Block 4 Flashcards
squamous papilloma = bpsse
what does this result in?
benign proliferation stratisfied squamous epitelium
papillary or verruciform mass
what induces squamous papilloma? How do you id it?
- Human Papilloma Virus 6 and 11
- ways:
- PCR
- immunohistochemistry analysis
- in situ hybridization
Sq pap is identified _____ in oral papilloma and _____ in normal mucosal cells
- 50 % oral papilloma
- 5% in normal mucosal cells
Clincal features of sq papilloma:
sppec
- s = soft
- p = painless
- p= pedunculated
- e = exophytic nodule with finger-like surface projections
- c = look cauliflower or wartlike
what is the most common SOFT TISSUE MASS arising from the SOFT PALATE?
squamous papilloma
sq pap occurs ____ in men and women and at any age but specifically at ages _____?
- equally among men and women
- 30 - 50 yo
Finger-like projections can be _____ or ____ and _____, _____, _____ in color depending on the amt of surface keratinization
- blunted or pointed
- white, slightly red, normal in color
what are the histo features of sq papilloma? 3 things
- psep = pedunculated surface epithelial proliferation
- fct = fibrovascular connective tissue core
- koilocytes
- virus altered epithelial clear cells
- with dark nuclei [pyknotic]
- seen high in prickle cell layer
true or false:
If left untreated, they rarely transform into malignancy, continuous enlargement, or dissemination to other parts of the oral cavity
true
true or false
- Conservative surgical excision [w/ base of the lesion] is adequate;
- recurrence is likely.
- true
- false, unlikely for recurrence
What are the 3 Oral warts?
1) Verruca Vulgaris
2) Condyloma Acuminatum
3) Focal Epithelial Hyperplasia
Verruca Vulgaris is Benign, virus-induced, ________plasia of stratified squamous epithelium.
focal hyperplasia
true or false
HPV types 2, 4, 6, and 40 are found in virtually all examples of verruca vulgaris
and what are found for HPV 6 and 11?
- true
- squamous papilloma
Verruca vulgaris is Contagious, can spread to other parts of a person’s _______ or ______ by way of autoinoculation.
- skin
- mucous membranes
true or false
- Verruca vulgaris frequently develops on oral mucosa,
- extremely common on the skin
- false, infrequently develops on oral mucosa
- true
define Cutaneous horn/keratin horn which is a clinical feature of verruca vulgaris
- extreme accumulation of compact keratin
- results in hard projection several millimeters in height
- = keratin horn aka cutaneous horn
what are 3 other cutaneous lesions that creates cutaneous horns?
SAS
1) seborrheic keratosis,
2) actinic keratosis,
3) squamous cell carcinoma.
what are the 3 histofeatures of the verruca vulgaris ?
1) hyperkeratotic stratisfied squamous epithelium
2) elongated rete pegs at the EDGES of the lesion that converge at the CENTER
3) koilocytes in the upper epithelial layer
Skin verrucae – topical _____ acid, topical ______ acid, or liquid ________.
salicylic acid
lactic acid
nitrogen cyrotherapy
true of false verruca vulgaris
Surgical excision is always indicated for cases with an__________ in which the dx is uncertain.
false, ONLY FOR atypical clinical presentation for dx uncertain
typical cases use:
salicylic acid, lactic acid, or lq nitrogen cyrotherapy
Verruca vulgaris, Oral lesions – uses what 4 treatments?
surgical excision,
laser,
cryotherapy,
electrosurgery
verruca vulgaris, Recurrence – seen in a _____ portion of treated cases
small
w/out treatment, verrucae ____ transform into malignancy, and ____ will disappear spontaneously w/in 2 years
do NOT
2/3s disappear spontaneously in 2 years
what is the most common skin wart?
verruca vulgaris
waht is another name for condyloma acuminatum?
veneral wart
condyloma acuminatum, Virus-induced proliferation of stratified squamous epithelium of the 4______?
genitalia
perianal region
mouth
larynx
waht 2 types of HPV are often found in veneral wart? and waht it similar to?
6 and 11 just like squamous papilloma
condyloma acuminatum, Represents ___ of all STDs diagnosed in STD clinics and may be an indicator of sexual abuse when diagnosed in ____
20%
young children = may be an indicator of sexual abuse
true of false can veneral wart
be passed from mother to child in utero.
true
condyloma acuminatum can occur in:
mouth
larynx
genitalial
perianal region,
but specifically for the papillary lesions in the mouth, which 3 areas?
lingual frenum
labial mucosa
soft palate
4 veneral wart clinical features?
1) Sessile,
2) pink,
3) well-demarcated,
4) nontender exophytic mass w/ short, blunted surface projections.
Histo features of condyloma acuminatum, _______stratified squamous epithelium forming a ______ projection
Koilocytes in the ______ [arrows]
acanthotic stratisfied squamous epi
blunted projections
koilocytes in the spinous layer
what are the 2 treatments for ORAL condyloma acuminatum?
conservative surgical excision
laser ablation
what are the cons of laser ablation?
what treatment is this used for?
- causes aerosolized microdroplets
–> to airborne spread of HPV
- ORAL condyloma acuminatum
veneral wart, treatment of Anogenital, non-oral lesions = Nonsurgical, patient-applied topical agents 2___?
imiquimod
podophyllotoxin
true or false
Condyloma infected w/ ____ or ____ are associated w/ an increased risk of malignant transformation to squamous cell carcinoma
HPV-16 or HPV-18
true
true of false
veneral wart, Should be removed b/c it is contagious and can spread to other oral surfaces and to other persons through direct (sexual) contact
what else is also contagious?
true
verruca vulgaris
what is typically low risk lesions of HPV 6 and 11 and are dome shaped?
condyloma acuminatum
“accumulation of little hills”
veneral wart
waht is another name for multifocal epithelial hyperplasia?
Heck’s disease
multi focal epi hyperplasia, Virus-induced, localized proliferation of oral squamous epithelium is induced by?
HPV 13 and 32
multifocal epi hyperplasia
May be related to eithery _______ or _____ transmitted by _________ .
Association w/ ________.
genetic suscpetibility
HPV transmitted by
family members
HLA-DR4 allele
what are the risk factors of multifocal epi hyperplasia?
lower socioeconomc status
crowded living conditions
poor oral hygiene
multifocal epithelial hyperplasia
Lesions arise more often in people with ____.
aids
multifocal epi hyperplasia
Usually _______ condition, but can affect young and middle-aged adults
Slight ______ predilection, or no significant gender bias
childhood
female
Common sites of multifocal epi hyperplasia?
Rarely seen?
common:
labial, buccal, lingual mucosa
gingival, palatal, and tonsillar regions
rarely:
conjunctiva region
what are the histo features of multifocal epi hyperplasia?
- acanthotic epithelium with broad and elongated rete pegs
- mitosoid cells containing altered nuclei in otherwise mature and well-differentiated stratisfied squamous epithelium
true or false of mutlifocal epi hyperplasia
Spontaneous regression of these lesions has been reported after months or years and is inferred from the rarity of the disease in adults.
true
4 backgound information of molluscum contagiosum
- epithelial hyperplasia
- molluscum contagiousum virus [DNA pox virus]
- sexual and non sexual transmission
- lesions have predilection for warm skin and recent injury
what are the non sexual ways for transmission of molluscum contagiosum
bathing
swimming
wresting
sharing clothing
who does molluscum contigosum affect?
immunocompromised
HIV [5 - 18%}
atopic dermatitis pt
Darier’s Disease
children and young adults
molluscum contagiosum is like verruca vulgaris in two ways
what are the two ways
- like verruca vulgaris and condyloma acuminatum - multiple papules [non solitary]
- like verruca vulgaris **commonly **affects SKIN - skin of head, neck eyelids, trunk and genitial
- oral involement is - buccal mucosa, lips, gingiva or palate
like multifocal epi hyperplasia, molluscum contagiousum is similar for the treatment
no TX
spontaneous regression in 6 - 9 MONTHS
tx can be given to decrease risk of transmission or provide symptomatic relief
Leukoplakia is what?
- white plaque or patch that cant be rubbed off
- CAN NOT be clinically or pathologically identified as another disaese
leukoplakia is waht type of term?
clinical term, NOT a specific tissue alteration
waht are the clinical COLORS of leukoplakia?
- thickened keratin surface epi [white when wet]
- thickened spinous layer [masks vascularity of underlying CT]
4 causes of leukoplakia
- tobacco [highly correlated]
- UV radiation [caustive factor for leukoplakia on the vermillion border of the lower lip]
- micro-o = HPV 16 and 18
- sanguinaria [maxillary vestibule and alveolar max mucosa]
what is the most common INDICATOR of evolving or actual malignancy
leukoplakia
most common ORAL precancer or premalignant lesion
leukoplakia
who does leukoplakia affect
+40
5
70%
> +40 yo
prevalence increases with age
found to occur 5 years earlier than SCC
70% vermillion border, buccal mucosa, and gingiva
give me the order of change in leukoplakia from plaque to projections
early grary plaque
mild/thin leukoplakia
homogenous/ thick leukoplkia [leathery]
granular / nodule leukoplakia
verrucous / verruciform leukoplakia [projections]
what is PVL and what are the info
Proliferative VERRUCOUS leukoplakia
- high risk, slowly spread
- development of multiple keratotic plaque with rough surface projections
- GINGIVA FREQ involved
- STRONG FEMALE predilection
- looks like verrucous carcinoma, but this will have dysplastic changes and in 8 year will turn to SCC
- simple flat hyperkeratosis -> persistent growth -> exophytic and verruca in nature
development of multiple keratotic plaque with rough surface projections, is what?
proliferative verrucous leukoplakia
speckled leukoplakia aka waht and give the descriptio
erythroleukoplakia
- intermixed red and white lesion
- lesions ahve scattered red patches
- epi cells are immature or atrophic cant make keratin
- reveals advaced dysplakia on biopsy
waht is reveals advaced dysplakia on biopsy
speckled leukoplakia
Hyperkeratosis
thickened surface keratin epithelium with or WITHOUT acanthosis = thickened spinous layer
Leukoplakia four description
- hyperkeratosis
- chronic inflammatory cells in the subadjacent CT
- underlying epi can be thinning or atrophic even with hyperkatosis
- keratin layer can be parakeratin [nuclei but no granular cell layer] or orthokeratin [granular cell layer but no nuclei]
Alterations of dysplactic epithelial cells
- large nuclei and cells
- large and prominent nucleolus
- incraesed nucleus to cytoplasm ratio
- hyperchromatic [dark stain nuceli
- pleomorhphic [abnormal cells and nuceli]
- dyskeratosis = premature keratinization
- abnrmal mitotic activity [tripolar]
- increased mitotic activity
- bulbous and tear shaped RETE RIDGES
- loss of polarity [lack proliferation maturation towards surface
- keratain and epithelial pearls
spectrum of epithelial dysplasia
mild = basal or parabasal layer
moderate = basal -> mid spinous layer
severe = basal -> mid epithelial layer
carcinoma in situ = entire thickness of epi
ductal dysplasia = down the duct of minor salivary glands
waht is the FIRST STEP of tx for leukoplakia
biopsy
___ % of oral leukoplakia turns in to SCC
4%
what factors INCREASE the risk of cancer in leukoplakic lesions
- non smoker
- female
- persistence over many years
- on the ORAL FLOOR OR VENTRAL TONGUE
what are the risk factors for INCREASED MALIGNANT TRANSFORMATION for leukoplaskic lesions
- loss of heterogenicity
- microsatellite instability
- incrase telomerase activity
- change in expression of biomarkers
true or false
change in expression of biomarkers = increase malig trans
- on the oral floor or ventral tongue = incrase malig trans
- true
- false, increase risk of cancer in leukoplastic lesions
what 2 things can eliminate or reduce leukoplakia
- iso tre ti noin
- betacarotene
what other diseases have white plaques
- leukoedema
- leukoplakia
- frictional keratosis
- tobacco pouch keratosis
- white sponge nevus
- nicotinic stomatitis
- lichen planus
- mor sica tio
waht is erythroplakia
red patch that CAN NOT be clinically or pathologically identifed as another diease
____ is LESS common than leukoplakia but has a ___ potential to be SEVERELY DYSPLATIC CHANGES at the time of biopsy or invasive malignancy later in time
erythroplakia is less common than leukoplakia
greater potential for severely dysplastic
waht is asymptomatic and associated with erythroleukoplakia
erythroplakia
clincal features of erythroplakia
- altered mucosa and well demarcated
- erythematous MACULE or PLAQUE
- with soft velvety texture
- assymptomatic
- associated with erythroleukoplakia
- biopsy REQUIRED to distinguish bt psoriasis and candidiasis
true or false
biopsy is required for erythroplakia to distinguish bt psoriasis and candidiasis
true
what are the histofeatures of erythroplakia
90% erythroplakic lesions represent S C Sscc
- severly epithelial dysplasia
- carcinoma in situ
- superficially invasive squamous cell carcinoma
2. epi of erythroplakia lacks keratin production, thin, and shows underlying vasculature = red
3. underlying CT has chronic inflammatory cells
treatments of erythroplakia
- biopsy
- if moderat dsyplasia or worst need to:
- completely destroy
- remove
by means of leukoplakia methods
- reoccurence = common
mom = multifocal oral mucosal involvement = common
true of false
long term follow up is necessary for erythroplakia because of reoccurence is common
true
Nicotine stomatitis is a general- ized white palatal alteration that seems to be a hyper- keratotic response to the _______ by tobacco smoking (usually a pipe), rather than a _______ .
HEAT from the tobacco smoke
NOT response to the carcinogens within the smoke
true or false nicotine stomatitis malignant transformation is low
true
true or falase
- Erythroplakia also may occur in conjunction with leukoplakia
- has been found concur- rently with a large proportion of early invasive oral carcinomas.
true
true
waht are the 3 most common types of smokeless tobacco
chewing tobacco
snuff:
- dry snuff
- moist snuff
waht is the most popular type of snuff
moist
true or false
- chronic users of smokless tobacco are carcinogenic
- its more carcinogenic than cigs
- true
- false LESS CARCINOGNEIC than cigs
resorption of smokless tobacco of nicotine and other molecues through _____
resorption through oral mucosa
local oral alterations in chronic users of smokless tobacco
- most common = gingival recession
- halitosis [bad breath]
- destruction of facial surface of alveolar bone
- DENTAL CARIES
- localized or generalized wear on occlusal and incisal surfaces
- smokeless tobacco keratosis [white plaque where you put the tobacco
- mucosal is fissured and rippled
- soft velvety texture to mucosa
- lesions thickens appear leathery
are induration, pain, and ulceration assocaited with smokless tobacco
no
the epithelium of smokless tobacco appears?
- hyperkeratosis
- acanthosis
- chevron formation
waht is chevron formation and where do you see this
- pointed projections ABOVE or WITHIN superficial epithelial layers
- seen with smokelss tobacco
true or false
smokeless tobacco,
- epithelial dsyplasia is uncommon
- significant dysplasia and SCC can be present
true
true
in smokeless tobacco when is biopsy ONLY need?
- severe lesions
- if lesion remains after 6 WEEKS without tobacco contact
waht is the treamtnet for smokeless tobacco
NO TX
unless, dsyplasia or malignant
waht are the pros and cons of alterating smokeless tobacco use
pro = reduce smokeless tobacco keratosis [white plaque lesions]
con = 2 sites instead of 1
waht is the most common malignancy with smokeless tobacco
SCC
smokless tobacco, habit cessation leads to normal mucosa appearance in ___ %
98%
what condition involves chronic progressive scarring
oral submucous fibrosis
oral submucous fibrosis involves
____ risk,
pre cancerous condition
oral mucosa
high risk
oral submucous fibrosis
chronic placement of betel quid in the mouth, prevalence in these people:
indians
SEA
southern China
taiwan
4 Conditions characterized by oral submucous fibrosis
- mucosal rigidity
- fibro-elastic hyperplasia with
- changes to:
- superficial CT - submucosal changes from areca nut: [cytokines, growthfactors, and copper]
- epithelial changes and CARCINOGENSIS from tobacco contact
The underlying pathogenetic mechanism for oral submucous fibrosis is hypothesized to involve the role of the areca nut in disrupting the _____.
homeostatic equilib- rium between
synthesis and degradation of the
extra- cellular matrix
waht is the main chief complaint for oral submucous fibrosis
trismus and associated with mucosal pain
an 20 cm interincisal distance = severe
which sex is more suceptible to oral submucosal fibrosis
females
clinical features of oral submucous fibrosis
- first found in young adults chewing betel quid
- females > males
- chief complaint trismus and some mucosal pain [20 mm interincisal distance or less = severe]
- signs and symptoms: X Men S VP
- X = xerostomia
M = melanosis
S = stomatopyrosis [generalized oral burning sensation]
V = vesicles
P = petechiae
waht are the most common areas affected by oral submucous fibrosis
- buccal mucosa
retromolar area
soft palate
3 Histo features of oral submucous fibrosis
- submucosal deposition
DENSE and HYPOvascular
collagenous CT
with chronic inflammatory cells
- hyperkeratosis, basilar hyperplasia, fibrosis of LAMINA PROPRIA
- ragged keratinaceous surface
covered by
encrusted betel quid ingredients
Unlike ____, oral submucous fibrosis does NOT regress with habit cessation.
tobacco pouch keratosis,
- Frequent evaluation for development of oral SCC
is essential because a ______ YEAR malignant transformation 2. At a rate of ___ % has been determined for betel quid users in India.
17 years
8%
people with oral submucous fibrosis are ___ x more likely to develop oral cancer than people without
19 times
true or false
nicotinic stomatitis is a generalized MUCOSAL alteration to the hard palate
true
true or false
Once a common mucosal change of the hard palate, nicotine stomatitis has become less common as cigar and pipe smoking have lost popularity.
true
white keratotic change
with tobacco smoking
nicotinic stomatitis
nicotinic stomatitis, does have a premalignant nature
false DOES NOT have premalignant in nature
true or false
nicotinic stomatitis, reverse smokers palate has potential to develop to dysplasia or carcinoma
true, reverse smokers plalate can turn to dysplasia or carcinoma
waht are the 3 clinical features of nicotinic stomatitis
- WE GIS of hard palate
- white kertotic changes
- extensive leathery
- generalized mucosal alteration
- inflamed salivary duct openings which represent
- sprinkled red papules - ducts have white keratotic rings surrounding them
- gingival mucosal also keratotic
what are the 2 histofeatures of nicotinic stomatitis
- hyperkeratosis and acanthosis
PALATAL epithelium
- squamous METAplasia of
minor salivary gland ducts
true or false
- nicotinic stomatitis is completely reversible
- also, non precancerous lesion and not malignant, so thus doesnt need treatment
true
true
nicotinic stomatitis
any white lesion of the PALATAL MUCOSA persisting 1 month after cessation is considered a true _____ and should be ____ for tx.
leukoplakia and should be biopsied for treatment
actinic keratosis is a ____ ___ lesion and is ______ in nature
cutaneous premalignant lesion
and
precancerous is nature
waht is actinic keratosis caused by?
CUMULATIVE UV radiation
sun exposed skin
esp fair skinned people
actinic keratosis
lesions develop on the skin of more than ___% ___ adults with SIGNIFICANT LIFETIME SUN EXPOSURE
50% ALL white adults
with
significant lifetime sun exposure
clinical features of actinic keratosis
- seldom occurs in people YOUNGER than 40 yo
- common sites:
- face and neck
- scalp of balding men
dorsum of hands
forearm
- **irregular scaly plaques **
VARY IN COLOR
can be superimposed on erythematous background
- keratotic scales can PEEL OFF
- palpation reveals rough, sandpaper feel
- minimal elevation, but may produce cutaneous horn
waht are the 4 histofeatures of actinic keratosis
- hyperPARAkeratosis and acanthosis
- excessive amount of parakertain on the surface epithelium
- tear drop rete ridges
- hyperchromatic and pleomorphic epidermal cells
what are 4 ways to destroy actinic keratosis
- lq nitrogen cyrotherapy
- electrodessication
- surgical excision
- CURETTAGE
true or false actinic keratosis
- reoccurance is likely
- additonal lesions freq arise in adj sun damaged skin
false, recurrence is RARE
true add lesions can arise in adj sun damaged skin
just like erythroplakia, actinic keratosis has long term follow up?
true
what is actinic cheilosis
- premalignant lesion of
lower lip vermillion border
- caused by: excessive UV radiation from sun
- mostly confined to fair skin people and people that sunburn easily
- outdoor jobs: sailer’s lip and farmer’s lip
actinic cheilosis, lesions develop rapidly
true or false
false, lesions develop SLOWLy that pts are NOT aware of changes
what are the clinical changes of actinic cheilosis
- EARLIEST CHANGE:
- **atrophy **lower lip vermillion border
- smooth surface
- blotchy pale areas - **blurring **of margin bt vermillion zone and cutaneous portion of lip
- rough scaly areas develop
lesion progress
thicken and appear like LEUKOPLAKIC LESION
waht are the 4 histofeatures of actinic kertaosis
- atrophic SSE w/
marked keratin production
- hyperkeratosis and epithelial atrophy
- mild chronic INFLAMMATORY INFILTRATE present
subadjacent dysplastic epithelium
- underlying CT shows:
solar [actinic]
elastosis
waht is elastosis and which diseaease do you see it in the underlying CT histofeatures
- elastosis = UV light induceed alteration of COLLAGEN and ELASTIC FIBERS
- actinic cheilosis
true or false actinic cheilosis
- many changes are irreversible
- to prevent further damage use lip balm with sunscreen
true IRREVERSIBLE for ACTINIC CHEILOSIS
true
actinic cheilosis
any areas with 4_____ should be biopsy
- induration
- ulceration
- thickening
- leukoplakia
SHOULD BIOPSY
