red and white lesions and the relationship with oral cancer

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lecture given 9/11/2026

Last updated 2:11 AM on 9/12/26
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85 Terms

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demarcated hyperkeratosis with epithelial dysplasia

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gingival cyst of the adult

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focal cemento-osseous dysplasia

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central giant cell granuloma

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leukoplakia

white plaque of questionable risk having excluded (other) known diseases or disorders that carry no increased risk for cancer

clinical term, diagnosis is modified after histopathologic evaluation

most common potentially malignant oral lesion with higher risk of malignant transformation over time

DO NOT WRITE THIS TERM ON THE EXAM- IT IS WAY TOO BROAD

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leukoedema

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leukoedema

delicate grayish change involving buccal mucosa; disappears on stretching (edema)

may be secondary to mild topical injury

remove inciting agent if identified

no further management

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linea alba

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frictional keratosis or morsicatio

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frictional keratosis

non keratinized mucosal lesions- linea alba, morsicatio mucosae oris, usually not sharply demarcated, local mild trauma from nibbling

keratinized mucosal lesions- benign alveolar ridge keratosis (BARK), white plaque on the alveolar ridge, painless, may be rough; poorly demarcated, often in the area of previously extracted mandibular third molar (wisdom tooth)

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smokeless tobacco keratosis

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smokeless tobacco keratosis

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smokeless tobacco keratosis

asymptomatic grey-white opalescent area with parallel ridges where tobacco is placed

likely caused by contact irritation and gradient effect

reversible unless leukoplakia develops

manage by discontinuing habit

counsel pt regarding other adverse effects- periodontal disease, staining of dentition

cancer risk is 2x; low compared to cigarettes

follow up

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nicotinic stomatitis

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nicotinic stomatitis

pebbly, red and white change on palate

caused by heat; typically from pipes, reverse smoking

management via pt education, discontinue habit

reverse smoking may have malignant potential; too few to know

follow up

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candidiasis

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candidiasis

pseudomembranous type (thrush); white, curdy plaques that may or may not wipe off

hyperplastic candidiasis- do not wipe off easily, often associated with muco-cutaneous disease

treatment- nystatin, clotrimazole, fluconazole, if necessary scraping for cytology, biopsy

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leukoplakia

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what causes a white lesion to appear white lesion to appear white?

thickened keratin

thickened epithelium

altered epithelial cells- keratinocyte edema, coagulation/degeneration of cells, epithelial dysplasia, squamous cell carcinoma

scar/fibrosis below epithelium (no surface change)

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potentially malignant/premalignant

morphologically altered tissue in which cancer is more likely to occur than its apparently normal counterpart

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developmental white lesions

white sponge nevus

other congenital genodermatoses

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reaction to mild local injury white lesions

leukoedema

contact desquamation

frictional keratoses

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autoimmune white lesions

lupus erythematosus

chronic graft vs host disease

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tobacco-associated white lesions

smokeless tobacco keratosis

nicotinic stomatitis

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infectious white lesions

candidiasis

hairy leukoplakia (EBV- associated)

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immune mediated white lesions

lichen planus/lechenoid lesions

migratory glossitis

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pre-neoplastic / neoplastic white lesions

dysplasia

squamous cell carcinoma

verrucous carcinoma

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leukoplakia

localized- homogenous vs non-homogenous (verrucous/nodular leukoplakia, erytheroleukoplakia (speckled leukoplakia))

proliferative (multi-focal) leukoplakia- homogenous vs non-homogenous (verrcous/nodular leukoplakia, erythroleukoplakia (speckled leukoplakia))

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how common is leukoplakia (white), and how often does it become dysplasia or carcinoma?

common

43-47% dysplasia or carcinoma

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how common is speckled leukoplakia (red and white), and how often does it become dysplasia or carcinoma?

less common

50-80% dysplasia or carcinoma

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how common is erythroplakia (red), and how often does it become dysplasia or carcinoma?

least common

90% dysplasia or carcinoma

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what sites are high risk for oral squamous cell carcinoma?

lateral tongue, ventral tongue, floor of mouth, retromolar tongue, soft palate

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high risk leukoplakia

lesional presence in high risk areas such as the floor of the mouth, ventral tongue, and soft palate have a higher association with dysplasia or carcinoma than other sites

sharp demarcation at least in parts of the lesion is a worrisome sign

red, raised, or ulcerated component

pt with exoegenous risk factors such as tobacco and alcohol use

non smoker and unknown etiology of lesion

non-reversible type

microscopic atypia

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leukoplakia and transformation

when clinical leukoplakia shows histoplathologic dysplasia or carcinoma in situ, the malignant transformation rate is 5-36%

higher risk of malignant transformation in lesions involving lateral-ventral tongue, floor of mouth, and soft palate sites, and non-homogenous lesions

clinical leukoplakia with initial histopathologic findings of hyperkeratosis, unclear if reactive may transform to cancer; not all lesions with histopathologic findings of dysplasia will transform

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what level of risk of cancer development is acceptable to watch for a leukoplakic lesion?

overall 10-18% of leukoplakias undergo malignant transformation

in leukoplakic lesions with dysplasia malignant transformation in 5-36% of lesions

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squamous cell carcinoma

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what are common myths about pre-malignant and malignant oral lesions?

the lesion doesn’t look like cancer

the lesion is not white enough to be cancer

the lesion is too small to be oral cancer

the pt is too young to have oral cancer

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epithelial dysplasia

morphologically altered tissue in which cancer is more likely to occur than its apparently normal counterpart

OR

the sum of various disturbances of epithelial proliferation as evidence by histopathologic evaluation

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what are morphologic features of dysplasia?

drop shaped rete ridges

basal cell hyperplasia

irregular epithelial stratification

nuclear hyperchromatism

increased nuclear-cytoplasmic ratio

enlarged nucleoli

individual cell keratinization

loss or reduction of cellular cohesion

cellular pleomorphism

loss of basal cell polarity

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how are epithelial dysplasias graded and treated?

mild, moderate, or severe / carcinoma in situ

no invasion of the underlying connective tissue has occurred

treat with complete surgical excision

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normal

A?

<p>A?</p>
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mild

B?

<p>B?</p>
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moderate

C?

<p>C?</p>
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severe/carcinoma in situ

D?

<p>D?</p>
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invasive SCCa

E?

<p>E?</p>
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normal

what grade is this?

<p>what grade is this?</p>
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moderate

what grade is this?

<p>what grade is this?</p>
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squamous cell carcinoma

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dysplasia

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squamous cell carcinoma, sharply demarcated

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how should benign hyperkeratosis be re-evaluated?

is it at least partially well demarcated?

has it ever resolved completely?

has it grown larger?

could it be frictional?

if unlikely to be frictional, what can be causing the hyperkeratosis? early dysplasia?

are there exogenous risk factors?

is this a high risk site?

is it verrucous?

what would you do if this was in your mouth and biopsy was benign hyperkeratosis?

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what questions should you ask to weigh no treatment vs treatment?

what is likelihood that this will become invasive?

how long will it take to become invasive?

how morbid, difficult, expensive is removal?

is the pt healthy and what age?

can we safely watch and see what happens?

if we watch with the option to remove it later, have we lost valuable time?

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how is localized leukoplakia managed?

all dysplastic lesions should be excised, preferably with clear margins

even if not dysplastic, conservative or narrow excision should be considered, if no clear etiology is identified

wide excision of recurrent lesions

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how should you manage an oral leukoplakia?

eliminate the possible cause

if the lesion disappears- definable lesion, manage accordingly

if the lesion does not change- biopsy

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squamous cell carcinoma


<p></p>
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what are factors that affect squamous cell carcinoma?

extrinsic factors- cigarette smoking, alcohol use, betal quid and areca nut use, immunosuppression, history of previous cancer, family history of cancer, HPV, sunlight, age

exophytic, endophytic, leukoplakic, erythroplakic

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squamous cell carcinoma

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normal epithelium

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dysplasia, bulbous rete ridges

what is this, and what is it demonstrating?

<p>what is this, and what is it demonstrating?</p>
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dysplasia

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carcinoma

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carcinoma

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carcinoma

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carcinoma

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squamous cell carcinoma

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squamous cell carcinoma

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squamous cell carcinoma

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squamous cell carcinoma

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squamous cell carcinoma

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what is the 5 year survival rate for squamous cell carcinoma?

50%

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how is squamous cell carcinoma treated?

combination surgery, radiotherapy, and chemotherapy

altered fractionated radiotherapy

chemo-radiotherapy

immunotherapy

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proliferative (verrucous) leukoplakia

extensive, irregular white plaques

involves multiple mucosal sites

persistent growth, exophytic, and verrucous

may lead to dysplasia, squamous cell carcinoma

female predilection (4:1 vs males)

<50% with tobacco habit

multifocal lesions, non-contiguous

transform in 50-100% of cases over time

homogenous type is rare

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tldr localized leukoplakia

mostly in men

high association with cigarette smoking

single site, usually ventral tongue, floor of mouth

malignant transformation: 10-18%

easy to ablate/excise because localized

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tldr proliferative leukoplakia

mostly in women

low association with smoking

multifocal

malignant transformation 50-100%

difficult to treat bc multifocal

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what are the common histopathologic findings in proliferative leukoplakia?

typically multiple biopsies

usually early biopsies show benign hyperkeratosis with no evidence of dysplasia

not reliable- should re-evaluate clinically

follow closely

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proliferative leukoplakia

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proliferative leukoplakia

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proliferative leukoplakia

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proliferative leukoplakia

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erythroplasia

least common and appears as a well demarcated erythematous area with a velvety texture

floor of the mouth, tongue, and soft palate are common locations

90% of changes exhibit carcinoma in situ or invasive squamous cell carcinoma at diagnosis

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bruising trauma, not erythroplasia

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pt on blood thinners, not erythroplasia

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squamous cell carcinoma

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t/f once you treat a lesion like squamous cell carcinoma once, no need to follow up, it won’t come back

false- life long follow up at routine intervals is indicated

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t/f there is a fancy machine that can help diagnose squamous cell carcinoma

true HOWEVER nothing is better than the unaided eye