Chapter 10 Flashcards
1
Q
A
Squamos Papilloma
Benign proliferation of STRATIFIED SQUAMOUS epithelium
Caused by: HPV 6 & 11 (DNA virus)
Low virulence and infectivity rate
MOST COMMON - intraoral
2
Q
Sites of predilection of Squamous Papilloma
A
Tongue
Lips
Soft Palate
3
Q
What are the clinical manifestations of Squamous Papilloma?
A
Pedunculated
Painless
White, red, or mucosal colored
5mm
4
Q
Squmous Papilloma Differentials
A
Verruca Vulgaris
Condyloma acuminatum
Verruciform xanthoma
5
Q
A
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
6
Q
A
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)
7
Q
Condyloma Acuminatum Differential Diagnosis
A
Squamos papilloma
Verruca Vulgaris
Verruciform xanthoma
8
Q
HPV 16 and HPV 18
Condyloma acuminatum
A
increased risk for malignant transformation to squamos cell carcinoma
_** anogenital region – NOT ORAL LESIONS **_
9
Q
HPV 6 and 11
A
Squamous Papilloma
(may be Condyloma acuminatum)
10
Q
HPV 2, 4, 6, 40
A
Verruca Vulgaris
11
Q
HPV 2, 6, 11, 16, 18, 31, 53, 54
A
Condyloma Acuminatum
12
Q
Multifocal Epithelial Hyperplasia
A
HECK’S DISEASE
HPV 13 & 32
CHILDHOOD
Multiple lesions
Painless
Flattened or rounded papules –> Cobblestone
Mucosal colored
13
Q
Treatment for Heck’s Disease?
A
Spontaneously regress
Conservative surgical excision
Risk of recurrence
No risk of malignancy
14
Q
Heck’s Disease
A
Multifocal Epithelial Hyperplasia
15
Q
A
Sinonasal Papillomas
Benign - localized proliferation of respiratory mucosa
Three histological patterns
Arise from:
* Lateral nasal wall
* Septum
* Sinuses
16
Q
Sinonasal Papilloma Histological Forms (3)
A
Fungiform
Inverted
Cylindrical
17
Q
A
Mulluscum Contagiosum
DNA POXVIRUS
virally-induced epithelial hyperplasia
Sessile, papules
Umbilicated lesions
Skin-colored
Smooth surface
18
Q
Molluscum contagiosum histology
A
Molluscum bodies (Henderson-paterson bodies)
Virally infected epithelial cells (glossy appearance)
19
Q
Treatment of Molluscum Contagiosum
A
Remission occurs in 9 months
Treat to decrease risk of transmission
Remove by curettage or cryotherapy
20
Q
A
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
21
Q
Verrucifrom Xanthoma differential diagnosis
A
Squamous papilloma
Verruca vulgaris
Condyloma acuminatum
22
Q
Treatment of Verruciform Xanthoma
A
Conservative surgical excision
Recurrence is rare
No risk of malignant transformation
23
Q
A
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
24
Q
Dermatosis papulosa nigra
A
Seborrheic Keratosis that occurs in AFRICAN AMERICANS
Genetic inheritance (AD)
Multiple black 2mm papules
Scattered around zygomatic and periorbital region
25
Dermatosis Papulosa Nigra
26
**Leser-Trelat Sign**
Sudden appearance of NUMEROUS seborrheic keratosis
**_Associated with INTERNAL MALIGNANCY_** (not good!)
27
**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
28
**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
29
**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
30
Color intensity in UV light:
Increases --\> ?
Stays the same --\> ?
Ephelis
Actinic Lentigo (appearance induced by sun)
Lentigo simplex (found in sunless areas)
31
**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
32
**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
33
**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_*
34
Labial melanotic macule
oral melanotic macule
"oral freckle" found on the vermillion border
35
**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**
36
**Acquire melanocytic nevus -** MOLE
_Benign localized proliferation of cells from the NEURAL CREST_
***Most common ADULT TUMOR***
\* Junctional, Compound, Intradermal\*
37
Junctional aquired meloncytic nevus
earliest presentation
Dark macule - less than 6mm
38
Compound acquired meloncytic nevus
nevus cells proliferate
Slightly elevated, smooth surface
Pigmentation decreases
39
Intradermal acquired meloncytic nevus
Papillomatous surface
hairs grow from center
Losses most or all of it's pigmentation
40
Intraoral melonocytic nevi
Uncommon
Appearance similar to skin nevi
PALATE
41
**Congenital Melanocytic Nevus**
1% of newborns
Small or Large
42
Large congenital melanocytic nevus
hypertrichosis
(excess hair)
May undergo malignant transformation into MELANOMA
Should be removed or closely followed
43
**Halo Nevus**
Melanocytic nevus with a surrounding pale HYPOPIGMENTED BORDER
Nevus cell destruction by immune cells - no color
44
**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
45
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**
46
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
47
White lesions
Keratin, microbial colony, scar tissue, necrosis are blocking the redness of the underlying vascular tissue
48
White lesions that can be scraped off (5)
Materia Alba
White coated tongue
Burn (thermal, chemical, cotton roll)
Pseudomembranous candidiasis
Sloughing from toothpaste
49
Leukoplakia Etiology (6)
Tabacco
Alcohol
Sanguinaria
Microorganisms
Trauma
50
Tobacco
| (Smokeless)
80% -- leukoplakia smoke
smokeless tobacco --\> tobacco pouch keratosis
51
Sanguinaria
Toothpaste and mouthrinses
**Maxillary vestibule or alveolar mucosa of the maxilla**
80% of pts with leukoplakia have history of using sanguinaria
52
UV radiation
Causes luekoplakia on the lower lip vermillion
53
Microorganisms
Treponema pallidum --\> 3rd stage, glossitis
Candida albicans
HPV 16 and 18
EBV - hairy leukoplakia
54
Trauma
Not precancerous
Not true leukoplakia
Nicotene stomatitis and Frictional keratosis
55
Most common LOCATION for leukoplakia
Lower lip vermillion border
Buccal mucosa
Gingiva
56
common location for DYSPLASIA or CARCINOMA
Lip vermilion - lower lip
Lateral/ventral tongue
Floor of mouth
57
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
58
Erythroleukoplakia
Red and white intermixed lesions
Advanced dysplasia
59
**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_
60
Leukoplakia Histopathology
Hyperkeratosis
Hyperparakeratosis (No granular layer, nuclei retained)
Hyperorthokeratosis (Granular layer, nuclei lost)
Acanthosis (thickened spinous layer)
61
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
62
Factors that increase the risk of cancer in leukoplakia ( 4)
Persistence over several years
Female patient
Nonsmoker
Oral floor or ventral tongue lesions
63
**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
64
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
65
**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
66
Most commonly affected sites of oral submucosal fibrosis
Buccal mucosa
Retrmolar areas
Soft palate
67
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_***
68
**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\*\*
69
**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_***
70
Actinic keratosis treatment and prognosis
Treatment --\> Destroyed or excised
Prognosis --\> 10% will progress to SCCA in 2 years
71
**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
72
Treatment for Actinic Cheilisis
Chnages are irreversible
Use lip balms with sunscreens to prevent further damage
**_10% of patients --\> SCCA_**
73
When should an Actinic Cheilisis be biopsied?
Induration
Thickening (leukoplakia)
Ulceration
74
**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_
75
Etiology of SCCA
Tobacco
Alcohol
Phenolic agents
Radiation
Ifron deficiency
Vitamin A deficiency
Sphyillis
Oncogenic viruses
Immunosuppression
Oncogenes
Tumor suppresor genes
SCC
76
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
77
SCAA Alcohol
Significant risk factor when combined with tobacco
78
SCC Phenolic agents
Phenoxyacetic acids -- rood mills
79
SCC radiation
UV radiation
X ray radiation increase the risk
80
SCC Iron deficiency
Iron is required for --\> NORMAL function of epithelial cells
**_Plummer-Vinson Syndrome_** -- severe, chronic form
Iron deficiency -- impaired cell mediated immunity
81
SCC vitamin A defiency
Excessive keratinization
Normal levels are protective
82
SCC syphillis
**tertiary stage**
DORSAL tongue
83
SCC oncogenic viruses
HPV 16, 18, 31, 33
84
SCC Tumor suppressor genes
Allow tumor production when they become inactivated
85
SCC most common location --\>
second most common --\>
Third --\>
Fourth --\>
Tongue -- lateral and vertical
Floor of mouth -- associated with leukoplakia or erythroplakia
Soft palate
Gingiva
86
SCC oropharyngeal
Soft palate or tonisllar areas
87
Tumor staging
Best indicator of patient prognosis
T = size of primary local tumor in cm
N = involvement of local lymph nodes
M = distant metastasis
88
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
89
What guides treatment for intraoral lesions?
Clinical staging
90
Best therapy for SCC
Wide surgical excision and/pr radiation therapy
91
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
92
Field Cancerization
Tendency toward development of multiple mucosal cancers
93
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**
94
Verrucous Carcinoma
**Low grade variant of oral SCC**
Can be caused by smokeless tobacco
Common sites:
Mandibular vestibule
Gingiva
Deceptively **benign microscopic appearance**
95
Malignant transformation potential (most to least)
PVL
Nicotine stomatitis
Erythroplakia
Oral submucous fibrosis
Erythroleukoplakia
Granular leukoplakia
Actinic Cheilosis
96
Nasopharyngeal Carcinoma
Group of malignancies that arise from lining epithelium in the nasopharynx
## Footnote
**Associated with EBV**
97
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
98
Most common form of BCC
Nodular (noduloulcerative)
99
Clinicopathologic varieties of BCC
Nodular
Pigmented
Sclerosing
Superficial
Those associated with nevoid BCC
100
Treatment of BCC
Less than 1 cm are excised with 3-5 mm margins
101
Melanoma
Malignant neoplasm of melanocytic origin
**Acute sun exposure** is a major causative factor (big time burns)
Third most common skin cancer - MOST DEATHS
102
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%
103
Melanoma growth patterns
Radical = malignant cells spread horizontally through basal layer
Vertical = malignant cells invade underlying CT
104
ABCDE of Melanoma
Asymmetry
Border irregularity
Color variation
Diameter greater than 6 mm
Evolving lesions
105
Treatment - Melanoma
Surgical excision with 3-5 cm margins
Radioresistant
106
Squamous Cell Carcinoma
107
Basal Cell Carcinoma
\*\* DOES not occur in the MOUTH \*\*
**Telangiectactic blood vessels**
108
Telangiectactic blood vessels
Superficial capillaries
Found on Basal Cell Carcinoma Lesions
109
Prognosis of oral melanoma \>.5mm
POOR
Survival rate decreases with DEPTH of lesion
110
Melanoma areas with WORST prognosis? (4)
**BANS**
**B -** interscapular area of back
**A -** posterior arm
**N** - Posteriot and lateral NECK
**S -** Scalp
111
Benign vs Malignant
Benign -- not a cancerous tumor
Malignant - cancerous tumor, out of controlled growth of tissue?
112
Does seborrheic keratosis occur in the mouth?
No
