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Medsci 312 > Lecture 27; Metabolic Bone diseases > Flashcards

Lecture 27; Metabolic Bone diseases Flashcards

1
Q

What are the types of bone?

A

Spongy (trabecular)

Compact (osteon) (cortical bone)

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2
Q

What sort of tissue is bone?

A
  • Connective Tissue

- Dynamic balance between reabsoprtion and deposition

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3
Q

What happens to bone with age?

A

Menopause / really old (60) age in men results in bone reabsoprtion > Deposition

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4
Q

Give a brief description of bone?

A

Made of collagen fibres that have become part of a calcified matrix.

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5
Q

When looking macroscopically at bone what can be seen?

A

Smooth = Bone covered in lining cells derived from osteobasts

Rough = Osteoclast activity / bone remodelling site

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6
Q

How do osteoclasts function?

A

Release HCl = removes mineral structures

Releases proteolytic enzymes = removes collagenous structures

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7
Q

What do osteoblasts do?

A

Deposit collagen (osteoid) this becomes mineralised

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8
Q

How often is the entire skeleton replaced?

A

~10 years

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9
Q

What happens in osteoporosis?

A

When bone reabsoprtion exceeds bone deposition

  • Less bone
  • Less robust plates
  • If a trabeculae rod is punched through the middle then the remaining partial rods will waste away as they are not load bearing.
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10
Q

What is the actual definition of osteoporosis?

A

Thinning of bone and destruction of the micro architecture.

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11
Q

What have clinical trials shown regarding trying to manipulate osteoclast activity in osteporosis?

A

Huge clinical trial that pharmacologically switched off osteoclasts reduced the number of fractures compared to the placebo group

  • but no increase in bone density

However the microarchitecture was preserved.

Therefore prevention is better overall than a cure and it is never too late to intervene.

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12
Q

What does age do to bone?

A

Reduces its density and porosity esp. in women.

Bone, trabeculae thin, eventually reduction in trabeculae numbers.

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13
Q

What does the thinning of bone of age lead to?

A

Vertebral compression fractures are common as the bone can no longer bear load

This can result in kaposis (curved back) as front of vertebrae break more than back

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14
Q

When looking at bone density across a population what is it important to note?

A
  • Bone density is normally distributed and remains this way with age even though whole population at older age has lower bone density
  • Young adults / most people are not osteoporotic
  • 50 = hardly any changes
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15
Q

When looking at the bone density on a population scale what is seen at 50-90?

A
  • Ongoing bone loss
  • Females by 80, 50% will have bone densities in the osteoporotic range
  • Doesnt guarantee fracture but increases risk.
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16
Q

Describe the fracture risk of women in the us;

A
  • Colles fracture risk inc. @50-60 then plateaus
  • Spine fracture risk inc. throughout life
  • Hip osteoporotic fractures at 75+ rapidly increases in risk
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17
Q

Describe the fracture risk of men in the US

A

Hip + Spine 80+ fracture risk increases rapidly

18
Q

What is a hip fracture associated with?

A
  • loss of independence

- 20% mortality

19
Q

How many women will have an osteoportic fracture by death?

A

50%

20
Q

How do we access fracture risk?

A

Bone densitometry

Clinical Risk Factors

21
Q

What are the clinical risk features for fractures?

A

Age

Weight (low weight

22
Q

What is a major osteoporotic fracture?

A

Major osteoporotic fracture is hip fracture, clinically evident vertebral fracture, proximal humerus fracture and distal forearm fracture. This is about half of total fractures

23
Q

Does being physically active prevent fractures?

A

Mixed evidence

Reality might be that fit people are better are preventing falls.

24
Q

What do osteocytes monitor and how do they regulate osteoclasts and osteoblasts?

A

Osteocytes = Have processes to monitor degree of bone loading, then can regulate osteoclasts (RANKL - turns them on) and osteoblasts (Sclerosin-turns them off)

= ALL IN RELATION TO LOAD BEARING

25
Q

Describe the role of PTH in bone regulation;

A

PTH is secreted in response to lowered serum Ca levels and increases osteocyte secretion of RANKL

i.e it boosts Ca release form bone to increase sCa

Drugs can be used to inhibit PTH

26
Q

What does exercise do to osteocytes?

A

Inhibits Sclerosin release.

27
Q

Can an increase in dietary Ca increase bone density?

A

No Ca is homeostatically regulated such that an increase in dietary intake does not correlate with increased bone density.

28
Q

What happened to bone density when ca supplementation was given?

A

Yes at 1 year there was a 1.5% increase in bone density but this was the same at 3 years.

Thus doesnt prevent fractures nor decrease the relative risk

29
Q

What are activated Vit D levels assocated with?

A

UV exposure

30
Q

How does PTH regulate vit D activation?

A

PTH regulates Vit D (1,25 D) activation to increase ca absorption in gut

31
Q

What happens when people were given Vit D supplementation?

A

No net benefit of giving vit D supplementation in terms of spinal bone density and no significant changes in fracture risk.

32
Q

When was vit D supplementation effective?

A

When supplementing people who were deficient it increased bone density

i.e those people who dont see much sun

33
Q

What are the non-pharmacal interventions for addressing fracture risk?

A

Address risk factors for bone loss (smoking, low weight, alcohol)
Address risk factors for falls (hazards, vision, pills)
Exercise
Minimize impact (hip protectors, soft floors)

34
Q

What are the pharmacological interventions for osteoclasts?

A

Principle treatment of osteoporosis = bisphosphonates

-ve charge makes it very attracted to bone but only 4% absorption (it poisons the osteoclasts)

However injected into the bone the 50% of it remains in the bone for years as it is not metabolised.

35
Q

How could we treat osteoporosis?

A 
Ca supplements (not really)
Vit D supplements (to those deficient)
PTH inhibition
Bisphosphonates
Exercise (inhibits sclerosin release)

Denosumab (inhibits RANKL)
Cathepsin K inhibitor (inhibits osteoclasts)
Antisclerosis antibodies

36
Q

What are the conclusions of Ca supplementaiton?

A

Calcium supplements reduce bone turnover
Effects on fracture remain uncertain
Poor compliance with supplements limits their effectiveness
Calcium supplements increase risk of vascular events, stones, and GI events

37
Q

What are the implications for Ca homeostasis practise?

A

Aim for dietary calcium intake of >400 mg/day
Use interventions with proven anti-fracture efficacy if fracture prevention is the goal
Calcium supplements are NOT a safe way to promote bone health

38
Q

What are some side effects of bisphosphonates?

A

Common AEs:
Gastrointestinal
APR (acute phase reaction (ill))
IV BPs require satisfactory vitamin D and renal status

Rare AEs: 
ONJ (osteo necrosis jaw)
Sub-trochanteric fractures
AF
Oesophageal cancer
Mortality
39
Q

What does bisphosphonates do to bone density and fracture risk?

A
  • Rapid decrease in bone reabsorption
  • Dose related
  • Increase bone density

50% decrease in hip frac. risk
~50% decrease in vert. frac. risk
Not particular 20-30 reduction in no vertebral fracture risks

40
Q

How do new drugs target RANKL?

A

RANKL regulates the development of osteoclasts

Denosumab ; Directs ABs against RANKL = decreased osteoclast development

41
Q

How is TeriparatidePTH used?

A

Teriparatide PTH regulates osteoblast and osteoclast activity to stimulate bone formation.

42
Q

What does anti-sclerosin AB do?

A

Antisclerosin AB

  • Increased Bone density (best yet)
  • Decreased fractures

Medsci 312 (28 decks)

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