Membership of the Joint Dental Faculties (MJDF) Periodontology and Oral Medicine Flashcards

24 sample cards from the Periodontology and Oral Medicine deck

Sampled from the end of the deck, so these are different cards from the ones shown on the syllabus page.

1. What immunofluorescence patterns are seen in pemphigus vulgaris versus pemphigoid?

   Pemphigus vulgaris: direct immunofluorescence shows intercellular IgG and C3 in a 'fishnet'/'chicken-wire' pattern around keratinocytes. Pemphigoid: linear IgG and C3 deposition along the basement membrane zone. Biopsy for DIF should include perilesional tissue.

2. Describe the clinical presentation of primary herpetic gingivostomatitis and its management.

   Caused by HSV-1 (primary infection), usually in children: fever, malaise, lymphadenopathy, and widespread painful vesicles that ulcerate on gingivae, tongue, lips, and mucosa, with markedly inflamed swollen gingivae. Management: supportive — fluids/hydration, soft diet, analgesia/antipyretics, chlorhexidine; aciclovir if severe, immunocompromised, or early presentation. Self-limiting (~10–14 days). The virus then becomes latent in the trigeminal ganglion.

3. What is herpes labialis and its triggers, and how do shingles and herpangina relate to oral viral infections?

   Herpes labialis ('cold sore') is reactivation of latent HSV-1 from the trigeminal ganglion, producing recurrent vesicles at the lip vermilion border; triggers include sunlight/UV, stress, illness, immunosuppression. Treated with topical aciclovir if caught in the prodrome. Herpes zoster (shingles, VZV reactivation) follows a trigeminal dermatome (unilateral, does not cross midline). Herpangina (Coxsackie A) causes vesicles/ulcers on the soft palate/fauces.

4. List the clinical forms of oral candidosis.

   Acute pseudomembranous (thrush — wipeable white plaques leaving an erythematous base); acute erythematous/atrophic (e.g. antibiotic sore mouth); chronic erythematous (denture stomatitis); chronic hyperplastic (candidal leukoplakia — non-wipeable, potentially malignant); plus Candida-associated angular cheilitis and median rhomboid glossitis.

5. What predisposing factors and treatment apply to oral candidosis (including denture stomatitis)?

   Predisposing factors: immunosuppression (HIV, steroids — including inhaled corticosteroids, chemotherapy), diabetes, broad-spectrum antibiotics, xerostomia, denture wearing/poor denture hygiene, iron/B12/folate deficiency, extremes of age. Treatment: address the cause, antifungals — topical nystatin or miconazole gel, or systemic fluconazole for resistant/extensive cases; for denture stomatitis emphasise denture hygiene, leave dentures out at night, and disinfect dentures.

6. List the major risk factors for oral squamous cell carcinoma.

   Tobacco (smoked and smokeless/chewing), alcohol (synergistic/multiplicative with tobacco), betel quid/areca nut (and paan), HPV (especially type 16, oropharyngeal), sunlight/UV (lip cancer), age >40, male sex, immunosuppression, poor diet, chronic immune/inflammatory conditions, and potentially malignant disorders (leukoplakia, erythroplakia, OSMF, lichen planus).

7. What are the high-risk intraoral sites for oral cancer and typical presenting features of an oral SCC?

   High-risk sites: lateral/ventral tongue and the floor of mouth ('coffin/horseshoe' area), also the retromolar region and soft palate complex. Features: non-healing ulcer >3 weeks, rolled/indurated everted edges, exophytic or fungating mass, red/white/speckled patch, fixation to underlying tissue, abnormal mobility of teeth, persistent pain/numbness, and cervical lymphadenopathy.

8. List the main oral potentially malignant disorders (OPMDs).

   Leukoplakia (esp. non-homogeneous/proliferative verrucous), erythroplakia, oral submucous fibrosis, oral lichen planus (erosive), actinic cheilitis, chronic hyperplastic candidosis, dyskeratosis congenita, and lupus-related lesions. Erythroplakia and proliferative verrucous leukoplakia carry the highest transformation risk.

9. What is oral submucous fibrosis — cause, features, and significance?

   A chronic progressive scarring condition caused chiefly by areca/betel nut chewing. Features: blanching and stiffening of the mucosa, fibrous bands, burning sensation, and progressive trismus/limited mouth opening. It is a potentially malignant disorder with a significant risk of transformation to SCC, and the fibrosis is largely irreversible.

10. What is the urgent suspected cancer (2-week-wait) referral pathway for suspected oral cancer in the UK?

    Any patient with features suggestive of oral cancer — an unexplained oral ulcer or red/white/speckled patch persisting >3 weeks, a persistent unexplained lump in the mouth or neck, or unexplained tooth mobility >3 weeks — should be referred urgently under the 2-week-wait (urgent suspected cancer) pathway to an oral/maxillofacial or head and neck specialist. NICE NG12 guidance underpins this.

11. What is the principle of biopsy site selection and technique for a suspicious oral lesion?

    Incisional biopsy is used for large/suspected malignant lesions (to obtain a representative sample including the most clinically suspicious area and a margin of adjacent tissue); excisional biopsy for small benign lesions. Avoid biopsying only necrotic/sloughy centre; include the lesion edge with normal tissue. Definitive surgical management of confirmed malignancy is led by the head and neck MDT after histological diagnosis and staging.

12. What staging system is used for oral cancer and what does it describe?

    The TNM system: T = primary tumour size/extent, N = regional (cervical) lymph node involvement, M = distant metastasis. These combine into overall stages I–IV, guiding prognosis and treatment (surgery, radiotherapy, chemotherapy) decided by the head and neck multidisciplinary team.

13. Define temporomandibular disorders (TMD) and list the cardinal clinical features.

    TMD is an umbrella term for musculoskeletal and neuromuscular conditions affecting the temporomandibular joint, masticatory muscles, and associated structures. Cardinal features (Okeson triad): pain in the muscles of mastication/preauricular region, joint sounds (clicking/crepitus), and limited or deviating mandibular movement. Often associated with parafunction (bruxism), stress, and trauma.

14. What is the first-line ('conservative/reversible') management of temporomandibular disorders?

    Conservative and reversible measures first: patient reassurance/education, soft diet, jaw rest, avoiding wide opening/parafunctional habits, masticatory muscle exercises and physiotherapy, heat, stress management, analgesia/NSAIDs, and a soft/stabilisation occlusal splint (bite guard). Irreversible treatments (occlusal adjustment, surgery) are reserved for refractory cases.

15. How does clicking due to anterior disc displacement with reduction differ from displacement without reduction?

    Disc displacement WITH reduction: the disc is displaced anteriorly but recaptures on opening, producing a click (often reciprocal clicks on opening and closing) with generally normal mouth opening. Displacement WITHOUT reduction ('closed lock'): the disc does not recapture, causing limited mouth opening (often <30 mm), deviation to the affected side, and absence of click but possible pain.

16. Describe the classic features and management of trigeminal neuralgia.

    Trigeminal neuralgia: sudden, severe, brief (seconds), electric-shock-like/lancinating unilateral pain in the distribution of the trigeminal nerve (commonly V2/V3), triggered by light touch, chewing, cold, or wind, with refractory periods between attacks. First-line treatment: carbamazepine (anticonvulsant); alternatives oxcarbazepine, lamotrigine, gabapentin. Refractory/secondary causes (e.g. vascular compression, MS) may need MRI and surgery (microvascular decompression).

17. Why is MRI indicated in trigeminal neuralgia, and what red flags suggest a secondary cause?

    MRI excludes secondary causes such as a neurovascular conflict (e.g. superior cerebellar artery compressing the trigeminal root), tumour at the cerebellopontine angle, or multiple sclerosis. Red flags: age <40, bilateral symptoms, sensory deficit/numbness, other cranial nerve signs, or features of MS — these warrant imaging and neurology referral.

18. What characterises persistent idiopathic facial pain and burning mouth syndrome (neuropathic/chronic orofacial pain)?

    Persistent idiopathic facial pain (atypical facial pain): chronic, poorly localised, dull/aching facial pain not following nerve boundaries, with no identifiable organic cause and normal investigations. Burning mouth syndrome: a chronic burning sensation of the oral mucosa (often tongue) with clinically normal-appearing mucosa, more common in postmenopausal women. Both are managed with reassurance and neuropathic agents (e.g. tricyclics such as nortriptyline, gabapentin) and exclusion of local/systemic causes.

19. List the major causes of dry mouth (xerostomia).

    Drugs (commonest — anticholinergics, antidepressants/tricyclics, antihistamines, diuretics, opioids, antihypertensives); dehydration; salivary gland disease/Sjögren's syndrome; radiotherapy to head and neck; diabetes; anxiety/somatisation; and ageing/mouth breathing. Sjögren's and irradiation cause true reduced salivary flow (hyposalivation).

20. What is Sjögren's syndrome and how is it investigated?

    An autoimmune exocrinopathy causing lymphocytic destruction of salivary and lacrimal glands, giving dry mouth and dry eyes (keratoconjunctivitis sicca). Primary = sicca alone; secondary = with another connective tissue disease (e.g. rheumatoid arthritis, SLE). Investigations: anti-Ro (SSA) and anti-La (SSB) antibodies, rheumatoid factor/ANA, Schirmer test, salivary flow rates, sialography, and labial gland biopsy (focal lymphocytic sialadenitis). It carries an increased risk of MALT lymphoma.

21. How is xerostomia managed and what oral complications must be prevented?

    Management: address the cause/review medications, frequent sips of water, sugar-free chewing gum to stimulate flow, saliva substitutes/sprays, and salivary stimulants (e.g. pilocarpine if gland function remains). Complications to prevent: rampant/cervical caries (intensive fluoride, dietary advice), candidosis, mucosal soreness, and difficulty with dentures/speech.

22. Compare causes of acute versus chronic salivary gland swelling.

    Acute: infective — bacterial sialadenitis (ascending, often Staph. aureus in a dehydrated/obstructed gland) or viral (mumps — bilateral parotid swelling, paramyxovirus). Recurrent/chronic: obstructive (sialolithiasis/stones, commonly submandibular/Wharton's duct), chronic sialadenitis, Sjögren's, sialosis (sialadenosis — bilateral non-inflammatory enlargement from diabetes/alcoholism/bulimia), and neoplasms (e.g. pleomorphic adenoma).

23. Why are most salivary stones found in the submandibular gland, and how do they present and get managed?

    ~80% of salivary calculi occur in the submandibular gland because its saliva is more mucinous/alkaline (higher calcium/phosphate) and Wharton's duct runs upward against gravity with a tortuous course. Presentation: pain and swelling at mealtimes ('mealtime syndrome'). Management: hydration, sialogogues, gland massage; stones may be removed via the duct, by sialendoscopy, or by gland excision; radiographs/sialography/ultrasound aid diagnosis.

24. What is sialadenitis, and what features distinguish bacterial from obstructive causes?

    Sialadenitis is inflammation of a salivary gland. Acute bacterial sialadenitis: painful, tender, enlarged gland (often parotid) with overlying erythema and purulent discharge from the duct on massage, fever — managed with antibiotics, hydration, and sialogogues. Obstructive sialadenitis: recurrent mealtime swelling/pain due to a stone or stricture, with pus only if secondarily infected; managed by relieving the obstruction.

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