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Module 204 MSK & Immune system > T2 L12 Physiology of bone repair > Flashcards

T2 L12 Physiology of bone repair Flashcards

1
Q

What are the functions of the skeleton?

A 
Maintaining bone structure
Locomotion
Haematopoiesis
Ca2+ / mineral homeostasis
Protection of inner organs
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2
Q

What is the consequence of too much bone resorption?

A

Osteoporosis
Osteopenia
Rickets

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3
Q

What is the consequence of too little formation?

A

Osteopetrosis

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4
Q

What is the definition of bone resorption?

A

Solid bone dissolved by physiological processes

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5
Q

Why is bone resorption important?

A

Repair of broken bones
Remodelling of bones as person grows
Remodelling of bone for specific stresses

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6
Q

What is the definition of demineralisation?

A

Breaking down bone by making hydroxyapatite soluble

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7
Q

What is osteopenia?

A

Condition were bone mineral density is lower than normal

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8
Q

What are the uses of measuring bone mineral density?

A

Identify osteoporosis
Determine risk for fractures
Measure response to osteoporosis treatment

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9
Q

What is osteopetrosis?

A

One of several diseases where bones harden in excess
Bone becomes hard, lacks flexibility, easily fractures
Autosomal recessive disease

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10
Q

What is rickets?

A

Disease of bone development usually due to malnutrition

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11
Q

What does rickets result in?

A

Bone deformities
Increased tendencies for fractures
Spinal deformity

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12
Q

How is bone classified on macroscopic level?

A 
Cortical bone
Cancellous bone (spongy)
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13
Q

What is cortical bone?

A

Thick bone organised in osteons
Associated with or connected to outer surface of bone
High turnover to remodel according to stress across bone
Spicules
Trabeculae

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14
Q

What is cancellous bone?

A

Bony structs organised into loose network with blood / bone marrow between struts
30-90% is porous and contains bone marrow

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15
Q

What happens to cancellous bone in osteoporosis?

A

Increased porosity

Less strong, less ridge, more elastic

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16
Q

How is bone organised microscopically?

A

Lamellar

Woven

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17
Q

Describe lamellar organisation of bone?

A

Secondary bone which is created by remodelling woven bone
Organised and stress oriented
Stronger and less flexible than woven bone
Osteons

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18
Q

Describe woven organisation of bone

A

Immature
Disorganised
Not stress orientated
More osteocytes, higher rate turnover, weaker and more flexible than lamellar bone

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19
Q

What are the 3 principle cell types in bone?

A

Osteoblasts
Osteocytes
Osteoclasts

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20
Q

Describe osteoblasts

A

Form new bone and release signalling substances
Produce protein components of acellular matrix which regulates bone growth and degradation
Located on developing bone surfaces
Post-mitotic - most will undergo apoptosis

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21
Q

What are osteoblasts derived from?

A

From mesenchyme

Precursor cells in bone marrow storm

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22
Q

Describe the histology of osteoblasts

A

20-25 microns
Round and regular shape
Mononucleate

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23
Q

Describe osteocytes

A

Quiescent mature cells embedded in bone matrix
Function is maintenance and detection of environmental and ageing stresses
Within osteoid

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24
Q

What are osteocytes derived from?

A

Osteoblasts

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25
Q

Describe the histology of osteocytes

A

Long and thin
Extensive branches that travel through canaliculi
Main cell body inside lacunae is 20x5microns
Mononucleate

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26
Q

Describe osteoclasts

A

Function is bone degradation and remodelling bone

Can proliferate

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27
Q

What are osteoclasts derived from?

A

Same precursor as monocytes (haematopoietic stem cells)

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28
Q

Describe the histology of osteoclasts

A

40-100micrometre diameter
15-20 closely packed oval-shaped nuclei
Regular, cube-like shape with ruffled border

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29
Q

What does the ruffled border on osteoclasts do?

A

Has integrins to surround region of resorption
Prevents dilution of acid
Prevents loss of proteases

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30
Q

What is an osteoid?

A

Unmineralised, organic portion of bone matrix that forms prior to maturation of bone tissue

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31
Q

What are the organic components that make up the matrix?

A

Proteins e.g. collagen and elastin
Polysaccharides
Glycosaminoglycans

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32
Q

What are the inorganic components that make up the matrix?

A

Ca2+
Phosphate
Hydroxyapatite
Magnesium

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33
Q

Wha types of components are found in the matrix?

A

Organic components
Inorganic components
Growth factors

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34
Q

Describe glycosaminoglycans

A

Long unbranched polysaccharides
Highly negative
Resist compression
Abundant in cartilage

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35
Q

Describe the role of growth factors

A

Revealed by osteoclast action which stimulates and attracts osteoblasts leading to proliferation and mineralisation
Bone remodelling leading to bone turnover and activation-resorption-formation sequence

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36
Q

What is the Haversian system?

A

One type of microscopic organisation of bone tissue

Communication system between cells is immobilised in bone matrix

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37
Q

What is the Haversian canal?

A

Longitudinal canal within bone tissue
Runs parallel to surface and along long-axis of bone
Surrounded by lamellae to form Haversian system

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38
Q

What are canaliculi?

A

Microscopic canals between lacunae of ossified bone

Radiating processes of osteocytes projects into these canals

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39
Q

What is compressive strength?

A

Ability to resist compression without collapsing or expanding to point of failure

40
Q

What provides compressive strength in bone?

A

Hydroxyapatite

41
Q

What is tensile strength?

A

Ability to resist stretching without breaking

42
Q

What provides tensile strength?

A

Collagen

43
Q

Where do osteoclasts resorb bone?

A

In Howship’s lacunae

44
Q

What is Howship’s lacunae?

A

Space on edge of bony spicule which has been made by and contains osteoclast

45
Q

What controls activation-resorption-remineralisation sequence?

A

Surface osteoblasts

Detect mechanical factors (stresses on that bone) and hormonal factors that initially trigger bone remodelling

46
Q

What are the 2 ways bone can form?

A

Intramembranous

Endochondral

47
Q

What is intramembranous bone formation?

A

Bone formation without cartilage model

48
Q

Describe the mechanism of intramembranous bone formation

A

Osteoblasts lay down osteoid and bone mineralisation
Form tiny bony spicules
Join with nearby spicules
Form trabeculae (woven bone)

49
Q

What is endochrondral bone formation?

A

Bone formation based on cartilage model. Cartilaginous template made from mesenchyme

50
Q

Describe the mechanism of endochondral bone formation

A

Chondrocytes proliferate and secrete extracellular matrix and proteoglycans
Osteoblasts arrive
Osteoid laid down
Mineralisation begins

51
Q

What factors govern bone remodelling?

A

Recurrent mechanical stress

Calcium homeostasis

52
Q

What happens to bone trabeculae under recurrent mechanical stress?

A

Becomes dense and prominent to strengthen bone

53
Q

How does recurrent mechanical stress govern remodelling?

A

Surface osteoblasts and osteocyte network detect stresses

Inhibits bone resorption and promotes deposition

54
Q

What are bisphosphonates used for?

A

Osteoporosis to diminish bone resorption by osteoclasts

55
Q

Give an example of a bisphosphonae

A

Alendronate

56
Q

What is the mechanism of bisphosphonates?

A

Inhibit osteoclast-mediated bone resorption
Related to inorganic pyrophosphate
- pyrophosphate is endogenous regulator of bone turnover
- accumulates on bone as it binds to calcium, ingested by osteoclasts which interferes with osteoclast metabolism

57
Q

Give an example of a drug that encourages osteoblast formation of bone

A

Teriparatide

58
Q

What drug prevents osteoclast maturation?

A

Denosumab

59
Q

What is densoumab?

A

Monoclonal antibody that targets RANK ligand

- mimics action of OPG to prevent activation and differentiation of osteoclasts

60
Q

What is RANK ligand?

A

Member of TNF cytokine family

Functions as key factor for osteoclast differentiation and activation

61
Q

What is the molecular mechanisms in osteopetrosis?

A

Osteoclasts can’t remodel bone
Defective vacuolar proton pump which can’t make Howship’s lacuna acidic so bone isn’t resorbed
Defective chloride channel

62
Q

What are the consequences of osteopetrosis?

A 
Fatal within 10 years
Brittle (dense) bones
Blindness
Deafness 
Severe anaemia
63
Q

What is the treatment for osteopetrosis?

A

Bone marrow transplant - only partially effective

64
Q

How long does fracture healing take in adults?

A

2 to 3 weeks in upper body

At least 4 weeks in lower body

65
Q

What are the 4 phases of fracture healing?

A

1) Reactive phase - haematoma and inflammation
2) Soft callus formation
3) Hard callus formation
4) Remodelling

66
Q

Describe the reactive phase of fracture healing

A

Blood cells enter wound and haematoma forms
Inflammatory cells invade to form granulation
Bone precursor cells arrive from periosteum

67
Q

Describe the soft callus formation stage of fracture healing

A

Woven bone (or hyaline cartilage) joints pieces of broken bone

  • woven bone is near blood vessels
  • fibrocartilage is further away

Fast process

68
Q

Describe the hard callus formation stage of fracture healing

A

Lamellar bone replaces woven bone

Slow process resulting in stronger bones

69
Q

Describe the remodelling phase of fracture healing

A

Endochondral (lamellar) bone is replaced by trabecular bone

Trabecular bone is remodelled into original bone shape

70
Q

Where is calcium stored?

A 
Bone
Sequestered inside cells / SR
Protein bound
Complexed with anions
Free calcium
71
Q

Where is PTH made?

A

By parathyroid chief cells

72
Q

What does PTH do to calcium?

A

Increases plasma calcium

73
Q

Where does PTH act?

A

Bone
Kidney
Gastrointestinal tract

74
Q

What effect does PTH have on kidney?

A

Reduces kidney secretion of calcium and increases secretion of phosphate

75
Q

What effect does PTH have on bone?

A

Stimulates bone to mobilise calcium
Detected by osteoblasts and osteocytes –> mobilise sequestered calcium and release cytokines
Increased differentiation and activity e.g. osteoclasts

76
Q

Where is vitamin D made?

A

Skin
Liver
Kidney

77
Q

What effect does vitamin D have on calcium?

A

Increases plasma Ca2+ for longer time than PTH

78
Q

Where is calcitonin made?

A

Thyroid C cells

79
Q

What effect does calcitonin have on calcium?

A

Decreases blood calcium as more is taken up by bone

80
Q

What does OPG (osteoprotegrin) do?

A

Binds to RANK ligand to prevent RANK binding

Inhibits differentiation of precursor osteoclast into mature osteoclast

81
Q

Describe the negative feedback of calcium in lactation

A

Lactation –> low plasma Ca2+
Calcium-sensitive receptor in parathyroid chief cells detect low calcium
Chief cells release PTH
Kidney increases Ca resorption at DCT, enterocytes increase calbindin –> Ca absorption, bone mobilises Ca to plasma
Plasma calcium increases

82
Q

Describe the steps of vitamin D production and activation

A

1) Cholecalciferol in skin
2) 25-OH cholecalciferol
3) 1,25-di-OH-cholecalciferol (calcitriol)
4) Increase calbindin in gut enterocytes
5) Increase intestinal absorption of calcium
6) Increase calcium reabsorption in kidney
7) Increase plasma Ca2+

83
Q

What are the effects of vitamin D?

A

Increase intestinal calcium absorption - increases calbindin
Stimulates kidneys to reabsorb calcium
Indirectly stimulates osteoclasts
Facilitates bone remodelling

84
Q

What is calbindin?

A

Calcium-binding protein that increases intestinal calcium absorption

85
Q

How is vitamin D production controlled via negative feedback?

A

25-OH-cholecalciferol feeds back on liver to reduce production of 25-OH-cholecalciferol from cholecalciferol
Calcium feeds back on parathyroid gland to reduce PTH production –> reduces kidney’s activation of 25-OH-cholecalciferol to 1,25-di-OH-cholecalciferol

86
Q

What are the causes of low plasma calcium?

A 
Pregnancy, lactation
Kidney dysfunction
Low intake
Parathyroid dysfunction
Drugs
87
Q

What drugs can cause low calcium?

A

Magnesium

Anticonvulsants

88
Q

What are the consequences of chronic hypocalcaemia?

A 
Skeletal deformities
Increased tendency towards bone fractures
Impaired growth
Short stature
Dental deformities
89
Q

Describe the skeletal deformities in chronic hypocalcaemia

A 
Bowlegs
Forward projection breastbone
Asymmetrical or odd-shaped skull
Soine deformities e.g. scoliosis
Pelvic deformities
90
Q

What are the consequences of acute hypocalcaemia?

A

Convulsions
Arrhythmias
Tetany

91
Q

What is Chvostek’s sign?

A

Latent tetany

Tapping master leads to twitch on same side of face

92
Q

What is Trousseau’s sign?

A

Carpopedal spasm with lateral tetany

93
Q

What is DiGeorge syndrome?

A

Rare genetic anomaly

Typically has issues with mediastinum that lead to absent thymus and underdeveloped parathyroid glands

94
Q

Why does hypocalcaemia make membranes less stable?

A

More excitable
Sodium is more able to leak through
Explains late tetany

95
Q

Why does hypercalcaemia make membranes more stable?

A

Reduces excitability

Increases intracellular calcium which inactivates channels to reduce calcium inflow in muscle cells

96
Q

What are the signs and symptoms of hypercalcaemia?

A 
Can be asymptomatic
Reduced excitability 
 - constipation
 - depression
 - confusion
 - kidney stones
Abnormal heart rhythms
 - short QT interval
 - no ST segment
 - widened T wave
97
Q

What are the signs of severe hypercalcaemia?

A

Coma

Cardiac arrest

Module 204 MSK & Immune system (44 decks)

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