Malignant White/Red Lesions Flashcards
List the white/red oral malignancies
-Squamous Cell Carcinoma
-Verrucous Carcinoma
Why does the term “oral cancer” generally denote SCC?
Because 90% of oral cancers arise from the surface epithelium
List other primary oral cancers
-Salivary gland carcinomas
-Lymphomas
-Melanoma or sarcoma (rare)
List the secondary cancers
A metastasis to the oral cavity from a distant site (e.g. carcinoma, sarcoma, lymphoma/leukemia etc.)
Oral Cancer Epidemiology
- 2% of all cancers in US
-Most common cancer in India (men)
-Male:Female (2:1)
-Highest risk for white men >65yrs and black men in middle age
-Increasing incidence overall if oropharynx is included
-No significant improvement has been made in early diagnosis
Oral Squamous Cell Carcinoma (SCC) Demographics
> 90% of all oral cancers are SCC
SCC Risk Factors
-Similar to premalignant oral lesions
- 80% associated with tobacco with or w/o alcohol
-(20-25%) no identifiable risk factor - lateral tongue young adults (especially women) or gingiva (older women)
-Heredity does not appear to play a major role
SCC Clinical
-Irregular shape, mixture of red and white
-Often ulcerated center with “rolled” border
-Exophytic (growing out) or endophytic (growing in) growth pattern
-Often much firmer (indurated) than surrounding tissues
-Early lesions = asymptomatic; pain is usually a late feature
-Ragged radiolucency is characteristic of bone involvement
List the high risk sites for oral SCC
-Lateroventral tongue
-Floor of mouth
-Soft palate/tonsillar pillar
-Lip vermilion
SCC Lip
-One of the more common sites of involvement, not really intraoral
-Secondary to ultraviolet light exposure
-Arises in the setting of actinic cheilitis
- 90% lower lip
-Crusted, nontender, indurated ulceration, typically <1cm when discovered
-Slow-growing, usually well-differentiated lesions
-Relatively good prognosis
SCC Tongue
-Lateroventral tongue - most common intraoral site:
1. majority of pts have history of cigarette smoking and alcohol abuse
2. When oral SCC is seen in younger pts (<40yrs), it almost always develops at this site
-Dorsal tongue - uncommon
SCC Floor of Mouth
-Second most common site for oral SCC
-Most pts have history of cigarette smoking and alcohol abuse
-Most likely location to develop from preexisting white/red lesion
-Often associated with 2nd primary malignancy
SCC Gingiva/Alveolar Mucosa
-Intermediate risk site (3rd most common) for oral SCC
-More common in women at this site (2:1) and those without identifiable risk factors
-Most likely site for misdiagnosis as it may mimic benign/reactive gingival lesions (e.g.pyogenic granuloma) or periodontal disease
SCC Palate
-Hard palate SCC is rare (unless reverse smoking)
-May develop in the maxillary sinus and invade through the sinus floor
-Most SCCs affecting the palate arise on the lateral soft palate. They likely show a visible premalignant lesion
-Most oropharyngeal carcinomas arise from the tonsillar region w/o a visible precursor lesion:
1. symptoms –> dysphagia, persistent sore throat, dull/sharp pain may be referred to ear, odynophagia
SCC Buccal Mucosa
-“low risk” (uncommon) site for oral SCC in the western world
-Very common in the setting of betel quid use
Clinical differential diagnosis for oral SCC
-Non-specific ulcer (i.e. traumatic)
-Specific infections: tuberculosis, deep fungal, syphilis
-Immune-mediated conditions: granulomatosis with polyangiitis, crohn disease
SCC Radiographic
-Direct tumor invasion of bone (usually a late phenomenon) causes a “moth-eaten” radiolucency with ragged/ill-defined borders
-Pathologic fracture is possible
Histopathology of malignant lesions
-Invasive cords and nests of malignant squamous epithelial cells arising from dysplatic surface epithelium
-Tumor cells show an increased nuclear/cytoplasmic ratio, cellular and nuclear pleomorphism, and mitotic activity
-Varying degrees of keratin production (keratin pearls) and dyskeratosis
-Desmoplasia - tumor-induced fibrosis
Grading of malignant lesions
-“Superficially invasive” or “microinvasive” - very early lesions
-Multiple classification schemes
-Somewhat subjective interpretation of histologic differentiation:
1. Well differentiated (grade I; low grade)
2. Moderately differentiated (grade II; intermediate grade)
3. Poorly differentiated (grade III; IV; high grade)
T/F: Differentiation does influence staging
FALSE!
Differentiation does NOT influence staging
Describe the microscopic features that do affect stage and prognosis:
- Depth of invasion (>5mm) correlates with increased risk for nodal metastasis
- Extracapsular spread outside a lymph node, “extranodal extension” (ENE), is associated with a worse prognosis
HPV Detection
-All oropharyngeal SCCs REQUIRE high-risk HPV (HRHPV) testing b/c affects staging
-Don’t do HRHPV testing on oral cancers
Which HPV test should be used?
-Presence of HPV E6, E7 indicates transcriptionally active HPV infection so gold standard is to test for this. More expensive
-p16 immunohistochemistry (inexpensive, sensitive surrogate marker for HRHPV) is the routine test used
After biopsy proven oral SCC (or other H/N cancer), what next?
- Complete head and neck exam
- Dental exam: PANX - will need to treat any unresolved dental issues
- Imaging to evaluate the primary tumor, any second primaries, and nodal disease (MRI or CT with contrast, chest CT)
- Multidisciplinary consultations as needed
