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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
What is atypia
* changes in the cell
26
What is the criteria of diagnosis for dysplasia based on
architechtural changes cytological abnormalities (cellular atypia)
27
What do the cytological abnormalities represent
* changes in individual cells reflecting abnormal dna content in the nucleus, failure to mature and keratinise correctly and increased proliferation
28
What are the different cytological abnormalities that may be seen
* 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
29
What does architectural changes represent
changes in organisation of maturation and normal layer of the epithelium
30
What are the different architechtural changes that may be seen
* 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
31
What is the WHO 2005 classification of dysplasia
* basal hyperplasia * mild dysplasia * moderate dysplasia * severe dysplasia
32
What are the architectural changes in basal hyperplasia
*increased number of basal cells in basal compartment * regular stratification * basal compartment is larger
33
What are the cytological abnormalities in basal hyperplasia
nil
34
Slide of basal hyperplasia
35
What are the architectural changes seen in mild dysplasia
* in lower third * basal cell hyperplasia
36
What is the cytological changes seen in mild dysplasia
* mild atypia * pleomorphism * hyperchromatism
37
What is pleomorphism
* nuclei and cells are different shapes and sizes
38
What is hyperchromatism
* increased dna content causes darker staining of nuclei
39
Mild dysplasia is often reactive, what does this mean
* caused by trauma, infection, smoking etc * removal of cause will most likely result in regression
40
Mild dysplasia slide
41
What are the architectural changes in moderate dysplasia
* extent into middle third * loss of intercellular adhesion * drop shaped rete pegs
42
What are the cytological changes in moderate dysplasia
moderate atypia pleomorphism hyperchromatism
43
Moderate dysplasia slide
44
What are the architectural changes in severe dysplasia
* extend into upper third
45
What are the cytological changes in severe dysplasia
* severe atypia * numerous mitoses- abnormally high * pleomorphism * hyperchromatism * loss of polarity
46
Severe dysplasia slide
47
What is carcinoma in situ
theoretic concept all layers of epithelium involved malignant but no invasion to underlying connective tissue not beyond the basement membrane
48
What are the architectural changes in carcinoma in situ
* full thickness of viable cell layers
49
What are the cytological changes in carcinoma in situ
* pronounced cytological atypia * mitotic abnormalities frequent
50
# What does malignancy trigger What would we expect to see in the underlying tissue in carcinoma in situ
immune response
51
Carcinoma in situ slide
52
Summarise the different histopathological features of epithelial dysplasia
* 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)
53
What 2 factors does carcinogenesis depend on
* genetic (changes) * carcinogens (environment)
54
How do genetics and environment come together to form malignancy
* damage causes mutation at genetic level * damage results in altered gene expression * results in inactivation or overexpression and this alters cell function
55
What are the stages of carcinogenesis
1. initiation 2. promotion 3. transformation 4. progression
56
What is intiation
mutation
57
What is promotion | stages of carcinogenesis
* 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
What is transformation
* further mutations are acquired * they cannot be repaired due to the damage to the dna repair system
59
What is progression
formation of malignant tumour
60
What are the changes to genes that can occur
* changes to chromosome e.g translocation * genes e.g mutation, deletion, amplification * epigenetic changes
61
What are proto-oncogenes
* normal genes * regulat cell division
62
What does mutation in proto-oncogenes result in
* oncogenes
63
What do oncogenes do
* produce oncoproteins * these encourage tumour growth by dysregulating cell growth, proliferation and division
64
What are tumour suppressor genes
* inhibit cell division and growth * act as anti-oncogenes * when these become mutated, there is nothing to prevent cell division
65
What is the safety net with tumour suppressor genes
* requires loss of both alleles to become insufficient * known as knudson's two hit hypothosis
66
What is an example of a tumour suppressor gene
TP53 produces p53
67
What are the genes that are important in malignancy
* oncogenes * tumour suppressor genes * genes that regulate apoptosis and are involved in dna repair * miRNA
68
What is miRNA
* noncoding part of mRNA * similar to onco/TS genes
69
What are the hallmarks of cancer
* self sufficiency in growth signals * insensitivity to antigrowth signals * tissue invasion and metastasis * limitless replicative potential * sustained angiogenesis * evading apoptosis
70
What is the field change theory
* 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
What is a synchronous tumour
within 6 months of primary
72
What is a metachronous tumour
* after 6 months of primary
73
What does a pathology report contain
* diagnosis * differentiation/grading * pattern of invasive front related to nodal spread
74
What are the different grades of differentiation
* well differentiated - best prognosis * moderately differentiated * poorly differentiated * anaplastic
75
What are the patterns of invasive fronts
cohesive non cohesive
76
What is cohesive
cells advancing at same rate better prognosis
77
What is non-cohesive
* advancing in strands * more implicated with lymph node involvement * worse prognosis
78
What is the common pattern of spread with OSSC
1. local extension of disease 2. lymphatic spread 3. haematogenous spread
79
What is local extension of disease
* mucosal extension * muscle * bone * nerve
80
How can OSSC spread to bone in the edentulous px
via gaps in cortex
81
How can OSSC spread to bone in the dentate patient
via PDL be wary of mobile teeth with no explanation
82
What is the significance of perineural spread
* spread involving small nerves at advancing edge predicts nodal spread * hard to eradicate when reaches nerves * usually spreads via myelin sheath
83
What are the two ways carcinoma can spread to lymphatics
* permeation * embolism
84
What is permeation
* tumour grows in lymphatic vessels
85
What is embolism
* grows outside the node, breaks off, travels in the lymphatics and then grows again
86
What is extracapsular spread
grows outside lymph and spreads to surrounding areas
87
What is sentinal node biopsy
used in staging often used for earlier stages not used for everyone
88
When do we see haematogenous spread
* late feature * likely enters veins in neck * may metastases to other areas e.g neck and spine
89
What are the OSCC subtypes
* verrucous * basaloid * spindle
90
What are the features of verrucous OSCC
* better prognosis * outward growing * thick * slow invasion * metastasis rare
91
What are the features of basaloid OSCC
* assoc with HPV * looks like basal cells
92
What is spindle OSCC
* aggressive * looks like fibroblasts * poor prognosis, rare
93
What is oral cancer defined by
international classification of disease for oncology ICD-O
94
What are the two main groups of oral cancer
* oral cavity * oropharyngeal
95
Describe the epidemiology of oral cavity cancer
* more common than OPC * more common in males (ratio starting to become more equal)
96
Describe the epidemiology for oropharyngeal cancer
* more common in males * increasing younger cases - hpv link * hpv type 16 most commonly implicated
97
Why is the gender ratio for oral cancer equalising
* tobacco use in men decreasing * tobacco use in women increasing
98
What are the common high risk sites for oral cancer
* fom * lateral border of tongue * retromolar region * soft/hard palate * gingiva * buccal mucosa
99
What sites are oropharyngeal cancer
* base of tongue (post 2/3) * tonsils * soft palate * side and back walls of throat
100
What sites are oral cavity cancer
* lips * gingiva * anterior 2/3 of tongue * buccal mucosa * FOM * hard palate
101
What are the definite risk factors for oral cancer
* smoking * alcohol * smoking & alcohol (synergistic effect) * betel quid * socioeconomic status
102
Describe the impact of smoking (without alcohol) on oral cancer risk
* 2 x risk * increases with quantity, frequency and **DURATION** * smoker risk generally greater for larynx cancer
103
What is the impact of drinking (without smoking) on oral cancer risk
* 2x the risk * 3-4 drinks a day * frequency most important * risk for OCC and OPC
104
What is the impact of smoking and drinking on oral cancer risk
* 5x risk * synergistic effect * frequency and duration increases risk * no safe lower limit
105
What is the impact of betel quid on oral cancer risk
3x risk mixture of substances including areca nut mixed with or without tobacco, wrapped in betel leaf and placed in mouth
106
What is the impact of socioeconomic status on oral cancer risk
*2x risk even without other risk factors, risk still increased * likely due to stressful circumstances * can be assessed using SIMD or DEPCAT
107
What are uncertain risk factors
* family history * oral health * sexual activity
108
What is the criteria for sexual activity that increases oral cancer risk
>6 sex partners >4 oral sex partners <18 YO on first sexual encounter most likely linked to HPV
109
When do the benefits of quitting smoking emerge
1-4 years of quitting risk reduced close to baseline after 20 years
110
When do the benefits of alcohol quitting emerge
takes longer for risks to reduce post quitting benefits can take up to 20 years to emerge
111
What is the benefit of a good diet on oral cancer risk
* obesity not linked * high intake of fresh fruit and veg reduces risk by 50%
112
On what type of mucosa do most oral carcinoma arise in (UK)
normal
113
On what type of mucosa do most oral carcinoma arise in (high incidence areas e.g India)
potentially malignant lesions
114
What is leukoplakia
* white patch * cant be rubbed off * no other attributable disease
115
What is the risk of malignant change in leukoplakia
<4%
116
What is candidal leukoplakia
* 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
What is hairy leukoplakia
* 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
When is biopsy strongly indicated for leukoplakia
* current / previous HN cancer * non-homogenous e.g verrucous * high risk site e.g FOM or tongue * symptomatic * no obvious aetiology
119
What is erythroplakia
* less common * red lesion - unexplained * much higher risk of dysplasia and cancer * up to 50% already carcinoma * be suspicious of these lesion
120
What are the histological prognostic factors
* pattern of invasion * depth of invasion * perineural invasion * invasion of vessels
121
How does pattern of invasion impact prognosis
* bulbous rete pegs infiltrating at same level (cohesive) = better prognosis * widely infiltrating small islands (non-cohesive) = worse prognosis
122
How does depth of invasion impact prognosis
* risk of metastases 4x greater * greater if >4mm
123
How does perineural invasion infact prognosis
* seen in 60% OSCC * most significant when at large nerve distant from main tumour mass
124
What is the impact of invasion on prognosis
widely thought to be associated with lymph node metastases poor prognosis
125
How is the cancer staged
TNM tumour node involvement metastases staged 1-4
126
What is the treatment options for HN cancer
* surgery * chemotherapy * radiotherapy * immunotherapy * may be combined
127
What is the ideal tx of choice
* surgical resection * may not be possible
128
Why may surgical resection not be possible
* depends on margins * size and site of tumour * prognosis, px health, nutritional status
129
What is the aetiology of lip cancer
* sunlight UVB * smoking
130
What is the behaviour of lip SCC
* slow growth * local invasion * rarely metastasise to nodes * good prognosis as usually detected early
131
What do we consider when thinking of screening methods
* benefit vs harm * undetected lesion vs false positive * cost of screening vs cost of disease * cost of screening vs disability of disease
132
What are the different oral cancer screening methods
* hpv16 screening * toluidine blue * VELscope * clinical screening by GDP
133
What is toluidine blue
* stains markers in cells * false positive: highlights area of trauma and inflammation
134
What is VELscope
uses autofluorescene with blue light theoretically, loss of fluorscence equates to change
135
What does clinical screening by GDP consist of
* soft tissue exam * risk factor reduction
136
When should we refer
* 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
What guidelines do we follow for oral cancer
scottish referral guidelines for suspected cancer
138
What are the guidelines for suspected cancer referral in scottish referral guidelines
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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