Oral Pathology Flashcards
Define cyst
Pathological cavity filled with fluid, semi-fluid or gas freq. lined by epithelium
Never filled with pus
Classification of cysts
Epithelial
- odontogenic
- non-odontogenic
Non-Epithelial
Sub classification of odontogenic cysts
Inflammatory
- radicular; apical, lateral
- residual
Developmental
- odontogenic keratocyst
- dentigerous; follicular, eruption
- lateral periodontal
Sub-classification of non-odontogenic cysts
Fissure (developmental)
- nasopalatine
- nasolabial
- median palatine
Soft tissue
- mucous extravasation
- mucous retention
- dermoid
- lymphoepithelial
- thyroglossal duct
Non-epithelial cysts
Bone
- simple; solitary, haemorrhagic, traumatic
- aneurysmal
3 requirements for cyst pathogenesis
- Epithelial source
- Stimuli for cavitation + epithelial proliferation
- Mechanism(s) for continued growth + bone resorption
Discuss epithelial source of cysts
Inflammatory Cysts
- remnants of Hertwig’s Epithelial Root Sheath
— ensheath’s root dentine
- form epithelial cell rests of Malassez
- throughout PDL, entrapped in periapical granuloma
Dentigerous - reduced enamel epithelium — forms epithelial ‘cover’ for enamel — protects enamel during development + eruption - split b/w REE + enamel -> cyst
Odontogenic keratocyst
- remnants of dental lamina
— initial buds of oral epithelium
- Glands of Serres
Discuss stimulus for cavitation and epithelial proliferation of cysts
Inflammation
- inflammatory cysts usually stim. by inflammation
- site specific: pulp necrosis -> periapical granuloma -> cyst
- PD pocket -> lat. PD inflammatory cyst
- cytokines + growth factors stim. epithelial proliferation
— IL-1+6, TNF, EGF, TGF-beta
Genetic
- possible genetic defect in tumour suppressor gene
- odontogenic keratocyst linked to Gorlin’s syndrome
Discuss mechanisms for continued epithelial growth and bone resorption
Hydrostatic: inflammatory + dentigerous
- protein accumulation in cyst
- wall acts as semi-permeable membrane
- fluid accumulates in cyst lumen creating +ve pressure in cyst
Bone Resorption
- cyst releases cytokines stim. bone resorption
- IL1, TNF, PGE2
Epithelial Growth Factors
- EGF + TGF-beta May cause pronounced epithelial proliferation
- odontogenic keratocyst: pronounced mural growth
— epithelial cells over proliferate
— don’t have lots of expansion
General radiographic presentation of cysts
Well defined round/oval radiolucency
- keratocyst: scalloped margin
Usually, well corticated margin (radiopaque)
- except solitary bone cyst
- infection = loss of definition
Shape
- round due to hydrostatic growth
- keratocyst (+ solitary bone) grow through bone cf expand jaw
Locularity
- true (multiple cavities): keratocyst
- large cysts appear multilocular due to ridges in bony wall
General clinical findings of cysts
Swelling Pain Fluctuance Eggshell cracking Tooth displacement/loosening
Clinical + radiographic findings of radicular cyst
Clinical
- S: non-viral tooth, UIs common
- develop within periapical granuloma (>10mm = cyst)
- regular growth limited; B expansion late
- long standing: displacement + loosening
Radiographic
- unilocular, oval/round
- well corticated
- @ apex non-vital tooth
- continuous w/ lamina dura
Epidemiology + Tx of radicular cyst
Epidemiology: 4-5th decade
Most common cyst; 65%
Tx: RCT, XLA
Discuss residual cysts
Epithelial odontogenic inflammatory cyst
Derived from rests of Malassez
S: edentulous area; retained radicular cyst post-XLA
Radiographic: well defined, oval/round
Histology of radicular/residual cysts
Lumen
- pale pink serious exudate (white if removed)
- macrophages, desquamated epithelial
- inflammatory cells
- cholesterol clefts + foreign body giant cells (if RF; GP, amalgam)
Epithelial
- non-keratinised stratified squamous
- variable thickness, often arcading (hyperplastic rete processes)
- long-standing: thin, attenuated
Capsule: thick wall fibrous + granulation tissue
Inflammatory infiltrate: acute + chronic cells
Clinical + radiographic findings of dentigerous cysts
Clinical
- S: 3s, 8s common
- attached @ CEJ surrounding crown of UE tooth
— confirmed surgically/pathologically (not X-ray)
- envelop crown symmetrically
- late B expansion
Radiographic
- unilocular, well corticated
- crown associated lies centrally in cyst
Epidemiology + Tx of dentigerous cysts
Epidemiology: 3-4th decade
20% of jaw cysts
Tx: uncover tooth, XLA
- no recurrence
Histology of dentigerous cysts
Lumen
- pink serious exudate
- cholesterol clefts
Epithelial
- non-keratinised stratified squamous
- flat basement membrane
- thin (2-5 cells), uniform
- resembles REE
Cyst Wall
- variably thick
- blueish myxoid appearance (like dental follicle)
If becomes inflamed, indistinguishable from inflammatory cyst
Clinical + radiographic findings of odontogenic keratocyst
Clinical: S: Md; angle, ramus
Radiographic - usually multilocular - poss. associated w/ UE tooth - little expansion - grows through medullary bone; late B expansion — root resorption possible
Epidemiology and Tx of odontogenic kerarocyst
Epidemiology: 2-3rd decade
5% jaw cysts
Tx: XLA
- recurrence common due to daughter cysts
Histology of odontogenic keratocyst
Lumen: pink, keratin filled
Epithelial - para/keratinised corrugated surface - flat basement membrane (developmental) - basal cells — reverse nuclear polarity (towards lumen) — darkly staining
Wall: thin, fibrous
Small daughter cysts poss. in wall
- due to epithelial growth grows into marrow spaces
- lots = syndromic
Discuss lateral periodontal cysts
Any cyst in lat. PD area
Epithelial: derived from remnants dental lamina
Clinical: lat. roots vital teeth
Radiographic
- unilocular, well corticated
- round, small (<1cm)
- B expansion if v large
Histology of lat. PD cyst
Epithelial
- non-keratinised stratified squamous
- thin (2-5 cells), not uniform
- thickened areas for swirled plaques
- flat basement membrane
Wall
- thin, fibrous
- scattered glycogen rich clear cells
Clinical + radiographic findings of nasopalatine cyst
Clinical
- S: midline, ant. Mx; vital UIs
- size: >6mm
- asymptomatic
Radiographic
- unilocular, well corticated
- round/oval
- apices of U1s
Histology of nasopalatine cyst
Lumen
- serous exudate
- variable inflammatory infiltrate
Epithelium
- non-keratinised stratified squamous
- ciliated pseudo-stratified respiratory
- both
Wall
- fibrous
- neurovascular bundles
Discuss solitary bone cyst
Non-epithelial non-odontogenic cyst
Usually <20y
Aetiology: unknown, poss. trauma
Clinical
- S: Md body
- asymptomatic
Radiographic
- unilocular, well corticated
- irregular outline; extend b/w roots
Histology of solitary bone cyst
Fibrovascular tissue only
Lumen: usually empty
Epithelial: none
Wall: none/thin fibrous
- occ. giant cells
- haemosiderin pigment; blood vessels were present
Discuss aneurysmal blood cyst
Epidemiology: child, young adult
Aetiology: unknown
Soft tissue lesion; also classified as giant cell lesion
- blood filled cystic spaces
Clinical: S: Md
Radiographic
- multilocular, well corticated
- cortical expansion (ballooning)
- partially cystic, partially solid
Histology of aneurysmal bone cyst
Giant cell lesion
Giant cells in hypervascular, hypercellular background
Localised proliferative lesion of vascular tissue w/ giant cells + granulation tissue
Blood filled cystic spaces
Discuss mucous extravasation and retention cysts
Extravasation - younger - aetiology: trauma - S: L lip - histology — lumen: extravasated mucin — epithelial: none — wall: granulation tissue
Retention - older - S: L lip less common - related to duct obstruction - histology — dilated salivary duct filled w/ mucin — has epithelial lining
Discuss lympho-epithelial cyst
Epidemiology: late childhood, early adulthood
Epithelial: remnants within lymphoid tissue
- stimuli for proliferation unknown
Clinical
- unilateral, fluctuant swelling
- S: lat. neck, ant. sternocleidomastoid
Histology
- attenuated epithelium surrounded by lymphoid stroma
Discuss dermoid cyst
Developmental anomaly
Rare
- F=M
- 15-35; may present earlier/later
Clinical: S: midline FoM, above mylohyoid
Histology
- epithelial: epidermis
- wall: skin appendages (sebaceous glands, hair follicles)
Discuss thyroglossal cyst
Developmental
Occurs when thyroglossal tract left from descent of thyroid doesn’t breakdown
Clinical: S: midline
Histology
- epithelium: attenuated or respiratory
- wall: thyroid follicles (req. for Dx)
Briefly describe tooth development
Neural crest cells (from ectoderm) migrate + clump beneath oral ectoderm
- induce formation 1ry epithelial band
- gives rise to tooth germs
Pre-ameloblast induce odontoblasts
- form dentine which induce ameloblasts
- form enamel of crown
Following fragmentation of Hertwig’s root sheath, dentine formation during root development induce cementoblasts
General features of odontogenic tumours
Derived: odontogenic epithelium (oral ectoderm) +/- mesenchyme
Neoplasm
- abnormal/uncontrolled growth/proliferation
- unrelated to stimuli
- benign or malignant
Hamartoma
- developmental malformation
- normal tissue, incorrect proportion or morphological arrangement
Most odontogenic tumours are benign
- more hard tissue content (mature) = more benign
Classification of odontogenic tumours
Epithelium only
Epithelium + mesenchyme +/- hard tissue
Mesenchyme only
Odontogenic epithelium only tumours
Ameloblastoma: benign, v aggressive Calcifying epithelial: benign Squamous: benign Clear cell: malignant Adenomatoid: enamel, cystic
Odontogenic epithelial + mesenchyme tumours
Ameloblastic fibroma: no hard tissue, both epithelium + mesenchyme neoplastic
Calcifying odontogenic cyst: dentine + enamel like material, cystic
Odontoma: all hard tissues formed
Odontogenic mesenchyme only tumours
Benign cementoblastoma
Odontogenic fibroma: only mesenchyme neoplastic
Myxoma: destructive potential
Epidemiology, freq., origin + Tx ameloblastoma
Benign odontogenic neoplasm
Epidemiology: 20-50y
Freq.: 1% all tumours
Origin: cell rests of enamel organ or dental lamina
Tx
- surgical removal w/ margin (invasive)
- long term follow up due to recurrence
Clinical + radiographic findings of ameloblastomas
Clinical
- S: Md 80% (angle); Mx 20%
- behaviour: slow growing, locally aggressive
- late Dx + incidental finding as mucosa appears normal
- early: asymptomatic
- late
— expansion of cortical plates, egg shell cracking
— extension into soft tissues
— root resorption, painless
— if left: destruction of Md
Radiographic
- multilocular ‘soap bubble appearance’
- well corticated; slow growing, Mx less so
- round/oval, scalloped edge
Histology of ameloblastoma
Solid/cystic/both
Epithelium: resembles ameloblasts
- tall, columnar
- reverse nuclear polarity (prominent basal cells)
Follicular
- epithelial islands
- filled w/ loose stellate reticulum-like cells
- some cystic degeneration (not true cyst)
Plexiform
- interlacing epithelial strands
- less stellate-like cells
Discuss unilocular ameloblastoma
Freq.: 10-15% of ameloblastomas
Radiographic: unilocular
- resembles dentigerous/radicular cyst
Often associated w/ crown UE8
Epidemiology, freq., origin + Tx of calcifying epithelial odontogenic tumours
Benign, solid neoplasm
Epidemiology: 20-60
Freq.: rare, 1% of odontogenic tumours
Origin: odontogenic epithelium, poss. cells of stratum intermedia
Tx: surgical excision w/ margin
Clinical + radiographic features of calcifying epithelial odontogenic tumours
Clinical
- S: Md body 75% (P/M)
- behaviour: slow growing, locally invasive
— usually small; v. large if undetected
- early: asymptomatic
- late: cortical plate expansion, root resorption
Radiographic
- uni/multilocular
- scatter radiopacities; esp. around UE crown
- often associated w/ UE tooth
- ill/well defined, irregular/round
Histology of calcifying epithelial odontogenic tumours
Epithelial
- islands
- pleomorphic, hyperchromatic, prominent nucleoli
- bizarre atypia
- no mitosis, no necrosis
Calcifications
- concentric circles
- laminated
- basophilic
- no pre-dentine layer; abrupt
Epidemiology, freq., origin + Tx ameloblastic fibroma
Benign neoplasm
Epidemiology: <20
Freq.: rare;
Clinical + radiographic findings of ameloblastic fibroma
Clinical
- S: Md body 80%
- behaviour: slow growing
- asymptomatic
- B+L expansion w/ tooth displacement
- 50% associated w/ UE (mistaken for dentigerous)
Radiographic
- resembles ameloblastoma
- small: unilocular, smooth, well corticated
- large: multilocular
Histology of ameloblastic fibroma
Similar to ameloblastoma
Epithelial
- tall, columnar basaolid (ameloblast-like)
- islands + strands
- filled w/ stellate-like cells
Hypercellular mesenchyme in connective tissue (fibroma); usually dominant feature
- looks primitive; too many cells for mature cell
No hard tissues
Epidemiology, freq., origin + Tx of adenomatoid odontogenic tumour
Benign lesion, epithelium + variable hard tissue
Epidemiology: <30
Freq.: v rare
Origin: odontogenic epithelium
Tx: curettage
Clinical + radiographic findings of adenomatoid odontogenic tumour
Clinical
- S: Mx ant., usually associated w/ UE
- behaviour: slow growing, locally expansive
- early: asymptomatic
- late: root resorption, displacement, bony destruction (expansion)
Radiographic
- unilocular, round/oval
- well corticated
- early: resemble dentigerous cyst, extends apical to CEJ
- late: small radiopacities within lesion
Histology of adenomatoid odontogenic tumour
Solid or cystic
Intra-osseous or extra-osseous (gingival swelling-like)
Epithelium
- tall, columnar cells resemble ameloblasts
- from duct-like structures + rosettes (whirls of cells)
Calcifications
- abrupt, basophilic deposits within epithelium
- immature enamel, dentine
- like calcifying epithelial odontogenic tumour
Epidemiology, freq., origin + Tx of calcifying odontogenic cyst
Benign cystic tumour; epithelium + hard tissue
Epidemiology: <40
Freq.: rare
Origin: odontogenic epithelium
Tx: enucleation
Clinical + radiographic findings of calcifying odontogenic cyst
Clinical
- S: Md ant. 80%
- behaviour: slow growing
- early: asymptomatic
- late: local expansion
Radiographic
- unilocular, well corticated
- occ. associated w/ UE/odontome
- radiopacities within lesion
Histology of calcifying odontogenic cyst
Cystic (majority), some solid
75% intra-osseous
Epithelium
- tall, columnar, reverse nuclear polarity
- ameloblast-like
Suprabasal: loose stellate reticulum-like layer Ghost cells (lack nuclei), may calcify
Calcifications: dysplastic dentine
Resembles ameloblasts, diff. by ghost cells + calcifications
Epidemiology, freq., origin, Tx of odontomes
Hamartoma, developmental abnormality (WHO)
Epidemiology: <20
Freq.: most common
Origin: odontogenic epithelium
Tx: XLA
Type of odontome
Compound
- small tooth-like denticles
- tooth shapes of normal radiodensity
Complex
- irregular, haphazard mass
- similar radiopacity to normal
Clinical + radiographic findings of odontomes
Clinical
- S: Mx
- behaviour: slow growing
- asymptomatic, delay eruption/impacted
- local expansion
Radiographic
- similar radiopacity to normal tissue
- associated w/ UE/impacted tooth
- radiolucent line around lesion
Histology of odontome
Resemble developing teeth
- enamel space (white)
- dentine + pre-dentine
- pulp tissue
Compound: organised, separated structures
Complex: irregular, haphazard arrangement
Epidemiology, freq., origin, Tx of odontogenic myxoma
Benign neoplasm, mesenchymal
Epidemiology: young adult, F>M
Freq.: rare
Origin: mesenchyme (fibroblasts)
Tx: excision
Clinical + radiographic findings of odontogenic myxoma
Clinical
- S: Md (angle) > Mx
- behaviour: locally invasive + expansive
- early: asymptomatic
- late: expansion
Radiographic - multi/unilocular — poss. soap-bubble appearance - occ. associated w/ UE - smooth, well defined
Histology of odontogenic myxoma
Hypercellular myxoid ground substance
- contains spindle/stellate cells
- stellate reticulum-like
Epithelium: scattered rests, not neoplastic
Epidemiology, freq., origin + Tx of benign cementoblastoma
Benign neoplasm, mesenchymal
Epidemiology: 10-70; 50% <20
Freq.: rare
Origin: cementoblasts
Tx: excision/enucleation
Clinical + radiographic findings of benign cementoblastoma
Clinical
- S: Md > Mx; P/M
- behaviour: slow growing
- local enlargement + expansive
- root resorption
Radiographic
- well defined dense mass @ apex
- radiolucent margin
- continuous w/ root
Histology of benign cementoblastoma
Cellular cementum - attached to root - resting + reversal lines — mark changes in growth direction — usually indicate fast growing lesion
Fibrous capsule
Histology of alveolar osteitis
Dry socket
Excessive acute inflammatory infiltrate
- lots of neutrophils
- localised to socket wall
Bacterial aggregates
Irregular necrotic bone
Histology of osteomyelitis
Acute - acute inflammatory infiltrate — densely packed neutrophils form pus - necrotic bony islands; acellular — resorbed by osteoclasts
Chronic
- mixed inflammatory infiltrate
- fibrosis
Radiographic findings of osteomyelitis
Ill defined/poorly corticated; loss of cortication
Mottled/moth eaten appearance
Bony sequestra floating
Mixed radio-density
Histology of ORN
Completely acellular bone
- lacunae empty; lack osteocytes
- no osteoblasts on periphery
Bacterial aggregates
- periphery
- bone marrow spaces
Mixed inflammatory infiltrate
Necrosis
Fibrin
Epidemiology and aetiology of fibrous dysplasia
Benign skeletal anomaly
Normal bone replaced by immature disorganised bone + fibrous tissue
Epidemiology
- children, young adults (bones growing)
- F>M
Clinical + radiographic findings of fibrous dysplasia
Clinical: depends on bone(s) affected - S: Mx > Md - behaviour: slow growing, self limiting — stops once bones stop growing - facial asymmetry - tooth displacement + malocclusion
Radiographic
- ground-glass appearance
- ill defined; extends to cortex
- roots + bone appear continuous (not)
- loss of lamina dura
- narrowing of PDL
- early: radiolucent (fibrous)
- late; radiopaque (calcified)
Histology of fibrous dysplasia
Highly cellular fibrous stroma
Bony islands deposited in fibrous tissue
- immature, woven bone
- no osteoblast rim; secreted by fibroblasts
- irregular, curved, haphazard morphology
Epidemiology, freq. and Tx of cemento-ossifying fibromas
Benign neoplasms of jaws + craniofacial skeleton
Epidemiology: 40-59, F>M
Freq.: rare
Tx: excision; recurrence rare
Clinical + radiographic findings of cemento-ossifying fibroma
Clinical - S: Md (P/M) - behaviour: slow growing — no malignant transformation - B+L expansion - painless
Radiographic
- well corticated
- mixed radiodensity
- no fusion b/w roots + bone
Histology of cemento-ossifying
Highly cellular fibrous stroma
Pseudo-capsule: reactive bone
Mineralised tissue deposited within stroma
- reactionary, woven bone
- lamellar bone
- cementum-like tissue
Epidemiology of cemento-osseous dysplasia
Non-neoplastic fibro-osseous condition affecting alveolar bone
Epidemiology
- middle aged
- F
- Afrocaribbean
Types of cemento-osseous dysplasia
PA: PA region, Md, ant.
Focal: single tooth
Florid: multiple sites, multi-Qs
Familial gigantiform cementoma: autosomal dominant, multifocal
Clinical + radiographic findings of cemento-osseous
Clinical
- PA/Focal: asymptomatic, incidental finding
- Florid: minor bony expansion
- FGC: bony expansion, facial deformity
Radiographic
- well defined
- thin radiolucent rim
- mixed radiodensity
- no fusion w/ roots
Mx of cemento-osseous dysplasia
PA/Focal: none, monitor Florid: risk osteomyelitis, regular recall FGC: surgery - risk recurrence - 2ry infection
Histology of cemento-osseous dysplasia
High cellular fibrous stroma Mineralised deposits - woven/lamellar/cementum-like - haphazard, irregular - fuse to from islands - many reversal lines
Epidemiology, freq., aetiology + Mx of Paget’s disease
Epidemiology: >40 Freq.: 1.5-8% popn Aetiology: unknown - genetic - environmental: paramyxovirus
Mx: bisphosphonates
Phases of Paget’s disease
- Osteoclastic: excessive resorption, fibrovascular tissue deposited
- Osteoblastic: new bone formation within fibrous tissue
- Osteosclerotic: bone coalesces -> dense, sclerotic bone
Clinical presentation of Paget’s disease
Jaws rare: Mx > Md
Mx
- widening of alveolar process
- palate flattening
- malocclusion: retroclination UIs, P tipping post.
Md: expansion -> facial deformity
Enlargement Pathological # (weak) Deformity of weight bearing bones Compression of cranial nerves - deafness - visual disturbance - vertigo
Radiographic findings of Paget’s disease
- Radiolucent
- Mixed radiodensity, cotton wool appearance, ill defined
- Very dense, radiopaque
Dental implications of Paget’s disease
Early: highly vascular stroma -> inc. risk post-XLA bleeding
Late: irregular bone + min. vascularity -> inc. risk infection
Hypercementosis: difficult XLA
Histology of Paget’s disease
Mosaic pattern
- haphazard, irregular arrangement of bone
Prominent, basophilic reversal lines
Mature: less vascular
Aetiology of cherubism
Benign, autosomal dominant disorder of childhood
Aetiology: mutation of binding protein gene
Clinical presentation of cherubism
Presents: 2-4y, usually normal @ birth
S: Md > Mx Behaviour: slow growing, self limiting Bilateral, symmetrical expansion Facial deformity - characteristic retracted skin, upwards gaze
Tooth displacement + loosening
Delayed eruption + premature loss
Speech + visual impairments
Radiographic findings + Mx of cherubism
Radiographic
- hypercellular + hypervascular fibrous stroma
— replaces bone
— numerous multinucleate osteoclast giant cells
- abundant haemosiderin (b/d of RBC)
- perivascular hyalinisation
Mx - detect + Tx UE - OH - orthognathic: facial deformity + malocclusion — once stopped growing
Aetiology/types of hyperparathyroidism
1ry
- adenoma (benign tumour) 80%
- carcinoma (malignancy) 5%
- idiopathic hyperplasia 15%
2ry: hyperplasia 2ry to renal disease/intestinal malabsorption
3ry: hyperplasia, gland behaves as autonomous adenoma following removal
Pathogenesis of hyperparathyroidism
Parathyroid glands detect + regulate serum Ca2+ conc.
Excess PTH prod. from adenoma/hyperplasia
Stim. osteoclasts -> Ca2+ mobilised from bone
Ca2+: tubular re-absorption, intestinal absorption
PO4-: renal excretion
PTH: inc.
ALP: inc.
Clinical features of hyperparathyroidism
Bone - brown tumours (giant cell lesions) - osteoporosis - joint pain Renal stones GIT irregularity Depression Fatigue, nausea Muscle weakness
Radiographic findings + Mx of hyperparathyroidism
Radiographic
- well defined
- variable: radiolucent -> densely sclerotic
- irregular radiopacities
Mx
- 1ry: removal
- 2ry: Tx underlying cause
Histology of hyperparathyroidism
Similar to cherubism
Hypercellular, hypervascular fibrous stroma
- multinucleate osteoclast giant cells
Haemosiderin
Bony destruction, modular appearance
Types of giant cell granuloma
Central
Peripheral
Epidemiology + Mx of central giant cell granuloma
Localised, benign osteolytic lesion of jaws
Epidemiology: F > M
Mx - curettage - intralesional/systemic medication — steroid — calcitonin — interferone — RANKL inhibitors
Clinical + radiographic findings of central
Clinical - S: Md > Mx, ant. - behaviour: slow growing, expansile - asymptomatic - 30% locally aggressive — pain — resorption + displacement — perforate cortex, involve soft tissue
Radiographic
- well defined radiolucency
- advanced: multilocular
Histology of central giant cell granuloma
Hypercellular, hypervascular fibrovascular stroma
Numerous multinucleate osteoclast giant cells
Haemosiderin
Aetiology of peripheral giant cell granuloma
Localised reactive proliferation of gingiva/alveolar mucosa
Aetiology
- 2ry reactive process
- localised mucoperiosteum/coronal PDL irritation
- plaque/calculus/overhanging restoration
Clinical + radiographic findings, Mx of peripheral giant cell granuloma
Clinical
- S: Md > Mx, gingiva, edentulous ridge
- sessile/pedunculate soft pink/purple-blue lump
- smooth/ulcerated/papillomatous surface
Radiographic: no bony invasion (poss. erosion of alveolar bone)
Mx: surgical removal, recurrence low
Syndromes that may lead to central giant cell granulomas
Neurofibromatosis type 1
Noonan
LEOPARD (noonan w/ lentigines)
General features of abscesses
Develop @ apices of tooth w/ necrotic/infected RC
May occur in deep PPD along affected tooth
Presents: pain + swelling, poss. discharge
- spread along fascial/muscle planes -> cellulitis, Ludwig’s angina
Causes of pulpitis/abscess
Caries Trauma # Deep PPD: lat. +/- accessory canals Extension of PA infection from adjacent tooth Blood stream (anachoresis)
Sequelae of pulpitis
Pulpitis -> acute chronic
- > PA periodontitis -> acute chronic
- > dento-alveolar abscess PA granuloma
- > inflammatory dental cyst -> abscess -> distant spread
Obligate anaerobes commonly associated w/ pulpitis
Gram- rods
- porphyromonas gingivalis
- prevotella intermedia
- fusobacterium nucleatum
Gram+ rods
- eubacterium
- lactobacillus
- actinomyces
Gram+ cocci: peptostreptococci
Gram- cocci: veillonella
Facultative anaerobes commonly associated w/ pulpitis
Gram+ cocci
- strep. mitis, oralis, intermedius
- enterococcus faecalis
Gram- cocci: neisseria
Gram+ rods
- corynebacterium
- lactobacillus
Tx of pulpitis
Debridement: remove necrotic + infected tissue from RC
Antimicrobial: RC dressing, occ. systemic
RCT
Apicoectomy: if infection persists
Clinical features of abscesses
Pain: rapid onset Erythema Swelling Tenderness: TTP, palpation Mobility
Routes for pus drainage from abscess
RC/PDL
Cancellous bone + perforate cortex
Into OC/facial skin through sinus tract
Palate: discrete swelling due to dense mucoperiosteum
Mx of periapical abscess
Drainage Remove source (RCT) AB - req. — no drainage — spread to soft tissues — pt febrile - amoxicillin - metronidazole: failure to respond within 48h
What is a periodontal abscess?
Abscess caused by acute/ bronco destructive process in periodontium
Results in localised formation of pus communicating w/ OC through PDL and/or periodontal sites
Doesn’t arise from necrotic pulp
Classification of periodontal abscesses
Gingival: localised soft gingival tissues; margin, interdental papilla
Periodontal: larger, extends apically
Pericoronal: associated gingiva of UE/E tooth (usually periocoronitis)
What causes periodontal abscesses to form? Mx?
Occlusion or trauma to PPD orifice causing bacteria to become trapped
- infection spread; pocket -> soft tissues
Mx
- drainage
- debridement
- AB: if pyrexia or cellulitis
Define abscess
Pathological cavity w/ pyogenic membrane + pus filled
Local + systemic signs of inflammation
Local
- pain
- swelling
- redness
- heat
- loss of function
- lymphadenopathy
Systemic - fever - inc. HR - altered bloods — Inc.: WBC (PMN), serum protein, ESR
Clinical presentation of acute abscess
Soft tissue swelling
- usually B
- U2/6 P
Pain: poorly localised
- affected tooth painful if post-PA PD
Mobility (post-PD)
X-ray changes: may take few days
Tx for acute abscesses
Drain pus
Remove cause
- RCT/XLA/incise + drain
What can happen if abscesses are left unTx’d?
Spontaneous drainage will occur -> chronic abscess
Why may an infection to spread? What determines direction of spread?
Cause
- host usually maintain balance b/w defence + bacteria
- imbalance -> spread
— opportunistic infection
— inadequate/no Tx
— immunocompromised: cold, fatigue, insomnia
Direction
- can spread in any direction
- take path of least resistance
Stages of infection/abscess
Cellulitis
- diffuse swelling due to tissue oedema
- red + shiny
- firmness depends on amount of fluid
- spreading in potential connective tissue spaces
- suppurations @ source, accumulates if unTx’d
Suppurative - once infection peaked - pus accumulation @ centre - position depends on — gravity — pressure — heat — muscle activity
Source of dental infections
Odontogenic infections: any dental infectious disease
- abscess: PA, PD
- pericoronitis
Less common
- AUG
- infected cysts
- MRONJ/ORN/osteomyelitis
- fungal infection
- cancrum oris
Potential maxillary spaces for spread of infection
Buccal space: sup. to buccinator Buccal sulcus: inf. to buccinator Palatal Lat. pharyngeal Sinus Canine fossa
Potential mandibular spaces for spread of infection
Sublingual Submandibular Submental Labial sulcus Submasseteric Pytergomandibular Lat. pharyngeal Peritonsillar Buccal space Buccal sulcus
Differentiate b/w sublingual + submandibular space
Sublingual: sup. to mylohyoid
Submandibular: inf. to mylohyoid
Mylohyoid is lower ant., higher post.
- most post. infection will be sublingual
What are the submasseteric and pytergomandibular spaces?
Submasseteric: b/w lat. border ramus (lat., post.) + masseter (ant., medial)
Pytergomandibular: b/w medial border ramus (lat., ant.) + medial pterygoid (post., medial’)
What are the peritonsillar and lat. pharyngeal spaces?
Lat./parapharyngeal
- b/w carotid sheath (post., lat.) + medial pterygoid (ant., medial)
- sup. to constrictor
Peritonsillar: inf. to constrictor
Differentiate b/w submental + labial sulcus space and buccal space + sulcus in Md
Submental
- chin
- inf. to mentalis
Labial sulcus: sup. to mentalis
Buccal
- space: inf. to buccinator
- sulcus: sup. to buccinator
What factors affect the spread of infection?
Ability to
- bacteria: no., virulence
- failure to drain
- pt health
Anatomical
- site
- drainage site
- natural barriers
Discuss Ludwig’s angina
Bilateral submental, submandibular, sublingual infections
Clinical
- raised, swollen tongue
- pyrexia
- dysphagia
- dyspnoea
- dysarthria
Tx
- drainage
- IV AB
- poss. tracheostomy for airway
Indications urgent referral to hospital is req. for abscess
Rapidly swelling Pyrexia Raised FoM: dysphagia, dysarthria, dyspnoea (Ludwig’s) Deviated uvula: Ludwig’s Immunocompromised/DM Severe trismus High pulse, raised WBC Toxic appearance Malaise
Difference b/w premalignant lesion and condition
Lesion: morphologically altered tissue in which cancer more likely cf normal counterpart
Condition: generalised state associated w/ significantly inc. risk developing cancer
What is leukoplakia?
Pre-malignant lesion characterised by white patches w/ questionable risk having excluded know diseases/disorders w/ no inc. risk
Epidemiology + aetiology of leukoplakia
Epidemiology
- middle age, inc. age
- M>F
Aetiology
- smoking: 90%
- idiopathic: 10%
Clinical presentation of leukoplakia
White patches S - B mucosa: 25% - Md gingiva: 20% - tongue: 10% - FoM: 10%
Discuss the two types of leukoplakia
Homogenous: no malignant change
- uniform flat appearance
- may have shallow cracks
- smooth/wrinkled/corrugated surface
- consistent texture
Non-homogenous: 26% malignant transformation
- predominately white or white/red lesion (erythroleukoplakia)
- irregularly flat/nodular/exophytic
— nodular: raised, rounded, red and/or white excrescences
— exophytic: irregular blunt or sharp projections
What is erythroplakia?
High risk pre-malignant lesion
Always associated w/ dysplasia/carcinoma
80% malignant transformation
Aetiology of erythroplakia
Tobacco + smoking
Snus: 60% users get keratoses
- associated w/ oral epithelial dysplasia
- rarely dysplastic
- malignancy: 0-1.2%/10y
Candida albicans: 30% associated
- chronic hyperplastic candidiasis
- dysplasia, speckled/nodular = high risk
- lesion may regress w/ Candida Tx
Clinical presentation of erythroplakia
Brightly red velvety plaque
Can’t be characterised as any other lesion
Oral signs of syphilis
1ry: oral chancre (rare, 2% extragenital)
2ry
- leukoplakia: D tongue
- condyloma lata
- mucosal patches
- ulcers
3ry
- gumma
- syphilitic leukoplakia
- atrophied glossitis
Malignancy risk of syphilis
2.5% pt have leukoplakia
10% OSCC
Clinical presentation of Plummer-Vinson syndrome and associated risk
Clinical - Fe anaemia — strophic glossitis — aphthous-like ulcers — mucosal pallor — sore tongue - post-cricoid oesophageal web - dysphagia
Risk factor for OSCC and oesophageal carcinoma
Discuss oral submucous fibrosis
Pre-malignant condition
Aetiology: Paan/Betel quid chewers
Clinical
- mucosal fibrosis + marbling
- trismus
- leukoplakia
- staining + attrition
30% develop OSCC
Discuss actinic keratosis
Aetiology: sunlight damage
Clinical
- speckled, rough scaly patch
- obliterates vermillion border
- lip crusting
- peri-oral freckles
Risk: 1%/yr SCC
- 60% SCC from AK
Cancer risk of LP
0.5-2.0%/5yr OSCC
Controversial
Define: keratosis, hyperkeratosis, orthokeratosis, parakeratosis
Keratosis: keratinisation of epithelium not normally keratinised
Hyperkeratosis: thickening of keratinised layer
Orthokeratosis: flat, anucleate superficial cells w/ homogenous eosinophilic cytoplasm
Parakeratosis: flat, homogenous eosinophilic cells w/ pyknotic nuclei
Define: acanthosis, atrophy, atypia, dysplasia
Acanthosis
- inc. no. cells in prickle cell layer
- inc. epithelial thickness
- broadening of Rete ridges
Atrophy
- dec. thickness due to less cells
- loss of Rete ridges
- epithelium uniform
Atypia: changes to individual cell
Dysplasia: changes to whole epithelium
Features of dysplasia
Nuclear hyperchromatism Nuclear + cellular pleomorphism Inc. nuclear:cytoplasm Inc. no. + bizarre mitoses Mitosis in prickle layer Premature keratinisation in prickle layer Loss of polarity of basal cells Loss of cell adherence Drop shaped Rete ridges Loss of epithelial stratification
Grading of dysplasia
None: epithelium normal
Mild: few epithelial cells in basal layer show atypia
Mod.: atypia in most basal cells + few suprabasal cells
Severe: almost all cells show atypia, basement membrane intact (no invasion)
Histology of leukoplakia
Para/hyperkeratosis (clinically white) Variable: hyperplasia, acanthosis Atrophy Candidal hyphae Inflammation Poss.: 1/+ dysplasia features
Histology of erythroplakia
Atrophy (clinically red)
Dysplasia
Inflammation
Management of dysplasia
Mild: review, advice, biopsy (repeat if req.)
Mod
- small: surgical excision
- large: multiple biopsies, review + monitor, repeat biopsy
Severe: excision
Relative freq., incidence, prevalence + death rate of oral cancer in UK
Freq.: % all malignancies
- WW: 10%
- UK: 1-2%
- India: 30-50%
- geographical variation due to aetiological factors
Incidence: new cases / 100000/yr
- UK: 4
Prevalence: cases within popn. @ T
- 0.05-0.1% (1 in 1000)
Mortality: 60% 5yr survival
- comparable to breast cancer
- > malignant melanoma, cervical Ca
Predisposing factors for oral cancer
Elderly M
M:F 3:1
- lip: 5-20:1
- tongue: 1:1
- other: 2:1
Age: 60-70
- > 50 85%
- > 40 98%
Prognosis of oral cancer
Poor prognosis depends on staging
Early: >80% 5 yr
Node involvement: >40%
Distant mets: <20%
Aetiology of oral cancer
Tobacco Alcohol Diet Viral infection Other infections
Discuss tobacco as risk factor for oral Ca
Smoking
- hydrocarbons in cigarettes broken down by salivary enzymes
- benzopyrene carcinogen of cigarette (tar)
- 80-90% oral Ca pt long term smokers, 2x risk
Smokeless:
- India, HK, Sri Lanka, SEA: buccal Ca
— association b/w site of betel quid + lesion
— dose T related
— Areca nut: oral submucous fibrosis, Ca not clear
- chewing: nitrosonornicotine (carcinogen)
Discuss alcohol as risk factor for oral Ca
80-90% oral Ca pt drink
Ethanol: inc. permeability of mucosa to carcinogens
- not carcinogen itself
Contaminants, colourants poss. carcinogenic
Discuss how diet can be risk factor for oral Ca
Fe2+ deficiency
- mucosal atrophy -> more susceptible to carcinogen
- Plummer-Vinson syndrome: Fe2+ deficiency + oesophageal web
VitA
- req. for normal epithelial differentiation
- may be factor in neoplasia
- retinoid Tx can cause remission of white lesions
What virus are associated w/ oral Ca? How may viruses cause Ca?
Mechanism
- activate cellular oncogenes by
— initiation of mutations OR
— inserting own genome close to oncogene
Associated
- HPV16/18: oropharyngeal, cervical
- EBV: nasopharyngeal, Burkitt’s lymphoma
What other infections may be involved in oral Ca?
Syphilis
- limited evidence
- leukoplakia D tongue -> Ca D tongue
Candida
- associated w/ premalignant white patches
- leukoplakia w/ Candida more freq. malignant transformation
- tumour promoter
- enzymes prod. catalyse: nicotine -> nitrosamines
3 factors influence mortality rate of oral Ca
Site
Size
Stage
Discuss impact of size on oral Ca survival
Further ant. better
Lip: 90% 5yr survival
FoM: 45%
Tongue: 40%
B mucosa: 40%
Discuss impact of size of tumour on mortality
Larger: inc. risk metastases, worse prognosis
Depth invasion worse cf surface size + pattern
Perineural + vascular spread poor prognosis
Most common sites for oral Ca
Gutter: 80%
Tongue: 30%
FoM: 15%
Retromolar: 15%
Regional features of oral Ca
Lymphadenopathy
Metastatic deposits cause enlargement
Firm, painless
Fixed if spread beyond capsule
Infected nodes: painful soft/firm, not fixed
Local features of oral Ca
Leukoplakia
Speckled leukoplakia
Erythroplakia
Ulceration
Fungation (exophytic tumour)
Fixation
Destruction
Painless
Loss of function
Ix may be req. for oral Ca
Biopsy: fine needle aspirate of lumps
X-ray: bony involvement
CT: soft/hard tissue involvement for staging + Tx plan
MRI: soft tissue, better resolution cf CT
MET: shows ‘hot spots’ of activity, detect occult 1rys
Systemic features of oral Ca
Weight loss
Cachexia
Symptoms due to distant metastases
- lung: coughing blood, shortness of breath
Discuss pathology of oral Ca
Epithelial malignancy
Malignant cells invade underlying CT
Spread via lymphatics to regional lymph nodes
- becomes established within node
- replace normal structure
- may spread out of capsule into neck tissue
Rare: vascular spread to distant sites
Histology of oral Ca
Epithelial island invasion of
- connective tissue
- muscle
- salivary glands
- bone
Cellular atypia
- nuclear hyperchromatism
- nuclear + cellular pleomorphism
- inc. nuclear:cytoplasm
- inc. + abnormal mitoses
Inflammatory infiltrate: lymphocytes, plasma cells
Principles of Ca surgery
Resection
- remove Ca
- 1cm clear margin
Reconstruction
- reshape damaged/destroyed structures
- skin graft: radial forearm flap, pectoralis major flap
- microvascular surgery
Rehabilitation
- speech + language therapist
- oral competence
- chewing
- palatal competence
- dental rehabilitation: teeth, implants etc
How does radiotherapy work?
X-ray beams directed at site which cause damage to cells w/ high turnover
Adverse affects of radiotherapy
Acute
- mucositis
- dysgeusia
- weight loss
- fatigue
Late: >90d post-Tx
- xerostomia
- oedema
- ORN
- telangiectasia
- fibrosis
- atrophy
Difference b/w palliative and curative surgery
Palliative
- doesn’t remove Ca
- alleviate pain/discomfort
- improve QoL
Curative
- removes malignant tissue
- aims to cure Ca
Aetiology + risk factors for acute bacterial sialadenitis
Aetiology
- Strep. pyogenes
- Staph. aureus
Predisposing
- red. salivary flow
- dehydrated
- immunocompromised
- acute exacerbation of chronic
Clinical features + Mx of acute sialadenitis
Clinical
- S: parotid, submandibular (common), unilateral
- gland: tender, swelling
- erythema: skin, mucosa
- suppurative
- fever, malaise, trismus
- lymphadenopathy
Mx
- antimicrobial: Tx infection
- target predisposing factor
Discuss chronic sialadenitis
Non-specific inflammation of gland
Associated w/ red. saliva flow -> low-grade ascending infection
Clinical
- S: submandibular, unilateral
- recurrent tenderness + swelling
- duct orifice: erythema, suppurative (acute exacerbation)
- early: enlarged
- late: small, firm, no saliva prod. when massaged
Ix: US, sialography
- determine predisposing: calculus, stricture
Histology of sialadenitis
Progressive glandular atrophy
- acinar destruction
- fibrous replacement
- ductal ectasia
Inflammatory infiltrate
Discuss sialolithiasis
Salivary gland stones Predisposing - red. saliva flow - dehydration - chronic sialadenitis - Sjögren’s
Clinical
- S: submandibular (80-90%)
- pain + swelling associated w/ meal times
Mx
- Tx acute infection (if present)
- surgical removal
— strategy depends on site
Aetiology, epidemiology + Mx of mumps associated sialadenitis
Aetiology: paramyxovirus
Epidemiology: childhood usually, any age poss.
Mx
- supportive: hydration, OH, analgesic
- vaccine: 88% effective
— immunity long lasting thus recurrence low
Clinical presentation + complications of mumps associated sialadenitis
Clinical
- S: parotid (70% bilateral)
- prodromal: fever, malaise
- painful swelling 1/+ glands
Complications
- orchitis
- meningoencephalitis
- pancreatitis
- arthritis
Histology of mumps sialadenitis
Dense interstitial lymphoplasmacytic infiltrate
Acinar destruction
Duct dilation
Discuss cytomegalic inclusion disease
Aetiology: CMV (HHV5)
Clinical
- asymptomatic
- neonates, immunocompromised: severe disseminated disease
- salivary disease usually incidental finding
Histology: viral inclusions in epithelial nucleus + cytoplasm
Clinical features of HIV sialadenitis
Diffuse cystic enlargement of major salivary glands
S: bilateral Gradual, non-tender enlargement 1/+ Cervical lymphadenopathy Nasopharyngeal swelling Xerostomia
Histology of HIV sialadenitis
Cystic spaces - lined by squamous epithelium Associated w/ reactive lymphoid stroma Florid follicular hyperplasia Loss of mantle zones Lymphoepithelial islands
Epidemiology + aetiology of necrotising sialometaplasia
Epidemiology: middle age
Aetiology: unknown
- local ischaemia (trauma) -> minor gland infarction
Clinical features + Mx of necrotising sialometaplasia
Clinical
- S: hard palate
- deep crater-like ulcer
- erythematous edge
- preceded: indurated swelling
- mistaken for malignancy
Mx
- reassure
- supportive
- spontaneous resolution: 4-10/52
Histology of necrotising sialometaplasia
Mucosal ulceration - lobular necrosis minor glands Reactive squamous metaplasia Ductal hyperplasia Mucus extravasation -> inflammation
What is sarcoidosis? Clinical features
Mutlisystem, systemic granulomatous disorder
Clinical
- S: parotid (bilateral), minor glands
- painless, persistent enlargement
- indurated swellings: gingiva, tongue
- multiple asymptomatic submucosal nodules
- xerostomia
Mx of sarcoidosis
Medications
- steroids
- azathioprine
- methotrexate
- cyclophosphamide
May remain stable/regress spontaneously/progressively worsen
- mortality: <5%
Histology of sarcoidosis
Non-necrotising granulomatous inflammation
Hyalinisation
Calcification
Aetiology, Mx + histology of tuberculosis
Aetiology: mycobacterium tuberculosis
Mx: anti-mycobacterial
Histology: necrotising granulomatous inflammation
Clinical features of oral TB
S: parotid Mycobacterial lymphadenitis - peri/intra-parotid lymph node enlargement - due to lymphatic drainage Painless, discrete nodule(s) in gland Deep, punched-out ulcers - erythema - swelling
Histology of Sjögren’s syndrome
Lymphocytic infiltrate
- formation of punctate lymphocytic foci
- peri-acini/ductal/vascular distribution
Exocrine gland atrophy
What is Küttner tumour? Epidemiology, risk factors + Mx
IgG4-related salivary gland disease
Chronic sclerosing sialadenitis
Benign, fibroinflammatory process affecting submandibular gland in pt w/ IgG4 disease
Epidemiology: >50, M
Mx: surgical excision
Clinician features of Kuttner tumour
S: submandibular common
Non-tender firm swelling
Mimics neoplasia
Histology of Kuttner tumour
Dense lymphoplasmacytic infiltrate
Storiform pattern of fibrosis
Obliterative phlebitis
Clinical features of pleomorphic adenoma
Benign epithelial salivary gland neoplasm
Clinical
- S: parotid, minor glands
- behaviour: slow growing
- asymptomatic
- smooth, mobile mass
Mx + prognosis of pleomorphic adenoma
Mx: excision
- incomplete capsule makes difficult
- may req. parotidectomy
Prognosis
- low of complete removal
- recurrence aggressive
- malignant transformation: 6%
Histology of pleomorphic adenoma
Pleomorphism: epithelial, connective tissue
Formation bilayered ducts
- ductal epithelium: inner layer
- myo-epithelium: outer layer
Stroma: myxochondroid/myxoid/chondroid + mucin
Clinical features of Warthin’s tumour
Benign epithelial salivary gland tumour
Clinical
- S: parotid, peri-parotid lymph nodes
- behaviour: slow growing
- asymptomatic, fluctuant swelling
- multifocal, bilateral
Mx + prognosis Warthin’s tumour
Mx: excision w/ margin
Prognosis
- recurrence low (5%): incomplete removal, multifocal
- malignant transformation: rare
Histology of Warthin’s tumour
Double layer epithelial cells
Lymphoid stroma
Cystic spaces
Oncocytic columnar cells w/ discontinuous basal cells
Epidemiology + clinical features mucoepidermoid carcinoma
Epidemiology: <20
Clinical - S: parotid — P, submandibular, minor - cystic, mimic mucocele - soft/firm circumscribed/infiltrative mass
Difference b/w low + high grade of mucoepidermoid carcinoma
Grading based on epidermal:mucous cells
Low/intermediate
- less aggressive
- good prognosis
- Tx: surgical excision
High Grade
- aggressive
- regional metastases
- Tx: resection +/- neck dissection + post-op radiotherapy
- 10y survival 25%
Histology of mucoepidermoid carcinoma
Mucinous, epidermoid + intermediate cells in varying amounts
Solid -> cystic growth pattern
Cysts mucin filled
High grade
- less mucous cells
- solid/infiltrative growth
- perineural spread
- vascular invasion
- cytological anaplasia
- necrosis
Discuss adenoid cystic carcinoma
Malignant epithelial salivary gland neoplasm
Epidemiology: >50, elderly Clinical - S: major glands — most common submandibular tumour - behaviour: slow growing, locally invasive - painless relentless swelling/mass - ulceration: skin, mucosa - numbness/paraesthesia/pain
Mx: excision +/- radiotherapy
Prognosis
- distant metastases common: >50%
- 10y survival: 50-70%
Histology of adenoid cystic carcinoma
Biphasic: ductal epithelial + albuminal myoepithelial
- myoepithelial: basaloid appearance; dark, angulated nucleus + scant cytoplasm
Architecture: cribriform (myoepithelial w/ globules), tubular (tubules) or solid (sheets of basaloid cells)
Acellular basophilic + hyalinised matrix incorporeal into micro-cystic islands
Peri/intraneural spread
High grade
- solid growth
- cellular atypia
- inc. mitoses
- necrosis
Epidemiology + Mx of acinic cell carcinoma
Malignant salivary gland neoplasm
Epidemiology: 50, F
Mx
- excision
- high grade: neck dissection +/- radiotherapy
Clinical features of acinic cell carcinoma
S: parotid
Behaviour: slow growing, infiltrative
Solitary, unfixed mass
Poss. multi-nodular +/- fixed
Histology of acinic cell carcinoma
Usually sheets of neoplastic acinar cells
Non-encapsulated
Pushing or frankly infiltrative
Prominent lymphoid stroma,basophilia
Aggressive: perineural invasion, stromal hyalinisation
Indications for salivary gland surgery
Overproduction -> drooling
Neoplasia
Obstruction
Trauma -> cyst
What is Wilkie’s procedure?
Surgical rerouting of parotid and/or subMd ducts
Indicated: overproduction of saliva -> drooling
Tx of benign salivary gland tumour
Surgical excision
Minor glands: local excision
Superficial parotidectomy
Total parotidectomy; if deep
Extracapsular dissection
Discuss parotidectomy; structures + complications
Structures
- CN7
- great auricular nerve (sensory)
- retromandibular vein
Complications - sensory disturbance — CN7: temp 30%, perm 1-3% - facial hollowing - sialocele - Frey’s syndrome
What is Frey’s syndrome?
Disorder associated w/ parotid gland and great auricular nerve
Clinical
- erythema + sweating of cheek adjacent to ear
— distribution of great auricular nerve
- usually associated w/ meal times
What is extracapsular dissection?
Surgical technique for Tx gland tumours aims to preserve CN7
Dissection outside of tumour capsule
Benefits
- red. CN7 weakness
- red. Frey’s syndrome
Not suitable for all tumours
Discuss Mx of malignant salivary gland tumours
Surgical excision w/ wide margin
CN7 preserved if poss.
May req. neck dissection + removal of other structures
- ear, skin, Md
Difference b/w mucous extravasation cyst and mucous retention cyst
Extravasation
- damaged duct
- spillage of mucous into surrounding tissues
Retention
- duct obstruction/stricture
- red. mucous secretion from gland
Tx for mucocele and ranula
Mucocele: excision + closure
Ranula
- marsupialisation: suture edges open to allowing drainage
- resection: sublingual/subMd, OE approach
- sclerotherapy: inject drug to shrink vessel, red. production
Tx options for submandibular gland obstruction
Papillotomy Endoscopic removal Duct removal Gland removal Hilar exploration Extracorporeal lithotripsy Radiographically assisted basket removal
Complications of submandibular gland removal
Sensory alteration
- CN7, Md branch: lip/chin muscles
- CNV3: lingual branch, sensory ant. 2/3 tongue
- CN12: muscles of tongue
Sialolithiasis
Scarring