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Oral Pathology Exam 1 > 7 Benign/Premalignant Epithelial Lesions > Flashcards

7 Benign/Premalignant Epithelial Lesions Flashcards

1
Q

HPV

  • # of subtypes?
  • # of type identified in lesions affected the head and neck?
  • # of genuses of the family
  • 2 major groups:
  • basic structure?
A
  • 200 subtypes
  • ~24 that affect head/neck
  • 5 genuses of the Papillomaviridae family
  • 2 groups: cutaneous and mucosal
  • circular dsDNA
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2
Q

most common sexually transmitted infection in the US, but not all are sexually transmitted

A

HPV

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3
Q

How does HPV infects cells?

A

Virus is epitheliotropic –> enters through wounds/abrasion and infects basal cells (only actively dividing cells in the epithelium)

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4
Q

low risk HPV

A
  • viral genome remains separate in the host nucleus
  • replication of the viral genome occurs in parallel with host genome replication
  • stable viral copy number distributed among daughter epithelial cells
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5
Q

low risk HPV types

A

6, 11 (squamous papilloma, condyloma aacuminatum)

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6
Q

benign papillary proliferation of squamous epithelium, all ages, any location

A

squamous papilloma

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7
Q

Clinical findings: -

  • “wart-like”
  • exophytic
  • soft
  • pedunculated or sessile
  • finger-like projections
  • pink or white
A

squamous papilloma and verruca vulgaris

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8
Q

tx of squamous papilloma

A

surgical removal

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9
Q

aka common wart

A

verruca vulgaris

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10
Q

benign papillary proliferation of squamous epithelium, any location but skin is most common

A

verruca vulgaris (common wart)

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11
Q

single papillary lesion (2)

A

squamous papilloma

verruca vulgaris

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12
Q

clinical findings: exophytic, soft, pedunculated or sessile, rough papillary surface, can see multiple lesions, pink or white

A

verruca vulgaris

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13
Q

tx for verruca vulgaris

A

surgical removal (oral), cryotherapy (skin)

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14
Q

any age but most commonly adolescents and young adults, multiple lesions

A

condyloma acuminatum

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15
Q

incubation period of condyloma acuminatum

A

1-3 months from time of sexual contact

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16
Q

caused by HPV 6, 11

A

squamous papilloma

condyloma acuminatum

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17
Q

causes 90% of genital warts

A

condyloma acuminatum

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18
Q

Clinical findings: more likely sessile, pink, well-demarcated, nontender exophytic mass, short, blunted surface projections (cauliflower like

A

condyloma acuminatum

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19
Q

tx of condyloma acuminatim

A

surgical excision

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20
Q

tx for all intraoral warts

A
  • recommend surgical removal
  • laser ablation has been used (airborne secretions of HPV possible)
  • some lesions may resolve on their own
  • recommend removal given risk of spread (discuss risk of spread with patients)
  • not routinely evaluated by the pathologist for the presence of high-risk HPV genotypes
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21
Q

caused by HPV 13, 32

A

multifocal epithelial hyperplasia (Heck’s disease)

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22
Q

initially reported in Native Americans and Innuits

A

multifocal epithelial hyperplasia (Heck’s disease)

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23
Q

age group affected by multifocal epithelial hyperplasia (Heck’s disease)

A

children most common

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24
Q

most common sites affected by multifocal epithelial hyperplasia

A

labial, buccal, and lingual mucosa

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25
Q

Clinical findings:

  • 3-10 mm lesions
  • multiple, usually clustered
  • coalescing (merge together)
  • soft
  • nontender
  • flattened or rounded papules
  • color of normal mucosa
  • spontaneous regression after months or years
  • rarely seen in adults
A

multifocal epithelial hyperplasia (Heck’s disease)

26
Q

tx for Heck’s disease

A

biopsy for dx, monitor, remove lesions subject to recurrent trauma, remove for aesthetic purposes

27
Q

HPV vaccine

A

Gardasil 9-9vHPV

28
Q

Gardasil

  • Age given recommended?
  • Age range given?
  • Expanded age range?
A

11-12 yo
9-26 yo
27-45

29
Q

CDC guideline for the decision on whether or not to give the gardasil vaccine to pts 27-45

A

shared clinical decision making

30
Q

benign OR premalignant

A

smokeless tobacco keratosis

31
Q

formation of a white plaque where the mucosa directly contacts the tobacco product

A

smokeless tobacco keratosis

32
Q

appearance is wrinkled, fissured, or rippled (“sand on a beach at ebbing tide”)

A

smokeless tobacco keratosis

33
Q

state that uses the most smokeless tobacco

A

West Virgina
Wyoming
Mississippi

34
Q

Smokeless tobacco contains ____ carcinogens.

A

28

35
Q

forms of smokeless tobacco

A

Chewing tobacco

Snuff- dry or moist, fire cured

Snus- steam pasteurized

36
Q

consequences of smokeless tobacco use

A
  • caries due to high sugar levels
  • gingival recession/bone loss
  • staining of teeth
  • halitosis
  • cardiovascular disease
  • oral cancer increases with long term use
37
Q

ADA reports ___x greater risk for oral cancer for those who use smokeless tobacco than never users

A

4x

38
Q

Which is better? wet or dry snuff

A

wet snuff

39
Q

histo: hyperkeraotic, acanthotic (thickened, hyperplastic) epithelium, fibrosis of CT, dysplasia may be seen

A

smokeless tobacco keratosis

40
Q

tx for smokeless tobacco keratosis

A
  • counsel pt to quit
  • if unwilling, have them move product to different site
  • lesion should resolve in 2-6 weeks following cessation
  • biopsy if lesion persists after 6 weeks without tobacco use
41
Q

What does a severe biopsy look like?

A

intensely white, sharply defined borders, verrucous surface, ulceration, erythematous appearance, induration (palpable mass under the surface) or mass

42
Q

High risk sites for premalignant/malignant lesions:

What percentage of all oral cancers occur in these location?

A

lateral/ventral tongue, roof of mouth, soft palate/oropharynx (lower lip also but develops from UV exposure so very different behavior)

90% of oral cancers occur in these locations!!

43
Q
  • white plaque that cannot be diagnosed clinically as another entity
  • cannot be wiped off
  • has a risk to develop into cancer
  • more commonly has sharply defined borders
  • a clinical term only, have to biopsy to know what it is (may be benign, premalignant, or malignant)
A

leukoplakia

44
Q

cannot be wiped off

A

leukoplakia

45
Q

average age of leukoplakia

A

60

46
Q

Patients at increased risk for cancer development within a leukoplakia include:

A
  • female patients
  • nonsmokers
  • persistent lesion over several years
  • lesion on the floor of mouth or ventral tongue
47
Q

After biopsy, leukoplakia may be:

A
  • hyperkeratosis
  • atypia (atrophy, acanthosis, hyperplasia)
  • mild, moderate, or severe dysplasia
  • carcinoma in-situ
  • SCC
48
Q

What does normal squamous look like?

A
  • cells above the basal layer show progressive flattening of the cell body
  • nuclear condensation as the cell differentiates/matures
  • mitoses are almost never seen above the basal layer
49
Q

histo appearance of dysplasia

A
  • enlarged nuclei and cells
  • large and prominent nucleoli
  • increased nuclear-to-cytoplasmic ratio
  • hyperchromatic nuclei (darkly staining)
  • pleomorphic nuclei and cells
  • dyskeratosis- premature keratinization
  • increased mitotic activity
  • abnormal mitotic figures
  • mitotic figures above the basal layer
  • bulbous (teardrop) shaped rete ridges
  • lack of maturation toward surface
50
Q

mild vs moderate vs severe vs full thickness dysplasia

A

Mild = extends to basilar 1/3 of the epithelium

Moderate = extends to basilar 1/2 of the epithelial thickness

Severe = extends beyond 1/2 of the epithelial thickness but not full thickness

Full thickness = carcinoma in-situ, almost cancer or “intra-epithelial neoplasm”

*The closer the cellular changes are to the surface, the worse the dysplasia

51
Q

intra-epithelial neoplasm

A

carcinoma in-situ (or almost cancer)

52
Q

histo: tissue with dysplastic epithelial cells that extend from the basal layer to the epithelial surface, “top-to-bottom” change, no invasion has occurred yet, basement membrane is intact

A

carcinoma in-situ

53
Q

entire epithelial thickness exhibits dysplastic changes, basement membrane is intact

A

carcinoma in-situ

54
Q
  • persistent red patch that cannot be classified as anything else
  • sharply demarcated borders
  • frequently asymptomatic
  • less common than leukoplakia
  • biopsy for definitive diagnosis
  • final tx dictated by microscopic diagnosis
A

erythroplakia (erythroleukoplakias)

55
Q

~90% are severe dysplasia, carcinoma in-situ, or SCC

A

erythroplakia

56
Q
  • an aggressive form of oral leukoplakia
  • persistent
  • often multifocal, slowly spreading plaques
  • rough surface projections
  • high risk of recurrence
  • high risk of malignant transformation
A

proliferative verrucous leukoplakia

57
Q

etiology unknown, not associated with tobacco, alcohol, HPV, or other virus

A

PVL/PL

58
Q

management of pts with PVL/PL

A
  • photographs at every visit and submitted with biopsy specimens
  • reassess every 3-6 months
  • if biopsy shows hyperkeratosis, atrophy, or acanthosis –> followed
  • if biopsy shows mild/moderate dysplasia –> excised
  • severe dysplasia or CIS –> complete excision
59
Q

management protocol for pts with diagnosed oral premalignancy

A
  • removal of precancer
  • discontinue tobacco and/or heavy alcohol
  • upper aerodigestive tract evaluation
  • clinical re-evaluation every 3-6 months
  • repeat biopsy if clinically indicated
60
Q

leukoplakia vs PVL/PL

A

Leukoplakia

  • single site
  • men > women
  • 5th decade and beyond
  • higher correlation with tobacco and alcohol
  • ~40% have dysplasia at first biopsy
  • moderate rate of malignant transformation (3-15%)

PVL/PL

  • multifocal
  • women > men
  • 6th-8th decades
  • lower correlation with tobacco and alcohol
  • < 10% have dysplasia on first biopsy
  • high rate of malignant transformation (70-100%)
61
Q

malignant transformation potential from high to low

A 
PVL
erythroplakia 
erythroleukoplakia 
granular leukoplakia 
actinic chelitis 
smooth thick leukoplakia 
smokeless tobacco 
smooth thin leukoplakia

Oral Pathology Exam 1 (16 decks)

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