Oral Biology & Pathology Flashcards

What is the pathogenesis of ANUG (acute necrotising ulcerative gingivitis)?

Answer: Polymicrobial infection dominated by spirochaetes and fusiform bacteria (Treponema, Fusobacterium) causing necrosis of interdental papillae in immunocompromised or stressed patients

ANUG is characterised by painful necrosis of interdental papillae with punched-out crater formation. It is caused by synergistic anaerobic bacterial infection (spirochaetes, Fusobacterium, Prevotella) in predisposed individuals (stress, smoking, malnutrition, HIV).

What is the clinical feature that distinguishes an aphthous ulcer from a herpetic ulcer?

Answer: Aphthous ulcers are solitary/few, non-keratinised mucosa, no vesicle stage, no systemic viral features; herpes causes clusters from vesicles, initially on keratinised mucosa, with systemic features in primary infection

Aphthous ulcers are non-viral, occur on non-keratinised mucosa (buccal, labial, floor of mouth), no preceding vesicle, and no systemic illness. Herpetic ulcers arise from vesicles, affect keratinised/non-keratinised mucosa, and have viral prodromal features.

What is 'taurodontism' and with which syndromes is it associated?

Answer: Enlarged pulp chambers with apical displacement of the root furcation (bull-tooth morphology) — associated with Klinefelter's syndrome, Down's syndrome, and tricho-dento-osseous syndrome

Taurodontism features enlarged pulp chambers with the furcation displaced apically. It is seen in isolation and in association with Klinefelter's syndrome, Down's syndrome, and tricho-dento-osseous syndrome. Important in endodontic treatment planning.

What does IL-1β (interleukin-1 beta) do in periodontal disease?

Answer: A pro-inflammatory cytokine produced by macrophages that stimulates bone resorption (via RANKL pathway) and collagenase production — a key mediator of periodontal tissue destruction

IL-1β is a pivotal pro-inflammatory cytokine in periodontitis. It stimulates osteoclast activity through RANKL upregulation causing bone loss, promotes collagenase (MMP) production destroying collagen, and perpetuates the inflammatory cycle.

What is the oral manifestation of Stevens-Johnson syndrome relevant to dentistry?

Answer: Severe mucositis with haemorrhagic crusting of lips, widespread oral ulceration, and target lesions on skin — potentially triggered by drugs (e.g., carbamazepine, allopurinol) or infections

Stevens-Johnson syndrome (severe form of erythema multiforme) presents with extensive haemorrhagic lip crusting, painful widespread oral ulceration, and skin/ocular involvement. Drug triggers include AEDs, antibiotics, and allopurinol.