9 - Bone pathology Flashcards

1
Q

What are the key components of bone?

A
  • osteon (Haversian system)
  • interstitial, concentric and circumferential lamellae
  • periosteum
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2
Q

What are Haversian canal?

A

Bony canal that contains blood vessels

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3
Q

What are volksman’s canal?

A

Bony canal that runs perpendicular to Haversian canal that contains blood vessel

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4
Q

What cells are contained within lacunae?

A

Osteocytes

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5
Q

How does bone histology change as it matures?

A

Becomes less cellular

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6
Q

What stimulates bone remodelling?

A
  • mechanical stimuli
  • systemic hormones
  • cytokines
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7
Q

What systemic hormones stimulate bony remodelling?

A
  • PTH
  • vitamin D3
  • oestrogen
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8
Q

How does oestrogen influence bone?

A
  • acts like a brake on osteoclasts
  • when oestrogen levels drop, osteoclasts become more active
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9
Q

What special tests can be done for bone biochemistry?

A
  • can’t take biopsy
  • serum alkaline phosphatase
  • osteocalcin
  • PTH
  • vitamin D assays
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10
Q

What is a torus?

A
  • developmental exostosis
  • palatinus/mandibularis
  • thickening of cortical bone
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11
Q

What is osteogenesis imperfecta?

A
  • type 1 collagen defect
  • inheritance varied
  • weak bones, multiple fractures
  • associated with dentinogenesis imperfecta
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12
Q

What is achondroplasia?

A
  • autosomal dominant condition
  • poor endochondral ossification
  • causes dwarfism
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13
Q

What is osteopetrosis?

A
  • lack of osteoclast activity
  • bone fails to resorb and marrow is obliterated
  • bone becomes very dense like stone
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14
Q

What is fibrous dysplasia?

A
  • uncommon gene defect
  • slow growing, asymptomatic bony swelling where bone is replaced by fibrous tissue
  • stops progressing after growth period
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15
Q

What are the different types of fibrous dysplasia?

A
  • monostotic
  • polyostotic
  • syndromic (Albright’s syndrome)
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16
Q

What is monostotic fibrous dysplasia?

A
  • single bone (continues to grow)
  • most common phenotype
  • maxilla>mandible
  • causes facial asymmetry
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17
Q

What is polyostotic fibrous dysplasia?

A

Many bones affected by fibrous dysplasia

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18
Q

What is Albright’s syndrome?

A

Characterised by multiple bones with fibrous dysplasia, early puberty and increased melanin pigment

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19
Q

Describe the radiographic appearance of fibrous dysplasia.

A
  • “ground glass”, “cotton wool”, “orange peel”
  • lacks trabecular pattern
  • margins blend into surrounding bone
  • bone maintains approximate shape
  • becomes more radiopaque as lesion matures
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20
Q

Describe the histology of fibrous dysplasia.

A
  • “fibro-osseous” lesion
  • fibrous replacement of bone
  • cellular fibrous tissue around metaplastic or woven bone which increases in density
  • no capsule
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21
Q

What is rarefying osteitis?

A
  • localised loss of bone in response to inflammation
  • process rather than disease
  • occurs secondary to another form of pathology
  • if at apex of tooth, consider apical periodontitis, periapical granuloma or periapical abscess
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22
Q

What is sclerosing osteitis?

A
  • localised increase in bone density in response to low grade inflammation
  • most common around apex of tooth with necrotic pulp
  • periapical radiopacity that is poorly defined
  • can cause external root resorption
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23
Q

What is idiopathic osteosclerosis?

A
  • localised increase in bone density of unknown cause
  • most common in premolar/molar region of mandible
  • asymptomatic
  • no bony expansion or effect of adjacent structures
24
Q

What is alveolar osteitis?

A
  • dry socket
  • complication of extraction
  • causes severe pain, loss of clot and bone sequestra
25
Q

What is osteomyelitis?

A
  • endogenous infection
  • acute or chronic (suppuration is rare)
  • presents similarly to sequestra, actinomycosis, chronic diffuse sclerosing osteomyelitis or periostitis
26
Q

What is Garre’s sclerosing osteomyelitis?

A
  • only seen in children
  • any infection can cause
  • suppuration present
  • painful hard swelling
27
Q

What are the different aetiologies of bone necrosis?

A
  • osteomyelitis
  • avascular necrosis (age related ischaemia or anti-resorptive medication)
  • irradiation (ORN)
28
Q

What are the different types of metabolic bone disease?

A
  • osteoporosis
  • rickets/osetomalacia
  • hyperparathyroidism
29
Q

What is osteoporosis?

A
  • bone atrophy (resorption>formation)
  • endosteal net bone loss
  • quantitive deficiency (bone that is formed is normal)
  • symptomless, weak bones, sinus enlargement
30
Q

What are the radiographic features of osteoporosis?

A

Loss of normal bone markings

31
Q

What is the aetiology of osteoporosis?

A
  • sex hormone status
  • age
  • calcium status and physical activity
  • secondary osteoporosis caused by hyperparathyroidism, cushings, thyrotoxicosis, diabetes, long term steroids
32
Q

What is rickets/osteomalacia?

A
  • rickets in children, osteomalacia in adults
  • osteoid forms but fails to calcify
  • qualitative deficiency
33
Q

What is the aetiology of rickets/osteomalacia?

A

Vitamin D deficiency

34
Q

How does rickets present?

A
  • children with bow legs
  • poor endochondral bone
  • law calcium and raised alkaline phosphatase
35
Q

What is hyperparathyroidism?

A
  • increased levels of parathyroid hormone
  • calcium is mobilised from bones causing generalised osteoporosis, brown tumours and metastatic calcification in kidneys
36
Q

What are the different types of hyperparathyroidism?

A
  • primary (neoplasia/hyperplasia)
  • secondary (hypocalcaemia due to vit D deficieny)
  • tertiary (hyperplasia due to prolonged secondary)
37
Q

What is the incidence of primary hyperparathyroidism?

A
  • 1 in 100
  • postmenopausal women
  • 3:1 F:M
  • 90% caused by parathyroid adenoma
38
Q

What is osteitis fibrosa cystica?

A
  • aka brown’s tumour
  • giant cell lesions which with mulitnucelated giant cells and blood vessels which give brown colour
39
Q

What are the different types of giant cell lesion in the jaw?

A
  • peripheral giant cell epulis
  • central giant cell granuloma
40
Q

What is a central giant cell granuloma?

A
  • grows along jaw
  • mandible>maxilla
  • 10-25 years
  • central lesion may “burst” out which is first clinal sign
41
Q

What is cherubism?

A
  • rare condition in children
  • autosomal dominant inheritance (FH important)
  • multicystic/locular lesions in multiple quadrants
  • grow before 7 years then regress after puberty
  • vascular giant cell lesions
42
Q

What is the management of cherubism?

A
  • no active management
  • may require orthodontic treatment to realign once condition is resolved
43
Q

What is Paget’s disease?

A
  • presents with bone swelling, pain and nerve compression
  • unknown aetiology
  • monostotic or polystotic
  • > 40 years M>F
44
Q

Describe the radiographic appearance of Paget’s disease.

A
  • bone pattern changes as disease progresses
  • osteoporotic in early stages, becoming osteosclerotic in mature disease
  • causes loss of lamina dura, hypercementosis and migration
45
Q

Describe the histology of Paget’s disease.

A
  • active increased bone turnover
  • osteoblastic and osteoclastic activity next to each other which indicates disordered turnover
46
Q

What are the complications of Paget’s disease?

A
  • infection
  • pathological fracture
  • tumours (osteosarcoma)
47
Q

What is an osteoma?

A
  • solitary bone tumour
  • if multiple, consider Gardner syndrome which has high polyp cancer risk
48
Q

What is an osteoblastoma?

A
  • rare bone tumour
  • very active growth
49
Q

What is an ossifying fibroma?

A
  • slow growing bone tumour
  • affects wide age range
  • mandible
  • radiologically well defined as has capsule
50
Q

Describe the histology of an ossifying fibroma.

A
  • cellular fibrous tissue
  • immature bone
  • acellular calcifications
51
Q

What are the different types of cementum lesions?

A
  • cementoblastoma
  • cemento-osseous dysplasia
52
Q

What is a cementoblastoma?

A
  • neoplasm attached to root
  • commonly found in lower 4 anteriors
  • histology same as osteoblastoma
  • PDL space is continuous on radiograph
53
Q

What is a cemento-osseous dysplasia?

A
  • not neoplastic
  • periapical COD (lower 4 anteriors)
  • focal COD (one)
  • florid COD (all quadrants)
  • starts as radiolucency then calcifies
54
Q

What complication is associated with cemento-osseous dysplasia?

A

Risk of osteomyelitis if extraction is carried out in area of COD

55
Q

What is an osteosarcoma?

A
  • rare tumour
  • 30s, if older Paget’s related
  • mandible>maxilla
  • local destruction
  • recurrence is high and metastasis common