Bone

Question 1

Bone remodelling

Answer 1

• Stress induced micro-fracture appears
• Osteocytes usually secrete sclerostin which inhibits Wnt so are quiescent.
  Activation: Osteocytes undergo apoptosis, secrete GH, NO attracting pre-osteoclasts
  Osteocytes no longer under sclerostin inhibition, attract pre-osteoblasts
  Pre-OBs activate pre-OCs by RANKL
  Resorption: Osteoclasts digest mineral matrix (2 weeks)
  Reversal: Pre-OBs secrete OPG (decoy receptor) stopping OC activity
  Formation: Osteoblasts synthesise bone matrix, becomes mineralised (3-4 months)
  Primary min: 100 days
  Secondary min: 1 year
  Quiescence: Osteoblasts become resting bone lining cells on newly formed bone surface

Question 2

OP: treatments

Answer 2

Antiresorptive (reduces bone turnover): 
Bisphosphonates e.g. alendronate 
HRT 
Denosumab 
Strontium ranelate 

Anabolic (increases bone formation):
Teriparatide (PTH)
Strontium ranelate

Question 3

Indirect fracture healing

Answer 3

Fracture haematoma and inflammation 6-8 hrs

• Blood clot forms
• Swelling and inflammation at fracture site

Repair -
Fibrocartilage (Soft callus) - 3 weeks
- New capillaries organise fracture haematoma into granulation tissue - pro callus forms
- Fibroblasts and osteogenic cells migrate into pro-callus
- Chrondrocytes secrete fibrocartilage

Hard callus - after 3 weeks, takes 3 months
Osteoblasts make woven bone

Remodelling - 6 months
Osteoclasts remodel bone into compact and trabeculae bone

Question 4

Direct fracture healing

Answer 4

Direct formation of bone without callus formation, in unique surgical situations, until skeletal continuity is restored
- OC resorption and OB formation