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musculoskeletal > metabolic bone disorders - histopathology > Flashcards

metabolic bone disorders - histopathology Flashcards

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1
Q

what are the functions of bone

A

structure - give structure and shape to the body

mechanical - sites for muscle attachment, allow movement of the structure

protective - vital organs and bone marrow, eg skull and ribs. by protecting marrow bones support preoduction of blood and stroma cells

metabolic - reserve of ca and other minerals

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2
Q

what is the composition of bone *

A

inorganic - 65%

  • ca hydroxyapatite
  • is a storehouse for 99% of ca in body, 85% phosporus, 65% Na and mg
  • release these minerals to systems that need them

organic - 35%

  • bone cells and protein matrix (ECM proteins, collagen fibres and linking proteins needed to form, shape and repair the bone)
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3
Q

what are the features of typical bones

A

have condyles which are on articular surfaces and synovial joints

pully shaped region - trochlea

fovea - small dip/depression on bone eg on femoral head - where it is a ligament attachment

underneath the articular surface have the subchondral bone - provide support for the cartilage

epiphysis line - separates the epiphysis from the bulk of the bone

main bulk is in the diaphysis

medulla is surrounded by the cortex that is surrounded by the periosteum

metaphysis - join the epiphysis to teh diaphysis - during growth this contains the cartilaginous growth plate - allows linear growth of bones. area where trabecular bone is found - provides strength and involved in turnover of minerals

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4
Q

what can be seen on the x-ray *

A

poorly circumscribed lytic lesion - in diaphysis of bone that has eroded the cortex - see no bone here

periosteal reaction - new bone outside of the normal bone

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5
Q

what can be seen on the x-rau *

A

well circumscribed lytic lesion in metaphysis of tibia that has broken through the cortex

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6
Q

what are the types of anatomical bone

A

flat - eg skull/rib, protective

long - eg femer/tibia, for weight support, linear growth and movement

short/cuboidal - eg carpal/tarsal, stabalise and fascilitate movement

irregular - vertebrae/pelvis, protect specific organs

sesamoid - in tendons

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7
Q

what are the classifications for macroscopic structure of bone *

A

trabecular/cancellous/spongy - criss cross through medullary cavity

cortical/compact

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8
Q

what are the classifications for microscopic bone structure *

A

woven bone - immature

lamellar bone - mature

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9
Q

describe cortical bone *

A

make up the outside of the shaft

is the bulk of the long bones and appendicular skeleton

makes up 80% of the skeleton

80-90% calcified

has a low turnover

mainly structural, mechanical and protective

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10
Q

describe trabecular bone *

A

make up bulk of vertebrae and pelvis and axial skeleton

15-25% calcified - low mineralisation

20% of skeleton

metabolic function - high turnover - large SA fasciliates this

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11
Q

describe cortical bone microanatomy *

A

made of parallel osteons (0.2mm diameter) that surround the conversion canal containing bv

osteons are circular structures of lamella bone

in periosteum get circumfrential lamellae that go all around all of bone

interstitial lamellae - are between the osteons

in trabeculae have lamellae but they are in layers not in osteons

osteocytes have dendritic Canalicular Networks throughout the lamellae structure

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12
Q

describe woven bone *

A

disorganised

it is found in the developing skeleton - initial bone that is layed down before it is replaced

when there is rapid growth or pathological high turnover

weak bone

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13
Q

what are the 3 types of bone cell *

A

osteoclasts

osteoblasts

osteocytes

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14
Q

describe osteocytes *

A

90% of bone cells

live 25yrs

form a mechanosensory network and tell other cells what to do

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15
Q

describe osteoclasts *

A

multinucleated

form haemopoetic lineage

the resorb/remove bone

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16
Q

describe osteoblasts *

A

mononuclear

produce osteoid to form new bone

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17
Q

describe the bone remodelling cycle

A

osteoblasts make RANKL and M-CSF which are the key osteoclastic factors that cause cells to differentiate into osteoclasts

blasts also make a decoy receptor for RANKL

blasts control amount of clasts that are forming

osteocytes sense damage/new stresses - signal for osteoclasts to come to site that needs to be remodelled/removed

osteocytes signal by apoptosing and so releaseing RANKL - signal for osteoclasts to form here

osteoclasts resorb away bone

osteoclasts die away as reversal phase occurs

osteoclasts are recruited to site and produce osteoid to replace lost bone

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18
Q

describe this image *

A

multinuclear cell resorbing bone

cuboidal cell on surface is an osteoblast

osteocyte is in the osteocytic lacunae

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19
Q

why perform a bone biopsy *

A

to confirm the diagnosis of a bone disorder

when you need histological evidence

to find the cause of or evaluate ongoping bone pain/tenderness - when bone marker/histological evidence has not been useful

investigate abnormality seen on x-ray

for bone tumour diagnosis - benign v malignant

to determine cause of unexplained infection

to evaluate therapy performance

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20
Q

risk of biopsy *

A

low risk

chance of infection/fracture - if can avoid them then you should

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21
Q

explain the 2 types of bone biopsy *

A

closed - core biopsy with jamshidi needle inserted into bone, returns with a core of bone

open - for sclerotic/inaccessible bone - scleroti means it ahs thickened so cant get in. Or if you need a large sample. There is more risk

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22
Q

why do you do a transiliac bone biopsy *

A

see all the types of bone here - cortical and trabecular in the core of bone

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23
Q

describe this histological image *

Study These Flashcards
A

articular cartilage

trabecular bone

cortical bone

subchondral bone

24
Q

describe what histological stains show *

Study These Flashcards
A

H & E stain on decalcified samples

masson-goldner trichrome - look at amount of mineralised V unmineralised

tetracycline - dynamic histopathology, rate of bone turnover

25
what can be seen in the cortical bone \*
osteocytes
26
what can be seen in this image of top of femoral head cavity \*
articular surface dots are cartilage cells subchondral bone trabecular bone medullary cavity
27
what can be seen in this image \*
mineralised bone is green osteoid is orange
28
when is it useful to use masson-goldner stain \*
osteomalacia
29
what can be seen with tetracycline labelling \*
stain is incorporated into mineralising front - mike flurescent line then few days later another injection given get another line can measure amount of mineral layed down between the 2 injections areas with single lines were only undergoing mineralisation during one of the injections compare distance between lines and proportion of bone labelled, you can determine the amount of bone formed between injections - bone formation rate mineral apposition rate - distance between 2 lines see if mineralisation is fast or slow and if there is a defect
30
what is a metabolic bone disease \*
a gp of bone diseases that cause reduced bone mass and strength due to imbalance of chemicals in body - vits, hormones, minerals cause altered bone cell activity, rate of mineralisation or changes in bone structure
31
what are common met bone diseases
osteoporosis osteomalacia/rickets primary hyperparathyroidism renel osteodystrophy paget's disease
32
what is osteoporosis \*
bone mineral density T-scoe of -2.5 or lower - means 2.5 standard deviations different from mean BMD at peak bone mass aged 25 diagnosed radiologically by DEXA primary - no external cause, because of age/ 5-7 yrs post menopause secondary - something has caused it eg drugs/systemic disease (genetic, endocrine, nutritional defects, metabolic disorders) happens because more resorption than formation 2 types - high turnover/low turnover impacts trabecular bone because it is metabolically active
33
what is the difference between high and low bone turnover osteoporosis \*
high - both made and resorbed increased, but resorbed more low - both making and resorption decrease, making more
34
what can be identified in osteoporotic bone \*
holes the trabeculae that are left are thinner and less connected = weaker as condition continues see thinning of cortical bone, compression fractures in spine and low impact fragility fractures in long bones
35
osteoporosis histologically \*
trabecular are thinner some are free floating wont determine high/low bone turnover - would need to do tetracycline staining or histomorphometric studies - most cases serum markers are better for interpreting in this image - high turnover because lots of regions of unmineralised bone
36
what is osteomalacia \*
defective mkineralisation of normally synthesised bone matrix rickets in children 2 types - deficiency of vit D and def of phosphate vit d dif = hypocalcaemia low phos/ca = unable to form hydroxyapatite crystals
37
effect of vit D \*
increases ca absorption in SI increases ca reabsorption in kidney
38
how does this image show osteomalacia \*
huge areas of osteoid - weak bone,
39
symptoms of osteomalacia \*
painful and tender bones weak bones prox myopathy fractures bone deformity
40
signs of rickets \*
widening growth plate bowing of legs - remodel to spread weight so deform
41
explain looser zones in osteomalacia \*
pseudofractures at areas of high tensile stress in body only extend part way through bone at R angle to cortex irregular sclerotic margins from new bone growth around it
42
what is hyperparathyroidism\*
excess PTH = increased Ca and phos excretion in urine hypercalcaemia hypophosphtaemia skeletal changes of osteitis fibrosa cystica
43
what is osteitis fibrosa cystica \*
resorption of bone and replacement with fibrous tissue forms brown tumours
44
describe the control of ca metabolism \*
4 parathyroid glands that produce PTH- increase ca - released from store in bone, increased reabsorption from kidney, increased absorption from SI increase ca and reduce phos ca reduces PTH by -ve feedback
45
causes of primary hyperparathyroidism \*
parathyroid adenoma - 85-90% chief cell hyperplasia
46
causes of secondary hyperparathyroidism \*
chronic renal deficiency - cant exrete phos or activate vut d vit d deficency
47
symptoms of hyperparathyroidism \*
stones - ca oxalate renal stones bones - osteitis fibrosa cystica, bone resorption - seen less because condition diagnosed before this abdo groans - acute pancreatitis psychic moans - psychosis, depression
48
x ray of hyperthyroidism \*
periosteal bone erosions
49
histology of hyperparathyroidism \*
centre of trabeculae has been resorbed away - tunnel reabsorption - osteoclasts penetrate centre of trabeculae and resorb central channel
50
histology of brown cell tumour \*
bone resorbed away and replaced by giant cell reparative granuloma giant cells surrounded by fibrous tissue reactive bone forming next to them
51
describe osteodystrophy \*
comprises all the skeletal changes resulting from chronic renal disease: * increased bone resorption - osteitis fibrosa cystica * osteomalacia - due to hypercalcaemia * osteosclerosis - increase in bone mass * growth retardation * osteoporosis because of failure to excrete phos and activate vit d - secondary hyperparathyroidism
52
describe paget's disease \*
onset \>40yrs - affects 3-8% caucasions \>50yrs M\>F rare in asians and africans mono-ostotic - 15% remainder poly-ostotic aetiology unknown familial cases show autosomal pattern of inheritance with incomplete penetrance (mutations in SQSTM1 or RANK) parvomyxovirus type particles gave been seen in EM - doubt this is the cause overuse/previous bone injury
53
3 stages of paget's disease \*
osteolytic - focal bone loss osteolytic-osteosclerotic - reactive phase where blasts respond to bone loss quiescent osteosclerotic - blasts react then both cell types burn out - get disorganised lamellae structure
54
clinical symptoms of paget's disease \*
pain microfractures nerve compression - inc spinal nerve and cord skull changes put medulla at risk deafness +/- haemodynamic changes, cardiac failure hypercalcaemia development of sarcoma in area of involvement
55
sites where pagents is common and the 3 phases
pic
56
histology of paget's disease
thick cortices - sclerosis course disorganised trabeculae in medullary canal small lytic regions in medullary canal photograph - active phase - osteoclasts resorb trabeculae last pic - mosaic image - cement line left from blasts repairing bone

musculoskeletal (12 decks)

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