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BDS 3: Oral Diseases > L27 Mouth cancer: epidemiology and aetiology > Flashcards

L27 Mouth cancer: epidemiology and aetiology Flashcards

1
Q

What are the most frequent sites of mouth cancer?

A
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2
Q

List some head and neck cancers.

A
  • Skin
  • Nose and sinuses
  • Nasopharynx
  • Oropharynx
  • Oral cavity
  • Pharynx
  • Larynx
  • Associated bone
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3
Q

What malignant diseases affect skin and mucosa?

A

Skin:
- SCC
- BCC
- Malignant melanoma

Mucosa:
- SCC
- Soft tissue sarcomas (fibrosarcoma, liposarcoma)
- Malignant lymphoma

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4
Q

Describe the epidemiology of mouth cancer.

A
  • Relatively rare
  • Twice as common in men
  • 2386 deaths in the UK in 2014
  • Predominantly a disease of the elderly but in recent years has become more common in younger people
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5
Q

What is the most common oral malignant neoplasm?

A

Squamous cell carcinoma (accounts for more than 90% of oral malignant neoplasms)

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6
Q

What is the 10 year survival rate for intra-oral SCC?

A
  • 19-59%
  • Poor prognosis
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7
Q

What is the average size of intraoral SCC ar presentation?

A

3-4cm (large)

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8
Q

Where is mouth cancer more common?

A

More common in India.

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9
Q

How does social class relate to mouth cancer?

A
  • Oral cancer 3 times more common in social class V (most depriveed) than social class I
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10
Q

Name some aetiological factors for mouth cancer.

A
  • Tobacco
  • Alcohol
  • UV light (lip cancer)
  • Betel chewing
  • Infection
  • Irradiation
  • Diet and nutrition
  • Dental factors
  • Immunosuppression
  • Occupation
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11
Q

Explain how tobacco is a risk factor for mouth cancer.

A
  • Over 90% of patients with oral cancer use tobacco in some form
  • Pipes, cigars cigarettes
  • Reverse smoking
  • Oral tobacco products (snuff/snus) were banned in the UK in 1992
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12
Q

Explain how betel chewing is a risk factor for mouth cancer.

A
  • Areca nut wrapped in betel leaf with added tobacco
  • Users develop leukoplakia
  • Can also develop submucous fibrosis (mottled, marbled, thick mucosa)
  • Carcinoma develops in area of leukoplakia
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13
Q

Explain how alcohol is a risk factor for mouth cancer.

A
  • 75-80% of pts frequently consume alcohol
  • Dose/time relationship
  • Drinking+smoking = highest risk
  • Carcinogens found in distilled spirits (vodka, gin, rum, tequila, whiskey)
  • Alcohol increases permeability of oral mucosa
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14
Q

What infections are risk factors for mouth cancer?

A
  • Viral infection: Herpes simplex, HPV, EBV, HIV
  • Candida
  • Syphilis
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15
Q

Explain how HPV is a risk factor for mouth cancer.

A
  • HPV related oropharyngeal cancer commonly affects tonsils, base of tongue and soft palate
  • Associated with HPV-16 and -18
  • Affects a younger age group
  • Significant increase over the past decade
  • Significantly better prognosis for HPV positive pts (up to 80% 5-year survival rate) than tonsillar cancer in non-HPV related cases
  • More sensitive to chemo and radiotherapy than SCC
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16
Q

Explain how candida is a risk factor for mouth cancer.

A
  • Clinical association between candidosis and oral cancer
  • Iron deficiency is associated with oral candidosis
  • Immunodeficiency is associated with oral candidosis

Chronic hyperplastic candidosis as a premalignant lesion:
- Leukoplakia so has premalignant potential
- Frequently clinically speckled (speckled leukoplakia are more often dysplastic or malignant than homogenous leukoplakia)

17
Q

Explain how irradiation is a risk factor for mouth cancer.

A
  • Strongly associated with cancer of the lower lip
  • More common in men than women
  • More common in people with outdoor occupations
  • Rare in races with darker skin
  • May be preceded by solar keratosis (actinic keratosis)
18
Q

Explain how diet and nutrition are risk factors for mouth cancer.

A
  • Emerging area of interest
  • Dietary deficiencies, particularly of vitamin A (and related carotenoids), vit C, vit E, iron, selenium, folate and other trace elements have been linked to increased risk of mouth cancer
  • Many studies have found that oral cancer patients have a history of low fruit and vegetable intake
  • Intervention studies where diets have been supplemented have some shown some beneficial effect on pre-malignant conditions and reducing the risk of a second oral cancer but further research is necessary
19
Q

Explain how dental factors may act as risk factors for mouth cancer.

A
  • Poor oral hygiene, sharp teeth, sharp restorations, ill fitting dentures have all been implicated in the aetiology of oral cancer
  • Many patients with oral cancer have poor dentitions
  • Difficult to determine a causal relationship, lots of confounding factors
  • Little real evidence for a causative association
  • However, mechanical irritation can act as a promotor in experimental carcinogenesis
20
Q

Explain how immunosuppresion can act as a risk factor for mouth cancer.

A
  • Increased incidence of mouth cancer in renal transplant patients
  • Possible increased incidence in those with HIV infection
  • Smoking, alcohol and iron deficiency suppress cell mediated immunity
21
Q

Explain the pathology of oral squamous cell carcinoma.

A
  • SCC is a malignant neoplasm derived from the stratified squamous epithelium of the oral mucosa
  • Histologically the tissues are well differentiated (obviously squmaous epithelium)
  • As SCC progresses, it invades the lamina propria, underlying tissues, muscles, salivary glands and bone
22
Q

Describe how oral SCC spreads.

A
  • Cancer invades nerves and spreads down the sheath
  • Invades the bone of the mandible and fills marrow spaces
  • Spreads through lymphatics and reaches nodes of neck

Aka perineural invasion, lymphatic permeation and vascular invasion

Blood borne metastases (to lung, liver, bone etc) tends to be a late phenomenon.

23
Q

Describe the histological pressentation of oral SCC.

A
  • Islands, strands and branching trabeculae of squamous cells
  • Budded architecture
  • Usually well-defined basal layer, bulk consists of prickle cells; often central keratinisation
  • Cells are clearly cytologically malignant: cellular and nuclear pleomorphism, increased mitoses, abnormal mitoses
  • Variable inflammatory reaction in surrounding fibrous stroma
  • Keratin present
24
Q

What are the 2 ways that oral SCC advances?

A
  • Cohesive: cancer invades on broad front (better prognosis)
  • Non-cohesive: separate islands of tumour extending along the advancing edge, poorer prognosis
25
Q

How is oral SCC managed?

A
  • Surgical excision
  • Non-surgical:
  • Radiotherapy +/- chemotherapy
  • Primary management following surgical excision, except for oropharyngeal which is primary radio/chemotherapy initially and then potentially surgery
26
Q

What is the 5 year survival rate for oral SCC?

A

56%

27
Q

What factors affect prognosis following oral SCC diagnosis?

A
  • Site (lip has best prognosis)
  • Size
  • Degree of differentiation
  • Lymph node metastasis (poorer prognosis if lymph node involvement already present at initial appointment)
  • Age of patient, co-morbidities, general level of fitness
28
Q

Is there a better prognosis for well differentiated or poorly differentiated oral SCC?

A

Well differentiated (grade I) = better 5 year survival rate

29
Q

What factors influence risk of metastasis?

A

Size, site and thickness of tumour dictates risk of metastasis.

Deeper penetration (thickness) of tumour = higher risk of metastasis and poorer survival.

30
Q

How is oral SCC staged?

A

TNM system
T = tumour size
N = lymph nodes
M = metastasis

BDS 3: Oral Diseases (13 decks)

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