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BDS4 Radiology > Bone Pathology > Flashcards

Bone Pathology Flashcards

1
Q

What are the components of compact bone?

A

Compact bone- made up of osteons (Haversian system)

Haversian canal- centre of osteon, inside this we have blood vessels, bone is laid down around canal as concentric lamellae

Osteoblasts form bone- after formation they go into lacunae and become osteocytes

Interstitial lamellae

Volkmans canals allow communication of HS

Canals between osteocytes allow information exchange about environment and stimuli affecting formation

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2
Q

What is the periosteum and what does it contain?

A

Soft tissue overlying bone
-> contains pain receptors, blood vessels, osteo-progenitor cells

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3
Q

What is found in woven bone?

A

Osteoblasts- oval in shape, sit in rows over the bone (once they have formed bone and become surrounded they become cytes

Osteoclasts (multinucleated)- break down bone to release calcium if required
-> sit on surface of bone in howship lacunae

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4
Q

What factors affect bone remodelling?

A

Mechanical stimuli- muscular loading, orthodontic forces (resorption and deposition)

Hormones- most have some effect on bone metabolism (direct or indirect)
-> PTH, Vit D3, Oestrogen

Cytokine
-> IL-1 and IL-6 are released in response to inflammation and can activate osteoclasts and cause bone resorption

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5
Q

What is the issue with biopsying bone, what tends to be done instead?

A

Difficult access/Difficult healing
-> Use special tests- bone biochemistry

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6
Q

What are the different bone biochemistry tests and their normal ranges?

A

Blood calcium (2.20 to 2.60 mmol/L)

Osteoblast activity (bone formation)
-> serum alkaline phosphatase (30 to 130 U/L)
-> Osteocalcin (Vit K dependent) (< 15 ng/L)

Osteoclast activity (bone resorption)
-> collagen degradation urine & blood

Parathyroid hormone (1.6 to 7.5 pmol/L)

Vitamin D assays (>50 nmol/L adequate)

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7
Q

What is a torus?

A

Developmental exostosis

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8
Q

What are the types of Tori?

A

Torus palatinus- midline of palate

Torus mandibularis
-> bilateral on lingual aspect of mandible at premolar region (can meet at midline)

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9
Q

What are the issues with Tori?

A

Can impede flanges of dentures due to lack of space

May get trauma to them from denture or eating causing discomfort

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10
Q

What is a potential cause of torus formation?

A

Clenching- increased bone pressure could be leading to increased bone thickness

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11
Q

What are the features of Tori when seen on CBCT?

A
  • Found incidentally
  • Found in body of mandible as bony protuberances (not growing into bone, growing off of it)
  • Cortical bone- solid
  • In palate- seen as dense lump of bone in midline (flat normally)
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12
Q

What type of Osteogenesis imperfecta is related to dentinogenesis imperfecta?

A

Type 3

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13
Q

What is the most severe type of OI?

A

Type 2- tend to die young

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14
Q

What types of OI are related to blue sclera?

A

Type 1 and 3

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15
Q

What are some of the implications of OI?

A

Weak bones- prone to fracture

Lasting scarring can occur after fractures

Patient may be wheel chair bound

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16
Q

What is achondroplasia?

A

Issue with formation of long bones (defect in endochondral ossification)
-> Shorter limbs, normal head and thorax (dwarfism)

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17
Q

What pattern of inheritance does Achondroplasia follow?

A

Autosomal dominant

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18
Q

What is Osteopetrosis?

A

Lack of osteoclast activity (resorption failure) with excess osteoblast activity leading to denser bones
-> marrow can become lost (obliterated) and can lead to anaemia

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19
Q

What are the dental implications of Osteopetrosis?

A

Difficult to extract teeth due to bone density

Delayed healing- lack of blood supply

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20
Q

What causes fibrous dysplasia?

A

Gene defect

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21
Q

What occurs in fibrous dysplasia?

A

Slow growing swelling in bone- bone is replaced by fibrous tissue

Stops when patient stops growing (treat after this finishes)

Serum biochemistry is normal

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22
Q

What is the difference between monostotic and polystotic Fibrous Dysplasia?

A

Monostotic- single bone (more common)
-> can affect head- maxilla > mandible
-> increasing facial asymmetry occurs

Polyostotic- many bones (usually part of Albrights syndrome)

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23
Q

What are some of the other features of Polystotic fibrous dysplasia (Albright’s)?

A

Melanin pigmentation

Precious puberty (may start at age 2-3)

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24
Q

What are the radiographic features of Fibrous Dysplasia?

A

Ground glass/orange peel appearance

Amorphous- loss of trabecular pattern

Base on clinical presentation and fact that it looks abnormal

Margins are poorly defined (helps distinguish from other fibro-osseous lesions)

Becomes more radiopaque as it matures

Bone maintains approximate shape initially

On OPT it may be seen as bulging of alveolar crest that drops below opposite side (enlarged tuberosity with loss of trabeculae)

Usually no root resorption of displacement of teeth (can happen as it progresses)

Secondary lesions can occur- Solitary bone cysts

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25
Q

What are the histological features of Fibrous dysplasia?

A

Fibro-osseus appearance- cellular fibrous tissue background with bone within it (usually woven and as it matures can increase in size)

Metaplasia- spicules of bone present

No capsule- not separated from surrounding normal bone (nothing present to demarcate it from bone)

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26
Q

What is the treatment if Fibrous dysplasia is not deemed to be too deforming?

A

Leave it and do nothing

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27
Q

What is rarifying osteitis?

A

Process rather than pathology- localised loss of bone in response to inflammation

Bone breaks down leaving area without bone or less mineralised bone (radiolucent on radiographs)

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28
Q

What pathologies is rarifying osteitis be associated with?

A

PA abscess, granuloma, periodontitis
-> seen in failed RCT

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29
Q

What is sclerosing osteitis?

A

Abnormal hardening- increase in bone density in response to low grade inflammation

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30
Q

How does scleroisng osteitis appear radiographically?

A
  • Seen as radiopacity
  • Poorly defined
  • May form alongside rarefying
  • Increased density in trabeculae
  • Tends to occur alongside non-vital teeth
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31
Q

What is Idiopathic osteosclerosis?

A

Localised increase in bone density of unknown cause
-> Seen as island of Dense bone

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32
Q

What are the features of idiopathic osteosclerosis?

A
  • Commonly occurs in premolar region of mandible
  • Always asymptomatic- if any issues this is not diagnosis
  • No expansion
  • No displacement of teeth or canal (shows it is not a bony tumour)
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33
Q

How is Idiopathic osteitis distinguished from sclerosing osteitis?

A

Carry out sensibility tests on teeth involved- if tooth NV its likely to be SO

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34
Q

What is the technical term for Dry Socket?

A

Alveolar osteitis

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35
Q

What are the risk factors for dry socket?

A

Mandible

Further back in mouth

Difficult extractions

Female sex

Smokers

OCP use

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36
Q

What is thought to occur which results in Dry socket?

A

Clot is lost from socket too soon (loss of temporary plug)- perhaps by rinsing too soon (tell patient not to brush?)

-> Patient may say it is sorer than toothache they were experiencing

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37
Q

How is dry socket managed?

A

LA
-> try and create new clot by gently traumatising

Irrigate with saline

Apply packs with medicament to socket
-> helps stop pain but can delay healing process

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38
Q

What is Osteomyelitis?

A

Endogenous infection of the bone itself
-> as removal of tooth creates compound fracture which is exposed to oral environment

39
Q

What other focal lesions is OM associated with?

A

Sequestrum

Actinomycosis

Chronic diffuse sclerosing osteomyelitis

Periostitis (productive)
-> Garre’s

40
Q

How does OM present?

A

Swelling

Pain for weeks

Multiple draining sinuses

41
Q

What are the radiographic features of OM?

A
  • Inflammation causes SO making it more radiopaque
  • May appear as breach in cortical plate (rarefying osteitis)
  • CBCT-seen as sclerotic area underneath bone
42
Q

What are the features of Garre’s Sclerosing OM?

A
  • Seen in younger patients
  • Tend not to get pus or pain
  • Presents as bony swelling in patient’s jaw
  • Tends to be minor low grade source of infection
    -> NV carious tooth
43
Q

How does GSOM appear radiographically?

A

Seen as faint bulging of bone on radiographs (periosteal bone reaction- new bone formed in response to inflammation in periosteum)

44
Q

How does GSOM appear radiographically?

A

Seen as faint bulging of bone on radiographs (periosteal bone reaction- new bone formed in response to inflammation in periosteum)

45
Q

How is GSOM treated?

A

Manage source of infection

46
Q

What are the causes of bone necrosis (death)?

A

Osteomyelitis
-> Acute or chronic

Avascular necrosis
-> Age-related ischaemia
-> Anti-resorptive medication

Irradiation- patients now made dentally fit
-> Osteoradionecrosis
-> Prone to infections

47
Q

What conditions may patients take osteoclast inhibitors for?

A

Paget’s

Bony metastases- prostate and breast cancer

Osteoporosis

Osteogenesis Imperfecta

48
Q

What are the features of MRONJ?

A
  • More likely in people who take stronger associated medications for longer (esp IV)
  • Associated with extraction or rubbing denture (trauma)
  • More likely in mandible- poorer blood supply
49
Q

What are the treatments for MRONJ?

A
  • Sharp areas- smooth down
  • Adjacent tissues to dead bone can become infected (long term antibiotics)
  • Treatment is supportive
  • Mostly seen in very ill patients (may be least serious of patient problems)
  • Monitor if treatment would impact quality of life (maintain dignity?)
50
Q

What are the symptoms of MRONJ?

A
  • Not usually any pain as bone is dead (unless infected)
  • Can have multiple sinuses and lots of pus
51
Q

What occurs in Osteoporosis?

A

Bone atrophy (quantitive loss)- resorption exceeds formation
-> net loss of bone

52
Q

What are the clinical features of osteoporosis?

A

Symptomless
-> may be noticed after trauma (hip fracture)

Weak bones

53
Q

What are the radiographic features of OP?

A

Enlarged antrum- also seen in sinusitis

Loss of bone markings and trabecular

54
Q

What are the causes of primary OP?

A

Sex hormone status

Age

Calcium status

Lack of physical activity

55
Q

What are the secondary causes of OP?

A

Hyperparathyroidism

Cushing’s syndrome

Thyrotoxicosis

Diabetes mellitus

56
Q

What is the dental issue with patients who have OP?

A

They take medications that can cause MRONJ

57
Q

What occurs to bone in rickets/osteomalacia?

A

Osteoid forms but does not calcify

58
Q

What is the cause of Vitamin D deficiency which is associated with rickets and osteomalacia?

A

Lack of sunlight – daylight hours

Diet

Malabsorption

Renal causes

59
Q

What are the clinical features of osteomalacia/rickets?

A

Poor endochorndral bone

Low Ca

High alkaline phosphatase

60
Q

What is rickets?

A

Same disease as osteomalacia but occurs in childhood during formation of bone

-> seen as bow legs

61
Q

What occurs as a result of mobilisation of Calcium in patients with hyperparathyroidism?

A

Generalised osteoporosis

Osteitis fibrosa cystica (‘Brown Tumours’)

Metastatic calcification - kidney

62
Q

What are the types of hyperparathyroidism?

A

Primary – Neoplasia / hyperplasia
-> associated with adenoma

Secondary – Hypocalcemia (due to Vit D Deficiency)

Tertiary – prolonged secondary results in hyperplasia

63
Q

What are the epidemiological features of primary hyperparathyroidism?

A

1 in 1000 population

Mainly postmenopausal women
-> F:M 3:1

90% parathyroid adenoma (inc. PTH)
-> Hypercalcaemia
-> Increased bone turnover

64
Q

What are the radiogrpahic features of hyperparathyroid oral lesions?

A
  • Thin cortical margins (difficult to see)
  • Wispy septa in between
  • Seen as bulges in the bone- expansion
  • Pushes teeth out the way
  • Loss of lamina dura around teeth
  • Loss of trabeculation
  • Radiolucent
  • Multilocular
  • Pulp stone- excess calcium
  • Brown tumour (only 10% get this)
  • Do not always shrink on treatment (tend to infill with sclerotic bone)
65
Q

What are the histological features of osteitis fibrous cystica?

A
  • Brown Tumour (refers to colour)- contains red blood cells which have haemorrhaged/extravasated into mass of soft tissue (break down to release components giving brown colour)
  • Microfractures- formation of granulation tissue (contains giant cells)
  • Can be cyst like lesions present
  • Generalised OP
  • Focal osteolytic lesions
66
Q

What other bone conditions involve Giant cells?

A

Giant cell granuloma

Giant cell epulis- can be stand alone or caused by central giant cell granuloma which goes through bone and presents as peripheral lesion
-> grows in AP direction, along the length of it- reaches large size before it becomes apparent clinically

Aneurysmal bone cyst- multilocular, can look similar to central giant cell granuloma

Giant cell tumours- very rare

Cherubim- vascular giant cell lesion

67
Q

Why is it good to take a radiograph for GC epulis?

A

As it usually appears in attached mucosa clinically- so this helps us check if it is a central lesions presenting peripherally

68
Q

What are the features of a giant cell granuloma?

A

Age 10-25

Mandible>maxilla

May be multilocular

69
Q

What are the features of cherubism?

A
  • Occurs in children until age 7 then after puberty tends to regress
  • Autosomal dominant- affects gene that regulates bone turnover
  • Seen as multilocular/multicystic radiolucency within jaw (can be multiple quadrants)
  • Orbit can be pushed up
70
Q

What patients are most likely to get Paget’s disease?

A

Over 40s

Males > Females

71
Q

What are the aetiological factors involved in Paget’s?

A
  • Racial predilection- associated with people from UK
  • Virus- cytomegaly virus?
72
Q

What occurs in Paget’s disease?

A

Disturbed turnover of bone- deposition and resorption can occur simultaneously
-> results in swelling and enlargement
-> can be monostotic or polystotic

73
Q

What happens to serum biochemistry in patients with Paget’s?

A

Alkaline phosphatase goes up to 250-300 units

74
Q

How does Paget’s present clinically?

A

Pain

Bone swelling and enlargement of bone

Deposition can result on pressure on nerves emerging from foramina (can result in blindness, deafness, palsy)

Chief complaint- dentures are getting smaller (unusual as dentures tend to get looser)

75
Q

What are the issues with extraction in Paget’s patients?

A

Depends on phase:
- If extraction in lytic phase- bleed a lot
- Osteosclerotic- prone to dry socket and more difficult extractions

76
Q

What are patients with Paget’s more prone to?

A

Infection

Malignancy
-> Osteosarcoma

77
Q

What are the radiographic features of Paget’s?

A
  • Cotton wool appearance in diploic bone between tables of skull
  • Patches of radiopacity
  • Osteoporotic, mixed, osteosclerotic
  • Bone is enlarged
  • Hypercementosis if mandible and maxilla are affected (bulging of the root)
  • Loss of lamina dura
  • Displacement of teeth can occur
78
Q

What are the histological features of Paget’s?

A

Disorganised bone remodelling- increased turnover

Osteoblasts are forming bone with osteoclasts resorbing bone side by side (usually one side there is resorption, and one side is deposition)

Reversal lines in bone become prominent (dark blue lines give mosaic appearance)

79
Q

What are the features of osteoma?

A
  • Excess growth of cortical bone
  • Usually solitary
  • May interfere with dentures- may need to be trimmed down
80
Q

What condition is suggested by presence of multiple Osteomas, what can be done to diagnose this?

A

Gardener’s syndrome- can be associated with polyps in colon that may undergo malignant change
-> Genetic test and colonoscopy can be used to diagnose

81
Q

What are the features of Osteoblastoma?

A
  • Tumour of osteoblasts- overgrowth and hyperfunction
  • May be caused by giant osteoid osteoma
  • Very active growth- lots of deposition
82
Q

What other syndrome that causes colonic polyps can be found around the oral tissues?

A

Peutz-jeghers
-> freckles around mouth

83
Q

What is an ossifying fibroma caused by?

A

Fibrous tissue becomes calcified by bone or cementum or both
-> benign

84
Q

What are the clinical features of Ossifying fibroma?

A

Slow growing- can be aggressive in children

Affects only mandible- rare in jaw, tends to happen elsewhere

Continuous- growth does not stop like in FD

85
Q

What are the histological features of Ossifying fibroma?

A

Cellular fibrous tissue
-> sometimes has capsule

Immature bone

Acellular calcifications

Resembles FD but is more well defined

86
Q

How does Ossifying Fibroma appear radiographically?

A

Well defined

Bone appears abnormal- radiolucent in early stages, becomes more radiopaque as it matures, can result in sclerotic mass

87
Q

What are the clinical features of a cementoblastoma?

A
  • Benign
  • Attached to root
  • Rare
  • Younger patients
  • Involves cementum around tooth
  • Dull aching pain
88
Q

How does a cementoblastoma appear radiographically?

A

Radiolucent margin continuous with PDL
-> PDL space does not go around the root (it becomes continuous with mass)
-> hard to say where root stops and mass starts

89
Q

What is the issue with nomenclature of cemento-osseus dysplasia?

A

Not tumours but they seem to be a reaction

90
Q

What are the types of cemento-osseus dysplasia?

A

Periapical COD
-> Starts as radiolucency
-> Later calcification
-> affects vital lower 4 incisors- appears like granuloma

Focal COD- not related to lower 4 incisors

Florid COD

91
Q

What are the radiographic features of Focal COD?

A
  • occurs at particular points
  • Around tooth apices- may be around multiple teeth
  • Can appear like radicular cysts
  • Radiolucent margin around but you can still see PDL space around roots of tooth (occurs superficial to PDL space)
  • Looks like SO- but teeth are vital
  • Different from idiopathic as they wouldn’t have radiolucent lesion
92
Q

What are the radiographic features of Florid COD?

A
  • Can be difficult to see due to spine and expansion being out with focal trough
  • Can get lesions with different maturities in the same patient
  • Expands buccal and lingually (can be excessive)
93
Q

How does Florid COD appear?

A

Masses that resemble bone or cementum

94
Q

What are the features of osteosarcoma?

A
  • Tends to occur in younger people (in their 30s)
    -> So if patient is older then it suggests paget’s
  • Rare
  • Mandible is more commonly affected
  • Sunburst appearance in radiograph
  • Cause bone destruction- can cause unexplained mobility of teeth
  • Can metastasise

BDS4 Radiology (8 decks)

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