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BDS4 Radiology > Bone pathology > Flashcards

Bone pathology Flashcards

(106 cards)

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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
What is monostotic fibrous dysplasia
single bone effected
26
What is polyostotic fibrous dysplasia
many bones effected
27
How does monostotic fibrous dysplasia present
the more common one more common in mandible may present as asymmetry on one side
28
What is polyostotic fibrous dysplasia
* usually part of a syndrome
29
What syndrome is polyostotic fibrous dysplasia associated with
**Albright's syndrome** * also present with melanin spots * girls can experience early puberty
30
How does fibrous dysplasia appear radiographically
* cotton wool appearance * ill defined margins which blend into bone * bone maintains approximate shape initially * becomes more radiopaque as the lesion matures
31
What are the histological features of fibrous dysplasia
* 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
32
Why should other tests be done for fibrous dysplasia
* it can involve other bone conditions * should do other tests to take them into account
33
What is rarefying osteitis
* localised loss of bone in response to inflammation * it is a process, not a pathology
34
What causes rarefying osteitis
* 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
35
What is sclerosising osteitis
* localised increase in bone density in response to low grade inflammation * most common around apex of a tooth with a necrotic pulp
36
How does sclerosing osteitis present
* periapical radiopacity * often poorly defined * may eventually lead to external root resorption if chronic *also known as condensing osteitis
37
What is idiopathic osteosclerosis
* localised increase in bone density of unknown cause
38
Where is idiopathic osteosclerosis most common
* premolar/molar region of mandible
39
How does idiopathic osteosclerosis present
* always asymptomatic * no bony expansion * no effect on adj structures * similar to sclerosising osteitis - vitality test and look out for symptoms
40
What is alveolar osteitis aka
dry socket complication of XLA
41
What is alveolar osteitis due to
clot being lost too early should be recognised as part of healing process leaves behind bony sequestra
42
How does alveolar osteitis present
sevrere pain
43
What are risk factors for alveolar osteitis
* smoking * OCP * difficult XLA * mandible * posterior * rinsing too soon
44
What is the management of dry socket
* can use medicaments e.g alveogyl however can slow healing * best management = encourage healing and allow new clot formation
45
What is osteomyelitis
rare endogenous infection
46
What is the theory surrounding the cause of osteomyelitis
* compound fracture creation when performing XLA which exposes the fracture to the air * can be acute or chronic *
47
What may osteomyelitis present with
* sequestreum * actinomycosis * chronic diffuse sclerosing osteomyelitis * periostitis productive - inflammation of the periosteum
48
What are the 2 main types of osteomyelitis
supparitve garre's ostemyelitis - periostitis productive
49
What is supparative osteomyelitis
* 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
What are the symptoms of acute osteomyelitis
fever malaise swelling pain trismus
51
What are symptoms of chronic osteomyelitis
swelling pain chronic suppuration
52
What is Garre's ostemyelitis
* 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
What are other causes of bony necrosis
avascular necrosis - reduction of blood supply irradiation
54
What can avascular necrosis be further split into
age related ischaemia antiresorptive medications
55
What are examples of metabolic bone diseases
* osteoporosis * rickets and osteomalacia * hyperparathyroidism
56
What is osteoporosis
bone loss > bone apposition
57
What are the greatest risk factors for osteoporosis
* sex hormone status - post menopausal women * age - bone apposition reduces with age * calcium status and physical activity * secondary osteoporosis
58
What conditions result in secondary osteoporosis
cushing's primary hyperparathyroidism thyrotoxosis
59
How does osteoporosis present
* 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
How will osteoporsosis appear on xray
* normal trabeculae lost * will appear as loss of bone markings
61
What is significant about the medications taken for osteoporosis
MRONJ risk
62
What is rickets and osteomalacia
* osteoid laid down but not fully calcified
63
What is the cause of osteomalacia/rickets
lack of vitamin d usually due to * diet * lack of sunlight * malabsorption * renal causes
64
What may a px with rickets present with
* poor endochondral bone * low calcium * raised alkaline phosphatase
65
How does the body try to increase serum calcium
* increased calcium absorption into the gut * increased calcium resorption in the kidney * stimulate osteoclast activity
66
How does hyperparathyroidism present
* 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
What are the types of hyperthyroidism
* primary - neoplasio//hyperplasia * secondary - hypocalcaemia e.g vitamin D deficiency * tertiary - prolonged secondary results in hyperplasia
68
How does primary hyperthyroidism present
* 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
What is brown's tumour
* 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
What is the radiographic appearance of primary hyperparathyroidism
* may show no detectable changes or a generalized osteoporosis * partial loss of lamina dura
71
What is the radiographic appearance of browns tumour
* sharply defined round or oval radioluceny area * may appear mutlilocular * more common in mandible
72
What are the 2 types of giant cell lesions
peripheral giant cell epulis central giant cell granuloma
73
How does peripheral giant cell epulis present
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
Which age group is central giant cell granuloma most common in
10-25 YO most common in mandible
75
How does central giant cell granuloma present
* 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
How does a central giant cell granuloma appear histologically
* multinucleate osteoclast giant cells are present
77
What is the differential diagnosis for giant cell lesions
* browns tumour * aneurysmal bone cyst * giant cell tumour
78
What is cherubism
* rare condition * autosomal dominant inheritance
79
How does cherubism present
* multicystic/multilocular lesions in multiple quadrants * painless swelling * lesions grow until 7 YO then regress * histologically: vascular giant cell lesion
80
What age group and gender does Paget's disease effect
>40 YO M>F
81
What is the aetiology of Pagets
* racial deposition - more common in British Migrants e.g AUS * viral - measles? * no real known cause atm
82
What is monostotic paget's
one bone involved
83
What is polystotic paget's
>1 bone involved
84
What will blood tests for paget's show
raised alkaline phosphotase
85
What will paget's present with
* bony swelling - look for changes in facial profile and oclcusion * pain * nerve compression * motor and sensory disturbance if skull involved
86
How does Paget's present radiographically
variable bone pattern * changes as disease progresses * osteoporotic/mixed/osteosclerotic * can have cotton wool appearance Dental changes * loss of lamina dura * hypercementosis * migration
87
What is the histology of Paget's
* 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
What are reversal lines (Paget's)
* junctions where there has been reversal of osteoclastic resorption to osteoblastic deposition
89
What are complications of paget's
* infection * MRONJ - px usually on implicated medication * tumour - rare complications = osteosarcoma and other bone tumours
90
What is the main benign bone tumour
osteoma
91
How does osteoma present
* slow growth * excess growth of cortical bone * usually solitary but can have multiple
92
What is multiple osteomas a sign of
Gardner's syndrome genetic disorder
93
What is an important feature of gardner's syndrome that should be checked out
polyposis coli tendency to become malignant refer to GI
94
What is the main malignant bone tumour
* osteosracoma
95
How does osteosarcoma present
* 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
What is ossifying fibroma
* well demarcated, occasionally encapsulated benign neoplasm
97
What is the clinical presentation of ossifying fibroma
* slow growing * wide age range * mainly mandible * radiologically well defined - may have calcium deposits
98
How does ossifying fibroma present histolofically
* pretty much same as fibrous dysplasia * cellular fibrous tissue containing immature bone and acellular calcification
99
What differentiates ossifying fibroma to fibrous dysplasia
fibrous dysplasia does not have well defined margins, ossifying fibroma does
100
What are the main 2 cementum lesions
cementoblastoma cemento-osseous dysplasia
101
What is cementoblastoma
neoplasm attached to root histologically same as osteoblastoma
102
What is cementoosseous dysplasia unlikely to be
neoplastic
103
What are the 3 types of cemento-osseous dysplasia
peripheral focal florid
104
What is peripheral COD
* usually lower incisors effected (teeth are vital) * starts as well defined radiolucency resembling PA granuloma
105
What is focal COD
* localised * no more than 1 in 1 area
106
What is florid COD
widespread

BDS4 Radiology (8 decks)

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