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BDS4 Radiology > Bone pathology > Flashcards

Bone pathology Flashcards

1
Q

What is spongy bone

A
  • trabeculae
  • contains bone marrow
  • contains canaliculi
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2
Q

What are canaliculi

A

communication between adjacent cavities

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3
Q

What is compact bone

A
  • osteons are functional units
  • the central haversion canal is encased in lamella
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4
Q

What is the outermost layer of bone

A

periosteum

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5
Q

What are osteoclasts

A

remove bone
found in howship’s lacunae

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6
Q

What are osteoblasts

A
  • facilitate mineralization of osteoid matrix
  • interconnected via dendritix extensions
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7
Q

What are osteocytes

A

differnetiated osteoblasts
trapped in bone matrix
contain cytoplasmic projections with osteoblasts and osteocytes

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8
Q

What stimuli can impact bone deposition and resorption

A
  • mechanical
  • systemic
  • cytokines
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9
Q

What systemic hormones impact bone resorption/deposition

A
  • PTH
  • vitamin d3
  • oestrogen
  • growth hormone
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10
Q

How does PTH impact bone remodelling

A
  • secretion controlled by serum calcium
  • reduced serum calcium results in increased PTH
  • increased PTH increases bone resorption
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11
Q

How does oestrogen impact bone remodelling

A
  • inhibits bone resorption
  • this is why women are more prone to OP in menopause
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12
Q

What are examples of developmental bone abnormalities

A
  • torus
  • osteogenesis imperfecta
  • achondroplasia
  • osteopetrosis
  • fibrous dysplasia
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13
Q

What is a torus

A
  • exostosis
  • torus palatinus = midline of palate
  • torus mandibularis = in mandible
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14
Q

What is an exostosis

A

defined as an extra growth of bone that extends outward from existing bone

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15
Q

Where is tori mandibularis usually seen

A
  • lingual aspect of mandible
  • premolar region
  • generally unproblematic unless px wants denture
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16
Q

What is osteogenesis imperfecta

A
  • type 1 collagen defect
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17
Q

What are the 4 main types of osteogenesis imperfect

A

numbered 1-4
type 1 = most mild
type 2 = most severe
type 3 = dentally related

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18
Q

How do osteogenesis imperfecta px present clinically

A

weak bones
multiple fractures
sometimes associated with dentinogenesis imperfecta

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19
Q

What is achondroplasia

A
  • autosomal dominant
  • problem with long bone formation
  • poor endochondral ossification
  • no significant dental related problems
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20
Q

What is osteopetrosis

A
  • lack of osteoclast activity
  • failure of resorption
  • leads to marrow obliteration
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21
Q

What is the dental significance of osteopetrosis

A
  • difficult extractions
  • delayed healing
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22
Q

What is fibrous dysplasia

A
  • due to gene defect
  • slow growing, asymptomatic bony swelling where bone is replaced by fibrous tissue
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23
Q

What age group do we see fibrous dysplasia

A
  • active in under 20s
  • usually stops growing after active growth period
  • surgery should be delayed until after growth
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24
Q

What are the types of fibrous dysplasia

A
  • monostotoic
  • polyostotic
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25
Q

What is monostotic fibrous dysplasia

A

single bone effected

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26
Q

What is polyostotic fibrous dysplasia

A

many bones effected

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27
Q

How does monostotic fibrous dysplasia present

A

the more common one
more common in mandible
may present as asymmetry on one side

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28
Q

What is polyostotic fibrous dysplasia

A
  • usually part of a syndrome
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29
Q

What syndrome is polyostotic fibrous dysplasia associated with

A

Albright’s syndrome
* also present with melanin spots
* girls can experience early puberty

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30
Q

How does fibrous dysplasia appear radiographically

A
  • cotton wool appearance
  • ill defined margins which blend into bone
  • bone maintains approximate shape initially
  • becomes more radiopaque as the lesion matures
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31
Q

What are the histological features of fibrous dysplasia

A
  • fibro-osseous appearance
  • fibrous replacement of bone with cellular fibrous tissue
  • bone is metaplastic or woven but will remodel and increase in density
  • no capsule, not seperated from adj bone
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32
Q

Why should other tests be done for fibrous dysplasia

A
  • it can involve other bone conditions
  • should do other tests to take them into account
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33
Q

What is rarefying osteitis

A
  • localised loss of bone in response to inflammation
  • it is a process, not a pathology
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34
Q

What causes rarefying osteitis

A
  • inflammatory factors coming from necrotic pulp and resorb the apex
  • if at the apex of the tooth, consider PA periodontitis, periapical granuloma or periapical abscess
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35
Q

What is sclerosising osteitis

A
  • localised increase in bone density in response to low grade inflammation
  • most common around apex of a tooth with a necrotic pulp
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36
Q

How does sclerosing osteitis present

A
  • periapical radiopacity
  • often poorly defined
  • may eventually lead to external root resorption if chronic
    *also known as condensing osteitis
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37
Q

What is idiopathic osteosclerosis

A
  • localised increase in bone density of unknown cause
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38
Q

Where is idiopathic osteosclerosis most common

A
  • premolar/molar region of mandible
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39
Q

How does idiopathic osteosclerosis present

A
  • always asymptomatic
  • no bony expansion
  • no effect on adj structures
  • similar to sclerosising osteitis - vitality test and look out for symptoms
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40
Q

What is alveolar osteitis aka

A

dry socket
complication of XLA

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41
Q

What is alveolar osteitis due to

A

clot being lost too early
should be recognised as part of healing process
leaves behind bony sequestra

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42
Q

How does alveolar osteitis present

A

sevrere pain

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43
Q

What are risk factors for alveolar osteitis

A
  • smoking
  • OCP
  • difficult XLA
  • mandible
  • posterior
  • rinsing too soon
44
Q

What is the management of dry socket

A
  • can use medicaments e.g alveogyl however can slow healing
  • best management = encourage healing and allow new clot formation
45
Q

What is osteomyelitis

A

rare endogenous infection

46
Q

What is the theory surrounding the cause of osteomyelitis

A
  • compound fracture creation when performing XLA which exposes the fracture to the air
  • can be acute or chronic
    *
47
Q

What may osteomyelitis present with

A
  • sequestreum
  • actinomycosis
  • chronic diffuse sclerosing osteomyelitis
  • periostitis productive - inflammation of the periosteum
48
Q

What are the 2 main types of osteomyelitis

A

supparitve
garre’s ostemyelitis - periostitis productive

49
Q

What is supparative osteomyelitis

A
  • source of infeciton = teeth e.g abscess
  • anaerobic predominate
  • mandible most ocmmon
  • vascular supply reduced
  • organisms proliferate in the marrow space - acute inflammatory reaction
  • necrosis and suppuration ensue
  • sequestreum may exfoliate or be removed surgically
50
Q

What are the symptoms of acute osteomyelitis

A

fever
malaise
swelling
pain
trismus

51
Q

What are symptoms of chronic osteomyelitis

A

swelling
pain
chronic suppuration

52
Q

What is Garre’s ostemyelitis

A
  • most common in children and adults
  • periosteal osteosclerosis presenting clinically as a bony hard swelling on the outer surface of hte mandible
  • periosteal reaction is thought to result from the spread of a low grade, chronic apical inflammation through the cortical bone
  • xray will show overgrowth of bone
53
Q

What are other causes of bony necrosis

A

avascular necrosis - reduction of blood supply
irradiation

54
Q

What can avascular necrosis be further split into

A

age related ischaemia
antiresorptive medications

55
Q

What are examples of metabolic bone diseases

A
  • osteoporosis
  • rickets and osteomalacia
  • hyperparathyroidism
56
Q

What is osteoporosis

A

bone loss > bone apposition

57
Q

What are the greatest risk factors for osteoporosis

A
  • sex hormone status - post menopausal women
  • age - bone apposition reduces with age
  • calcium status and physical activity
  • secondary osteoporosis
58
Q

What conditions result in secondary osteoporosis

A

cushing’s
primary hyperparathyroidism
thyrotoxosis

59
Q

How does osteoporosis present

A
  • usually symptomless until something bad happens
  • weak bone (normal composition, reduced quantity)
  • in edentulous px may only be thin strip of bone left
  • antrum enlargred
60
Q

How will osteoporsosis appear on xray

A
  • normal trabeculae lost
  • will appear as loss of bone markings
61
Q

What is significant about the medications taken for osteoporosis

A

MRONJ risk

62
Q

What is rickets and osteomalacia

A
  • osteoid laid down but not fully calcified
63
Q

What is the cause of osteomalacia/rickets

A

lack of vitamin d
usually due to
* diet
* lack of sunlight
* malabsorption
* renal causes

64
Q

What may a px with rickets present with

A
  • poor endochondral bone
  • low calcium
  • raised alkaline phosphatase
65
Q

How does the body try to increase serum calcium

A
  • increased calcium absorption into the gut
  • increased calcium resorption in the kidney
  • stimulate osteoclast activity
66
Q

How does hyperparathyroidism present

A
  • calcium mobilised from bone
  • generalized osteoporosis
  • osteitis fibrosa cystic - aka browns tumour
  • metastatic calcification of the kidney due to increase calcium in the blood
67
Q

What are the types of hyperthyroidism

A
  • primary - neoplasio//hyperplasia
  • secondary - hypocalcaemia e.g vitamin D deficiency
  • tertiary - prolonged secondary results in hyperplasia
68
Q

How does primary hyperthyroidism present

A
  • usually due to parathyroid adenoma
  • mainly post menopausal women
  • blood tests will show hypercalcaemia and increased bone turnover
  • 10% present with brown’s tumour
69
Q

What is brown’s tumour

A
  • focal area of bone resorption results in formation of lesions called browns tumour
  • large number of multinucleate, osteoclast like giant cells are scattered in a highly cellular vascular fibroblastic connective tissue stroma
  • hemosiderin pigment present
70
Q

What is the radiographic appearance of primary hyperparathyroidism

A
  • may show no detectable changes or a generalized osteoporosis
  • partial loss of lamina dura
71
Q

What is the radiographic appearance of browns tumour

A
  • sharply defined round or oval radioluceny area
  • may appear mutlilocular
  • more common in mandible
72
Q

What are the 2 types of giant cell lesions

A

peripheral giant cell epulis
central giant cell granuloma

73
Q

How does peripheral giant cell epulis present

A

swelling on gingiva
may be a sole lesions
may be a central giant cell granuloma which bursts out of the bone and presents as a peripheral giant cell epulis

74
Q

Which age group is central giant cell granuloma most common in

A

10-25 YO
most common in mandible

75
Q

How does central giant cell granuloma present

A
  • may be multilocular
  • possible swelling of bone
  • tends to grow along length of the jaw so often gets quite large before becoming apparent
  • may thin, expand or perforate the cortex
  • teeth may be displaced and their roots resorbed
76
Q

How does a central giant cell granuloma appear histologically

A
  • multinucleate osteoclast giant cells are present
77
Q

What is the differential diagnosis for giant cell lesions

A
  • browns tumour
  • aneurysmal bone cyst
  • giant cell tumour
78
Q

What is cherubism

A
  • rare condition
  • autosomal dominant inheritance
79
Q

How does cherubism present

A
  • multicystic/multilocular lesions in multiple quadrants
  • painless swelling
  • lesions grow until 7 YO then regress
  • histologically: vascular giant cell lesion
80
Q

What age group and gender does Paget’s disease effect

A

> 40 YO
M>F

81
Q

What is the aetiology of Pagets

A
  • racial deposition - more common in British Migrants e.g AUS
  • viral - measles?
  • no real known cause atm
82
Q

What is monostotic paget’s

A

one bone involved

83
Q

What is polystotic paget’s

A

> 1 bone involved

84
Q

What will blood tests for paget’s show

A

raised alkaline phosphotase

85
Q

What will paget’s present with

A
  • bony swelling - look for changes in facial profile and oclcusion
  • pain
  • nerve compression
  • motor and sensory disturbance if skull involved
86
Q

How does Paget’s present radiographically

A

variable bone pattern
* changes as disease progresses
* osteoporotic/mixed/osteosclerotic
* can have cotton wool appearance
Dental changes
* loss of lamina dura
* hypercementosis
* migration

87
Q

What is the histology of Paget’s

A
  • increased bone turnover
  • osteoblastic and osteoclastic activity next to each other
  • disorganized remodelling results in bony trabeculae showing numerous criss-crossing, resting and scalloped reversal lines giving a mosaic appearance
88
Q

What are reversal lines (Paget’s)

A
  • junctions where there has been reversal of osteoclastic resorption to osteoblastic deposition
89
Q

What are complications of paget’s

A
  • infection
  • MRONJ - px usually on implicated medication
  • tumour - rare complications = osteosarcoma and other bone tumours
90
Q

What is the main benign bone tumour

A

osteoma

91
Q

How does osteoma present

A
  • slow growth
  • excess growth of cortical bone
  • usually solitary but can have multiple
92
Q

What is multiple osteomas a sign of

A

Gardner’s syndrome
genetic disorder

93
Q

What is an important feature of gardner’s syndrome that should be checked out

A

polyposis coli
tendency to become malignant
refer to GI

94
Q

What is the main malignant bone tumour

A
  • osteosracoma
95
Q

How does osteosarcoma present

A
  • rare in jaws
  • usually seen in younger px, if elderly, consider pagets
  • usually presents as swelling with pain adn paraesthesia
  • may be a giant osteoid sarcoma
  • often v active growth
96
Q

What is ossifying fibroma

A
  • well demarcated, occasionally encapsulated benign neoplasm
97
Q

What is the clinical presentation of ossifying fibroma

A
  • slow growing
  • wide age range
  • mainly mandible
  • radiologically well defined - may have calcium deposits
98
Q

How does ossifying fibroma present histolofically

A
  • pretty much same as fibrous dysplasia
  • cellular fibrous tissue containing immature bone and acellular calcification
99
Q

What differentiates ossifying fibroma to fibrous dysplasia

A

fibrous dysplasia does not have well defined margins, ossifying fibroma does

100
Q

What are the main 2 cementum lesions

A

cementoblastoma
cemento-osseous dysplasia

101
Q

What is cementoblastoma

A

neoplasm attached to root
histologically same as osteoblastoma

102
Q

What is cementoosseous dysplasia unlikely to be

A

neoplastic

103
Q

What are the 3 types of cemento-osseous dysplasia

A

peripheral
focal
florid

104
Q

What is peripheral COD

A
  • usually lower incisors effected (teeth are vital)
  • starts as well defined radiolucency resembling PA granuloma
105
Q

What is focal COD

A
  • localised
  • no more than 1 in 1 area
106
Q

What is florid COD

A

widespread

BDS4 Radiology (8 decks)

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