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Oral Pathology Exam 1 > 2. Premalignant Lesions of Surface Epithelial Origin > Flashcards

2. Premalignant Lesions of Surface Epithelial Origin Flashcards

1
Q

What is the normal histology of the oral mucosa?

A

parakeratinized, stratified squamous epithelium

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2
Q

What part of the oral mucosa isn’t parakeratinized?

A

Palate and Gingiva, which is orthokeratinized

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3
Q

Dysplasia involving the entire thickness of the epithelium with: no maturation and no keratin.

A

CIS - highest grade of dysplasia

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4
Q

What do all grades of dysplasia except CIS show?

A

Some keratin production on the surface

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5
Q

Why are dysplasia and CIS not considered cancer?

A

There is no invasion with access to blood and lymphatics

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6
Q

What are the 4 histological architectural changes that occur with dysplasia and CIS?

A
  • Bulbous or teardrop-shaped rite ridges
  • Loss of polarity
  • Keratin or epithelial pearls
  • Loss of epithelial cell cohesiveness, but intact bm b/c no invasion
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7
Q

What are the 6 histological cytologic changes that occur with dysplasia and CIS?

A
  • Enlarged cells, nuclei and nucleoli
  • Increased nuclear:cytoplasmic
  • Hyperchromatism
  • Pleomorphism (cellular and nuclear)
  • Increased, altered and displaced mitoses
  • Dyskeratosis (premature keratinization of individual cells)
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8
Q

Where do up to 50% of oral malignancies occur, that are associated with reverse smoking?

A

Hard palate

This is an unusual location

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9
Q

How many years after cessation does it take, before your cancer risk is that of non-smokers?

A

10 years

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10
Q

Risk for what is 2-6x greater than of those that quit smoking after their 1st cancer?

A

2nd primary UADT Carcinoma

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11
Q

What is the Clinical Appearance of Smokeless Tobacco Keratosis?

A
  • A reactive change to placement of the product
  • Gray/white, translucent plaque with rippled appearance and blending borders,
  • Probably isn’t a true leukoplakia
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12
Q

What is the presence of dysplasia seen with Smokeless Tobacco?

A

Infrequently ~3%, compared to 5-25% for Leukoplakia

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13
Q

What in Betel Quid or Paan Quid causes euphoria by enhancing the alkaloids released from the areca nut?

A

Slaked lime

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14
Q

What is the lifetime risk for developing oral cancer due to betel chew or paan quid use?

A

8%

Even tobacco-free Paan increases risk

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15
Q

What is Oral Submucous Fibrosis associated with?

A

Habit of Betel Nut Chewing

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16
Q

What is Oral Submucous Fibrosis?

A
  • A chronic progressive scarring disease of the oral mucosa
  • High-risk Precancerous Condition
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17
Q

In the pathogenesis of Oral Submucous Fibrosis, what does the areca nut primarily due?

A

Stimulates Fibrosis

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18
Q

In the pathogenesis of Oral Submucous Fibrosis?

A
  • Alkaloid from the areca nut –>
  • Stimulates fibroblasts to synthesize collagen
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19
Q

In the pathogenesis of Oral Submucous Fibrosis, what effect do high levels of copper have?

A

increase collagen cross-linking

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20
Q

What is the initial clinical presentation of Oral Submucous Fibrosis?

A
  • Vesicles
  • Petechiae
  • Xerostomia
  • Generalized Oral Burning Sensation (Stomatopyrosis) with Intolerance to spicy foods
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21
Q

What gradually forms as Oral Submucous Fibrosis progresses? (3)

A
  • Formation of fibrous bands with oral pallor and stiffness
    • Lose depth of the vestibule due to scaring
    • Soft palate has a pale look due to all of the collagen laid down
  • Leading to increasing Trismus
  • Develop Leukoplakic lesions, with dysplasia that have a tendency to undergo malignant transformation
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22
Q

What is the Histology of Oral Submucous Fibrosis?

A
  • Hyperkeratosis with epithelial atrophy & atypia is seen
  • Pronounced collagen deposition in submucosal CT
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23
Q

What may be used to improve mild cases & severe cases of trismus associated with Oral Submucous Fibrosis?

A
  • Intalesional corticosteroids
  • Surgical splitting of fibrous bands, with skin grafts & mouth props, physiotherapy
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24
Q

Does cessation of betel nut habit stop Oral Submucous Fibrosis?

A

No, but the pt should still d/c betel nut habit

This is in contrast to the cessation of smoking tobacco

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25
Q

What percent of Oral Submucous Fibrous cases show dysplasia at initial biopsy?

A

~10%

  • All pts should be biopsied to confirm dx & assess for dysplasia
  • Biopsy even if they don’t have a Leukoplakia
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26
Q

What percent of Oral Submucous Fibrosis cases undergo malignant transformation to SCCA in a 17 yr period?

A

~8%

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27
Q

How much of an increased risk do Oral Submucous Fibrosis pts have for developing Oral Cancer?

A

19x

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28
Q

What carcinogens does marijuana release at a 50% higher levels than tobacco?

A

Polycyclic hydrocarbons & Acetaldehyde like tobacco

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29
Q

What is a promotor of tobacco, creating a synergistic effect to develop cancer (RR=15)

A

Alcohol

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30
Q

What is the pathogenesis of alcohol?

A
  • Ethanol turns to acetaldehyde (carcinogenic)
  • Carcinogenic impurities in alcoholic drinks
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31
Q

What is the HPV type that is associated with OPSCC?

A

mostly HPV 16

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32
Q

HPV-associated OPSCC has increased dramatically in what groups of pts? (4)

A
  • ~10 yrs younger
  • Higher socioeconomic group
  • Increased % in whites (men)
  • Strong assoc with sexual behavior
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33
Q

What HPV associated ds has a more favorable prognosis (~30%) than those associated with tobacco and alcohol, that don’t have HPV in their tumor?

A

HPV associated OPSCC

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34
Q

What is the Gold Standard for determining clinically relevant HPV infection of the Oral Cavity?

A

Expression of viral oncogenes E6 and E7 mRNA

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35
Q

What is the prevalence rate of HPV in oral cancers?

A

6%

it is not recommended to routinely test for HPV in Oral Cancers, because there is such a small % that have it

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36
Q

What does Therapeutic Irradiation increase the risk of?

A

NEW primary malignancy, either sarcoma or carcinoma

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37
Q

What is the pathogenesis of therapeutic irradiation?

A

Decreases immune response, and causes alterations in DNA

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38
Q

What conditions cause mucosal atrophy, with predisposition to develop cancer? (5)

A
  • Oral Submucous Fibrosis
  • Atrophic Lichen Planus/Lichenoid Dysplasia
  • Discoid Lupus Erythematosus
    • more so if it effects the lips
  • Plummer-Vinson Syndrome
  • Tertiary Syphilis
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39
Q

What population is affected with Plummer-Vinson Syndrome?

A

Women 30-50 years old with Scandinavian/Northern European background

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40
Q

What are the signs and symptoms of Plummer-Vinson Syndrome? (4)

A
  • Iron Deficiency Anemia
  • Papillary atrophy of the tongue
  • Esophageal Web Formation
  • Koilonychia = spoon-shaped nails
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41
Q

What is there an increased risk for with Plummer-Vinson Syndrome?

A

5-50% increased risk of UADT Carcinoma, mostly esophagus

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42
Q

What is Tertiary Syphilis strongly assocaited with?

A

Dorsal Tongue Carcinoma, before antibiotics when arsenic was used for tx

NOT a Proven RF

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43
Q

What are 5 uncommon etiologies of oral cancer/precancerous lesions?

A
  • Vitamin A Deficiency
  • Cheilitis Glandularis
  • Dyskeratosis Congenita
  • Mate Drinking
  • Sanguinaria
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44
Q

What is the pathogeneis of Vitamin A Deficiency?

A

Excess mucosal keratinization, leads to Leukoplakias

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45
Q

What is Cheilitis Glandularis?

A

Rare inflammatory condition of minor salivary glands

46
Q

What does Cheilitis Glandularis cause?

A
  • Swelling causes eversion of lower lip, the mucosal side is exposed to sunlight causing Actinic Cheilitis
  • 18-35% develop SCC of the lower lip
47
Q

What is the etiology of Dyskeratosis Congenita?

A
  • Recessive X-linked (more common in men)
  • Mutation in telomerase
48
Q

What does the mutation of telomerase in Dyskeratosis Congenita lead to the development of?

A

Leukoplakia on the Tongue and UADT

Promotes the cell to continue to divide

49
Q

Why is it important to watch pts with Dyskeratosis Congenita and to biopsy any changes?

A
  • ~1/3 of lesions transform over 10-30 years
50
Q

What effect does Mate Drinking have on the risk for Oral Cancer?

A

2x increased risk

51
Q

What is Sanguinaria?

A

Herbal extract from blood-root plant

  • possesses anti-microbial/anti-inflammatory properties
  • Use to be put into mouthwashes and toothpastes (Viadent)
  • Not a proven risk factor for oral cancer development
52
Q

What is the clinical characteristic that > 80% of pts with a history of Sanguinaria use, it is a dead giveaway?

A

Maxillary Vestibule Leukoplakia

Maxillary Alveolar Mucosal Leukoplakia

(this is a strange place to have a leukoplakia)

53
Q

What can Tumor Suppressor Genes exhibit?

A
  • Loss of Heterozygosity
  • TP53 Mutation
  • Hypermethylation (p16)
    • Cyclin dependent kinase inhibitor leads to inactivation and tumor growth
54
Q

In Molecular Carcinogenesis what causes the cell cycle to be uninhibited causing increased growth?

A
  • Overexpression of:
    • EGFR
    • Telomerase
    • Cyclin D1
55
Q

What makes oral tissues look white? (5)

A
  • Increased keratinization
  • Acanthosis
  • Edema
  • Thermal or Chemical Injury
  • Extrinsic Coatings
    • Debris and/or bacterial/fungal organisms (plaque, candida) that adhere but can be rubbed off the oral mucosa
56
Q

What 10 diagnoses must be ruled out before a dx of Leukoplakia can be made?

A
  • Leukoedema
  • Cheek Chewing
  • Frictional Keratosis
  • Nicotine Stomatitis
  • Tobacco Pouch Keratosis
  • Chemical Burn
  • Candidiasis
  • Lichen Planus
  • White Sponge Nevus
  • Cinnamon Reaction
57
Q

Where do 90% of leukoplakias that show dysplasia come from?

A
  • Tongue, Lip Vermilion, and FOM
58
Q

What population do Leukoplakia’s have a predilection for?

A
  • Males (70%), usually greater than 40 yrs old
  • Increase with age, average age of 60 years
59
Q

What is the clinical appearance of Leukoplakia’s?

A
  • Often sharply demarcated, white patch or plaque with variable surface textures
    • Thick or Thin
    • Smooth Granular-Nodular or Verrucous
    • Homogenous vs. Non-homogenous
60
Q

If a red component is present in leukoplakia what is it called?

A

Speckled Leukoplakia or Erythroleukoplakia

61
Q

What are the phases of Leukoplakias?

A
  • Normal Mucosa
  • Thin, smooth leukoplakia (hyperkeratosis)
  • Thick, fissured leukoplakia (mild/moderate dysplasia)
  • Granular, verruciform leukoplakia (moderate/severe dysplasia)
  • Erythroleukoplakia/CIS
    • Becomes thinner
    • Starts to look red, not making keratin
    • May ulcerate
62
Q

What is the histology of Leukoplakias?

A

Some degree of Hyperkeratosis or Acanthosis

63
Q

What are the High Risk Sites of Leukoplakia?

A
  • Latero-Ventral Tongue
  • FOM
  • Retromolar Pad/Tonsillar Pillar/Soft Palate area
64
Q

What percent of high risk sites of leukoplakia shows dysplasia?

A

24-42% show dysplasia

65
Q

What are the Low Risk Sites of Leukoplakias?

A
  • Buccal Mucosa
  • Hard Palate
  • Dorsal Tongue
66
Q

What percent of low risk sites of leukoplakia shows dysplasia?

A

11-18% show dysplasia

67
Q

What percent of leukoplakias show dysplasia for all sites?

A

5-25% all of Leukoplakias will show dysplasia

68
Q

How long does it take for transformation of leukoplakias to occur?

A

2-4 years, but can be variable from months to several years

69
Q

Why do leukoplakias need to be followed closely?

A

~1/3 of Leukoplakias recur after excision

70
Q

What is the tx for leukoplakias with mild dysplasia or hyperkeratosis with atypia?

A
  • Tx varies
  • D/C carcinogenic habits (smoking) may lead to resolution
  • May remove OR observe very closely based on size, location, etc.
71
Q

What is the tx for leukoplakias with Moderate Dysplasia or Worse (Severe Dysplasia, CIS)?

A
  • Remove by most convenient means available
    • Usually excision
    • Large lesions use laser, electrocautery, cryosurgery
72
Q

What is the Malignant Transformation Risk (by clinical appearance) of thin leukoplakias?

A

Sledom transforms without clinical alteration

73
Q

What is the Malignant Transformation Risk (by clinical appearance) of thick, homogenous leukoplakias?

A

1-7%

74
Q

What is the Malignant Transformation Risk (by clinical appearance) of Granular or Verruciform Leukoplakia?

A

4-15%

75
Q

What type of Leukoplakias have the highest Malignant Transformation Risk (by clinical appearance)?

A
  • Non-Homogenous = higher risk
  • Erythroleukoplakia = 28%
76
Q

What is the Malignant Transformation Risk for Severe Dysplasia?

A

20-43%

77
Q

What is the Malignant Transformation Risk for all dysplasia combined?

A
  • <2% per year
  • 12% over time
78
Q

What are other risk factors for malignant transformation of Leukoplakias? (6)

A
  • Female
  • Older Age
  • Nonsmoking Status
  • Lesion Persistence
  • Large Size
  • Ventro-Lateral Tongue/FOM (16-39%)
79
Q

In summary what features increase risk for leukoplakia to progress to cancer?

A
  • High risk sites
  • Non-homogenous, red/speckled or ulcerated are higher risk (appearance)
  • Presence of dysplasia
  • Increased grade of dysplasia
80
Q

What is the follow-up for an excised leukoplakia with dysplasia?

A

Every 3 months

81
Q

What is the follow-up for leukoplakia without dysplasia?

A

Every 6 months

UNLESS other risk factors are present, then see every 3 months

82
Q

What are the sites usually affected in Erythroleukoplakia?

A
  • Lateral Tongue
  • FOM
  • Soft Palate

These are high risk sites for Leukoplakia

83
Q

What is the red appearance of Erythroleukoplakia due to?

A
  • Lack of surface keratin production
  • Epithelial atrophy
84
Q

What are the differences of Erythroleukoplakia and Leukoplakia? (2)

A

Erythroleukoplakias…

  • More advanced when detected
  • 90% show Severe Epithelial Dysplasia or worse (CIS) at the time of biopsy
85
Q

What is Proliferative Verrucous Leukoplakia?

A
  • Multiple leukoplakias, often extensive, that spread and thicken over time
86
Q

What is the most common site affected in PVL?

A

Gingiva, other sites may be affected as well

87
Q

What is the population affected by PVL?

A
  • Female predilection (4:1), only 1/3 have traditional RFs
    • Mean female age = 65 yrs
    • Mean male age = 49 yrs
88
Q

What is the Histology of PVL?

A

Hyperkeratosis/Hyperplasia with variable dysplasia, often verrucous surface

89
Q

What is the tx for PVL?

A
  • Optimal tx remains to be determined
  • Surgical or Ablative Therapy, but recurrence is common
90
Q

What is the malignant transformation of PVL?

A

64% of pts develop SCCA, with a mean follow-up of 7.4 yrs

  • Traditional Leukoplakias, transform much faster, usually within 2-4 yrs
  • Highest Risk Leukoplakia for malignant transformation, 40% died from cancer
91
Q

Which adjunct to clinical evaluation/biopsy is not recommended as indications for use would also require scalpel biopsy?

A

Brush Biopsy

92
Q

Which adjunct to clinical evaluation/biopsy has limited application on red lesions?

A

Cytology

93
Q

Which adjunct to clinical evaluation/biopsy is most useful in red lesions?

A

Toluidine Blue

94
Q

Which adjunct to clinical evaluation/biopsy may help visulize subtle leukoplakias, but has limited application?

A

Vizilite

95
Q

Which adjunct to clinical evaluation/biopsy has some application in margin delineation but insufficient evidence for use as a screening device?

A

Velscope

96
Q

What is Actinic Keratosis (AK)?

A

Premalignant sun-induced skin lesion caused by UV light exposure - precursor to SCCA

97
Q

Where are common locations for Actinic Keratosis?

A
  • Facial skin and vermilion zone (AC) of the lips of fair-skinned persons, over 40 years old
98
Q

What is the clinical appearance of Actinic Keratosis?

A
  • Red base with white scaly plaque with sandpaper texture
99
Q

What is the Histology of Actinic Keratosis?

A
  • Hyperkeratosis, usually parakeratin
  • Some degree of epithelial dysplasia or even superficially invasive SCC
  • Solar Elastosis - degeneration of CT from UV damage with increased elastic fibers (stains blue)
100
Q

What is the average time to progression of Actinic Keratosis?

A

2 years

101
Q

What is the prognosis for Actinic Keratosis if sun exposure is reduced?

A

25% may regress

102
Q

What population has a strong predilection for developing Actinic Cheilosis (Cheilitis)?

A
  • Male
103
Q

What is the Clinical Progression of Actinic Cheilosis?

A
  • Atrophy (blotchy pale), dryness, fissures
  • Scaly/crusty and thickening
  • Leukoplakia
  • Ulceration (when cancer forms)
104
Q

After tx of Actinic Cheilosis via vermilionectomy what is now a potential problem?

A

Developement of Cheilitis Glandularis, due to exposed lip mucosa

105
Q

Why is long term follow up of Actinic Cheliosis recommended?

A
  • 2x increased risk for lip cancer
  • Transforms at >2x the rate that occurs with Actinic Keratosis
    • Good news: takes a long time to transform, mets late, and typically well-differentiated, slower growing lesion
106
Q

What is Bowen Disease?

A
  • Skin equivalent of CIS
    • Not always related to sun exposure
107
Q

What is the clinical appearance of Bowen Disease?

A

Erythematous and scaly, well-defined, irregular plaque on keratinized skin

108
Q

What is Erythroplasia of Queyrat?

A

A clinical variant of CIS of the penis

109
Q

What is the clinical appearance of Erythroplasia of Queyrat?

A

Velvety red plaques on penile mucosa

110
Q

What occurs in a pt years after exposure to arsenic, in pts with Arsenical Keratosis?

A
  • Keratosis of palms and soles
    • palms look pigmented and have scaly plaques
  • Skin pigmentation
  • Skin tumors
  • Increased risk for Internal Malignancy

Oral Pathology Exam 1 (8 decks)

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