Oral Cancer Clinical Presentation Flashcards

1
Q

Clinical presentation of early, low stage oral squamous carcinoma

A
  • red patch
  • speckled patch
  • soft or minimally firm
  • flat or slightly depressed
  • superficially non-healing ulcer
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2
Q

Clinical presentation of established carcinoma (high stage or late)

A
  • Indurated (firm and hard as a result of inflammation, fibrosis and infiltration of tissues)
  • ulcerated
  • rolled ulcer margins
  • nerve pain
  • paraesthesia or anaesthesia
  • loose teeth
  • bone loss
  • pain
  • reduced mobility of tissue/tongue
  • spontaneous bleeding
  • non healing tooth socket
  • palpable lymph node in neck
  • may find enlarged cervical lymph nodes
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3
Q

Common sites of oral cancer

A
  • Tongue is most frequently affected particularly lateral borders and ventral tongue
  • FOM and lingual aspect of alveolus and retromolar region
  • Forms a U-shaped area extending back to oropharynx (possibly due to pooling of carcinogens in saliva)
  • Also: buccal mucosa, soft palate, lip
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4
Q

Less common sites of oral cancer

A
  • Gingivae
  • Dorsal tongue
  • Hard palate
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5
Q

When does metastasis of carcinomas of the tongue occur and what route does it take?

A
  • Carcinomas of the tongue only have to invade 1cm before they enter muscle
  • Unpredictable spread; growth is directed along muscle bundles which radiate in all directions
  • Metastases at an early stage
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6
Q

When does metastasis of carcinomas of the FOM occur and what route does it take?

A
  • Spread laterally producing broad superficial tumours
  • Treatment is difficult
  • Poor prognosis
  • Often poorly differentiated, and metastases occur early
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7
Q

When does metastasis of carcinomas in the retromolar region occur and what route does it take?

A
  • May spread to underlying bone, medial to the ramus and pharynx, laterally into the cheek or up to the tuberosity region and infratemporal fossa
  • Treatment is difficult
  • Half of cases present with metastasis
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8
Q

When does metastasis of carcinomas in the alveolar ridge and gingivae occur and why is diagnosis of gingivae carcinomas often delayed?

A
  • Tend to be well differentiated and more slowly growing than tongue carcinomas but erode bone at an earlier stage, making tx more complex
  • Gingival carcinoma often delayed diagnosis, being mistaken for inflammatory periodontal disease or denture trauma
  • Important not to extract teeth adjacent to such a carcinoma as it allows carcinoma to spread into medullary cavity
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9
Q

How does the carcinoma on the buccal mucosa spread?

A
  • Erode the soft tissue and eventually penetrate through to skin
  • Some are associated with betal quid chewing
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10
Q

What are the symptoms of carcinomas

A
  • Pain considered little value in dx
  • Early carcinoma is often painless, but can experience burning or sharp stinging pain localised to carcinoma (possibly associated with ulceration)
  • Pain increases with carcinoma size and is typically severe only in the late stages (can get referred pain to ear)
  • Involved nerves produce neuropathic pain, paraesthesia or anaesthesia in that nerves distribution
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11
Q

What is the pathology of SCC: how do the epithelial cells grow into the lamina propria

A

Invasion:

  • Cells become spindle shaped and motile
  • They induce surrounding fibroblasts and endothelial cells to produce fibrous tissue that is easy to migrate through (tumour stroma)
  • They induce growth of new vessels (angiogenesis) to supply the increased nutrient requirements of the malignant cells
  • Lesion appears red clinically
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12
Q

How to cells with metastatic ability emerge from SCC

A
  • Each carcinoma comprises many genetically different clones of cells
  • Each clone can only survive with nutrients or signals from its neighbouring cells
  • With time and continuous proliferation of the genetically damaged cells, a diverse population of clones of cells develops with different properties
  • Eventually, a clone with metastatic ability emerges
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13
Q

What are the histological features of SCC and how are SCCs graded? Which grade has the better prognosis and what is the exception?

A
  • Features of malignancy: large and irregularly shaped nuclei, darkly stained nuclei, abnormal mitosis
  • SCC graded according to its degree of differentiation; the degree to which the malignant cells differentiate to form prickle cells and keratin (poorly differentiated show little evidence of prickle cell differentiation or keratinisation)
  • Poorly differentiated carcinomas are more likely to metastasise and carry a poorer prognosis (exception is HPV carcinoma which is poorly differentiated but is responsive to tx unless untreated which makes it aggressive and metastasise early)
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14
Q

How do carcinomas spread and how does this affect the prognosis

A
  • Spread is by direct invasion of surrounding tissues and by lymphatic metastasis
  • Prognosis deteriorates sharply with local spread and nodal involvement
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15
Q

How do carcinomas spread locally on a cellular level?

A
  • Invading cells grow into the tissues by direct extension
  • Poorly differentiated carcinomas, single cells and small clusters of cells detach along invasive front (discohesive invasive front) - higher risk of metastasis than cohesive front
  • Aggressive carcinomas show perineurial infiltration or vascular invasion (vascular invasion more likely to metastasise)
  • Tumour cells invade and eventually destroy all tissues (muscle fat nerves and bone).
  • Induces resorption of bone until it can invade medullary cavity
  • Invading cancer cells excite and inflammatory and immune reaction and become surrounded by lymphocytes and plasma cells which kill the carcinoma cells but provides no significant protection
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16
Q

Which two methods do carcinomas metastasise (distant spread)?

A
  1. Lymphatic metastasis to regional lymph nodes is most likely form of distant spread
  2. Bloodstream metastasis (uncommon)
    - mainly after tx
    - develop most frequently in the lungs, followed by liver and bone
17
Q

How does lymphatic metastasis occur? What is the normal path of metastasis?

A
  • Clones of cells in the tumour eventually acquire ability to migrate, penetrate lymphatics, survive as single cells during transit, lodge in a lymph node and proliferate to form a metastasis
  • Specific sites of metastasis depend on drainage of tumour site, but submandibular and jugludigastric nodes are most freq affected
  • Metastases develop progressively down the jugular lymphatic chain, reaching level IV supraclavicular lymph nodes
18
Q

How can lymphatic metastasis present clinically and why?

A
  • Metastatic carcinoma is initially limited to the affected node but then grows through the capsule into the tissues of the neck (Excision is then difficult, thus reducing chances of survival)
  • Forms a hard mass when small,
  • In larger masses the central area becomes necrotic and the centre may then break down so becomes cystic and fluctuant
19
Q

Features that suggest poorer prognosis

A
  • Pattern of invasion
    1. small islands that spread diffusely with smaller nests has poorer prognosis
    2. more cohesive and well demarcated with cells joining together = better prognosis
  • Invasion of lymphatics and blood capillaries
    1. Lymph-vascular invasion has a poorer prognosis
    2. Extra-capsular spread outside of lymph nodes further worsens prognosis
  • Infiltration along nerves = less likely to be excised and more likely to recur
  • Invasion of bone
  • Spread to neck