Oral Medicine Flashcards
(195 cards)
How is Oral cancer classified?
International Classification of Disease for Oncology- ICD-O
What makes classification of cancer difficult?
Makes comparison difficult Makes epidemiology difficultMakes treatment planning difficult
Name the 2 distinct disease patterns for oral cancer?
Oral Cavity Cancer (OCC) Oro-Pharyngeal Cancer (OPC)
Describe the epidemiology of OCC?
2.5 per 100,000 pop (2012)Almost HALF (48.7%) in south central AsiaMale 2:1 Female Incidence not increasing worldwide- Decreasing in men, increasing in women- Linked to reduction in tobacco useScottish Cancer Registry- 10% increase 2001-2012
Name the 6 common sites for mouth cancer?
Floor of the mouthLateral border of the tongueRetromolar regionsSoft and hard palateGingivaeBuccal mucosa
Name the 3 higher sites for SSC in drinkers and smokers?
FoMLat. border of the tongueSoft palate
Name the 8 sites of oral cancer?
LipsPalateTonsilsFoMOther throatTongueOropharynxGums
Describe the epidemiology for OPC?
1.4 per 100,000 popMost in North America and south central AsiaMale 4.8:1 FemaleRates rapidly rising, especially in High Income areas (North America)- Linked to rising HPV epidemicScottish Cancer Registry- 85% increase 2001-2012 – highest increase for any cancer
Name the 5 main risk factors and their associations to Oral Cancer? - how much does each RF multiply the risk of OC?
Smokers who don’t drink x2 risk- 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 cancerDrinkers (3-4 drinks/day) x2 risk- Never smoked population- Frequency more important than duration – more drinks each day key- alcohol drinking for oral cavity and pharyngeal cancersSmoke and Drink x5 risk- Increases with frequency and duration of smoking and alcohol consumption- No safe lower limitBetel quid (paan) x3 risk- mixture of substances including areca nut with or without tobacco wrapped in a betel leaf and placed in the mouth Socioeconomic Status x2 risk- Even without other risk factors- Low educational attainment
Name the 3 risk factors that have not been confirmed as certain to increase the overall risk of Oral cancer?
Family History- 1st degree relative with H&N cancer may be importantOral Health- Early data suggests poor oral health may be associated with an increased cancer risk – small effectSexual 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)
What are the benefits of reducing smoking and alcohol intake?
Benefits seen between 1-4 yearsRisks 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.
What are the benefits of improving SE status?
Socioeconomic status- 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
What are the benefits of reducing poor diet choices?
- 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)
Name 4 potentially malignant lesions?
White lesions (leukoplakia)Red lesions (erythroplakia)Lichen planus- Candidal Leukoplakia- Chronic Hyperplastic CandidiasisOral Submucous Fibrosis
Describe the epidemiology of white lesions in OC?
incidence 0.2 - 4%- wide variation in different populations- Reliability of data not clearmalignant change- varied reports, most under 4%- period prevalence2.5% in 10 years, 4% in 20 yearsMost oral carcinomas in UK arise in initially clinically normal mucosaMost cancer in high incidence areas (e.g. India) from potentially malignant lesionWorldwide leukoplakia is 50 to 100 times more likely to progress to cancer than clinically normal mucosa
Name 3 types of descriptions of white lesions?
HomogenousErosiveNon-homogenous on atrophic background
How does erythroplakia compare to leukoplakia?
much less frequent than leukoplakiamuch higher risk of cancergreater dysplasia risk- Up to 50% already be carcinomano good follow-up studies available
What are the common characteristics of dysplasia and the new categorisation of severity?
Based on:- Cellular Atypia- Epithelial Architectural OrganisationNew categorisation- Low grade- high grade- carcinoma-in-situ
Describe the histological low grade of oral mucosal dysplasia?
Easy to identify that the tumour originates from squamous epitheliumArchitectural change into lower third Cytological atypia or dysplasia may not be prominent Shows a considerable amount of keratin productionEvidence of stratificationWell formed basal cell layer surrounding the tumour islands Tumour islands are usually well defined and are often continuous with the surface epithelium Invasion pattern with intact large branching rete pegs ‘pushing’ into underlying CT(Where there is architectural change into middle third, depending on the level of cytological atypia will be classified into low grade or high grade)
Describe the histological high grade of oral mucosal dysplasia?
Show little resemblance to a normal squamous epitheliumArchitectural change upper third Usually show considerable atypiaInvade in a non-cohesive pattern with fine cords, small islands and single cells infiltrating widely through the CTMitotic figures are prominent and many may be abnormal Degree of differentiation used to predict prognosis
Describe the histological carcinoma in situ of oral mucosal dysplasia?
Theoretical conceptCytologically malignant but not invadingAbnormal architecture- Full thickness (or almost full)- Severe cytological atypiaMitotic abnormalities frequent
Name the histoloigcal prognostic facors which give information on survivability?
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 tumours greater than 4mm was 4x greater than for a tumour less than 4mmmPerineural Invasion- Is seen in up to 60% of OSCCs but is most significant when a tumour is seen within a large nerve at a site some distance from the main tumour massInvasion of Vessels- Widely thought to be associated with lymph node metastaes and a poor prognosis
Describe the Field Cancerisation concept?
Multiple primaries possible over time- up to 15 to 20 in some patientsConcept of “field cancerisation”- high cancer risk in 5cm radius of original primary - that’s most of the mouth/pharynxSynchronous or metachronous lesions- Can occur at the same time as the primary or at later times
Name the multiple variables for clinical cancer staging of OC?
site size (T)spread (N&M)