Oral Cancer & Precursor Lesions Flashcards
1
Q
Premalignant lesions
A
- Leukoplakia
- Proliferative verrucous leukoplakia
- Smokeless tobacco keratosis
- Oral submucosal fibrosis
- Actinic cheilitis
- Erythroplakia
2
Q
Malignant lesions
A
- Squamous cell carcinoma
- Verrucous carcinoma
- Basal cell carcinoma
3
Q
Leukoplakia
A
- White patch that cannot be characterized clinically or pathologically as any other disease (strictly clinical, not dx’c term)
- 80% of pts are smokers
- Smokers > non-smokers
- Heavy smokers > light smokers
- May resolve after cessation
- Synergistic effect w/ tobacco (oral cancer)
- Mouth rinses >25% alcohol
- Grayish plaques (not true leukoplakia)
- Affect those >40yo
- 70% found on lip vermillion, buccal mucosa, gingiva
- Tongue, lip vermillion, floor of mouth: 90% dysplasia or cancer
- Lesions may have varied appearance and change over time
- Microscopic dx of leukoplakia would be:
-
Hyperkeratosis = benign callus
- Increased thickness of keratin layer
- Uniform maturation of squamous cells
-
Dysplasia = abnormal growth/cells
- Variation in size, shape, staining of nuclei
- Can regress or progress
-
Carcinoma in situ
- Will progress to invasive carcinoma
- Entire epithelium is dysplastic
- Superficially invasive carcinoma
- Squamous cell carcinoma
- Keratin pearl: Keratin should be towards superficial surface, but it’s towards the basement layer, where it doesn’t belong
-
Hyperkeratosis = benign callus
- Many leukoplakias are hyperkeratosis
- 2-4% of leukoplakias are carcinoma in situ or SCC @ time of discovery
- Up to 6% of leukoplakias progress to carcinoma
4
Q
Proliferative Verrucous Leukoplakia
A
- Special high risk form of leukoplakia
- Characterized by multiple white plaques w/ rough, warty surface projections
- Multiple plaques tend to spread slowly
- Significantly increased tendency to develop into SCC
- Req’s close follow up
- Management: Incisional biopsies
- Microscopic dx: SCC arising in proliferative verrucous leukoplakia
- Tx: Monitor. Difficult to tx b/c it’ll just keep coming back even though we know it’s on its way to cancer
5
Q
Smokeless Tobacco Keratosis
A
- Wide variety of “smokeless tobacco”
- Moist snuff
- Dry snuff
- Chewing tobacco
- Dry & chewing are declining in popularity, but moist is on the rise
- Main concern:
-
Gingival recession - characteristic painless loss of gingival tissues in the area of tobacco contact
- Gingival recession w/o perio recession
- High sugar content also causes caries
-
Gingival recession - characteristic painless loss of gingival tissues in the area of tobacco contact
- Clinical findings:
- Smokeless tobacco keratosis: gray-white “translucent” plaque w/ border that blends into surrounding area
- Cancer risk
- Smokeless tobacco has 1-9% the risk of smoking cigarettes
- SCC may develop after use of several decades, if at all
- Higher risk of cancer
- Dx can often be achieved on clinical basis
- Biopsy for lesions w/ worrisome presentation (i.e. ulcerated)
- Tx: Depends on biopsy
- Habit cessation
6
Q
Oral Submucous Fibrosis
A
- Chronic, progressive, high-risk, precancerous condition
- Asia
- Placement in mouth of a betel quid or paan
- Wrap of areca tree nut & slaked lime, usually w/ tobacco
- Users chew from early age, 16-24hr/day
- CC: Trismus
- Buccal mucosa, retromolar pad, soft palate most common sites
- Betel chewer’s mucosa: Brown-red color (not precancerous)
- Does not regress w/ habit cessation
- Surgery & meds can improve fibrosis
- Freq evaluation for development of cancer
- Pts are 19x more likely to develop oral cancer
7
Q
Actinic Cheilitis
A
- Common premalignant change of lower lip vermillion
- Due to long-term excessive exposure to UV light
- Seen in most people w/ fair skin that burn easily
- Rare in 45yo, 10x more common in males
- Cancer develops in 6-10% of cases
- Features:
- Slow development
- Atrophy of vermillion border
- Smooth surface and paleness
- Blurring of vermillion margin
- Rough, scaly areas develop
- Leukoplakia areas appear
- Scaly material can be peeled off
- Multifocal ulcers develop
- Tx:
- Many changes are reversible
- Encourage pts to use lip balms to prevent further damage
- Biopsy req’d for areas of ulceration, induration, or whitening
- Severe cases, vermilionectomy may be performed
8
Q
Erythroplakia
A
- Red patch that cannot be clinically or pathologically dx’d as any other condition
- AKA erythroplakia of Queyrat: Initially described in male genital
- Same causes as cancer (esp smoking)
- Less common than leukoplakia
- Greater potential for malignancy
- Disease of middle-aged to older adults
- Floor of the mouth, tongue, soft palate
- Well-demarcated macule/plaque, velvety texture
- Erythroleukoplakia: when associated w/ leukoplakia
- R/O candidiasis, vascular lesions, psoriasis, mucositis
- Red lesions should be viewed w/ suspicion & biopsied
- Floor of mouth and lateral/ventral tongue
- If trauma is apparent, may wait 2wks to see if it regresses
- Tx depends on biopsy results (degree of dysplasia)
- Recurrence and multifocal involvement common: long term follow up
9
Q
Squamous Cell Carcinoma
A
- 95% oral cancer
- ~35K new cases/yr; males > female
- Px: ~58% of all pts w/ OSCC survive 5yr
- Only 33% AA pts survive 5yr
- 5yr survival rate for OC is relatively low, compared to cancer in other locations
- Why is px so poor?
- By the time it’s dx’d, usually in advanced stages
- Risk factors
- Tobacco
- 80% pts are smokers
- 8x increased risk
- Risk of secondary carcinomas
- EtOH
- 30% of pts are drinkers
- 20% have cirrhosis
- 15x increased risk
- Tobacco + EtOH greatly increases risk
-
HPV
- Oral cancer: 3-5%
- Genetic mutations & epigenetic events
- People w/o risk factors CAN & DO still develop OC
- Tobacco
10
Q
Clinical features of OSCC
A
- Intraoral Locations
- Tongue: 50%
- Floor of mouth: 35%
- OC can happen anywhere in the oral cavity
- Lips
- Found in light-skinned persons
- Due to UV damage
- 70% pts outdoor occupation
- 90% lower lip
- Metastases are rare
- Clinical features of advanced OC
- Indurated tumor mass
- Ulceration/bleeding
- Pain
- Cervical lymph node enlargement
11
Q
Early detection of OSCC
A
- Challenge: Detecting OSCC in its EARLY stages or as a precancerous lesion
- Early OSCC
- Most OSCC arises from clinically visible precursor lesions
- Evolution from precursor lesion to invasive cancer is often a slow process
- Most OCs are preventable or curable if detected early in development
- Common Presentations of Early OSCC
- Persistent, localized
- Asymptomatic red lesion (erythroplakia)
- Asymptomatic white lesion (leukoplakia)
- Asymptomatic red & white lesion (erythroleukoplakia)
- Not ulcerated or painful
- Pt unaware of lesion
12
Q
Tx for OSCC
A
If a single ulcer shows no sign of healing 14 days after the putative cause is removed, it should be considered malignant until proven otherwise
- Tx:
- Smaller lesions tx’d by surgery alone
- Larger lesions tx’d w/ surgery and/or radiation
- Neck dissection when lymph nodes involved
- Chemotherapy usually palliative
13
Q
TNM staging system for OSCC
A
T: Tumor
N: Nodes
M: Metastasis
14
Q
Malignancy potential
A
15
Q
Verrucous Carcinoma
A
- Slowly growing cancer w/ a writhe, rough, warty surface
- Low grade malignancy
- Rarely metastasizes; good Px