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MSK > 5 - Bone structure, growth and repair > Flashcards

5 - Bone structure, growth and repair Flashcards

1
Q

What do I need to know?

A
  • features of bone, types, structure
  • how primary and secondary osteons are formed
  • how bones undergo remodelling
  • how the epiphyseal plate increases the length of the bones
  • how fractures heal
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2
Q

What are the 4 essential features of bone?

A

It resists tension, pressure and torsion
Light (fresh bone feels heavy due to bone marrow)
Strong
Dynamic and can and does remodel consistently

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3
Q

How does it differ from other CTs?

A

Differs due to hydroxyapatite in the ECM that resists pressure and torsion. It is a calcium phosphate mineral that is deposited ON collagen fibrils with a crystalline structure. It is a very dense mineral so when it covers the fibrils you can’t see them

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4
Q

What are the three types of bone?

A
  1. Fine cancellous
    In fetuses and young children where the collagen fibres are arranged in a half hazard fashion in all 3 directions (woven bone)
  2. Coarse Cancellous
  3. Compact

In adults the fibrils are layed down in layers (lamellar bone)

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5
Q

Describe membrane bone?

A

Membrane bone where the bone has formed out of mesenchymal tissue (CT) and the cells take on osteogenic properties and the bone forms from NO precursor for example the flat bones of the skull

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6
Q

How are most of the bones in the body preceded with the exception of membrane bones?

A

By cartilage - this is cartilage bone. Bones are not made of cartilage and the cartilage does not turn into bone, the bone replaces the cartilage

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7
Q

How do the trabeculae in cancellous bone arrange themselves?

A

The trabeculae align themselves perpendicular to the compressive forces that arise at the compact bone at the epiphysis of the bones. The trabeculae then transmit the forces from the head of the bone to the shaft/diaphysis and distributes the forces from a wide platform in the joint onto the outside of the shaft
- they are aligned to the lines of compression in the bone

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8
Q

Describe a histological section of a slice of vertebral bone

A
  • the volume of actual cancellous bone is small relative to the volume of tissue as it is very strong and don’t need much. Increases as you go down column but not much
  • On the surface of compact bone is a fibrous layer 1/2 a dozen cell layers thick that are spaced far apart due to collagen called the periosteum
  • thinner fibrous layer with flattened cells is endosteum that lines inside of compact bone and lines
  • in COMPACT bone the larger holes are blood vessels not osteocyte lacunae
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9
Q

Mature bone cell? Primitive bone cells and where are they found?

A

Osteocytes. Osteoblasts - found mostly on the surfaces of bone in the osteogenic layers (peri/endosteum)

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10
Q

How does bone grow?

A

By appositional growth at the periosteal and endosteal surfaces

  • osteoblasts divide and the progeny closest to the bone secrete and surround themselves with new bone matrix (collagen and hydroxyapatite) adding it to the existing surface of bone
  • the cells then become osteocytes
  • those away from the bone surface remain the peri/endosteum and will divide again
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11
Q

How are osteocytes linked?

A

By cell processes passing through canaliculi which join lacunae

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12
Q

How do deeper osteocytes get their nutrients?

A

Capillary at endosteal/periosteal surface
They receive their nutrients by the cell processes as they can’t diffuse through the dense hydroxyapatite mineral
Means the deeper cells will be most deprived

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13
Q

How far can nutrients pass before the last cell becomes deprived?

A
  • 0.2mm. This means a trabeculum can be 0.4mm with a BV/endosteum on either side
  • compact bone can be several mm meaning a blood supply must be enclosed WITHIN the bone
  • bones are full of blood so when you fracture them you get a blood clot around the fractured surface
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14
Q

How do blood vessels get inside compact bone?

A

Two ways

  1. At the periosteal and endosteal(less) surface there are capillaries. As the bone grows by appositional growth the blood vessel doesn’t move and the bone grows around it (primary osteon)
  2. The blood vessels invade the channels in bone bored out by osteoclasts (secondary osteon)
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15
Q

Describe primary osteon formation

A
  1. Surface of the bone/shaft is not smooth but has ridges and grooves
  2. The periosteum over the ridges forms bone by appositional growth to make the ridges higher - then ridges then meet and fuse and the groove becomes a tunnel
  3. The periosteum of the groove now becomes the endosteum of the tunnel
  4. The endosteum is still active and the osteoblasts continue putting down bone matrix in a lamellar fashion until the tunnel closes just big enough for the blood vessel forming a Haversian System/Osteon
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16
Q

How can you see lamellae in osteons?

A

Under polarised light (light in one direction)

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17
Q

What is outer circumferential lamellae?

A

The outer and outer lamella of compact bone aren’t circular or in osteons because they are within 0.2mm of the BVs in the periosteum or endosteum

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18
Q

How do osteons get a blood supply?

A

Via BVs in the periosteum. These infiltrate through holes in the bone, through perpendicular Volkmann’s Canals and parallel Haversian Canals to the osteon.

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19
Q

How does bone remodel and repair?

A

By a combination of removing the bone from the inside (usually not always) and add it to the outside of the bone via appositional. Means the shape and proportions stay the same

20
Q

How is bone removed?

A
  • By Osteoclasts - large multinucleated cells that eat/digest at bone all the time slowly
  • The osteoclast sits in a Howships Lacunae which is a concave area that has had the bone removed
  • the osteoclast takes out mineral, canniliculi, cell processes and osteocytes
  • They release enzymes and acids with a low pH which you don’t want seeping out into tissues so you create a collar around the edge to attach to the bone that keeps these in a concentrated pool
  • this keeps the secretions at high concentration and efficiency by increasing its absorption and secretion surface area by a ruffled border (foldings)
21
Q

What is the sequence of the degradation of bone?

A
  1. Decalcification of the soluble hydroxyapatite by organic acids (carbonic, citric, lactic)
  2. Digestion of extracellular materials (collagen) by acid hydrolases (enzymes) such as cathepsins that digest EXPOSED collagen fibrils
22
Q

How to osteoblasts contribute to bone removal?

A

They prepare the surface of bone for osteoclasts by digesting the OSTEOID they put down. There is co-operation as the osteoblast is usually on the surface so has to move

23
Q

What are the two main hormones involved in the hormonal control of bone removal?

A

PTH (parathyroid hormone)

Calcitonin

24
Q

Give an example of how mechanical forces influence bone removal and repair

A

Braces - move the root of the tooth by digesting and rebuilding bone slowly.

25
Q

What does parathyroid hormone do (PTH)?

A

Increases both osteoblast and osteoclast activity resulting in decreases bone mass

26
Q

What does Calcitonin do?

A

Only decreases osteoclast activity. Reduces membrane ruffling, number of osteoclasts, movement of osteoclasts

27
Q

What are the 3 things that PTH and calcitonin act on to control osteoclast activity?

A
  1. RANK receptor on primitive osteoclasts
  2. RANKL - RANK Ligand on osteoblasts
  3. OPG (Osteoprotegerin) - this is a decoy molecule that fits over and caps the RANKL on osteoblasts. It is also released by osteoblasts so these control the whole process of remodelling

RANK + RANKL leads to differentiation of primitive osteoclast to mature osteoclast

28
Q

Why is OPG clinically significant?

A

OPG prevents bone removal so is important with the ageing population as everyone starts to lose bone (osteoporosis)

29
Q

How can you decrease PTH and so decrease bone loss?

A

Ca supplements and vitamin D can increase Serum Calcium and this will decrease Parathyroid Hormone

30
Q

What pharmacotherapy will decrease osteoclast activity?

A

Biphosphonates
Hormone Replacement Therapy (increases estrogen)
Cathepsin K inhibitors (affects the enzyme production)

31
Q

What pharmacotherapy will decrease RANKL

A

Denosumab (binds/acts like OPG)

32
Q

What does sclerostin normally do?

A

Stops osteoblasts producing bone

33
Q

What pharmacotherapy will decrease sclerostin?

A

Anti-sclerostin antibodies

Exercise

34
Q

Where can osteoclasts remove bone?

A

On flat surfaces and they can remove bone inside compact bone by drilling holes and this allows bone to remodel

35
Q

Briefly describe secondary osteon formation

A
  • osteoclasts dig down from the surface and a blood vessel follows into the cavity
  • periosteal cells (osteoblasts) also follow the invading BV and osteoclasts and become the endosteum
  • in a cross section of a secondary osteon you will normally see 2 blood vessels as it loops into the cavity and only 1 in a primary osteon
36
Q

What type of osteon is most adult bone composed of?

A

Secondary osteons as the original primary osteons have been replaced. Bone is replaced at 2% per year

37
Q

Where does growth in length occur in long bones?

A

Near the ends of the bones at the cartilaginous plates called the epiphyseal plates which stains blue
- during puberty the appositional growth like at width ins’t fast enough

38
Q

How does growth at the length of long bones occur?

A

The cells in the cartilaginous plates divide and one slips under the other forming columns. This means the cartilage plate grows upwards (and at other end of the bone) and you grow in height

39
Q

Why doesn’t the epiphyseal plate thicken as you grow?

A
  • At the other side of the plate towards the bone, the cartilage cells die after hypertrophy
  • The matrix around these cells breaks down and allows small blood vessels to invade from the bone into the dead cartilage
  • the BVs bring with them osteoblasts which start to lay down bone over the fragments of collagen left behind
40
Q

When and why do you get closure of the epiphyseal plates?

A

Until 18 the rate of growth of epiphyseal plate EQUALS the loss of cartilage
Later the rate of growth slows and rate of loss stays the same so plates get thinner until it disappears and you get closure
Leaves an epiphyseal line that is prone to fracture in youth until it remodels and strengthens

41
Q

What are the zones of the epiphyseal plate?

A 
Resting
Proliferation
Maturation
Hypertrophy
Calcification 
New Bone
42
Q

Where do the cells come from for healing of bone fractures?

A

Peri/endosteum are a source of new bone cells/osteogenic cells for healing

43
Q

How do fractures heal?

A
  1. the peri/endosteum will proliferate and act as a source of new bone cells for healing which migrate to the fracture site
  2. often bleeding/haematoma which forms a blood clot that is soft so we need support/casts
  3. at the osteoblasts move FASTER than the blood vessels they initially produce CARTILAGE this is because a osteoblast in low oxygen will act as a chondrocyte
  4. later when the BV infiltrates and oxygen increases new bone is laid down, replacing the cartilage, in a COLLAR around the fracture site called a BONE CALLUS
  5. this lumpiness around the fracture site will be remodelled as osteoclasts dig out channels and form secondary osteons to knit the bone ends together
  6. Post fracture sites are actually very strong
44
Q

When is assisted healing/external support needed in the healing of bone fractures?

A
  • metal plates and screws can help with the ALIGNMENT of the broken bone and prevents CALLUS formation as the metal rod will take its place for extra support during healing
45
Q

What is a downside to assisted healing of bone fractures?

A

The fractures are weaker when the plates and screws are removed and take longer to heal

46
Q

What is a callus?

A

A callus is bony and cartilaginous material forming a connecting bridge across a bone during fracture

MSK (29 decks)

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