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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5510_Библиотеки_им_академика_М_И_Перельмана.pdf
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- •Preface
- •Essays
- •Viva questions
- •Dedication
- •Acknowledgement
- •1 Evidence-based practice
- •Overview
- •1.1 Decision-making
- •Evidence-based medicine
- •Best research evidence
- •Clinical expertise
- •Using this book
- •Patient values
- •Benefits and limitations of evidence-based medicine
- •1.2 Randomised controlled trials
- •Components of the randomised controlled trial
- •Randomisation and allocation concealment
- •Philosophy of the book
- •Layout and contents
- •Approaching assessment
- •The main types of assessment
- •Multiple choice questions
- •Single best answer questions
- •Short notes
- •Blinding
- •Completeness of follow-up
- •Sample size calculation
- •Inclusion and exclusion criteria
- •Estimate of effect
- •Different types of randomised controlled trial
- •Phase I, II and III trials
- •Parallel, cross-over, and split-mouth design
- •Bias and assessment of randomised controlled trials
- •Bias
- •Assessing the quality of randomised controlled trials
- •1.3 Other research methods
- •Cohort studies
- •Case-control studies
- •Cross-sectional surveys
- •Case reports
- •1.4 Systematic reviews
- •1.5 How to read a paper
- •Appraisal questions
- •Consort
- •1.6 Clinical practice guidelines
- •Implementation of guidelines
- •Problems with guidelines
- •2 Assessing patients
- •Overview
- •2.1 History
- •The complaint
- •History of the complaint
- •Past dental history
- •Social and family history
- •Medical history
- •2.2 Extra-oral examination
- •Lymph node examination
- •Temporomandibular joint
- •Salivary glands
- •Problem-specific examination
- •Swelling/lump
- •Paraesthesia/anaesthesia
- •Paralysis/motor disturbance
- •2.3 Intra-oral examination
- •2.4 Special investigations
- •Chairside laboratory investigations
- •Evidence-based laboratory medicine
- •Microbiology
- •Viruses
- •Bacteria
- •Fungi
- •Aspiration biopsy
- •Incisional/excisional biopsy
- •Excisional biopsy
- •Incisional biopsy
- •Haematology
- •Biochemistry
- •Immunology
- •Imaging
- •Conventional radiography
- •Contrast investigations
- •Computed tomography
- •Cone beam computed tomography
- •Diagnostic ultrasound
- •Radioisotope imaging
- •Magnetic resonance imaging
- •2.5 Writing a referral letter
- •3 Human disease and patient care
- •Overview
- •3.1 Medical assessment
- •Medical history
- •Physical examination
- •Cardiac failure
- •Management
- •Arrhythmias
- •Management
- •Angina and myocardial infarction
- •Management
- •The respiratory system
- •The upper airway
- •Chronic obstructive pulmonary disease
- •Management
- •Asthma
- •Management
- •Other respiratory diseases
- •Upper or lower respiratory tract infections
- •Cystic fibrosis
- •Pulmonary tuberculosis
- •Haematological disorders
- •Anaemia
- •Management
- •Sickle cell anaemia
- •Leukaemia
- •Management
- •Lymphoma
- •Management
- •Bleeding disorders
- •Management
- •Thrombocytopenia
- •Emergency management of a bleeding patient
- •Anticoagulant therapy
- •Management
- •Antiplatelet therapy
- •Endocrine disease
- •Diabetes mellitus
- •Management
- •Hypothyroidism and hyperthyroidism
- •Management
- •Hypoparathyroidism and hyperparathyroidism
- •Hypoparathyroidism
- •Hyperparathyroidism
- •Hepatic disease
- •Clotting dysfunction
- •Drugs
- •Cross-infection
- •Renal disease
- •Gastrointestinal disease
- •Bone disease
- •Radiotherapy
- •HIV/AIDs
- •Management
- •Cross-infection
- •Neurological disorders
- •Epilepsy
- •Management
- •Psychiatric disorders
- •Organic pathology
- •Psychological origin
- •The psychoses
- •The neuroses
- •Personality disorders
- •Other psychiatric disorders
- •Medications
- •Routine medication
- •Steroid drugs
- •Contraceptive pill
- •Allergies
- •Pregnancy
- •Treatment
- •3.3 Medical emergencies
- •Emergency drugs and equipment
- •Common medical emergencies
- •Syncope
- •Signs and symptoms
- •Cause
- •Principles of treatment
- •Further management
- •Hyperventilation
- •Signs and symptoms
- •Cause
- •Principles of treatment
- •Postural hypotension
- •Signs and symptoms
- •Causes
- •Principles of treatment
- •Choking and aspiration
- •Signs and symptoms
- •Cause
- •Principles of treatment
- •Further management
- •Diabetic emergencies: Hypoglycaemia
- •Signs and symptoms
- •Cause
- •Principles of treatment
- •Further management
- •Epileptic seizure
- •Signs and symptoms
- •Cause
- •Principles of treatment
- •Further management
- •Signs and symptoms
- •Cause
- •Hospital setting
- •Medical risk assessment
- •3.2 Dental relevance of the medical condition
- •The cardiovascular system
- •Congenital and rheumatic heart disease
- •Hypertension
- •Management
- •Principles of management
- •Further management
- •Acute asthma
- •Signs and symptoms of acute severe asthma
- •Signs and symptoms of life-threatening asthma
- •Cause
- •Principles of treatment
- •Further management
- •Anaphylaxis
- •Signs and symptoms
- •Principles of treatment
- •Further management
- •Stroke
- •Signs and symptoms
- •Cause
- •Principles of treatment
- •Further management
- •Benzodiazepine overdose
- •Signs and symptoms
- •Cause
- •Principles of treatment
- •Further management
- •Psychiatric emergencies
- •Signs and symptoms
- •Cause
- •Principles of treatment
- •Angina and myocardial infarction
- •Signs and symptoms
- •Angina
- •Myocardial infarction
- •Cause
- •Principles of treatment
- •Further management for severe angina or myocardial infarction
- •Cardiorespiratory arrest
- •Signs and symptoms
- •Causes
- •Principles of treatment
- •Further management
- •ALS for cardiac arrest
- •Advanced airway management
- •Adrenaline (epinephrine)
- •Hospital transfer
- •3.4 Drug delivery
- •Self-assessment questions
- •True/false
- •Case history question
- •Oral examination questions
- •Self-assessment answers
- •True/false
- •Case history answer
- •Oral examination answers
- •4 Control of pain and anxiety
- •Overview
- •4.1 Systemic analgesia
- •Nociception and pain
- •Nociception
- •Pain
- •The pain system
- •Acute pain
- •Chronic pain
- •Pain control
- •Dental pain and pain after surgery
- •Dosing schedules
- •Preemptive analgesia
- •Preoperative patient preparation
- •Patient-controlled analgesia
- •Route of drug administration
- •Pain and the mind
- •4.2 Local anaesthesia
- •Mechanism of action
- •Amino-esters
- •Amino-amides
- •Potency
- •Speed of onset
- •Duration of action
- •Metabolism and excretion
- •Failure of anaesthesia
- •Complications
- •General complications
- •Psychogenic
- •Toxic
- •Allergic
- •Local complications
- •Soft-tissue trauma
- •Nerve trauma
- •Intravascular injection
- •Complications of inferior alveolar nerve block
- •Types of LA drugs
- •Topical LAs
- •Intraoral
- •Skin
- •Application method
- •Vasoconstrictors
- •Adrenaline (epinephrine)
- •Felypressin (octapressin)
- •Common drugs in dentistry
- •Lidocaine (lignocaine)
- •Prilocaine
- •Articaine
- •Bupivacaine
- •Drug dose for safety
- •4.3 Conscious sedation
- •Assessment for conscious sedation
- •Dental indications
- •Medical and behavioural indications
- •Dental contraindications
- •Medical contraindications
- •Allergy
- •Systemic disease
- •Respiratory disease
- •Pregnancy
- •Liver and kidney disease
- •Muscle disease
- •Obesity
- •Psychiatric disorders
- •Drug interactions
- •Physical status
- •Indicator of sedation need
- •Sedative drugs
- •Nitrous oxide
- •Elimination
- •Undesirable effects
- •Teratogenicity
- •Nausea or vomiting
- •Increased pressure in gas-containing body spaces
- •Benzodiazepines
- •Mechanism of action
- •Undesirable effects
- •Respiratory depression
- •The elderly
- •Elimination
- •Diazepam
- •Midazolam
- •Temazepam
- •Legal status
- •Flumazenil
- •Sedation techniques
- •Oral sedation
- •Inhalation sedation
- •Intravenous sedation
- •Dosage
- •Venous access
- •Amnesia
- •Analgesia
- •Discharge
- •Preoperative starvation
- •Intranasal sedation
- •Monitoring sedated patients
- •4.4 General anaesthesia
- •Patient assessment
- •Social history
- •Smoking
- •Alcohol
- •Home circumstances
- •Drug abuse
- •Previous anaesthetic history
- •Hereditary problems
- •Porphyria
- •Malignant hyperpyrexia
- •Suxamethonium apnoea
- •Physical examination
- •Special investigations
- •Haemoglobin concentration
- •Urinalysis
- •Sickle test
- •Urea and electrolyte (U&E) concentrations
- •Blood glucose concentration
- •Liver function tests (LFTs)
- •Clotting studies
- •Chest X-ray
- •Cervical spine X-ray
- •Electrocardiogram (ECG)
- •Pulmonary function tests
- •Weight
- •Risk assessment
- •Grading of physical status
- •Cardiovascular disease
- •Hypertension
- •Respiratory disease
- •Preoperative medication
- •Preoperative starvation
- •GA technique
- •Maintenance
- •Recovery
- •Monitoring during anaesthesia
- •Cardiovascular system
- •Respiratory system
- •Neuromuscular junction
- •Body temperature
- •Depth of anaesthesia
- •Self assessment questions
- •True/false
- •Single best questions
- •Case histories questions
- •Case history 1
- •Case history 2
- •Self assessment answers
- •True/false
- •Single best answers
- •Case histories answers
- •Case history 1
- •Case history 2
- •Overview
- •5.1 Pulpitis
- •Acute pulpitis
- •Clinical features
- •Radiology
- •Pathology
- •Management
- •Chronic pulpitis
- •Clinical eatures
- •Radiology
- •Pathology
- •Management
- •Acute periapical periodontitis
- •Clinical features
- •Radiology
- •Pathology
- •Management
- •Chronic periapical periodontitis (periapical granuloma)
- •Clinical features
- •Radiology
- •Pathology
- •Management
- •Pathoses associated with periapical inflammation
- •Hypercementosis
- •External resorption
- •5.4 Soft tissue infections of the face
- •Infection sited at a tooth
- •Acute alveolar abscess
- •Clinical features
- •Radiology
- •Pathology
- •Management
- •Spread of infection to facial tissues
- •Lymphatic spread of infection
- •Spread of infection through tissue spaces
- •Floor-of-mouth tissue spaces
- •Other tissue spaces of importance
- •Buccal spaces
- •Pharyngeal tissue spaces
- •Hard palate area
- •Types of facial infection
- •Maxillary infections
- •Mandibular infections
- •Cellulitis
- •Cavernous sinus thrombosis
- •Management of infections about the face
- •Drainage
- •Chronic infection
- •Actinomycosis
- •Clinical features
- •Pathology
- •Management
- •Osteomyelitis
- •Acute osteomyelitis
- •Clinical features
- •Radiology
- •Pathology
- •Management
- •Chronic osteomyelitis
- •Clinical features
- •Radiology
- •Pathology
- •Management
- •Clinical features
- •Radiology
- •Pathology
- •Management
- •Osteoradionecrosis
- •Clinical features
- •Radiology
- •Pathology
- •Management
- •Medication related osteonecrosis of the jaw (MRONJ)
- •Clinical features
- •Radiology
- •Pathology
- •Management
- •Periostitis
- •Self-assessment questions
- •True/false
- •Single best questions
- •Case history questions
- •Case history 1
- •Case history 2
- •Case history 3
- •Case history 4
- •Viva questions
- •Self-assessment answers
- •True/false
- •Single best answers
- •Case history answers
- •Case history 1
- •Case history 2
- •Case history 4
- •Clinical features
- •Radiology
- •Likely diagnosis
- •Viva answers
- •6 Removal of teeth and surgical implantology
- •Overview
- •6.1 Dental extractions
- •Assessment for extraction
- •Indications for dental extraction
- •History and clinical examination
- •Radiographic examination
- •Treatment planning
- •Consent
- •Infection control
- •Reducing risk of errors in surgery
- •Surgical removal of teeth
- •Surgical flap design
- •Postoperative care
- •Complications of dental extractions
- •Postoperative pain
- •Postoperative swelling
- •Trismus
- •Fracture of teeth
- •Excessive bleeding
- •History
- •Examination
- •Achieve haemostasis
- •Postoperative infection
- •Osteomyelitis
- •Damage to soft tissues
- •Damage to nerves
- •Opening of the maxillary sinus
- •Loss of tooth
- •Loss of tooth fragment
- •Fracture of the maxillary tuberosity
- •Fracture of jaw
- •Dislocation of the mandible
- •Displacement of tooth into the airway
- •Surgical emphysema
- •6.2 Impacted and ectopic teeth
- •Assessment
- •Third molars
- •Impacted maxillary canines
- •Impacted lower second premolars
- •History and clinical examination
- •Radiological examination
- •Diagnosis
- •Treatment options
- •Indications for removal of third molars
- •Surgical techniques
- •Lower third molar surgery
- •Upper third molar surgery
- •Maxillary canines
- •Mandibular second premolars
- •Supernumerary teeth
- •Complications of treatment of impacted and ectopic teeth
- •6.3 Preprosthetic surgery
- •Retained teeth/roots removal
- •Denture irritation hyperplasia
- •Tori
- •Muscle attachments
- •Alveolar ridge augmentation
- •Sulcus deepening
- •Nerve repositioning
- •6.4 Dental implant surgery
- •Assessment
- •Indications for implant treatment
- •Assessment for oral implant surgery
- •Clinical examination
- •Presurgical investigations
- •Imaging
- •Periapical view
- •Panoramic view
- •Lateral cephalometric radiograph
- •Cone beam computed tomography (CBCT)
- •Surgical techniques
- •Bone augmentation
- •Autogenous bone
- •Alloplastic materials
- •Ceramics
- •Allografts
- •Xenografts
- •Bone grafting techniques
- •Onlay grafting
- •Interpositional grafting
- •Sinus elevation or lift
- •Stimulation of bone regeneration
- •Guided bone regeneration (GBR)
- •Distraction osteogenesis
- •Implant placement
- •Implant exposure
- •Immediate loading of implants
- •Postoperative care
- •Soft tissue surgery
- •Timing of implant placement
- •Immediate implant placement
- •Delayed immediate implants
- •Zygoma implants
- •Implant success
- •Self-assessment questions
- •True/false
- •Case history questions
- •Case history 1
- •Case history 2
- •Viva questions
- •Self-assessment answers
- •True/false
- •Case history answers
- •Case history 1
- •Case history 2
- •Viva answers
- •7 Diseases of bone and the maxillary sinus
- •Overview
- •7.1 Diseases of bone
- •Normal jaw skeleton
- •Benign fibro-osseous lesions
- •Fibrous dysplasia
- •Clinical features
- •Pathology
- •Radiology
- •Management
- •Cemento-ossifying fibroma
- •Clinical features
- •Pathology
- •Radiology
- •Management
- •Paget’s disease of bone
- •Cemento-osseous dysplasias
- •Giant-cell granuloma (central giant-cell granuloma)
- •Osteoporosis
- •Hyperparathyroidism
- •Genetic disorders
- •Bone tumours
- •7.2 Diseases of the maxillary sinus
- •Anatomy
- •Histology
- •Anomalies
- •Inflammation (“sinusitis”)
- •Chronic maxillary sinusitis
- •Acute maxillary sinusitis
- •Mucosal cysts of the antrum
- •Benign tumours
- •Osteoma
- •Odontogenic cysts and benign tumours
- •Malignancy
- •Antral response to inflammation of dental origin (odontogenic sinusitis)
- •Displacement of roots into the sinus
- •Oro-antral communication
- •Fracture of the maxillary tuberosity
- •Self-assessment questions
- •True/false
- •Single best questions
- •Case history questions
- •Case history 1
- •Case history 2
- •Case history 3
- •Case history 4
- •Case history 5
- •Viva questions
- •Self-assessment answers
- •True/false
- •Single best answers
- •Case history answers
- •Case history 1
- •Case history 2
- •Case history 3
- •Case history 4
- •Case history 5
- •Viva answers
- •Overview
- •8.1 Assessment of the injured patient
- •Primary survey
- •Airway
- •Breathing
- •Circulation
- •Disability
- •Exposure and environmental control
- •Radiographic examination
- •Secondary survey
- •Documentation
- •Children
- •Adult domestic violence and abuse
- •8.2 Dental injuries
- •Management
- •8.3 Facial soft tissue injuries
- •Aetiology
- •Clinical presentation
- •Radiology
- •Surgical management of lacerations
- •Surgical management of burns
- •8.4 Facial fractures
- •Aetiology
- •Clinical presentation
- •Radiological examination
- •Principles of facial fracture management
- •Dento-alveolar fractures
- •Mandibular fractures
- •Zygoma (or malar) fractures
- •Orbital fractures
- •Maxillary fractures
- •Nasal/nasoethmoidal fractures
- •Techniques for facial fracture management
- •Closed reduction and indirect fixation in the mandible
- •Acrylic splints
- •Disadvantages of IMF fixation
- •Peralveolar and circumandibular wiring
- •Gunning-type splints
- •Closed reduction and indirect fixation in the maxilla
- •Suspension wires
- •Extraoral craniomandibular fixation
- •Open reduction and direct fixation in the mandible and maxilla
- •Plating with mini- and micro-plating systems
- •Titanium mesh
- •Biodegradable plates and screws
- •Transosseous and intraosseous wiring
- •Bone screws
- •8.5 Gunshot wounds
- •Weapons
- •Management
- •Initial
- •Imaging
- •Soft tissues
- •Hard tissues
- •8.6 Dislocation of the mandible
- •8.7 Complications of facial injury
- •Complications of dental injury
- •Primary teeth
- •Permanent teeth
- •Complications of facial soft tissue injury
- •Complications of facial fractures
- •Self-assessment questions
- •True/false
- •Single best questions
- •Case history questions
- •Case history 1
- •Case history 2
- •Case history 3
- •Case history 4
- •Viva questions
- •Self-assessment answers
- •True/false
- •Single best answers
- •Case history answers
- •Case history 1
- •Case history 2
- •Case history 3
- •Case history 4
- •Viva answers
- •9 Dentofacial and craniofacial anomalies
- •Overview
- •9.1 Congenital anomalies
- •Aetiology and types
- •Clinical management
- •History
- •Clinical examination
- •Investigations
- •Imaging
- •Cephalometric analysis
- •Diagnosis
- •Treatment planning
- •9.2 Orthognathic surgery
- •Preoperative stage
- •Preoperative planning
- •Preoperative care
- •Treatment
- •Mandibular surgery
- •Genioplasty
- •Maxillary surgery
- •Postoperative care
- •Airway management
- •Analgesia
- •Follow-up
- •9.3 Cleft lip and palate surgery
- •9.4 Craniofacial surgery and osteodistraction
- •Osteodistraction techniques
- •Technique
- •9.5 Cosmetic facial surgery
- •Self-assessment questions
- •True/false
- •Single best questions
- •Viva questions
- •Self-assessment answers
- •True/false
- •Single best answers
- •Viva answers
- •10 Cysts and odontogenic tumours
- •Overview
- •10.1 General features
- •Cyst growth
- •Classification of cysts
- •Other cysts
- •Odontogenic cysts
- •10.2 Examination
- •General clinical features
- •Radiological examination: General principles
- •Maxilla
- •Mandible
- •Radiological signs
- •Margins
- •Shape
- •Locularity
- •Effects on adjacent structures
- •Effect on unerupted teeth
- •Radicular cyst
- •Radiology
- •Pathology
- •Residual radicular cyst
- •Radiology
- •Pathology
- •Inflammatory collateral cysts
- •Radiology
- •Pathology
- •Dentigerous cyst
- •Radiology
- •Pathology
- •Eruption cyst
- •Radiology
- •Pathology
- •Odontogenic keratocyst
- •Radiology
- •Pathology
- •Lateral periodontal and botryoid cysts
- •Radiology
- •Pathology
- •Gingival cysts
- •Glandular odontogenic cyst
- •Radiology
- •Pathology
- •Calcifying odontogenic cyst
- •Radiology
- •Pathology
- •Orthokeratinising odontgenic cyst
- •Radiology
- •Pathology
- •Nasopalatine cyst
- •Radiology
- •Pathology
- •Nasolabial cyst
- •Radiology
- •Pathology
- •Solitary bone cyst
- •Radiology
- •Pathology
- •Aneurysmal bone cyst
- •Radiology
- •Pathology
- •10.4 Surgical management of cysts
- •Enucleation
- •Marsupialisation
- •Surgical management of particular cysts
- •Radicular cysts
- •Odontogenic keratocyst
- •Eruption cysts
- •Solitary bone cyst
- •Aneurysmal bone cyst
- •Malignant odontogenic tumours
- •Ameloblastoma
- •Odontomes
- •Mesenchymal odontogenic tumours
- •10.7 Surgical management of odontogenic tumours
- •Self-assessment questions
- •True/false
- •Single best questions
- •Case history 2
- •Case history 3
- •Short note questions
- •Essay questions
- •Viva questions
- •Self-assessment answers
- •True/false
- •Single best answers
- •Case history answers
- •Case history 1
- •Case history 2
- •Case history 3
- •Short note answers
- •Essay question answers
- •Viva answers
- •11 Mucosal diseases
- •Overview
- •11.1 Normal oral mucosa
- •Normal structures
- •Leukoedema
- •11.2 Conditions related to friction or trauma
- •Smoker’s palatal keratosis
- •Fibrous hyperplasia and neoplasia
- •Fibroepithelial polyp
- •Denture irritation hyperplasia
- •Connective tissue neoplasms
- •11.3 Ulceration
- •Traumatic ulceration
- •Drug-related ulceration
- •Recurrent aphthous stomatitis: Aphthous ulceration
- •Aetiology
- •Diagnosis
- •Management
- •11.4 Infections
- •Bacterial infections
- •Viral infections
- •Herpes simplex
- •Primary herpetic gingivostomatitis
- •Herpes labialis (cold sores)
- •Herpes zoster
- •Coxsackievirus
- •Epstein–barr virus
- •Human papillomavirus
- •Kaposi’s sarcoma
- •Hairy leukoplakia
- •Erythematous candidiasis
- •HIV-related gingivitis
- •HIV-related periodontitis
- •Other mucosal manifestations in HIV infection
- •Fungal infections
- •Angular cheilitis
- •Chronic hyperplastic candidiasis
- •Clinical features
- •Histopathological features (fig. 11.12)
- •Median rhomboid glossitis
- •11.5 Lichen planus
- •Clinical features
- •Oral lesions
- •Skin lesions
- •Lichenoid mucositis
- •Histopathological features
- •Aetiology
- •Management
- •11.6 Pigmented lesions
- •Black hairy tongue
- •Amalgam tattoos
- •Melanotic lesions
- •Discrete melanin-pigmented lesions
- •Malignant melanoma
- •Diffuse oral melanosis
- •Other lesions
- •11.7 Vesiculo-bullous lesions
- •Immune-mediated conditions
- •Mucous membrane pemphigoid
- •Pemphigus vulgaris
- •Other autoimmune conditions
- •Erythema multiforme
- •Genetic disorders
- •Angina bullosa haemorrhagica
- •11.8 Granulomatous disorders
- •Causes of granulomas
- •Foreign body
- •Orofacial granulomatosis
- •Crohn’s disease
- •Sarcoidosis
- •11.9 Other mucosal conditions
- •White sponge naevus
- •Diagnosis
- •Management
- •Geographic tongue
- •Diagnosis
- •Management
- •Epulides
- •Fibrous epulis
- •Vascular epulis
- •Giant-cell epulis (peripheral giant-cell granuloma)
- •Self-assessment questions
- •True/false
- •Single best questions
- •Case history questions
- •Case history 1
- •Case history 2
- •Case history 3
- •Case history 4
- •Case history 5
- •Viva questions
- •Self-assessment answers
- •True/false
- •Single best answers
- •Case history answers
- •Case history 1
- •Case history 2
- •Case history 3
- •Case history 4
- •Case history 5
- •Viva answers
- •12 Oral potentially malignant disorders and oral cancer
- •Overview
- •12.1 Oral potentially malignant disorders
- •Leukoplakia
- •Erythoplakia
- •Oral lichen planus
- •Oral lichenoid reactions
- •Oral lesions of graft-versus-host disease
- •Oral lupus erythematosus
- •Chronic hyperplastic candidosis and candidal leukoplakia
- •Proliferative verrucous leukoplakia (PVL)
- •Types of oral cancer
- •Minor salivary gland cancers
- •Malignant melanoma
- •Malignant lymphoma
- •Leukaemia
- •Metastatic deposits
- •Rare neoplasms
- •Squamous cell carcinoma
- •Aetiology
- •Smoking
- •Paan and other tobacco use
- •Alcohol
- •Ultraviolet light
- •Diet
- •Viruses
- •Clinical features
- •The lip
- •Intra-oral surfaces
- •Head and neck
- •Pathology
- •Histopathological features
- •Bone invasion
- •Metastasis
- •Grading and staging
- •Histological grading: Prognostic features
- •Imaging of oral squamous cell carcinoma
- •Treatment
- •Exophytic verrucous hyperplasia
- •Oral submucous fibrosis
- •Palatal lesions in reverse smokers
- •Genetic mucosal lesions
- •Clinically normal susceptible mucosa
- •12.2 Pathology, dysplasia grading and management
- •Epithelial dysplasia
- •Grading of dysplasia
- •Molecular pathology of opmds
- •12.3 Management of opmds
- •12.4 Oral cancers
- •Epidemiology
- •Global incidence and trends
- •Morbidity and mortality
- •Surgery
- •Radiotherapy
- •Chemotherapy
- •12.5 Role of the dentist in prevention, detection and treatment
- •Prevention
- •Early diagnosis and screening
- •Referral
- •Dental care prior to radiotherapy
- •Post-treatment care
- •Self-assessment questions
- •True/false
- •Single best questions
- •Case history questions
- •Case history 1
- •Case history 2
- •Case history 4
- •Viva questions
- •Self-assessment answers
- •True/false
- •Single best answers
- •Case history answers
- •Case history 1
- •Case history 2
- •Case history 3
- •Case history 4
- •Viva answers
- •13 Facial skin and neck
- •Overview
- •13.1 Facial skin lesions
- •Non-melanoma skin cancer
- •Malignant melanoma
- •13.2 Neck swellings
- •Lymphadenopathy
- •Examination and investigation of lymph nodes
- •Bacterial infections
- •Viral infections
- •Fungal and protozoal infections
- •Sarcoidosis
- •Haematological malignancy
- •Secondary malignancy
- •Other causes of lymphadenopathy
- •Cysts of the neck
- •Self-assessment questions
- •True/false
- •Case history questions
- •Case history 1
- •Case history 2
- •Self-assessment answers
- •True/false
- •Single best answers
- •Case history answers
- •14 Salivary gland disease
- •Overview
- •14.1 Anatomy
- •Minor salivary glands
- •Submandibular gland
- •Parotid gland
- •14.2 Investigations
- •History and clinical examination
- •Sialometry
- •Radiology
- •Is there a calculus present?
- •Plain radiographs, or ultrasound
- •Parotid glands
- •Submandibular gland
- •Ultrasound
- •Is there an obstruction in the duct system? What is the condition of the duct system?
- •Sialography
- •Sialoendoscopy
- •Is there a mass present?
- •Ultrasound
- •Is there an abnormality of gland function?
- •Radio-isotope imaging
- •Biopsy
- •14.3 Salivary gland disorders
- •Obstructive salivary disorders
- •Extra-ductal obstruction
- •Duct wall thickening
- •Intra-ductal obstruction
- •Acute sialadenitis
- •Viral sialadenitis
- •Bacterial sialadenitis
- •Chronic sialadenitis
- •Bacterial sialadenitis
- •Relapsing parotitis
- •Radiation sialadenitis
- •Chronic sclerosing sialadenitis
- •Sarcoidosis
- •Sialosis
- •Sjögren’s syndrome
- •Diagnosis
- •Management
- •Systemic disorders and salivary function
- •Salivary gland tumours
- •Benign tumours
- •Pleomorphic adenoma
- •Warthin’s tumour
- •Other adenomas
- •Soft tissue salivary tumours
- •Malignant tumours
- •Adenoid cystic carcinoma
- •Mucoepidermoid carcinoma
- •Acinic-cell carcinoma
- •Secretory carcinoma
- •Polymorphous adenocarcinoma
- •Carcinoma arising in pleomorphic adenoma
- •Other carcinomas
- •Other malignant tumours
- •Molecular pathology of salivary glands
- •Salivary gland cysts
- •Mucous extravasation mucocoele
- •Mucous retention mucocoele
- •Ranula
- •14.4 Surgery
- •Minor salivary glands
- •Submandibular salivary gland
- •Self-assessment questions
- •True/false
- •Single best questions
- •Case history questions
- •Case history 1
- •Case history 3
- •Case history 4
- •Case history 5
- •Case history 6
- •Viva questions
- •Self-assessment answers
- •True/false
- •Single best answers
- •Case history answers
- •Case history 1
- •Case history 2
- •Case history 3
- •Case history 4
- •Case history 5
- •Case history 6
- •Viva answers
- •15 Facial pain
- •Overview
- •15.1 Assessment of a patient suffering from orofacial pain
- •Social history
- •Trigeminal neuralgia
- •Clinical presentation
- •Nature
- •Duration
- •Site
- •Initiating factors
- •Associated signs and symptoms
- •Special investigations
- •Medical management
- •Surgical management
- •Painful trigeminal neuropathies
- •Painful trigeminal neuropathy attributed to herpes zoster (preherpetic neuralgia)
- •Clinical presentation
- •Nature
- •Duration
- •Site
- •Associated signs and symptoms
- •Special investigations
- •Medical management
- •Trigeminal postherpetic neuralgia
- •Clinical presentation
- •Nature
- •Duration
- •Site
- •Accompanying signs and symptoms
- •Special investigations
- •Medical management
- •Surgical management
- •Glossopharyngeal neuralgia
- •Clinical presentation
- •Nature
- •Duration
- •Site
- •Initiating factors
- •Associated signs and symptoms
- •Special investigations
- •Medical management
- •Surgical management
- •15.3 Primary and secondary headaches
- •Migraine
- •Clinical presentation
- •Nature
- •Duration
- •Site
- •Initiating factors
- •Associated signs and symptoms
- •Special investigations
- •Medical management
- •Tension type headache
- •Clinical presentation
- •Nature
- •Duration
- •Site
- •Initiating factors
- •Associated signs and symptoms
- •Special investigations
- •Medical management
- •Trigeminal autonomic cephalalgias
- •Clinical presentation
- •Nature
- •Duration
- •Site
- •Initiating factors
- •Associated signs and symptoms
- •Special investigations
- •Medical management
- •Secondary headaches
- •Giant-cell arteritis (cranial arteritis, temporal arteritis)
- •Clinical presentation
- •Nature
- •Duration
- •Site
- •Initiating factors
- •Associated signs and symptoms
- •Special investigations
- •Medical management
- •15.4 Idiopathic orofacial pain
- •Persistent idiopathic facial pain (PIFP)
- •Clinical presentation
- •Nature
- •Duration
- •Site
- •Initiating/ameliorating factors
- •Associated signs and symptoms
- •Clinical examination
- •Medical history
- •Social history
- •Special investigations
- •Medical management
- •Persistent idiopathic dentoalveolar pain (atypical odontalgia)
- •Burning mouth syndrome
- •Clinical presentation
- •Nature
- •Duration
- •Site
- •Initiating/ameliorating factors
- •Associated symptoms
- •Clinical examination
- •Special investigations
- •Medical management
- •Self-assessment questions
- •True/false
- •Single best questions
- •Case history questions
- •Case history 1
- •Case history 2
- •Case history 3
- •Case history 4
- •Essay question
- •Self-assessment answers
- •True/false
- •Single best answers
- •Case history answers
- •Case history 1
- •Case history 2
- •Case history 3
- •Case history 4
- •Case history 5
- •Essay answer
- •16 Disorders of the temporomandibular joint
- •Overview
- •16.1 Anatomy and examination
- •Anatomy
- •Components
- •The mandibular condyle
- •The mandibular (glenoid) fossa
- •Interarticular disc (meniscus)
- •Capsule
- •Ligaments
- •Joint movement
- •Examination
- •Clinical examination
- •Joint examination
- •Movement
- •Pain on palpation
- •Auscultation
- •Muscle examination
- •Radiology
- •Arthroscopy
- •16.2 Temporomandibular joint disorders (TMDs)
- •What are TMDs?
- •Clinical features
- •Radiology
- •Management
- •Internal derangement
- •Disc displacement with reduction
- •Clinical features
- •Radiology
- •Management
- •Disc displacement without reduction
- •Clinical features
- •Radiology
- •Management
- •Surgical treatment of internal derangement
- •16.3 Other conditions affecting the joint
- •Degenerative joint disease
- •Clinical features
- •Radiology
- •Management
- •Rheumatoid arthritis
- •Clinical features
- •Radiology
- •Management
- •Juvenile idiopathic arthritis (juvenile chronic arthritis)
- •Malignancy mimicking a TMD
- •Rare disorders of the TMJ
- •Trauma
- •Effusion
- •Clinical features
- •Radiology
- •Management
- •Dislocation
- •Clinical features
- •Radiology
- •Management
- •Ankylosis
- •Self-assessment questions
- •True/false
- •Single best questions
- •Case history questions
- •Case history 1
- •Case history 2
- •Case history 3
- •Case history 4
- •Viva questions
- •Self-assessment answers
- •True / false
- •Single best answers
- •Case history answers
- •Case history 1
- •Case history 2
- •Case history 3
- •Case history 4
- •Viva answers
- •17 Radiation protection
- •Overview
- •17.1 Ionising radiation and its effects
- •Interaction with matter
- •Somatic and genetic effects of X-rays
- •Doses and risks in dental radiography
- •17.2 Radiation protection
- •Protection of patients
- •Selection of bitewing radiographs
- •Selection of periapical radiographs
- •Selection of panoramic radiographs
- •Selection of cone beam CT examinations
- •Dose limitation
- •Quality assurance
- •Protection of staff
- •Position
- •Workload
- •Local rules
- •‘Good practice’ guidelines
- •Administration of radiation protection
- •Employer (legal person)
- •Registration
- •Referrer
- •Practitioner
- •Operator
- •Radiation protection supervisor
- •Radiation protection adviser (RPA)
- •Medical physics expert (MPE)
- •Self-assessment questions
- •True/ false
- •Single best questions
- •Essays
- •Viva questions
- •Self-assessment answers
- •True /false
- •Single best answers
- •Essay plans
- •Viva answers
- •Index

12 • Oral Potentially Malignant Disorders and Oral Cancer
193
of PVL sufferers develop oral cancer and progressive increase
in dysplasia grade is frequently seen in sequential biopsies.
Close follow-up is undertaken as the mucosal lesions are often
too large to permit laser excision and the aim is to detect oral
cancer as early as possible. Sometimes multifocal synchronous and nonsynchronous oral cancers occur.
Exophytic Verrucous Hyperplasia
This is a recently recognized disorder described by an expert
group in Southeast Asia. It is characterized by verrucous or
papillary growth, sometimes on a background of submucous fibrosis that lacks any downward growth of the hyperplasic oral epithelium. The natural history is uncertain and
there may be overlap with PVL and other verrucous mucosal lesions. Patients with exophytic verrucous hyperplasia
should be regarded as having an oral potentially malignant
disorder until larger studies become available
ORAL SUBMUCOUS FIBROSIS
Oral submucous fibrosis is related to using paan, which is a
leaf quid containing areca nut. Many types exist, including
fresh products consumed in the Indian subcontinent and
Southeast Asia, as well as packed proprietary products.
Tobacco, slaked lime, spices and other ingredients may be
added; in Southeast Asia, areca nuts are often chewed fresh.
The mucosa and teeth become stained orange–brown because paan is held in the mouth for long periods. The
affected mucosa becomes pale in colour and feels firm on
palpation (Fig. 12.2). Fibrous bands may develop in the buccal mucosa and a pale, constricting fibrosis typically involves
the palate. Mouth opening becomes restricted and swallowing may be difficult. The risk of developing oral carcinoma
has been estimated at around 5%, although the risk of submucous fibrosis itself cannot be separated from the risks
posed by carcinogenic substances in paan. In biopsy material, a subepithelial band of fine fibrillary collagen is seen in
the lamina propria and the oral epithelium can be reduced
to only a few cell layers in thickness. Keratinisation and
chronic inflammation may be present in some cases. Where
areas of erythroplakia and leukoplakia are present, biopsies
may show epithelial dysplasia or even carcinoma.
PALATAL LESIONS IN REVERSE SMOKERS
Reverse smoking is prevalent in countries such as Sri Lanka,
Venezuela, Sardinia, Panama and India, particularly in the
state of Andhra Pradesh. The smoker puts the lit end of a
type of cheroot into the oral cavity, then inhales the smoke
from the burning end. Palatal lesions are consequently
common and are known to undergo malignant transformation over time.
GENETIC MUCOSAL LESIONS
The rare disorders tylosis, epidermolysis bullosa and dyskeratosis congenita predispose to the development of OPMDs and oral cancer. Keratotic and red lesions may also be
found in Fanconi’s anaemia and these are known to have a
high transformation rate to oral cancer. Patients with these
disorders should be followed up at least 6 month intervals.
CLINICALLY NORMAL SUSCEPTIBLE MUCOSA
It is recognized that in certain conditions the oral mucosa
has increased susceptibility to oral cancer even if no clinical
abnormality can be observed in the oral cavity. The oral
mucosa in such instances is therefore considered as an
OPMD. Chronic iron deficiency results in generalised mucosal atrophy because iron is an essential growth requirement
for the oral epithelium. Sideropenic dysphagia is a known
risk factor for oral cancer but can be mitigated by treating
medically. Genetic disorders (as mentioned in the previous
section) such as Fanconi’s anaemia may also have a phase
where the oral mucosa is clinically normal, though visible
lesions may develop during surveillance.
12.2 Pathology, Dysplasia Grading and Management
LEARNING OBJECTIVES
You should:
• know the features of epithelial dysplasia.
• understand the significance of dysplasia grade.
• be aware of the biology and molecular pathology of
OPMDs.
Fig. 12.2 Submucous fibrosis showing tethering bands involving the
buccal mucosa.
EPITHELIAL DYSPLASIA
The term dysplasia is used in a variety of contexts in pathology and means literally ‘abnormal growth’. In the context
of OPMDs, it refers to a combination of cytological changes
and disturbances of cellular arrangements seen during the
process of malignant transformation. Epithelial dysplasia is
currently categorized by oral and maxillofacial pathologists
into mild, moderate and severe grades (Figs. 12.3 and
12.4). An alternative binary grading system that classifies
‘low grade’ and ‘high grade’ dysplasia may be used. Such
binary systems are widely used in pathology for potentially
malignant disorders in sites other than the oral cavity. The
architectural and cellular features seen in dysplasia are
given in Table 12.2.

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Fig. 12.3 Mild epithelial dysplasia, with subtle cytological atypia
Fig. 12.4 Moderate epithelial dysplasia, some oral pathologists might
grade this as severe epithelial dysplasia, but would agree that it is a
high-grade dysplasia.
Table 12.2 Microscopic Features of Epithelial Dysplasia
HISTOLOGICAL ARCHITECTURAL FEATURES SIGNIFICANCE
Irregular epithelial stratification Keratinisation may be seen in the lower layers of oral epithelium; orderly maturation is disturbed
Loss of polarity of basal cells Loss of the intrinsic symmetry in the shape, structure and organisation of basal cells.
Drop shaped rete processes Basal cell proliferation and accumulation alter the interface morphology
Increased number of mitotic figures Molecular changes to oncogenes, tumour suppressor genes and transcriptional factors drive
Abnormally superficial mitotic figures Mitotic figures are normally seen in basally located stem cells and their amplifying progeny. Arrested
Premature keratinisation in single cells
(dyskeratosis)
Keratin pearls within rete processes Keratinisation in concentric layers of cells results in a whorl or keratin pearl; this can be a reactive
Loss of epithelial cell cohesion Loss of intercellular cohesion between keratinocytes (acantholysis) causes cell separation and round-
HISTOLOGICAL CELLULAR FEATURES SIGNIFICANCE
Anisonucleosis Abnormal variation in nuclear size resulting from abnormal nuclear structural and activity
Nuclear pleomorphism Abnormal variation in nuclear shape resulting from changes in nuclear structure and activity
Anisoscytosis Abnormal variation in cell size
Cellular pleomorphism Abnormal variation is cell shape Keratinocytes may become spindle-shaped in HPV-related dysplasia
Increased nuclear to cytoplasmic ration Often results from increased nuclear size and dysregulation of nuclear and cytoplasmic processes
Atypical mitotic figures Atypical mitotic figures have an abnormal chromosomal distribution or an excessive number
Increased number and size of nucleoli Nucleoli are the sites of ribosome biogenesis and their increase may reflect greater protein
Nuclear hyperchromasia Dark staining by haematoxylin may be the result of increased nuclear DNA content
FEATURES SEEN IN CYTOLOGY PREPARATIONS SIGNIFICANCE
Nuclear changes Clumping and irregular distribution of chromatin, nuclear crowding, irregularities of nuclear
Image analysis of nuclear features DNA ploidy is a powerful predictor of malignant transformation
Cytoplasmic changes Keratinisation, tadpole-shaped, spindle-shaped and bizarre cytoplasmic outlines
Alteration of basal-apical polarity may be a cause of tumour initiation and may reflect early
epithelial-mesenchymal transition
increased cell proliferation
mitotic figures (mitosoid bodies) are seen in the superficial layers in HPV-related dysplasia
Dyskeratosis is caused by premature keratin formation resulting in compacted eosinophilic
cytoplasm and change in cell shape in the lower cell layers
feature
ing of shape. It is a feature of some immune-mediated and inflammatory diseases as well as dysplasia
changes impacting on chromatin packing
of mitotic spindles resulting in multipolar appearance
synthesis; however, abnormality of their many other functions may be important drivers of
dysplasia
membrane, micronuclei and nuclear moulding may be seen in addition to nuclear features
observed in histological sections
HPV, Human papilloma virus.

Grading of Dysplasia
Studies on histopathological grading show poor agreement between even specialist pathologists. This problem
arises partly because of lack of scientific evidence for
weighting the various features of dysplasia. For example,
drop-shaped rete processes are generally accepted as a sinister feature, whereas increased mitotic rate may be seen in
reactive processes. Both inter- and intraobserver variability
rates are high and the biological behaviour of an individual OPMD does not always correlate with its grade. A
meta-analysis study showed that mild (low grade) dysplasia was associated with an annual malignant transformation rate of 1.7%, whereas combined moderate and severe
(high grade) dysplasia had a 3.7% annual transformation
rate. Problems with grading may also arise because of
nonrepresentative sampling at the time of biopsy. It is important to select the area of greatest clinical suspicion for
biopsy of an OPMD and sometimes multiple punch biopsies
can reveal where the most florid changes are present. In
contrast to biopsy of a suspected oral cancer, there is no
requirement to include the margin with normal tissue.
Although histopathological grading is intrinsically unreliable, the presence of dysplasia in a suspicious lesion remains the best-known predictive indicator of malignant
change.
12 • Oral Potentially Malignant Disorders and Oral Cancer
Fig. 12.5 Human papilloma virus (HPV)–related dysplasia, showing
mitosoid bodies high in the epithelium and disordered maturation.
195
differentiated lesions that are low risk. Further research is
required, and it is likely that a combination of biomarkers
will come into clinical use in the future. Clinical assessment
by experienced specialists remains the gold standard for the
diagnosis and management of OPMDs currently.
MOLECULAR PATHOLOGY OF OPMDS
A complex pattern of accumulation of gene mutations
and transcriptional dysregulation leads to transformation
from normal tissue to a cancer. Large scale sequencing
studies have shown that OMPDs show similar molecular
changes to those found in oral cancer, but with lower mutational rates. The most frequent mutations in OMPDs are
found in TP53, CDKN2A, NOTCH1 and PIK3CA, though
numerous other genes are known to be mutated but at
much lower frequency. The mutational burden increases
with progression of dysplasia grade and is highest in oral
cancer. Commonly, T.C substitutions in the sequence
context 59-ATN-39 correlate with tobacco exposure.
Alterations in mRNA transcripts have also been found and
may have predictive value when combined into a molecular signature.
High-risk HPV has been found in a subset of OMPDs
clinically diagnosed as leukoplakia, erythroleukoplakia
or erythroplakia, most often occurring in the floor of the
mouth or ventral tongue. Severe dysplasia with characteristic histological features, including intraepithelial
spindle cells and mitosoid bodies, is found and the diagnosis can be confirmed by HPV testing (Fig. 12.5). Malignant transformation has been described in HPV-related
dysplasia, but more evidence is needed to determine
whether it behaves differently from its non-HPV–related
counterparts.
Biomarkers have been extensively researched to aid in
risk stratification of OPMDs. Ploidy analysis can detect relatively gross changes to DNA and is a useful tool that can
supplement dysplasia grading. It can be difficult to recognize early dysplasia where minimal changes are present
and only hyperkeratosis is seen in the biopsy. Immunohistochemical staining for cytokeratin 13 can be used to identify
12.3 Management of OPMDs
Clinical risk factors for malignant change include tobacco
habit, high alcohol intake and possibly poor diet. Clinical
factors that must also be taken into account are:
n
female gender
n
extensive or spreading lesions
n
lesions in the floor of mouth/ventral tongue, retromolar
area, palate or pillar of fauces
n
red, speckled, verrucous or nodular appearance
n
presence of multifocal lesions.
Most important is the presence of epithelial dysplasia.
Management should include:
n
clear information and explanation of the significance of
the lesion to the patient
n
intervention to stop tobacco habit, paan use and limit
alcohol intake
n
treat anaemia, Candida infection or other underlying
factors if present
n
surgical or laser excision or drug treatment may be
considered
n
regular review and observation, and intraoral photography can be useful
n
prompt investigation if signs or symptoms of cancer appear.
Referral to a specialist centre is usually advisable for patients presenting with white or red mucosal patches, or
other suspicious lesions. Biopsy is normally required for diagnosis and to determine whether epithelial dysplasia is
present. Occasionally biopsy may show invasive cancer in a
white or red patch at the outset. Patients with OMPDs may
be followed up in primary or secondary care settings or
through shared care pathways.

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12.4 Oral Cancers
LEARNING OBJECTIVES
You should:
• know the global epidemiology and types of oral cancers.
• know the clinical and pathological features of squamous
cell carcinoma,
• understand the principles of management of squamous
cell carcinoma,
Most oral cancers do not arise in a clinically identified oral
potentially malignant disorder and are diagnosed as primary
cancerous lesions. They are typically painless, unless infected
or advanced, and often cause no symptoms. For this reason,
the need to conduct a careful systematic examination for
every patient cannot be stressed too much. Extra-oral examination should include both visual inspection of the face and
neck and palpation of the neck (see Chapters 2 and 16). The
patient’s head should be tilted forwards and the lymph nodes
in the neck palpated in relaxed tissue. A routine technique
should be adopted, perhaps starting with the submental
nodes and then moving to more posterior node groups. The
oral mucosa and oropharynx should be examined carefully.
The tongue should be protruded to detect lateral deviation
and then relaxed and lifted to allow examination of its ventral surface and the floor of the mouth. Correct positioning
and the use of good illumination and mirrors are important
factors. When oral cancer is detected, prompt referral is essential. The importance of attending at the hospital should
be stressed, without provoking undue anxiety. Until a biopsy
result is available, providing a definitive diagnosis should be
avoided. Any ulcer that fails to heal within a 3-week period
should be regarded as suspicious, and the patient should be
referred to a specialist.
EPIDEMIOLOGY
Global Incidence and Trends
The global incidence of oral and oropharyngeal cancer has
been estimated at over 400,000 new cases per year. The
incidence of oral squamous carcinoma is 9 per 100,000 in
the UK resulting in around 6800 new cases every year.
There is marked geographical variation in distribution,
with the highest incidence in the Indian subcontinent and
Southeast Asia, because of the particular use of paan and
tobacco. Oral cancer ranks in the top ten in the global
prevalence tables of cancer. The incidence of oral cancer is
rising and more cases are seen in younger age groups. The
male to female ratio of around 2.5:1 is also changing, with
an increasing oral cancer incidence in women, particularly
involving the tongue.
Morbidity and Mortality
Overall, 5-year survival for oral cancer is just over 50% but
depends very much on the stage at initial diagnosis and
clinical factors. Squamous cell carcinoma of the lip has a
better prognosis than intraoral carcinoma. In general,
prognosis is worse when tumours arise in the more posterior parts of the oral cavity than in the anterior area. Midline carcinomas in the floor of the mouth and ventral
tongue may, however, spread to both sides of the neck.
Staging is a system used to describe the degree of spread or
tumour ‘load’ and the most widely used TNM (tumour,
lymph node, metastases) system is described in Table 12.3.
Survival at 5 years for TNM stage I oral carcinoma is
around 80%, whereas survival is reduced to 15% for stage
IV. Morbidity refers to a reduction in function, both physical
and psychological. Again, morbidity tends to relate to stage,
as large tumours may require removal of a large amount of
tissue or radical radiotherapy, sometimes combined with
Table 12.3 Staging Using the TNM8 System
T—PRIMARY TUMOUR
T1 Tumour 2 cm or less in greatest dimension and 5 mm or less
depth of invasion
T2 Tumour 2 cm or less in greatest dimension and more than
5 mm but no more than 10 mm depth of invasion or tumour
more than 2 cm but not more than 4 cm in greatest dimension
and depth of invasion no more than 10 mm
T3 Tumour more than 4 cm in greatest dimension or more than
10 mm depth of invasion
T4a (Lip) Tumour invades through cortical bone, inferior alveolar
nerve, floor of mouth or skin (of the nose or chin)
T4a (Oral cavity) Tumour invades through cortical bone of the
mandible or involves the maxillary sinus, or invades the skin of
the face
T4b (Lip and oral cavity) Tumour invades the masticator space,
pterygoid plates, or skull base, or encases internal carotid artery
N—REGIONAL LYMPH NODES
N0 No regional lymph node metastasis
N1 Metastasis in a single ipsilateral lymph node, 3 cm or less in
greatest dimension without extranodal extension
N2a Metastasis in a single ipsilateral lymph node, more than 3 cm
but less than 6 cm in greatest dimension, without extranodal
extension
N2b Metastasis in multiple ipsilateral lymph nodes, none more
than 6 cm in greatest dimension, without extranodal extension
N2c Metastasis in bilateral or contralateral lymph nodes, none
more than 6 cm in greatest dimension, without extranodal
extension
N3a Metastasis in a lymph node more than 6 cm in greatest
dimension without extranodal extension
N3b Metastasis in a single or multiple lymph nodes with clinical
extranodal extension
M—DISTANT METASTASIS
M0 No distant metastases
M1 Distant metastases
STAGE GROUPING
Stage I T1 N0 M0
Stage II T2 N0 M0
Stage III T3 N0 M0
T1, T2, T3 N1 M0
Stage IVA T4a N0, N1 M0
T1, T2, T3, T4a N2 M0
Stage IVB Any T N3 M0
T4b Any N M0
Stage IVC Any T Any N M1

chemotherapy and neck dissection. Hospital re-admission
is frequent during treatment and, in many cases, tumours
prove refractory to all forms of therapy. Quality of life can
be assessed and is an important measure of morbidity. Good
dental health is a significant factor.
TYPES OF ORAL CANCER
Squamous cell carcinoma accounts for around 95% of all
oral cancers. It arises from the epithelial lining of the oral
cavity. It is described in detail in the next section. A number of other forms of malignant disease also arise in the
oral cavity.
12 • Oral Potentially Malignant Disorders and Oral Cancer
197
MINOR SALIVARY GLAND CANCERS
These tend to occur in the palate and upper lip and they
present as rubbery nodules, sometimes ulcerated and painful. They are described in Chapter 14.
MALIGNANT MELANOMA
This typically occurs in the palatal and gingival mucosa.
A spreading, brown-pigmented patch or a raised ulcerated nodule, surrounded by pigmented mucosa, may be
seen (Fig. 12.6). Prognosis is poor in nodular malignant
melanoma.
MALIGNANT LYMPHOMA
Extranodal lymphoma arises principally in the oropharynx
in the area of Waldeyer’s ring including the soft palate, base
of tongue and tonsils. Nodular infiltration of the mucosa is
seen and lymph nodes in the neck may become involved.
LEUKAEMIA
Leukaemia may present with oral signs such as persistent
gingival haemorrhage and oral ulceration. Acute myeloid
leukaemia and childhood leukaemia may cause gingival
enlargement because of direct infiltration of leukaemic
cells (Fig. 12.7).
Fig. 12.7 Generalised gingival enlargement caused by acute leukaemia.
METASTATIC DEPOSITS
Metastasis from primary cancers in the kidney, gastrointestinal tract, lung, breast, prostate and other sites occur in the
oral cavity. Deposits of metastatic tumour often present as
gingival nodules or as destructive bone lesions. Metastatic
lesions in the jaws are usually radiolucent, but prostate and
some breast metastases appear as sclerotic lesions in bone.
RARE NEOPLASMS
Malignant primary soft tissue and bone tumours can arise
in the oral cavity and jaws. Odontogenic malignant
tumours are known but are very rare.
SQUAMOUS CELL CARCINOMA
Aetiology
Smoking
Cigarette smoking is the most important aetiological factor
for intra-oral cancer in the Western world. Risk increases
with cumulative dose, which is measured in ‘pack-years’.
There are no safe levels. The risk is greatest when combined
with high alcohol intake. It is believed that carcinogens in
tobacco smoke accumulate in the floor of the mouth, accounting for the increased risk of squamous carcinoma at
that site.
Fig. 12.6 Malignant melanoma of the palate.
Paan and Other Tobacco Use
Paan, also known as betel quid, is used throughout the Indian subcontinent. Leaf of the betel piper vine is used to
form a rolled-up quid, into which areca nut is placed. Areca
is thought to contain alkaloid carcinogenic precursors. In
addition, tobacco, spices and slaked lime may be added. The
quid is held in the oral cavity for a considerable time and is
habit-forming. Buccal and labial cancers are commonly associated with paan use. Other tobacco habits exist, including smearing tobacco paste into the mouth and reverse
smoking, which has been linked to palatal cancer. In recent
times, areca nut has become popular in Southeast Asia.
Alcohol
Alcohol is a cause of oral cancer and is an important co factor when combined with smoking. Acetaldehydes which

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cause DNA damage are produced by metabolism of alcohol.
In the oral cavity, alcohol may directly increase epithelial
permeability, allowing greater access of carcinogenic substances to the basal cells. The oral cancer risk is similar with
all forms of alcoholic drink and other chemicals in the beverage called congeners are thought to add to the risk, particularly in certain home distilled products.
Ultraviolet Light
Ultraviolet B is an important factor in lip cancer. Fairskinned races in tropical latitudes are particularly at risk
from sunlight. Protection, using measures such as sun
block and wearing a wide-brimmed hat, is advocated where
there is high risk.
Diet
Evidence is accumulating that a poor diet with low antioxidant action (deficient in fresh vegetable content) is an
important contributory factor.
Viruses
HPV is an important factor in oropharyngeal cancer and is
thought to drive the increasing incidence in men despite
falling smoking rates. Oropharyngeal carcinoma arises
mostly in the tonsil, soft palate and base of the tongue and
is thought to originate from the reticular epithelium in the
folds of the lymphoid tissue. In contrast, HPV-related oral
cavity cancer is very rare and routine testing for HPV is not
undertaken on mouth cancers. Some authors have suggested a possible viral aetiology for oral cancer in those
cases where no risk factors are identified. No viral sequences have been identified to date in that group although
the immune signature in such cases suggests that a virus
may have triggered early changes and then been cleared.
Clinical Features
The Lip
Although the lip is the most common site for oral cancer, intraoral cases are detected more often by dentists. The lower
lip is almost exclusively affected, often to one side of the midline (Fig. 12.8). Shallow ulceration, crusting or thickening
are typical presentations. Spread to the submental nodes
tends to be slow; if detected early, this cancer has the best
prognosis.
Intra-oral Surfaces
The floor of the mouth, ventral tongue and lateral anterior
tongue are most commonly involved. All too frequently, intraoral cancer is symptomless and reaches an advanced
stage before detection. The classical description is of a hard,
fixed ulcer, with raised rolled margins and a necrotic base
(Fig. 12.9). It is vital to remember that squamous carcinomas may also present as white or red mucosal patches,
fleshy polyps, punched-out ulcers, indurated plaques or by
tethering mucosa. The tongue may become fixed to the
floor of the mouth, making it difficult for the patient to raise
it. Alternatively, the tongue may deviate to the side of an
oropharyngeal tumour on protrusion (Fig. 12.10). Sometimes patients present with nodal metastasis in the neck
from an occult primary lesion, particularly from the oropharynx. Nodal deposits of metastatic squamous carcinoma in the neck are tested for HPV and Epstein-Barr virus
(EBV, indicating likely origin from the oropharynx or
nasopharynx, respectively).
Squamous cell carcinoma also arises on the gingivae, alveolar ridge, buccal mucosa and palate, albeit less commonly
(Fig. 12.11). Bone invasion is an early feature of carcinoma
arising in mucoperiosteum and extension through the cortex
to invade marrow spaces is an adverse feature
Head and Neck
Dentists should also be aware of extra-oral cancers. Basal
cell carcinomas, squamous cell carcinomas and malignant
melanomas are common on the facial skin (Chapter 13).
Squamous cell carcinoma arises in the maxillary sinus
(Chapter 7), nasopharynx (where is often associated with
EBV) and larynx. Persistent hoarse voice can be a presenting sign of laryngeal cancer and should trigger referral to
an otolaryngologist.
Pathology
Histopathological Features
Microscopically, squamous cell carcinoma comprises sheets
of squamous epithelial cells supported by a fibrous stroma
Fig. 12.8 An early squamous cell carcinoma on the lower lip.
Fig. 12.9 A squamous cell carcinoma of the floor of the mouth show-
ing the typical raised rolled borders. The lesion was painless and the
patient presented requesting new dentures.

12 • Oral Potentially Malignant Disorders and Oral Cancer
Fig. 12.12 The margin of a squamous cell carcinoma, the normal margin is on the right side and islands of atypical squamous cells can be
seen invading the connective tissue on the left of the photograph.
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Fig. 12.10 Tongue deviation on thrusting. This patient had an oro-
pharyngeal cancer on the left side that tethered the tongue causing
deviation to the left.
Fig. 12.11 A gingival squamous cell carcinoma.
containing the tumour vasculature. The squamous cells
can be recognised by their tendency to form flattened layers
held together by prominent intracellular bridges (desmosomes). Often, individual cells undergo keratinisation and
the most conspicuous feature is the formation of keratin
pearls or whorls (Figs. 12.12 and 12.13). The vast majority
Fig. 12.13 Squamous cell carcinoma showing a keratin pearl and cytological atypia.
of tumours are moderately differentiated, though examples
of well-differentiated and poorly differentiated carcinomas
occur. Increased mitotic activity is seen and bizarre mitotic
figures are often present. Nuclear and cellular pleomorphism and nuclear hyperchromatism are typical features.
Necrosis is present in some cases due to tumour cell growth
outstripping nutritional supply and is usually associated
with poor prognosis driven by chronic hypoxia. A key feature is invasion of the adjacent tissues by detachment and
movement of the carcinoma cells. Invasion may be on a
cohesive front or a diffuse non-cohesive front (Fig. 12.14).
Carcinoma spreads along anatomical planes. Adverse histological features that are recognised are spread along
nerves (perineural invasion), vascular channels (lymphovascular invasion) or into the sarcolemmal sheaths of muscle fibres (Figs. 12.15 and 12.16). A chronic inflammatory
response is usually seen at the invasive front. Many carcinomas are thought to arise in a wide field of mucosal
change. Second primary cancers can arise at the same time

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Fig. 12.14 Invasive margin of a squamous cell carcinoma showing
small groups and individual cells in the connective tissue. This is a
noncohesive invasive pattern indicating an adverse prognosis.
(synchronous) or more than 6 months later than the presenting cancer (metachronous) and are a significant cause
of poor outcome. Over a 15-year span, around 25% of
patients may develop a second primary cancer.
When an incisional biopsy is undertaken on clinically
suspicious mucosal lesions, it is important to include the
margin of the ulcer. The biopsy must be of sufficient depth
and crush damage must be avoided. Failure to sample
appropriately may lead to misdiagnosis.
Bone Invasion
In addition to local spread into soft tissues, oral squamous
cell carcinoma can spread into adjacent bone. At first the
periosteum acts as a barrier but cortical resorption can lead
to entry of the carcinoma cells to marrow spaces and bone
destruction. Radiographs show irregular bone destruction
and teeth may be displaced or resorbed. Contrast enhanced
computed tomography (CT), and magnetic resonance imaging (MRI) scanning are used in combination to determine the extent of bone and soft tissue spread (Figs. 12.17
and 12.18). Spread of squamous carcinoma through the
bone cortex to invade the medullary cavity is an adverse
histological finding (Fig. 12.19).
Fig. 12.15 Lymphovascular invasion. A cord of carcinoma may grow in
the lumen of a lymphatic vessel.
Fig 12.16 Neural invasion. Groups of atypical squamous cells surround
the nerve sheath and are seen here infiltrating between the nerve
fibres.
Metastasis
Carcinoma spreads to regional lymph nodes via the lymphatics. The primary site is important: lip cancers spread
to the submental nodes, whereas intra-oral tumours are
more likely to spread to the cervical nodes (see Chapter 2,
Fig. 2.1). Involved lymph nodes become first palpable and
then fixed and hard. With increasing tumour growth,
nodes may become cystic as a result of central necrosis or
even matted together to form a craggy mass. Spread of the
neoplastic cells outside the lymph node capsule is known
as extranodal extension and is a powerful predictor of adverse outcome (Fig. 12.20). Tumours in the anterior floor
of the mouth and tongue may metastasise to both sides of
the neck. Imaging can also identify suspicious nodal metastasis to help treatment planning. Fine-needle aspiration and core biopsies can be used to detect cancer in
equivocal nodes.
Distant metastasis is a relatively late event but spread
may occur to the lungs, brain, viscera and bone. Chest radiography, isotopic bone scans and whole-body CT or PET
may be used to detect distant metastasis.
Grading and Staging
Histological Grading: Prognostic Features
Histological grading refers to those features seen in the
microscope that can be related to the biological behaviour
of the tumour. The degree of differentiation is not a particularly good indicator of prognosis in oral squamous cell
carcinoma. Pattern of invasion is more important;
tumours that invade tissue on a noncohesive front (single
cells or narrow strands) have a worse prognosis than
those that invade on a broad front. Perineural and lymphovascular invasion are also indicators of poor prognosis. As yet, no molecular markers are in routine use for
prediction of outcome or to guide therapy in oral cancer.
As described above, markers for high-risk HPV are mandatory for oropharyngeal carcinomas where HPV signals a
more favourable prognosis.

12 • Oral Potentially Malignant Disorders and Oral Cancer
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A B
Fig. 12.17 A buccal squamous cell carcinoma shown by (A) CT and (B) contrast-enhanced MRI scans invading and destroying the right maxillary
tuberosity.
A B
Fig. 12.18 (A) and (B). MRI scanning is used here to map the extent of a primary squamous cell carcinoma arising from the retromolar trigone.
Staging: TNM Classification
Clinical and pathological staging refers to determination of
the extent of tumour size and spread. The patient is examined carefully and imaging is used to aid in the detection of
involved neck nodes. The TNM (Table 12.3) system is widely
used. Pathological staging (pTNM) is undertaken on surgically resected specimens and is more accurate than clinical
staging. Pathologists record detailed information on the
neck dissection, including the levels containing lymph
nodes involved by metastatic disease (Fig. 12.21).
Imaging of Oral Squamous Cell Carcinoma
The role of imaging in oral cancer management includes:
n
identifying tumour size and anatomical extent
n
detection of regional nodes (staging)
n
detection of distant metastases
n
post-treatment follow-up.
Plain radiographs have a very limited role to play in assessment and management of oral squamous cell carcinoma.
Advanced lesions on the floor of the mouth may cause gross

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Fig. 12.19 Bone invasion by carcinoma. The tumour is seen top right
and it stimulates osteoclasts to erode the bone surfaces, leaving scalloped outlines.
Fig. 12.21 The levels of the neck agreed by consensus used for recording staging as part of the dataset for neck dissections.
Fig. 12.20 A lymph node from the neck containing a deposit of metastatic squamous cell carcinoma from an oral primary lesion. Note that
there is florid extracapsular spread with neoplastic cells extending into
adjacent fibro-adipose tissue. Extra-nodal extension is the most powerful predictor of adverse outcome in neck metastatic disease.
bone destruction in the adjacent mandible, but detection of
early bony involvement has poor sensitivity. CT using bone
windows provides a good diagnostic sensitivity for detection
of bone involvement. Panoramic radiographs are useful for
preoperative assessment of patients who require dental interventions prior to receiving radiotherapy.
Imaging of oral squamous cell carcinoma relies upon
cross-sectional techniques (i.e., CT or MRI). Thin-slice
(3–5-mm) CT sections are usually performed through the
oral region and neck. Intravenous iodinated contrast is
given and the scans are repeated, because neoplastic lesions
of the floor of the mouth and tongue base tend to enhance,
which improves the delineation between normal and abnormal tissues. Contrast also highlights vessels, allowing
them to be more easily distinguished from nodes. PET can
be used to detect small deposits of metastatic carcinoma
and can often localise ‘unknown’ primary sites. However,
MRI scanning is often the best at defining the leading edge
and margins of a primary carcinoma within soft tissue, especially if that tissue also enhances with contrast, for example the tonsils. In addition, specific sequences of MRI
enable early detection of perineural spread, not possible
with other imaging modalities. Unfortunately, bone changes
are not as easily evaluated on MRI as on CT, and the longer
scan time presents a risk of patient movement which will
spoil the imaging.
When examining images of submandibular and jugulodigastric nodes of the internal jugular chain, those nodes
with a diameter exceeding 1.5 cm are abnormal; in other
parts of the neck, 1 cm is the maximum size of normal
nodes. A low-density centre in nodes of normal shape is
most likely to represent the adipose tissue of the hilum and
may be found in normal, hyperplastic and inflamed nodes.
Central enhancement of a lymph node is suggestive of
metastatic tumour. When lymph nodes appear enlarged,
round and possess a low density centre, the combination of
features is typical of tumour necrosis and indicates metastatic disease. Imaging can provide an indication of extracapsular extension of the tumour. In addition, imaging
contributes to the clinical staging process not least because
it shows deeply situated nodes (e.g., retropharyngeal,
hilar and pretracheal) beyond the scope of clinical (or
endoscopic) examination.
Treatment
The treatment of oral cancer is usually surgery. The patient
is normally discussed at a multidisciplinary team meeting
(MDTM) where the margin clearance, any adverse histological findings and patient factors such as the patients
views and comorbidities are considered. Surgery may be
followed by adjunctive radiotherapy, sometimes combined
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