Week 11 - Bone Biology Clinic + extra slides Flashcards

(18 cards)

1
Q

Where does bone remodeling and repair occur

A

o Periosteal surface (outer bone layer)
o Endosteal surface (inner layer)

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2
Q

function of osteocytes

A

act as mechanosensors:
o Detect stress and release signals that regulate osteoblasts & osteoclasts

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3
Q

what happens to bone exposed to increased mechanical stress

A

o Undergoes strengthening/remodelling.

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4
Q

what happens to bone with decreased stress

A

o Undergoes resorption (weakened).

more sensitive to parathyroid hormone → more resorption

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5
Q

tooth loss leads to

A

o Loss of alveolar bone function
o Progressive bone loss in the jaw

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6
Q

what drives bone resorption

A
  1. Mechanical stress
  2. Calcium homeostasis
  3. Inflammation (pathological) – other
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7
Q

what stimulates osteoclast activity

A

activated T-lymphocytes

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8
Q

What is perodontitis

A
  • A chronic inflammatory disease of the supporting structures of teeth.
  • Progresses from gingivitis.
  • Leads to:
    o Destruction of connective tissue attachment
    o Loss of supporting alveolar bone (hallmark)- the major cause of tooth loss in adults
    o Major cause of adult tooth loss
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9
Q

how is inflammation involved in bone loss

A
  • Bacterial infection triggers immune response.
  • However it is the inflammatory response that plays a critical role - Inflammation reaches alveolar bone:
    o Requires high local concentrations of inflammatory mediators.
  • Inflammatory mediators stimulate osteoblasts to express:
    o RANKL (Receptor Activator of NF-κB Ligand)

o Cytokines from immune response (e.g., ILs, TNF-α) impact RANKL/OPG balance.
o High inflammatory signals → ↑ RANKL → ↑ osteoclast activity → bone loss.

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10
Q

function of OPG

A

a decoy receptor produced by osteoblasts:
o Binds RANKL, preventing it from binding RANK.
o Inhibits osteoclast formation and induces apoptosis of mature osteoclasts. – prevents excessive activation of osteoclasts

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11
Q

what happens if there’s high OPG

A

bone deposition

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12
Q

what is osteoporosis

A
  • Most common bone disease in adults – particularly older age groups
  • Results from diminished bone matrix because of decreased osteoblastic activity
    Could be caused by:
  • lack of exercise
  • Malnutrition
  • Hormonal changes – decreased oestrogen
  • Aging – decreased protein anabolic functions
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13
Q

what do normal levels of glucocorticoids do

A

Support osteoblast differentiation.

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14
Q

what do high levels of glucocorticoids lead to

A

o Inhibit osteoblasts.
o Promote osteoclast activity.
o Suppress OPG and increase RANKL expression.
* Result: Increased bone resorption and risk of osteoporosis (e.g., in Cushing’s disease).

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15
Q

What is the impact of oestrogen

A
  • Promote OPG production.
  • Can operates as both osteoblasts and osteoclasts
  • Inhibit RANKL and cytokines that recruit osteoclasts.
  • Help oppose PTH-induced resorption.
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16
Q

what does postmenopausal estrogen deficiency cause

A

less OPG, more bone resorption → osteoporosis.

17
Q

what does * SERMs selective oestrogen receptor modulators (e.g., raloxifene): do

A

Mimic estrogen in bone, inhibit in breast/uterus.

18
Q

what detects mechanical stress

A

osteocytes → promotes adaptive remodelling.