Oral Pathology/ Radiology Flashcards

1
Q

Which odontogenic epithelial cysts have their epithelial lining derived from:

  1. Rests of Malassez?
  2. Reduced Enamel Epithelium
  3. Remnants of Dental Lamina?

What is the site for 1 & 2?

A
  1. Radicular & Residual cysts (Inflammatory)
  2. Dentigerous & Eruptions cysts
  3. All other developmental cysts (OK, LPC, GCoA & GOC)

Rests of Malassez derived from proliferation of Remnants of Hertwig’s Root Sheath.
Site = Throughout PDL & trapped within the periapical granuloma

REE Site = On top of enamel (cyst formation due to split between REE & underlying enamel - usually at CEJ where tightest)

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2
Q

What are the 3 main pathogenesis stages/ requirements for cyst formation & growth?

A
  1. Source of Epithelium
  2. Stimulus for epithelial cell proliferation & cavitation
  3. Mechanism(s) for continued cyst growth & accompanying bone resorption
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3
Q

What is the main stimulus for epithelial cell proliferation in cyst formation?

What is an alternative mechanism?

A

Inflammation

Inflammatory cells secrete cytokines (IL-1, IL-6, TNF & GF) inducing Epidermal GF & Transforming GF Beta

Alternatively, possibly Genetic defects in tumour suppressor gene (e.g. Gorlin Goltz Syndrome)

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4
Q

What are the 3 mechanisms for continued cyst growth?

A
  1. Internal Hydraulic Pressure
  2. Bone Resorption
  3. Epithelial Proliferation (particularly important in Odontogenic Keratocyst)
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5
Q

What are 5 clinical features of cysts?

A
  1. Swelling
  2. Pain
  3. Displacement or loosening of teeth
  4. Egg-shell crackling (breaking of periosteal bone overlying cyst)
  5. Fluctuance (if cyst lies within soft tissue or perforates overlying bone)
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6
Q

What 5 things do you want to assess for on a cyst?

A
  1. Location
  2. Size & Locularity
  3. Shape
  4. Margin
  5. Effect on adjacent structures
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7
Q

What are the main indications for:

  1. Aspiration
  2. Excisional Biopsy
  3. Internal Biopsy
A
  1. Looking for blood, infection (e.g. pus) or keratin (by smear onto cytology slide or soluble protein estimation)
  2. Small lesion amenable for excision
  3. Large extensive lesion or reason to believe not a simple cyst
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8
Q

When completing aspiration for an odontogenic keratocyst - Is the soluble protein estimation high or low?

A

LOW soluble protein (less than 4g/100ml)

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9
Q

Cyst margins are often well defined & well-corticated, what are 2 exceptions to this?

A
  1. Solitary bone cyst (NON-corticated)
  2. Infections (loss of well defined margins)
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10
Q

Most cysts grow through hydrostatic mechanism (interna hydraulic pressure), what are 2 exceptions to this?

A
  1. Odontogenic Keratocyst - primarily via Epithelial proliferation
  2. Solitary Bone Cyst - Bone resorption
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11
Q

Explain the 3 cyst growth mechanisms…

A

1) Internal Hydraulic Pressure

  • Protein in cyst wall acts as semi-membrane
  • Fluid accumulation in cyst lumen → Positive pressure in cyst → Bone resorption from outwards pressure

2) Bone Resorption

​Cyst secretion of pro-infammatory cytokines, TNF & PGE2 (fibroblasts) → Bone resorption

3) Epithelial Proliferation

Growth factors (e.g. EGF & TGFß) → Pronounced cyst epithelium proliferation

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12
Q

What are 3 key histological features in soft tissue cysts?

A
  1. Epithelial lining
  2. Mucin (positive purple stain)
  3. Lymphoid stroma
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13
Q

What are 6 cysts of soft tissues in the mouth, face and neck?

A
  1. Mucous Extravasation Cyst (minor SG)
  2. Mucous Retention Cyst (SG cyst)
  3. Ranula (SG cyst)
  4. Lymphoepithelial (Branchial) Cyst
  5. Dermoid & Epidermoid Cyst
  6. Thyroglossal Cyst
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14
Q

Which cyst might you suspect in a:

  1. Vital tooth?
  2. Non-vital tooth?
A
  1. Vital = Lateral Periodontal Cyst
  2. Non-Vital = Residual Cyst
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15
Q

What cyst histologies would you expect to see the following in?

  1. Cholesterol Clefts
  2. Mucous Metaplasia
  3. Hyaline Bodies
  4. Flat basement membrane
A
  1. Radicular cysts & Dentigerous (in lumen)
  2. Dentigerous cysts
  3. Odontogenic cysts (Radicular most often)
  4. ALL Developmental Odontogenic Cysts!
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16
Q

In histology of a Radicular cyst, what 5 things does the lumen contain?

A
  1. Pale pink serous exudate
  2. Cholesterol clefts
  3. Inflammatory cells
  4. Macrophages
  5. Desquamated epithelial cells
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17
Q

Name 4 inflammatory bone disorders (that u need to know for path)…

A
  1. Dry Socket (Localised Alveolar Osteitis)
  2. Osteomyelitis
  3. Osteoradionecrosis
  4. Medication-related Osteonecrosis (MRONJ)
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18
Q

Name 4 fibro-osseous bone disorders (that you need to know for oral path)…

Which one is neoplastic?

A
  1. Fibrous Dysplasia
  2. Ossifying/Cemento-Ossifying Fibroma (COF) - NEOPLASTIC
  3. Cemento-Osseous Dysplasia
  4. Paget’s disease
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19
Q

What is the definition of a:

  1. Premalignant Lesion? (Give 2 examples)
  2. Premalignant Condition?
A
  1. Premalignant Lesion = Morphologically altered tissue where cancer is more likely to occur than in “normal” tissue counterpart
    E.g. Leukoplakia (Homogenous/Non-Homogenous) or Erythroplakia
  2. ​Premalignant Condition = Generalised state associated with significantly increased malignancy risk
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20
Q

What are 5 Premalignant Conditions?

A
  1. Lichen Planus (~0.2-5%)
  2. Syphilis
  3. Submucus Fibrosis
  4. Patterson-Kelly / Plummer-Vinson Syndrome (Sideropenic Dysphagia)
  5. Actinic Keratosis
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21
Q

What is seen histologically in Leukoplakia? (6)

A
  • Hyper- or Para-keratosis (→ white appearance)
  • Variable hyperplasia and acanthosis (increased prickle cell layer thickness)
  • Atrophy
  • Inflammation
  • +/- Candidal Hyphae (30%)
  • +/- Dysplasia
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22
Q

What 3 things occur in acanthosis?

A
  • Increased number of cells → Thickening in prickle cell layer
  • Broadening of rete ridges
  • Thicker epithelium
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23
Q

What are 3 main aetiological factors associated with pre-malignant lesions?

(HINT: think SH & Infectionsx2)

A
  1. Tobacco (Betel/Areca or Smoking)
    * Associated with 90% of Leukoplakias*
  2. Candida
    * Seen in 30% of Leukoplakias*
  3. HPV (HPV16 + 18)
24
Q

30% of Leukoplakias are associated with Candida infection,

  • How does it often appear clinically (site and shape/colour)?
  • How can it be treated/managed?
A

Appearance:

  • Often corner of mouth
  • Speckled or Nodular appearance - Dysplasia

Treatment:

  • Lesion may regress with systemic candida tx:
    6 weeks of Fluconazole (often resistant to therapy)
  • Biopsy - review based on degree of dysplasia
    (Increased dysplasia = Increased malignancy risk)
25
Q

What is the best measure of malignancy potential in a pre-malignant lesion?

What pre-malignant lesions are therefore often the most high risk?

A

The degree of DYSPLASIA on biopsy

Higher dysplasia = Higher malignancy risk

ERYTHROPLAKIA (over 90% = severe dysplasia or carcinoma on 1st biopsy)

26
Q

What are the 4 main sites affected by Leukoplakia? (include %)

A
  1. Buccal mucosa (25%)
  2. Mandibular gingivae (20%)
  3. Tongue (10%)
  4. Floor of mouth (10%)
27
Q

What is the main gender and age group Leukoplakia affects?

What is the MAIN risk factor (associated with 90% cases)?

A

Middle aged (increased prevalence with age) MALES

Main risk factor = Tobacco/Areca nut use

28
Q

What are the 2 main forms of leukoplakia?

How do they appear and what is their malignant potential (%)?

A

1. HOMOGENOUS (~0%)

  • White
  • Uniform + smooth OR Wrinkled (shallow cracks)

2. NON-HOMOGENOUS (~26%)

  • Predominantly white OR white/red (“Speckled Erythroleukoplakia”)
  • Irregularly flat + outward growing:
    Nodular = raised, round, red/white outgrowths
    Exophytic = blunt or sharp outgrowths
29
Q

How does the management differ in Leukoplakia vs. Erythroplakia?

A

Erythroplakia = MUCH more high risk malignancy potential (~80%)

  • URGENT OMF referrel
  • Hospital = Biopsy + excise (tx based on findings)

Leukoplakia

  • Refer to OMF - URGENT referral if suspicious (e.g. speckled red/white, nodular/rasied, older pt or “gutter” site)
  • Hospital = Biopsy
30
Q

In a biopsy, what 2 types of tissue do you want to obtain?

Based on lesion size, when would you do an:

  1. Incisional biopsy?
  2. Excisional biopsy?
A

The suspicious affected area AND normal tissue (so edge often best)

  1. Incision = larger lesion
  2. Excisional = smaller lesion
31
Q

Leukoplakia is a diagnosis of exclusion, what are 9 other differentials for a white patch lesion?

A
  • Frictional keratosis
  • Candida
  • Lichen Planus
  • Lichenoid Reaction
  • (Discoid) Lupus Erythematosis
  • Graft vs. Host Disease
  • Epithelial Dysplasia
  • Fordyce’s Spots (normal anatomy - enlarged glands)
  • Smokers Keratosis (seen on palate)
32
Q

What is erythroleukoplakia

What 3 things are observed on its histology?

Why do we need to refer this urgently?

A

“Pre-malignant, bright red, velvety plaque which cannot be characterised as any other condition” - diagnosis of exclusion

Histology:

  • Inflammation
  • Atrophy
  • DYSPLASIA !

Urgent referral because it is extremely high risk, ~80% malignancy potential

33
Q

What social history factor is “Submucus Fibrosis” closesly linked with?

What 2 features (complications) might the patient present with?

A

Paan/Betel Chewers!

  1. Trismus (difficulty opening)
  2. Dysphagia (difficulty swallowing)
34
Q

Sideropenic Dysphagia = “Plummer-Vinson” or “Patterson-Kelly” Syndrome

It is a PRE-MALIGNANT condition for Pharyngeal + Oral Cancer… What are the main presentations of the patient? (5)

(HINT: 1 in name and think about age/person)

A
  • Middle-aged female
  • Iron-deficient anaemia
  • Glossitis
  • Mucosa atrophy
  • Post-cricoid oesophageal web (mechanical block) → Dysphagea (difficulty swallowing)
35
Q

What are the 10 histological changes seen in Dysplasia?

(Dysplasia Looks Like Mini People Having Lunch In Poplar Market)

A
  1. Drop-shaped rete ridges
  2. Loss of cell adhesion
  3. Loss of epithelial stratification
  4. Mitosis in prickle cell layer
  5. Pleomorphism (nucelar and cellular)
  6. Hyperchromatism (nuclear - increased DNA)
  7. Loss of basal cell polarity
  8. Increase in nuclear to cytoplasm ratio
  9. Premature keratinisation in prickle cell layer
  10. Mitosis = Increased number and abnormality
36
Q

Whats the difference between (definition of):

  • Keratosis?
  • Hyperkeratosis?
  • Parakeratosis?
  • Orthokeratosis?
A

Keratosis = Keratinisation in normally non-keratinised epithelium

Hyperkeratosis = Increased keratin layer thickness

Parakeratosis = Flat, homogenous eosinophilic superficial cells BUT with pyknotic nuclei (dense and compact)

Orthokeratosis = Flat, anucleate superficial cells with homogenous eosinophilic cytoplasm

37
Q

Amount of dysplasia in a premalignant lesion is the best indicator for malignancy potential.

How can we grade dysplasia? (4 catagories none → severe)

A

NONE = Normal epithelial cells

MILD = Few epithelial cells in basal layer show atypia

MODERATE = Most cells in basal layer show atypia

SEVERE = Almost all cells show atypia (but no invasion into underlying tissues)

38
Q

How do we manage pre-malignant lesions based on the outcome of their dysplasia?

  • Mild/Moderate?
  • Moderate?
  • Severe?
A
39
Q

What are 8 aetiologies/risk factors for oral cancer?

A
  1. Tobacco (smoking)
  2. Tobacco (smokeless) - Betel/Paan
  3. Alcohol
  4. Malnutrition
  5. Viral (HPV16/18 and EBV)
  6. Bacterial (Syphilis → Premalignant lesion on tongue)
  7. Fungal (Candidal Leukoplakia = premaligant)
  8. Congenital (e.g. Falconi)
40
Q

What are 3 ways in which malnutrition can be a risk factor for oral cancer?

A
  1. Iron deficiency → Muscle atrophy → Increased mucosa permeability to carcinogens
  2. Vit A deficiency → Neoplasia
  3. Plummer-Vinson/Patterson-Kelly Syndrome = Iron deficiency and Oropharyngeal Carcinoma
41
Q

What is the relative risk in malignancy with smoking alone and smoking with drinking alcohol?

A

Smoking = x2 risk

Smoking AND drinking = x6 risk !

42
Q

What is the carcinogen in:

  1. Smoked Tobacco?
  2. Smokeless Tobacco (Paan/Betel)?
A
  1. Benzopyrenes (formed from salivary gland breakdown of polycyclic hydrocarbons)
  2. Nitrosonornicotine
43
Q

Is the malignancy risk higher for Paan containing tobacco or without tobacco?

A

With tobacco = x30 risk (higher)

Without tobacco = x3 risk

(N.B. Smoking tobacco = x2)

44
Q

What is the classic presentation (sentence with 7 buzz words) of oral cancer?

A

Persistent, non-healing ulcer which is indurated (firm), often painless and has raised, rolled borders.

45
Q

What are 6 features of advanced oral cancer?

A
  • Painful (initially painless)
  • Bleeding/Haemorrhage
  • Paraesthesia
  • Fixed
  • Pathological fracture risk
  • Dysphagia
46
Q

What are 7 features of a SUSPICIOUS (CANCEROUS) lesion?

(HINT: think site, size, shape, colour, surface, surroundings and history)

A
  1. “Gutter area” (tongue, FoM..)
  2. Large
  3. Raised, well-demarcated, non-healing ulcer
  4. Speckled or Red
  5. Indurated
  6. Destruction or fixation to surroundings
  7. History: RFs, older pt, pre-malignant lesion or loss of function
47
Q

What is:

  • 1 regional
  • 3 systemic

clinical features of oral cancer?

A

Regional:

Lymphadenopathy

(Early = Painless and palpable, Later = Fixed and if Infected = Painful and movable)

Systemic:

  • Weight loss (unexplained)
  • Weakness
  • Secondary features from distant mets (e.g. haemoptysis if lungs affected)
48
Q

What are the 3 main distant metastatic spread sites of OSCC?

A

3 L’s

  1. LNs
  2. Lungs
  3. Liver
49
Q

What are the 4 treatment options for OSSC?

A
  1. Surgery +/- radiotherapy
  2. Radiotherapy
  3. Chemotherapy
  4. Palliative care
50
Q

What are the “3R’s” of surgery for OSCC?

What are 4 side effects of the last R?

A

Resection → Reconstruction → Rehabilitation

Rehabilitation:

  • Difficulty speaking
  • Difficulty swallowing
  • Difficulty eating
  • Oral/palatal competency issues
51
Q

What are 10 local features of OSCC (seen in the mouth)?

A
  • Red/white patches on oral mucosa
  • Leukoplakia, Speckled Leukoplakia or Erythroplakia*
  • Ulceration
  • Fungation (excess epithelial proliferation → outward growth)
  • Induration
  • Fixation to surrounding structures
  • Rolled borders
  • Bleeding
  • Painless (initially)
  • Loss of function (e.g. Dysphagia or change in voice)
  • Tooth mobility
52
Q

How is the mortality rate of an OSCC affected by:

  1. Site?
  2. Size?
  3. Stage (TMN)?
A
  1. Further forward (e.g. lip) = better prognosis (earlier detection)
  2. Larger and deeper = Worse prognosis
  3. Higher stage (1-4) = Worse prognosis
53
Q

What are 5 different special investigations for OSCC?

A
  1. Biopsy (Fine needle aspiration or Incisional)
  2. Radiographs (bony involvement)
  3. CT
  4. MRI
  5. PET scan
54
Q

What are the main histological features seen in OSCC? (2 but elaborate on 1)

A
  1. Epithelial cell atypia
  • Nuclear hyperchromatism
  • Nuclear and Cellular pleomorphism
  • Increased nuclear to cytoplasm ratio
  • Increased rate of mitosis
  • Mitosis abnormality
  1. Lymphocyte and Plasma cells
55
Q

As an alternative staging to TMN,

how can OSCC be staged (3 grades) by histology?

A
  1. Well-differentiated
    * Larger keratin islands (abundant keratin), less atypia and reduced mitosis*
  2. Moderately differentiated
  3. Poorly differentiated (WORST PROGNOSIS)
    * Smaller keratin islands, more atypia and more frequent mitosis.*
56
Q

After a diagnosis of OSSC, what is the role of the GDP:

  1. Pre RT treatment? (3)
  2. Post RT treatment? (3)
A

1) PRE

  • Restore any caries
  • Extract poor prognosis teeth (6+ weeks before tx starts)
  • Prevention! (High F paste, F rinse, F varnish)

2) POST

  • Prevention!! (Xerostomia so high caries risk)
  • Regular recall and maintenance (6 month xrays)
  • Refer any XLA (avoid)
57
Q

What are the:

  1. ACUTE (4)
  2. CHRONIC (90+ days after) (6)

side effects of Radiotherapy (for OSCC)?

A

1. ACUTE

  • Mucositis → Pain and Dyspahgia
  • Taste changes
  • Weight loss
  • Fatigue

2. CHRONIC

  • Xerostomia
  • ORN (and increased pathological # risk)
  • Oedema
  • Atrophy
  • Fibrosis
  • Telangectasia