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Block 4 > Bone Structure, Formation, Growth & Repair > Flashcards

Bone Structure, Formation, Growth & Repair Flashcards

1
Q

What are the constitutes of connective tissue?

A
  1. Cells: fibroblasts (secrete ECM), adipocytes, osteoblasts/osteocytes (bones), chrondroblasts/chrondrocytes (cartilage) + immune cells
  2. ECM: fibrous proteins (e.g. collagen/elastin) + ground substance (proteoglycans, glycoproteins + water) - composition determines tissues physical properties
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2
Q

What is bone?

A

A specialised type of connective tissue

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3
Q

What is the function of proteoglycans?

A

Consist of repeat dissacharide units called GAGs bound to core of protein that are hydrophilic and attract water so tissue can resist compressive forces

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4
Q

What is the function of glycoproteins?

A

Allows cells to adhere to underlying ECM

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5
Q

What are the 2 main features of bone and what gives it these properties?

A

Need a BALANCE of:

  1. Rigidity: deals with force via mineralised ECM (hydroxyapatite)
  2. Resilience: absorb energy from impact, change slightly then return to original form via type I collagen fibres
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6
Q

What are the functions of bone?

A 
Movement
Mineral homeostasis
Support
Protection
Site of haematopoiesis
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7
Q

What is periosteum?

A

Non-calcified dense irregular connective tissue layer covering bone helping bones to grow in thickness (as it contains osteoprogenitor cells and osteoblasts), protects bone, assists fracture repair, helps nourish bone tissue and is attachment point for tendons and ligaments

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8
Q

What are the 2 layers of periosteum?

A
  1. Outer fibrous layer

2. Inner cellular layer

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9
Q

What are the 2 different microscopic types of bone?

A
  1. Woven: immature primary weak bone formed at any site during development (also sites of fracture healing) where collage fibres are arranged randomly and quickly
  2. Lamellar: mature bone formed by remodelling of collagen fibres from woven bone into an orderly arrangement increasing strength
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10
Q

What are the 2 different types of lamellar bone structure?

A

Need a BALANCE of:

  1. Cortical: dense, strong and heavy giving rigidity
  2. Trabecular/spongy bone: less dense with holes like a sponge giving resilience
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11
Q

What are the different types of cortical (compact) bone?

A
  1. Outer circumferential lamellae
  2. Haversian systems (osteons)
  3. Interstitial lamellae (result of bone remodelling + formation of new Haversian systems)
  4. Inner circumferential lamellae
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12
Q

Define lamellae.

A

Bony plates made up of irregularly arranged collagen fibres in parallel

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13
Q

What are Haversian systems (osteons)?

A

Concentric lamellae around a central Haversian canal which contains blood vessels, lymphatic vessels and nerves

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14
Q

What is the function of Volkmann’s canals?

A

Run transversely or obliquely to Haversian canals allowing communication between Harversian canals, periosteum, the marrow cavity and itself

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15
Q

What is trabecular/cancellous/spongy bone?

A

3D network of beams and struts of lamellar bone orientated along lines of stress (more likely to be remodelled in stress) making up large areas of interconnecting marrow spaces for haematopoiesis

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16
Q

Why do bones need a good vascular supply? Why is this clinically relevant?

A

Because a lot of remodelling occurs regularly - fractures can break blood vessels causing bleed and access can be gained to these vessels to give drugs in emergencies

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17
Q

What types of arteries supply bone?

A

Epiphyseal
Metaphyseal
Periosteal
Nutrient

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18
Q

How are bone cells formed?

A

From mesenchymal stem cells which form osteoprogenitor cells which become osteoblasts then osteocytes

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19
Q

What do osteoblasts do?

A

Line the surface of bones synthesizing and secreting organic bone matrix (osteoid)/ECM which is subsequently mineralised outside of the cell - once surrounded by matrix they become OSTEOCYTES

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20
Q

What does osteoid contain?

A 
Type I collagen 
Proteoglycans
Glycoproteins
ALK P (forms hydroxyapatite)
Osteocalcin (Ca2+ binding)
Osteopontin
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21
Q

What are periosteal cells?

A

Resting osteoclasts lining bone with important role in fracture healing

22
Q

What are osteocytes?

A

Mature bone cells (do not divide) occupying lacunae and surrounded by bone matrix - their dendritic processes pass through canaliculi which radiate from lacunae and anastamose with those from other lacunae where gap junctions allow transfer of ions and nutrients so there main functions are matrix maintenance/Ca2+ homeostasis and mechanotransduction (detection of force/stress + laying down of new bone in response)

23
Q

What are osteoclasts?

A

Large multinucleated cells with ruffled border derived from monocyte-macrophage system (haemtopoietic origin) that function in resorption of bone matrix via synthesis and secretion of enzymes and acid (form Howship’s lacunae) but also, remodelling, growth and repair

24
Q

What is bone remodelling?

A

Continual process throughout life in response to changing mechanical stress or microfractures of bone whereby there is coupling and balance of bone resorption (osteoclasts) and formation (osteoblasts)

25
Q

How is bone remodelled?

A
  1. Osteoclasts form cone-shaped tunnels into compact bone (Howship’s lacunae)
  2. Tunnel is invaded by blood vessels, osteoblasts + osteoprogenitor cells
  3. Osteoblasts lay down new bone in concentric lamellae around blood vessels forming new Haversian systems closing the cone
26
Q

How is bone remodelling regulated?

A

Osteoblasts secrete:

  1. RANKL which binds to RANK receptor on osteoclasts activating bone resorption
  2. OPG is a non-signalling decoy receptor of RANKL mopping it up and decreasing bone resorption

RANKL:OPG important in determining degree of resorption along with cytokines, hormones + drugs

27
Q

What hormone favours bone formation?

A

Oestrogen via increasing OPG levels

28
Q

What hormones favour bone resorption?

A

Calcitriol + PTH via stimulation of osteoblasts to release RANKL which acts on RANK receptor on osteoclasts to activate bone resorption

29
Q

What are the 2 ways in which bones can develop?

A
  1. Intramembranous ossification: direct replacement of mesenchyme by bone tissue with NO cartilage precursor (e.g. flat skull bones, clavicle + mandible)
  2. Endochrondral ossification: bone develops from mesenchyme but with a cartilage precursor in weight-bearing bones (e.g. long bones, vertebrae + pelvis)
30
Q

What are the steps of intramembranous ossification?

A
  1. Primary ossification centre: mesenchyme membrane differentiates directly into osteoprogenitor cells then osteoblasts then osteocytes
  2. Osteoblast secrete osteoid which is then calcified
  3. Blood vessels invade and trabecula of woven bone is formed whilst mesenchyme condenses to form fibrous periosteum
  4. Bone collar is formed (compact bone) and spongy bone cavities (diploe) now contain red marrow
31
Q

What are the steps of endochrondral ossification of the diaphysis?

A

Primary (diaphyseal) ossification centre:

  1. Mesenchyme develops into chondroblasts which form a mini hyaline cartilage model
  2. Cartilage cells in centre of diaphysis hypertrophy die and become calcified leaving large open spaces in cartilage (future marrow cavity)
  3. Osteoblasts secrete matrix and form subperiosteal bony collar around edge of diaphysis
  4. Vascularisation of perichondrium transforms it to periosteum
  5. Blood vessels invade cartilage model with osteoprogenitor cells which differentiate into osteoblasts
  6. Osteoblasts secrete bone matrix on surface of calcified cartilage scaffold
32
Q

How does endochondral ossification occur in the epiphysis?

A

Similar process forming secondary ossification centres but there is no bony collar and bone is not laid down at articular surface or epiphyseal plate

33
Q

When do different ossification centres appear?

A
  1. Primary ossification centres in diaphysis develop in foetal life (14 weeks)
  2. Secondary ossification centres in epiphyses develop after birth in an ordered way related to age (X-rays can determine if a child’s skeleton is developing appropriately with age as a result)
34
Q

What are the 2 different types of bone growth?

A
  1. Longitudinal: at epiphyseal growth plate of weight bearing long bones where there is proliferation of cartilage cells followed by endochondral ossification
  2. Appositional: growth in width where new bone is formed under periosteum
35
Q

What are the different zones of the epiphyseal growth plate?

A
  1. Resting (quiescent): cartilage cells resting + ready to be used
  2. Growth (proliferation): cartilage cells proliferate under influence of ILGF produced by hepatocytes in response to GH (epiphyseal aspect)
  3. Hypertrophic: chrondocytes stacked in columns like coins, mature + hypertrophy
  4. Calcification: hypertrophied chrondrocytes die + cartilage matrix is calcified which is removed by osteoclasts
  5. Ossification (osteogenic): osteoblasts form new bone (diaphyseal aspect) and epiphyseal growth plate closes
36
Q

When does the epiphyseal growth plate close? What can be left in its place?

A

18-25 years when rate of proliferation zone decreases and ossification zone overtake other zones - may be marked by an epiphyseal line where the marrow cavity of the epiphysis and diaphysis have joined up = no growth in length is possible at this point

37
Q

What is growth plate activity and closure influenced by?

A

A range of hormones e.g. GH and oestrogen

38
Q

Why does the thickness of growth plates remain the same?

A

The rate of proliferation of cartilage cells is the same as the rate of new bone production at the opposite end of the growth plate

39
Q

What is the clinical significance on growth plates?

A

Weak point particularly if subject to shearing forces which can cause:

  • Salter-Harris fractures of growth plates causing deformities in developing bone (e.g. shortening/angulation)
  • Disorders of bone mineralisation (e.g. Rickets can affect size/shape of growth plates)
40
Q

What is a fracture?

A

Breach in the integrity of part OR the whole of a bone

41
Q

What are the stages of fracture healing for long bone?

A
  1. Haematoma
  2. Granulation tissue
  3. Callus
  4. Woven bone
  5. Lamellar bone
  6. Remodelling
42
Q

What is the difference in fracture healing of other bones?

A

Bones with more trabecular bone have a better blood supply so there is usually less necrosis and callus formation

43
Q

What occurs in the haematoma stage of fracture healing?

A

Rupture of vessels in region of fracture site forming a haematoma so there is necrosis of bone fragments - this initiates an inflammatory reaction where phagocytes migrate to the area to remove necrotic tissue

44
Q

What occurs in the granulation tissue stage of fracture healing?

A

Blood clot is invaded by small capillaries and fibroblasts from surrounding connective tissue to form granulation tissue - cytokines, signalling molecules and GFs induce subperiosteal/endosteal cellular proliferation as they attract cells to the site

45
Q

What occurs in the callus stage of fracture healing?

A

Bridge formed between fractured bone ends to form a soft fibrocartilaginous callous made up of fibrous tissue, inflammatory cells and cartilage

46
Q

What occurs in the woven bone stage of fracture healing?

A

Osteoprogenitor cells proliferate and differentiate into osteoblasts to form woven bone which strengthens the callus giving it rigidity forming a bony callus - when it is sufficiently firm that movement no longer takes place at fracture site it is clinically united

47
Q

What occurs in the lamellar bone stage of fracture healing?

A

Osteoclasts remove woven bone and osteoblasts gradually replace it with lamellar bone although its laid down quick so it is not that strong

48
Q

What occurs in the remodelling stage of fracture healing?

A

Osteoclasts and osteoblasts remodel lamellar bone in response to stresses and excessive callus is reabsorbed also re-establishing the marrow cavity

49
Q

What factors aid fracture healing?

A

Stability of fracture (can be clinically enhanced by fixations)

Apposition of bone ends (dont want foreign material/tissue between bone ends - want bones to be as close as possible)

Adequate blood supply

50
Q

What factors delay fracture healing?

A

Excessive movement of bone ends
Poor blood supply
Infection
Foreign bodies

51
Q

What can happen if fracture healing goes wrong?

A
  1. Malunion: healing in unsatisfactory position
  2. Delayed union: takes longer than expect to unite
  3. Non-union: can lead to fibrous union of pseudoarthrosis (fake joint)

Block 4 (33 decks)

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