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Oral Pathology Exam 1 > 3. Malignant Epithelial Lesions > Flashcards

3. Malignant Epithelial Lesions Flashcards

1
Q

What are the Risk Factors for OSSC?

A
  • 80% associated with tobacco, with or without alcohol
  • 20-25% show no identifiable RFs, increasing incidence in:
    • Young Adults , especially females on Lateral Tongue
    • Older Women on Gingiva
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2
Q

What is the Clinical Differential Diagnosis for Oral SCC? (6)

A
  • Non-Specific Ulcer:
    • Traumatic Granuloma
  • Specific Infections:
    • TB
    • Deep Fungal Infection
    • Syphilis
  • Immune-Mediated Conditions:
    • Wegener’s Granulomatosis
    • Chron’s Ds
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3
Q

What are the best indicators of prognosis, and what guides tx, in Oral SCC?

A

Staging

  • Tumor Size
  • Extent of Metastatic Spread

The TNM System, except for nodal involvement

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4
Q

What is the most important prognostic factor in Oropharyngeal CA?

A

HPV status, rather than stage

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5
Q

Why do HPV+ tumors respond better to chemo?

A

Lack p53 mutations and field cancerization

  • 60% reduction in risk of death
  • 30% greater 5 yr survival than HPV - tumors
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6
Q

What gives the best locoregional control and disease-free survival for advanced stages: 3, 4a, 4b-no distant mets OSCC?

A

Post-operative concurrent chemoradiation therapy

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7
Q

What is the tx for OSCC with Distant Mets?

A

Single/multi-agent Chemotx

Not going to radiate it becuase it is throughout the entire body!

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8
Q

What drugs are using in OSCC Chemotherapy?

A
  • Cisplatin or Carboplatin
  • 5-fluorouracil
  • Taxanes (paclitaxel, docetaxel)
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9
Q

What OSCC Radiation, targets the tumor site and mimimizes damage to surrounding tissue?

A

Intesity-Modulated Radiation Therapy (IMRT)

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10
Q

What OSCC Radiation involves the placement of tiny radioactive seeds, used for small intraoral tumors or with IMRT to increase dosage?

A

Brachytherapy

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11
Q

What is the Clinical appearance of OSCC?

A
  • Irregular shape, mixture of red and white
  • Ulcerated center with elevated rolled border, that is much firmer (indurated) than surrounding tissues
  • Early lesions are Aysmptomatic (don’t hurt)
    • Pain is a late feature
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12
Q

What occurs with bone involvement in OSCC?

A
  • “Moth-Eaten” Ragged RL
  • Osteomyelitis
  • Pathologic Fracture
  • Bone Loss
    • Faster than perio bone loss
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13
Q

How does SCC of the Lip develop?

A
  • Sun induced, not tobacco induced
  • In the setting of Actinic Cheilitis; changes in months
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14
Q

What is the clinical appearance of SCC of the Lip?

A
  • 90% Lower Lip
  • Crusted, non-tender, indurated ulceration
  • < 1cm when discovered
  • Slow-growing, well-differentiated lesion = better prognosis
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15
Q

What is the most common site of involvement for OSCC (>50%)?

A

Lateroventral Tongue

(mostly posterior)

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16
Q

In what population is SCC of the Tongue typically seen in?

A
  • Younger people (< 40 yrs old)
    • Almost always at this site
  • Majority have a history of tobacco and alcohol abuse
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17
Q

What OSCC is most likely to develop from preexisting white/red lesion?

A

SCC of the FOM

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18
Q

What is SCC of the FOM often associated with?

A

2nd Primary Malignancy

Ask the pt if they have a history of oral cancer

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19
Q

What is the incidence for SCC of the FOM?

A
  • Almost equals Lateral Tongue as a common site for OSCC (~35%)
  • Majority have a history of of tobacco and alcohol abuse
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20
Q

In what population is the prevelance of Oral Cancer the highest in?

A

Adult Disease

  • White Men > 65 yrs
  • Middle Aged Black Men
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21
Q

In what population is SCC of the Gingiva/Alveolar Mucosa most prevelant in?

A
  • Women (2:1)
  • Those w/o identifiable RFs
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22
Q

What is the clinical appearance of SCC of the Gingiva/Alveolar Mucosa?

A
  • Epithelium will have a speckled (red and white), pebbly, granular surface
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23
Q

What can SCC of the Gingiva/Alveolar Mucosa mimic?

A

Benign Reactive Lesions of Gums

  • Pyogenic Granulomas
    • Can appear big and red, ~ inflammation
  • Perio Ds
    • Smooth surfaced, and pink
    • Bone loss will occur faster than in PD
    • Biopsy if PD doesn’t respond to tx after a month
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24
Q

Where do most SCC of the Palate arise?

A

Lateral Soft Palate - Oropharyngeal

Hard to tell if it arised in the max sinus and invaded down

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25
Q

Where do most Oropharyngeal Carcinomas arise from?

A

70% from Tonsillar Region

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26
Q

What are the Symptoms associated with Oropharyngeal Carcinoma (SCC of Palate)?

A
  • Persistant Sore Throat
  • Dysphagia (difficulty swallowing)
  • Odynophagia (pain on swallowing)
  • Dull/Sharp Pain Referred to Ear

Pt may think they have a toothache so ask about these symptoms

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27
Q

In what population does SCC of the Buccal Mucosa occur?

A
  • Very common in India due to betel quid use
  • Not very common site for OSCC in the western world
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28
Q

What can SCC of the Buccal Mucosa be confused for?

A
  • Aphtous Ulcer, but it will be:
    • Firm
    • Persistant > 2 weeks
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29
Q

What is the Histology of OSCC? (3)

A
  • Invasive cords/nests of malignant squamous epithelial cells arising from, but not connected to, dysplastic surface epithelium
  • Varying degrees of Keratin Production (keratin pearls) and Dyskeratosis
  • Desmoplasia = tumor induced fibrosis
    • Why the lesions feel firm
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30
Q

What Histology do the Tumor Cells of OSCC show? (3)

A
  • Increased nuclear:cytoplasmic
  • Cellular and nuclear pleomorphism
  • Mitotic activity
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31
Q

What determins the stage in OSCC?

A

TNM System

  • T = Tumor Size
  • N = Nodal Involvement
  • M = Metastasis (distant spread)
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32
Q

What is the Prognosis for OSCC? (3)

A

Poor​

  • ~2/3 of pts present in Stage III or IV
    • LN spread = Stage III (minimum)
  • ~3-5% improved 5 yr survival over the last decade, but still 1 of the worst prognoses of any major cancer
  • Even with tx: significant disfiguarment, disability, pain
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33
Q

What is the Follow-Up Needed for pts with OSCC? (4)

A
  • Necessary for Life of the Patient
  • Field Effect = Must check Entire Mouth
  • Most recurrences will occur within the first 2 years
  • May require biopsy of multiple areas
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34
Q

What population is Verrucous Carcinoma common in?

A
  • Elderly Males
  • With Historical Smokeless Tobacco (Snuff) Association
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35
Q

What may give rise to Verrucous Carcinoma of OSCC?

A

Proliferative Verrucous Leukoplakia (PVL)

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36
Q

In the Grading of OSCC, what microscopic features correlate with increased risk for nodal metastasis?

A

Tumor Thickness or Depth of Invasion

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37
Q

In the Grading of OSCC, what feature is associated with a worse prognosis?

A

Extracapsular Spread in a Lymph Node

38
Q

What is the Location, Clinical Appearance, and Growth Pattern of Verrucous Carcinoma? How is this different from OSCC?

A
  • Diffuse white or red and white plaque
    • ​OSCC has an ulcerated center with an indurated rolled border
  • Low-Risk Sites: Hard Palate, Alveolar and Buccal Mucosa
    • OSCC is in High Risk Sites
  • Grows Laterally, invading with a “pushing margin”, but doesn’t infiltrate or show mets
    • OSCC infiltrates and can mets
39
Q

How does Verrucous Carcinoma appear microscopically? How is this different from OSCC?

A

Appears very bland/benign, with no features of dysplasia and no cytologic atypia

  • OSCC arises from a dysplastic surface epithelium, with features of cytologic atypia:
    • ​Increased Nuclear:Cytoplasm, Pleomorphism, and Mitotic acitivity
40
Q

What is the diagnosis of Verrucous Carcinoma based off of?

A
  • Overall Architecture of the Tumor
  • How it Invades “pushing margin”

Not based on individual cell appearance because they look pretty normal

41
Q

What is the Histology of Verrucous Carcinoma?

A
  • Thick, abundant keratin production, and a papillary or verrucous surface
  • Parakeratin Plugs = parakeratin fills in the clefts between the surface projections (dark pink)
  • Wide, elongated rete ridges that invade by pushing into CT
  • Often intense chronic inflammatory infiltrate in the CT (same as OSCC​)
42
Q

What is the Treatment for Verrucous Carcinoma?

A
  • Surgical Excision
    • Not as aggressive as what is needed for OSCC, because it grows laterally.
    • 90% ds free 5yrs after surgery
43
Q

What is Carcinoma of the Maxillary Sinus?

A

SCC that arise in the Sinus

44
Q

What is the Etiology for Carcinoma of the Maxillary Sinus?

A
  • Unknown cause for most
    • Weak tobacoo link
    • Some may have HPV
    • 1 type shows strong assoc to occupational exposure to wood/leather dust
45
Q

What is the Clinical Appearance of Carcinoma of the Maxillary Sinus?

A
  • Mostly aymptomatic until tumor fills and perforates the sinus
  • Symptoms depend on direction of tumor growth
    • Lateral: painful facial swelling
    • Medial: chronic unilateral nasal obstruction/bleeding
    • Inferior: palatal mass/ulceration
    • Superior: eyeball protrusion
46
Q

What is the radiographic appearance of Carcinoma of the Maxillary Sinus?

A
  • Loose Teeth
  • Moth-eaten Bone
  • Cloudy Sinus on PANX
47
Q

In what population is Nasopharyngeal Carcinoma more common?

A
  • 20-55x more common in Southern China
  • Middle-Aged Males (3:1), but can be any age
48
Q

What is the etiology/pathogenesis of Nasopharyngeal Carcinoma?

A
  • Primary tumor may be small and arise from Waldeyer’s Ring
  • Assoc with EBV infection, although etiology is multifactorial
49
Q

What are the symptoms of Nasopharyngeal Carcinoma?

A
  • Epistaxis
  • Obstruction of 1 side of nose
50
Q

What are the 2 possible histologies of Nasopharyngeal Carcinoma?

A
  • SCC with or without keratin production
  • Undifferentiated Type - lesional cells blend with stromal lymphocytes = Lymphoepithelioma
51
Q

What is the treatment for localized Nasopharyngeal Carcinoma?

52
Q

What is the treatment for Metastatic Nasopharyngeal Carcinoma?

A

Radiation with concomitant Chemotx

53
Q

What does BCC arise from?

A
  • Basal cells of epidermis, OR
  • Germ cells of hair follicles
54
Q

What is the most common skin cancer?

55
Q

What population of pts are affected by BCC?

A
  • > 40 yrs
  • Fair complexion
  • History of chronic sun exposure
56
Q

What is the molecular pathogenesis of BCC?

A
  • Dysregulation of hedgehog signaling pathway
  • TP53 mutations in 50%
57
Q

Where is BCC located on the skin?

A

Middle 3rd of face

58
Q

What is the most common subtype of BCC?

A

Nodulo-Ulcerative (45-60%)

Located in the head and neck region

59
Q

What subtype of BCC is found on the trunk?

A

Superficial BCC (15-35%)

60
Q

What is the characteristics of Sclerosing (morpheaform) BCC?

A
  • Mimics scar tissue, but:
    • No previous history of trauma
    • Continues to grow
    • In the Head and Neck Region
61
Q

What is the clinical appearance of BCC?

A
  • Umbilicated (depressed) papule that may show central ulceration, with a rolled pearly white border
    • May see telangiectastic vessels
  • Lacks adnexal skin structures (no hair)
  • “Rodent Ulcer”
    • Untx lesions continue to enlarge slowly, with ulceration and destruction of underlying structures
62
Q

What is the Histology of BCC?

A
  • Basaloid cells that appear to “drop off” of the basal cell layer of the epidermis
  • Nodulo-Ulcerative BCC:
    • Characteristic large lobules of tumor cells
63
Q

What is the prognosis for BCC?

A
  • Excellent
    • > 95% of pts cured after 1st tx
  • More aggressive lesions require Mohs’ surgery:
    • Larger, recurrent, or in embryonic planes of fusion
64
Q

Why is Follow-Up of BCC important?

A
  • Same concept as the Field Effect in the mouth from smoke
    • 44% chance of 2nd BCC
    • 6% chance of SCC within 3 yrs
65
Q

What is the etiology of Cutaneous SCC?

A
  • Pre-exisiting AK
  • Chronic sun (UV light) exposure
66
Q

Where is Cutaneous SCC typically found?

A
  • Face
  • Helix of Ear
  • Dorsum of Hands
  • Arms
67
Q

What is the treatment and prognosis for Cutaneous SCC?

A
  • Surgical Excision
    • Actinically-induced SCC are well-differentiated and grow slowly
  • Prognosis is Very Good, if ID early
68
Q

In what population is Cutaneous Melanoma predominate in?

A
  • Slight Male predominance
  • Fair-skinned
  • 40-70 yrs old
69
Q

What is the most frequent site for Cutaneous Melanoma in men?

70
Q

What is the most frequent site for Cutaneous Melanoma on women?

A

lower extremity

71
Q

What are the Risk Factors for Cutaneous Melanoma? (6)

A
  1. History of increased # of sunburns
  2. Indoor occupation, with outdoor recreation
  3. Family history of melanoma
  4. Personal history of melanoma
  5. Dysplastic or Congenital Nevus
  6. > 100 Common Nevi
72
Q

What is the most common mutation associated with Cutaneous Melanoma, and what other 2 are sometime seen?

A

BRAF mutation

  • CDKN2A mutation
  • CDK4 mutation
73
Q

What mutation is associated with Mucosal Melanomas?

A

KIT mutations

74
Q

What population does Cutaneous H/N Melanoma occur in?

A
  • Sun-exposed skin of older adults, mainly mid-face region
75
Q

What does Cutaneous H/N Melanoma develop from?

A
  • A premalignant precursor called Lentigo Maligna (Hutchinson Freckle)
  • Melanoma in-situ
76
Q

What is the clinical appearance of Cutaneous H/N Melanoma?

A
  • Slowly expanding (radial growth phase = 15 yrs)
  • Variegated macule with irregular borders
77
Q

What is the treatment for Cutaneous H/N Melanoma?

A

Surgical Excision with 1-2cm margins

78
Q

What is the treatment for Aggressive or Recurrent Cutaneous H/N Melanoma?

A

Radiation or Immunotherapy (IFN-a, checkpoint inhibitors)

79
Q

What is the treatment for Metastic Cutaneous H/N Melanoma?

A

BRAF Inhibitor (vemurafenib) and T-Cell Promotor (ipilimumab)

80
Q

What is the single most important prognostic indicator for Cutaneous H/N Melanoma?

A

Breslow Tumor Thickness

81
Q

What is the prognosis for Cutaneous H/N Melanoma, and what factors increase the prognosis?

A
  • 92% 5 yr survival
  • 3-5% develop a 2nd melanoma = follow-up
  • Better Prognosis for:
    • Females
    • Younger
    • Not High Risk Areas (BANS)
    • No Ulceration
82
Q

What is the most common melanoma variant in the oral cavity?

A

Acral Lentiginous

83
Q

Where are Oral (Mucosal) Melanomas found?

A

70-80% on hard palate, maxillary alveolus

84
Q

What is the Clinical Appearance of Oral (Mucosal) Melanomas?

A
  • Early Lesions:
    • ​brown/black/blue macules with irregular borders
    • A minority are colorless
  • Late Lesions:
    • ​Nodular
    • May ulcerate
85
Q

What does bone involvement in Oral (Mucosal) Melanomas appear as?

86
Q

What is the histological appearance of Oral (Mucosal) Melanomas?

A
  • Invasive cells are spindle-shaped, pleomorphic melanocytes making brown pigment
    • ​They are invading up into the lamina propria

​​

87
Q

In what type of melanoma is invasion of blood vessels and lymphatics more common, Oral or Cutaneous?

A

Oral Melanoma

88
Q

What is the prognosis for Oral (Mucosal) Melanomas?

A
  • Much worse once depth > 0.5mm
  • 10-25% 5 yr survival
    • Much worse than the 92% for cutaneous melanoma
  • Pts usually die due to mets rather than local extension
89
Q

What are components of Melanoma Staging?

A
  • Breslow Thickness
  • Clark Level
90
Q

What does Breslow thickness measure?

A

From the granular cell layer to depth of invasion (mm)

91
Q

What does Clark Level indicate in Melanomas?

A

Anatomic extension of the tumor

  • I - epithelium
  • II - penetrating papillary dermis
  • III - filling papillary dermis
  • IV - invasion of reticular dermis
  • V - invasion of subcutaneous fat

Oral Pathology Exam 1 (8 decks)

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