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Locomotor > Bone Function, Structure and Development > Flashcards

Bone Function, Structure and Development Flashcards

1
Q

What is bone?

A

A mineralized collagen-rich matrix which is very rigid and strong while still retaining some degree of flexibility

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2
Q

What are the properties of bone that enables its function?

A
  • Resistance to compression: inorganic content

- Resistance to tension: organic matrix

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3
Q

What are the functions of bone?

A
  • Houses bone marrow
  • Calcium homeostasis
  • Protects vital organs
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4
Q

What are the different types of bone cells?

A
  • Osteoblasts
  • Osteocytes’
  • Bone lining cells
  • Osteoclasts
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5
Q

What is the bone structure?

A
  • Bone matrix/ mineralisation
  • Bone remodelling
  • Bone development: intramembranous, endochondral
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6
Q

What are the different parts of long bone anatomy?

A 
Top to bottom:
-Epiphysis
-Metaphysis
-Diaphysis
(symmetrical)
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7
Q

What is the Epiphyseal Growth Plate?

A
  • Specialised zone of cartilage
  • Lies between epiphysis and metaphysis
  • Site of longitudinal growth
  • ‘Closes’ at/ after puberty
  • Long bone growth stops
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8
Q

Describe the macroscopic organisation of bone

A
  • Cortical (70%)= compact

- Trabecular (30%)= cancellous, medullary, spongy bone

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9
Q

What type of bone is each part of long bone made of (macroscopic organisation)?

A
  • Proportion of cortical/ cancellous bone varies in different parts and types of bone
  • Mid bone/ diaphysis= most cortical, little cancellous bone
  • End of bone/ epiphysis= predominantly cancellous bone
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10
Q

Describe compact/ cortical bone

A
  • Provides most structural support

- Resists bending and torsion stresses (thicker in mid part of bone)

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11
Q

Describe the microscopic structure of cortical bone

A 
Osteons/ Haversian canals
-Main structural unit of cortical bone
-Bone cylinders 2-3mm long
-8-15 concentric lamellae 0.2mm wide
-Axis parallel to long axis of bone
-Central cavity with blood vessels and nerve
Volkmann's canals
-Carry blood vessels from periosteum to Haversian system
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12
Q

Describe the microscopic structure of cancellous/ trabecular/ spongy bone

A
  • Found inside cortices
  • Forms interconnecting network of plates/ trabeculae
  • Provides large surface area for metabolic functions
  • Marrow space between bone trabeculae
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13
Q

Describe cancellous/ trabecular bone

A
  • Provides strength without disadvantage of weight
  • Organisation of trabecular plates is purposeful
  • Arranged along lines of maximum mechanical stress (allows transmission of loads, support areas of maximum stress)
  • More metabolically active than cortical bone (larger surface area)
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14
Q

What are mechanical loads transmitted through?

A

Hip joint to the trabecular bone of the femoral head towards the femoral cortical bone

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15
Q

Describe the composition of bone

A
  • Organic 35% (osteoid)= Type 1 collagen, non collagenous proteins
  • Inorganic 65%= calcium hydroxyapatite
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16
Q

What is osteoid?

A
  • Unmineralised bone matrix= produced by osteoblasts
  • Type 1 collagen (90%)
  • Non collagenous proteins= osteocalcin (marker of bone formation), osteonectin, osteopontin, growth factors
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17
Q

Describe the microscopic organisation of bone matrix

A

Lamellar bone
-Type 1 collagen fibres laid down in parallel sheets/ lamellae
-Structurally very strong
Woven bone
-Collagen fibres randomly arranged
-Mechanically weak
-Formed when bone is being produced rapidly e.g. foetus or fracture

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18
Q

Describe what each bone cell types do

A
  • Osteoblasts= bone-forming cells
  • Osteocytes= a mature osteoblast surrounded by bone matrix
  • Osteoclasts= function in resorption and degradation of existing bone
  • Osteoprogenitor cells= osteoblast precursors
19
Q

How are osteoblasts created?

A
  • Derived from osteoprogenitor cells
  • Formation and proliferation of preosteoblast cells from stem cells requires signalling through the Wnt-frizzled-Lrp5-beta-catenin signalling pathway
  • Osteoblast differentiation is controlled by the transcription factors Runx2 and osterix
  • In the absence of either Runx2 or osterix, no osteoblasts are formed
  • Mesenchymal to bipotential to preosteoblast to osteoblast
20
Q

What are the functions of osteoblasts?

A
  • Produce and deposit osteoid
  • Regulate osteoclast differentiation/ function= RANKL-RANK interactions
  • RANKL= Receptor Activator of Nuclear Factor K B ligand
21
Q

What is the fate of the osteoblast?

A

Life span 6 months

  • Osteoid production
  • 10-15% entombed in bone- differentiate into osteocytes
  • Others die by apoptosis or differentiate into lining cells on quiescent bone
22
Q

What are osteocytes?

A
  • Most common cell in bone
  • Reside in lacunae in cortical and trabecular bone (connect to other osteocytes, osteoblasts and osteoclasts via long cytoplasmic processes)
23
Q

What are the functions of osteocytes?

A 
Regulation of bone remodelling
Calcium homeostasis (responds to increasing PTH levels by inducing rapid calcium release= osteocytic osteolysis)
24
Q

What happens in regulation of bone remodelling?

A
  • In response to local (biomechanical) or systemic e.g. parathyroid hormone (PTH) signals
  • Increases osteoclast formation by increased expression of RANKL = bone resorption
  • Inhibits osteoblast formation by production of Sclerostin= decreased bone formation (Sclerostin production inhibited by PTH and mechanical loading= increased bone formation)
25
Q

What are osteoclasts?

A
  • Monocyte/ macrophage derived multinucleate giant cells
  • Formation regulated by growth factors and interactions between RANK (expressed by osteoclast lineage) and RANKL expressed by stromal cells/ osteoblasts/ osteocytes
26
Q

Describe RANK-RANKL interactions

A

M-CSF and TNF produced by stromal cells induces expression of RANK by osteoclast precursors

  • induce precursor cell fusion and increase osteoclast activity
  • Regulated by Osteoprotegerin (OPG) a decoy receptor that binds RANKL and inhibits osteoclast formation preventing excessive bone resorption
  • OPG secreted by osteoblasts and stromal cells
27
Q

What are the actions of osteoclasts?

A
  • Bind to mineralised bone surface (integrins)
  • Resorb bone by production of: acid to release calcium, proteases to breakdown organic matrix
  • By-products of bone breakdown and osteoclast enzymatic activity are used as markers of bone resorption: detected in blood or urine, Type 1 collagen fragments (N- and C- terminal cross-linked telopeptides), Tartrate-resistant acid phosphatase (expressed by osteoclasts)
28
Q

What are the mechanisms of bone formation and skeletal development?

A
  • Intramembranous ossification= osteoid laid down by osteoblasts within loose fibroconnective tissue of a fibrous membrane
  • Endochondral ossification= osteoid deposited on cartilage scaffolds
29
Q

Describe intramembranous ossification

A
  • Formation of skull, maxilla parts of clavicle/ mandible
  • Subperiosteal bone growth
  • Fracture repair
30
Q

Describe the process of Intramembranous Ossification

A

A: Mesenchymal stem cell proliferation in fibrous tissue, Formation of cluster/ nodule
B: Differentiation into osteoblasts- formation of ossification centre, Production of osteoid (woven)
C: Mineralisation of matrix (osteoid), Osteoblasts embedded in matrix- osteocytes
D: Blood vessels become entrapped/ grow in, Bone remodelled into lamellar trabecular bone

31
Q

Describe the process of Endochondral Ossification

A
  • Osteoid deposited on preformed cartilage: development of most of the skeleton, growth plates, fracture repair
  • Programmed changes in chondrocyte: hypertrophy, matrix vesicles, type X collagen secretion, chondrocyte death
32
Q

What are the primary centres of ossification?

A

Genetically predetermined sites and times of ossification in diaphysis of cartilage bones in utero

33
Q

How are the primary centres of ossifications created?

A
  • Hyaline Cartilage ‘Model’
  • Periosteum forms
  • Formation of a bony collar
  • Chondrocyte hypertrophy
  • Matrix calcification
  • Osteoprogenitor and blood vessel ingrowth
  • Primary centre of ossification
34
Q

How are secondary centres of ossification formed?

A
  • Ossification in epiphysis at or after birth
  • Similar process to that of primary centre formation
  • Line of cartilage between primary and secondary centres= epiphyseal growth plate
35
Q

How does the epiphyseal growth plate work?

A

-Site of continued enchochondral ossification during growth
Longitudinal growth:
-Regulated by complex networks of nutritional, cellular, paracrine, and endocrine factors (including growth hormones, IGF-1, thyroid hormone, glucocorticoids, androgens and oestrogens)
-Rapid growth occurs at puberty and when there is plentiful nutrition

36
Q

Describe longitudinal bone growth

A
  • The cartilage model grows in length by continuous proliferation of chondrocytes
  • Chondrocytes differentiate and hypertrophy
  • Cartilage matrix calcifies
  • Blood vessels/ chondroclasts invade and remove calcified cartilage
  • Osteoblasts deposit bone on residual cartilage struts
37
Q

What are the zones of the epiphyseal growth plate?

A
  • Resting Zone= normal chondrocytes
  • Proliferative Zone= chondrocytes proliferate, form stacks
  • Hypertrophic Zone= chondrocytes enlarge, secrete alkaline phosphatase, Type X collagen
  • Calcification Zone= chondrocytes die, matrix becomes calcified
  • Ossification Zone= osteoprogenitor cells and blood vessels invade calcified cartilage, new bone laid down
  • Remodelling Zone= struts if cartilage with bone remodelled into trabecular bone
38
Q

Describe cessation of bone growth

A

Growth stops when the epiphyseal growth plates close
Varies at different sites
Genetically determined (inherited height)
-Oestrogens/ Androgens initially increase GH secretion in early puberty and increase bone growth but later induce closure of growth plates
-Premature closure of a growth plate results in a shortened bone

39
Q

What are the pathological causes of growth arrest?

A 
Local hyperaemia
-Infection: osteomyelitis
-Juvenile chronic arthritis
-Arteriovenous malformation
Trauma
Metabolic conditions
40
Q

Describe growth plate abnormalities

A

Defects in chondrogenesis give rise to skeletal dysplasias and short stature
-Achondroplasia
-Achondrogenesis type 2
-Multiple epiphyseal dysplasias
Endocrine abnormalities can give rise to increased or decreased bone growth
-Giantism
-Hypopituitarism

41
Q

What is Achondroplasia?

A
  • Mutation in fibroblast growth factor receptor 3 (FGFR3)
  • Receptor constitutively active
  • Decreased chondrocyte proliferation and hypertrophy
42
Q

What is Gigantism?

A
  • Excess growth hormone production before puberty

- Increased longitudinal bone growth

43
Q

What is Acromegaly?

A
  • Excess GH production
  • Growth plates closed
  • Increased bone formation

Locomotor (20 decks)

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