Dysplasia & OC P2 Flashcards
Potentially malignant lesions
- previously termed premalignant/ precancerous
- important to inform pt so they know if they can turn malignant
- are they en-route to becoming cancer?
- much more likely to be cancer?
- potentially malignant?
Examples of potentially malignant lesions?
- White lesions- leukoplakia
- Red lesion- erythroplakia
- Lichen planus
- ulcerative and erosive LP
- candidal leukoplakia??
- chronic hyperplastic candidiasis?? - Oral submucous fibrosis
Leukoplakia
- white patch that cannot be rubbed off
- undiagnosed white patch, higher risk of cancer developing than normal mucosa
- not all white patches have the same levels of malignancy
** clinical description and should not be used as a pathological diagnosis for pt
Erythroplakia
- red patch
- much more common to malignant change
- erythema may represent vascular change consequent to malignant change
** clinical description and should not be used as a pathological diagnosis for pt
Incidence of OC in white lesions
0.2 - 4%
- very small
Oral cancer in White lesions
- 0.2 - 4%
- wide variation in different pop
- diet, smoking habits, genetics
- malignant change is at most 4%
- 2.5% in 10 years and 4% in 20 years
**pt needs to know there is a risk of malignant change, and lesions need to be monitored.
OC in white lesions in UK
- most arise initially as clinically normal mucosa
- most cancer in higher incidence areas are from potentially malignant lesions
- worldwide leukoplakia is 50-100 times more likely to progress to cancer than clinically normal mucosa
White lesions example
Erythroplakia
- higher risk of malignancy
- much less frequent than leukoplakia which does not have an explaination
- higher risk of cancer
- greater dysplasia risk
- no good followup studies
Dysplasia to assess cancer risk?
- Based on
- cellular atypia
- epithelial architectural organisation
Previous categorisation of dysplasia
- mild
- moderate
- severe
- carcinoma- in- situ
** moderate sometimes can proceed to severe or mild -> affecting tx
New categorisation
- low grade
- high grade
- carcinoma-in-situ
Histological grading of Oral Mucosa Dysplasia
Low grade dysplasia
- easy to identify that tumour originates from squamous epithelium
- architectural change into lower third
- cytological atypia/ dysplasia may not be prominent
- considerate amount of keratin production
- evidence of stratification
- well formed basal cell layer surrounding tumour islands
- tumour islands are usually well defined and often continuous with surface epithelium
- invasion pattern with intact large branching rete pegs pushing into underlying CT
**when there is architectural changes into middle 3rd, depending on level of cytological atypia, will then be classified either into low/ high grade
High grade dysplasia
- show little resemblance to a normal squamous epithelium
- architectural change upper third
- show considerable atypia
- invade in a non-cohesive pattern with fine cords, small islands and single cells infiltrating widely through CT
- mitotic figures are prominent and many may be abnormal
- loss of stratification
Degree of differentiation is widely used to predict prognosis and shows a significant correlation to survival
Carcinoma in situ
- cytologically malignant but not invading
- abnormal architecture
- full thickness
- severe cytological atypia
- Mitotic abnormalities frequent
Prognostic factors
- Pattern of invasion
- Bulbous rete pegs infiltrating at same level is considered of a better prognosis than widely infiltrating small islands and single cells - Depth of invasion
- risk of metastases for a tumour greater than 4mm was 4x greater than a tumour less than 4mm - Perineural invasion
- up to 60% of OSCC, most significant when a tumour is seen within a large nerve at a site some distance from main tumour mass - Invasion of vessels
- associated with lymph node metastases and poor prognosis
How does cancer happen?
- it is a multi-stage promotion
Field Cancerisation concept
Definition
- where a cancer develops inside the mouth, it is not the only part of mouth which has been subject to changes and stimuli that lead to cancer
- coalesce in cancer area and produce change at the time
- may be progressing at other parts at a slower stage
** has a risk of developing cancer in a later time at diff parts
- higher risk in 5cm radius of original primary
- hence important to consider the whole mouth
- review pt
- look for other lesions that may have been missed
Synchronous/ Metachronous lesions
- can occur at the same time as primary but different places at a later times
Oral cancer staging
Multiple variables for clinical staging of oral cancer
- site
- size (T)
- spread (N & M)
Oral cancer prognosis
1/3 patients present at stage1/2
- Stage 1: 80% cure rate
- Stage 2: 65% cure rate
- later than this is 5 year survival of <50%, cure 30%
- if untreated, with metastases, survival is about 4 months
Surgery/ radiotherapy/ chemo/ immunotherapy
- choice will depend on pt choice and health/ prognosis
- tumour location, size and nutritional status
For resectable tumours, primary surgery offers best outcome
- post surgical radiotherapy/ chemotherapy
Lip cancer
Lower lip
- non- healing ulcer/ swelling
- normally detected early as it is visible, hence good prognosis
- Aetiology is sunlight UVB or smoking
- slow growth
- local invasion
- rarely metastasise to nodes
Oral cancer detection
- difficult process
- Oral cancer Recognition Toolkit by Cancer Research UK and British Dental Association
Oral Cancer Screening
- looking specific for a lesion at early stage or before lesion is malignant
- benefit vs harm
- undetected lesions vs false positive
- cost of screening vs cost of disease
- cost of screening vs disability from disease
Different forms of screening processes
- HPV16 screening
- Toluidine blue
- VELscope
- Photodynamic diagnosis (PDD)
- clinical judgement of experienced clinician
- oral brush cytology
Toluidine Blue
- which apply to oral mucosa
- stain particular markers within cells
- show areas of change in dysplasia
- also shows area of inflammation and trauma
- not particularly helpful, as it widespread
- false positive in inflammatory lesions
- not a good tool to detect oral malignant lesions
VELscope
- autofluorescence of tissues with blue light
- loss of fluorescence equates to change
- change can be cancer or can be other changes
- ie: show area with reduce fluorescence, but with no cause why, may lead to biopsy of false positive test
PDD
- Photodynamic diagnosis
- use Psoralen, UV light which can be attracted to area of dysplasia/ cancer
Oral cancer screening
- most cost effective and reliable screening tool is experienced dental practitioner
Oral cancer in primary care
- part of general CPD requirement now
- primary prevention in pts attending for regular oral care
Dentist must be familiar with and competent in
1. smoking cessation advice
2. alcohol reduction advice
3. healthy diet promotion- will help in long term
- can present in any age in any pt
Referral for OC
- dentist has to make decision about the referral threshold for potentially malignant lesions
- monitor with photographs and education, ie: smoking and alcohol reduction
- remove local factors where ulcer may be due to trauma and review
2 week rule for referral to clinic for hospital (maxillofacial department- local health board pathway- suspicion of cancer)
- pt must be initially seen within this time- lesion can be promptly assess
- 62 days referral to tx time for cancer pt
Desquamative gingivitis
- OHI
- Topical Tacrolimus: topical immunosuppressant
