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

What does Step 2 of periodontal therapy involve?

Step 2 (cause-related/subgingival): subgingival instrumentation (root surface debridement / scaling and root planing) to remove subgingival biofilm and calculus, with or without adjuncts (e.g. local/systemic antimicrobials in selected cases). Performed at sites with pockets, after Step 1.

What is the recommended toothbrushing technique and interdental cleaning advice in standard oral hygiene instruction?

Modified Bass technique: bristles angled at $45^{\circ}$ to the gingival margin, small vibratory/circular motions, twice daily for 2 minutes with fluoride toothpaste. Daily interdental cleaning: interdental brushes (TePe) where spaces allow are more effective than floss for plaque removal; floss for tight contacts. Spit, don't rinse, after brushing.

In non-surgical periodontal treatment, when is systemic antibiotic adjunctive therapy generally indicated, and what is a commonly cited regimen?

Systemic antibiotics are generally reserved for younger patients with Grade C (rapidly progressing/Stage III–IV molar-incisor) periodontitis, not as routine adjuncts. A commonly cited regimen is amoxicillin 500 mg + metronidazole 400 mg three times daily for 7 days alongside subgingival instrumentation. Routine use is discouraged due to antimicrobial resistance.

How long after non-surgical periodontal treatment should re-evaluation be performed, and why that interval?

Re-evaluation is typically performed 6–12 weeks (commonly 8–12 weeks) after subgingival instrumentation. This interval allows healing, formation of a long junctional epithelium, resolution of inflammation, and recession/maturation of tissues so that probing depths and bleeding reflect the true treatment response.

At periodontal re-evaluation, what clinical endpoints indicate a successful response and which sites require further intervention?

Success: reduced BoP (<10% ideally), pocket depths $\leq 4$ mm with no BoP, improved plaque scores, and stability. Sites with residual pockets $\geq 5$ mm (or $\geq 4$ mm with BoP) after good Step 1–2 therapy are candidates for re-instrumentation (Step 2 repeat) or Step 3 (surgery/referral).

What is supportive periodontal therapy (SPT / maintenance) and how is recall interval determined?

SPT (Step 4) is ongoing maintenance after active treatment: regular review of plaque control, risk factors, BoP, probing, and professional supra/subgingival debridement to maintain stability. Recall interval is risk-based (commonly every 3 months for higher-risk, up to 6–12 months for stable low-risk patients), guided by tools such as the Periodontal Risk Assessment.

List the main indications for periodontal surgery.

Persistent deep pockets ($\geq 6$ mm) with BoP that fail to respond to non-surgical therapy and good OH; access for debridement of deep/complex defects; regeneration of intrabony or furcation defects; correction of mucogingival defects/recession; crown lengthening; and management of furcation involvement. Surgery is considered only after Steps 1–2 and adequate plaque control.

What are the general criteria for referral of a periodontal patient to a specialist?

Referral is indicated for: complex cases (Stage III/IV), Grade C / aggressive/rapidly progressing disease especially in young patients, periodontitis as a manifestation of systemic disease, cases not responding to initial therapy, those requiring complex surgery (regeneration, mucogingival), and diagnostic uncertainty. The BSP referral framework guides complexity-based referral.

Describe Miller's classification of gingival recession (the classic system).

Class I: recession not extending to the mucogingival junction (MGJ); no interdental bone/soft tissue loss — full root coverage predictable. Class II: recession extends to/beyond MGJ; no interdental loss — full coverage predictable. Class III: recession to/beyond MGJ with interdental bone/soft tissue loss — partial coverage. Class IV: severe interdental loss/malposition — root coverage not achievable.

What is the Cairo classification of recession (RT1–RT3) based on interproximal attachment?

RT1: no interproximal attachment loss (CEJ not detectable interproximally) — full root coverage expected. RT2: interproximal CAL $\leq$ buccal CAL — full coverage possible. RT3: interproximal CAL $>$ buccal CAL — full root coverage not achievable. This system is based on interproximal CAL and is more predictive than Miller's.

What is the predominant surgical technique for treating gingival recession, and when is grafting needed?

The coronally advanced flap (CAF), often combined with a connective tissue graft (CTG) — the 'gold standard' for root coverage. CTG is added to increase keratinised tissue width/thickness and improve predictability, especially in thin biotypes. Other options: lateral pedicle flap, free gingival graft (to increase keratinised tissue), and tunnel techniques.

What are the main aetiological factors of gingival recession?

Toothbrushing trauma (overzealous/horizontal), thin gingival biotype, plaque-induced inflammation/periodontitis, tooth malposition/orthodontic movement out of the bony envelope, frenal pull, high muscle attachment, and iatrogenic factors (restoration margins, piercings). Often multifactorial.

Describe the clinical features and microbiology of necrotising ulcerative gingivitis (NUG).

NUG presents with painful, punched-out/ulcerated necrotic interdental papillae covered by a grey pseudomembranous slough, spontaneous gingival bleeding, halitosis, and a metallic taste. Microbiology: fusospirochaetal — Fusobacterium species, Treponema (spirochaetes), Prevotella intermedia. Predisposing factors: smoking, stress, immunosuppression (notably HIV), poor OH, malnutrition.

How is necrotising gingivitis/periodontitis managed in the acute and definitive phases?

Acute: gentle debridement, oral hygiene measures, hydrogen peroxide or chlorhexidine mouthwash, analgesia; metronidazole 400 mg TDS for 3 days if systemic involvement/spreading or marked symptoms. Definitive: address predisposing factors (smoking cessation, stress, nutrition), thorough professional cleaning, and review. Necrotising periodontitis involves attachment/bone loss; necrotising stomatitis extends beyond into bone/soft tissue (often severely immunocompromised).

What is a periodontal (lateral) abscess and how does it differ from a periapical abscess?

A periodontal abscess is a localised collection of pus within the gingival wall of a periodontal pocket, usually in a tooth with a vital pulp and existing periodontitis, presenting with a deep pocket, swelling, and tenderness to lateral pressure. A periapical abscess arises from a non-vital pulp (pulp necrosis), with the tooth typically non-responsive to vitality testing and tender to vertical percussion/apical palpation.

List the major categories of causes of oral ulceration.

Traumatic (mechanical, thermal, chemical); recurrent aphthous stomatitis; infective (herpes, HIV, syphilis, TB); systemic/GI disease (coeliac, Crohn's, ulcerative colitis); haematological/nutritional deficiency (iron, B12, folate); mucocutaneous (lichen planus, pemphigus/pemphigoid); drug-induced; and malignancy (squamous cell carcinoma). A single ulcer persisting >3 weeks must be considered malignant until proven otherwise.

Describe the three clinical types of recurrent aphthous stomatitis (RAS).

Minor (most common, ~80%): <10 mm, round/oval, grey-yellow base with erythematous halo, non-keratinised mucosa, heal in 7–14 days without scarring. Major: >10 mm, deeper, last weeks–months, can scar, may affect keratinised mucosa. Herpetiform: multiple (10–100) tiny 1–2 mm ulcers that coalesce, despite the name not herpes-related.

What investigations and management are appropriate for recurrent aphthous stomatitis?

Exclude haematinic deficiency (FBC, ferritin, B12, folate), coeliac screen, and ask about GI symptoms; correct any deficiency. Management: avoid triggers (e.g. SLS-free toothpaste, trauma), topical corticosteroids (e.g. hydrocortisone oromucosal tablets, betamethasone mouthwash), chlorhexidine, benzydamine for symptom relief; refer/systemic immunomodulators for severe major RAS.

How are white patches in the mouth classified, and which require biopsy?

White patches may be rubbed off (pseudomembranous candidosis) or not (keratotic). Causes: frictional keratosis, leukoplakia, lichen planus, hairy leukoplakia, white sponge naevus, smoker's keratosis, candidal leukoplakia. Leukoplakia is a clinical diagnosis of exclusion ('a white patch that cannot be characterised as any other definable lesion') and is potentially malignant — it warrants biopsy. Speckled (non-homogeneous) leukoplakia carries higher malignant risk.

What is erythroplakia and why is it clinically important?

Erythroplakia is a fiery red velvety patch that cannot be attributed to any other condition. It is the oral potentially malignant disorder with the HIGHEST risk of malignant transformation/already harbouring dysplasia or carcinoma (a large proportion show severe dysplasia or invasive SCC on biopsy). It mandates urgent biopsy and referral.

Describe the clinical types and features of oral lichen planus (OLP).

Reticular (most common): asymptomatic white lacy Wickham's striae, typically bilateral on buccal mucosa. Other forms: papular, plaque-like, atrophic/erythematous, erosive/ulcerative, and bullous. Erosive/atrophic forms are painful. OLP is a T-cell mediated condition; the erosive/atrophic types carry a small (~1%) risk of malignant transformation and warrant monitoring.

How is oral lichen planus distinguished from a lichenoid reaction, and what is the histology?

Lichenoid reactions are clinically similar but often unilateral/asymmetric and related to an identifiable cause: dental amalgam (contact lesion), drugs (e.g. NSAIDs, beta-blockers, ACE inhibitors, antimalarials), or graft-versus-host disease. Histology of both: band-like (lichenoid) subepithelial T-lymphocyte infiltrate, basal cell liquefaction/degeneration, saw-tooth rete ridges, and Civatte (apoptotic) bodies.

Compare pemphigus vulgaris and mucous membrane pemphigoid (level of split, antibody target, Nikolsky, prognosis).

Pemphigus vulgaris: INTRA-epithelial split (suprabasal, acantholysis), antibodies against desmoglein 1/3 (desmosomes), positive Nikolsky sign, fragile bullae, potentially life-threatening — oral lesions often the first sign. Mucous membrane (cicatricial) pemphigoid: SUB-epithelial split (basement membrane), antibodies against hemidesmosomal antigens (BP180/BP230, laminin), more robust blisters, can cause ocular scarring/symblepharon.

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.

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.

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.

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.

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.

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).

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.

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.

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.

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.

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.

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.

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.

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.

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.

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).

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.

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.

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).

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.

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.

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).

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.

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.