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Oral Path > Premalignant White/Red Lesions > Flashcards

Premalignant White/Red Lesions Flashcards

1
Q

Premalignant/Precancer lesion

A

A lesion which has a greater than normal risk of transformation to cancer

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2
Q

Premalignant/Precancerous condition

A

A disease or habit associated with greater than normal risk to develop a premalignant lesion or cancer in tissues affected

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3
Q

Describe normal oral mucosa histoloy

A

Mostly parakeratinized, stratified squamous epithelium except for gingiva and palate which is orthokeratinized

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4
Q

Describe normal skin histology

A

Orthokeratinized, stratified squamous epithelium

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5
Q

To be histologically premalignant, a lesion must show….

A

“epithelial dysplasia” = alteration of epithelial maturation (dysmaturation)

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6
Q

Epithelial Dysplasia

A

The thickness of the altered epithelium affected determines the “grade”
-Mild dysplasia (lower 1/3)
-Moderate dysplasia (lower 1/2)
-Severe dysplasia (lower 2/3)
-Carcinoma in situ (CIS) - full thickness dysplasia with no maturation (no keratin, cells at bottom = cells at top)

**Note: dysplasia and CIS are NOT cancer as there is no invasion with access to blood and lymphatics

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7
Q

What are the architectural changes (overall, low-power appearance) seen histologically with dysplasis/CIS?

A

-Bulbous, tear-drop shaped rete ridges
-Loss of polarity (maturation to the surface)-cells are crowded and jumbled
-Keratin or epithelial pearls (concentrically layered keratinized cells)
-Loss of epithelial cell cohesiveness (but intact basement membrane - lack of invasion)

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8
Q

What are the cytologic changes (how single cells are altered) seen histologically with dysplasis/CIS?

A

-Enlarged cells, nuclei and nucleoli
-Increased nuclear/cytoplasmic ration
-Hyperchromatism
-Pleomorphism (cellular and nuclear)
-Increased, altered and displaced mitoses
-Dyskeratosis - premature keratinization of individual cells

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9
Q

Describe the histologic gray area

A

Some clinical white lesions don’t show dysplasia but are still microscopically abnormal. They may be diagnosed as:
1. “hyperkeratosis” - thickened keratin layer
2. “hyperkeratosis and atypia” - thickened keratin and basal and parabasal cell layers are altered
3. “epithelial hyperplasia” or “acanthosis” - spinous layer is thickened

**Based on the clinical presentation, some may have premalignant potential, and require follow up.

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10
Q

Smokeless tobacco keratosis

A

-Gray/white, translucent plaque with rippled appearance and blending borders
-Probably not a true leukoplakia - small increased risk for oral cancer for moist snuff, chewing tobacco
-Resolution expected within 6weeks (usually 2-3wks) of changing placement site of product
-Biopsy leathery or nodular areas

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11
Q

Oral Submucous Fibrosis (OSF)

A

Chronic progressive scarring disease and high-risk precancerous condition associated with betel nut chewing

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12
Q

OSF clinical

A

Signs/symptoms may occur as soon as 2-3yrs (commercial paan) with 2-5 quids/day with daily frequency being more important that duration.
-Vesicles, petechiae, xerostomia and generalized oral burning sensation (stomatopyrosis) with intolerance to spicy foods
-Gradual collagen deposition causes fibrous bands with oral pallor and stiffness leading to increasing trismus
-Some patients also develop leukoplakia that can become dysplastic or turn into oral cancer

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13
Q

OSF management

A

-Patients should discontinue the betel nut habit. Cessation doesn’t stop OSF though
-Cancer risk:
1. All patients with oral submucous fibrosis should be biopsied to confirm the diagnosis and assess for dysplasia (approx. 8% undergo malignant transformation to SCC)
-If there is trismus:
1. Intralesional corticosteroids may improve mild cases
2. Severe cases may require surgical splitting of fibrous bands, with skin grafts and mouth props, physiotherapy

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14
Q

Leukoplakia definition

A

Leuko=white; plakia=patch
-WHO original definition: “a white patch or plaque that cannot be characterized clinically or pathologically as any other disease”
-Clinical term only. Should be used after exclusion of known entities that produce white patches/plques
-When defined this way (i.e. other clinical entities are excluded), leukoplakia can be considered a premalignant lesion
-Male predilection, usually >40yrs

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15
Q

Diagnoses that must be excluded: NOT leukoplakia

A

-Leukoedema
-Cheek chewing
-Frictional keratosis
-Nicotine stomatitis
-Smokeless tobacco keratosis
-Chemical burn
-Candidiasis
-Lichen planus
-Contact reaction

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16
Q

What is the most common oral premalignant lesion?

A

Leukoplakia

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17
Q

Describe how Leukoplakia looks

A

-Often sharply demarcated white patch or plaque
-Variable surface texture:
1. thin or thick
2. smooth or rough
3. granular/nodular or verrucous
4. homogeneous vs. non-homogeneous
-If red component is present, called “speckled leukoplakia” or “erythroleukoplakia”

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18
Q

Describe the Leukoplakia phases

A
  1. Normal mucosa
  2. Thin, smooth leukoplakia –> hyperkeratosis, acanthosis, lymphocytes
  3. Thick, fissured leukoplakia –> hyperkeratosis, acanthosis, lymphocytes, dysplasia (mild/moderate)
  4. Granular, verruciform leukoplakia –> irregular hyperkeratosis, bulbous rete pegs, lymphocytes, moderate/severe dysplasia, congested vessels, candida hyphae
  5. Erythroleukoplakia (speckled leukoplakia) –> irregular hyperkeratosis, bulbous and crowded rete pegs, epithelial atrophy, lymphocytes, severe dysplasia, carcinoma in situ, congested vessels
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19
Q

Leukoplakia Histology

A

-Some degree of hyperkeratosis (wet keratin appears white) and/or thickening of the spinous cell layer (acanthosis)
-Demonstration of epithelial dysplasia histologically proves lesion is premalignant
-….but if dysplasia is not seen does NOT mean that it doesn’t have premalignant potential (clinical correlation needed)

20
Q

Leukoplakia Tx

A

-Moderate dysplasia or worse: remove by the most convenient means available (excision, laser, elctrocautery, cryosurgery, etc.)
-Mild dysplasia or hyperkeratosis with atypia - tx varies:
1. D/C carcinogenic habits (smoking) may lead to resolution
2. Mild dysplasia may remove or observe very closely based on size, location, etc.

21
Q

Leukoplakia malignant transformation risk

A

The higher grade you go, the higher the cancer risk (think of the phases photo)

22
Q

White (leukoplakia) or red (erythroplakia) patches/plaques show variable risk to show dysplaisa or SCC based on the location where they occur.

List the high risk sites, intermediate risk sites, and low risk sites.

A

High Risk:
-lateroventral tongue
-floor of mouth
-soft palate/tonsillar pillar
-lip vermilion

Intermediate Risk:
-gingiva

Low Risk:
-buccal mucosa
-hard palate
-dorsal tongue

23
Q

List the features that increase the risk that leukoplakia will progress to cancer

A

-The site (high-risk sites more than low-risk sites)
-The appearance (non-homogenous, red/speckled or ulcerated lesions are higher risk)
-Presence of dysplasia
-Increasing dysplasia grade

24
Q

Erythroplakia

A

Erythro=red, plakia=patch/plaque
-A red patch/plaque that cannot be clinically or pathologically diagnosed as any other condition
-Prevalence = <1.0%
-Velvety red, well-demarcated patch, usually affecting the lateral tongue, floor of the mouth or soft palate
-Red appearance is due to the lack of surface keratin production and epithelial atrophy

25
Q

List the risk factors, histologic appearance, tx and prognosis for Erythroplakia

A

Risk Factors:
-same risk factors as leukoplakia, but generally more advanced when detected

Histologic Appearance:
-Microscopically, 90% of these lesions are severe epithelial dysplasia or worse at the time of biopsy

Tx and Prognosis:
-Similar for that of leukoplakia having a similar degree of epithelial dysplasia
-Surgical excision often preferred to rule out cancer

26
Q

Proliferative Verrucous Leukoplakia (PVL)

A

-Uncommon, high-risk presentation of leukoplakia
-NOT associated with HPV
-Multiple leukoplakias, often extensive, that spread and thicken over time
-Often involve the gingiva. Other sites may be affected as well
-Female predilection, mean age 65yrs
-Hyperkeratosis/hyperplasia with variable dysplasia, often verrucous surface

27
Q

Proliferative Verrucous Leukoplakia Tx

A

-Optimal tx remains to be determined
-Surgical or ablative therapy, but recurrence common
-Malignant transformation is a frequent complication, even in lesions without previous biopsy evidence of dysplasia

28
Q

Red or white lesions that persist for more than 2-3wks that cannot be ascribed to any known causes must get a….

A

BIOPSY

29
Q

Actinic Cheilosis (Cheilitis)

A

-Term for actinic keratosis involving the vermillion zone of the lower lip
-Strong male predilection
-Clinical progression: atrophy (blotchy pale), dryness, fissures –> scaly/crusty and thickening –> leukoplakia –> ulceration
-Tx: typically excision (scalpel or laser)
-Prognosis: long term f/up recommended as 2x increased risk for cancer of the lip

30
Q

Hairy Leukoplakia

A

-Epstein-Barr Virus (EBV) induced lesion often with superimposed candidiasis
-Usually HIV-infected or other immune compromise. Rare in healthy pts.
-Non-removable white plaque(s) of the lateral tongue
-Faint vertical strands to thick furrowing with shaggy keratotic surface
-Tx: usually resolves with control of HIV infection

31
Q

Histopathology of Hairy Leukoplakia

A

-Thick, irregular parakeratin
-Candida infection
-Hyperplastic (thicker) epitherlium with “balloon cells” that show EBV by in situ hybridization
-No dysplasia
-Minimal inflammation

32
Q

List the etiology of oral cancer and oral precancerous lesions

A

-Tobacco (smoked/smokeless)
-Alcohol
-HPV
-Radiation (UV or therapeutic)
-Immunosuppression
-Uncommon causes - won’t discuss

33
Q

What is the value in smoking cessation?

A

-Leukoplakias with no or mild dysplasia may shrink
-10 yrs after cessation, cancer risk approximates that of non-smokers
-Risk for 2nd primary upper aerodigestive tract carcinoma = 2-6x greater in those that continue to smoke compared to those that quit after first cancer

34
Q

Reverse Smoking

A

-Placing burning end inside mouth
-Up to 50% of oral malignancies in these populations occur on the hard palate

35
Q

Marijuana association

A

Recent research can’t confirm or refute association between head and neck cancer and marijuana use

36
Q

Alcohol association

A

-Heavy alcohol use (4+ beverages/day) = 2-14 fold increase risk
-With tobacco there is a synergistic effect to develop cancer, RR = 15
-Pathogenesis:
1. ethanol –> acetaldehyde (carcinogenic)
2. carcinogenic impurities in alcoholic drinks
3. may increase permeability to epithelium and solubility of carcinogens

37
Q

HPV - oral cavity

A

-Role in oral cavity carcinogenesis is uncertain
-Expression of viral oncogenes E6 and E7 mRNA is not the gold standard for determining clinically relevant HPV infection. HPV16 is the predominant type

38
Q

HPV testing

A

-All OPSCC or cervical lymph node metastases of unknown primary should be tested for high-risk HPV
-It is NOT recommended to routinely test for HPV in oral cancers

39
Q

Radiation

A

-UV radiation (sun exposure) - chronic exposure is main cause of actinic cheilitis –> lip cancer
-X-irradiation:
1. decreases immune response and causes alterations in DNA
2. increased risk of new primary malignancy (either carcinoma or sarcoma)

40
Q

Immunosuppresion

A

Increased risk for oral SCC and other H&N malignancies for patients
-with AIDS
-on immunosuppressive tx for malignancy
-having received an organ transplant

41
Q

Sanguinaria

A

-Antimicrobial/anti-inflammatory herbal extract added to OH products
-Strong association with maxillary vestibule or Mx alveolar mucosal leukoplakia
-Unknown if increases risk of cancer development (not proven)

42
Q

List things that are NOT a cause of premalignancy or oral cancer

A

-Oral sepsis - bad OH
-Broken teeth
-Dentures
-Galvanism
-Mouthwashes
-Routine dental radiography

43
Q

How does other bacteria play a role?

A

-Not a proven risk factor
-Oral bacteria may interact with tobacco and alcohol increasing acetaldehyde
-Periodontal bacteria association with oral cancer not confirmed

44
Q

How does Candida play a role?

A

-Not a proven risk factor
-Can overlay leukoplakias but not causing them
-Link to oral cancer not shown

45
Q

Molecular Carcinogenesis

A

-Tumor suppressor genes can exhibit loss of heterozygosity, mutation or hypermethylation which can lead to inactivation and tumor growth
-EGFR, telomerase, and Cyclin D1 overexpression lead to increased growth
-Increasing polysomy

46
Q

Leukoplakia and Dysplasia Tx consideration

A

-1/3 of leukoplakias recur after excision
-Transformation usually occurs within 2-4yrs but can be variable so follow closely
-Typical follow-up plan (3-6mo):
1. Every 3mo for an excised leukoplakia with dysplasia
2. Every 6mo for leukoplakia w/o dysplasia

47
Q

List the Diagnostic Techniques (oral premalignant and malignant lesions)

A

-Scalpel biopsy: gold standard - adjunct to clinical evaluation/biopsy
-Cytology: limited application on red lesions
-Toluidine Blue: most useful in red lesions
-Vizilite: may help visualize subtle leukoplakia, but limited application
-Velscope: some application in margin delineation but insufficient evidence as a screening device
-Brush Biopsy: not recommended as indications for use would also require scalpel biopsy

Oral Path (17 decks)

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