Bone structure, growth and Repair Flashcards

1
Q

Bone remodelling is done by which cell type?

A

Osteoclasts

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2
Q

Howships lacunae are?

A

Depressions in which osteoclasts are active

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3
Q

What do osteoclasts secrete and what does this secretion do? What is this process called?

A

1) Acids - digest hydroxyapitite
2) Enzymes - digest collagen

‘Decalcification’

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4
Q

Focal decalcification

A

Done by organic acids

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5
Q

Extracellular digestion

A

by acid hydrolysis

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6
Q

Calcitonin

A

Produced by C-cells in the thyroid. A hormone that causes a DECREASE in osteoclast activity, number, movement and a decrease in membrane ruffling (so a lower SA for secretion).
Bone mass increases

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7
Q

Parathyroid Hormone (PTH)

A

From the parathyroid in the neck. A hormone that INCREASES osteoblast/clast activity.

Bone mass DECREASES

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8
Q

“______ can remove bone at flat surfaces”

A

Osteoclasts

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9
Q

What are the three molecules that control osteoclast activity?

A

RANK (on primitive osteoclast)
RANKL (on osteoblast)
Osteoprotegerin (OTP)

OTP is a decoy molecule that stops bone reabsorbtion by ‘capping’ RANKL and stopping RANK from binding

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10
Q

Formation of a Secondary Osteon

A

1) Osteoclasts drill through bone
2) Blood vessel develops and loops into the hole
3) Osteoblasts from periosteum crawl out and line the hole
4) these osteoblasts grow the hole inwards to the capillaries

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11
Q

Adult bone is comprised manly of which type of osteon

A

Secondary osteon, as the original primary osteons have been replaced

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12
Q

At what rate is bone replaced per year?

A

2%

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13
Q

Where does growth occur often in long bones?

A

The epiphyseal plates

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14
Q

what are the sites of epiphyseal growth?

A

resting cartilage/proliferation/maturation/hypertrophy/calcification/newbone

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15
Q

How do the epiphyseal plate eventually stop growing?

A

The rate of cartilage growth is surpassed by the rate of bone formation, the plate fuses and epiphyseal line is left

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16
Q

Steps of healing bone fractures

A

1) Hematoma (blood clot) forms,
2) Periosteum moves in and covers blood clot
3) Capillaries lag so the O2 levels are low and cells around this degenrate into chondrocytes
3) Eventually cappilaries invade, chondrocytes to osteoblasts
4) new bone is laid in a collar around the fracture site, called a ‘bone callous’
5) eventually this callous is broken down by osteoclasts, and secondary osteons invade

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17
Q

why is there blood/blood clots after a fracture

A

Because there is a blood vessel in every osteon.

18
Q

What allows bone to resist tension?

A

Collagen fibres

19
Q

What allows bone to resist torsion and compression?

A

Hydroxyapitite

20
Q

What Extracellular materials are in bone?

A
Collagen fibres - resist tension
Decorin (PG) - aligns collagen fibres
Osteonectin (glycoprotein)
tissue fluid (little bit)
Hydroxyapitite
21
Q

What cells are in bone

A

Osteoblast

osteocytes

22
Q

What are the types of bones?

A

Fine Cancellous- fetal, seen via microscope
Coarse cancellous - adult
Compact Bone - solid bone

23
Q

Fine Cancellous?

A

Membrane bone (by intramembranous ossification)
- flat bones of skull. NOT preceded by cartilage, form fibrous sheets
Cartilage Bone (by endochondral ossification)
-all other bones in body. Trabeculare have core of cartilage surrounded by woven bone

24
Q

The trabeculae arrangement in Long bone

A

Arranged so the force on the head of the bone is directed down the shaft of the bone and to the surface, dispersing some of the force.

25
Q

Trabeculae arrangement in general

A

Thicker trabecaulae have a common alignment and are supported by smaller trabeculae at right angles to it

26
Q

Appositional Growth

A

Bone grows on the osteogenic surfaces.
Osteoblasts secrete CF and hydroxyapitite that seeds onto bone.
osteoblasts divide, daughter cell closest to the bone buries itself in matrix to become an osteocyte
Remaining daughter cell will maintain the Osteogenic layer and later divide again.

27
Q

What is something that protects the osteoblasts

A

A layer of unmineralised matrix surrounding the osteoblast, giving it ‘wiggle room’. This has CF but NO hydroxyapitite. This is arround osteocytes also

28
Q

What is an osteocyte process for and what does it lie in?

A

To deliver nutrients and remove waste from osteocytes. They lie in canniculi

29
Q

Why is the size of bone limited?

A

As each cell passes on nutrients whilst taking what it needs, there comes a point where not enough will be passed on = deprivation of the cell. The max width in which this will not occur in 0.2mm

30
Q

Max size of trabueculae

A

0.4mm as can only get nutrients from the peri/endosteum.

31
Q

Max thickness of compact bone

A

Much larger, due to the presense of blood vessels enclosed within the bone. On each side there is also a clear zone of vessels as the peri/endosteum can supply instead.

32
Q

What are the two ways to get a blood vessel into a bone?

A

1) Primary osteon - grows around blood vessel lying on surface
2) Secondary osteon - burrows hole by osteoclasts and vessel follows.

33
Q

Which form of osteon is more common in adults

A

Secondary as bone has stopped growing so much

34
Q

What are interstitual lamellae?

A

Bit of leftover bone from old osteons that are left from the formation of secondary osteons. they will eventually be burrowed out.

35
Q

What happens when RANK binds with RANKL

A

It acts as a signal to the primitive osteoclast to differenciate in to an active osteoclast

36
Q

High RANK, RANKL and low OPG

A

more bone reabsorbtion (bad for elderly)

37
Q

Low RANK, RANKL and high OPG

A

less bone reabsorbtion

38
Q

What experiment showed that growth didn’t occur centrally in long bones?

A

Man put two holes in the centre of a chicken leg.

39
Q

What experiment discovered epiphyseal plates?

A

Man feed his pigs beetroot, stained plates red

40
Q

How could you avoid a bony calous and whats the disadvantage of this?

A

A screw and plates. Disadvantage is that this bone is weaker without the callous, more likely to fracture again