MJDF Oral & Dental Pathology 3 — Questions and Answers
Question 1: What is the most common cause of a periapical abscess?
- Bacterial infection of the pulp due to deep caries causing pulp necrosis (Correct answer)
- Periodontal disease alone
- Trauma without pulp necrosis
- Iatrogenic root perforation
Correct answer: Bacterial infection of the pulp due to deep caries causing pulp necrosis
Periapical abscess most commonly results from bacterial infection of a necrotic pulp (secondary to deep caries), spreading through the apical foramen to cause periapical inflammation and pus formation.
Question 2: What differentiates a true cyst from a pseudocyst histologically?
- A true cyst has an epithelial lining; a pseudocyst lacks epithelial lining (Correct answer)
- Size difference only
- Location in the jaw
- Type of fluid content
Correct answer: A true cyst has an epithelial lining; a pseudocyst lacks epithelial lining
By definition, a true cyst has a cavity lined by epithelium surrounded by connective tissue; a pseudocyst (e.g., aneurysmal bone cyst) lacks this epithelial lining.
Question 3: Which stain is used to identify Candida hyphae in a mucosal biopsy?
- Periodic acid-Schiff (PAS) stain (Correct answer)
- Haematoxylin and eosin only
- Ziehl-Neelsen
- Gram stain
Correct answer: Periodic acid-Schiff (PAS) stain
PAS stain highlights the polysaccharide-rich cell walls of Candida hyphae and pseudohyphae in a bright magenta colour, making it the standard histochemical stain for fungal identification in tissue sections.
Question 4: What is the histological difference between hyperkeratosis and dysplasia in oral leukoplakia?
- Hyperkeratosis is excess keratin without cellular atypia; dysplasia involves cellular and architectural atypia (Correct answer)
- They are identical
- Dysplasia always shows hyperkeratosis
- Hyperkeratosis always progresses to dysplasia
Correct answer: Hyperkeratosis is excess keratin without cellular atypia; dysplasia involves cellular and architectural atypia
Hyperkeratosis is increased keratin production without cytological atypia and has a lower malignant potential; dysplasia involves both architectural and cellular abnormalities and is the true precancerous change.
Question 5: What is the mechanism of bone resorption in a dentigerous cyst?
- Prostaglandins and cytokines (IL-1, TNF) from the cyst lining stimulate osteoclast activity (Correct answer)
- Direct pressure alone
- Infection causing bone loss
- Cyst fluid pH causing demineralisation
Correct answer: Prostaglandins and cytokines (IL-1, TNF) from the cyst lining stimulate osteoclast activity
Cyst expansion is driven by osmotic pressure and prostaglandins/cytokines released by the cyst lining, which stimulate osteoclasts at the bone-cyst interface to resorb alveolar bone.
Question 6: What is the recurrence rate of an odontogenic keratocyst compared to a dentigerous cyst?
- OKC has a high recurrence rate (25–60%); dentigerous cyst rarely recurs after enucleation (Correct answer)
- Both have equal recurrence
- Dentigerous cysts recur more often
- Neither recurs after enucleation
Correct answer: OKC has a high recurrence rate (25–60%); dentigerous cyst rarely recurs after enucleation
OKCs have a high recurrence rate (25–60%) due to satellite cysts, the origin in rests of dental lamina, and thin fragile epithelium prone to tearing during enucleation, leaving remnants behind.
What is the most common cause of a periapical abscess?