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The Locomotor System > Bone: Function, Structure and Development > Flashcards

Bone: Function, Structure and Development Flashcards

1
Q

What are the functions of bone

A
  • Resistance of compression and tension (locomotion)
  • Calcium homeostasis
  • Houses the bone marrow.
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2
Q

Which element of bone aids resistance of compression

A

The inorganic content (hydroxyapatite)

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3
Q

Which element of bone aids resistance of tension

A

The organic matrix (collagen)

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4
Q

What are the three types of bone cells

A
  • Osteoblasts
  • Osteoclasts
  • Osteocytes
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5
Q

What are the two types of ossification of bone

A
  • Intramembranous ossification

- Endochondral ossification

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6
Q

What are the three parts of long bones from the ends to the centre

A

Epiphysis, metaphysis and diaphysis.

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7
Q

Where is the growth plate of long bones situated

A

Between the epiphysis and the diaphysis.

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8
Q

What determines when the growth plate closes

A

Genetics - this is why people have different heights.

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9
Q

What are the two types of bone

A
  • Cortical/compact bone

- Trabecular/ cancellous/ spongy bone.

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10
Q

What is there more of in the body, compact or cancellous bone

A

Compact bone.

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11
Q

Where is the compact/cortical bone in long bones

A

The diaphysis of the bone is mostly cortical bone. There is very little trabecular bone here.

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12
Q

Where is the cancellous bone in long bones

A

The epiphysis is mostly made up of cancellous bone.

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13
Q

What is the role of compact/cortical bone

A

It provides most of the structural support and resists bending stresses which is why it is thicker in the mid part of the bone.

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14
Q

What are osteons/haversian canals in cortical bone

A

These are bone cylinders with an axis parallel to the long axis of the long bone. They have a central cavity with blood vessels and a nerve.

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15
Q

What are Volkmann’s canals in cortical bone

A

These carry blood vessels from the periosteum to the .haversian system

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16
Q

What is the role of the haversian canals

A

To provide strength and nutrients to the bone.

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17
Q

What is the function of trabecular bone

A

Trabecular bone provides a large surface area for the metabolic function of bone. Most metabolic activities occur here.

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18
Q

How are the trabeculae in cancellous bone organised

A

Along lines of maximum mechanical stress. This allows the transmission of weight to the thicker cortical bone.

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19
Q

What can change the organisation of the trabeculae in cancellous bone

A

Alteration in the stress on the bone can change the organisation of trabeculae.

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20
Q

What is the main component of bone - organic or inorganic

A

Organic (osteoid)

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21
Q

What are the two elements of the osteoid (the organic part of the bone)

A

Type I collagen and non-collagenous proteins

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22
Q

What makes up the inorganic part of the bone

A

Calcium hydroxyapatite.

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23
Q

What is the osteoid

A

The unmineralised bone matrix.

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24
Q

What is the main component of osteoid

A

Type I collagen

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25
Q

What are the non-collagenous proteins that are also part of the osteoid

A

Osteocalcin, osteonectin and osteopontin

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26
Q

What are the two descriptions of bone matrix dependent on how the collagen fibres are laid down

A

Lamellar bone or woven bone.

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27
Q

How is collagen laid down in lamellar bone

A

Type I collagen fibres are laid down in parallel sheets called lamellae. This is a very organised structure and is very strong.

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28
Q

How is collagen laid down in woven bone

A

In woven bone, collagen is randomly arranged. Woven bone is the structure that tends to arise when bone is bring produced very rapidly such as in the foetus. It tends to be pathological if found in adults.

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29
Q

What is the role of osteoblasts

A

These are bone forming cells. They secrete osteoid.

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30
Q

What is the role of osteocytes

A

Osteocytes are mature osteoblasts which are laid down and become surrounded by bone matrix.

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31
Q

What is the role of osteoclasts

A

Osteoclasts function in resorption and degradation of existing bone.

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32
Q

What are osteoprogenitor cells

A

Osteoprogenitor cells are osteoblast precursors. Osteoblasts are derived from osteoprogenitor cells.

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33
Q

Which signalling pathway is required for the formation and proliferation of preosteoblast cells

A

The Wnt-frizzled-Lrp5-beta-catenin signalling pathway pathway

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34
Q

Which two transcription factors control osteoblast differentiation

A

Runx2 and osterix. if these are not present, no osteoblasts are formed.

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35
Q

What interaction between osteoclasts and osteoblasts regulates osteoclast differentiation and function

A

RANK ligand (on osteoblasts) and RANK (on osteoclasts) interactions.

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36
Q

What happens to osteoblasts after they secrete and deposit osteoid

A

Some become part of the bone matrix as osteocytes while some die by apoptosis or differentiate into bone lining cells.

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37
Q

What are the most common cells in the bone

A

Osteocytes

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38
Q

How do osteocytes connect to other osteocytes, osteoblasts and osteoclasts

A

By long cytoplasmic processes.

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39
Q

What is the function of osteocytes

A

They regulate bone remodelling

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40
Q

How do osteocytes regulate bone remodelling

A

They respond to local (biomechanical) or systemic (PTH) signals

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41
Q

What does signalling from RANKL do

A

RANKL is expressed on osteoblasts while RANK is expressed on osteoclasts. RANKL increases osteoclast formation.

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42
Q

What does signalling from sclerostin do

A

It inhibits osteoblast formation.

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43
Q

What is the production of sclerostin inhibited by

A

Sclerostin production is inhibited by PTH and mechanical loading.

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44
Q

What is PTH

A

Parathyroid hormone

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45
Q

What is the role of PTH

A

It causes rapid calcium release.

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46
Q

Which cells are osteoclasts derived from

A

Monocytes/macrophages.

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47
Q

What is the formation of osteoclasts regulated by

A

RANK-RANKL interactions and growth factors.

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48
Q

How do RANK and RANKL interactions increase osteoclast activity

A

RANK-RANKL interactions induce precursor cell fusion and this increases osteoclast activity.

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49
Q

What is the function of osteoprotegerin

A

Osteoprotegerin is a decoy receptor that binds RANKL and inhibits osteoclast formation. This means osteoprotegerin regulates RANK-RANKL interactions.

50
Q

What is the name of the molecule which regulated RANK-RANKL interactions

A

Osteoprotegerin (OPG)

51
Q

What two substances do osteoclasts produce

A

Acid and proteases

52
Q

What does the acid released by osteoclasts do

A

Releases calcium from bone

53
Q

What do proteases released by osteoclasts do

A

Breakdown organic matrix.

54
Q

What is the main method of calcium regulation

A

The breakdown of bone by osteoclasts.

55
Q

What are the two major routes by which bone is formed in utero

A

Intramembranous and endochondral ossification

56
Q

What happens in intramembranous ossification

A

Osteoid is laid down within loose fibroconnective tissue of a fibrous membrane.

57
Q

What happens in endochondral ossification

A

Osteoid is deposited on cartilage scaffolds.

58
Q

Which bones are formed by intramembranous ossification

A

The skull, the maxilla, parts of the clavicle, parts of the mandible, subperiosteal bone growth, fracture repair

59
Q

Which type of ossification forms the skull

A

Intramembranous ossification

60
Q

Which type of ossification is seen in fracture repair

A

Intramembranous ossification or endochondral ossification

61
Q

In intramembranous ossification what is bone trabeculae formed from

A

Mesenchyme

62
Q

What happens in the process of intramembranous ossification

A

Mesenchymal stem cells proliferate. These differentiate into osteoblasts to form the ossification centre. Osteoid is produced and laid down as woven bone. The matrix is mineralised and the osteoblasts become embedded in the matrix as osteocytes. Blood vessels grow in and the bone is remodelled into lamellar trabecular bone.

63
Q

By which method is most of the skeleton produced

A

Endochondral ossification

64
Q

By which method are the growth plates produced

A

Endochondral ossification

65
Q

What happens in endochondral ossification

A

Osteoid is deposited on preformed cartilage.

66
Q

Where does endochondral ossification in long bones start

A

Endochondral ossification starts from the diaphysis and extends out towards the metaphyses. The ephiphyses remain as cartilage in the foetus.

67
Q

What is formed by endochondral ossification

A
  • Most of the skeleton
  • Growth plates
  • Fracture repair.
68
Q

What is required in terms of the chondrocytes in order for endochondral ossification to occur

A

Programmed changes in the chondrocyte. The chondrocytes first proliferate and become hypertrophic. they then form type X collagen before dying.

69
Q

What is the stages of the process of endochondral ossification

A
  • The perichondrium transforms to the periosteum.
  • There is formation of a bony collar
  • Chondrocyte hypertrophy
  • Matric calcification
  • Osteoprogenitor and blood vessel in growth.
70
Q

When does ossification of the epiphysis occur

A

After birth.

71
Q

Where are the secondary ossification centres

A

The epiphyses

72
Q

Where are the primary ossification centres

A

The diaphysis

73
Q

What is the line of cartilage between the primary and secondary ossification centres known as

A

The epiphyseal/growth plate.

74
Q

When does growth stop

A

When the growth plates close.

75
Q

What determines the cessation of growth

A

Genetics

76
Q

Which gland control growth of bones

A

The pituitary gland which produces growth hormones.

77
Q

What is achondroplasia

A

Achondroplasia is a growth plate abnormality which causes short stature.

78
Q

What causes achondroplasia

A

Achondroplasia is caused by a mutation in fibroblast growth factor receptor 3 - FGFR3. It causes decreased chondrocyte proliferation and hypertrophy so while bones like the skull are of normal size (since they are reliant on intramembranous ossification), bones dependent on growth plates are short.

79
Q

Which is gigantism

A

Tall stature.

80
Q

What is gigantism caused by

A

Excess growth hormone production before puberty.

81
Q

What is acromegaly

A

This is increased growth hormone production after puberty (growth plates of long bones will have closed) and it results in large bones of the face (not dependent on growth plates).

82
Q

What happens with remodelling in normal bone

A

The amount of new bone laid down is the same as the amount of bone that was removed.

83
Q

When is bone remodelling normal

A

Bone remodelling happens all the time to repair micro-damaged bone and to reinforce bone in areas subject to increased stress to strengthen the bone depending on load.

84
Q

How much of the skeleton is replaced each year

A

18%

85
Q

What is quicker - removal of bone or formation of bone

A

Removal of bone is a lot quicker than formation of new bone.

86
Q

What factors are involved in regulation of bone remodelling

A
  • Mechanical load
  • Systemic hormones - PTH, Vitamin D, endocrine hormones
  • Local cytokines.
87
Q

What is the first stage of bone remodelling

A

Activation.

88
Q

What happens in activation

A

Osteoclasts are activated due to RANK-RANKL interactions between the osteoclast and osteoblasts/osteocytes.

89
Q

What happens if the resorption stage of bone remodelling

A

Osteoclasts adhere to the bone via integrins. They form a ruffled border and secrete acid and proteases into the space between the bone and the ruffled border.

90
Q

How do osteoclasts die

A

Apoptosis

91
Q

What are osteoclasts replaced by

A

Mononuclear cells which lay down the cement line

92
Q

What is the cement line laid down by the mononuclear cells which replace the osteoclasts

A

The cement line is the glue which allows new osteoid to be deposited.

93
Q

What happens in the reversal stage of bone remodelling

A

Osteoblasts differentiate from bone marrow stromal cells.

94
Q

What happens in the formation stage of bone remodelling

A

Osteoblasts lay down osteoid and the osteoid is mineralised. Osteoblasts become entrapped in the matric and become osteocytes.

95
Q

What is the name of a molecule which inhibits bone formation

A

Sclerostin.

96
Q

What Pi/PPi ratio promotes mineralisation

A

A high Pi/PPi ratio promotes mineralisation.

97
Q

What Pi/PPi ratio inhibits mineralisation

A

A low Pi/PPi ratio inhibits mineralisation

98
Q

What does osteopontin - the non-organic protein - do

A

Osteopontin inhibits mineralisation.

99
Q

When is peak bone mass achieved

A

Peak bone mass is achieved in young adulthood - in a persons 20s-30s.

100
Q

What is peak bone mass determined by

A
  • Genetic factors
  • Physical activity
  • Muscle strength
  • Diet - calcium intake
  • Hormonal state
101
Q

What are three bone remodelling disorders

A
  • Osteoporosis
  • Paget’s disease of the bone
  • Osteopetrosis
102
Q

What happens in osteoporosis

A

Resorption happens at a faster rate than formation so bone density decreases (resorption > formation)

103
Q

What happens in Paget’s disease of the bone

A

Bone resorption and formation are both increased.

104
Q

What happens in osteopetrosis

A

Resorption is decreased - there is too much formation.

105
Q

What are three examples of metabolic bone diseases

A
  • Vitamin D deficiency (rickets, osteomalacia)
  • Hyperparathyroidism
  • renal osteodystrophy
106
Q

What are the three stages of Pagets Disease

A
  • Lytic - bone is removed
  • Mixed - there is bone absorption and formation
  • Sclerotic - there is lots of active bone remodelling
107
Q

What are the consequences of Pagets disease

A

Weak deformed bone and nerve compression. Bone is thickened but is still weak.

108
Q

How could deafness result from Pagets disease

A

Due to nerve compression as a result of thickened bone.

109
Q

What is the presentation of osteopetrosis (marble bone disease)

A

Hard dense bone.

110
Q

What causes osteopetrosis

A

A decrease in the number or activity of osteoclasts.

111
Q

What is a primary cause of hyperparathyroidism

A

Parathyroid adenoma

112
Q

What are secondary causes of hyperparathyroidism

A

Chronic renal disease (leading to low calcium), low serum calcium and phosphate induce parathyroid hyperplasia.

113
Q

What does hyperparathyroidism bring about in bones

A

Increased bone turnover due to increased osteoclastic activity and increased osteoblastic activity.

114
Q

What are the sources of vitamin D

A

The skin, however this requires sunlight to be activated, as well as dietary intake.

115
Q

What is the role of vitamin D

A

It helps the body to absorb calcium.

116
Q

What are the 5 causes of vitamin D deficiency

A
  • Lack of sunlight
  • Dietary
  • GI disease leading to malabsorption (such as is crohns disease)
  • Liver disease
  • Kidney disease.
117
Q

What is the result of vitamin D deficiency in the blood

A

Decreased serum calcium levels as calcium cannot be absorbed as well.

118
Q

What is the name given vitamin D deficiency

A

In children - rickets

In adults - osteomalacia.

119
Q

What happens in osteomalacia

A

There is decreased mineralisation of the bone.

120
Q

What happens in rickets

A

Children have soft bones that deform easily - bow legs (varus)

The Locomotor System (13 decks)

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