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LCRS Musculoskeletal > Metabolic Bone Disease: Histopathology > Flashcards

Metabolic Bone Disease: Histopathology Flashcards

1
Q

what are the main functions of bone?

A

o Mechanical – support and muscle attachment.
o Protective – vital organs and bone marrow.
o Metabolic – calcium reserve.

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2
Q

what is the inorganic composition of bone?

A

65%

calcium hydroxyapatite-99% of body calcium
85% of phosphorus
65% of Na, Mg

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3
Q

what is the organic composition of bone?

A

35%

bone cells and protein matrix

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4
Q

what are the two functional classifications of bone?

A

cortical: long bones
cancellous: vertebrae/pelvis

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5
Q

what are the anatomical types of bone?

A
  • flat e.g. skull
  • long e.g. femur
  • short/cuboid e.g. carpals
  • irregular e.g. vertebrae
  • sesamoid e.g. patella
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6
Q

how calcified is cortical bone?

what function does it serve?

A

80-90%

mainly protective/mechanical

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7
Q

how calcified is cancellous bone?

what function does it serve?

A

15-25%

mainly metabolic, with large surface

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8
Q

what are the main distinguishing features of cortical bone?

A
  • osteons containing Haversian canals
  • Volkmann’s canals (horizontal)
  • Howship’s lacunae (lacunae left by osteoclasts)
  • canaliculi
  • concentric layers of lamellae
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9
Q

what are the main features of cancellous bone?

A 
trabecular bone (avascular- lack blood vessels) 
no osteons
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10
Q

what separates the diaphysis and epiphysis?

A

metaphysis

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11
Q

what part of the skeleton is cortical bone? how much of the skeleton?

A

80% of the skeleton making the appendicular skeleton

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12
Q

what part of the skeleton is cancellous bone? how much of the skeleton?

A

20% of the skeleton making the axial skeleton

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13
Q

what is the diameter of an osteon?

A

0.2mm

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14
Q

when must a bone biopsy be done?

A 
o	Evaluate bone pain.
o	Investigate x-ray abnormalities – e.g. brown lesions.
o	Bone tumour diagnosis.
o	Cause of unexplained infection.
o	Evaluate medical therapy.
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15
Q

what are the two types of bone biopsy?

A

closed: (Jamshidi needle) into the core of the bone
open: for sclerotic or inaccessible lesions

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16
Q

what is the role of osteoblasts?

A

build bone by laying osteoid

surface osteoblasts become osteocytes

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17
Q

what is the role of osteoclasts?

A 
resorb bone (crush) 
multinucleate cell removes bone
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18
Q

what is the role of osteocytes?

A

osteoblast-like cells that sit-in lacunae. 90% of all bone cells works as the mechanosensory network

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19
Q

where is RANK found?

A

on the osteoclast precursors in response to stimulation via M-CSF

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20
Q

what is competitive inhibitor of RANK?

A

OPG (osteoprotegrin) inhibits RANK and RANKL binding therefore inhibiting osteoclastogenesis

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21
Q

how does mature bone compare to woven bone in organisation?

A

more well organised

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22
Q

what type of ossification occurs in flat bones?

A

intramembranous

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23
Q

what type of ossification occurs in long bones?

A

endochondral except clavicle

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24
Q

what are the two architectural classifications of bone?

A

woven (immature)

lamellar (mature)

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25
Q

where is woven bone found?

A

at the base of teeth

only physiological in fracture healing

26
Q

what is metabolic bone disorder?

A

disorder of bone turnover due to imbalance of chemicals in bone

overall effect: reduced bone mass (osteopenia) leadings to pathological features

27
Q

what are stains that can be used in bone biopsy?

A

H&E stain
Masson-Goldner trichrome
tetracycline/calcein binding

28
Q

what are the 3 main categories of MBD?

A
  • endocrine abnormalities e.g. Vit D, PTH
  • non-endocrine e.g. age-related osteoporosis
  • disuse osteopenia e.g. astronauts
29
Q

when is the Masson-Goldner trichrome stain appropriate?

A

to see calcification levels in samples i.e. non mineralised vs mineralised bone

result:
mineralised –>green
non-mineralised–> orange

30
Q

when is the tetracycline/calcein binding stain appropriate?

A

see the rate of bone formation and bone turnover

fast or slow
produces fluorescent lines upon IV injections over bone and a later second injection reveals the time it to to lay new bone by looking at the distance between the lines

31
Q

what are the two types of osteoporosis aetiology?

primary and secondary causes

A

1) primary- age, post-menopause (physiological)

2) secondary- drugs, systemic disease (pathological)

32
Q

what is osteomalacia?

A

defective bone mineralisation of normally synthesised bone

33
Q

what is osteoporosis?

A

reduced bone density

T score < or = -2.5 SD

34
Q

what is high bone turnover?

A

increased bone formation and resorption but resorption is greater than formation

35
Q

what is low bone turnover?

A

decreased bone formation and resorption but a greater reduction in formation

36
Q

what are the two types of osteomalacia causes?

A

deficiency of Vit D

deficiency in phosphate

37
Q

what does the bone anatomy of osteoporosis look like?

A

large areas of trabecular bone is thinner and goes missing

they are less well connected leading to the thinning of cortical bone

38
Q

what is the role of vit D in osteomalacia?

A

role in PTH secretion

  • a deficiency in Vit D leads to increased PTH secretion and therefore bone resorption (calcium is taken from bone)
  • Vit D def is the most common cause of hypocalcaemia

results in proximal myopathy aswell

39
Q

how does low level of calcium manifest itself?

A

muscle spasms, twitches and tingling and numbness

High Na+ influx

40
Q

what is osteomalacia in children?

how does it present?

A

rickets

widening of growth plates and leg bowing to spread the weight

41
Q

what are the features of osteomalacia?

A

o Sequelae.
o Bone pain/tenderness.
o Fractures – e.g. horizontal fractures in Looser’s zone
o Proximal myopathy.
o Bone deformity – e.g. bowing in rickets.

42
Q

what are Looser’s Zones?

A

perpendicular fractures to cortex in areas of high tensile stress

43
Q

what stain can be used in examining osteomalacia?

A

MG trichrome to see the mineralisation level of the bone

44
Q

how is hyperparathyroidism defined?

A

excess PTH

45
Q

what are the features resulting from excess PTH?

A

o Increased Ca2+ and PO42- excretion in the urine.
o Hypercalcaemia due to increased calcium resorption
o Hypophosphatemia due to increased phosphate excretion
o Osteitis fibrosa cystica – skeletal changes including brown tumours and kidney stones.

46
Q

what is the role of vitamin D in calcium metabolism?

A

The major function of vitamin D is to optimize intestinal calcium and phosphorus absorption for proper formation of the bone mineral matrix.

Channels are dependent on vitamin D e.g. TRPV6

47
Q

what are the four organs involved with PTH?

A

Parathyroid glands
bones
kidneys
proximal small intestine

48
Q

what are the two forms of hyperparathyroidism?

A

primary- due to PT adenoma (85-90%) resulting in chief cell hyperplasia

secondary- accompanying a primary disease like chronic renal def resulting Vit D def

49
Q

what are the symptoms of hyperparathyroidism (and hypercalcaemia)?

A

1) stones (CA oxalate renal stones)
2) bones (osteitis fibrosa cystica)
3) abdominal groans (acute pancreatitis)
4) psychic moans (psychosis & depression)

50
Q

what is renal osteodystrophy?

A

comprises of all the skeletal changes of chronic renal disease

failure to excrete phosphate

51
Q

what are the skeletal changes that occur in chronic renal disease?

A 
o	Increased bone reabsorption (osteitis fibrosa cystica) – shows multiple lytic lesions on x-ray.
o	Osteomalacia.
o	Osteosclerosis.
o	Growth retardation.
o	Osteoporosis.
52
Q

what are the biochemical markers of renal osteodystrophy?

A

o PO4 retention/hyperphosphataemia.
o Hypocalcaemia – because of low vitamin D.
o Secondary hyperparathyroidism – low calcium due to low vitamin D so reflex hyperparathyroidism.
o Metabolic acidosis.
o Aluminium deposition.

53
Q

why does PTH remain high in hypercalcaemia of hyperparathyroidism?

A

negative feedback has been switched off

54
Q

what are the x-ray findings in hyperparathyroidism?

A

periosteal bone erosion

channel resorption in the trabecular (middle parts missing)

55
Q

what is Paget’s disease?

A

disorder of bone turnover

bone resorption followed by compensatory bone formation

56
Q

what are the 3 stages of Paget’s?

A

o Osteolytic stage – rapid breakdown of bone.
o Osteolytic-osteosclerotic – bone formation.
o Quiescent osteosclerotic – quiescent stage.

57
Q

what does formation breakdown in paget’s affect the bone?

A

produces a mosaic effect in the bone

58
Q

what is the epidemiology of Paget’s?

A

o Onset >40yo (but only 3% greater than 55yo).
o Equally affects males and females.
o Rare in Asians and Africans.
o Only affects one bone in 15% (most are poly-ostotic

59
Q

what is the aetiology of paget’s ?

A

o Mainly unknown.
o Familial cases – autosomal – mutation 5q35-qter – sequestosome 1 gene.
o Parvomyxovirus found in Pagetic bone.

60
Q

what are the clinical symptoms of Paget’s?

A

o Pain.
o Micro fractures and bowing of tibia.
o Nerve compression.
o Skull changes may put the medulla at risk.
o Deafness.
o Haemodynamic changes and possible cardiac failure.
o Hypercalcaemia.
o Development of sarcoma (in area of involvement).

LCRS Musculoskeletal (11 decks)

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