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7/28/2019 1- Lab Infections of the Oral Mucosa
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Infections of the Oral
Mucosa
LAB 1
Dr. Tahani Abualteen
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Viral Infections
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The following viruses may cause oral infections or oral manifestations:
1. Herpes viradae (or Human Herpes viruses)
2. Coxsackie A virus causing Herpangina and hand, foot & mouth
disease
3. Paramyxovirus causing measles and mumps (may be associated
with non-specific stomatitis)
4. Human Papilloma Virus (HPV) causing warts/epithelial
hyperplasias
5. Human Immunodeficiency Virus (HIV)
6. Influenza Viruscausing influenza (may be associated with non-specific stomatitis)
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Herpes viradae (or Human Herpes viruses):
Generally speaking, these viruses tend to produce an initial primary infection, get
latent somewhere in the body and then they may be reactivated for a reason or
another to cause recurrent or secondary infections
These viruses include:
1. Herpes Simplex (HSV) type 1 causing herpetic stomatitis (primary/recurrent)
ofskin & oral mucosa
2. Herpes Simplex (HSV) type 2 causing herpetic stomatitis (primary/recurrent)
ofgenitalia3. Varicella Zoster (VZV) causing chickenpox (primary) & shingles"herpes zoster"
(recurrent)
4. Epstein-Barr virus (EBV) causing infectious mononucleosis "glandular fever
(primary) and hairy leukoplakia (recurrent) (may be associated with non-
specific stomatitis)5. Cytomegalovirus (HHV5) causing cytomegalovirus infection(may be
associated with non-specific stomatitis)
6. Human Herpes Virus 6 (HHV6) not common
7. Human Herpes Virus 7(HHV7) not common
8. Human Herpes Virus 8(HHV8) thought to be associated with Kaposis sarcoma
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This 12 years old child is presented to the dental
clinic with Multiple vesicles and ulcers affecting
both keratinized and non-keratinized mucosae and
widespread gingival inflammation
Knowing that the patient is having this situation for
the first time in his lifetime and his little brother hadthe same situation 1 week earlier
The histopathological picture is shown below
1- Whats the most likely diagnosis?!
2- Whats the causative agent?!
3- How did the condition probably spread from thelittle brother to the patient?!
4- Describe the clinical course of the disease?!
5- Is this condition usually clinical or subclinical?!
6- Do lesions only occur intraorally?! And if can occur
extraorally, then where?!
7- Does the immunity gained after this primary
infection protect against farther secondary
infections?!
8- Describe the histopathological appearance?!
9- What happens to the virus at the end of this
primary infection?!10- Whats the treatment?!
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Mild Circumoral crusting
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Herpes virus maybe transmitted to
fingers causing a
primary infection
which is extremely
painful known asHerpetic
whitlow
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Primary herpetic gingivostomatitis
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Tzank cells
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Intraepithelial
vesicle
Multinucleated epithelial cells
Tzanck
Cell
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Balloon cell
degeneration
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This 24 years old female patient is presented to the
dental clinic with clusters of vesicles on the lips
and adjacent skin
She stated that these lesions started to appear
few hours after local Prodromal symptoms ofitching or tingling
Knowing that the patient had this situation before
The histopathological picture is shown below
1- Whats the most likely diagnosis?!
2- Whats the causative agent?!3- How did the condition probably develop?! And
what factors participate?!
4- Describe the clinical course of the disease?!
5- What can the patient do before these vesicles and
ulcers appear to minimized symptoms?!
6- Do lesions only occur extraorally?! And if can
occur intraorally, then where?!
7- If this patient contacts another patient, will she be
spreading the infection to someone else?!
8- Describe the histopathological appearance?!
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Thi 10 ld hild i d h d l
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This 10 years old child is presented to the dental
clinic with Multiple vesicles and ulcers affecting
the skin & the oral mucosa
Skin lesions are pruritic while mucosal lesions are
asymptomatic
Knowing that the patient is having this situation forthe first time in his lifetime and his little brother
had the same situation 1 week earlier
The histopathological picture is shown below
1- Whats the most likely diagnosis?!
2- Whats the causative agent?!3- How did the condition probably spread from the
little brother to the patient?!
4- Describe the clinical features of the disease?!
5- Does the immunity gained after this primary
infection protect against farther secondary
infections?!6- Describe the histopathological appearance?!
7- What happens to the virus at the end of this
primary infection?!
8- Whats the treatment?!
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Intraepithelial
vesicle
Multinucleated epithelial cells
Tzanck
Cell
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Pharyngitis lymphadenopathy
Petechia
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Bacterial Infections
This 25 years old male is presented to the
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This 25 years old male is presented to the
dental clinic with this unique clinical
appearance of the gingiva
1- Describe the clinical presentation?!2- Whats the most likely diagnosis?!
3- Whats the causative agent?!
4- Describe the clinical features of the
disease?!
5- What are the predisposing factorsinvolved in the etiology of this condition?!
6- How to diagnose such condition?!
7- Give me one differential diagnosis?!
8- What is the possible complication?!
9- Whats the treatment?!
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Noma (Cancrum Oris)
Severe and rapidly destructive gangrene of the
orofacial tissue and jawsUsually preceded by NUG followed by rapid spread of
necrosis from gingiva to cheeks
Almost all cases appear in developing countries
(especially Africa) particularly in malnourished
children whose resistance has been lowered by
concurrent infections such as measles or malaria(i.e. immunosuppressed individuals)
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Actinomycosis
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Neutrophils Actinomyces colonies
Actinomycosis
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Primary Syphilis (Chancre)
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Secondary Syphilis (Mucous Patches)
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Secondary Syphilis (Snail-track ulcers)
Snail-track ulcers flat areas ofulceration that coalesced
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Tertiary Syphilis (Atrophic Glossitis)
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Congenital Syphilis (Dental anomalies)
Hutchinsons
Incisors
Mulberry Molars
This 45 years old male is presented to
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y p
the dental clinic with indurated painless
undermined ulcer affecting his tongue
He is also present with granulating
gingival hyperplasia in the lowerright quadrant and granulating
cervical lymph nodes
1- Whats the most likely diagnosis?!
2- Whats the causative agent?!
3- How does the causative agent usually
infect the mouth?!
4- Describe the clinical features of this
condition?!
6- How to diagnose the condition?!7- Whats the treatment?!
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Tuberculosis
Granulating
gingival
hyperplasia
Tuberculous
Lymphadenitis
This 60 years old male is presented to
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the dental clinic with nodular masses of
the skin which cause facial deformity
and tend to ulcerate occasionally
Similar masses are found on anterior
maxillary Gingivae, tongue and palate
1- Whats the most likely diagnosis?!
2- Whats the causative agent?!
3- How many forms of the condition are
there?!4- Within which form oral lesions
occur?!
How does the causative agent usually
infect the mouth?!
4- Describe the clinical features of this
condition?!
6- How to diagnose the condition?!
7- Whats the treatment?! are
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Gonorrhea Neisseria gonorrhea
Mainly Tonsillar and soft palatal lesions Oral lesions are non-specific, presenting as:
Erythema, vesicles, ulcers, pain on speaking
and swallowing
Granulomatous infections:
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Granulomatous infections:
Actinomycosis:
Endogenous polymicrobial infection
Submandibular swelling
Chronic suppuration
Multiple sinuses draining pus
Sulphur granules in pus
Syphilis:
Primary chancre
Secondary snail-track ulcers, mucous patches
Tertiary Gumma, lingual leukoplakia
Congenital Hutchinson incisors, mulberry molars, dished face
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Tuberculosis:
Oral usually secondary to pulmonary Painless chronic lingual ulcer
Leprosy:
Oral lesions in Lepromatous type
Secondary to nasal involvement
Nodular masses on palate/anterior maxillary gingiva
Granulomatous infections:
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chronic ulcer:InfectiousDifferential diagnoses of an
1. Syphilis
2. TB
3. Cytomegalovirus in immune-compromised patients4. Deep fungal infection
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specific oral lesions:-Causes of non
1. Gonorrhea
2. Infectious mononucleosis (Glandular fever)
3. Cytomegalovirus infection4. Paramyxovirus infection
5. Influenza
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Fungal Infections
Fungal infections of oral mucosa frequently encountered are those
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Fungal infections of oral mucosa frequently encountered are those
due to species of the genus " Candida"
" Candida albicans"is the principle species associated with oral
infection,but other species such as: C. glabrata, C. tropicalis, C.
parapsilosis, C. krusei are also pathogenic
Candida species (especially C. albicans) is characterized by the
following:
Commensal microorganism in the mouth of about 40% of the
population
** Commensalism = benefiting from living in the oral cavity
without harming the host or the flora present there
Dimorphic (exists in two forms; the bud form "present as small
oval yeasts in carriers", and hyphal form "present as elongatedrod-like or ribbon-like structure in patients)Multiply bybudding (production of buds from ovoid yeast cells,
buds then separate and grow to form hyphae)
Variable carriage rates
Candida species (especially C albicans) is characterized by the following:
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Candida species (especially C. albicans) is characterized by the following:The primary oral reservoir for the organism in carriers is the posterior
dorsum of the tongue (probably due to its rough surface)
There is overlap in the candidal counts in saliva from carriers and from
individuals showing infection and so isolation of Candida from the mouth of
an adult is not confirmatory evidence of fungal infectionIt is presumed that Candida has a direct etiological relationship with a
lesion if hyphae are present in smears or in histological sections of the
lesion** The pathogenic form of Candida is the hyphal form that if noticed in theoral cavity it indicates active fungal infection
** The presence of yeasts alone "bud form" not being regarded as
confirmatory evidence for fungal infection but it might indicate a carrier
state
** So to diagnose a patient with fungal infection (candidosis) we cantsimply rely on the presence of Candida nor on their count, BUT insteadwe
need to see the hyphal form histologically and the lesion clinicallyOpportunistic pathogen that is waiting for a chance to cause infection
whenever the balance between the host and the organism is disturbed by
different local or systemic factors
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Factors predisposing to candidal infection:
Local factors: trauma, denture hygiene, tobacco
smoking, carbohydrate-rich diet
Age neonates or elderly people they may not have a
competent immune system
Drugs: broad spectrum Antibiotic (kill the bacteria anddisturb the balance between bacteria and fungi and this favors
candidal growth and proliferation), steroids (cause immunesuppression and disturb the balance between host and fungi
and this favors candidal growth and proliferation), Cytotoxic
drugs
Xerostomialeads to decreased washing effects ofsaliva and this might enhance the adherence of Candida
to the oral mucosa
Systemic diseases
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Protection against candidal infection
Non specific factors: shedding of epithelium,
salivary flow, Commensal bacteria (oral flora)
Specific factors (targeting the Candida specifically):
Serum antibodies is less important
Secretory antibodies (e.g. IgA) is more
important (it decreases adherence of Candida to
oral epithelium)
Cell mediated immune responses
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Pathogenesis of Candidal infection:
Adherence
Secretion of enzymes (such as proteineases)
which enable the hyphae to invade the oral
epithelium
Invasion of epithelium by hyphae
Secretion of nitrosamine compounds which
may play a role in oral carcinogenesis
? Type 4 hypersensitivity to candidal pathogens
Classifications of oral and Perioral candidosis:
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Classifications of oral and Perioral candidosis:
Group 1: primary oral candidosis (candidosis confined to oral & Perioral
tissues)
Acute:PsuedomembranousErythematous (atrophic)ChronicPsuedomembranousErythematous (atrophic)Hyperplastic (candidal leukoplakia)Candida associated lesions:Denture stomatitisAngular cheilitisMedian Rhomboid glossitis** In here Candida may be found in association with these mucosal lesions, but acausal relationship has not been fully established
Group 2: secondary oral candidosis (oral candidosis is a manifestations of a
generalized systemic candidosis)Systemic mucocutaneous candidosis
This 45 years old female is presentedt th d t l li i ith thi k hit
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to the dental clinic with thick white
plaque/coating on the buccal mucosa,
that can be wiped away/scraped off
leaving a red inflamed & bleeding base
The patient complains ofpain and
burning sensation sometimes
The patient is diabetic
1- Whats the most likely diagnosis?!
2- Whats the causative agent?!3- What are the predisposing factors?!
4- What do we call these white
plaques?! And what are they made
from?!
5- How to diagnose the condition?!
Acute Psuedomembranous
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Acute Psuedomembranous
candidosis (Thrush)
Thick white plaque/coating (psuedomembrane) on affected
mucosa, that can be wiped away/scraped off leaving a red
inflamed & often bleeding base
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PAS stain
PAS (Periodic Acid Schiff) stain is a special dye that stains the
carbohydrate-rich wall in Candida with a red or pink color
This 40 years old female is presentedt th d t l li i ith ddi h
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to the dental clinic with reddish
painful depapillated dorsum of the
tongue
The patient complains ofgeneralized
pain, discomfort and burning
sensation most of the time
The patient is on antibiotic regimen
since 2 years
1- Whats the most likely diagnosis?!2- Whats the causative agent?!
3- What are the predisposing factors?!
4- Where is this condition seen most
commonly?!
5- How to diagnose the condition?!
Acute Erythematous candidosis
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Acute Erythematous candidosis
(antibiotic sore tongue)
Red atrophic area of oral mucosa causing generalized pain,
discomfort or burning sensation
This 47 years old male is presented to thedental clinic with reddish painless palatal
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dental clinic with reddish painless palatal
mucosa delineated by the outline of upper
removable partial denture
1- Whats the most likely diagnosis?!2- Whats the causative agent?!
3- What are the predisposing factors
increasing the probability of such condition
in denture wearers?!
4- Where is this condition seen mostcommonly?! Upper or lower dentures?!
5- How to diagnose the condition?!
6- What is the unique thing about the
histopathological findings?!
7- How many patterns are there?!
This 35 years old male is presented to thedental clinic with reddish painless
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dental clinic with reddish painless
depapillated lesion in the middle of the
dorsum of the tongue just anterior to
foramen cecum
The lesion is roughly rhomboidal in shape
1- Whats the most likely diagnosis?!
2- Whats the causative agent?!
3- What are the predisposing factors
increasing the probability of such conditionin denture wearers?!
4- What can we clinically find in some
patients?!
5- How to diagnose the condition?!
6- Give me one differential diagnosis?!
M di Rh b id Gl i i
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Median Rhomboid Glossitis
Median (occurs in the midline), Rhomboid (due to its shape),
glossitis (inflammation of the tongue)
This 62 years old female is presented tothe dental clinic with cracks fissures
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the dental clinic with cracks, fissures,
crusts, and pain in the commissure area
bilaterally
The patient is denture wearer
1- Whats the most likely diagnosis?!
2- Whats the causative agent?!
3- Whom patients are mainly affected?!
4- What are the types of candidosis thiscondition is usually related to?!
5- What are the predisposing factors
increasing the probability of such
condition?!
5- How to diagnose the condition?!
A l Ch liti
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Angular Chelitis
Angular (occurs at the corners of the mouth),
chelitis (inflammation of the lips)
This 25 years old female is presented tothe dental clinic with triangular
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the dental clinic with triangular,
bilateral, white patch on the buccal
mucosa at the commissure area
The white patch seems speckled and
cant be scrapped off
The patient is a smoker
1- Whats the most likely diagnosis?!
2- Whats the causative agent?!
3- Whom patients are mainly affected?!4- What is the type of candidosis this
condition is usually related to?!
5- What are the local predisposing
factors increasing the probability of such
condition?!6- Whats the most commonly affected
site?!
7- Can this lesion be multifocal?! Whats
the term used to describe such a case?!
This 50 years old female is presented tothe dental clinic with triangular
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the dental clinic with triangular,
bilateral, white patch on the buccal
mucosa at the commissure area
The white patch seems speckled and
cant be scrapped off
The patient is a smoker
8- Give me one differential diagnosis
clinically?!
9- How to diagnose the condition?!10- Describe the histopathological
presentation?!
11- Is it considered a premalignant
lesion?! Why?!
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This 50 years old female is presented to
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the dental clinic with multiple white
patches affecting oral mucosa, skin and
nails
The white patches cant be scrapped off
1- Whats the most likely diagnosis?!
2- Is oral mucosa frequently involved in
this condition?!
3- What type of candidosis do orallesions of this condition resemble?!
4- Can this lesion be multifocal?!
Oral manifestations of the deep fungal infection (deep visceral
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Oral manifestations of the deep fungal infection (deep visceral
mycoses):
Oral lesions are uncommon, but may present as non-specificulceration or as nodular granulomatous areas
Lesions are NOT caused by Candida (Candida cause
superficial lesions only)Examples ofdeep fungal infections which may be associated
with oral lesions are:
BlastomycosisHistoplasmosisZycomycosisCoccidiodomycosis
Deep Fungal Infection
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Blastomycosis
Deep Fungal Infection
Deep Fungal Infection
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Histoplasmosis
Deep Fungal Infection
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HIV infection & AIDS
Transmission of the HIV virus may be
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Transmission of the HIV virus may be
followed by the following stages:
Sero-conversion: Detection of HIV antibodies in blood Within 3 months of exposure Few patients may have also acute symptoms
Sero-postitive: Symptom free for many years
Later on: Persistent generalized lymphadenopathy
AIDS related complex: persistent pyrexia, lymphadenopathy,diarrhea, weight loss, fatigue and malaise
Fully developed AIDS: Opportunistic infections, Kaposi sarcoma, non Hodgkin's
lymphoma.
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Classification of oral lesions associated with HIV infection(fully developed AIDS)
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(fully developed AIDS)Group 1 "lesions strongly associated with HIV"
Candidosis (erythematous, psuedomembranous, hyperplastic)
Hairy leukoplakia (EBV) HIV-associated periodontal disease (HIV-gingivitis, NUG, HIV-periodontitis,
necrotizing stomatitis)
Kaposis sarcoma
Non-Hodgkin's lymphoma
Group 2 "lesions less commonly associated with HIV" Atypical ulceration (oropharyngeal)
Idiopathic thrombocytopenic purpura
Salivary glands disorders (dry mouth, decreased salivary flow rate, uni- or bilateral
swelling of major glands)
Viral infections "other than EBV"(HSV, VZV, CMV, HPV)Group 3 "lesions possibly associated with HIV"
Bacterial infections other than gingivitis/periodontitis
Fungal infections other than candidosis
Melanotic hyper-pigmentation
Neurological disorders (facial palsy, trigeminal neuralgia)
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This 55 years old male is presented to thedental clinic with bilateral vertical white
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folds on lateral border of the tongue
The white folds cant be scrapped off
Histopathological presentation is shown
below
1- Whats the most likely diagnosis?!
2- Whats the causative agent?!
3- Whom patients might be affected with
such kind of condition?!4- Describe the clinical features?!
5- What other microorganism can be
isolated from the surface of the lesion?!
What is its role?!
6- Is it premalignant?!7- Describe how does this condition
usually occur?!
8- Give me one factor that might influence
the location of this condition?!
This 55 years old male is presented to thedental clinic with bilateral vertical white
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folds on lateral border of the tongue
The white folds cant be scrapped off
Histopathological presentation is shown
below
9- What serological finding this patient
might have?!
10- Whats the most commonly affected
site?!11- Describe the histopathological
presentation?!
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Kaposis Sarcoma
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Kaposi s Sarcoma
K i
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Kaposi sarcoma
Proliferating endothelialcells
Cleft like vascular channels
Extravasated RBC
Inflammation
Occasional atypical cells Later stages more atypical
cells
Early stages difficult todifferentiate it from other
vascular lesions
Slit-like vessels
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HIV associated periodontal diseases:HIV-gingivitis (linear gingival Erythema)NUGNUP** Prevalence is less than 10% of all cases
(prevelanact is now low, particular for
patients on HAART)
This 25 years old male is presented tothe dental clinic with Linear band ofErythema on the free gingival margin
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Erythema on the free gingival marginthat doesnt appear to be related to theaccumulation of dental plaque (patient
has excellent oral hygiene)The Erythema is NOT responsive toplaque control
1- Whats the most likely diagnosis?!
2- Whats the mechanism by which this
condition occur?!
3- What microorganism can be
associated with such condition?!
Acute Necrotizing Ulcerative
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Gingivitis
In HIV-infected patients, the lesions may be persistent and
extensive & may NOT respond to conventional treatment
Necrotizing Ulcerative
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g
Periodontitis Severe rapidly destructive
process
Necrosis of gingival andperiodontal tissues
Exposure of alveolar bone
and sequestration Due to sever impairment of
local defensive mechanismslike reduction in CD4 cells
Defects usually localized
Not responsive toconventional periodontaltherapy
Other oral manifestations of HIV
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Non Hodgkin's lymphomaNeurological disturbances:HIV is neurotropic may directly involve CNSFacial nerve palsy
Atypical ulceration: resemble aphthous stomatitis may beassociated with CMV
Salivary gland disease:xerostomiaSalivary gland enlargement associated with lymphocytic
infiltrateLymphoepithelial cysts
Idiopathic thrombocytopenic purpura:
Present as superficial bleeding spots due to reduction in the
platelets count by an autoimmune response
infection
HIV associated HSV infection
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HIV associated HSV infection
HIV associated HZV infection
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HIV associated HZV infection
HIV thrombocytopenic purpura,
7/28/2019 1- Lab Infections of the Oral Mucosa
95/97
y p p p
autoimmune response
HIV oral ulceration
7/28/2019 1- Lab Infections of the Oral Mucosa
96/97
HIV oral ulceration
7/28/2019 1- Lab Infections of the Oral Mucosa
97/97