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3rd Year - Module 5 > Bone Biology > Flashcards

Bone Biology Flashcards

1
Q

State the roles of calcium

A

Bone and teeth rigidity
Muscle contraction
Membrane potential stability
Neurotransmitter release
secretory processes
blood clotting
intracellular 2nd messenger
enzyme regulation

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2
Q

What does a decrease in free ECF Ca2+ concn (severe hypocalcaemia) cause?

A

An increase in Na+ permeability, depolarisation of membrane potential closer to threshold which results in muscle spasm

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3
Q

What does an increase in cytosolic Ca2+ cause?

A

Contraction. Whereas an increase in free ECF Ca2+ decreases neuromuscular excitability

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4
Q

What does an increase in free ECF Ca2+ cause?

A

A decrease in neuromuscular excitability and therefore a decreased likelihood of contraction

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5
Q

What is the plasma Ca2+ concentration?

A

2.2-2.6mmol/L

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6
Q

What is the intracellular Ca2+ concentration?

A

around 0.1micromol/L

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7
Q

What are two important roles of phosphate?

A

Component of ATP
Crucial in activation and deactivation of enzymes (kinases and phosphatases)

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8
Q

How are calcium and phosphate linked?

A

Both are components of hydroxyapatite crystals in bone
Both are regulated by the same three hormones

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9
Q

What three hormones regulate calcium and phosphate?

A

Parathyroid hormone (PTH)
1,25-dihydroxyvitamin D (calcitriol)
Calcitonin

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10
Q

How many parathyroid glands do humans have?

A

4

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11
Q

Where are the parathyroid glands located?

A

2 on the posterior surface of the left lobe of the thyroid gland and two more on the right lobe

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12
Q

What are the parathyroid glands composed of?

A

Chief cells which synthesise and secrete PTH

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13
Q

What do parathyroid glands secrete?

A

Parathyroid hormone (PTH)

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14
Q

What is the main regulator of PTH?

A

Plasma calcium concentration

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15
Q

What stimulates release of PTH?

A

a decrease in plasma calcium concentration (hypocalcaemia)

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16
Q

What kind of hormone is PTH?

A

a peptide hormone

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17
Q

What is the significance of PTH being a peptide hormone?

A

It circulates freely in the plasma and is rapidly metabolised

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18
Q

What are the net effects of PTH on the kidney and bone?

A

To increase plasma calcium concentration and to lower plasma phosphate concentration

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19
Q

Describe the effect of hypocalcaemia

A

hypocalcaemia stimulates secretion of PTH from chief cells. PTH then acts on the kidney and bone resulting in an increase in plasma calcium and a simultaneous decrease in plasma phosphate

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20
Q

What do the kidneys form when they filter plasma?

A

Tubular fluid

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21
Q

At what point is tubular fluid referred to as urine?

A

the fluid that leaves the collecting duct at the end of the nephron is referred to as urine and excreted from the body

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22
Q

How much of the calcium ion filtered by the kidneys is reabsorbed and where?

A

around 65% is reabsorbed in the proximal convoluted tubule (PCT) and around 25% in the thick ascending limb.
another 5-10% is absorbed in the distal nephron

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23
Q

What percentage of filtered calcium ions are excreted from the body in the urine?

A

around 0.5%

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24
Q

How does PTH increase plasma calcium concentration?

A

PTH stimulates the reabsorption of calcium in the distal nephron, reducing the amount excreted in the urine and therefore raising plasma concentration

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25
Q

Why does PTH modify transepithelial transport?

A

1) stimulate reabsorption of calcium ions in the distal nephron of the kidney
2) inhibit renal phosphate absorption in the proximal convoluted tubule

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26
Q

Where does the synthesis of 1,25-dihydroxyvitamin D occur?

A

mitochondria of cells in the proximal convoluted tubule

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27
Q

What are the 3 actions of 1,25-dihydroxyvitamin D?

A

1) enhance renal calcium reabsorption
2) enhance calcium reabsorption by the small intestine
3) modulate movement of calcium and phosphate in and out of bones

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28
Q

What is the net effect of a persistent increase in plasma parathyroid hormone concentration?

A

Stimulation of bone resorption

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29
Q

What impact does PTH have on osteoclasts?

A

PTH indirectly increases both the number and activity of osteoclasts

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30
Q

What is the net effect of an intermittent increase in plasma parathyroid hormone concentration?

A

Stimulation of bone deposition

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31
Q

What impact does the intermittent increase in PTH have on osteoblasts?

A

Promotes osteoblast differentiation and inhibition of osteoblast apoptosis

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32
Q

In what two forms does vitamin D exist in in the body?

A

Vitamin D3
Vitamin D2

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33
Q

How is vitamin D3 synthesised?

A

synthesised by the skin if sufficient UV light is absorbed

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34
Q

How is vitamin D2 obtained?

A

only obtained from the diet - vegetables

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35
Q

How do vitamin D2 and D3 differ?

A

Only differ on the side chain of ring D

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36
Q

Why can vitamin D also be considered a hormone?

A

because it is endogenously synthesised

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37
Q

How is vitamin D activated?

A

the addition of 2 hydroxyl groups to form 1,25dihydroxyvitamin D

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38
Q

What is the activated form of vitamin D and what does it have a role in?

A

1,25-dihydroxyvitamin D
Role in calcium balance

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39
Q

What is the action of 1,25-dihydroxyvitamin D?

A

to raise the plasma concentrations of both calcium and phosphate

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40
Q

What sites does 1,25-dihydroxyvitamin D impact on?

A

the small intestine (duodenum) and kidney to raise plasma calcium

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41
Q

What impact does 1,25-dihydroxyvitamin D have on the small intestine?

A

up-regulates the reabsorption of calcium by increasing expression of epithelial calcium channels, pumps and binding proteins
also stimulates synthesis of a NaPi cotransporter to increase phosphate absorption

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42
Q

What impact does 1,25-dihydroxyvitamin D have on the kidney?

A

acts synergistically with PTH to enhance calcium reabsorption in the distal tubule and promotes phosphate reabsorption.
Less dramatic effects than PTH

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43
Q

What medical condition can be caused in children with vitamin D deficiency and why?

A

Rickets
Vitamin D deficiency leads to impaired intestinal absorption of calcium and therefore hypocalcaemia.
Hypocalcaemia causes increase in PTH secretion, PTH leads to increased bone resorption so bones soften and deform.

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44
Q

What is the equivalent of rickets in adults?

A

Osteomalacia

45
Q

What kind of hormone is calcitonin?

A

Peptide hormone

46
Q

What cell produces calcitonin?

A

C cells (aka clear or parafollicular cells) of the thyroid gland

47
Q

What triggers calcitonin secretion?

A

an increase in the extracellular calcium concentration above normal (hypercalcaemia)

48
Q

What is the main action of calcitonin?

A

To lower plasma calcium concentration

49
Q

What impact does calcitonin have on osteoclasts?

A

calcitonin inhibits the resorptive activity of osteoclasts, slowing the rate of bone turnover

50
Q

Is the action of calcitonin hyper or hypocalcaemic?

A

HYPOcalcaemic

51
Q

How does calcitonin cause phosphaturia?

A

It results in mild phosphaturia by inhibiting phosphate transport in the proximal convoluted tubule

52
Q

Which of the three regulatory hormones has the smallest role in calcium ion homeostasis?

A

Calcitonin

53
Q

What sites does PTH act on?

A

Kidney, bone and small intestine

54
Q

What site does 1,25-dihydroxyvitamin D act on?

A

Kidney and small intestine

55
Q

What site does calcitonin act on?

A

kidney and bone

56
Q

What is the composition of bone?

A

60% mineral (largely hydroxyapatite)
25% organic (90% type 1 collagen, 10% non-fibrous extracellular matrix)
15% water

57
Q

In the microscopic bone structure, where are circumferential lamellae?

A

outside of most cortical bone

58
Q

In the microscopic bone structure, where are concentric lamellae organised?

A

organised in Haversian systems/osteons

59
Q

In the microscopic bone structure, what are interstitial lamellae?

A

remnants of old lamellae

60
Q

What are the three stages of endochondral ossification?

A

cartilage
calcified cartilage
bone

61
Q

What is intramembranous ossification?

A

bone develops directly from sheets of mesenchymal connective tissue

62
Q

What are osteoblasts derived from?

A

Mesenchymal or ectomesenchymal derived

63
Q

What do osteoblasts produce?

A

Osteoid matrix

64
Q

Where are osteoblasts found?

A

On bone surface - periosteum, endosteum

65
Q

What are osteocytes?

A

trapped osteoblasts, linked by gap junctions

66
Q

Are osteocytes vital?

A

Yes

67
Q

What are osteoclasts derived from?

A

Haemopoietic source - macrophage/monocyte line

68
Q

Where are osteoclasts found?

A

Howships lacunae

69
Q

What do osteoclasts do?

A

dissolve bone mineral - acid
breakdown organic matrix - enzymes

70
Q

What weight of calcium is present in the body?

A

1kg

71
Q

How is calcium regulated QUICKLY?

A

rapid exchanges between bone and ECF

72
Q

How is calcium regulated SLOWLY?

A

intestinal absorption and renal excretion

73
Q

How does PTH increase plasma calcium concentration?

A

Withdraws calcium from the bone bank

74
Q

What are the five phases involved in bone remodelling?

A

1) activation
2) osteoclast recruitment and resorption
3) reversal
4) osteoblast recruitment and bone formation
5) termination - quiescence

75
Q

What is osteogenesis imperfecta?

A

defective collagen formation, effects whole skeleton

76
Q

What is osteopetrosis?

A

defective osteoclastic bone resorption

77
Q

Name three metabolic bone diseases

A

Hyperparathyroidism
Pagets disease
Fibrous dysplasia

78
Q

What happens to bone following an extraction?

A

Physiological osteoclastic bone resorption

79
Q

Following extraction, in what dimension is there the largest bone resorption?

A

greatest amount of bone loss in the horizontal dimension mainly on the buccal aspect of the ridge

80
Q

What is the net effect of resorption following extraction on the ridge?

A

results in a narrower and shorter ridge and also the relocation of the ridge to a more palatal/lingual position

81
Q

How long does the bone remodelling process take?

A

6 months

82
Q

What types of drugs can impact on bone remodelling? (Name 4 types)

A

Bisphosphonates
Denosumab and anti-angiogenics
steroids
NSAIDs

83
Q

What are bisphosphonates?

A

Non-metabolised analogues of pyrophosphate

84
Q

What is the function of bisphosphonates?

A

They are capable of localising to bone and inhibiting osteoclastic function

85
Q

What do bisphosphonates bind avidly to?

A

exposed bone mineral around resorbing osteoclasts so therefore there can be a high level of bisphosphonate in the resorption lacunae

86
Q

What does the fact that bisphosphonates are not metabolised mean?

A

high concentrations are therefore maintained in bone for long periods of time

87
Q

Are bisphosophonates anti-angiogenic?

A

Yes

88
Q

What are the two classes of bisphosphonate?

A

non-nitrogen containing
nitrogen containing

89
Q

Name a non-nitrogen containing bisphosphonate

A

Clodronate

90
Q

Name a nitrogen containing bisphosphonate

A

Alendronate

91
Q

How do non-nitrogen containing bisphosphonates function?

A

resemble pyrophosphate so are incorporated into phosphate chain of ATP rendering it unusable for energy production in osteoclasts

92
Q

How do nitrogen-containing bisphosphonates function?

A

preventing formation of key lipids in osteoclasts which anchor proteins to the cell membrane.
Without these cell death occurs

93
Q

Name four conditions treated with bisphosphonates

A

osteoporosis
multiple myeloma
prostate cancer
breast cancer

94
Q

What bisphosphonate patients are considered low risk?

A

not yet started taking them
taking them for prevention or management of osteoporosis

95
Q

What bisphosphonate patients are considered high risk?

A

previous diagnosis of MRONJ
Taking as management of malignant condition
for other non-malignant condition of the bone eg. Paget’s disease
under care of specialist for rare condition eg. osteogenesis imperfecta
concurrent use of corticosteroids or immunosuppressants
radiotherapy, chemotherapy, coagulotherapy

96
Q

What is the SDCEP management advised for low risk patients?

A

if unavoidable then atraumatic extractions, raising flaps, achieve good haemostasis, review at 4 weeks.
If not healing at 4-6 weeks refer to oral/maxfax surgeon

97
Q

What is the SDCEP management advised for high risk patients?

A

contact oral/maxfax surgeon for advice on primary care or referral

98
Q

What are the three criteria for MRONJ?

A

1) Current or previous bisphosphonates, anti-angiogenic drugs or RANKL inhibitors
2) exposed bone or bone that can be probed that has persisted for more than 8 weeks
3) no history of radiation therapy to jaws

99
Q

What are the signs and symptoms of MRONJ?

A

area of exposed necrotic bone
internal or external discharging fistulas
painful generally
loose mobile teeth
bony sequestrae
paraesthesia
usually mandible (60-70% cases)

100
Q

How do you treat established MRONJ lesions?

A

no definitive guidelines.
Conservative management, irrigation, antibiotics, do not curette, remove small/loose sequestrae, stop bisphosphonate if safe to do so

101
Q

What is denosumab (prolia)?

A

Human monoclonal antibody that inhibits osteoclastic function

102
Q

What is the timescale of denosumab effect?

A

osteoclast function inhibited within 6 hours of SC injection and function returns 6 months later

103
Q

How does denosumab work?

A

inhibits receptor activator of nuclear factor kappa B ligand (RANKL), a protein which acts as primary signal for bone removal

104
Q

What is everolimus and what is its action?

A

a serine-threonine kinase, inhibits mammalian target of rapamycin resulting in reduced growth of cells, angiogenesis and survival of cells

105
Q

What is the impact of corticosteroids administered systemically and in strong doses?

A

Delay healing

106
Q

What drugs can affect absorption of calcium from the stomach?

A

Anti-seizure drugs eg. carbamazepine, phenytoin and long term proton pump inhibitors

107
Q

What drugs increase the renal excretion of calcium?

A

Diuretics

108
Q

What drugs reduce androgen and oestrogen levels?

A

drugs for treatment of breast and prostate cancer

3rd Year - Module 5 (12 decks)

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