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OKC Flashcards

1
Q

What is the origin of OKC?

A

Derived from dental lamina remnants.

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2
Q

How does the WHO classify OKC in 2017?

A

As an odontogenic cyst (previously a neoplasm in 2005 WHO classification).

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3
Q

What genetic mutation is linked to OKC?

A

PTCH1 gene mutation (Hedgehog signaling pathway).

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4
Q

Which syndrome is associated with multiple OKCs?

A

Nevoid Basal Cell Carcinoma Syndrome (NBCCS) (Gorlin Syndrome).

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5
Q

What is the most common site for OKC?

A

Posterior mandible (angle and ramus region).

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6
Q

What is the usual age range for OKC?

A

2nd–4th decades (younger in syndromic cases).

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7
Q

Describe the typical radiographic appearance of OKC.

A

Unilocular or multilocular radiolucency with well-defined, scalloped borders, minimal expansion.

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8
Q

Does OKC commonly cause root resorption?

A

Less common compared to dentigerous cysts.

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9
Q

Describe the epithelial lining of OKC.

A

Thin, 6-8 cell thick parakeratinized stratified squamous epithelium with palisaded basal cells.

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10
Q

What is a key microscopic feature responsible for OKC recurrence?

A

Daughter cysts and satellite cells in the fibrous wall.

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11
Q

What is the first-line treatment for OKC?

A

Enucleation + curettage, sometimes with Carnoy’s solution.

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12
Q

What is the recurrence rate of OKC?

A

25–60% (higher than other odontogenic cysts).

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13
Q

Why is long-term follow-up important for OKC?

A

Recurrence can occur 5–10 years post-treatment.

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14
Q

What are three key features that differentiate OKC from other odontogenic cysts?

A

a. High recurrence rate
b. Minimal buccal expansion
c. Association with NBCCS (Gorlin Syndrome)

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15
Q

Why is OKC considered aggressive?

A

a. High recurrence (25-60%)
b. Locally invasive growth pattern
c. Tendency to perforate bone

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16
Q

Which radiographic feature helps distinguish OKC from ameloblastoma?

A

OKC usually has scalloped borders and minimal expansion, while ameloblastoma tends to show cortical expansion.

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17
Q

What is the most common location for OKC?

A

Mandibular ramus and posterior body.

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18
Q

What type of keratinization is seen in OKC?

A

Parakeratinization (typically), sometimes orthokeratinized.

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19
Q

How do the basal cells appear histologically in OKC?

A

Palisaded, hyperchromatic, and columnar.

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20
Q

What is the significance of satellite (daughter) cysts in OKC?

A

a. Increase recurrence risk
b. Contribute to difficulty in complete removal
c. Present more in syndromic cases

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21
Q

How does the lining of an OKC differ from a dentigerous cyst?

A

a. OKC: Thin, uniform 6-8 cell layer, parakeratinized
b. Dentigerous cyst: Thicker, non-keratinized, inflamed epithelium

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22
Q

What syndrome is associated with multiple OKCs?

A

Nevoid Basal Cell Carcinoma Syndrome (NBCCS/Gorlin Syndrome).

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23
Q

What are key systemic features of NBCCS?

A

a. Multiple OKCs
b. Bifid ribs
c. Palmar and plantar pits
d. Basal cell carcinomas
e. Calcification of falx cerebri

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24
Q

At what age do OKCs present earlier—syndromic or non-syndromic cases?

A

Syndromic cases (often in childhood/teens), non-syndromic cases appear in the 2nd-4th decade.

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25
What genetic mutation is responsible for NBCCS?
PTCH1 mutation (tumor suppressor gene, chromosome 9q22.3).
26
How does an OKC typically appear on a panoramic radiograph?
a. Unilocular or multilocular radiolucency b. Well-defined corticated borders c. Scalloped margins d. Minimal or no expansion
27
What feature of OKC can mimic dentigerous cysts?
Association with an impacted tooth (especially the mandibular third molar).
28
What radiographic sign suggests an aggressive OKC?
Perforation of the cortical bone.
29
What imaging modality is best to assess soft tissue extension of OKC?
CBCT or MRI (MRI for detecting soft tissue involvement).
30
What is the first-line treatment for small OKCs?
Enucleation + curettage.
31
What solution is often used to reduce OKC recurrence?
Carnoy’s solution (fixative to eliminate residual cells).
32
When is marsupialization preferred over enucleation?
a. Large OKCs b. Lesions close to vital structures (e.g., inferior alveolar nerve)
33
Which surgical approach has the lowest recurrence rate?
Resection with margins (used for aggressive or recurrent cases).
34
Why is follow-up necessary for OKC cases?
Recurrence can occur 5-10 years post-surgery.
35
What percentage of OKCs recur after simple enucleation?
Up to 60%.
36
Which type of OKC has a lower recurrence rate: parakeratinized or orthokeratinized?
Orthokeratinized (less aggressive, lower recurrence rate).
37
Can OKC undergo malignant transformation?
Rarely, but has been linked to squamous cell carcinoma (SCC).
38
What is the typical age range for non-syndromic OKC cases?
20-40 years old (peak in 2nd-4th decade).
39
What gender is more commonly affected by OKC?
Males > Females (slight male predilection).
40
What percentage of jaw cysts are OKCs?
About 10-15% of all odontogenic cysts.
41
What embryologic tissue does OKC originate from?
Remnants of the dental lamina.
42
Which syndrome must always be ruled out in a patient with multiple OKCs?
Nevoid Basal Cell Carcinoma Syndrome (NBCCS).
43
Why is OKC considered a cystic neoplasm by some researchers?
Aggressive, infiltrative growth; High recurrence rate; Genetic mutations (PTCH1) associated with neoplasia
44
How does OKC expand compared to other odontogenic cysts?
Grows along the medullary bone with minimal buccal-lingual expansion.
45
What is the primary mode of spread in OKC?
Anteroposterior spread within the cancellous bone.
46
What key feature differentiates OKC from ameloblastoma in terms of cortical perforation?
OKC tends to perforate earlier despite minimal expansion.
47
What is the doubling time of OKC epithelial cells compared to other cysts?
Faster than radicular or dentigerous cysts, leading to its aggressive nature.
48
What is the most common radiographic pattern of OKC?
Unilocular, well-defined radiolucency with scalloped borders.
49
When does OKC present as a multilocular lesion?
a. Larger lesions b. When located in the posterior mandible c. In recurrent cases.
50
What feature of OKC can mimic an odontogenic myxoma?
Multilocular 'soap bubble' or 'honeycomb' appearance.
51
How does OKC behave when associated with an impacted tooth?
Mimics a dentigerous cyst but with a more irregular border.
52
What is a key radiographic sign of aggressive OKC?
Cortical bone perforation and root resorption.
53
Name three lesions that resemble OKC radiographically.
1. Ameloblastoma (multilocular, but more expansion) 2. Dentigerous cyst (if OKC is pericoronal) 3. Odontogenic myxoma (honeycomb pattern)
54
What histopathologic feature distinguishes OKC from unicystic ameloblastoma?
OKC has a uniform parakeratinized epithelial lining, whereas unicystic ameloblastoma has ameloblastic islands.
55
What key histologic feature differentiates OKC from an orthokeratinized odontogenic cyst (OOC)?
OKC is parakeratinized with basal palisading; OOC is orthokeratinized without palisading.
56
What feature can help distinguish OKC from a radicular cyst?
Radicular cysts show chronic inflammation, while OKCs have a thin, uniform epithelium with minimal inflammation.
57
Which condition should be suspected if OKC is bilateral?
Nevoid Basal Cell Carcinoma Syndrome (NBCCS).
58
What are the primary treatment options for OKC?
a. Small OKC: Enucleation with curettage b. Large OKC: Marsupialization followed by enucleation c. Aggressive/recurrent cases: Resection
59
What adjunctive therapy is commonly used to prevent recurrence?
Carnoy’s solution (fixative) or liquid nitrogen cryotherapy.
60
What is the recurrence rate of OKC after simple enucleation?
25-60%.
61
Which surgical technique has the lowest recurrence rate?
Resection with 5 mm margins.
62
How often should post-surgical follow-up be performed for OKC?
Every 6 months for at least 5 years due to late recurrence.
63
What genetic mutation is linked to OKC?
PTCH1 (tumor suppressor gene on chromosome 9q22.3).
64
How does PTCH1 mutation contribute to OKC pathogenesis?
Leads to uncontrolled Hedgehog signaling, promoting aggressive growth.
65
What syndrome is caused by a germline PTCH1 mutation?
Nevoid Basal Cell Carcinoma Syndrome (NBCCS).
66
How can PTCH1 mutation be detected?
Genetic testing (PCR, sequencing).
67
What is the significance of Ki-67 staining in OKC?
High Ki-67 index indicates high proliferative activity and aggressive behavior.

Pathology (1 decks)

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