dysplasia and oral cancer Flashcards
what is used to define oral cancer
classification
International Classification of Disease for Oncology
ICD-O
Many different sites
* Makes comparison difficult
* Makes epidemiology difficult
* Makes treatment planning difficult
Congregated into
* OC – oral cavity cancer
* OP – oropharyngeal cancer
epidemiology of oral cancer
BDJ Ref Vol 225 No. 9 (November 9 2018) - useful
2 distinct disease patterns
* Oral Cavity Cancer (OCC)
* Oro-Pharyngeal Cancer (OPC)
each have Different populations, outcomes, risks
Female: Male divide
Country divide
Change over time – male predominency reduce
INHANCE
The International Head and Neck Cancer Epidemiology Consortium (INHANCE)
Collaboration of research groups of large epidemiological (case-control) studies
Investigating the risk factors for head and neck cancer including (separately) oral cavity and oropharyngeal cancer subsites
* 35 studies – 25,000 patients, 37,000 controls
oral cavity cancer
prevalance
2.5 per 100,000 pop (2012)
Almost HALF (48.7%) in south central Asia
Male 2:1 Female
Incidence not increasing worldwide
* Decreasing in men, increasing in women
* Linked to reduction in tobacco use (falling in men, rising in women)
Scottish Cancer Registry
* 10% increase 2001-2012
* Unclear why
common/high risk sites for oral cavity cancer
6
Floor of the mouth
Lateral border of the tongue
Retromolar regions
Soft and hard palate
Gingivae
Buccal mucosa
tongue and tonsillar area
It is well known that there are geographic and regional differences in the intraoral distribution of oral cancer
red highlighted area represents ~20% of the mouth, but ~70% of oral cancers are found here
3 specific sites are more predisposed to developing SSC in drinkers and smokers - FOM, lateral border of the tongue, soft palate
Don’t ignore others
oral cancer sites division
red highlighted area represents ~20% of the mouth, but ~70% of oral cancers are found here
oro-phayngeal cancer
prevalance
1.4 per 100,000 pop
Most in North America and south central Asia
Male 4.8:1 Female
More males than females, significant difference
Rates rapidly rising, especially in High Income areas (North America)
* Linked to rising HPV epidemic
Scottish Cancer Registry
* 85% increase 2001-2012 – highest increase for any cancer
OCC and OPC trends
OCC slowly increase (red dash line)
OPC biggest rise over last period (Red line)
5 key risk factors for oral cancer
smoking
drinking alcohol
both smoking and drinking
betel quid (paan)
socieoeconomic status
smokers who don’t drink oral cancer risk
Smokers who don’t drink x2 risk (compared to nonsmokers who don’t drink)
* Increases with quantity, duration and frequency of tobacco use
* Fewer cigarettes for longer duration worse than high number, short term
* Smoking risks were generally greater for larynx cancer
drinking alcohol oral cancer risk
Drinkers (3-4 drinks/day) x2 risk (same as smokers who don’t drink)
* Never smoked population
* Frequency more important than duration – more drinks each day key
* alcohol drinking for oral cavity and pharyngeal cancers
smoking and drinking alcohol oral cancer risk
Smoke and Drink x5 risk
* Increases with frequency and duration of smoking and alcohol consumption
* No safe lower limit
betel quid (paan) use oral cancer risk
x3 risk
mixture of substances including areca nut with or without tobacco wrapped in a betel leaf and placed in the mouth
socioeconomic statis oral cancer risk
x2 risk (SIMD 4/5)
* Even without other risk factors
* Key factor in many other diseases
* Same risk as smoking
* More likely to smoke and/or drink too- compound
* Low educational attainment
3 things that may impact oral cancer risk - but not yet certain currently
Family History
* 1st degree relative with H&N cancer may be important
Oral Health
* Early data suggests poor oral health may be associated with an increased cancer risk – small effect
Sexual Activity
* a slight increased risk for oropharyngeal cancer with:
* six or more lifetime sexual partners
* four or more lifetime oral sex partners
* early age (<18 years) of sexual debut (INHANCE)
* Probably link to HPV
benefits of stopping smoking and alcohol
INHANCE
Demonstrable benefits of quitting smoking were identified within one to four years after stopping smoking
* Quicker
* Smoker prevention more important when time limit on social health intervention (compared to drink)
risks reduced and reached a similar level to those who had never smoked after 20 years of quitting.
In contrast, the risk effects associated with quitting heavy alcohol consumption take 20 years to begin to emerge.
SE status compared to smoking/alcohol oral cancer risk
SE status is on a par with smoking and alcohol in terms of magnitude (two-fold increased risk)
* specifically low educational attainment and low income.
These risks were not fully explained by smoking and alcohol consumption (‘the cause of the cause’)
* have a more direct effect associated with socioeconomic circumstances
diet and oral cancer risk
There is limited new evidence in relation to dietary factors beyond confirming that a high intake of fresh fruits and vegetables were associated with reducing by half the oral cancer risk
obesity was not associated with an increased oral cancer risk
* young people (aged 30-years or less) oral cancer was more likely in those who self-reported a low body mass index (BMI)
potentially malignant disorders examples
4
White lesions (leukoplakia)
Red lesions (erythroplakia)
Lichen planus
* Candidal Leukoplakia
* Chronic Hyperplastic Candidiasis
Oral Submucous Fibrosis
leukoplakia
white pathc that cannot be rubbed off and not attributable to any other disease
PMD
oral cancer in white lesions
incidence 0.2 - 4%
* wide variation in different populations
* Reliability of data not clear
malignant change
* varied reports, most under 4%
* period prevalence
3.2.5% in 10 years, 4% in 20 years
biopsy where possible to assess dysplasia
oral cancer in red lesions
much less frequent than leukoplakia
much higher risk of cancer
greater dysplasia risk
* Up to 50% already be carcinoma
no good follow-up studies available
grading of oral mucosa dysplasia
histologically
based on cytological and architectural changes
* not all features needed for dysplasia to be occuring
* more features present, the higher the grade of dysplasia reported
multi stage promotion
from normal to PMD to OCC
process takes time
can happen at different stages at different parts of mouth depening on what environmental stimuli playing a role
field cancerisation concept
Multiple primaries possible over time
up to 15 to 20 in some patients
Concept of “field cancerisation”
high cancer risk in 5cm radius of original primary - that’s most of the mouth/pharynx
synchronous or metachronous lesions
* Can occur at the same time as the primary or at later times
Need to follow up for rest of life as at risk of another oral cancer
oral cancer staging
clinical
mutliple variable for clinical staging
site
size (T)
spread (N&M)
TNM
oral cancer staging
Tumour
Nodes
Metasis
lip cancer
location
aetiology
behaviour and prognosis
Lower lip
* non-healing ulcer or swelling
Aetiology
* Sunlight UV-B
* smoking
Behaviour
* slow growth
* local invasion
* rarely metastasise to nodes
Good prognosis as early detection
