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204-theme 2 -anatomy > L12: The Physiology of Bone > Flashcards

L12: The Physiology of Bone Flashcards

1
Q

what are the 2 opposing processes occurring in bone and how can they cause disease

A

Bone-resorption- Imbalance this side leads to
Osteoporosis
Osteopenia, Rickets

Bone formation: Imbalance this side
Osteopetrosis

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2
Q

how do you classify bone structure

A

Classifications:
long bone
short bone

Macroscopic:
-Cortical Bone
-Cancellous (spongy)
Spicules, trabeculae

Microscopic

  • Lamellar
  • Wover
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3
Q

what is bone composed off

A

1-Osteoclasts

-Extracellular
Matrix
(osteoid)

2-Osteocytes

3-osteoblasts

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4
Q

what are the functions of the 3 principle cells

A

osteoblasts – on surface bone, produce protein component acellular matrix – regulate bone growth and degradation

osteocytes – quiescent mature cells embedded in bone matrix. They maintain bone.

osteoclasts – responsible for bone degradation and remodelling

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5
Q

describe the difference between organic and inorganic bone material

A

Organic – cells and proteins
Inorganic – minerals, eg Ca2+ & PO4- (hydroxyapatite)

bone dominated by extracellular matrix – few cells

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6
Q

what is the Haversian system in lamellar bone

A

one type of microscopic organisation of bone tissue (the other is woven bone)

look at slide 8

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7
Q

describe how osteocytes arrive from osteoblasts

A

From mesenchyme:
-From precursor cells in bone marrow stroma

Osteoblasts are post-mitotic:

  • Most osteoblasts will undergo apoptosis
  • Number of osteoblasts  with age

A low % of osteoblasts will become osteocytes locked in lacuna

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8
Q

describe the function and features of Osteoclasts

A

Function: Resorption
Multinucleate
40-100 micrometer in diameter.
(large )

Same precursor as monocytes (haematopoietic stem)

Phagocytose (bone matrix & crystals)

Secrete Acids

Secrete proteolytic enzymes from lysosomes

ruffled border = where bone resorption occurs

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9
Q

what is the ruffle border

A

= a specialized part of osteoclast cell membrane that touches the surface of the bone tissue at a site of active bone resorption. It facilitates the removal of the bony matrix by increasing surface area interface for bone resorption. It is a sign that resorption is actively taking place

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10
Q

3 characteristics of bone

A
  • Extracellular matrix is 70% minerals
  • Plus abundant proteins and sparse cells
  • High compressive strength and tensile strength
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11
Q

what are the acellular elements of bone

A

collagen fibres – protein, flexible but strong

hydroxyapatite – mineral, provides rigidity-calcium/phosphate crystals > 50 %

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12
Q

describe glycosaminoglycans

A
  • long polysaccharides
  • Highly negative
  • Attract Water
  • Repel each other
  • Resists compression

Abundant in Cartilage

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13
Q

what are the growth factors effects on bone

A

They are revealed by osteoclast action

Which leads to proliferation & mineralisation

bone remodelling = bone turnover = the activation-resorption-formation sequence

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14
Q

How is bone remodelled

A

Osteoclasts resorb bone in Howships lacuna

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15
Q

Describe the bone remodel model

A

Osteoclasts (controlled by the signalling of osteoblasts), resorb bone in Howships lacuna

The osteoblasts deposit the bone onto pre-existing bone and does so forming osteons in different directions .

In adult life osteoblasts bring about bone deposition as part of remodelling and they secrete bone matrix directly onto pre-existing bone

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16
Q

what occurs in the active resorption remineralisation sequence of bone

A

Surface osteoblasts control activation-resorption-mineralisation, because they detect the mechanical factors (stresses on that bone) and hormonal factors (from elsewhere in the body) that initially trigger bone remodelling.

They do this via IL-6 and other cytokines into the osteoclast which causes them to be activated (causing bone-resorption)

They signal back via liberated matrix bound growth factors

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17
Q

How can bone be formed

A

bone forms either as compact or cancellous and by either intramembranous or endochondral bone formation –

18
Q

what is endochondral bone ossification

A

Endochondral ossification = bone formation based on a cartilage model. Chondrocytes proliferate and secrete extracellular matrix and proteoglycans. Osteoblasts (derived from osteoprogenitor cells) arrive and then osteoid is laid down and mineralisation begins. Precise modelling of the final bone is done by osteoclasts.

19
Q

what occurs in intramembranous ossification

A

Intramembranous ossification = bone formation without a cartilage model. Osteoblasts (derived from osteoprogenitor cells) lay down osteoid and begin mineralisation, forming tiny bony spicules. Nearby spicules join together into trabeculae (woven bone).

20
Q

what are the factors governing remodelling

A

1-Recurrent mechanical stress

2- calcium homeostasis
-Plasma calcium is essential in maintaining structural integrity of skeleton

21
Q

what are the effects of mechanical stress on the bone

A

1-inhibits bone resorption and promotes deposition (surface osteoblast and osteocyte network detect stresses)

2- without weight bearing bone rapidly weakens -(skeleton reflects forces acting on it )

3- eg, bed rest , lack of gravity

22
Q

what are the role of bisphosphonates in bone remodelling

A

For osteoporosis

E.g. Alendronate

inhibit osteoclast-mediated bone-resorption

the endogenous regulator of bone turnover
Accumulate on bone & ingested by osteoclasts
Interfere with osteoclasts metabolism

23
Q

describe the drugs used for osteoporosis treatment

A

Encourage osteoblast formation of bone:

  • Teriparatide
  • portion of human parathyroid hormone (PTH)
  • Intermittent application activates osteoblasts more than osteoclasts

Prevent osteoclast maturation:

  • Denosumab
  • -Monoclonal Antibody that targets RANKL
24
Q

Describe the process of osteopetrosis

A

Molecular Mechanism
Osteoclasts cannot remodel bone

Defective Vacuolar proton pump or

Defective Chloride channel

Excess bone growth
Bone growths at foramina press on nerves

Brittle (dense) bones
Blindness
Deafness
Severe anaemia

25
Q

what are the secondary effects of excess bone growth

A

Brittle (dense) bones
Blindness
Deafness
Severe anaemia

26
Q

osteoclasts secrete acid

A

enables them to destroy bone. without the chloride channel this cant occur

27
Q

describe phases 1 and 2 of fracture healing

A

1)Reactive Phase: Haematoma & Inflammation:

-Blood cells enter wound
-Haematoma forms
-Inflammatory cells invade
-Granulation tissue formed:
Aggregation of
Blood vessels &
Fibroblasts

Bone Precursor cells arrive
from Periosteum

2) Soft callus formation:
Woven bone (or hyaline cartilage) join the pieces

Woven bone near BVs

Fibrocartilage further away

28
Q

what are the Phases of Fracture Healing: Stages 3 & 4

A

1) Hard callus formation:
- Lamellar bone replaces woven bone

2) Trabecular bone replaces (endochon.) lamellar bone

Original bone shape

Compact bone formed where appropriate

29
Q

what are the Hormones of calcium regulation

A

1) PTH – parathryoid hormone, parathormone
- Parathyroid chief cells
- Increases plasma Ca2+

2) Vitamin D: 1,25-di-OH cholecalciferol (calcitriol)
- Made in stages: Skin  Liver =Kidney
- Increases plasma Ca2+

3) Calcitonin
- Made by thyroid C cells
- “tones down” blood calcium
- –Calcium goes into bone
- –Used as a treatment for osteoporosis

30
Q

how does PTH stimulate resorption via osteoblasts

A

It does this via :

  • binding to PTH receptor on osteoblast , activating it, releases RANK Ligand
  • this binds onto the RANK of an osteoclast precursor cell,
  • causes it to differentiate into an activated osteoclast which can now perform bone resorption
31
Q

describe how PTH release can cause different effects

A

PTH applied continuously results in bone loss via increased osteoclast activity, but intermittent PTH results in increased osteoblast number and osteoblast mineralisation activity in osteoporosis; the net effect of intermittent PTH is bone strengthening.

32
Q

Describe Vitamin D production and activation

A

SKin- Choleciferol (D3) is hydroxylised in the liver forming 25-oh-cholecalciferol.

This once it goes through the kidneys are transformed into 1,25-di-OH cholecalciferol (calcitrioil)

  • this leads to increased levels of calbindin in the gut enterocytes
  • this increases intestinal absorption of ca2+ and in the kidneys too

this leads to an overall increase in plasma ca2+

33
Q

what are the overall effects of vitamin d in the body

A

Increases intestinal Ca2+ absorption
Increases calbindin

Stimulates kidneys to reabsorb calcium

stimulates osteoclasts indirectly
via osteoblasts
This is a comparatively weak effect

Vitamin D facilitates bone remodelling and thus increases serum Ca2+

34
Q

how does vitamin D stimulate osteoclasts

A

stimulates osteoclasts indirectly via osteoblasts.
osteoblast is principle target of vitamin D
stimulates osteoblasts to produce cytokines that accelerate maturation of osteoclasts thus facilitating bone remodelling
Thus, vitamin D remodels bone and increases serum Ca2+

35
Q

What are the causes of low plasma calcium

A

Loss:

  • Pregnancy
  • Lactation
  • Kidney dysfunction

Low Intake:

  • Insufficient ingestion of Calcium
  • Rickets (low vit D)

Parathyroid dysfunction

36
Q

what are the effects of chronic hypocalcaemia

A

Skeletal deformities

Increased tendency toward bone fractures

Impaired growth

Short stature (adults less than 5 feet tall)

Dental deformities

37
Q

what are the effects of acute hypocalcaemia

A

Excitability

B – Bleeding
A – Anaesthesia
D – Dysphagia 
C – Convulsions
A – Arrhythmias
T – Tetany
S – Spasms and stridor

BADCATS-mneumonic

38
Q

what are the signs that we can test for acute hypocalcaemia

A

Chvostek’s sign = Tapping masseter leads to twitch on same side of face

Trousseau’s sign /Carpopedal spasm = Trousseau’s sign = Hand spasm after 3 minutes with blood pressure cuff in place (above systolic pressure)

DI-George syndrome: rare (1:4000) genetic anomaly caused by the absence of the long arm of one of the two 22nd chromosomes. The resulting developmental anomaly presents in many different ways, but typically there are issues with the mediastinum that lead to an absent thymus (poor T cell function) and underdeveloped parathyroid glands

39
Q

why does low plasma calcium lead to excitability

A

Hypocalcaemia makes membranes “more excitable” and “less stable”
Sodium is more able to leak through it
Explains latent tetany and its signs

40
Q

does hypercalcaemia cause excitability

A

Hypercalcaemia paradoxically reduces excitability

By making membranes more stable

41
Q

what are the signs and symptoms of hypercalcaemia

A

Can be asymptomatic

Reduced excitability
Esp. –Constipation
-Depression + other psychiatric

Abnormal heart rhythms:

  • Short QT interval,
  • ST segment gone
  • Widened T wave

Severe hypercalcemia

  • Coma
  • Cardiac arrest

204-theme 2 -anatomy (15 decks)

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