16 - Bone Function and Repair Flashcards

1
Q

Long bones require a ……… template to develop by …………….. ossification

A

Cartilage

Endochondral

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2
Q

Flat bones develop from ………… ………. …….. by …………….. ossification

A

Mesenchymal Stem Cells

Intramembranous

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3
Q

Intramembranous ossification contributes to the development of flat bones but also to …….

A

Thickening of long bones at their periosteal surfaces (appositional growth)

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4
Q

Describe the process of intramembranous ossification.

A
  1. Mesenchymal stem cells aggregate and differentiate into osteoblasts
  2. Ossification begins (lays down osteoid containing type I collagen) and bone expands as spicules into surrounding tissue
  3. As the spicules interconnect, they trap blood vessels within the bone (creates trabeculae)
  4. Bone assumes the structure of spongy (cancellous) bone

Areas of spongy bone can later be removed to create marrow cavities or remodelled into compact bone.

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5
Q

During endochondral ossification, bone is added to the ………. but the height of the ………. does not change

A

Diaphysis

Cartilage (only gets pushed upwards)

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6
Q

In the foetal skull, the periosteum is not fully formed and still contains osteoprogenitor cells for bone deposition. What is this called and why is it useful?

A

Fontanelle’s of the skull

Skull can compress as bones can slide over each other slightly - allows the baby to move through the birth canal

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7
Q

In mature flat bones, what structures form that normally arise from endochondral ossification? How does this differ in a child from an adult?

A

Osteons (with Haversian and Volkmann’s canals)

In a child there is less osteon structure (no concentric lamellae) - takes ~24 years to develop fully

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8
Q

How does the structure of immature and mature compact bone differ?

A

Immature - osteocytes in random arrangemenrts

Mature - osteocytes in concentric lamellae of osteons (occurs by remodelling)

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9
Q

What is found in cancellous bone instead of vessel canals?

A

Red bone marrow with sinusoid nutrient arteries and central veins

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10
Q

How is osteoid and collagen laid down in cancellous bone?

A

In parallel lines forming rings of bone

Collagen is laid in the same direction due to gravity –> without this bones are weakened

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11
Q

How do bones resist fracture?

A
  • Great tensile and compressive strength with a small degree of flexibility
  • Main force lines are through the cortical bone
  • Lamellae are thought to be able to slip relative to each other to resist fracture
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12
Q

The activity of what cells affect bone stability?

A
  • Osteocytes (osteoid recycling)
  • Osteoblasts (bone deposition - stimulated by calcitonin)
  • Osteoclasts (bone resorption - stimulated by PTH)
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13
Q

What vitamins affect bone stability?

A
  • Vitamin D3 - produces calcitriol for calcium absorption
  • Vitamin C - collagen synthesis
  • Vitamins K and B12 - synthesis of bone proteins
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14
Q

Summarise the process of fracture repair.

A
  1. Hematoma formation - Blood clot forms and granulation tissue arises (fibroblasts and capillary-rich)
  2. Fibrocartilaginous callus formation - Granulation tissue replaced by fibrocartilage where bony trabeculae begin to develop
  3. Bony callus formation - Endochondral and intramembranous ossification form the cancellous bone
  4. Bone remodelling - Cancellous bone begins to remodel into cortical bone, material bulging out the outside is removed
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15
Q

What is:

  • A cutting cone?
  • A closing cone?
A

Cutting cone - osteclasts make a wide tunnel in the bone

Closing cone - osteoblasts make a smaller tunnel in the cortical bone

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16
Q

What is osteoid?

A

Unmineralised, organic content of bone (90% collagen and 10% ground substance)

17
Q

How does osteogenesis imperfecta affect the bones?

A
  • Mutation in COL1A gene
  • Incorrect production of collagen I fibres
  • Weak bones and increased fracture risk
  • Shortened height and stature
18
Q

What is rickets and how does it affect the bones?

A
  • Mainly affects children
  • Vitamin D deficiency
  • Poor calcium mobilisation and ineffective mineralisation
  • Bones are weak/soft (characteristic bowing of the legs)
19
Q

What is osteomalacia?

A
  • A form of rickets in adults
  • Vitamin D deficiency due to malnutrition
  • Low mineralisation and increased osteoid
  • Increased calcium resorption
20
Q

What is osteoporosis?

A

A condition of the bones making them weak and fragile

21
Q

How does type 1 primary osteoporosis occur?

A
  • In postmenopausal women

- Increase in osteoclast number due to loss of oestrogen after the menopause

22
Q

How does type 2 primary osteoporosis occur?

A
  • Occurs in older men and women
  • Due to loss of osteoblast function as a result of loss of oestrogen and androgen
  • As osteoclasts break down bone for remodelling the osteoblasts can no longer fill in the bays properly
23
Q

What can cause secondary osteoporosis?

A
  • Drug therapies (e.g. corticosteroids)
  • Malnutrition
  • Prolonged immobilisation or weightlessness (e.g. space travel)
  • Metabolic bone diseases (e.g. hyperparathyroidism)
24
Q

What are the modifiable risk factors for osteoporosis?

A
  • Insufficient calcium intake (for postmenopausal women = 700mg/day)
  • Exercise - immobilisation leads to accelerated bone loss
  • Cigarette smoking - correlated with increased risk of osteoporosis in women
25
Q

What causes achondroplasia and how does it present?

A
  • Mutation in FGF3 receptor gene
  • FGF promotes collagen formation from cartilage (only endochondral ossification is affected)
  • Results in short stature but normal sized head and torso - long bones cannot lengthen properly