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Oral Disease - Soft tissue > Oral Cancer > Flashcards

Oral Cancer Flashcards

1
Q

Define: prevalence

A

Number of people with a disease at any one time

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2
Q

Define: incidence

A

Number of new cases over a time period (usually a year)

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3
Q

What is the expected trend of oral cancer cases (in comparison to other smoking related cancers)

A

Oral cancer is projected to increase (postulated for 2030 in the UK) whereas other smoking related cancers (lung, larynx for eg) is expected to decrease

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4
Q

What is the most common cancer found in the oral cavity?

A

90% are squamous cell carcinomas

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5
Q

What makes up the 10% of oral cancers that are not squamous cell carcinomas

A

Salivary gland, lymphomas, melanomas and sarcomas

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6
Q

Where does oral squamous cell carcinoma arise?

A

Surface lining epithelium of the oral cavity

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7
Q

What areas classify as oral cavity cancer proper?

A

Cancers confined to the oral cavity

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8
Q

What areas do not classify as oral cavity cancers?

A

Nasopharyngeal, oropharyngeal, hypopharyngeal - these are head and neck cancers

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9
Q

List countries which have high rates of lip and oral cavity cancers?

A

Melanesia (Papua New Guinea)
South central asia
Australia/NZ

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10
Q

Gender predilection for oral cavity and oropharyngeal cancer?

A

Males > females

HOWEVER - female cases are increasing

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11
Q

What is the limitation of research data showing the rise in oral cavity cancers?

A

Data accumulates figures for incidence and prevelance for both oral cavity cancer proper and oropharyngeal cancers (head and neck cancer) - therefore it is difficult to predict the incidence and prevalence of oral cavity cancer alone

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12
Q

Describe how the number of cases of oral cavity and oropharyngeal cancers in males are changing

A

Both are increasing in the UK (and decreasing in USA), however in 2013, oropharyngeal cancers overtook oral cavity cancers (There are now more cases of OP cancers - HPV?)

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13
Q

Describe the link between socioeconomic background and oral cancer

A

Strong association between the two

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14
Q

Describe the link between age and oral cancer

A

Mean age around 40

Worldwide increase in the proportion of cases occurring in pts BELOW 45 especially in females

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15
Q

Describe the mortality risk of lip and oral cavity cancer

A

Better prognosis than most including lung, liver and pancreas (18th) - 5 year mortality rate is around half
HOWEVER risk of mortality is increasing in the UK

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16
Q

How does the stage of oral cancer affect survival rate?

A

The lower the stage, the better the prognosis (5 year)

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17
Q

Define specialist workforce

A

People able to treat the disease - e.g. in the case of cancer, it would be surgeons, doctors and nurses who specialise in cancer treatment

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18
Q

What is the risk of second primary cancer with oral cancers oropharyngeal cancers?

A

Very high risk of second primary cancers - likely in the head and neck or the lungs

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19
Q

What are the MAJOR MODIFIABLE risk factors of oral cancer

A 
Smoking 
Smokeless tobacco 
Betel quid habit 
Alcohol 
Sunlight (lip)
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20
Q

What are the unmodifiable risk factors of oral cancer

A

Age
Previous cancer
Genetic suscpetibility?
Immunodeficiency

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21
Q

How does the dose of smoking relate to the risk of oral cancer

A

Risk increases with the number of cigarettes smoked a day - very high risk with >20/day for >20 years

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22
Q

What is the risk of oral cancer in smokers compared to non smokers

A

30 times greater

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23
Q

Does the risk of oral cancer reduce once a smoker stops?

A

No - the risk reduces by 50% after 5 years

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24
Q

List the signs of a smoker

A
  • White patches with red dots on the palate (these are inflamed minor SG)
  • Hyperpigmentation or smokers keratosis
  • Pigmentation of the mucosa (Reactive change)
  • Nicotine stained teeth
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25
Q

Describe the risk of oral cancer with ecigs and vaping

A
  • Unknown since they are both new
  • Vape contains added chemicals thus carrying a potential risk
  • Toxicity paper in 2016 indicated chemicals can cause cytotoxicity of epithelial cells thus incr in breakage of DNA strands
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26
Q

List the risks of shisa smoking

A
  • Cross infection from sharing pipe - herpes or tb
  • Carbon monoxide from the charcoal
  • Tobacco risk?
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27
Q

How is smokeless tobacco used?

A

Tobacco is prepared and placed into the sulcus and is absorbed by the mucosa

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28
Q

List the names of smokeless tobacco

A

Betel quid, paan, gutka

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29
Q

What are the signs of use of smokeless tobacco?

A

Patch in the buccal sulcus

Heavily stained teeth

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30
Q

Where are hotspots for smokeless tobacco abuse

A

South Asia, India, Bangladesh and Pakistan

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31
Q

What is the most important effect of smokeless tobacco

A

Oral submucous fibrosis - OPMD

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32
Q

What is the risk of oral cancer with alcohol?

A
  • Increased risk which is dose dependent

- Synergistic effect with smoking (heavy smoking and alcohol increases risk greater than both alone)

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33
Q

What are oral potentially malignant diseases?

A

Pre-existing lesions occurring in the oral cavity that have the potential for malignant change

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34
Q

List the main OPMD

A
  • Dysplastic and non-dysplastic leukoplakia
  • Erythroplakia
  • Speckled leukoplakia
  • oral submucous fibrosis
  • Proliferative verrucous leukoplasia
  • Chronic candidosis
  • Lichen planus
  • DLE
  • Dyskeratosis congenita, fanconi anaemia
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35
Q

Which OPMD have the highest risk of malignant change?

A
  • Proliferative verrucous leukoplakia - almost 100% risk
  • Oral submucous fibrosis - 15-20%
  • Erythroplakia
  • Speckled leukoplakia
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36
Q

What is field change?

A

Clonal expansion of cells which harbor early, preneoplastic genetic lesions which predispose the tissue to tumour formation

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37
Q

What types of genetic changes are required to produce OPMD

A

Mutations or chromosomal changes e.g. deletions or duplications
- PI3K/AKT/mTOR, RAS/RAF/MAPK, JAK/STAT, WNT/βcatenin and/or TGF β pathways must occur in order to develop a cancer

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38
Q

Describe the regulation of pathways in OPMD and cancers

A
  • OMPD - downregulated, indicating further genetic change is required to produce a cancer
  • Cancer - upregulated
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39
Q

Aetiology of OPMD

A
  • Tobacco
  • Alcohol
  • Genetics
  • AI/idiopathic
  • HPV?
  • Candida?
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40
Q

List susceptibility factors for oral cancer

A
  • Inherited mutations
  • Carcinogens (cause mutations or chromosomal changes)
  • Irritants and infections (Cause promotional changes through proliferation)
  • Host response - degradation of epithelial cells
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41
Q

What are the two parts of risk assessing OPMD

A
  • Clinical risk assessment

- Histological risk assessment

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42
Q

List the features of clinical risk assessment of OPMD

A
  • Type of OPMD (some have higher risk)
  • Site
  • Colour
  • Extent - larger increased risk
  • Surface texture
  • Habits
  • Gender (f > m)
  • Malnourished
  • Time present/changes
  • History of cancer
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43
Q

List the sites where OPMD have a greater malignant risk

A
  • FOM
  • Lateral or ventral tongue
  • Tonsil
  • Retromolar region
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44
Q

What type of surface texture of OPMD have a greater risk

A

Lumpy or spiky

If indurated it is probably a carcinoma already

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45
Q

How does colour relate to risk of OPMD

A
  • Speckled lesions have the highest risk
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46
Q

What is assessed during histological risk assessment of OPMD

A
  • Degree of dysplasia

- DNA ploidy

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47
Q

What is dysplasia?

A

Histological feature of premalignancy, epithelial dysplasia occurs when there are disturbances to epithelial proliferation (YOU CANNOT SEE DYSPLASIA CLINICALLY)

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48
Q

Why do we assess for dysplasia?

A

It is the best indicator for future malignant change

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49
Q

List the histological changes indicating epithelial dysplasia

A
  • Loss of basal cell polarity
  • > 1 layer with basaloid appearance
  • Increase nuclear-cytoplasic ratio
  • Drop shaped rete-ridges
  • Irregular epithelial stratification
  • Increase mitotic figures +/- abnormal form or present in the superficial epithelium
  • Enlarged nucleoli
  • Loss of cell adherence
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50
Q

Describe the degree of dysplasia and risk of malignant change

A
  • Mild < mod < severe

the greater the dysplasia, the higher the risk of malignant change

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51
Q

What is DNA ploidy analysis?

A

Assessment of DNA content in tissues

52
Q

What is the NORMAL result of a ploidy analysis?

A
  • Diploid

- This means that the cells contain a complete set of chromosomes (2)

53
Q

What is an ABNORMAL result of ploidy analysis which indicates malignancy

A
  • Aneuploid

- This indicates abnormal number of chromosomes in the cells

54
Q

What are the small peaks on an otherwise normal diploid result on a dna ploidy analysis?

A

Cells undergoing cell division cycle (they contain double the dna therefore they appear as smaller peaks alongside the large diploid peak)

55
Q

What are the aims of biopsies?

A
  • Identify or exclude a specific diagnosis
  • Assess dysplasia and map it to plan tx
  • Assess invasion
  • DNA ploidy analysis
  • Baseline for follow up
  • Pt communication
56
Q

What is the difference between dysplasia and cancer?

A
  • Cancer involves invasion, metastases and molecular changes
57
Q

How is HPV transmitted?

A

Skin to skin contact - mainly through sexual contact

58
Q

How many types of HPV are there?

A

over 100

59
Q

Which subtypes of HPV are identified in oropharyngeal cancers?

A

Hpv 16 and 18
Hpv 33 to a lesser degree
*rmbr there are different subtypes which cause genital cancers

60
Q

How are the subtypes of hpv classified?

A

Based on risk - e.g. cause malignant neoplasms (high risk) or benign neoplasms (low risk)

61
Q

What % of healthy population have hpv 16 and 18 present in their saliva?

A

25% test positive - it only becomes an issue when hpv infection becomes persistent

62
Q

List sites commonly affected by HPV-positive oropharyngeal cancer

A
  • Originates at the base of the tonsillar crypt (not the surface)
  • Base of the tongue
  • Has a predilection for Waldeyer’s ring
63
Q

Why is HPV cancer very difficult for dentists to screen?

A
  • It originates at the base of the tonsillar crypt and there are no surface changes even in advanced changes
  • difficult to assess oropharynx without a fibre-optic probe
64
Q

What makes up Waldeyer’s ring?

A
  • Pharyngeal tonsil
  • Tubal tonsil
  • Palatine tonsil
  • Lingual tonsil
65
Q

What are the risk factors for HPV positive cancers

A
  • > 26 total lifetime partners
  • > 6 oral sex partners
  • Higher income and educated = higher risk
66
Q

Link between smoking and alcohol and HPV cancers

A

Inverse correlation - most are non-smokers

Alcohol possibly has an inverse correlation too but evidence is insufficient

67
Q

What is the main risk factor for HPV oral cancers

A

High number of oral sex partners

68
Q

Demographic for HPV positive oral cancers

A

Caucasian males, 50-55, well educated and high income

69
Q

What are the presenting signs for HPV positive oral cancers

A 
Neck lumps (50%) 
Variable oral lesions (15%) - includes retrmolar area, diffuse redness on depression of the tongue
70
Q

Describe the prognosis of HPV oral cancers with HPV-negative oral cancers

A
  • HPV positive oral cancers have a better prognosis (around 90% 5 year survival compared with 40%)
71
Q

List the reasons why the prognosis of HPV positive cancers is better than HPV negative cancers

A
  • Low rates of secondary primary cancer
  • Less cumulative genetic mutations compared to HPV negative
  • Pt factors - Younger, lack of comorbidity, usually non-smokers
  • HPV positive responds well to radiotherapy
72
Q

Compare HPV negative and HPV positive oral cancers

A

Site - Neg - FOM, lat tongue, retromolar area / Pos - tonsi, base of tongue, waldeyers ring

Age - Neg - 58-60 / Pos - 52-56

Incidence - Neg - decreasing / Pos - increasing

Risk factors - Neg - tobacco, alcohol / Pos - oral sex

Prognosis - Neg - <40% 5 year / Pos - 90% 5 year

73
Q

What type of cancer is on the rise due to HPV?

A
  • Oropharyngeal cancers

- It plays a minimal role for oral cavity cancer proper

74
Q

List the categories of cancer treatments

A 
Curative 
Salvage 
Palliative 
Neoadjuvant 
Adjuvant
75
Q

What is the purpose of curative treatment

A
  • Aims to cure patient

- there is usually one shot at curative tx

76
Q

What is the purpose of salvage treatment

A
  • Form of tx given after the patient does not respond to the first treatment
77
Q

What is palliative care?

A
  • Supporting the patient with needs - including relief of symptoms, improve QOL, control side effects of treatment
78
Q

List the modes of cancer treatment

A

Surgery
Chemotherapy
Radiotherapy (External beam, brachytherapy)
Targeted therapy (Immunotherapies, anti EGFR, tyrosine kinase inhibitors)
Multimodality treatment
Holistic treatment

79
Q

List the general steps of cancer diagnosis to monitoring

A
  • Diagnose
  • Assess extent (stage and grade)
  • Recommend ideal tx
  • Assess comorbidities
  • Educate, understand, consent
  • Dietetics and speech
  • Active tx
  • Surveillence
  • Manage recurrence and second primary caners
  • Survivorship
80
Q

What is survivorship

A

Management of pts who survive cancers - need to cope with the side effects for the rest of their lives

81
Q

What % of pts sent to the 2 week referral have cancer

A

3%

82
Q

What are the NICE guidelines for referral of a pt to a 2 week cancer pathway

A
  • Unexplained ulceration in the oral cavity lasting >3 weeks
  • Persistent and unexplained lump in the neck
  • Lump on the lip or oral cavity or a red or red/white patch in the oral cavity consistent with erythroplakia or erythroleukoplasia (if assessed by a dentist)
83
Q

How is staging and grading carried out?

A
  • Imaging e.g. CT, MRI, PET, USS

- Biopsies for grading, mapping biopsies or FNA or neck nodes

84
Q

What stage and grading system is commonly used?

A

TMN (tumour size, metastases and nodes metastases)

85
Q

What are the scores for N in the TMN grade/stage

A

N0 - no regional lymph node mets
N1 - mets in a single node, 3cm max diameter without extranodeal extension
N2a - same as N1 but with extranodal extension
pN2b - mts in multiple ipsilateral nodes <6cm max diameter without extranodal extension
pN2c - mets in bilateral or contralteral nodes, <6cm max dia without extranodal extension
N3a - mets in node >6cm without extranodal
N3b - mets >3cm dia with extranodal extension

86
Q

What are the scores for T in TMN

A

Tis - dysplasia only (in situ)
T1 - tumour <2cm dimension and <5mm depth of invasion
T2 - tumour <2cm with 5-10mm invasion OR 2-4cm with up to 10mm
T3 - >4cm or >10mm invasion
T4a - invades cortical bone of the mandible or max sinus, or invades skin on the face
T4b - invades masticator space, pterygoid plates, skunn base or encases internal carotid

87
Q

What is the TNM for stage 1 cancer?

A

T1 N0 M0

88
Q

What is the TNM for stage 2 cancer?

A

T2 N0 M0

89
Q

What is the TNM for stage 3 cancer?

A

T3 N0 M0

T1-3 N1 M0

90
Q

What is the TNM for stage 4 cancer

A 
T4a N0/1 M0 
T1-4 N2 M0 
Any T N3 M0 
T4b any N M0 
Any T any N M1
91
Q

What is an occult metastases

A

Mets that cannot be detected

92
Q

What type of oral cancer is prone to occult mets

A

Tongue cancer as it is prone to early mets

93
Q

What is the risk of treating oral cancers without treating the neck too?

A
  • Risk of leaving behind occult mets in the neck therefore there is a risk of recurrence
94
Q

What is the purpose of a sentinel node biopsy?

A
  • It traces the path from the tumour to the nodes to determine the closest node that the tumour drains into
  • (indicates the node most likely to have mets so it can be investigated)
95
Q

What is neoadjuvant radiotherapy

A

Aims to reduce tumour size before surgery

96
Q

What is adjuvant radiotherapy

A

Redcue change of tumour recurrence after surgery

97
Q

What types of cancers can be treated with radiotherapy alone? which ones cannot?

A
  • Head and neck cancers respond well to RT alone

- ORAL cancers cannot be treated with radiotherapy alone (except HPV positive oropharyngeal)

98
Q

How does radiotherapy work?

A 
Ionising radiation (most use xrays and gamma rays) 
The radiation is produced via photons and electrons mainly (small amount via protons, neutrons and ion beams)
99
Q

How does the radiation kill cancer cells?

A

Via RT induced cell death (lethal damage to DNA and mitotic cell death or direct killing via apoptosis)

100
Q

What type of dose is used in radiotherapy?

A

Sublethal dose (cancer cells are more sensitive to the RT than healthy cells, and healthy cells have the ability to repair themselves)

101
Q

What are the aims of RT

A
  • Achieve local tumour control via delivery of a curative dose to the tumour (and keeping dose to adjacent tissues as low as possible - follow dose limits )
102
Q

How is the dose of RT reduced whilst still keeping it high enough to achieve the aims?

A
  • Delivery of small fractions (sessions) over a period of time to limit the dose and prevent overloading
103
Q

What is the purpose of multi-leaf collimators?

A

Allow us to conform the beam and change the angle to face the target to give a higher dose to the tumour without affecting adjacent cells

104
Q

What is clinical delineation?

A

Process where target volumes and organs around the tumour are identified and risk assessed - they map out the adjacent structures to avoid important areas (mapping the dose)

105
Q

How long does RT appt take? how often?

A
  • 5-7min per appt and carried out daily monday-friday for 3-7 weeks depending on the cancer type and patient
106
Q

When do side effects of RT usually start? when do they settle?

A

Acute toxicity - 1-2 weeks post initiation of tx

Late toxicity - 3 months after start of treatment

107
Q

What is acute toxicity to radiotherapy?

A
  • Side effects occuring 2-3 weeks from the start of tx and settle within 4-6 weeks of start of tx
  • They are present to a degree in all patients and usually affects rapid turnover tissue (mucous membranes)
108
Q

List the symptoms of acute toxicity

A
  • Loss of taste or metallic taste
  • dry mouth
  • dysphagia and true weight loss
  • Patchy, haemorrhagic or confluent mucositis
  • Thick, stringy saliva or secretions which makes pts feel nauseous
  • Erythema, dry, peeling or moist skin
109
Q

What is late toxicity to RT?

A
  • Symptoms occuring >3months post RT
  • Tends to be permanent and progressive
  • 5-10% develop severe toxicity
110
Q

List the symptoms of late toxicity

A

Skin - odema, fibrosis, atrophy, dipigmentation or telangiectasia

  • SG - xerostomia (radiation caries)
  • Spinal cord - Lhermittes syndrome
  • Ear - chronic otitis externa or deafness
  • Laryngeal - cartilage necrosis or hoarse voise
  • Muscle and joints - trismus, shoulder pain or neck striggnesss
111
Q

What is the main side effect of RT of concern to dentists?

A
  • Osteoradionecrosis of the jaw
  • Xerostomia and radiation caries
  • Mucositits
112
Q

Compare RT mucositis and chemotherapy mucositits

A

RT - lasts longer (3-12 weeks) and is generally more severe

Chemo - lasts 3-12 days and is less severe

113
Q

Describe the management of mucositis

A
  • Oral hygiene
  • Topical agents - saline rinses, difflam, oxetacine mouthwash (painkiller)
  • Analgesics (paracetamol, co-codamol or opiates)
  • Nutritional support and oral fluid intake - may need feeding tube
  • Swallowing exercises
  • Smoking and alcohol cessation
114
Q

How to manage thick, stringy saliva as a side effect of RT?

A
  • Sodium bicarbonate mouthwash or hygrogen peroxide
  • Saline rinse or nebuliser
  • Steam inhalations
  • Antiemetics
115
Q

What mouthwashes are contraindicated for RT mucositis

A
  • Alcohol containing moutwashes - it will sting

- CHX mouthwash

116
Q

Tx of post-RT mucositis due to an infection

A
  • Antifungals given as soon as diagnosis is made - fluconazole 100mg for 7-14 days
  • NOTE: prophylaxis nystatin is no longer given
117
Q

Tx of RT xerostomoa

A
  • Artificial saliva sprays

- Never goes back to normal flow - needs long term management, freq visits etc

118
Q

What is osteoradionecrosis

A

Bone death due to radiation commonly affecting the mandible

119
Q

List the role of the dentist before patients receive high dose RT

A
  • Poor prognosis teeth are removed
  • Perio health stabilised
  • Fluoride therapy initiated
120
Q

Who is at risk of ORN?

A
  • Anyone who has had RT- the risk is there for life and someone who has had RT should have XLA under specialist care - never in practice
121
Q

What stage of cancer is indicated for surgery (reconstructive surgery)?

A

All stages - however later spages may need RT or chemotherapy as an adjunct

122
Q

What are the main morbities associated withreconstructive surgery for oral and oropharyngeal caners?

A

Speech and swallowing difficulties

123
Q

What is the importance of the neck in oral and oropharyngeal surgery?

A
  • Risk of occult disease so there may be elective neck dissection (lymph node dissection)
124
Q

List the levels of the nodes int the neck

A 
Level I - submental and submandibular 
Level II - Upper internal jugular nodes 
Level III - middle internal jugular nodes
Level IV - lower internal jugular nodes 
Level V - posterior triangle nodes
125
Q

What nodes are oral cavity cancers most likely to drain to?

A

IIa > I > III > IV

Rarely to level 5

Oral Disease - Soft tissue (12 decks)

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