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BDS4 Oral Medicine > Dysplasia & Oral Cancer > Flashcards

Dysplasia & Oral Cancer Flashcards

1
Q

What can potentially malignant disorders be subtyped into

A
  • potentially malignant lesion
  • potentially malignant condition
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2
Q

What is a potentially malignant lesion

A

altered tissue in which cancer is more likely to form

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3
Q

What is a potentially malignant condition

A
  • generalized state with increased cancer risk
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4
Q

What are examples of potentially malignant lesions/conditions

A
  • leukoplakia
  • erythroplakia
  • lichen planus
  • oral submucosa fibrosis
  • iron deficiency
  • teritary syphilis

LP, OSF, tertiary syphilis can be potential malignant lesion/condition

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5
Q

What are predictors of malignancy in luekoplakia

A
  • age
  • gender
  • site
  • clinical appearance
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6
Q

How does age effect risk of malignant transformation of leukoplakia

A

older px more likely

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7
Q

How does gender effect risk of malignant transformation of leukoplakia

A
  • female more at risk
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8
Q

How does site effect risk of malignant transformation of leukoplakia

A
  • buccal mucosa = low risk
  • FOM & tongue = high risk
  • sublingual keratosis occurs in FOM and is v high risk
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9
Q

How does clinical appeareance effect risk of malignant transformation of leukoplakia

A
  • homogenous vs non-homogenous surface
  • non-homogenous higher risk
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10
Q

What is a homogenous surface

A

same colour and consistency throughout lesion

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11
Q

What is a non-homogenous lesion

A

*e.g verrucous, ulcerated, leukoerythroplakia
should be biopsied

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12
Q

Which types of lichen planus are at most risk of malignant transformation

A
  • erosive/atrophic
  • lichen planus also at greater risk of developing candidal leukoplakia which increases risk of malignant transformation
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13
Q

What is oral submucous fibrosis

A
  • more common in china and india
  • linked to betel nut chewing
  • abnormal collagen is deposited in connective tissue in submucosa
  • results in fibrosis of tissues and muscles
  • limited mouth opening
  • produces epithelial atrophy and sometimes leuko/erythroplakia
  • 8% malignant transformation
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14
Q

How does iron deficiency increase risk of malignant transformation

A
  • oral epithelium thins
  • protection lost against carcinogens
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15
Q

What is tertiary syphilis

A
  • get gumma formation
  • can result in leukoplakia on tongue
  • high risk for transformation to SCC
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16
Q

What is the gold standard for assessing malignant potential

A

biopsy (histopathology)

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17
Q

What are the tissues assessed for in histopathology

A
  • dysplasia
  • atrophy
  • candida infection
  • biological markers (mostly in research atm)
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18
Q

What are some of the biological markers that are looked at

A
  • DNA content
  • p53
  • HPV
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19
Q

What does increased DNA contnet in leukoplakia suggest

biological marker in histopathology

A
  • cell is acquiring hallmarks of cancer
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20
Q

What is p53

A
  • guardian of the genome
  • activates when cell damage occurs
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21
Q

What does p53 do when there is cell damage

A
  • stops cell cycle to allow DNA repair
  • apoptosis where repair is not possible
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22
Q

What is often discovered about p53 in cancers

A
  • it has been inactivated
  • by mutation or by virus (oncogenic)
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23
Q

Which types of HPV are associated with oropharyngeal cancer

A

mainly type 16
also hpv 18 occasionally

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24
Q

What is dysplasia

A

disordered growth in a tissue

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25
Q

What is atypia

A
  • changes in the cell
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26
Q

What is the criteria of diagnosis for dysplasia based on

A

architechtural changes
cytological abnormalities (cellular atypia)

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27
Q

What do the cytological abnormalities represent

A
  • changes in individual cells reflecting abnormal dna content in the nucleus, failure to mature and keratinise correctly and increased proliferation
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28
Q

What are the different cytological abnormalities that may be seen

A
  • abnormal variation in nuclear size
  • abnormal variation in nuclear shape
  • abnormal variation in cell size
  • abnormal variation in cell shape
  • increased/altered nuclear cytoplasmic ratio
  • atypical mitosis figures
  • increased number and size of nucleoli
  • nuclear hyperchromatism
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29
Q

What does architectural changes represent

A

changes in organisation of maturation and normal layer of the epithelium

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30
Q

What are the different architechtural changes that may be seen

A
  • irregular epithelial stratification
  • loss/disturbed polarity of basal cells
  • drop-shaped rete ridges
  • increased and abnormal mitosies
  • premature keratinisation in single cells
  • abnormal keratinisation
  • keratin pearls within rete ridges
  • loss of epithelial cohesion/adhesion
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31
Q

What is the WHO 2005 classification of dysplasia

A
  • basal hyperplasia
  • mild dysplasia
  • moderate dysplasia
  • severe dysplasia
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32
Q

What are the architectural changes in basal hyperplasia

A

*increased number of basal cells in basal compartment
* regular stratification
* basal compartment is larger

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33
Q

What are the cytological abnormalities in basal hyperplasia

A

nil

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34
Q

Slide of basal hyperplasia

A
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35
Q

What are the architectural changes seen in mild dysplasia

A
  • in lower third
  • basal cell hyperplasia
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36
Q

What is the cytological changes seen in mild dysplasia

A
  • mild atypia
  • pleomorphism
  • hyperchromatism
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37
Q

What is pleomorphism

A
  • nuclei and cells are different shapes and sizes
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38
Q

What is hyperchromatism

A
  • increased dna content causes darker staining of nuclei
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39
Q

Mild dysplasia is often reactive, what does this mean

A
  • caused by trauma, infection, smoking etc
  • removal of cause will most likely result in regression
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40
Q

Mild dysplasia slide

A
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41
Q

What are the architectural changes in moderate dysplasia

A
  • extent into middle third
  • loss of intercellular adhesion
  • drop shaped rete pegs
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42
Q

What are the cytological changes in moderate dysplasia

A

moderate atypia
pleomorphism
hyperchromatism

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43
Q

Moderate dysplasia slide

A
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44
Q

What are the architectural changes in severe dysplasia

A
  • extend into upper third
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45
Q

What are the cytological changes in severe dysplasia

A
  • severe atypia
  • numerous mitoses- abnormally high
  • pleomorphism
  • hyperchromatism
  • loss of polarity
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46
Q

Severe dysplasia slide

A
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47
Q

What is carcinoma in situ

A

theoretic concept
all layers of epithelium involved
malignant but no invasion to underlying connective tissue
not beyond the basement membrane

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48
Q

What are the architectural changes in carcinoma in situ

A
  • full thickness of viable cell layers
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49
Q

What are the cytological changes in carcinoma in situ

A
  • pronounced cytological atypia
  • mitotic abnormalities frequent
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50
Q

What does malignancy trigger

What would we expect to see in the underlying tissue in carcinoma in situ

A

immune response

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51
Q

Carcinoma in situ slide

A
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52
Q

Summarise the different histopathological features of epithelial dysplasia

A
  • increased/abnormal mitoses
  • basal cell hyperplasia
  • drop shaped rete pegs
  • disturbed polarity of basal cells
  • alteration in nuclear/cytoplasm ratio
  • nuclear hyperchromatism
  • prominent and enlarged nuclei
  • irregular epithelial stratification/disturbed maturation
  • nuclear and cellular pleomorphism
  • abnormal keratinization
  • loss of reduction of intercellular adhesion (or cohesion)
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53
Q

What 2 factors does carcinogenesis depend on

A
  • genetic (changes)
  • carcinogens (environment)
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54
Q

How do genetics and environment come together to form malignancy

A
  • damage causes mutation at genetic level
  • damage results in altered gene expression
  • results in inactivation or overexpression and this alters cell function
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55
Q

What are the stages of carcinogenesis

A
  1. initiation
  2. promotion
  3. transformation
  4. progression
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56
Q

What is intiation

A

mutation

57
Q

What is promotion

stages of carcinogenesis

A
  • agent promotes proliferation
  • can be due to further mutation
  • mutation encourages cell division and disrupts genetic stability by damaging dna repair system
  • instability makes it more prone to further mutations
  • once cell division greater than other cells, it has reaches this stage
58
Q

What is transformation

A
  • further mutations are acquired
  • they cannot be repaired due to the damage to the dna repair system
59
Q

What is progression

A

formation of malignant tumour

60
Q

What are the changes to genes that can occur

A
  • changes to chromosome e.g translocation
  • genes e.g mutation, deletion, amplification
  • epigenetic changes
61
Q

What are proto-oncogenes

A
  • normal genes
  • regulat cell division
62
Q

What does mutation in proto-oncogenes result in

A
  • oncogenes
63
Q

What do oncogenes do

A
  • produce oncoproteins
  • these encourage tumour growth by dysregulating cell growth, proliferation and division
64
Q

What are tumour suppressor genes

A
  • inhibit cell division and growth
  • act as anti-oncogenes
  • when these become mutated, there is nothing to prevent cell division
65
Q

What is the safety net with tumour suppressor genes

A
  • requires loss of both alleles to become insufficient
  • known as knudson’s two hit hypothosis
66
Q

What is an example of a tumour suppressor gene

A

TP53
produces p53

67
Q

What are the genes that are important in malignancy

A
  • oncogenes
  • tumour suppressor genes
  • genes that regulate apoptosis and are involved in dna repair
  • miRNA
68
Q

What is miRNA

A
  • noncoding part of mRNA
  • similar to onco/TS genes
69
Q

What are the hallmarks of cancer

A
  • self sufficiency in growth signals
  • insensitivity to antigrowth signals
  • tissue invasion and metastasis
  • limitless replicative potential
  • sustained angiogenesis
  • evading apoptosis
70
Q

What is the field change theory

A
  • process where large no. of cells at a tissue surface or within an organ are affected by carcinogenic alterations (genetic instability)
  • more at risk of developing cancer despite appearing normal clinically
  • includes pharynx, larynx, resp tract
  • high risk sites are within 5cm of primary tumour
  • 20% may develop synchronous or metachronus tumour

aka field cancerisation

71
Q

What is a synchronous tumour

A

within 6 months of primary

72
Q

What is a metachronous tumour

A
  • after 6 months of primary
73
Q

What does a pathology report contain

A
  • diagnosis
  • differentiation/grading
  • pattern of invasive front related to nodal spread
74
Q

What are the different grades of differentiation

A
  • well differentiated - best prognosis
  • moderately differentiated
  • poorly differentiated
  • anaplastic
75
Q

What are the patterns of invasive fronts

A

cohesive
non cohesive

76
Q

What is cohesive

A

cells advancing at same rate
better prognosis

77
Q

What is non-cohesive

A
  • advancing in strands
  • more implicated with lymph node involvement
  • worse prognosis
78
Q

What is the common pattern of spread with OSSC

A
  1. local extension of disease
  2. lymphatic spread
  3. haematogenous spread
79
Q

What is local extension of disease

A
  • mucosal extension
  • muscle
  • bone
  • nerve
80
Q

How can OSSC spread to bone in the edentulous px

A

via gaps in cortex

81
Q

How can OSSC spread to bone in the dentate patient

A

via PDL
be wary of mobile teeth with no explanation

82
Q

What is the significance of perineural spread

A
  • spread involving small nerves at advancing edge predicts nodal spread
  • hard to eradicate when reaches nerves
  • usually spreads via myelin sheath
83
Q

What are the two ways carcinoma can spread to lymphatics

A
  • permeation
  • embolism
84
Q

What is permeation

A
  • tumour grows in lymphatic vessels
85
Q

What is embolism

A
  • grows outside the node, breaks off, travels in the lymphatics and then grows again
86
Q

What is extracapsular spread

A

grows outside lymph and spreads to surrounding areas

87
Q

What is sentinal node biopsy

A

used in staging
often used for earlier stages
not used for everyone

88
Q

When do we see haematogenous spread

A
  • late feature
  • likely enters veins in neck
  • may metastases to other areas e.g neck and spine
89
Q

What are the OSCC subtypes

A
  • verrucous
  • basaloid
  • spindle
90
Q

What are the features of verrucous OSCC

A
  • better prognosis
  • outward growing
  • thick
  • slow invasion
  • metastasis rare
91
Q

What are the features of basaloid OSCC

A
  • assoc with HPV
  • looks like basal cells
92
Q

What is spindle OSCC

A
  • aggressive
  • looks like fibroblasts
  • poor prognosis, rare
93
Q

What is oral cancer defined by

A

international classification of disease for oncology
ICD-O

94
Q

What are the two main groups of oral cancer

A
  • oral cavity
  • oropharyngeal
95
Q

Describe the epidemiology of oral cavity cancer

A
  • more common than OPC
  • more common in males (ratio starting to become more equal)
96
Q

Describe the epidemiology for oropharyngeal cancer

A
  • more common in males
  • increasing younger cases - hpv link
  • hpv type 16 most commonly implicated
97
Q

Why is the gender ratio for oral cancer equalising

A
  • tobacco use in men decreasing
  • tobacco use in women increasing
98
Q

What are the common high risk sites for oral cancer

A
  • fom
  • lateral border of tongue
  • retromolar region
  • soft/hard palate
  • gingiva
  • buccal mucosa
99
Q

What sites are oropharyngeal cancer

A
  • base of tongue (post 2/3)
  • tonsils
  • soft palate
  • side and back walls of throat
100
Q

What sites are oral cavity cancer

A
  • lips
  • gingiva
  • anterior 2/3 of tongue
  • buccal mucosa
  • FOM
  • hard palate
101
Q

What are the definite risk factors for oral cancer

A
  • smoking
  • alcohol
  • smoking & alcohol (synergistic effect)
  • betel quid
  • socioeconomic status
102
Q

Describe the impact of smoking (without alcohol) on oral cancer risk

A
  • 2 x risk
  • increases with quantity, frequency and DURATION
  • smoker risk generally greater for larynx cancer
103
Q

What is the impact of drinking (without smoking) on oral cancer risk

A
  • 2x the risk
  • 3-4 drinks a day
  • frequency most important
  • risk for OCC and OPC
104
Q

What is the impact of smoking and drinking on oral cancer risk

A
  • 5x risk
  • synergistic effect
  • frequency and duration increases risk
  • no safe lower limit
105
Q

What is the impact of betel quid on oral cancer risk

A

3x risk
mixture of substances including areca nut mixed with or without tobacco, wrapped in betel leaf and placed in mouth

106
Q

What is the impact of socioeconomic status on oral cancer risk

A

*2x risk
even without other risk factors, risk still increased
* likely due to stressful circumstances
* can be assessed using SIMD or DEPCAT

107
Q

What are uncertain risk factors

A
  • family history
  • oral health
  • sexual activity
108
Q

What is the criteria for sexual activity that increases oral cancer risk

A

> 6 sex partners
4 oral sex partners
<18 YO on first sexual encounter
most likely linked to HPV

109
Q

When do the benefits of quitting smoking emerge

A

1-4 years of quitting
risk reduced close to baseline after 20 years

110
Q

When do the benefits of alcohol quitting emerge

A

takes longer for risks to reduce post quitting
benefits can take up to 20 years to emerge

111
Q

What is the benefit of a good diet on oral cancer risk

A
  • obesity not linked
  • high intake of fresh fruit and veg reduces risk by 50%
112
Q

On what type of mucosa do most oral carcinoma arise in (UK)

A

normal

113
Q

On what type of mucosa do most oral carcinoma arise in (high incidence areas e.g India)

A

potentially malignant lesions

114
Q

What is leukoplakia

A
  • white patch
  • cant be rubbed off
  • no other attributable disease
115
Q

What is the risk of malignant change in leukoplakia

A

<4%

116
Q

What is candidal leukoplakia

A
  • aka chronic hyperplastic candidosis
  • c albicans can cause or colonize other keratoses and is likely to form speckled leukoplakia at the commissures
  • higher risk of malignant transformation
117
Q

What is hairy leukoplakia

A
  • caused by EBV
  • usually has a corrogated surface
  • affects margin of the tongue
  • seen in immunocompromsied and HIV px
  • tends to be benign and self limiting
118
Q

When is biopsy strongly indicated for leukoplakia

A
  • current / previous HN cancer
  • non-homogenous e.g verrucous
  • high risk site e.g FOM or tongue
  • symptomatic
  • no obvious aetiology
119
Q

What is erythroplakia

A
  • less common
  • red lesion - unexplained
  • much higher risk of dysplasia and cancer
  • up to 50% already carcinoma
  • be suspicious of these lesion
120
Q

What are the histological prognostic factors

A
  • pattern of invasion
  • depth of invasion
  • perineural invasion
  • invasion of vessels
121
Q

How does pattern of invasion impact prognosis

A
  • bulbous rete pegs infiltrating at same level (cohesive) = better prognosis
  • widely infiltrating small islands (non-cohesive) = worse prognosis
122
Q

How does depth of invasion impact prognosis

A
  • risk of metastases 4x greater
  • greater if >4mm
123
Q

How does perineural invasion infact prognosis

A
  • seen in 60% OSCC
  • most significant when at large nerve distant from main tumour mass
124
Q

What is the impact of invasion on prognosis

A

widely thought to be associated with lymph node metastases
poor prognosis

125
Q

How is the cancer staged

A

TNM
tumour
node involvement
metastases
staged 1-4

126
Q

What is the treatment options for HN cancer

A
  • surgery
  • chemotherapy
  • radiotherapy
  • immunotherapy
  • may be combined
127
Q

What is the ideal tx of choice

A
  • surgical resection
  • may not be possible
128
Q

Why may surgical resection not be possible

A
  • depends on margins
  • size and site of tumour
  • prognosis, px health, nutritional status
129
Q

What is the aetiology of lip cancer

A
  • sunlight UVB
  • smoking
130
Q

What is the behaviour of lip SCC

A
  • slow growth
  • local invasion
  • rarely metastasise to nodes
  • good prognosis as usually detected early
131
Q

What do we consider when thinking of screening methods

A
  • benefit vs harm
  • undetected lesion vs false positive
  • cost of screening vs cost of disease
  • cost of screening vs disability of disease
132
Q

What are the different oral cancer screening methods

A
  • hpv16 screening
  • toluidine blue
  • VELscope
  • clinical screening by GDP
133
Q

What is toluidine blue

A
  • stains markers in cells
  • false positive: highlights area of trauma and inflammation
134
Q

What is VELscope

A

uses autofluorescene with blue light
theoretically, loss of fluorscence equates to change

135
Q

What does clinical screening by GDP consist of

A
  • soft tissue exam
  • risk factor reduction
136
Q

When should we refer

A
  • potentially malignant lesions with no concerning features can be managed in primary care by monitoring with photos and risk reduction
  • if lesions worsens or is concerning then refer via cancer pathway
  • should be seen within 2 weeks of referral and tx should commence within 62 days
137
Q

What guidelines do we follow for oral cancer

A

scottish referral guidelines for suspected cancer

138
Q

What are the guidelines for suspected cancer referral in scottish referral guidelines

A

refer
* persistent unexplained head and neck lumps for >3 wks
* unexplained ulceration or unexplained swelling/induration of oral mucosa persisting >3 weeks
* all unexplained red/mixed red and white patches of the oral mucosa persisting for > 3 wks
* persistent (not intermittent) hoarseness lasting >3 weeks - if other symptoms are present, suspicion of lung cancer
* persistent pain in throat or pain on swallowing lasting for >3 weeks

BDS4 Oral Medicine (17 decks)

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