Overseas Registration Exam · Part 1

ORE Part 1 Trainer

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UK guidance crib sheet

The points overseas-trained dentists most often get caught on in Paper B — the current UK position where it commonly differs from practice elsewhere. Items marked ⚠ verify change from time to time; confirm against the linked source close to your exam.

This is a study aid written to UK guidance, not official exam material.

1 · Regulation & professionalism

  • The GDC regulates individual registrants; the CQC regulates the practice/premises (in England). You must work within your scope of practice and hold indemnity.
  • The GDC's nine Standards put patients' interests first: consent, confidentiality, clear communication, working with colleagues, raising concerns.
  • Duty of candour: be open and honest when something goes wrong, and apologise — this is a professional and statutory duty.
  • Raise concerns if patients may be at risk; keep clear, contemporaneous records.
GDC Standards for the Dental Team

2 · Consent & capacity (England & Wales)

  • Adults are presumed to have capacity (Mental Capacity Act 2005); assess it decision-by-decision. A capacitous adult may refuse even life-saving care.
  • Under-16s can consent if Gillick competent (mature enough to understand the decision).
  • 16–17-year-olds are presumed able to consent to their own treatment (Family Law Reform Act 1969).
  • If an adult lacks capacity, act in their best interests (least restrictive option) — not simply what a relative prefers.
  • Valid consent is voluntary and informed: options, material risks, benefits, costs and the option of no treatment (Montgomery standard).
Mental Capacity Act 2005

3 · Confidentiality & records

  • Keep patient information confidential; share only with consent or a lawful basis (Data Protection Act 2018 / UK GDPR).
  • Retain records for at least 11 years for adults, and for children until age 25 (whichever is longer). ⚠ verify
  • Records must be accurate and contemporaneous; amend by adding a dated note, never by obscuring the original.

4 · Medical emergencies (Resuscitation Council UK)

  • Anaphylaxis: adrenaline 500 micrograms IM (0.5 mL of 1:1000), repeat after 5 min if needed; call 999.
  • Hypoglycaemia: conscious → oral glucose/sugary drink; unconscious → glucagon 1 mg IM (or IV glucose); call 999.
  • Asthma: salbutamol via a spacer, repeated. Angina: GTN spray and rest. Seizure: protect from injury, don't restrain, time it; buccal midazolam if prolonged (>5 min).
  • Practices must keep the recommended emergency drugs and equipment and train the team regularly (BLS).
Resus Council UK — primary dental care

5 · Antibiotics & prescribing

  • Infective endocarditis prophylaxis is NOT routine (NICE CG64). For those at increased risk it may be considered on a shared-decision basis — a common difference from overseas practice. ⚠ verify
  • Most acute dental infection is treated by drainage/extraction/pulp removal, not antibiotics. Antibiotics only for spreading or systemic infection, or the immunocompromised.
  • First line: amoxicillin (or phenoxymethylpenicillin); add metronidazole for anaerobes. Penicillin allergy → metronidazole or clarithromycin — not clindamycin as routine first choice.
  • Codeine is contraindicated under 12 and when breastfeeding (MHRA). Follow antimicrobial stewardship — shortest effective course.
SDCEP Drug Prescribing for Dentistry

6 · Anticoagulants & medically compromised (SDCEP)

  • Do not routinely stop anticoagulants or antiplatelets for dental procedures — bleeding is usually controlled with local measures, and stopping risks clot/stroke.
  • Warfarin: check INR (ideally within 24–72 h); treat if INR below 4.0 with local haemostasis.
  • DOACs (apixaban, rivaroxaban, dabigatran, edoxaban): for higher-bleeding-risk procedures, consider missing or delaying the morning dose per SDCEP; use local measures. ⚠ verify
  • Antiplatelets (aspirin, clopidogrel, dual therapy): continue; local measures.
  • MRONJ risk (bisphosphonates, denosumab, antiangiogenics): don't stop the drug for routine extractions; use atraumatic technique and review; refer high-risk cases.
SDCEP anticoagulant guidance

7 · Radiography law (IRR & IR(ME)R 2017)

  • Two regulations: IRR 2017 protects staff and the public; IR(ME)R 2017 protects the patient.
  • IR(ME)R roles: referrer, practitioner (justifies the exposure) and operator (carries it out).
  • Every exposure must be justified and optimised (ALARP). No routine radiographs — use selection criteria. Use rectangular collimation and the fastest receptor.
IR(ME)R 2017

8 · Prevention (Delivering Better Oral Health)

  • Fluoride toothpaste: under 3 — smear of 1000+ ppm; 3–6 — pea-sized 1350–1500 ppm; 7+ — 1350–1500 ppm. Spit, don't rinse. ⚠ verify
  • Fluoride varnish (22,600 ppm) at least twice a year, more often for higher-risk patients.
  • Recall interval is risk-based (NICE CG19) — anywhere from 3 to 24 months, not a fixed 6 months.
  • Diet: keep free sugars under 5% of energy and reduce the frequency of sugary intake (SACN).
Delivering Better Oral Health (OHID)

9 · Infection prevention (HTM 01-05)

  • Standard precautions: treat every patient as potentially infectious.
  • Follow the decontamination cycle (clean → inspect → sterilise → store); single-use items are never reprocessed.
  • Sharps: never re-sheath by hand; dispose at the point of use.
HTM 01-05 decontamination

10 · Periodontology (BSP)

  • Screen with the BPE; diagnose using the 2017 classification (staging I–IV, grading A–C, and stability).
  • Manage step-wise (BSP S3): oral hygiene and risk-factor control (including smoking) → subgingival instrumentation → reassess before any surgery.
British Society of Periodontology

11 · Oral surgery & paediatric

  • Do not routinely remove asymptomatic, disease-free third molars (NICE).
  • Avulsed permanent tooth: re-implant as soon as possible (transport in milk or saliva). Avulsed primary tooth: do not re-implant.
  • Paediatric caries is prevention-led; preformed metal (stainless steel) crowns / Hall technique are standard for carious primary molars.
Dental Trauma Guide (IADT)

12 · More high-yield UK specifics

  • Suspected oral cancer: make an urgent (2-week-wait) referral for an unexplained ulcer, lump, or red/white patch lasting more than 3 weeks (NICE NG12).
  • Tooth whitening: only by, or under the direct supervision of, a dental professional; patient must be 18+; maximum 6% hydrogen peroxide (over-the-counter products are capped at 0.1%).
  • Dental amalgam: restricted for children under 15 and pregnant or breastfeeding women unless clinically necessary (mercury regulations); a wider phase-out is evolving. ⚠ verify
  • Local anaesthetic: maximum safe dose is weight-based — know the limit for the agent used and don't exceed it (e.g. lidocaine with adrenaline). ⚠ verify
  • Needlestick / sharps injury: encourage bleeding, wash with soap and water, cover, then report and get an occupational-health risk assessment.
  • Referrals: include the reason, relevant history and findings, and the urgency; keep the patient informed and get consent to share information.
NICE NG12 (suspected cancer referral)

Study notes

General revision aids collected from study material — broad medicine, not UK-specific guidance. Each set has been checked against standard references; anything that couldn't be verified is flagged, and gaps have been filled in.

A revision aid, not official exam material. For anything that guides real UK clinical practice, use the UK guidance crib sheet instead.

Leucoplakia

The most common potentially-malignant disorder of the oral mucosa. A diagnosis of exclusion (WHO).

Definition

  • A white patch/plaque that cannot be scraped off and cannot be characterised clinically or histologically as any other definable lesion.

Risk factors

  • Tobacco (smoked or smokeless) — most important
  • Alcohol (synergy with tobacco)
  • Betel quid / areca nut
  • Chronic irritation, sharp teeth, poor OH

Clinical types

  • Homogeneous — thin, flat, uniform white; lower risk
  • Non-homogeneous — nodular / verrucous / speckled (erythroleukoplakia); higher risk

Histology

  • Hyperkeratosis / parakeratosis, acanthosis
  • ± Dysplasia (mild → moderate → severe → carcinoma in situ) = malignant potential

Malignant potential

  • ~3–17% transform to SCC ⚠ range varies
  • Higher risk: non-homogeneous, floor of mouth / ventral tongue, long duration, dysplasia

Diagnosis & management

  • Confirm by incisional biopsy
  • Remove risk factors; review every 3–6 months
  • Excise if moderate/severe dysplasia

Differential diagnosis

  • Frictional keratosis, lichen planus, chronic candidiasis, leukoedema, white sponge naevus

Exam pearls

  • Cannot be wiped off (vs candidiasis)
  • Diagnosis of exclusion; SCC is the malignant change

Oral submucous fibrosis (OSMF)

A chronic, progressive scarring disease of the oral mucosa; a potentially-malignant disorder (Pindborg).

Definition

  • Chronic disease with juxta-epithelial inflammation and fibroelastic change of the lamina propria + epithelial atrophy → stiffness, trismus and inability to eat.

Aetiology

  • Areca nut (arecoline) — most important
  • Areca + tobacco, chilli/spices
  • Nutritional deficiency (iron, B-complex), genetic

Clinical features

  • Burning on spicy food, blanched mucosa
  • Palpable fibrous bands (buccal mucosa, soft palate, lips)
  • Progressive trismus (restricted opening), difficulty eating/speaking

Grading by mouth opening

  • Normal 35–45 mm; Mild 30–35; Moderate 20–30; Severe <20 mm
  • Clinical staging by Khanna & Andrade (I–IV)

Histology

  • Atrophic epithelium, juxta-epithelial hyalinisation, dense collagen, reduced vascularity

Malignant potential

  • ~7–13% transform to SCC ⚠ range varies
  • Spares gingiva/hard palate early; tongue usually spared

Management (multidisciplinary)

  • Stop areca nut & tobacco (most important) + counselling
  • Intralesional steroids + hyaluronidase, antioxidants/lycopene
  • Physiotherapy (mouth-opening exercises); surgery (band excision + graft) in severe; nutritional support

Differential diagnosis

  • Lichen planus, leukoplakia, chronic candidiasis, GVHD, scleroderma

Oral lichen planus (OLP)

A chronic T-cell-mediated inflammatory mucocutaneous disease (skin, mucosa, hair, nails).

Aetiopathogenesis

  • Cell-mediated (T-lymphocyte) attack on basal keratinocytes
  • Triggers: stress, genetics, hepatitis C, drugs and dental materials (amalgam) → lichenoid reactions

Clinical types

  • Reticular (most common) — Wickham's striae, lace-like, symmetrical
  • Papular, plaque
  • Atrophic (erythematous), erosive (ulcerative, painful), bullous, pigmented
Wickham's striae = white lines → crossing lines → net-like pattern.

Sites

  • Buccal mucosa (posterior, bilateral), tongue, gingiva (desquamative gingivitis), palate

Histology

  • Hyperkeratosis, saw-tooth rete ridges
  • Basal cell (liquefactive) degeneration
  • Band-like lymphocytic infiltrate at the basement membrane; Civatte (colloid) bodies

Malignant potential

  • Reticular/papular — little/no risk
  • Erosive/atrophic higher (~1–3%, up to more in some series) ⚠ verify; SCC is the malignant change

Management

  • Topical corticosteroids (mainstay)
  • Remove triggers (replace amalgam if lichenoid contact); calcineurin inhibitors; monitor

Differential diagnosis

  • Lichenoid reaction (drug/amalgam — unilateral, related to contact), leukoplakia, lupus, chronic candidiasis, frictional keratosis

Aphthous ulcer (recurrent aphthous stomatitis)

The most common ulcerative lesion of the oral mucosa; recurrent, non-contagious, on non-keratinised mucosa in otherwise-healthy people.

Clinical appearance

  • Round/oval ulcer, yellow-grey base + erythematous halo
  • Burning pain; on non-keratinised mucosa; no systemic involvement

Types

  • Minor (70–80%): <1 cm, shallow, heal 7–10 days, no scar
  • Major (10–20%): >1 cm, deep, indurated, heal 2–6 weeks, may scar
  • Herpetiform (5–10%): 10–100 tiny (1–2 mm), coalesce, no scar

Predisposing factors

  • Local trauma, stress, hormonal, foods (spicy/nuts)
  • Deficiency: iron, folate, B12, zinc; drugs; genetic

Differential diagnosis

  • Traumatic ulcer, primary herpes (vesicles, fever, keratinised mucosa)
  • Behçet's (oral + genital + uveitis), pemphigus, erosive lichen planus

Associated conditions

  • IBD (Crohn's, UC), coeliac disease, Behçet's, PFAPA

Management

  • Topical corticosteroid (e.g. triamcinolone in orabase), topical anaesthetic, chlorhexidine
  • Correct deficiencies; systemic therapy for severe/frequent

Exam pearls

  • Most common oral ulcer
  • Non-keratinised mucosa (vs herpes, which favours keratinised mucosa/gingiva)

Pemphigus (vulgaris)

A potentially life-threatening autoimmune intra-epithelial bullous disorder; the mouth is often the first site.

Pathogenesis

  • Autoantibodies against desmogleins (Dsg3 ± Dsg1)
  • Loss of cell–cell adhesion (acantholysis) → suprabasal split → flaccid bullae → erosions

Clinical features

  • Oral involvement in almost all cases
  • Flaccid bullae rupture easily → painful erosions
  • Nikolsky sign positive; heals without scarring

Histology

  • Suprabasal cleft; acantholytic (Tzanck) cells; basal cells intact ("row of tombstones")
  • Tzanck smear: round acantholytic cells with perinuclear halo

Types

  • Vulgaris (Dsg3±1, suprabasal — commonest/severe)
  • Foliaceus (Dsg1, superficial), Paraneoplastic (lymphoma/Castleman/thymoma)

Differential diagnosis

  • Mucous membrane pemphigoid (sub-epithelial split, scarring)
  • Bullous LP, erythema multiforme, SJS, linear IgA, HSV, aphthous

Management

  • Systemic corticosteroids (mainstay) + immunosuppressants (azathioprine, MMF)
  • Rituximab for refractory; topical steroids for oral lesions

Exam pearls

  • Nikolsky positive; oral involvement almost always
  • Intra-epithelial split (pemphigus) vs sub-epithelial (pemphigoid)

Herpes zoster (shingles) — oral relevance

Reactivation of latent varicella-zoster virus in a sensory ganglion; a unilateral, painful, dermatomal vesicular eruption.

Key concept

  • Unilateral, follows a single dermatome, and does not cross the midline
  • The only condition with a dermatomal oral distribution

Trigeminal involvement

  • V1 (ophthalmic) — Hutchinson's sign (nose-tip vesicles) → eye risk
  • V2 / V3 → unilateral facial & oral ulcers up to the midline

Ramsay Hunt syndrome

  • Geniculate ganglion (VII): facial palsy + vesicles in the ear

Clinical course

  • Prodrome: pain/tingling → grouped vesicles on erythematous base → crusting (heal 2–4 weeks)

Complications

  • Post-herpetic neuralgia (most common), secondary infection, ophthalmic involvement

Management

  • Antivirals ideally within 72 h (aciclovir/valaciclovir/famciclovir) + analgesia
  • Dental relevance: recognise unilateral oral ulcers respecting the midline; refer promptly for antivirals

Gingival enlargement

An abnormal increase in the size of the gingiva (also called gingival hypertrophy/hyperplasia).

Causes / types

  • Inflammatory (dental plaque) — most common
  • Drug-induced: phenytoin, ciclosporin, calcium-channel blockers (nifedipine, amlodipine)
  • Hormonal (puberty, pregnancy), systemic (leukaemia, diabetes), hereditary fibromatosis

Clinical features

  • Interdental papillae affected first
  • Soft/red in inflammatory type; firm/pink in fibrotic (drug-induced) type
  • May be generalised or localised; interferes with mastication/speech

Grades (severity)

  • Grade 0: none; Grade 1: confined to gingiva/papilla
  • Grade 2: covers up to 2/3 of crown; Grade 3: covers >2/3 of crown

Differential diagnosis

  • Pyogenic granuloma, peripheral giant cell granuloma, leukaemic infiltration, fibroma

Management

  • Remove local factors (OHI, scaling & root planing)
  • Drug substitution where possible; treat systemic cause
  • Gingivectomy/gingivoplasty if it persists

Exam pearls

  • Plaque is the most common cause
  • Know the three drug culprits: phenytoin, ciclosporin, CCBs

Ameloblastoma

A benign but locally aggressive epithelial odontogenic tumour, from odontogenic epithelium (dental lamina rests, enamel organ).

Who / where

  • Age 20–40, M ≈ F
  • 80–85% mandible (molar-ramus region)

Radiographic features

  • Multilocular "soap-bubble" / "honeycomb" radiolucency
  • Scalloped borders, root resorption, tooth displacement, cortical expansion
  • Unicystic type may mimic a dentigerous cyst

Types

  • Conventional (solid/multicystic) — commonest, most aggressive
  • Unicystic (younger, better prognosis), peripheral, desmoplastic

Histology

  • Follicular: islands with peripheral palisaded columnar cells, reverse polarity, stellate-reticulum-like centre
  • Also plexiform, acanthomatous, granular, basal, desmoplastic

Clinical & management

  • Slow painless jaw swelling, buccolingual expansion, paraesthesia in large lesions
  • Unicystic → conservative (enucleation ± curettage); conventional → wide resection (high recurrence)

Differential diagnosis

  • Odontogenic keratocyst (OKC), odontogenic myxoma (tennis-racket), central giant cell granuloma, dentigerous cyst, aneurysmal bone cyst

Exam pearls

  • Benign but locally aggressive; 80–85% mandible; high recurrence → wide excision
  • The most common odontogenic neoplasm (odontomas are commoner overall but are hamartomas)
Corrected: the screenshot's "most common odontogenic tumour" is only true once odontomas are excluded.

Fibrous dysplasia

A benign, non-neoplastic fibro-osseous lesion: normal bone is replaced by fibrous tissue and immature woven bone.

Pathogenesis

  • GNAS gene mutation → abnormal osteogenic differentiation

Types

  • Monostotic (70–80%, single bone) — most common
  • Polyostotic (20–30%)
  • McCune–Albright: polyostotic FD + café-au-lait spots + endocrinopathy (e.g. precocious puberty)

Radiographic features

  • Three stages: radiolucent → mixed → radiopaque
  • Characteristic "ground-glass" appearance; ill-defined margins that blend into normal bone

Clinical features

  • Painless slow expansion, facial asymmetry (craniofacial FD), tooth displacement
  • Maxilla > mandible

Histology

  • Irregular woven-bone trabeculae ("Chinese-letter"/C shapes) in fibrous stroma; no osteoblastic rimming

Management

  • No treatment if asymptomatic; cosmetic recontouring after skeletal maturity
  • Bisphosphonates for pain; avoid radiotherapy (sarcoma risk)

Differential diagnosis

  • Ossifying fibroma (well-defined), cemento-osseous dysplasia, Paget's (cotton-wool, raised ALP, older), osteosarcoma

Exam pearls

  • Ground-glass + GNAS; blends with normal bone (vs sharply-defined ossifying fibroma)
  • Maxilla is the commonest oral site; monostotic commonest overall

Myofascial pain dysfunction syndrome (MPDS)

The most common chronic orofacial pain disorder — a muscle problem, not a joint problem.

Aetiology

  • Parafunction (bruxism/clenching), occlusal disharmony, stress/anxiety, muscle overuse

Clinical features

  • Dull aching pain in masticatory muscles, worse on function (chewing/talking)
  • Morning jaw stiffness, restricted opening, muscle tenderness
  • Referred headache/earache/toothache-like pain; often stress/sleep issues

Trigger points

  • Hyperirritable spot in a taut muscle band that reproduces referred pain on palpation
  • Temporalis (temporal headache), masseter (toothache-like), pterygoids, SCM, trapezius

Diagnosis

  • Clinical: history + palpation of trigger points; no specific test
  • Exclude red flags: trismus from infection/malignancy, true TMJ intra-articular disease, neuralgia, systemic muscle disorders

Differential diagnosis

  • TMJ disorders (joint sounds, imaging changes), trigeminal neuralgia (electric-shock, no trigger points), neuropathic pain, dental pain (localised, objective findings), fibromyalgia (widespread)

Management

  • Reassurance & habit modification, soft diet, jaw rest
  • Physiotherapy (heat, TENS, massage, exercises)
  • NSAIDs, muscle relaxants, low-dose tricyclics (amitriptyline)
  • Occlusal splint (night guard); trigger-point therapy; stress management

Custom (special) tray

A tray made on a preliminary cast for an individual patient, to carry impression material uniformly for the final impression.

Objectives

  • Accurate final impression; uniform material thickness (2–3 mm)
  • Reduce distortion, improve retention, support & stability; patient comfort; save material

Components

  • Tray body, handle, spacer (2–3 mm), tissue stops, relief holes (perforations)
handle● tissue stops

Materials

  • Self-cure acrylic resin (most common), light-cure resin, shellac base plate, VLC resin

Spacer & tissue stops

  • Spacer: uniform 2–3 mm wax space → even material thickness and flow
  • Tissue stops: projections contacting tissue to seat the tray correctly and prevent over-seating

Fabrication steps

  • Primary impression → cast → outline → spacer wax → tissue stops → separating medium → adapt tray material → handle → cure → finish → remove spacer → relief holes

Indications & viva points

  • Complete denture, RPD, implant impressions, high gag reflex, when accuracy matters
  • Common viva: define; why spacer; function of tissue stops; advantages; materials; steps

10 must-know radiographic diagnoses

Read every radiograph systematically. Radiolucent = loss of mineral (dark); radiopaque = gain of mineral (white).

CariesRadiolucent on crown
Periapical lesionRadiolucency at apex
Dentigerous cystRadiolucency at CEJ

1 · Dental caries

  • Radiolucent area in enamel/dentine, interproximal or occlusal

2 · Periapical abscess

  • Radiolucency at the root apex + loss of lamina dura

3 · Chronic apical periodontitis

  • Well-defined periapical radiolucency on a non-vital tooth

4 · Periodontal bone loss

  • Reduced alveolar bone height (horizontal or vertical)

5 · Impacted third molar

  • Unerupted tooth in bone; mesioangular/vertical/horizontal/distoangular

6 · Root resorption

  • Irregular loss / discontinuity of root outline (internal or external)

7 · Pericoronitis

  • Radiolucency around the crown of a partially-erupted/impacted tooth

8 · Dentigerous cyst

  • Well-circumscribed radiolucency attached at the CEJ of an impacted tooth

9 · Hypercementosis

  • Bulbous enlargement of the root apex; PDL space & lamina dura intact

10 · Condensing osteitis

  • Localised radiopaque area at the apex; chronic pulpal inflammation

Cardiovascular drugs — what matters in dentistry

The full drug notes are general medicine; this is the dentally-relevant distillation. Tell me if you want the complete pharmacology pages added too.

Drug-induced gingival enlargement

  • Calcium-channel blockers (nifedipine, amlodipine), plus phenytoin and ciclosporin
  • Manage with OHI/scaling; ask the GP about substitution

Bleeding risk (do not stop routinely)

  • Antiplatelets (aspirin, clopidogrel) and anticoagulants (warfarin — INR <4; DOACs — apixaban, rivaroxaban, dabigatran, edoxaban)
  • Follow SDCEP; use local haemostasis. ⚠ see UK crib sheet

Local anaesthetic with adrenaline

  • Caution with non-selective beta-blockers and tricyclics; limit the dose in significant cardiovascular disease

ACE inhibitors

  • Dry cough; angioedema (can cause tongue/facial swelling — airway emergency); lichenoid reactions

Dry mouth & the dental chair

  • Diuretics and many antihypertensives → xerostomia (caries/candidiasis risk)
  • Orthostatic hypotension — raise the chair slowly (alpha-blockers, nitrates)

Other quick hits

  • Beta-blockers can mask hypoglycaemia; cause bradycardia
  • Statins → myalgia; NSAIDs interact with antihypertensives/anticoagulants — prescribe with care

Triads — emergencies & medically compromised

The dentally-relevant triads: chairside emergencies and conditions that affect dental care. (The general-medicine triads have been set aside — see the note at the end.)

Cardiac arrest

  • Unresponsiveness
  • Apnoea / no normal breathing
  • Absent pulse

Acute asthma

  • Wheeze
  • Dyspnoea
  • Cough

Whipple's triad Hypoglycaemia

  • Symptoms of hypoglycaemia
  • Low measured plasma glucose
  • Symptoms relieved when glucose is corrected

Cushing's triad Raised intracranial pressure

  • Hypertension (widening pulse pressure)
  • Bradycardia
  • Irregular respiration

Samter's triad Aspirin sensitivity

  • Asthma
  • Nasal polyps
  • Aspirin / NSAID sensitivity
Relevant when choosing analgesics.

Virchow's triad Thrombosis risk

  • Venous stasis
  • Hypercoagulability
  • Endothelial injury
Background for anticoagulated patients.

Triads — head, neck & orofacial

Clusters a dentist may meet in orofacial pain and head/neck assessment.

Horner's syndrome

  • Ptosis
  • Miosis
  • Anhidrosis (± enophthalmos)

Migraine with aura

  • Aura
  • Unilateral throbbing headache
  • Nausea / vomiting

Gradenigo syndrome Petrous apicitis

  • Abducens (VI) nerve palsy
  • Deep facial / retro-orbital pain
  • Otorrhoea

Ménière's disease

  • Episodic vertigo
  • Sensorineural hearing loss
  • Tinnitus

Triads — oral signs of systemic disease

Systemic conditions with tell-tale oral or dental features.

Hutchinson's triad Late congenital syphilis

  • Hutchinson (notched) incisors
  • Interstitial keratitis
  • Sensorineural (8th nerve) deafness
A classic dental sign — the teeth are part of the triad.

Addison's disease

  • Hypotension
  • Hyperpigmentation (including oral mucosa)
  • Hyponatraemia

Kawasaki disease

  • Fever >5 days
  • Non-purulent conjunctivitis
  • Polymorphous rash (oral: strawberry tongue, cracked lips)

Reactive arthritis

  • Arthritis
  • Urethritis
  • Conjunctivitis (oral ulcers may occur)

Bone tumours — differential + signs (general)

General bone-tumour differentials. Kept for background — the jaw-specific lesions are under Ameloblastoma and Fibrous dysplasia.

Signature signs
SunburstOsteosarcoma
Codman triangleOsteosarcoma
Onion-skinEwing sarcoma
Soap-bubbleGiant cell tumour
Popcorn calcificationChondrosarcoma
Chicken-wireChondroblastoma
Differential table

Osteochondroma <20 y · benign

  • Metaphysis around knee; exostosis pointing away from joint
  • Most common benign bone tumour

Enchondroma 20–40 y · benign

  • Small bones of hand & feet; stippled calcification
  • Ollier / Maffucci syndrome

Chondroblastoma 10–20 y · benign

  • Epiphysis; chicken-wire calcification

Chondrosarcoma >40 y · malignant

  • Pelvis/shoulder/ribs; popcorn calcification; most common malignant cartilage tumour

Osteosarcoma 10–20 y · malignant

  • Metaphysis around knee; sunburst + Codman triangle; RB1/TP53/Paget

Giant cell tumour 20–40 y

  • Epiphysis; soap-bubble; multinucleated giant cells; locally aggressive

Ewing sarcoma 5–20 y · malignant

  • Diaphysis; onion-skin; small round blue cells; t(11;22), CD99+

Oral manifestations of systemic disease

The mouth as a mirror of systemic health — high-yield for exam “spot the disease” questions.

Beefy-red (B12)Atrophic (iron)

Diabetes mellitus

  • Xerostomia, candidiasis, periodontitis, delayed healing, loose teeth

Iron-deficiency anaemia

  • Atrophic glossitis, angular cheilitis, pale mucosa, burning tongue

Leukaemia

  • Gingival enlargement, spontaneous bleeding, petechiae, ulcers, infection

Chronic kidney disease

  • Uraemic stomatitis, uraemic odour, metallic taste, xerostomia, enamel hypoplasia

Liver disease

  • Bleeding tendency (↓ clotting factors), jaundiced mucosa, petechiae, glossitis

Hypertension (drugs)

  • Drug-induced gingival enlargement (CCBs), lichenoid lesions, xerostomia

Vitamin B12 deficiency

  • Beefy-red tongue (glossitis), burning mouth, ulcers, pale mucosa

HIV / AIDS

  • Candidiasis, hairy leukoplakia (EBV), Kaposi sarcoma, ulcers, periodontal disease

Thyroid

  • Hyperthyroid → accelerated eruption, burning mouth; hypothyroid → macroglossia

Memory hooks

  • Anaemia → glossitis; B12 → beefy-red; leukaemia/CCB → gingival enlargement; CKD → uraemic stomatitis; liver → bleeding; HIV → candida; hypothyroid → macroglossia

Radiographic appearances → diagnosis

The examiner's favourite “pattern → lesion” pairings. Recognise the pattern, name the lesion. (A clue, not a rule — always correlate clinically.)

Multilocular patterns

  • Soap-bubble → Ameloblastoma
  • Honeycomb / tennis-racket → Odontogenic myxoma
  • Multilocular radiolucency → ameloblastoma, OKC, myxoma, CGCG

Bone texture

  • Ground-glass → Fibrous dysplasia
  • Cotton-wool → Paget's disease
  • Orange-peel → Cherubism
  • Moth-eaten → osteomyelitis / malignancy

Periosteal / marrow

  • Sunburst → Osteosarcoma
  • Onion-skin → Garré's osteomyelitis (Ewing in long bones)
  • Hair-on-end / step-ladder → thalassaemia, sickle cell

Calcification flecks

  • Driven-snow → CEOT (Pindborg tumour)
  • Snowflake → AOT (adenomatoid odontogenic tumour)
  • Target → sialolith

Shapes & teeth

  • Heart-shaped → nasopalatine duct cyst
  • Inverted-pear → globulomaxillary cyst
  • Floating teeth → Langerhans cell histiocytosis
  • Ghost teeth → regional odontodysplasia
  • Scalloping between roots → simple bone cyst
  • Unilocular at CEJ → dentigerous cyst

Exam trap

  • Honeycomb and tennis-racket both point to odontogenic myxoma
  • Ground-glass = fibrous dysplasia, not Paget's (that's cotton-wool)

Local anaesthetics

Core dental pharmacology. Drugs that cause reversible loss of sensation in a limited area without loss of consciousness.

Mechanism

  • Block voltage-gated Na⁺ channels → prevent depolarisation & impulse conduction
  • Unionised form crosses the nerve sheath → ionised form binds the channel from inside

Esters vs amides

  • Esters (procaine, tetracaine, benzocaine, cocaine): plasma esterase metabolism; PABA allergy possible
  • Amides (lidocaine, articaine, prilocaine, bupivacaine, mepivacaine): hepatic metabolism; more stable, less allergy
Mnemonic: amides have an “i” before -caine (li-do-caine, art-i-caine).

Why LA fails in an abscess

  • Inflamed tissue is acidic → more ionised drug → less crosses the sheath → poor block
  • Adding bicarbonate raises pH → faster onset

Order of fibre block

  • Autonomic / pain first → temperature → touch → pressure → motor last (small fibres before large)

Agents (dental)

  • Lidocaine — workhorse; articaine — good diffusion; prilocaine — methaemoglobinaemia at high dose; bupivacaine — long-acting; mepivacaine — little vasodilation (use plain)

Toxicity

  • CNS first: circumoral numbness, tinnitus, then seizures → CNS depression; CVS: hypotension, arrhythmia (esp. bupivacaine)
  • Antidote: IV lipid emulsion (Intralipid)

Vasoconstrictor (adrenaline)

  • Prolongs action, reduces bleeding & systemic absorption
  • Caution: significant CVD, non-selective beta-blockers, tricyclics

Max dose

  • Weight-based — know the limit for the agent (e.g. lidocaine, articaine) and don't exceed it ⚠ verify figures

Antibiotics — classes, mechanism & resistance

General pharmacology, distilled. Group by mechanism, then remember the dental first-lines.

Cell-wall inhibitors

  • β-lactams (penicillins, cephalosporins, carbapenems, monobactams), vancomycin, bacitracin — bactericidal

Protein-synthesis inhibitors

  • 30S: aminoglycosides (cidal), tetracyclines (static)
  • 50S: macrolides, clindamycin, chloramphenicol, linezolid
Mnemonic: “buy AT 30, CCEL at 50” — Aminoglycosides/Tetracyclines = 30S; Chloramphenicol/Clindamycin/Erythromycin/Linezolid = 50S.

Nucleic-acid & others

  • Fluoroquinolones (DNA gyrase), rifampicin (RNA polymerase), metronidazole (anaerobes)
  • Folate: sulfonamides + trimethoprim; membrane: polymyxins, daptomycin

-cidal vs -static

  • Cidal: β-lactams, aminoglycosides, fluoroquinolones, vancomycin, metronidazole
  • Static (“ECSTaTiC”): Erythromycin, Clindamycin, Sulfonamides, Tetracyclines, Trimethoprim, Chloramphenicol

Resistance

  • Enzyme inactivation (β-lactamases), altered target (altered PBP → MRSA), reduced permeability/efflux, bypass pathway
  • Spread: transformation, transduction, conjugation (plasmids)

Dental first-lines

  • Amoxicillin first-line; metronidazole for anaerobes; penicillin allergy → clarithromycin or metronidazole (not clindamycin routinely)
  • Most dental infections are drained, not treated with antibiotics

Pharmacokinetics (ADME)

“What the body does to the drug.” Absorption → Distribution → Metabolism → Excretion.

Bioavailability (F)

  • Fraction of a dose reaching the systemic circulation unchanged
  • IV = 100%; oral is reduced by first-pass

First-pass metabolism

  • Gut wall + liver metabolise the drug before it reaches the circulation → ↓ F
  • Bypassed by sublingual/buccal, rectal (partial), transdermal, parenteral routes
Dental: sublingual GTN and buccal midazolam work because they bypass first-pass.

Metabolism

  • Phase I (oxidation/reduction/hydrolysis, CYP450) — may activate prodrugs (codeine → morphine)
  • Phase II (conjugation, e.g. glucuronidation) — ↑ polarity, usually inactivates

CYP450 inducers vs inhibitors

  • Inducers (↓ drug levels): rifampicin, phenytoin, carbamazepine, chronic alcohol, smoking
  • Inhibitors (↑ drug levels): erythromycin, azole antifungals, cimetidine, grapefruit

Excretion

  • Mainly renal (filtration, secretion, reabsorption)
  • pH trapping: alkalinise urine to clear weak acids (aspirin); also biliary & pulmonary (volatile anaesthetics)

Pharmacodynamics

“What the drug does to the body” — receptors, agonists/antagonists, and dose-response.

Receptor types (speed)

  • Ion-channel (ms; nicotinic, GABA-A), GPCR (secs; β-adrenergic, muscarinic), enzyme-linked (insulin), nuclear (hours; steroid/thyroid)

Types of drug action

  • Agonist (binds + activates), partial agonist (submaximal), antagonist (binds, blocks), inverse agonist (opposite effect), allosteric modulator

Affinity vs efficacy

  • Affinity = how tightly it binds; efficacy/intrinsic activity = ability to activate
  • Binding without activation = antagonism

Dose-response

  • Graded vs quantal; ED50 = potency (position on x-axis), Emax = efficacy (height)
  • Left shift = more potent (lower dose needed)

Factors modifying action

  • Age, weight, sex, genetics, pregnancy, liver/renal disease, tolerance/tachyphylaxis, interactions, compliance

Drug interactions, antagonism, synergism & ADRs

How drugs combine, and how they cause harm.

Interaction levels

  • Pharmaceutical (before dosing, e.g. penicillin + aminoglycoside in one syringe)
  • Pharmacokinetic (ADME — warfarin displaced/enzyme effects)
  • Pharmacodynamic (at the receptor)

Synergism

  • Additive (1+1=2, paracetamol + ibuprofen); true synergism (1+1>2, trimethoprim + sulfamethoxazole)
  • Potentiation: adrenaline potentiates LA by ↓ absorption

Antagonism

  • Competitive/reversible (atropine vs ACh), non-competitive/irreversible, physiological, chemical (protamine neutralises heparin)

Key dental interactions

  • Warfarin + NSAIDs / metronidazole / miconazole → ↑ INR & bleeding
  • Adrenaline + non-selective β-blocker / tricyclic; erythromycin & azoles inhibit CYP → ↑ statin/warfarin

Adverse drug reactions

  • Type A (Augmented) — dose-related, predictable (~80%)
  • Type B (Bizarre) — idiosyncratic/allergic, not dose-related (e.g. anaphylaxis)
  • Manage: stop, treat, report (UK Yellow Card)

Autonomic (sympathetic) drugs

Adrenergic pharmacology — the basis of the adrenaline in your LA cartridge.

Receptors

  • α1: vasoconstriction, mydriasis, ↑ BP
  • α2: ↓ NA release (presynaptic)
  • β1: ↑ HR & contractility; β2: bronchodilation, vasodilation; β3: lipolysis
Mnemonic: β1 = 1 Heart; β2 = 2 Lungs.

Sympathomimetics (agonists)

  • Direct: adrenaline, noradrenaline, isoprenaline, dobutamine, salbutamol, phenylephrine
  • Indirect: amphetamine, tyramine; mixed: ephedrine

Sympatholytics (blockers)

  • α-blockers (prazosin), β-blockers (propranolol non-selective; atenolol/metoprolol β1), α+β (labetalol, carvedilol), central (clonidine, methyldopa)

Uses / dental relevance

  • Adrenaline — anaphylaxis & the vasoconstrictor in LA; salbutamol — asthma attack in the chair
  • Caution: adrenaline + non-selective β-blocker → unopposed α (↑ BP)

Antidotes

The high-yield poison–antidote pairs, with the dentally-relevant ones first.

Dental / chairside

  • LA toxicity → IV lipid emulsion (Intralipid)
  • Benzodiazepine (sedation) → flumazenil; opioid → naloxone
  • Paracetamol → N-acetylcysteine

Anticoagulant reversal

  • Heparin → protamine; warfarin → vitamin K
  • Dabigatran → idarucizumab; factor Xa inhibitors → andexanet alfa

Cardiac drugs

  • Digoxin → digoxin-specific antibody (Fab)
  • β-blocker → glucagon; calcium-channel blocker → calcium gluconate

Classic pairs

  • Organophosphate → atropine + pralidoxime; cyanide → hydroxocobalamin
  • Methanol/ethylene glycol → fomepizole; iron → deferoxamine
  • Methaemoglobinaemia → methylene blue; isoniazid → pyridoxine (B6)
  • Methotrexate → folinic acid; CO → 100% O₂/hyperbaric

Bleeding disorders & thalassaemia

Haematology a dentist meets through bleeding risk, anaemia and craniofacial signs.

Coagulation screen

  • PT/INR = extrinsic (warfarin); aPTT = intrinsic (heparin)
  • ↑ aPTT, normal PT → intrinsic (haemophilia A/VIII, B/IX, vWD)
  • ↑ PT, normal aPTT → factor VII / early liver / vitamin K
  • Both ↑ → liver disease, DIC, vitamin K deficiency

Mixing study

  • Corrects → factor deficiency; does not correct → inhibitor (e.g. lupus anticoagulant)

Dental relevance

  • Take a bleeding history; haemophilia → factor cover before extraction; use local haemostasis; liaise with haematology

Thalassaemia

  • Inherited defect of α/β globin → microcytic hypochromic anaemia, ineffective erythropoiesis
  • Craniofacial: marrow expansion → “chipmunk facies”, maxillary overgrowth, hair-on-end skull, pale mucosa
  • Management: transfusion + iron chelation

General anaesthetics

Reversible unconsciousness with analgesia, amnesia, immobility and muscle relaxation. In UK dentistry GA is hospital-only — chairside you use conscious sedation.

Classification

  • Inhalational — gases (nitrous oxide) & volatile liquids (halothane, isoflurane, sevoflurane, desflurane)
  • Intravenous — thiopentone, propofol, etomidate, ketamine, midazolam

MAC (potency)

  • Minimum alveolar concentration preventing movement in 50% of patients
  • Halothane 0.75 (potent); nitrous oxide ~105 (weak)
Mnemonic: low MAC = high potency.

Mechanism

  • Enhance inhibitory GABA-A, inhibit excitatory NMDA → dose-dependent CNS depression

Key IV agents

  • Propofol — rapid, anti-emetic, pain on injection
  • Thiopentone — ultra-short, ↓ BP
  • Ketamine — dissociative, analgesic, bronchodilator, ↑ BP/HR
  • Midazolam — sedation & amnesia

Adverse effects

  • Respiratory depression, hypotension, nausea/vomiting, post-op delirium
  • Malignant hyperthermia (volatiles / suxamethonium) → dantrolene

Dental relevance

  • Conscious sedation: inhalation N₂O/O₂ (“RA”) or IV midazolam
  • Recognise malignant hyperthermia as an emergency; know N₂O occupational-exposure limits

Autonomic (parasympathetic) drugs

The cholinergic “rest & digest” system — acetylcholine acting at muscarinic (M1–M5) receptors. Companion to the sympathetic notes.

Cholinomimetics (agonists)

  • Direct: acetylcholine, bethanechol, carbachol, pilocarpine
  • Indirect = AChE inhibitors: neostigmine, pyridostigmine, physostigmine, edrophonium (irreversible = organophosphates)

Cholinolytics (antimuscarinics)

  • Atropine, hyoscine (scopolamine), glycopyrrolate, ipratropium, tolterodine, oxybutynin

Muscarinic receptors

  • M1 — CNS, gastric acid
  • M2 — heart (↓ HR)
  • M3 — glands & smooth muscle (secretions, bronchoconstriction, miosis)

Cholinergic excess

  • SLUDGE: Salivation, Lacrimation, Urination, Defecation, GI motility, Emesis
Seen with cholinomimetics & organophosphate poisoning.

Antimuscarinic toxidrome

  • “Dry as a bone, red as a beet, hot as a hare, blind as a bat, mad as a hatter, full as a flask”

Dental relevance

  • Pilocarpine for xerostomia / Sjögren's (stimulates saliva)
  • Atropine / glycopyrrolate as antisialagogue to dry the field
  • Organophosphate poisoning → atropine + pralidoxime

H1 antihistamines

Block H1 receptors (inverse agonists) to reduce histamine-driven allergy. They do not relieve bronchospasm and do not treat anaphylaxis alone.

Generations

  • 1st gen (sedating, cross BBB, anticholinergic): chlorphenamine, diphenhydramine, promethazine, hydroxyzine, cyclizine
  • 2nd gen (non-sedating): loratadine, cetirizine, fexofenadine, desloratadine, levocetirizine
Mnemonic: 2nd gen don't cross the BBB → no drowsiness.

Main uses

  • Allergic rhinitis (hay fever), urticaria (1st-line), allergic conjunctivitis, insect bites, drug allergy (adjunct)

Motion sickness & antiemetic

  • 1st gen: cyclizine, cinnarizine, promethazine

Anaphylaxis

  • Adjunct only — after adrenaline, for skin/nasal symptoms; never delay adrenaline

Other

  • Short-term sleep aid (1st gen), appetite stimulant (cyproheptadine), premedication

Dental relevance

  • Adjunct for mild allergic reactions (materials, latex); sedative premed
  • Not a substitute for adrenaline in anaphylaxis
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