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cysts, tumours, bone pathology > bone pathology > Flashcards

bone pathology Flashcards

1
Q

what 3 types of lamellae are in an osteon-Haversian system?

A

circumferential
interstitial
concentric

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2
Q

where are blood vessels located in a Haversian system?

A

central (Haversian) canal

perforating (Volkman’s) canal

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3
Q

what overlies the surface of bone?

A

periosteum

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4
Q

where are osteocytes located?

A

in lacunae

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5
Q

what does the periosteum contain?

A

pain receptors and blood vessels

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6
Q

how is bone laid?

A

around Haversian canal

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7
Q

where do osteoblasts sit?

A

on periphery of trabeculae

once become enclosed in osteoid - osteocytes

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8
Q

what type of tissue is bone?

A

vital, dynamic tissue

appears static

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9
Q

mature and immature bone

A

mature cortical lamellar bone

immature woven bone

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10
Q

stimuli for bone remodelling

A

mechanical - muscle loading
systemic hormones - direct/indirect effects
- PTH, vit D3, oestrogen, others
cytokines
complex interactions promote growth of cells and bone matrix

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11
Q

what is the normal blood Ca?

A

2.2-2.6 mmol/L

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12
Q

how to test osteoblast activity - bone formation

A

serum alkaline phosphatase

osteocalcin (vit K dependent)

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13
Q

normal serum alkaline phosphatase

A

30-130 U/L

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14
Q

normal osteocalcin (vit K dependent)

A

<15ug/L

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15
Q

how to test osteoclast activity - bone resorption

A

collagen degradation urine and blood

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16
Q

normal PTH levels

A

1.6-7.5 pmol/L

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17
Q

normal vitamin D assays

A

> 50nmol/l adequate

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18
Q

developmental abnormalities

A 
torus
osteogenesis imperfecta
achondroplasia
osteopetrosis
fibrous dysplasia
rarefying osteitis
sclerosing osteitis
idiopathic osteosclerosis
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19
Q

torus

A

developmental exostosis - outgrowth of bone

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20
Q

when can torus be a problem?

A

with fitting dentures

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21
Q

torus palatinus

A

midline of palate

often single

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22
Q

torus/tori mandibularis

A

usually multiple
bilateral on lingual aspect of mandible (usually premolar region)
if unilateral may xray
if bilateral can usually just diagnose clinically

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23
Q

what are tori usually composed of?

A

dense cortical bone

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24
Q

osteogenesis imperfecta genetics

A

type 1 collagen defect

inheritance varied - 4 main types

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25
Q

OI clinical

A

weak bones, multiple fractures

sometimes associated with type 1 dentinogenesis imperfecta

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26
Q

achondroplasia inheritance

A

autosomal dominant

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27
Q

achondroplasia clinical features

A

poor endochondral ossification - limbs - dwarfism

frontal bossing - can use distraction osteogenesis

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28
Q

osteopetrosis

A

lack of osteoclast activity - failure of resorption
bone becomes v hard - increased density
marrow obliteration - can affect blood cell production

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29
Q

cause of fibrous dysplasia

A

uncommon - gene defect

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30
Q

clinical presentation of fibrous dysplasia

A

slow growing, asymptomatic bony swelling

- bone replaced by fibrous tissue

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31
Q

at what age is fibrous dysplasia active?

A

under 20yrs

stops growing after active growth period (usually)

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32
Q

what are the clinical phenotypes of fibrous dysplasia determined by?

A

the timing of the gene mutation

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33
Q

clinical phenotypes of fibrous dysplasia

A

monostotic

polyostotic

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34
Q

monostotic fibrous dysplasia

A

single bone (more common)

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35
Q

monostotic fibrous dysplasia in the jaws - where is it most commonly located?

A

maxilla>mandible

usually maxilla and unilateral

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36
Q

consequence of monostotic fibrous dysplasia in the jaws

A

facial asymmetry

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37
Q

polyostotic fibrous dysplasia

A

many bones

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38
Q

Albrights syndrome

A

Polyostotic fibrous dysplasia
melanin pigment
early puberty

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39
Q

consequence of fibrous dysplasia in maxilla

A

expansion of maxilla - early occlusion

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40
Q

radiographic appearance of fibrous dysplasia

A

variable
- ground glass (frosty, transparent)
- orange peel
- finger print whorl
- cotton wool
- amorphous
margins often blend into adjacent normal bone - no evident capsule/demarcation. wide zone of transition
bone maintains approximate shape (initially)
becomes more radiopaque as lesion matures

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41
Q

if teeth are involved in fibrous dysplasia what can the effects be?

A

narrowing of PDL
loss of LD
v rarely external RR

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42
Q

histology of active fibrous dysplasia

A

“fibro-osseous”
fibrous replacement of bone
- cellular fibrous tissue
- bone - metaplastic or woven, but will remodel and increase in density

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43
Q

rarefying osteitis

A

localised loss of bone in response to inflammation
always occurring secondary to another form of pathology
if at apex of tooth consider periapical periodontitis/granuloma/abscess

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44
Q

sclerosing osteitis

A

localised increase in bone density in response to low-grade inflammation

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45
Q

most common area of sclerosing osteitis

A

around apex of tooth with a necrotic pulp

  • periapical radiopacity, often poorly defined
  • may eventually lead to external root resorption if chronic

can also get due to chronic pericoronitis

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46
Q

idiopathic osteosclerosis

A

localised increase in bone density of unknown cause

- aka dense bone island

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47
Q

where is idiopathic osteosclerosis most common?

A

in premolar-molar region of mandible

if in maxilla would tend to be more anterior

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48
Q

is idiopathic osteosclerosis symptomatic?

A

no it is always asymptomatic

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49
Q

idiopathic osteosclerosis effect on adjacent structures

A

no bony expansion and no effect on adjacent teeth/structures

- IDC not displaced

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50
Q

how to distinguish between idiopathic osteosclerosis and sclerosing osteitis

A

carry out sensibility testing on tooth involved

51
Q

inflammatory diseases

A

alveolar osteitis
osteomyelitis
Garre’s sclerosing osteomyelitis (periostitis productive)
bone necrosis

52
Q

risk factors of alveolar osteitis (varied aetiology)

A 
rinsing too early
smoking
female
OCP
mandible
posterior tooth
53
Q

symptoms of alveolar osteitis

A

severe pain
loss of clot
bone sequestra
delays healing process

54
Q

osteomyelitis

A

rare endogenous infection

acute or chronic - suppuration is rare

55
Q

osteomyelitis - other focal lesions

A

sequestrum - bone necrotic - body thinks it is foreign
actinomycosis - rare, after ext, need long-term ABs
chronic diffuse sclerosing osteomyelitis
periostitis (productive)

56
Q

Garre’s sclerosis osteomyelitis (periostitis productive)

A

generally children due to caries (/perio)
mandible growing and expands
periosteum lays down layers of bone in response to chronic inflammation
often get sclerosis

57
Q

aetiology of bone necrosis

A

if blood supply affected in some way - mandible more prone

osteomyelitis - acute or chronic

avascular necrosis

  • age related ischaemia: blood supply decreases as age
  • anti-resorptive meds

irradiation

  • ORN - endarteritis obliterans
  • prone to infections
  • also pharyngeal cancer - beware if you extract molars
58
Q

mechanism of action and uses of bisphosphonates

A

osteoclast inhibitors

used in osteoporosis, Pagets, bone metastases (prostate and breast cancer have tendency to metastasise to bone)

59
Q

osteonecrosis and bisphosphonates

A

mandible>maxilla
60% associated with a dental procedure
- poor healing after any trauma - ext/denture rubbing/spontaneous

60
Q

management of bisphosphonates related osteonecrosis

A

conservative - extraction as a last resort
if established - supportive
manage any (super)infections - antibiotics
don’t tend to excise necrotic bone as causes further insult to healthy bone - chain

61
Q

metabolic bone disease

A

osteoporosis
rickets (children) and osteomalacia (adults)
hyperparathyroidism

62
Q

mechanism of osteoporosis

A 
bone atrophy - resorption exceeds formation
endosteal net bone loss
quantitative deficiency (bone formed is normal)
63
Q

clinical features of osteoporosis

A

symptomless (no pain)
weak bone (hip and spinal fractures)
antrum enlarged

64
Q

radiographic features of osteoporosis

A

loss of normal bone markings
radiolucent trabecular pattern
thinning of cortical bone
IDC and MF disappear

65
Q

aetiology of osteoporosis

A 
sex hormone status - oestrogen
age
Ca status
physical activity
secondary osteoporosis
66
Q

secondary osteoporosis

A

reduced bone density as a result of other conditions/meds e.g.

  • hyperparathyroidism
  • Cushing’s syndrome
  • thyrotoxicosis
  • diabetes mellitus
  • many other causes
67
Q

what are the causes of rickets and osteomalacia?

A

vit D deficiency

  • lack of sunlight - daylight hours
  • diet
  • malabsorption
  • renal causes - kidney involved in activating vit D
68
Q

mechanism of rickets and osteomalacia

A

osteoid forms but fails to calcify

defect within bone rather than lack of bone

69
Q

presentation of rickets

A

poor endochondral bone (may have short limbs)
low Ca
raised alkaline phosphatase
- generic marker so can’t use on its own to diagnose

70
Q

PTH

A

release Ca from bones

71
Q

effect of hyperparathyroidism

A

Ca mobilised from bones

  • generalised osteoporosis
  • osteitis fibrosa cystica (Brown tumours)
  • metastatic calcification (kidney)
72
Q

primary hyperparathyroidism

A

problem with parathyroid gland - neoplasm/hyperplasia

73
Q

secondary hyperparathyroidism

A

hypocalcemia e.g. due to vit D deficiency

74
Q

tertiary hyperparathyroidism

A

prolonged secondary results in hyperplasia

75
Q

incidence pattern of primary hyperparathyroidism

A

1 in 1000 pop
mainly postmenopausal women
F:M 3:1

76
Q

what are 90% of cases of primary hyperparathyroidism caused by?

A

parathyroid adenoma (increased PTH)

  • hypercalcemia
  • increased bone turnover
77
Q

radiographic presentation of hyperparathyroidism

A

expansive ballooning out
v thin cortices, thin wispy septa
teeth displaced but rarely get resorption, can get pulp stones
radiolucent appearance of bone

78
Q

what is osteitis fibrosa cystica?

A

characteristic cystic changes in bone due to prolonged unchecked hyperparathyroidism

79
Q

presentation of osteitis fibrosa cystica

A

generalised osteoporosis
focal osteolytic lesions
giant cell lesion (brown tumour)

80
Q

giant cell lesion (brown tumour)

A

area of significant resorption
granulation tissue fills spaces where bone was
lots of multinucleate giant cells
often bleeding into lesion - rbcs break down - haemosidrin - brown

81
Q

giant cell lesions of the jaws

A

peripheral giant cell epulis

central giant cell granuloma

82
Q

central giant cell granuloma presentation

A

age 10-25
mandible>maxilla
may be multilocular
tends to grow in an AP direction along mandible so large before symptoms - can cause a lot of destruction
can sit on gingiva and resemble peripheral - radiograph
could have hard to explain mobility - radiograph before extraction

83
Q

differential diagnoses of giant cell lesions

A

osteitis fibrosa cystica
aneurysmal bone cyst
giant cell tumours (v rare)

84
Q

what may happen to central giant cell lesions?

A

may “burst out”

85
Q

cherubism genetics

A

rare, autosomal dominant inheritance

86
Q

cherubism presentation

A

multi cystic/multilocular lesions in multiple quadrants
- resorption of bone and replacement by GC lesions
grow before about 7yrs and regress after puberty

87
Q

histology of cherubism

A

vascular giant cell lesions

88
Q

what can Paget’s disease of bone be treated with?

A

anti-resorptive meds

89
Q

incidence patterns of Paget’s disease of bone

A

age >40
M>F
3% of routine autopsies

90
Q

aetiology of Paget’s disease of bone

A

unknown
genetic?
racial predilection?
viral?

91
Q

types of Paget’s disease of bone

A

monostotic

polyostotic

92
Q

serum biochemistry for Paget’s disease of bone

A

raised alkaline phosphatase

93
Q

clinical S and S of Paget’s disease of bone

A

vary depending on which bones affected and which stage of disease (can often be subclinical)
bone swelling
pain
nerve compression - deafness/blindness/paralysis
dentures always getting tight - jaws increasing in size

94
Q

cause of Paget’s disease of bone

A

disordered bone turnover

95
Q

stages of Paget’s disease of bone

A

1 - lytic stage - bone resorption
2 - mixed stage - bone resorption and deposition
3 - sclerotic stage - bone deposition

initially bone soft and deformed then calcified

96
Q

extractions and Paget’s disease of bone

A

complications depend on which stage

  • lytic - lots of bleeding
  • sclerotic - barely any bleeding, risk of dry socket and even necrosis
97
Q

general radiographic appearance of Paget’s disease of bone

A

skull commonly affected (normally diploic): thickened and very irregular, cotton wool appearance
variable bone pattern
- changes as disease progresses
- osteoporotic/mixed/osteosclerotic

98
Q

dental changes in Paget’s disease of bone

A

loss of lamina dura
hypercementosis (PDL remains outside)
migration (due to bone enlargement)

99
Q

histology of Paget’s disease of bone

A

active - increased bone turnover
OC and OB activity
osteoclasts dark multinucleate giant cells - sit in Howship’s lacunae
- bone forming and resorbing on same side of trabecular
will burn out
reversal line: recognise changes between deposition and resorption, in Paget’s v dark

100
Q

complications of Paget’s disease of bone

A

infection of affected bone
osteosarcoma (tumour)
pathological fractures as abnormal bone

101
Q

in which stage of Paget’s disease of bone is the bone marrow often very vascular?

A

1st stages

102
Q

what happens to the blood vessels in the sclerotic stage of Paget’s disease of bone?

A

they decrease

103
Q

bone tumours

A 
osteoma
osteoblastoma
ossifying fibroma
cementoblastoma
(cemento)-osseous dysplasia
osteosarcoma
104
Q

osteoma

A

small, benign

solitary, mostly cortical

105
Q

if multiple osteomas, what syndrome should be suspected?

A

Gardner syndrome

106
Q

Gardener syndrome

A

colon polyps (polyposis coli)
osteomas
ST torso growths - dermoid cysts

GP referral, genetic testing/colonoscopy

107
Q

osteoblastoma

A

rare, benign but more aggressive
may be a giant osteoid osteoma
often v active growth
anywhere inc jaws

108
Q

which tumours have a nomenclature problem?

A

ossifying fibroma

(cemento)-osseous dysplasias - probably not neoplastic - more likely reactive lesions, benign

109
Q

clinical presentation of ossifying fibroma

A 
slow growing (in children often fast growth)
wide age range
mainly mandible
110
Q

radiographic appearance of ossifying fibroma

A

well-defined

often fibrous tissue capsule or well-separated from surrounding bone

111
Q

histology of ossifying fibroma

A

cellular fibrous tissue
immature bone
acellular calcifications

112
Q

where is a cementoblastoma always found?

A

jaws

113
Q

clinical presentation of cementoblastoma

A

neoplasm attached to root, often apex

late stage bony expansion

114
Q

histology of cementoblastoma

A

same as osteoblastoma

115
Q

radiographic features of cementoblastoma

A 
well-defined radiopacity with radiolucent margin
rim part of PDL space
lose definition of root, can get RR
often incidental finding
often posterior mandible
116
Q

types of osseous dysplasias

A

periapical
focal
florid

117
Q

periapical OD

A

starts as radiolucency, later calcification

affects L anteriors, VITAL teeth (differentiates from PA cyst)

118
Q

focal OD

A

one quadrant/area

119
Q

florid OD

A

all 4 quadrants affected or growing v rapidly/large

120
Q

which pts are usually affected by OD?

A

mostly adult females, Afro-Caribbean origin

121
Q

symptoms of OD

A

none
dull pain
swelling

122
Q

radiographic appearance of OD

A

radiolucent background with developing radiopacity, unusual shapes, apices of teeth

can still see PDL space between root and lesion

rarely RR

some resemble bone and cementum

123
Q

potential risk of OD

A

increased risk of dry socket/infection post-extraction?

124
Q

osteosarcoma

A 
malignant 
rare
usually younger adults - 30s
 - if elderly likely Paget's related
mandible>maxilla
varied clinical and xray presentation
local destruction
recurrence and metastasis

cysts, tumours, bone pathology (4 decks)

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