Exam 3 Flashcards
Basal Cell Carcinoma
80% of all skin cancer, about 1 million cases/year (equals incidence of all other
cancers combined)
1/5 people in US develop skin cancer, 1/3 Texans
90% affect sun exposed H&N, doesn’t occur orally
↑↑ with age, ↑ fair skinned
usually upper lip lesions are basal cell carcinoma and lower lip are squamous cell carcinoma
Etiology: Ultraviolet radiation from chronic sun exposure
low grade, slow growing, almost never metastasize
Most common clinical form - noduloulcerative, central often cratered ulceration with
rolled, raised borders with telangiectatic (dilated) vessels
Histologic features: Islands of basaloid epithelial cells showing invasive growth
Treatment: Excision or curettage with electrodessication; Radiation therapy
Prognosis: 90-95% 5 year survival
Nasopharyngeal Cancer-Syndrome
Trotter’s syndrome = Pain referred to tongue or jaw secondary to invasion of nasopharyngeal
carcinoma to base of skull with involvement of trigeminal nerve (V3) as it exits foramen ovale
Mesenchymal-Sarcoma
“bulky or fleshy” mass under surface skin or mucosa
about 1% of H&N malignancies are sarcomas = rare
affect broader age range.
grow deep
Angiosarcoma
Malignancy of vascular endothelium
↑ H&N, ↑ scalp and forehead, ↑ elderly
Kaposi’s Sarcoma
Malignancy of vascular endothelium
geographic distribution & multicentricity suggest infectious etiology
(HHV-8 [human herpes virus - Type 8] implicated)
classically occurs in debilitated or immunosuppressed patients (HIV)
lesions can be macular, patch or mass lesion, usually reddish to purple
approximately 50% of HIV + KS patients have oral lesions
multifocal, can be flat or a mass
↑ gingiva and palate
Histology: Variable but classical features are spindle cell proliferation
with slit-like vascular spaces, prominent RBC extravasation
Treatment: Radiation therapy, chemotherapy, excise, intralesion vinblastine
Rhabdomyosarcoma
Malignancy of skeletal muscle
most common soft tissue malignancy in children
↑ H&N, ↑ urogenital tract
sarcoma botryoides (grape like clusters off of surface mucosa)
Malignant peripheral nerve sheath tumor (neurogenic sarcoma)
Malignancy of nerve may arise in neurofibromatosis mass lesion often with pain and nerve deficit
Treatment & Prognosis of Sarcomas: Most surgery ± radiation therapy ± chemotherapy;
Prognosis variable
Metastasis to the Oral Cavity
Most common malignancy in bone is metastatic disease
2/3 to bone (Mx 20%, Md 80%, ↑ midbody); soft tissue: ↑ gingiva
primary site commonly:
Male: lung, kidney, liver, prostate
Female: breast, female genital organs, kidney, colorectal
approximately 23% precede diagnosis of primary
Clinical: pain, paresthesia, swelling, loosening of teeth (may be asymptomatic)
Radiographic finding: Usually destructive, invasive, poorly marginated lucency. Rarely stimulates production of bone or osteosclerosis (classically from prostate)
Histology: Usually carcinoma, 10 may not be obvious
Treatment: Often palliation
Hodgkins Disease (lymphoma)
Reid-Sternberg cell (80% have markers for B-cells)
classically presents with lymphadenopathy
75% cervical or supraclavicular
spread tends to be predictable to contiguous nodes oral involvement rare
PE, chest film, CT, MRI, lymphangiography “ laparotomy
A= Absence of systemic signs
B= Presence of fever, night sweats and/or unexplained loss of 10 percent or more of body weight during the 6-month period before diagnosis
Non-Hodgkins Lymphoma
Diverse group of immune system malignancies, usually B cell origin, but some T-cell and occasionally histiocytic,
tend to affect lymphoid tissues/ organs but spread more unpredictably and often affect nonlymphoid tissues i.e. oral present with lymphadenopathy or mass lesion orally,
commonly affects palate can affect bone: any stage IV disseminated lymphoma or as only manifestation (primary lymphoma of bone)
swelling of palate; often vascular
Histologic classification:
low grade, intermediate grade, high grade
- Burkitt’s lymphoma - Type of non-Hodgkin’s B-cell lymphoma; African jaw lymphoma - affects jaws of children
90% contain Epstein-barr virus. 80% show translocation of protooncogene from C8 to C14. very rapidly growing destructive lucency
American Burkitt’s - less jaw involvement, older patients, ↑ CNS and abdominal involvement
Histology: “Starry sky”, phagocytic cells interspersed in sea of small malignant lymphoid cells
Treatment: Aggressive chemotherapy, usually with cyclophosphamide
Treatment: Radiation ± chemotherapy
prognosis highly variable
Plasma Cell Dyscrasias
Group of monoclonal malignant proliferative diseases affecting plasma cells where cells remain functional and produce whole antibody molecule or part of it (light chains - Bence Jones proteinuria)
- Multiple Myeloma
- Extramedullary plasmacytoma
Extramedullary plasmacytoma
Soft tissue lesions
isolated or with multiple myeloma
Multiple myeloma
Most common primary malignancy of bone,
multifocal, occasionally soft tissue
↑↑ with age, ↑ males, tend to affect bones with most active marrow, vertebrae,
ribs, skull, pelvis, jaws 10%
Clinical features: bone pain, anemia, infection, renal insufficiency, fatigue
Monoclonal gammopathy, IgA, IgG, IgM, IgE or IgD as detected on serum protein electrophoresis ± light chains (Kappa or Lambda)
Radiographic features: Orally - destructive lucencies
Skull - punched out lucencies
Treatment: Chemotherapy ± immunomodulating agents ± stem cell or bone marrow transplantation
Prognosis: Poor, overall 5 year survival is about 33%
- Solitary myeloma
Single bone lesion of myeloma; many patients will develop multiple myeloma
Leukemia
Malignancies of bone marrow stem cells
Classification - myelocytic, lymphocytic, monocytic leukocytosis
acute or chronic course
Primary manifestation - generalized gingival enlargement due to malignant cells radiolucencies
Secondary manifestation -due to bone marrow pancytopenia (poverty of all normal cell lines) anemia
thrombocytopenia - bleeding
immunosuppression - infections
Squamous Cell Carcinoma:
Clinical Features/What does it look like
Earliest lesions do NOT show characteristic features that increase index of suspicion!!!
Advanced lesions:
Firm to hard (indurated)
Non-movable (bound down to adjacent tissues)
Irregular, exophytic growth with poorly defined margins
Non-healing ulceration
Rolled borders are particularly ominous
Pain
What does it look like? White plaque (leukoplakia) Red plaque-like (erythroplakia) Often with a smooth velvety appearing surface May have slightly raised margin May have white areas speckled over the surface Ulcer Often with a raised, rolled border Often with a very deep, central crater Exophytic mass Often with an irregular surface texture
Squamous Cell Carcinoma:
Sites of Origin
Oral Cavity Decreasing in frequency overall It can occur anywhere—no area is immune to development of cancer!! Dorsum of the tongue is very rarely affected Anterior portion of hard palate is relatively immune High risk sites: Lower lip Posterior lateral border of the tongue Floor of the mouth Males mostly Increasing incidence in females though Tonsillar pillars/soft palate margins Minimal association with HPV infection
Oropharynx Increasing in frequency Base of tongue and tonsillar regions in vast majority of cases Strong HPV association in a very high percentage of cases Risk factors are different Generally non-smokers Generally not alcohol abusers Sexual debut at an early age Multiple oral sex partners!!!
Potential complications of surgical treatment of SCC:
Functional deficit Impaired nutrition Usually the result of a functional deficit Post surgical infection at the site Speech impairment Drooling Facial deformity
Potential complications of chemotherapy of SCC:
Mucositis and ulceration Xerostomia Infection Fungal Viral Bacterial Bleeding Anemia Nausea, vomiting, diarrhea Loss of appetite Neurotoxicity
Potential complications of radiation therapy of SCC:
Immediate complications: Dermatitis Mucositis and ulceration Decreased salivary flow Difficulty swallowing Impaired nutrition Taste alteration Partially due to decreased salivary flow Infection Candidiasis Bacterial
Long Term Complications with SCC tx
Xerostomia Radiation caries/rampant caries Ease of mucosal ulceration Infections, particularly candidiasis Osteoradionecrosis Trismus/fibrosis Impaired nutrition Alopecia (hair loss) of overlying skin
Premalignant conditions
Sideropenic dysphagia
Submucous fibrosis
Lichen planus: controversial, risk is debatable
many cases represent misdiagnosed cases of dysplasia
Immunosuppression
Leukoplakia
Erythroplakia
Erythroplakia:
Definition, sites, histology, tx
A red patch which can’t be diagnosed as a specific condition. considerably less common than leukoplakia
Clinical features
- tendency for high risk sites: lower lip, lateral border and ventral surface of tongue, floor of mouth
- may produce symptoms
Histologic features
Dysplasia, carcinoma in situ or carcinoma (approaches 100) (Most early asymptomatic oral carcinomas are red or red and white lesions)
II. Treatment
Depends on biopsy to assess for presence or absence of dysplasia and its severity
Non-dysplastic:
* Modify risk factors and follow
Dysplastic:
* Mild - ? moderate: Modify risk factors ± excise
* Severe, CIS: Modify risk factors + excise
Resolution with tobacco cessation:
50% smoked; 95% spit/topical
Leukoplakia:
definition, etiology, histology
A white patch or plaque that won’t rub off and which can’t be diagnosed as any specific condition.
Etiology:
a. Frictional Keratosis - reversible hyperkeratosis secondary to physical irritant -not premalignant. Frictional keratosis has been taken out of the leukoplakia/premalignant category
b.Tobacco- Most leukoplakias are in tobacco users
smoked-not site specific
topical –chew is abrasive but low risk for oracl cancer development.
stomatitis nicotina - white palate, small red macules (inflamed ducts), not premalignant. Particularly with pipe smoking: heat and chemicals
Histologic features
80% Hyperparakeratosis: increased amount of parakeratin
on surface of epithelium Hyperorthokeratosis increased amount of orthokeratin on surface of epithelium Acanthosis increase in thickness of epithelium
17% Epithelial dysplasia or carcinoma in situ Process the
epithelium goes through prior to becoming malignant as
determined by cytologic alterations of the cells:
1. Increased and/or abnormal mitoses 2. Abnormal keratinization 3. Increased nuclear/cytoplasmic ratios 4. Cellular disorientation 5. Hyperchromatism (increased nuclear staining) 6. Pleomorphism (many different shapes)
3% Superficially invasive squamous cell carcinoma (Carcinoma In Situ). stuck at the epithelial layer→can eventually migrate
Anatomic site:
a. Floor of the mouth and ventral tongue (approaches 50%
dysplastic/invasive)
b. Lateral border of tongue (25% dysplastic/invasive)
c. Lower lip (actinic keratosis) (35% dysplastic/invasive)
(sun damage→)vermilion becomes atrophic and blends with skin, variably white ± erosion ± crusting (superficial ulceraction)
Clinical variations
a. Homogenicity
Homogeneous leukoplakia
Non-homogeneous leukoplakia (50% - 80% dysplastic/invasive)
Areas of redness, ulceration, pebbly or verrucous surface
1. Erythroleukoplakia (Erosive)
2. Nodular leukoplakia (Speckled leukoplakia)
3. Verrucous leukoplakia surface irregularities
b. Proliferative verrucous leukoplakia (PVL)
Rare form of progressive leukoplakia that is characterized by progression, multifocality, verrucous morphology, recurrence after excision, progression to SCC and death.
Not much you can do tx wise
Malignant transformation
4-6% overall
15% if dysplastic surgical intervention
1-3.5% if not dysplastic watch these pgs
