PMOL Flashcards
what is the most common malignant tumour to arise in the oral cavity?
squamous cell carcinoma
what are most OSCC not accompanied by?
recognised pre exciting mucosal lesions
> some mucosal lesions seem to show an increased association with subsequent OSCC than others, but inconsistent
what does potentially malignant mean?
the lesions are not “malignant” already and it is not inevitable that the OSCC will develop, there is a risk that tumour could arise, although that risk is difficult to evaluate for individual patients
what do PMOL generally look like?
> generally white, red or both
flat, nodular, warty or elevated
large or small
single or multiple
any site but lateral/ ventral of tongue, FOM
what are examples of white / red lesions which aren’t PMOL?
> inherited = white sponge naevus
irritational = frictional keratosis
immunological = LP/LR, LE, others
infective = caused by candida, Epstein-barr virus
iatrogenic = scars, skin grafts and flaps
idiopathic = leukoplakia
classification and definition of leukoplakia?
- homogenous = flat, possibly fissured
- non-homogenous = nodular, speckled or both
proliferative verrucous leukoplakia is believed to be a subset of non homogeneous leukoplakia
def - a white patch which cannot be classified as any other disease and is associated with an increased risk of malignancy
in other words - not = acute candidiasis, frictional keratosis, LP/LR, WSN
definition of erythroplakia?
- a white/red patch that can’t be diagnosed as anything else
- similar to leukoplakia but refers to a red patch
- sometimes called erythroplasia
- diagnosis is based on exclusion and thus needs properly assessed
what intra oral disease have an association with OSCC?
- OLP/ LR
- LE
- patterson Kelly brown syndrome
- submucous fibrosis
- dyskeratosis congenita
- epidermolysis bullosa
what risk is a homogenous leukoplakia in developing into a OSCC?
low risk
what risk is a non homogenous leukoplakia at developing into an OSCC?
high risk
what risk is an erythroplakia at developing into an OSCC?
highest risk
what is the epidemiology of an OSCC?
- variable and complicated
- much uncerctaintity in diagnosis
- rare
- middle age and elderly
- twice as common in males as females
- developing countries = lots of tobacco use = Lots of OSCC = lots of precursors
- less than 10 a year in NI
what are the common sites of OSCC?
- VT
- LT
- FOM
- RMP
what is the size of an OSCC?
- larger
- spanning multiple intraoral sites
what is the appearance of an OSCC?
non-homogenous
microscopic = dysplasia
when would you be more worried if someone had an OSCC?
- in non smokers (absence of risk factors)
what 3 things do you need to do to establish a diagnosis of an unknown lesion?
- history (duration, onset, habits, systemic disease?, medication, family history)
- examination
- special investigations
what do you have to note during an examination of a PMOL?
- the nature
- the size
- the site
- the extent
- that it isn’t anything else
- homo or non-homogenous
why is it important to palpate a PMOL?
to check for any change in the feel of the underlying, especially induration
what laboratory investigation do you complete for a PMOL?
- MICROBIOLOGICAL - candida isolation
- HAEMATOLOGICAL - haematinic deficiencies/ anaemia, biochemistry, autoantibodies
- HISTOPATHOLOGICAL - morphological
what makes a lesion white?
- thicker keratin (hyperkeratosis)
- thicker epithelium (hyperplasia)
- fibrosis in the lamina propia
what makes a lesion red?
- thinner keratin
- thinner epithelium (atrophy)
- vascularity in the lamina propia
what morphological changes may occur in a PMOL?
- hyperkeratosis
- epithelial thickness change
- change in rete peg architecture
- status of basal layer (hyperplasia, apoptosis)
- dysplasia
- changers in lamina propia
- candida present
what is dysplasia?
> a description of architectural and cytological changes in epithelium that resemble those of cancer but without invasion of the tissues
> a form of “intermediate step” in cancer development : a tissue disturbance that looks like a cancer but does not behave like a cancer
> the presence of dysplasia implies some disturbance of epithelial proliferation and/ or differentiation, its presence can assist in treatment
what are the features of dysplasia ?
- distorted rete peg architecture
- irregular stratification
- dyskeratosis
- basal cell hyperplasia
- loss of adherence
- loss of polarity
- hyperchromatism
- increased N : C
- anisocytsosis
- pleomorphism
- number, location and form of mitotic figures
what are the 4 sub divisions of dysplasia?
- mild
- moderate
- severe
- carcinoma-in-situ
- they’re are sometimes referred to low grade (mild) and high grade
what is the sequence of cancer formation?
= progressive worsening of dysplasia
- no dysplasia > mild
- mild > moderate
- mod > severe
- severe > invasion
what does the linear sequence of cancer formation never appear in real life?
- cancer is a genetic disease
- cellular morphology is a poor reflection of genetic changes
- biopsies are small
- the section biopsied will never turn to SCC
- the past is a poor guide to the future
- dysplasia assessment is too complex too be helpful
what is the risk factor in the presence of dysplasia in developing an OSCC?
x10
what is the chance of developing an OSCC from dysplasia from the different grades?
mild = <5%
mod = 10-20%
severe = 15-20%
what are the important features of epithelial dysplasia?
- some features are interrelated
- none of the features are specific
- not all the features are present
- assessment is very subjective
- sampling error is significant
why is there lots of uncertainty in studying dysplasia for OSCC diagnosis?
- studies are retrospective, intrinisicallu biased and not directly comparable
- number of cases are small
- OSCC may not develop for many years
Management of PMOL?
> long term follow ups = life long
> get rid of the lesion (at least the worst part)
stabilise the intracellular biology
observation
combination
what are the surgical treatment option of PMOL?
- scalpel excision
- laser excisions
- CO2 laser ablation
- photodynamic therapy
- cryotherapy
what are medical treatment options for PMOL?
- retinoids
- EGFR inhibitors/ antagonists (epidermal growth factor receptor)
- COX2 antagonists
- cell cycle interruption = p53 modulators
- topical anti cancer agents = bleomycin
what are the advantages of treatment?
> surgical = the most abnormal looking tissue can be removed or destroyed
medical = topical drug can be directed at the most abnormal site with less destruction and systemic medication may also manage other sites
what are the disadvantages of treatments?
> local side effect - pain, infection, slow healing
sytemic side effects
no therapy prevents new lesions or OSCC
what is the aim of management?
- preventing the development of OSCC
- detecting the patients first OSCC at the earliest opportunity
