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Oral Disease for FINALS > Bone lesions of the jaw > Flashcards

Bone lesions of the jaw Flashcards

1
Q

Bone structure (3)

A 
• Gross structure
• Blood supply
• Microscopic structure
– lamellar bone - mature
– woven bone - immature (see this in embryology and healing or in a lesion)
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2
Q

Bone histology (5)

A

Cortical/ compact bone on outside
Cancellous bone on inside
-haemopoetic marrow and fat
In centre of traversian systems/ osteon are Haversian canals (contain BVs)
Osteocytes contained in holes you see on histology
Osteoblasts lining surface of woven bone

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3
Q

Bone turnover (4)

A
  • Laid down by osteoblasts (some osteoblasts osteocytes)
  • Removed by osteoclasts
  • Turnover occurs in response to forces on bone
  • Results in resting and reversal lines
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4
Q

Bone remodelling overseen by (4)

A

• Mechanical stimuli
• Systemic hormones
– parathyroid hormone (PTH) to stimulate resorption of bone to increase serum cacium
– vitamin D3 increases calcium absorption from diet and net absorption of calcium into bone
– oestrogen good at maintaining bone mass (loss of this in menopause can result in osteoporosis i.e. loss of bone mass)
– others: e.g. calcitonin for osteoclast function
• Cytokines (stimulus for osteoclasts and osteoblasts)
• Complex interactions promote growth of cells and
bone matrix

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5
Q

Special tests - bone biochemistry (5)

A 
• Serum calcium - cheapest and simplest, analysis of bone metabolism
• Osteoblast activity (bone formation)
– serum alkaline phosphatase
– osteocalcin
• Osteoclast activity (bone resorption)
– collagen degradation urine & blood
• Parathyroid hormone: regulates serum calcium (specialised)
• Vitamin D assays (specialised)
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6
Q

Oral developmental abnormalities of bone: torus (5)

A 
• torus: developmental
exostosis (i.e. growing out from surface of bone)
• problem with fitting
dentures
• torus palatinus
– midline of palate
• torus mandibularis
– bilateral on lingual
aspect of mandible
Histology: compact bone
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7
Q

Oral developmental abnormalities of bone: osteogenesis imperfecta (4)

A 
– type 1 collagen defect
– inheritance varied - 4 main types
Clinical
– weak bones, multiple fractures
– sometimes associated with dentinogenesis
imperfecta
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8
Q

Oral developmental abnormalities of bone: achondroplasia (3)

A

– autosomal dominant
– dwarfism
– poor endochondral ossification

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9
Q

Oral developmental abnormalities of bone: osteopetrosis (4)

A

– lack of osteoclast activity
– failure of resorption
– marrow obliteration
Made of compact bone only, becomes very fragile and has a tendency to fracture

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10
Q

Infections of bone and their prevalence (4)

A

Dry socket: very common
Sclerosing osteitis: relatively common
Osteomyelitis: rare
Osteonecrosis: rare, but increasingly more common

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11
Q 
Dry socket (alveolar osteitis)
-what does it affect
-how is it caused
-how might this have happened 
(6)
A 
Usually affects molars, particularly impacted 3rd molars
• Caused by loss of or failure of the clot to develop in a socket.
This may be due to:
• Excessive rinsing
• Fibrinolysis of clot
• Poor blood supply due to
radiotherapy, Paget's disease
• Excessive use of vasoconstrictors
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12
Q

Dry socket (alveolar osteitis) what is happening in the socket? (4)

A

Localised inflammatory reaction in bone adjacent
to socket
• Bone adjacent to socket becomes necrotic and is
removed by osteoclasts.
• Healing is very slow
– Irrigation
– Antiseptic dressing
• Very rarely develops into osteomyelitis

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13
Q

Differential diagnosis for sclerosing osteitis (3)

A

Hypercementosis, cementoblastoma, osteoma

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14
Q

What is sclerosing osteitis and who/ where does it affect? (4)

A
  • Focal bone reaction to low-grade inflammation e.g. chronic pulpitis
  • Any age
  • Commonly affects mandibular molars
  • Asymptomatic, incidental finding
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15
Q

Sclerosing osteitis - radiography (2)

A
  • Uniform opacity at apex tooth,

* Often with peripheral lucency

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16
Q

Treatment for sclerosing osteitis (1)

A

Cause of inflammation

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17
Q 
Osteomyelitis 
-what is it?
-who does it affect?
-subtypes
(5)
A

• Inflammation within marrow cavities of bone
• Can affect any age
• Acute or chronic
Subtypes:
• Sclerosing osteomyelitis - nightmare for pt and to treat
• Proliferative periostitis (Garré’s osteomyelitis)

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18
Q

Causes of osteomyelitis (6)

A 
Problems with:
• Blood supply:
– Age related
– Paget's disease
– Radiotherapy
• Host response
• Immunosuppression
• Poor nutrition
• Other causes:
– bisphosphonates
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19
Q

Acute osteomyelitis aetiology (3)

A

Most commonly infectious (Staphylococci,
Streptococci)
• Extension of periapical abscess
• Physical injury/fracture

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20
Q

Acute osteomyelitis acute inflammatory response (4)

A

Pain, pyrexia, lymphadenopathy, malaise

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21
Q

Acute osteomyelitis histology (3)

A
  • Acute inflammatory infiltrate
  • ↑ Bone resorption
  • ↓ Bone formation
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22
Q

Chronic osteomyelitis aetiology (2)

A
  • Low-grade inflammatory reaction

* May be progression from acute osteomyelitis

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23
Q

Chronic osteomyelitis - Chronic inflammatory response associated with low-grade infection (4)

A

Pain, swelling, bone loss, sequestrae

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24
Q

Chronic osteomyelitis histology (4)

A
  • Chronic inflammatory infiltrate - lymphocytes and plasma cells
  • Both osteoclastic and osteoblastic activity
  • Reversal lines
  • Osteonecrosis
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25
Q

What is proliferative periostitis? (1)

A

chronic osteomyelitis with periosteal inflammation

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26
Q

Chronic osteomyelitis radiograph (3)

A

Radiolucency, focal opacity, ‘moth eaten’
Indistinct margins
Sequestrae

27
Q

Osteomyelitis - patient management (3)

A
  • Resolve source of infection
  • Remove infected bone
  • Hyperbaric oxygen
28
Q

Osteonecrosis of the jaws - causes (8)

A 
• Osteoradionecrosis
– Complication of irradiation
– Head and neck malignancies
– Compromised vasculature - endarteritis obliterans
• Bisphosphonate/Medication related osteonecrosis
of the jaws
– MRONJ, BRONJ, DRONJ
• Associated with certain medications
– Bisphosphonates
– Denosumab
• Diabetes
• Smoking
• Poor OH
• Prolonged drug use
• Dental extractions
29
Q

Osteonecrosis of the jaws - patient management

  • prevention (4)
  • low risk (2)
  • high risk (2)
A 
• Prevention
– Dental assessment
– Oral hygiene
– Smoking cessation
– Limiting alcohol
• Low risk
– Osteoporosis
– Atraumatic extractions
• High risk
– Malignancy/ Paget's/ immunosuppressed/ history of MRONJ
– Refer to OS/OMFS
30
Q

Types of bone neoplasms (4)

A

Benign: osteoma, osteoblastoma
Malignant: osteosarcoma, chondrosarcoma

31
Q

Osteoma - clinical (4)

A 
• Localised bony nodule on maxilla
or mandible
• Shows continued growth
• Distinguish from tori
• May be associated with
syndromes (multiple osteomas --> Gardener's syndrome - colon cancer)
32
Q

Osteoma - histopathology: composed of (2)

A

• Compact bone
• Compact and cancellous
bone

33
Q

Osteosarcoma (6)

A
  • Malignant tumour which produces bone
  • Very rare - 120 cases per year all sites
  • Most in long bones
  • 2% to 10% in the jaws
  • About 10 jaw lesions per year in UK
  • Young adults
34
Q

Osteosarcoma of the jaws (3)

A

• Age 20-40 years
• Males slightly more
common
• Mandible > maxilla

35
Q

Why is early dx essential in osteosarcoma of the jaws (3)

A
  • Rapidly growing swelling
  • Pain
  • Nerve involvement
36
Q

Osteosarcoma of the jaws - radiographic features (2)

A

• Radiolucency with
bone formation (sunray)
• Loss of lamina dura is an
important sign

37
Q

Osteosarcoma - patient management (3)

A
  • Neo-adjuvant chemotherapy
  • Wide local excision +/- radiotherapy
  • 5 year survival – about 50%
38
Q

Fibro-osseus lesions (1)

A

Lesions where the normal bone is replaced by fibrous

tissue in which abnormal bone is laid down

39
Q

Fibro-osseus lesions - radiographically (3)

A

• Initially radiolucent because of bone loss
• Later more mixed radiodensity lesion as the abnormal bone is laid down.
• the extent of this varies with the lesion and some lesions
are almost always radio-opaque or radiolucent

40
Q

Types of fibro-osseus lesions (4)

A 
• Neoplastic: (Cemento) ossifying fibroma
• Developmental: Fibrous dysplasia
• Reactive: (Cemento) osseous dysplasia
Osteodystrophy
• Idiopathic: Paget's disease
41
Q

Ossifying fibroma (6)

A

• Benign neoplasm composed of fibrous tissue
which forms spicules, islands or cementicles of
bone
-pattern of bone and cellularity is variable
-lesion has well defined margin and is separated from the cortical bone
• Age: 20-50, average 35 years
– Children may be affected
• Females > males (>3:1)
• Mandible overall most common site (65%)
– Premolar or molar region
– May be in craniofacial bones

42
Q

Ossifying pt management (3)

A 
• Conservative
enucleation
• Resection
• Low recurrence
rate
43
Q

Fibrous dysplasia (7)

A 
• Developmental disorder of bone
– Mutations in GNAS1, not inherited
• 25% affect head and neck
• Age: 15-30
• Males = females
• Painless smooth enlargement/swellings
• Maxilla most frequent site in H&N
• Poorly demarcated radiopacity
44
Q

Fibrous dysplasia - radiographically (2)

A

• Stippled “orange peel”
appearance
• Merges with the surrounding bone

45
Q

Clinical variants of fibrous dysplasia: monostotic (single bone involved) (5)

A
  • Single skeletal lesions
  • Ribs and femur most common site
  • 25% of lesions in head and neck
  • Age 15-30 (average 25)
  • Males = females
46
Q

Clinical variants of fibrous dysplasia: polyostotic (multiple bones involved) (5)

A
  • Multiple lesions
  • Head & neck involved in 50%
  • Age: <15
  • 75% in females
  • May be part of McCune-Albright’s syndrome
47
Q

Fibrous dysplasia: patient management (5)

A

• Growth stabilises over time (skeletal maturity)
• Debulking and contouring of bone
-recurrence if during growth phase
-can reactivate in pregnancy
• Surgical removal
• Orthodontics and orthognathic surgery
• Very low risk of malignant transformation

48
Q

Fibrous dysplasia vs ossifying fibroma (4)

A

Poorly defined vs well defined
No margin vs clear margin
M=F vs F>M
Often maxilla vs often mandible

49
Q

Cemento-osseus dysplasias (5)

A

• A clinicopathological spectrum of reactive lesions
• Age: 30-50
• Often females
• Often multiple radiopacities in the tooth bearing
areas of the jaws
• Composed of irregular trabeculae of woven bone
and ‘cementum’ in fibrous stroma

50
Q

Classification of osseus dysplasias (3)

A

Focal: single lesions
Perapical: multiple mixed radiodensity lesions at apex of teeth
Florid: multiple lesions throughout jaws

51
Q

Familial gingatiform cementoma (3)

A

• Usually described as a variant of Florid OD
-appears to be a different entity to Florid OD
-autosomal dominant inheritance pattern
• M=F
• Found in white patients

52
Q

Paget’s disease (4)

A
  • Rare disorder affecting all bones
  • Bone turnover is increased and no longer related to functional demands
  • Early stages bone becomes very vascular: may result in heart failure
  • Later stages bone becomes sclerotic and shows numerous resting and reversal lines
53
Q

Paget’s disease epidemiology (4)

A 
• More common in Western
Europe, USA, Canada,
Australia, New Zealand
• Rare in Asia, Africa
• Cause unknown.
• Possible
genetic/hereditary
association or infective
cause
54
Q

Paget’s disease clinical features (3)

A 
• Legs become bowed
• Enlargement of the skull
causing constriction of
foramen: deafness, hats
do not fit etc
• Jaws become enlarged:
tooth spacing and
dentures do not fit
55
Q

Paget’s disease: dental implications (4)

A 
• Bone sclerotic: difficulty with
extractions and prone to infections
• Hypercementosis: difficulty with extractions
• Bisphosphonates may complicate matters
• Increased incidence of
osteosarcomas and other bone malignancy
56
Q

Giant cell lesions of the jaws: what are they and types (4)

A 
Characterised by
replacement of bone by fibrous tissue containing numerous
multi-nucleate giant cells (osteoclasts)
• Cherubism
• Central giant cell
granuloma
• Hyperparathyroidism
57
Q

Cherubism (5)

A

• Developmental condition
• Autosomal dominant inheritance
• Bilateral expansion of posterior mandible
• May regress after puberty
Histology: vascular multinucleated giant cell lesions

58
Q

Giant cell lesions of the jaws (6)

A
  • Reactive or hyperplastic lesions
  • Benign but may be locally destructive
  • Age: 10-30
  • 60% in females
  • Usually mandible
  • Characterised by osteoclasts
59
Q

Central giant cell granuloma (3)

A
  • Well demarcated radiolucency
  • Composed of giant cells - osteoclasts
  • May be destructive
60
Q

Giant cell lesions of the jaws: patient management (4)

A
  • Blood biochemistry (serum calcium initially)
  • Curettage
  • Resection
  • 20% recurrence rate
61
Q

Hyperparathyroidism types and tests (5)

A 
Hyperparathyroidism:
– Primary: parathyroid adenoma (90%)
– Secondary: renal failure, malabsorption
– Hereditary: autosomal dominant
• Blood biochemistry:
– Raised serum Calcium, Phosphate
– Parathyroid hormone
62
Q

Hyperparathyroidism mnemonic (1)

A

Stones, bones, groans and moans

63
Q

Hyperparathyroidism giant cell lesion (3)

A

• Radiolucent lesion
• “Brown tumour”
– Identical to central giant cell granuloma
• Management:
– Treatment of hyperparathyroidism (surgery)

Oral Disease for FINALS (34 decks)

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