical features
Usually endemic with occurring typically in summer or early
autumn
Complain of malaise, fever, dysphagia and sore throat aftera short incubation period.
Intraorally a vesicular eruption appears on soft palate,
faucal pillars and tonsils, oropharynx and uvula.
Signs and symptoms are mild to moderate and last in a
week.
Herpangina
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Differential diagnosis
PHG
Aphthous ulcers
FAPA syndrome
E M
H F M
Gonococcal oropharyngitis
Streptococcal pharyngitis
Herpangina
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Etiology and Pathogenesis
Is a highly contagious viral infection cause by a member of
the paramyxovirus family
Related structurally and biologically to viruses of the
orthomyxovirus family which cause mumps and influenza.
The virus spread by airborne droplets through the
respiratory tract
5. Measles, Rubeola
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Measles , Rubeola
Kopliks spot : Pathognomonicsmall erythematous macules
with blues white necrotic
centers appear in the buccal
mucosa opposite molar
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Additional virus related to dentistry
Mumps Parotitis (not included in
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Etiology and Pathogenesis
Mumps is an acute, self
limiting infectious disease that
most frequently affect the
parotid gland of children 5-15
years of age.
The causative agent is a
paramyxovirus.
Transmission is by direct
contact with salivary droplets
Mumps, Parotitis (not included in
vesiculous-bulous disease)
Mumps Parot i t is
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Clinical features
Fever malaise, headache and chills and preauricular pain
The parotid swelling tends to be asymmetric at the outset,
reaching maximum proportion within 2-3 days
Stensen s duct may become partially occluded as the
gland swells
Affects males and females equally, especially young adults
and children.
Potentially serious complications is orchitis or oophoritis
can occur in adults.
Mumps , Parot i t is
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Salivary gland involvement
Parotid tenderness with overlying facial edema
Painful swelling of one or both of the parotids that last forabout 7 days
The auricula tend to raised up
Orifice of the Stenson duct is usually red and swollen
Variable swelling and tenderness of submandibular and
sublingual glands
Mumps , Parot i t is
M P ti t i
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Differential diagnosis
Acute suppurative parotitis
Calculi in the parotid ducts
Buccal cellulitis
Sjogren syndrom
Mikulicz syndrome
Sarcoidosis
HIV infection
Neoplasma
Mumps , Parot i t is
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June 2000
Oral Manifestations Of HIV
Infection:Clinical Characteristics,
Diagnosis, And Treatment
Recommendations
Joan A. Phelan, DDS
Di i Of HIV R l d O l
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Diagnosis Of HIV Related Oral
Lesions
Oral examination procedures are the samefor HIV patients as for all dental patients
Diagnostic procedures must be appropriate to
the identified problem
Treatment should be based on either aprovisional or definitive diagnosis
Diagnosis should be re-evaluated if treatmentis not effective
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Oral Manifestations Of HIV
Infection
Opportunistic diseases--manifestations
of immune deficiency or derangement. Not caused directly by HIV.
The same lesions occur in association
with other immune deficiency disorders.
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HIV-related Oral Lesions
Infections Fungal, Viral, Bacterial
NeoplasmsKaposis Sarcoma, Non-Hodgkins Lymphoma
Other
Non-specific or Aphthous-like Ulcers, Lichenoidor Drug Reactions, Salivary Gland Disease
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Oral Candidiasis
Pseudomembranous
Erythematous Hyperplastic
Accompanying angular cheilitis
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Hyperplastic Candidiasis
Appearance: as a leukoplakia (a whitelesion that does not rub off)
Definitive diagnosis requires:
Identification of fungal hyphae in the lesion
Response of the lesion(s) to antifungaltherapy
If unresponsive to antifungal therapy, biopsymust be considered
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76HIV AIDShyperplastica candidiasis
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June 2000 HIV AIDShyperplastica candidiasis
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June 2000
Angular Cheilitis
Appearance: erythema and/or fissuring at
the corners of the mouth Frequently accompanies intraoral
candidiasis
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Kaposis Sarcoma
Is an unusual neoplasm first describe 1872 byMoritz Kaposi.
Early 1980 it has become quite commonbecause of its propensity to develop in
individuals infected by HIV virus causes by herpes virus 8 (associated
herpesvirus)
The lesion arises from endothelial cells
Four clinical presentations are recognized:
1.classic (chronic), 2. endemic (African),
3. iatrogenic 4. AIDS related
Kaposis Sarcoma
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Kaposi s Sarcoma
Main clinical features :almost all oral sarcoma presents with similar clinicalsigns and symptoms :
painless or painful, rapidly or slowly growingswelling or mass
the mass may be soft or semi-hard or hard onpalpation with or without ulceration.
the color may be red, blue red, or normal
the tongue, palate, buccal mucosa, gingiva andthe jaws are more frequently affected.
bony swelling, loosening of teeth and paresthesia
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Kaposi sarcomapalatal-bucal
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Kaposis Sarcoma
Appearance: Oral lesions appear as reddishpurple, raised or flat
Size ranges from small to extensive
Behavior is unpredictable
Definitive diagnosis: biopsy and histologicexamination
No curative therapy--radiation treatment,
chemotherapy and sclerosing agents havebeen, used to control oral lesions
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Kaposis Sarcoma
KS typically evolves through 3 stages.
1. Patch (macular): characterized byproliferation of miniature vessels. Thelesional endothelial cells have a blandappearance and may be associated withscattered lymphocytes and plasma cells
2. Plaque
3. Nodular
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Kaposis Sarcoma
KS typically evolves through 3 stages.
2. Plaque : demonstrates further proliferationof vascular channels along with thedevelopment of a significant spindle cellcomponent
3. Nodular : the spindle cells increase to forma nodular tumorlike mass that mayresemble a fibrosarcoma or other spindlecell sarcomas.
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86
Kaposi sarcomadorsal
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87
Kaposi sarcomapalatal-bucal
Kaposis Sarcoma
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Kaposi s Sarcoma
Differential Diagnosis:
Soft tissue sarcomas
Soft tissue abses
Pyogenic granuloma
Hemangioma
Peripheral giant cell granuloma
Non-Hodgkin lymphoma Salivary gland tumors
Squamous cell carcinoma
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End session