Lecture 18 - Bone Function & Repair Flashcards

1
Q

What are the mechanical, synthetic and metabolic functions of bone?

A

Mechanical = protect important organs, provide overall framework for human body and form basis of levers involved in movement.

Synthetic = Haemopoiesis (holds and protects red bone marrow)

Metabolic = mineral storage (Ca2+ and PO4), fat storage, acid-base homeostasis

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2
Q

What are the 2 types of ossification and what types of growth do they display?

A

1) Endochondral ossification - formation of long bones from a cartilage template, continued lengthening by ossification at epiphyseal growth plates (appositional growth) - growth at edges
2) Intra-membranous ossification - formation of bone from clusters of mesenchymal stem cells in the centre of bone (interstitial growth) - growth from the middle out

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3
Q

What are the main differences between endochondral and intra-membranous ossification?

A

Intramembranous takes place within condensation of mesenchymal tissue, endochrondral by replacement of hyaline cartilage template.

Intramembranous ossification contributes to bone thickening of long bones, at their periosteal surfaces (appositional growth).

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4
Q

What is the difference between immature and mature bone?

A
  • Immature bone has osteocytes in random arrangements
  • Mature bone has osteocytes arranged in lamellae of osteons.
  • Resorption canals in mature bone run parallel with osteons’ long axis.
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5
Q

Which one of compact or cancellous bone contains Haversian’s and Volkmann’s canals?
What do these structures do?

A
  • compact bone HAVE them
  • cancellous/spongy bone do NOT HAVE them
  • They carry blood vessels, lymph vessels and nerves
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6
Q

Why does bone have great tensile and compressive strength?

A

Lamallae within cortical bone are able to slip relative to each other to resist fracture - although excessive load can still cause fractures.

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7
Q

What are the main factors affecting bone stability?

A
  • Mostly activity of osteoblasts (bone deposition) and osteoclasts (bone resorption), however osteocytes have some ocsteoblast/clast activity too.
  • Other important factors include nutrition - Vit D, Vit C and Vik K and B12.
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8
Q

Describe the 4 stages of bone repair after a fracture occurs.

A

1) Blood clot (haematoma) is formed in which granulation tissue arises, eventually removed by macrophage
2) Fibrocartilaginous callus is formed, first a procallus of granulation tissue is replaced by a fibrocalliganous callus in which bony trabeculae are developing.
3) Bonus callus formation - endochondral and intramemranous ossification give rise to a bony callus of spongy/cancellous bone.
4) Cancellous bone replaced by compact cortical bone until remodelling is complete

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9
Q

What is the genetic basis of Osteogenesis imperfecta?
What are the clinical features?
Who does it mainly affect?

A
  • Mutation in COL1A (collagen type 1) gene, leading to incorrect production of collagen 1 fibres.
  • Weak bones, increased risk of fracture, shortened stature, blue sclera
  • Neonates + children
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10
Q

What is rickets caused by?

What are the clinical symptoms?

A
  • Vit D deficiency, leading to poor Ca2+ mobilisation and ineffective mineralisation
  • Leads to soft bones, shortened heigh, bow legs, pain while walking

NB: Rickets in adults is called Osteomalacia.

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11
Q

What are the 2 main divisions of osteoporosis?

What is each one due to?

A

1) Primary - can be type 1, which occurs in postmenopausal women, due to increased osteoclast number (as there is a loss of oestrogen which keeps osteoclast number under control) or type 2, which occurs in the elderly, due to loss of osteoblast function (due to loss of oestrogen/androgen)
2) Secondary - result of drug therapy (corticosteroids), is a major risk factor for bone fracture in elderly.

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12
Q

What are 3 modifiable risk factors for osteoperosis?

A

1) Insufficient Ca2+ intake
2) Exercise - immobilisation of bone leads to accelerated bone loss, physical activity is required
3) Cigarette smoking

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13
Q

What is Achondroplasia caused by?
What does it consequently affect?
What does it result in?

A
  • Inherited mutation in the FGF3 receptor gene
  • FGF promotes collagen formation from cartilage, therefore endochondral ossification affected (but not intramembranous).
  • Results in short stature, but normal sized head and torso (long bones cannot lengthen properly, e.g.: femur!)
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