Bone - bio. properties and remodelling Flashcards

1
Q

Why do we have bones?

A
  • Calcium regulation
  • Mechanical support and locomotion
  • Protection of vital organs
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2
Q

How do we regulate calcium?

A
  • Calcitonin - decreases bone resorption
  • PTH - increases bone resorption, increases 1a-hydroxylase (increases active VitD), increases renal calcium reabsorption, increases phosphate clearance.
  • Vit D - increases intestinal calcium absorption
  • Oestrogen - decreases bone resorption
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3
Q

What is the composition of bone?

A
  • Protein- 25% (matrix largely composed of type 1 collagen, with glycoproteins, proteoglycans, and other proteins making up the rest)
  • Mineral (75%) - Calcium phosphate
  • Cells (osteoblasts/clasts/cytes, bone marrow cells)
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4
Q

What is osteogenesis imperfecta?

A

Brittle bone disease - lack of type 1 collagen in the bone’s protein matrix

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5
Q

Cortical vs Trabecular bone

A

Cortical has a higher density, lower surface area, lower remodelling rate, Haversian systems (rings)
- Trabecullar bone uses struts and plates and is metabolically active

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6
Q

What do osteoblasts do?

A

Synthesise matrix proteins, formation of bone mineral, derived from mesenchymal stem cells

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7
Q

What do osteoclasts do?

A
  • production of acid - dissolution of mineral
  • production of proteolytic enymes - digestion of matrix (cathepsin K, metalloproteinase)
  • transcellular removal of calcium, phosphate and matrix
  • derived from macrophage type cells
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8
Q

What is rickets?

A

A disease where there is demineralisation of bone - gives bow-leg as the bones bend under load

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9
Q

What is the bone remodelling cycle?

A
  • Quiescence
  • Resorption of bone by osteoclasts
  • formation of new bone by osteoblasts
  • mineralisation
  • quiesence
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10
Q

How does trabecular bone remodel?

A
  • Osteoclasts cause resorption pits, osteoblasts fill in the pit with unmineralised proteins, which they then mineralise
  • Move along the trabeculae
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11
Q

What changes in bone mass are there with age?

A
  • men have much more bone mass on average
  • both plateau at 30-40 and then decline gradually
  • women have a much lower bone mass in later life - more risk of fractures
  • there is accelerated bone loss in menopause (oestrogen usually inhibits osteoclasts)
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12
Q

What is Paget’s disease?

A

Excessive breakdown and formation of bone in a localised area - leads to disorganised bone.

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13
Q

What is osteoperosis?

A

Osteoclasts are over active - you have more resorption than bone formation
- Generalised reduction in bone

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14
Q

What hormones regulate bone density?

A

Increase: Oestrogens/androgens (suppress osteoclast bone resorption). Growth hormone (IgF). Calcitonin.

Decrease: thyroxine, glucocorticoids (too much = cushing’s), PTH.

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15
Q

How do fractures occur?

A
  • When force exceeds bone’s strength

- bone has good tensile and compressional strength, but weaker torsional strength.

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16
Q

What are the 3 stages of fracture healing?

A

1: macrophages remove debris. granulation tissue forms. fibrous tissue - vascularised
2: Soft callus formed by osteoblasts. Hard callus then formed when the bone mineralises
3: lamellar bone fromation and remodelling