Chapter 10 Flashcards
Squamos Papilloma
Benign proliferation of STRATIFIED SQUAMOUS epithelium
Caused by: HPV 6 & 11 (DNA virus)
Low virulence and infectivity rate
MOST COMMON - intraoral
Sites of predilection of Squamous Papilloma
Tongue
Lips
Soft Palate
What are the clinical manifestations of Squamous Papilloma?
Pedunculated
Painless
White, red, or mucosal colored
5mm
Squmous Papilloma Differentials
Verruca Vulgaris
Condyloma acuminatum
Verruciform xanthoma
Verruca Vulgaris
HPV 2, 4, 6, 40
CONTAGIOUS - common on skin (hands)
ORAL LESIONS –> always white
* Hyperkeratized layer
Pedunculated or sessile
5mm
Multiple or clusters are common
Condyloma Acuminatum
(Venereal Wart)
HPV 2, 6, 11, 16, 18, 31, 53, 54
Clinically –> Painless, Sessile (short blunted surface projection), Exophytic, Clustered
Large (2x as papilloma or verruca vulgaris)
Condyloma Acuminatum Differential Diagnosis
Squamos papilloma
Verruca Vulgaris
Verruciform xanthoma
HPV 16 and HPV 18
Condyloma acuminatum
increased risk for malignant transformation to squamos cell carcinoma
_** anogenital region – NOT ORAL LESIONS **_
HPV 6 and 11
Squamous Papilloma
(may be Condyloma acuminatum)
HPV 2, 4, 6, 40
Verruca Vulgaris
HPV 2, 6, 11, 16, 18, 31, 53, 54
Condyloma Acuminatum
Multifocal Epithelial Hyperplasia
HECK’S DISEASE
HPV 13 & 32
CHILDHOOD
Multiple lesions
Painless
Flattened or rounded papules –> Cobblestone
Mucosal colored
Treatment for Heck’s Disease?
Spontaneously regress
Conservative surgical excision
Risk of recurrence
No risk of malignancy
Heck’s Disease
Multifocal Epithelial Hyperplasia
Sinonasal Papillomas
Benign - localized proliferation of respiratory mucosa
Three histological patterns
Arise from:
* Lateral nasal wall
* Septum
* Sinuses
Sinonasal Papilloma Histological Forms (3)
Fungiform
Inverted
Cylindrical
Mulluscum Contagiosum
DNA POXVIRUS
virally-induced epithelial hyperplasia
Sessile, papules
Umbilicated lesions
Skin-colored
Smooth surface
Molluscum contagiosum histology
Molluscum bodies (Henderson-paterson bodies)
Virally infected epithelial cells (glossy appearance)
Treatment of Molluscum Contagiosum
Remission occurs in 9 months
Treat to decrease risk of transmission
Remove by curettage or cryotherapy
Verruciform Xanthoma
Hyperplastic condition - likely due to trauma
Lipid-laden histiocytes in the epithelium – XANTHOMA CELLS
Common on gingiva
Painless
Sessile (slightly elevated)
Papillary (roughened surface)
Mucosal, white, yellow, or red
<2cm
Multiple lesions possible
Verrucifrom Xanthoma differential diagnosis
Squamous papilloma
Verruca vulgaris
Condyloma acuminatum
Treatment of Verruciform Xanthoma
Conservative surgical excision
Recurrence is rare
No risk of malignant transformation
Seborrheic Keratosis
Benign proliferation of epidermal basal cells (aquired)
DOES NOT OCCUR IN THE MOUTH
SKIN of FACE, TRUNK, and EXTREMITIES
lesions more prevalent with AGE
Tan to brown macules
Dermatosis papulosa nigra
Seborrheic Keratosis that occurs in AFRICAN AMERICANS
Genetic inheritance (AD)
Multiple black 2mm papules
Scattered around zygomatic and periorbital region
Dermatosis Papulosa Nigra
Leser-Trelat Sign
Sudden appearance of NUMEROUS seborrheic keratosis
Associated with INTERNAL MALIGNANCY (not good!)
Sebaceous Hyperplasia
Localized proliferation of SEBACEOUS glands of the skin
** significant because –> Clinically similar to facial tumor – Basal cell carcinoma (BCCA) **
Compression of lesion – sebum is expressed
*Distinguishes from BCCA
Ephelis – FRECKLE
Hyperpigmented macule of skin
** increased of melanin production without the increase of melanocytes **
MORE PRONOUNCED WITH UV LIGHT - sun exposure
Light skinned individuals, bad chilhood sunburns
Actinic Lentigo
Benign brown macules resulting from chronic UV light damage to skin
Dorsal surface of hands, face, and arms
Uniformly pigmented
NO CHANGE IN COLOR INTENSITY WITH UV LIGHT
Does not undergo malignant transformation
Color intensity in UV light:
Increases –> ?
Stays the same –> ?
Ephelis
Actinic Lentigo (appearance induced by sun)
Lentigo simplex (found in sunless areas)
Lentigo Simplex
Benign cutaneous melanocytic hyperplasia
(increase in number of MELANOCYTES)
Occurs in skin NOT exposed to UV light (sun)
Color intensity does not change with sunlight
Do not undergo malignant transformation
Melasma
Aquired, symmetrical
Hormonally-driven hyperpigmentation of the sun exposed skin of the face
(Bilateral light brown macules)
Pregnant women (dark skinned more common)
Pigmentation can remain faint or darken over time
No risk of malignant transformation
Oral Melanotic Macule - oral ephelis (freckle)
Brown, asymptomatic macule
Focal increase in malanin deposition
NOT DEPENDENT ON SUN EXPOSURE
most common site –> vermillion border ( labial melanotic macule)
Biopsy is MANDATORY – cannot distinguish clinically from early melanoma
Labial melanotic macule
oral melanotic macule
“oral freckle” found on the vermillion border
Oral Melanoacanthoma
Aquired pigmentation of the oral mucosa due to ? –> TRAUMA
Seen almost exclusively in AFRICAN AMERICANS
Most common– 20-30yr females
** BIRTH CONTROL**
Buccal mucosa is the MOST COMMON SITE Incisional biopsy –> rule out MELANOMA
Acquire melanocytic nevus - MOLE
Benign localized proliferation of cells from the NEURAL CREST
Most common ADULT TUMOR
* Junctional, Compound, Intradermal*
Junctional aquired meloncytic nevus
earliest presentation
Dark macule - less than 6mm
Compound acquired meloncytic nevus
nevus cells proliferate
Slightly elevated, smooth surface
Pigmentation decreases
Intradermal acquired meloncytic nevus
Papillomatous surface
hairs grow from center
Losses most or all of it’s pigmentation
Intraoral melonocytic nevi
Uncommon
Appearance similar to skin nevi
PALATE
Congenital Melanocytic Nevus
1% of newborns
Small or Large
Large congenital melanocytic nevus
hypertrichosis
(excess hair)
May undergo malignant transformation into MELANOMA
Should be removed or closely followed
Halo Nevus
Melanocytic nevus with a surrounding pale HYPOPIGMENTED BORDER
Nevus cell destruction by immune cells - no color
Blue Nevus
Proliferation of dermal or intramucosal melanocytes
oral lesions almost always on the PALATE
Tyndall Effect
Oral lesions –> must be biopsied to rule out melanoma
malignant transformation is rare
Tyndall Effect
Melanin particles are deep to the surface, light reflected back must pass through overlying tissue.
Long wavelenghts are easily absorbed into tissue
Blue has a shorter wavelenght and is reflected
Leukoplakia
An intraoral white plaque that does not rub off and cannot be identified as any well known entity
*If can be rubbed off – not leukoplakia
considered a PREMALIGNANT LESION
85% of oral precancer
BIOPSY IS MANDATORY
Recurrences are FREQUENT – long term follow ups
White lesions
Keratin, microbial colony, scar tissue, necrosis are blocking the redness of the underlying vascular tissue
White lesions that can be scraped off (5)
Materia Alba
White coated tongue
Burn (thermal, chemical, cotton roll)
Pseudomembranous candidiasis
Sloughing from toothpaste
Leukoplakia Etiology (6)
Tabacco
Alcohol
Sanguinaria
Microorganisms
Trauma
Tobacco
(Smokeless)
80% – leukoplakia smoke
smokeless tobacco –> tobacco pouch keratosis
Sanguinaria
Toothpaste and mouthrinses
Maxillary vestibule or alveolar mucosa of the maxilla
80% of pts with leukoplakia have history of using sanguinaria
UV radiation
Causes luekoplakia on the lower lip vermillion
Microorganisms
Treponema pallidum –> 3rd stage, glossitis
Candida albicans
HPV 16 and 18
EBV - hairy leukoplakia
Trauma
Not precancerous
Not true leukoplakia
Nicotene stomatitis and Frictional keratosis
Most common LOCATION for leukoplakia
Lower lip vermillion border
Buccal mucosa
Gingiva
common location for DYSPLASIA or CARCINOMA
Lip vermilion - lower lip
Lateral/ventral tongue
Floor of mouth
Erythroplakia
Scattered red patches
In areas of leukoplakia –> sites where epithelial cells are so immature they CAN NO longer produce KERATIN
Most Advanced Dysplasia
Common locations: FOM, Ventral tongue, Soft palate
Biopsy is MANDATORY
recurrence and multifocal involvement is common
Erythroleukoplakia
Red and white intermixed lesions
Advanced dysplasia
Prliferative verrucous leukoplaki (PVL)
Special high-risk form of leukoplaki
Multiple keratotic palques with roughened surface projections
Lesions slowly spread through the mouth
–> carcinoma can devleop
HIGEST RISK FOR MALIGNANT TRANSFORMATION
No association with tobacco use
Leukoplakia Histopathology
Hyperkeratosis
Hyperparakeratosis (No granular layer, nuclei retained)
Hyperorthokeratosis (Granular layer, nuclei lost)
Acanthosis (thickened spinous layer)
Mild dysplasia -
Moderate dysplasia -
Sever dysplasia -
Carcinoma in situ -
Alterations in lower 1/3
Alterations in lower 1/2
Alterations above 1/2
Alterations through epithelium
Factors that increase the risk of cancer in leukoplakia ( 4)
Persistence over several years
Female patient
Nonsmoker
Oral floor or ventral tongue lesions
Smokeless Tobacco Keratosis
Common local change - painless loss of gingival tissue in area of tobacco contact
Gingival recession may accompany
Correlates with QUANTITY of daily use and duration of habit
White plaque on mucosa in DIRECT contact (faint) - may look similar to luekoplakia
may appear fissured or ripped
longer use – thicker tissue
Biopsy needed if sever lesions
Treatment for smokeless tobacco keratosis
Alternating the site of tobacco placement
Habit cessation – normal mucosa appears in 2 weeks.
After 6 weeks no normal mucosa appears –> BIOPSY
Oral Submucosa Fibrosis
Chronic
Progressive scarring (Fibrosis) –> SURFACE IS TYPICALLY WHITE
Mucosal Rigidity
Limits the ability to open wide –> causes trismus
High risk precancerous condition
Caused by: BETEL QUID or POAN Tobacco like found in Indian culture
Most commonly affected sites of oral submucosal fibrosis
Buccal mucosa
Retrmolar areas
Soft palate
Treatment of oral submucosal fibrosis
Lesion DOES NOT regress with habit cessation - no new scarring will occur
** Can make incisions in bucall mucosa to release fibrous fibers and allowed a wider opening **
Frequent follow up is MANDATORY –> 1 in 10 biopsies undergo malignant transformation
Nicotene Stomatitis
White keratotic change on the palate – red dots are salivary gland openings
DUE TO HEAT – long term exposure
Reverse Smoking –> significant potential for malignancy (requires biopsy)
COMPLETELY REVERSIBLE – palate will return to normal within 2 weeks of habit cessation
** if it doesn’t not return to normal in 2 weeks – BIOPSY**
Actinic Keratosis
cutaneous PREMALIGNANT LESION
developes in adults with significant lifetime sun exposure
Scaly, irregular plaques – keratin formation
Vary in color
Scale peels off but will recur
Sandpaper texture
Some dysplasia may be present in the biopsy
10% will progress to SCCA in 2 years
Actinic keratosis treatment and prognosis
Treatment –> Destroyed or excised
Prognosis –> 10% will progress to SCCA in 2 years
Actinic Cheilosis
Common PREMALIGNANT alteration of lower lip vermillion
Loss of vermillion border - blotchy pale areas
Scaly areas develop on the drier protion of the vermillion
Further progression suggests changes to SCCA
Caused by –> LONG TERM UV LIGHT EXPOSURE
Treatment for Actinic Cheilisis
Chnages are irreversible
Use lip balms with sunscreens to prevent further damage
10% of patients –> SCCA
When should an Actinic Cheilisis be biopsied?
Induration
Thickening (leukoplakia)
Ulceration
Squamous Cell Carcinoma
95% of oral cancers are Squamous cell carcinoma –> MOST COMMON CANCER INTRAORALLY
lingual carcinomas - painless, indurated masses or ulcers on the posterior lateral border of tongue
Causes – multifactorial
Exophytic (mass forming - fungatin)
Endophytic
Leukoplakia
Erythroplakic
Erytrholeukoplakic
Etiology of SCCA
Tobacco
Alcohol
Phenolic agents
Radiation
Ifron deficiency
Vitamin A deficiency
Sphyillis
Oncogenic viruses
Immunosuppression
Oncogenes
Tumor suppresor genes
SCC
SCCA - Tobacco
80% of patients with oral SCCA have a history of smoking
The risk increases the longer a perso smokes
Greatest risk –> Reverse smoking (no filter)
Pipe smoking, cigar smoking
SCAA Alcohol
Significant risk factor when combined with tobacco
SCC Phenolic agents
Phenoxyacetic acids – rood mills
SCC radiation
UV radiation
X ray radiation increase the risk
SCC Iron deficiency
Iron is required for –> NORMAL function of epithelial cells
Plummer-Vinson Syndrome – severe, chronic form
Iron deficiency – impaired cell mediated immunity
SCC vitamin A defiency
Excessive keratinization
Normal levels are protective
SCC syphillis
tertiary stage
DORSAL tongue
SCC oncogenic viruses
HPV 16, 18, 31, 33
SCC Tumor suppressor genes
Allow tumor production when they become inactivated
SCC most common location –>
second most common –>
Third –>
Fourth –>
Tongue – lateral and vertical
Floor of mouth – associated with leukoplakia or erythroplakia
Soft palate
Gingiva
SCC oropharyngeal
Soft palate or tonisllar areas
Tumor staging
Best indicator of patient prognosis
T = size of primary local tumor in cm
N = involvement of local lymph nodes
M = distant metastasis
Tumor grading
Histologic features (not as good of indicator as clinical staging)
Grade I - tumor resembles parent tissue, well-differentitated
Grade II - tumor somewhat resembles parent tissue, moderately differentiated
Grade III (or IV) - tumor doesn’t resemble parent tissue, poorly differentiated
What guides treatment for intraoral lesions?
Clinical staging
Best therapy for SCC
Wide surgical excision and/pr radiation therapy
Treatment SCC
Intraoral tumors >3 mm depth = radical neck dissection
RADICAL NECK DISSECTION –> removal of neck tissue from collarbone to lower jaw.
Lip carcinoma = wedge resection
Field Cancerization
Tendency toward development of multiple mucosal cancers
Metastasis of SCC
Spread largely via lymphatics
Tends to spread ipsilaterally
Nodes = firm/hard, painless, enlarged, fixed
Metastasis most commonly found in:
lungs
liver
bones
Verrucous Carcinoma
Low grade variant of oral SCC
Can be caused by smokeless tobacco
Common sites:
Mandibular vestibule
Gingiva
Deceptively benign microscopic appearance
Malignant transformation potential (most to least)
PVL
Nicotine stomatitis
Erythroplakia
Oral submucous fibrosis
Erythroleukoplakia
Granular leukoplakia
Actinic Cheilosis
Nasopharyngeal Carcinoma
Group of malignancies that arise from lining epithelium in the nasopharynx
Associated with EBV
Basal Cell Carcinoma
Most common of all cancers
Locally invasive and slow spreading
80% found in head and neck
Results from UV radiation
Metastasis is rare
Most common form of BCC
Nodular (noduloulcerative)
Clinicopathologic varieties of BCC
Nodular
Pigmented
Sclerosing
Superficial
Those associated with nevoid BCC
Treatment of BCC
Less than 1 cm are excised with 3-5 mm margins
Melanoma
Malignant neoplasm of melanocytic origin
Acute sun exposure is a major causative factor (big time burns)
Third most common skin cancer - MOST DEATHS
Risk factors of Melanoma
UV radiation - ACUTE
Fair complexion
Light hair
Tendency to sunburn easily
History of painful/blistering sunburns as a child
Personal history of melanoma
Personal history of dysplastic or congenital nevus
FAMILY HISTORY - increases chances by 8%
Melanoma growth patterns
Radical = malignant cells spread horizontally through basal layer
Vertical = malignant cells invade underlying CT
ABCDE of Melanoma
Asymmetry
Border irregularity
Color variation
Diameter greater than 6 mm
Evolving lesions
Treatment - Melanoma
Surgical excision with 3-5 cm margins
Radioresistant
Squamous Cell Carcinoma
Basal Cell Carcinoma
** DOES not occur in the MOUTH **
Telangiectactic blood vessels
Telangiectactic blood vessels
Superficial capillaries
Found on Basal Cell Carcinoma Lesions
Prognosis of oral melanoma >.5mm
POOR
Survival rate decreases with DEPTH of lesion
Melanoma areas with WORST prognosis? (4)
BANS
B - interscapular area of back
A - posterior arm
N - Posteriot and lateral NECK
S - Scalp
Benign vs Malignant
Benign – not a cancerous tumor
Malignant - cancerous tumor, out of controlled growth of tissue?
Does seborrheic keratosis occur in the mouth?
No
