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Oral medicine > key points OPMDs > Flashcards

key points OPMDs Flashcards

1
Q

OPMD definition

A

morphological alterations with an increased potential for malignant transformation
indicate a risk of likely future malignancies elsewhere in (clinically normal appearing) mucosa

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2
Q

what are OPMDs generally higher in?

A

Asians and males

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3
Q

major risk factors

A

tobacco (smoked and smokeless)
excessive alcohol consumption
chewing betel quid containing areca nut
HPV role still unclear

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4
Q

clinical features associated with an increased risk of malignant progression

A 
size >200mm2
texture non-homogeneous
red/speckled
tongue and FOM
F
>50yrs
non-smoker
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5
Q

histologic features associated with an increased risk of malignant progression

A

severe dysplasia
HPV16+
DNA aneuploidy
many genes involved

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6
Q

progression from dysplasia to cancer over what time frame

A

usually 2.5 - 8yrs (av 5yrs)

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7
Q

primary prevention

A

eliminate modifiable risk factors

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8
Q

secondary prevention

A

oral screening and periodic follow up

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9
Q

diagnostic tools

A 
COE
histopathology
adjunctive diagnostic tools
 - vital staining
 - light-based detection systems
 - optical diagnostic technologies
 - salivary biomarkers
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10
Q

describe LP

A

chronic, inflammatory, mucocutaneous immuno-mediated disorder of unknown aetiology

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11
Q

LP etiopathogenesis

A

unidentified trigger initiates cell/tissue damage and immune response
immune reaction to an unknown antigenic stimulus in the epithelium
T4 hypersensitivity (delayed type) = T cell mediated immune reaction
- early T4 helper, late T8 cytotoxic cells

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12
Q

LP potential triggers

A 
viral infections
bacterial products
food allergens
mechanical trauma
systemic drugs
locally delivered drugs
contact sensitivity
dysplasia
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13
Q

LP epidemiology

A

1-2% pop
mostly middle-aged adults
- slight F predominance
- no apparent racial predilection

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14
Q

LP oral sites involved

A

any
common - buccal mucosa bilaterally, borders and dorsum of tongue, gingiva
rarer - palate (hard/soft), lips, FOM

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15
Q

LP EO manifestations

A

genital lesions - 20% of those with oral

cutaneous lesions - rosy, papular, scaly, itchy, regress and recur, flexor surfaces - 15% of those with oral

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16
Q

which LP lesions tend to be most persistent and difficult to tx?

A

oral

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17
Q

clinical types of LP

A 
reticular
papular
plaque
atrophic
erosive (ulcerative)
bullous
desquamative gingivitis
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18
Q

3 conditions desquamative gingivitis is seen in

A

LP
pemphigus
pemphigoid

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19
Q

symptoms of LP

A

tends to be persistent
reticular/papular lesions rarely symptomatic
- only need tx if symptomatic
erythematous and erosive/ulcerative lesions usually result in varying discomfort/pain

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20
Q

T lymphocytes in LP

A

accumulate beneath epithelium of oral mucosa and increase rate of differentiation of SSE, resulting in hyperkeratosis and erythema +/- ulceration

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21
Q

LP - which clinical types have the highest malignant potential?

A

atrophic and ulcerative

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22
Q

LP histopathology

A

keratinised SSE (ortho/para)
atrophy or hyperplasia
“hugging band” of lymphocytes below epithelium
= epitheliotropism
apoptosis of basal cell layer
“liquefaction degeneration” in basal cell layer
saw tooth rete peg appearance
acantholysis
colloid bodies
well-defined zone of cellular infiltration confined to LP

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23
Q

LP clinical appearance

A

usually multiple and symmetrical
often white papules which gradually enlarge and coalesce to form reticular, annular or plaque pattern
Wickham’s striae: white lines radiating from the papules
reticular form - lacelike network of slightly raised grey white lines, often interspersed with papules or rings
sometimes erythema, atrophy, ulceration +/- erosions
- bullae rare

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24
Q

desquamative gingivitis

A

clinical - descriptive term
whole thickness of gingiva can be affected
most often LP - can be pemphigus or pemphigoid
SLS, flavour or preservatives

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25
Q

when should you biopsy LP?

A

smoker
symptomatic
erosive type

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26
Q

LP tx

A 
CS - topical/systemic
retinoids - topical/systemic
vit A
homeopathic/herbal
immunosuppressive agents
 - azathioprine
 - methotrexate
calcineurin inhibitors
 - cyclosporin
 - tacrolimus
biological agents
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27
Q

tx for desquamative gingivitis

A

change toothpaste (SLS free)
improve OH (plaque aggravates lesions)
topical steroids - MDI inhaler or gum shield filled with steroid
topical tacrolimus (immune modulation) rinse or cream
systemic immunosuppression rarely

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28
Q

erythroplakia definition

A

clinically descriptive term

a fiery red patch that cannot be characterised clinically or pathologically as any other definable disease

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29
Q

risk factors for erythroplakia

A

tobacco chewing
tobacco smoking
betel quid chewing
+/- tobacco and alcohol usage

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30
Q

erythroplakia epidemiology

A

much rarer than leukoplakia

varies 0.2-0.7%?

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31
Q

erythroplakia pathogenesis

A

unknown

indications that it may be related to lichenoid lesions, which would constitute precursors of erythroplakia

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32
Q

erythroplakia clinical features

A

usually asymptomatic
fiery red macule
sharply demarcated lesion situated at a slightly lower level than surrounding mucosa
smooth, uniform, homogenous colour
may have a velvety feel because of its soft consistency on palpation
rarely multiple/extensive
carries a v high risk of malignancy

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33
Q

histopathological predictors of malignancy

A

architectural changes - abnormal maturation and stratification
cytological abnormalities - cellular atypia

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34
Q

11 histological features of epithelial dysplasia

A 
increased and abnormal mitoses
basal cell hyperplasia
drop shaped rete pegs
altered basal cell polarity
increased area or vol nuclear:cytoplasmic ratio
nuclear hyperchromatism
enlarged nuclei
irregular epithelial stratification
pleomorphism
abnormal keratinisation
loss/reduction of intracellular adhesion
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35
Q

6 hallmarks of cancer

A 
evading apoptosis
self-sufficiency in growth signals
insensitivity to anti-growth signals
tissue invasion and metastasis
limitless replicative potential (immortality)
sustained angiogenesis
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36
Q

CHC clinical features

A

often buccal commissures/retrocommissural region
white rough patch, can’t be rubbed off, may be bits of red
stings on eating spicy food
well-demarcated, smooth, homogeneous, raised white plaque
can appear non-homogenous with a nodular or speckled aspect
rarely other oral sites - mainly tongue

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37
Q

chronic multifocal candidiasis

A 
tetrad
CHC
denture stomatitis
angular cheilitis
MRG and oval/circular erythematous lesion on palate corresponding (kissing lesion)
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38
Q

CHC risk/predisposing factors

A 
tobacco smoking and chewing
alcohol consumption
betel quid chewing
Fe deficiency
diabetes
immunocompromised
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39
Q

CHC management

A

biopsy
smoking cessation
fluconazole and follow up
surgical excision if persistent and dysplasia
tx of concomitant staph infection - topical mupirocin 2% cream

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40
Q

CHC clinical diagnosis

A

homogeneous/non-homogeneous leukokeratotic plaque-type lesions localised in the retrocommissural area, +/- involvement of the commissure (fissure) and pericommissural area

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41
Q

CHC histopathological diagnosis

A

hyperortho or hyperparakeratosis (usually without dysplasia in the homogeneous forms)
candidal hyphae invading epithelium
chronic inflammation in LP, polymorphonuclear leukocytes can form “microabscesses” associated with candidal hyphae

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42
Q

CHC malignant transformation

A

colonisation of the epithelium
ability to produce carcinogens and initiate carcinogenesis
ability to promote carcinogenesis in an initiated epithelium
ability to metabolise procarcinogens
ability to modify the microenv and induce chronic inflammation

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43
Q

actinic cheilitis - definition

A

chronic inflammatory process, affects mainly L lip, due to a chronic UV exposure

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44
Q

actinic cheilitis - significant and independent risk factors

A

age 60 or above
Fitzpatrick skin phototype 2
outdoor working for >25 years
prev history of non-melanoma skin cancer

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45
Q

actinic cheilitis - clinical features

A

dryness, scaliness, colour variation
can be associated with atrophy, swelling, erythema, ulceration and diminished demarcation of vermillion border
vertical folds of lip can become more pronounced
grey-white discolouration
fissures

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46
Q

actinic cheilitis - tx

A

biopsy
surgical tx 1st line
laser therapy appears best option among non-surgical approaches
heterogeneous, photodynamic therapy and imiquimod application are promising
no evidence of effective tx in preventing malignant transformations

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47
Q

actinic cheilitis - clinical diagnosis

A

painless thickening and whitish discolouration at borders of lips, may gradually become scaly and indurated

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48
Q

actinic cheilitis - histopathological diagnosis

A 
epithelial atrophy
hyperkeratosis
solar elastosis
 - loss of eosin staining, accumulation of thick irregular elastic fibres and tangled fibrillin
 - elastin replaces collagen
perivascular inflammation
\+/- dysplasia
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49
Q

actinic cheilitis - why is biopsy mandatory?

A

some are found to be severe dysplasia or OSCC on 1st biopsy

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50
Q

actinic cheilitis - prevention

A

sunscreen and UV protective clothing
wide-brimmed hats
lip balm containing UVA and B
sunscreen/zinc

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51
Q

proposed classification of cheilitis categories

A

mostly reversible
mostly persistent
in association with dermatoses and systemic diseases (common conditions)

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52
Q

modified WHO criteria for OLP and OLL - clinical

A

bilateral, more or less symmetrical lesions
reticular pattern: lace-like network of slightly raised grey-white lines
erosive, atrophic, bullous and plaque-type lesions only accepted as a subtype in the presence of reticular lesions elsewhere in the oral mucosa

= in all other lesions that resemble OLP but don’t complete above criteria, use term ‘clinically compatible with’

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53
Q

modified WHO criteria for OLP and OLL - histopathological

A

well-defined band-like zone of cellular infiltration confined to superficial part of CT (LP), consisting mainly of lymphocytes
‘liquefaction degeneration’ in basal layer
absence of epithelial dysplasia
= when histopathological features are less obvious, use term ‘histopathologically compatible with’

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54
Q

modified WHO criteria for OLP and OLL - final diagnosis

A

OLP - fulfilment of both clinical and histopathologic criteria
OLL - clinically/histopathologically ‘compatible’ with either or both

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55
Q

LP proposed criteria - clinical

A 
multifocal symmetric distribution
white and red lesions exhibiting 1 or more of the following forms:
 - reticular/papular
 - atrophic (erythematous)
 - erosive (ulcerative)
 - plaque
 - bullous
lesions not localised exclusively:
 - to the sites of smokeless tobacco placement
 - adjacent to and in contact with Rxs
lesion onset does not correlate with the:
 - start of a medication
 - use of cinnamon containing products
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56
Q

LP proposed criteria - histopathological

A

band-like or patchy, predominantly lymphocytic infiltrate in the LP confined to the epithelium-LP interface
basal cell liquefactive (hydropic) degeneration
lymphocytic exocytosis
absence of epithelial dysplasia
absence of verrucous epithelial architectural change

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57
Q

leukoplakia - definition

A

clinical term to describe a white plaque (that can’t be rubbed off) of questionable risk having excluded (other) known diseases/disorders that carry no increased risk of cancer
- doesn’t indicate what kind of white plaque lesion

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58
Q

leukoplakia - clinical parameters

A 
site
size
homogeneity
multifocality
duration > or < 5yrs
dysplasia
smoking habit
drinking habit
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59
Q

leukoplakia - predictive risk factors for malignant transformation - pt characteristics

A 
F
non-smoker
>60yrs
drinker
chronic alcohol MW use
history of H and N cancer
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60
Q

leukoplakia - predictive risk factors for malignant transformation - lesion characteristics

A 
dysplasia
<5yrs since diagnosis
lat tongue, FOM, RM trigone/SP
>200mm2
multifocal
non-homogeneous
infection with c albicans
DNA aneuploidy
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61
Q

leukoplakia - clinical types (surface colour and morphology)

A

homogeneous
- uniform colour, flat, thin, with/without a slightly corrugated surface
non-homogeneous
- speckled: white plaque mixed in w red areas
- nodular: small polypoid outgrowth, white or red
- verrucous: white plaque with a warty surface
- mixed lesions: red and white plaque

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62
Q

leukoplakia - differential diagnosis

A 
white sponge naevus
frictional keratosis
morsicatio buccarum
chemical injury
acute pseudomembranous candidosis
leukoedema
LP (plaque type)
lichenoid reaction
discoid lupus erythematosus
skin graft
hairy leukoplakia
leukokeratosis nicotina palate
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63
Q

leukoplakia - initial mandatory management

A

biopsy
make definitive diagnosis when any aetiological cause other than tobacco/areca nut use has been excluded and histopathology has not confirmed any other specific disorder

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64
Q

leukoplakia - results of biopsy

A

most histologically benign
- usually hyperkeratosis or chronic inflammation
up to 20% may show changes - dysplasia/carcinoma
- high risk sites tongue and FOM

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65
Q

KUS

A

a histopathological term: just indicates hyperkeratosis with minimal/no atypia i.e. hyperkeratosis without epithelial dysplasia

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66
Q

what may KUS transform into?

A

OSCC

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67
Q

KUS histological features

A

can have parakeratosis, epithelial atrophy/acanthosis +/- inflammation
histologically different from frictional and reactive keratoses

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68
Q

KUS aetiology

A

unclear
don’t appear to be reactive
not obviously dysplastic
unclear what the biologic behaviour of these lesions is

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69
Q

KUS location

A

many occur at sites that are high risk for epithelial dysplasia and OSCC - tongue, FOM, SP

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70
Q

why might KUS be a more appropriate term than “benign hyperkeratosis”?

A

significance is unknown

some may be reactive and some may progress to dysplasia and OSCC

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71
Q

non-reactive keratoses (true leukoplakia)

A

KUS
dysplasia
cancer OSCC

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72
Q

PVL features

A

disease of unknown origin
clinically often begins as single white lesion, over time tends to become multifocal
grows slowly and progressively, harder to control
elderly women
high recurrence rate after tx
v high rate of malignant change
all sites in oral cavity can be affected, doesn’t show any preference for specific oral subsites

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73
Q

PVL modified diagnostic criteria

A

1 - leukoplakia showing verrucous/wartlike areas, involving >2 oral subsites
2 - add all involved sites ≥3cm
3 - disease evolution at least 5yrs, spreading and enlarging and ≥1 recurrences in a prev treated area
4 - at least 1 biopsy to rule out verrucous carcinoma/SCC

= all 4 criteria should be met

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74
Q

PVL tx

A

surgical resection

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75
Q

PVL major criteria

A

A - leukoplakia lesion with >2 oral sites
- most freq gingiva, alveolar process and palate
B - verrucous area
C - spread/engrossed during disease development
D - recurrence in a prev txed area
E - histopathology
- from simple epithelial hyperkeratosis to verrucous hyperplasia, verrucous carcinoma or oral SCC (in situ/infiltrating)

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76
Q

PVL minor criteria

A

A - ≥3cm when adding all affected areas
B - F
C - pt (M/F) non-smoker
D - disease evolution >5yrs

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77
Q

PVL final diagnosis

A

3 major criteria (inc E)

2 major criteria (inc E) and 2 minor criteria

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78
Q

proliferative leukoplakia

A

NOT a form of non-homogeneous leukoplakia

may be a more appropriate term than PVL because 18% are fissured and 22% erythematous

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79
Q

proliferative erythroleukoplakia PEL

A

better describes PL with prominent erythema

has highest malignant transformation rate similar to erythroleukoplakia

80
Q

clinical diagnostic criteria PL

A

white/keratotic lesions - smooth/fissured/verrucous/erythematous +/- ulcer
multifocal non-contiguous lesions or one lesion >4cm involving one site, or one lesion >3cm involving contiguous sites
expand in size/develop multifocality over time

81
Q

histopathology diagnostic criteria PL

A

if doesn’t show dysplasia/carcinoma shows hyperkeratosis, parakeratosis, atrophy or acanthosis with min to no cytologic atypia (KUS)
+/- lymphocytic band or verrucous hyperplasia
these features must not support a diagnosis of frictional or reactive keratosis

82
Q

leukoplakia management

A

photos every visit - submit to pathologist with biopsy
follow-up every 3-6m
- depends on histopathological diagnosis
periodic biopsies esp when change in character of lesion
biopsies that show only KUS can be followed only
- tx gingival leukoplakias on a case-by-case basis as many other factors impact tx - age, health, degree of involvement, bone loss, tooth mobility, appearance/behaviour of lesion

83
Q

leukoplakia result of biopsy - mild/mod dysplasia

A

can likely be observed if it is felt that complete removal not possible due to extent/location of lesion
if area discrete excision can be attempted

84
Q

leukoplakia result of biopsy - severe dysplasia/CIS

A

excise esp if discrete with the understanding that the margin will likely show KUS or mild/mod dysplasia

85
Q

what should pathology reports for excisional biopsies always report on?

A

margins, eben if they show KUS

86
Q

tx of leukoplakia to prevent cancer

A 
surgical interventions
non-surgical
 - vit A/retinoids
 - beta carotene or carotenoids
 - NSIADs (ketorolac and celecoxib)
 - herbal extracts
 - bleomycin
 - Bowman-Birk inhibitor

currently no evidence of a tx that is effective for preventing development of oral cancer

87
Q

classification of OLLs

A

oral lichenoid contact lesions (OLCLs)
oral lichenoid drug reactions (OLDRs)
OLLs in GvHD (OLL-GvHD)
OLL unclassified

88
Q

Van der Waals OLLs classification

A

amalgam Rx
drug-related
cGvHD
unclassified

89
Q

OLCLs - when is histological confirmation recommended?

A

in clinically atypical cases (exclude dysplasia/malignancy)

- but histopathology alone can’t reliably distinguish between OLP and OLCL

90
Q

OLCLs tx

A

may do skin patch testing - take readings at days 3,7,14 or even later to avoid missing delayed reactions

removal/replacement/coverage of Rxs that are in direct physical contact with mucosal lesions and are thought to be playing a causative role

91
Q

why can it be difficult to establish a diagnosis in OLDRs?

A

lack of specific features that distinguish it from OLP
may be hazardous to replace/withdraw drug
may take several months to see clinical change after withdrawing drug

92
Q

OLL-GvHD - when is histological confirmation indicated?

A

in absence of S+S of involvement of other systems/organs
when investigations of other sites provide only negative/non-specific results
cases of atypical clinical presentation to exclude dysplasia/malignancy

93
Q

OLL-GvHD tx

A

1st line - topical CS (+/- topical antimycotics) as an adjunct to systemic therapy or for isolated lesions
2nd line tx - topical calcineurin inhibitors as an adjunct to systemic therapy or for isolated lesions
PUVA not recommended - oncogenic potential

94
Q

potential histologic difference between LP and LTR

A

perivascular cuffing/infiltrate in LTR - inflammatory cells round blood vessels
indicates delayed hypersensitivity reaction

95
Q

OSF definition

A

debilitating, progressive, irreversible, collagen metabolic disorder induced by the chronic chewing of areca nut and its commercial preparations, affecting the oral mucosa and occasionally the pharynx and oesophagus, leading to mucosal stiffness and fct morbidity, has a potential risk of malignant transformation

96
Q

OSF epidemiology

A

about 10-20% world pop chew betel quid
about 600m areca nut chewers globally
recently noticed in children and adolescents
- similar clinical presentation to adults: burning sensation and blanching of buccal mucosa

97
Q

OSF pathogenesis

A

chewing betel quid is main cause of OSF
betel quid interferes with collagen metabolism
- increases collagen synthesis
- reduces collagen clearance
the thick fibres injure the oral mucosa
- causes inflammation of epidermal cells and activates macrophages to secrete cytokines
changes in cytokines and GFs cause fibroblast proliferation and collagen synthesis near the site of injury - fibrosis

98
Q

OSF S+S

A

mucosal blanching
stiffness
fibrous bands with a gradual inability to open the mouth
shrunken and everted uvula
depapillated tongue
fibrosis of palate with subsequent nasal intonation

99
Q

OSF prodromal symptoms

A

*burning sensation in mouth on eating spicy food
*ulceration/recurrent stomatitis
excessive salivation
defective gustatory sensation
occ dryness with painful vesicles

100
Q

OSF late S+S

A

fibrosis of laryngopharynx, oesophagus, Eustachian tubes, dysphagia and even hearing impairment

101
Q

OSF malignant transformation to OSCC

A 
OSF pathogenesis is quite varied which makes its transformation to malignancy open to many varied mechanisms
areca nut as a potent carcinogen
 - arecoline, major alkaloid of areca nut, with its cytotoxic and genotoxic properties mediates carcinogenesis by many pathways
hypoxia
cell cycle alterations
angiogenesis
sensecence
alterations in oncosuppressor genes

= early diagnosis and tx only best possible way to control progression towards malignancy

102
Q

OSF Grade 1 clinical

A

involves <1/3 oral cavity

mild blanching, burning sensation, recurrent ulceration and stomatitis, dryness

103
Q

OSF Grade 1 fct

A

mouth opening up to 35mm

104
Q

OSF Grade 1 histopathological

A

stage of inflammation

105
Q

OSF Grade 1 tx

A

habit cessation
nutritional supplement
antioxidants
topical steroid ointment

excellent prognosis

106
Q

OSF Grade 2 clinical

A

1/3-2/3 involved

blanching with mottled and marble-like appearance, fibrotic bands palpable and involvement of SP and premolar area

107
Q

OSF Grade 2 fct

A

mouth opening 25-35mm

cheek flexibility reduced by 33%

108
Q

OSF Grade 2 histopathological

A

stage of hyalinisation

109
Q

OSF Grade 2 tx

A 
habit cessation
nutritional supplement
intralesional injection of placental extracts
hyaluronidase
steroid therapy
physio

prognosis good, recurrence rate low

110
Q

OSF Grade 3 clinical

A

> 2/3 of oral cavity
severe blanching
broad thick fibrous palpable bands at cheeks, lips and rigid mucosa
depapillated tongue and restricted tongue movement
shrunken bud like uvula
FOM involvement and lymphadenopathy

111
Q

OSF Grade 3 fct

A

mouth opening 15-25mm

cheek flexibility reduced by 66%

112
Q

OSF Grade 3 histopathological

A

stage of fibrosis

113
Q

OSF Grade 3 tx

A

surgical

prognosis fair, recurrence rate high

114
Q

OSF Grade 4 clinical

A

leukoplakia changes, erythroplakia

ulcerating and suspicious malignant lesion

115
Q

OSF Grade 4 fct

A

mouth opening <15mm or nil

116
Q

OSF Grade 4 histopathological

A

stages of malignant transformation: erythroplakia changes into SCC

117
Q

OSF Grade 4 tx

A

surgical and biopsy of suspicious lesion

prognosis poor, malignant transformation

118
Q

OSF tx

A

depends on degree of clinical involvement
early stage - habit cessation sufficient
medical tx is symptomatic and predominantly aimed at improving mouth movements
- steroids
- enzymes
- drugs
- nutritional interventions
advanced stage - surgical tx - where restricted mouth opening due to heavy fibrous bands in buccal mucosa

no reliable evidence for effectiveness of any interventions

119
Q

GvHD definition

A

post-allogenic transplant
develops when non-identical donor immune cells recognise the recipient tissue antigens (the host) as foreign, and the donated cells/bone marrow attack the body

120
Q

GvHD risk factors

A 
genetic factors
older donor and recipient age
multiparous F donor
advanced malignant condition at transplantation
donor type
donor haematopoietic cell source
121
Q

aGvHD pathogenesis

A

activation of APCs
donor T cell activation, proliferation, differentiation and migration
target tissue destruction

122
Q

2 forms of GvHD

A

acute or chronic
can get 1 form, both forms or neither
historically - time post-transplant (< or > 100 days)
now clinical manifestations guide whether the S+S of GvHD are acute or chronic

123
Q

major organs affected by aGvHD

A

skin (erythema)
GI (secretory)
liver

124
Q

aGvHD - 1st episode

A

classic acute

125
Q

aGvHD - subsequent episode

A

recurrent
persistent
new onset or late acute

126
Q

major organs affected by cGvHD

A 
skin (lichenoid, sclerotic)
mouth
nails and hair - loss
eyes - dry
lung - restrictive/obstructive
MS - myositis
haematopoietic - anaemia, neutropenia
GI (oesophageal) - strictures
liver - jaundice
other
127
Q

cGvHD with no sign of acute

A

classic chronic

128
Q

cGvHD with signs of acute

A

overlap syndrome
where there are mixed features of both acute and chronic
associated with adverse prognosis and increased disease burden

129
Q

acute GvHD skin

A

maculopapular skin rash

- most freq affected and usually first organ

130
Q

aGvHD GIT

A

nausea, diarrhoea, abdo pain

131
Q

aGvHD liver

A

cholestatic hyperbilirubinaemia

132
Q

aGvHD oral cavity

A

diffuse ulcerative and erythematous lesions +/- lip crusting

133
Q

aGvHD grading

A

1 mild
2 mod
3 severe
4 v severe

134
Q

chronic GvHD

A

by definition after day 100 but usually 3-18m post-BMT
major cause of late non-relapse death following allogenic BMT
no effective prophylaxis regimen

135
Q

cGvHD risk factors

A

prior acute GvHD
older recipient age
F donor (multiparous in particular) with a M recipient
use of peripheral blood SCs

136
Q

oral complications of cGvHD

A

OSCC
rampant caries
fibrosis

137
Q

oral manifestations (main ones) of cGvHD

A 
oral mucosal cGvHD
 - lichen type features
 - hyperkeratotic plaques
salivary gland cGvHD
sclerotic cGvHD
138
Q

NIH oral cGvHD clinical scoring

A

score mucosal changes: erythema, lichenoid, ulcers

- no evidence, mild, mod, severe

139
Q

GvHD tx

A 
oral mucosal
 - steroid solutions
 - lips - tacrolimus ointment
salivary gland
 - xerostomia - stimulants, moisturising agents
 - caries - OH, F, diet
 - candidiasis - fluconazole
sclerotic
 - physical therapy
 - intralesional steroid therapy
 - surgery to disrupt mucosal bands
140
Q

GvHD - oral cavity may be only clinical site affected in a subset of pts

A

initial activation of APCs may occur via a respiratory infection or other inflammatory insult to oral cavity

once APCs activate CD4 and CD8 T cells, they initiate a strong cytokine response and migrate into oral mucosa, causing tissue damage and a reactive hyperkeratosis

once cellular mediators (T cells, activated macrophages and NK cells) have chemotaxed into target tissues, their production of chemokine and cytokine mediators acts synergistically to enhance target tissue destruction - oral ulcerations

141
Q

potentially malignant lesion

A

altered tissue in which cancer is more likely to form

142
Q

potentially malignant condition

A

generalised state with increased cancer risk

143
Q

why should the term “potentially malignant disorder” be used rather than premalignant/precancerous/preneoplastic?

A

malignant change won’t definitely happen

144
Q

molecular markers in oral epithelial dysplasia

A 
signalling pathways EGFR
cell cycle Ki67, p53, pRB
immortalisation telomerase
apoptosis p53, 21
angiogenesis VEGF
COX 1 and 2 enzymes
proliferation and differentiation markers
viruses - HPV
loss of heterozygosity 3p 9p 13q (retinoblastoma) 17p

no markers, whether single or in combination, have been identified to help determine progression

145
Q

where do most oral carcinomas arise in the UK vs high incidence areas e.g. India?

A

UK - most in clinically normal mucosa

high incidence areas - from potentially malignant lesions

146
Q

how much more likely is leukoplakia to progress to cancer than clinically normal mucosa?

A

50-100x

- but not every leukoplakia will progress into cancer

147
Q

leukoplakia clinical predictors of malignancy

A

age and gender
idiopathic (non-smoker, low alcohol)
site - buccal mucosa low risk, FOM and tongue high risk
clinical appearance - non-homogeneous - verrucous, ulcerated leukoerythroplakia

148
Q

leukoplakia histopathological indicators of malignant change - gold standard

A

dysplasia
atrophy (esp if red lesion)
candida infection

149
Q

biological marker - why could the DNA content in leukoplakia be a potential future prognostic indicator?

A

DNA content in nuclei of dysplastic epithelial cells is higher than in normal epithelial cells

150
Q

dysplasia

A

disordered/abnormal maturation (growth) in a tissue

- has to show this to be considered potentially malignany

151
Q

atypia

A

changes in cells

- fct, appearance, arrangement to other cells

152
Q

criteria for diagnosis of dysplasia

A

assess architectural changes then cytology
boundaries between categories not well defined

architectural changes

  • abnormal maturation and stratification
  • how many layers
  • rete pegs

cytological abnormalities
- cellular atypia

153
Q

grading of epithelial dysplasia - WHO 2005

A 
hyperplastic
mild
mod
severe
carcinoma in situ
154
Q

hyperplastic (basal hyperplasia)

A 
increased basal cell numbers
rest of epithelium normal
architecture
 - regular stratification
 - basal compartment larger
no cellular atypia
155
Q

mild dysplasia

A

architecture: changes in lower 1/3
cytology: mild atypia (few cells)
- pleomorphism
- hyperchromatism
- foci of slight irregularity in the stratification of the epithelium as it matures towards surface
- occ superficial mitoses
- basal cells hyperplasia, crowding - slight dip to accommodate increase
- not high numbers of cells abnormal

most cases will regress esp if can identify a causative factor and address it e.g. smoking often a reactive change

156
Q

hyperchromatism

A

increased DNA in nuclei so they take up more stain

157
Q

mod dysplasia

A

changes extend into middle 1/3
cytology - mod atypia
- pleomorphism
- hyperchromatism

158
Q

severe dysplasia

A

architecture - changes extend to upper 1/3
cytology - severe atypia and numerous mitoses, abnormally high
- loss of polarity
- hyperchromatism
- pleomorphism
- most cells involved
- severe immune inflammatory reaction against changed epithelial cells/ulcer - change in antigenicity
- mitoses should only occur in basal cell layer, not high up in epithelium
high risk of malignant change

keratinised - clinically leukoplakia
areas where epithelium thin - erythroplakia
ulceration
= non-homogeneous

159
Q

carcinogenesis components

A

genetic

env (carcinogens)

160
Q

CIS

A

theoretic concept
malignant but not invasive
abnormal architecture
- full thickness (or almost full) of viable cell layers
- large rete pegs
pronounced cytological atypia
- mitotic abnormalities frequent
still located in epithelium - why not invasive SCC
inflammation in LP
- immune response larger in more severe dysplasia
- due to genetic changes happening in epithelial cells

161
Q

molecular basis of cancer

A

damage

altered gene expression - affects formation of protein (increased/silenced)

altered cell fct

162
Q

changes to genes may inc:

A

changes to chromosomes
- aneuploidy - abnormal number of chromosomes
- translocations - a part breaks off and may attach to another
- amplifications
genes
- mutations
- deletions
- amplifications
epigenetic changes
- chemical changes in DNA, such as methylation and modification of the histones that package DNA
- DNA itself isn’t changing but makes it more likely to be/not be silenced

163
Q

oral cancer genes involved

A 
oncogenes
TSGs
Tp53
genes that regulate apoptosis
genes involved in DNA repair
miRNA - micro RNA
viral component HPV16 and 18
164
Q

oncogenes

A

have normal roles within the cells, produce GFs, differing oncogenes activated

165
Q

TSGs

A

suppress the growth of cells

166
Q

Tp53 (a TSG)

A

checks cells - sends irreparable cells for apoptosis to prevent mutations being passed on
a TSG and an apoptosis gene
mutation or inactivation

167
Q

miRNA - microRNA

A

strands of non-coding RNA - don’t produce proteins

some can act as oncogenes/TSGs - can play a part in neoplastic transformation

168
Q

viral component - HPV16 and 18 (oncogenic types)

A

oropharyngeal and cervical

produce proteins which deactivate proteins produced by TSGs e.g. p53

169
Q

Knudson’s 2 hit hypothesis of carcinogenesis

A

TSGs - both alleles need to be inactivated before malignancy

170
Q

field change theory (field cancerisation)

A

all of area may be susceptible to developing oral cancer
- if they have oral cancer the rest of the oral cavity is at risk
genetic instability increases possibility of developing cancer
clinically may appear normal
difficult to estimate extent of field
multiple primaries 15-20%
- inc larynx, pharynx and resp tract

171
Q

6 hallmarks of cancer

A 
evading apoptosis
self-sufficiency in growth signals
insensitivity to anti-growth signals
limitless replicative potential (immortality)
sustained angiogenesis
tissue invasion and metastasis
172
Q

process of carcinogenesis

A

“multistep” - initiation, promotion, progression
sum of genetic changes (not order/number) important
cancer cell interacts with its env - gets other cells to produce factors to help it grow and metastasise

173
Q

features predicting LN involvement

A

non-cohesive front
perineural infiltration
malignant cells in lymphatic vessels and bv’s

174
Q

oral cancer pathology report points

A

diagnosis: SCC 90%
differentiation and grading
pattern of invasive front
local extension of disease

175
Q

what is the pattern of invasive front related to?

A

nodal spread

176
Q

differentiation and grading

A

how well tissue resembles normal and how much of its fct it can perform

177
Q

well-differentiated

A

can tell they are epithelial cells and produce keratin

better response, less recurrence, better prognosis

178
Q

moderately differentiated

A

80% can tell epithelial cells but no keratin production

179
Q

poorly differentiated

A

hard to tell whether epithelial cells

need tests

180
Q

anaplastic differentiated

A

virtually impossible (related to metastatic tumours)

181
Q

pattern of invasive front

A

related to nodal spread
cohesive front
non-cohesive front

182
Q

cohesive front

A

all cells advancing together at same rate, like a wave

183
Q

non-cohesive front

A

strands/individual malignant cells breaking off from main front
associated with LN spread (micrometastasis)

184
Q

OSCC subtypes

A 
verrucous carcinoma
 - better prognosis, slow growing, rarely recurs
basaloid squamous
 - HPV association
 - aggressive
spindle cell
 - aggressive
185
Q

causes of pigmentation

A 
physiological/natural/racial
mucosal melanoma
smoking
post-surgical pigmentation
inflammatory e.g. LP
medications (prolonged CHX MW)
Addisons
186
Q

spread of oral cancer

A

local extension of disease
lymphatic spread
haematogenous spread

187
Q

local extension of disease

A 
varies according to site
mucosal extension
muscle (tongue etc)
bone
 - edentulous: gaps in cortex
 - dentate: via PDL
nerve
188
Q

lymphatic spread

A

*embolism - in lymphatics to get to LNs
permeation - tumour grows through lymphatic system
tumour involved node with EC spread

189
Q

sentinal node biopsy

A

see if cancer has spread to LNs
identify principal LNs by special techniques
- remove and study under microscope for micrometastasis
- if clear don’t need to remove chain, if not remove

190
Q

haematogenous spread

A

late feature (lymphatic first)
? enter veins in neck
- veins more susceptible as thinner walls
metastasis to lungs, spine etc

191
Q

metastatic cascade

A 
intravasation
survive in circulation
arrest in organ/tissue
extravasation
survive extravasation
initial proliferation
established growth
192
Q

oral cancer histopathology

A

invasion - cells beyond usual boundary into CT and even muscle (likely LN spread) - hard/induration
individual cells and nuclei vary size and shape
LN - epithelium cells present - 2 reasons - either due to metastatic tumour or developmental anomaly
LN appears as dark lymphoid tissue - organised pattern and peripheral CT capsule (FNAB)
immune reaction with every malignancy
- non-self cells
- malignant cells: influence other immune cells to produce things which help them

193
Q

palatal lesions in reverse smokers

A

white and/or red patches affecting the HP in reverse smokers

freq stained w nicotine

194
Q

OLE

A

AI CT disease
may affect lip and oral cavity
erythematous area surrounded by whitish striae, freq with a target configuration
often palate

195
Q

dyskeratosis congenita

A

rare cancer-prone inherited bone marrow failure syndrome caused by aberrant telomere biology

196
Q

dyskeratosis congenita diagnostic triad

A

dysplastic nails
lacy reticular skin pigmentation
oral leukoplakia

Oral medicine (14 decks)

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