key points OPMDs Flashcards
OPMD definition
morphological alterations with an increased potential for malignant transformation
indicate a risk of likely future malignancies elsewhere in (clinically normal appearing) mucosa
what are OPMDs generally higher in?
Asians and males
major risk factors
tobacco (smoked and smokeless)
excessive alcohol consumption
chewing betel quid containing areca nut
HPV role still unclear
clinical features associated with an increased risk of malignant progression
size >200mm2 texture non-homogeneous red/speckled tongue and FOM F >50yrs non-smoker
histologic features associated with an increased risk of malignant progression
severe dysplasia
HPV16+
DNA aneuploidy
many genes involved
progression from dysplasia to cancer over what time frame
usually 2.5 - 8yrs (av 5yrs)
primary prevention
eliminate modifiable risk factors
secondary prevention
oral screening and periodic follow up
diagnostic tools
COE histopathology adjunctive diagnostic tools - vital staining - light-based detection systems - optical diagnostic technologies - salivary biomarkers
describe LP
chronic, inflammatory, mucocutaneous immuno-mediated disorder of unknown aetiology
LP etiopathogenesis
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
LP potential triggers
viral infections bacterial products food allergens mechanical trauma systemic drugs locally delivered drugs contact sensitivity dysplasia
LP epidemiology
1-2% pop
mostly middle-aged adults
- slight F predominance
- no apparent racial predilection
LP oral sites involved
any
common - buccal mucosa bilaterally, borders and dorsum of tongue, gingiva
rarer - palate (hard/soft), lips, FOM
LP EO manifestations
genital lesions - 20% of those with oral
cutaneous lesions - rosy, papular, scaly, itchy, regress and recur, flexor surfaces - 15% of those with oral
which LP lesions tend to be most persistent and difficult to tx?
oral
clinical types of LP
reticular papular plaque atrophic erosive (ulcerative) bullous desquamative gingivitis
3 conditions desquamative gingivitis is seen in
LP
pemphigus
pemphigoid
symptoms of LP
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
T lymphocytes in LP
accumulate beneath epithelium of oral mucosa and increase rate of differentiation of SSE, resulting in hyperkeratosis and erythema +/- ulceration
LP - which clinical types have the highest malignant potential?
atrophic and ulcerative
LP histopathology
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
LP clinical appearance
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
desquamative gingivitis
clinical - descriptive term
whole thickness of gingiva can be affected
most often LP - can be pemphigus or pemphigoid
SLS, flavour or preservatives
when should you biopsy LP?
smoker
symptomatic
erosive type
LP tx
CS - topical/systemic retinoids - topical/systemic vit A homeopathic/herbal immunosuppressive agents - azathioprine - methotrexate calcineurin inhibitors - cyclosporin - tacrolimus biological agents
tx for desquamative gingivitis
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
erythroplakia definition
clinically descriptive term
a fiery red patch that cannot be characterised clinically or pathologically as any other definable disease
risk factors for erythroplakia
tobacco chewing
tobacco smoking
betel quid chewing
+/- tobacco and alcohol usage
erythroplakia epidemiology
much rarer than leukoplakia
varies 0.2-0.7%?
erythroplakia pathogenesis
unknown
indications that it may be related to lichenoid lesions, which would constitute precursors of erythroplakia
erythroplakia clinical features
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
histopathological predictors of malignancy
architectural changes - abnormal maturation and stratification
cytological abnormalities - cellular atypia
11 histological features of epithelial dysplasia
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
6 hallmarks of cancer
evading apoptosis self-sufficiency in growth signals insensitivity to anti-growth signals tissue invasion and metastasis limitless replicative potential (immortality) sustained angiogenesis
CHC clinical features
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
chronic multifocal candidiasis
tetrad CHC denture stomatitis angular cheilitis MRG and oval/circular erythematous lesion on palate corresponding (kissing lesion)
CHC risk/predisposing factors
tobacco smoking and chewing alcohol consumption betel quid chewing Fe deficiency diabetes immunocompromised
CHC management
biopsy
smoking cessation
fluconazole and follow up
surgical excision if persistent and dysplasia
tx of concomitant staph infection - topical mupirocin 2% cream
CHC clinical diagnosis
homogeneous/non-homogeneous leukokeratotic plaque-type lesions localised in the retrocommissural area, +/- involvement of the commissure (fissure) and pericommissural area
CHC histopathological diagnosis
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
CHC malignant transformation
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
actinic cheilitis - definition
chronic inflammatory process, affects mainly L lip, due to a chronic UV exposure
actinic cheilitis - significant and independent risk factors
age 60 or above
Fitzpatrick skin phototype 2
outdoor working for >25 years
prev history of non-melanoma skin cancer
actinic cheilitis - clinical features
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
actinic cheilitis - tx
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
actinic cheilitis - clinical diagnosis
painless thickening and whitish discolouration at borders of lips, may gradually become scaly and indurated
actinic cheilitis - histopathological diagnosis
epithelial atrophy hyperkeratosis solar elastosis - loss of eosin staining, accumulation of thick irregular elastic fibres and tangled fibrillin - elastin replaces collagen perivascular inflammation \+/- dysplasia
actinic cheilitis - why is biopsy mandatory?
some are found to be severe dysplasia or OSCC on 1st biopsy
actinic cheilitis - prevention
sunscreen and UV protective clothing
wide-brimmed hats
lip balm containing UVA and B
sunscreen/zinc
proposed classification of cheilitis categories
mostly reversible
mostly persistent
in association with dermatoses and systemic diseases (common conditions)
modified WHO criteria for OLP and OLL - clinical
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’
modified WHO criteria for OLP and OLL - histopathological
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’
modified WHO criteria for OLP and OLL - final diagnosis
OLP - fulfilment of both clinical and histopathologic criteria
OLL - clinically/histopathologically ‘compatible’ with either or both
LP proposed criteria - clinical
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
LP proposed criteria - histopathological
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
leukoplakia - definition
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
leukoplakia - clinical parameters
site size homogeneity multifocality duration > or < 5yrs dysplasia smoking habit drinking habit
leukoplakia - predictive risk factors for malignant transformation - pt characteristics
F non-smoker >60yrs drinker chronic alcohol MW use history of H and N cancer
leukoplakia - predictive risk factors for malignant transformation - lesion characteristics
dysplasia <5yrs since diagnosis lat tongue, FOM, RM trigone/SP >200mm2 multifocal non-homogeneous infection with c albicans DNA aneuploidy
leukoplakia - clinical types (surface colour and morphology)
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
leukoplakia - differential diagnosis
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
leukoplakia - initial mandatory management
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
leukoplakia - results of biopsy
most histologically benign
- usually hyperkeratosis or chronic inflammation
up to 20% may show changes - dysplasia/carcinoma
- high risk sites tongue and FOM
KUS
a histopathological term: just indicates hyperkeratosis with minimal/no atypia i.e. hyperkeratosis without epithelial dysplasia
what may KUS transform into?
OSCC
KUS histological features
can have parakeratosis, epithelial atrophy/acanthosis +/- inflammation
histologically different from frictional and reactive keratoses
KUS aetiology
unclear
don’t appear to be reactive
not obviously dysplastic
unclear what the biologic behaviour of these lesions is
KUS location
many occur at sites that are high risk for epithelial dysplasia and OSCC - tongue, FOM, SP
why might KUS be a more appropriate term than “benign hyperkeratosis”?
significance is unknown
some may be reactive and some may progress to dysplasia and OSCC
non-reactive keratoses (true leukoplakia)
KUS
dysplasia
cancer OSCC
PVL features
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
PVL modified diagnostic criteria
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
PVL tx
surgical resection
PVL major criteria
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)
PVL minor criteria
A - ≥3cm when adding all affected areas
B - F
C - pt (M/F) non-smoker
D - disease evolution >5yrs
PVL final diagnosis
3 major criteria (inc E)
2 major criteria (inc E) and 2 minor criteria
proliferative leukoplakia
NOT a form of non-homogeneous leukoplakia
may be a more appropriate term than PVL because 18% are fissured and 22% erythematous
