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Musculoskeletal System > 5. BONE BIOLOGY > Flashcards

5. BONE BIOLOGY Flashcards

1
Q

the SKELETON makes up approximately how much of our BODY WEIGHT

A

17%

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2
Q

4 FUNCTIONS of BONE

A
  • SUPPORT of the body
  • PREOTECTION of ORGANS
  • Site for HAEMATOPOIESIS (blood cells from bone marrow)
  • Regulation for MINERAL HOMEOSTASIS
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3
Q

2 STRUCTURES in BONE

A
  • CORTICAL / CORTEX BONE
    outer, compact (no gaps)
  • TRABECULAR BONE
    gaps filled with bone marrow
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4
Q

CELLS of BONE (3)

A
  • OSTEOBLASTS : MAKE bone
  • OSTEOCLASTS : RESORB bone
  • OSTEOCYTES : final, inactive form of Osteoblasts, most abundant, embedded in Bone Matrix, MECHANOSENSOR CELL
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5
Q

which CELL type is the MOST ABUNDANT in BONE

A

OSTEOCYTES

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6
Q

OSTEOBLASTS ORIGIN

A

MESENCHYMAL CELLS

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7
Q

OSTEOBLASTS express HIGH LEVELS of which ENZYME

A

ALKALINE PHOSPHATASE

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8
Q

OSTEOBLASTS SECRETE and RESPOND to many…

A

CYTOKINES and GROWTH FACTORS

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9
Q

where are OSTEOBLASTS - active or inactive (flattened)

A

COVER MOST BONE SURFACES

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10
Q

what do OSTEOBLASTS SECRETE/form

A

OSTEOID - UNCALCIFIED BONE MATRIX

  • becomes MINERALISED/CALCIFIED

-> CALCIFIED BONE MATRIX

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11
Q

after SECRETING BONE MATRIX, OSTEOBLASTS BECOME

A

OSTEOCYTES embedded in MATRIX

have CELL PROCESSES that form huge networks into bone tissue

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12
Q

DIFFERENTIATION of MESENCHYMAL PROGENITOR to OSTEOBLAST is regulated by

A

TRANSCRIPTION FACTORS:
SOX9+
RUNX2+
RUNX2+ OSX+

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13
Q

SOX9+ TRANSCRIPTION FACTOR can also cause DIFFERENTIATION of MESENCHYMAL PROGENITORS into… (besides OSTEOBLASTS)

A

CHONDROCYTES

  • become HYPERTROPHIC CHONDROCYTES
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14
Q

what can MESENCHYMAL PROGENITORS also become
(besides osteoblasts, chondrocytes)

A

ADIPOCYTE

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15
Q

BONE ORGANIC COMPONENT is 90%…

A

TYPE 1 COLLAGEN

(produced by osteoblasts)

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16
Q

why is bone 90% TYPE 1 COLLAGEN (what is it)

A
  • STRUCTURAL PROTEIN providing STRENGTH, FLEXIBILITY
  • MAJOR Structural Protein in the body
  • also present in Tendon, Ligaments, Skin, Scar Tissue
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17
Q

REMAINING 10% of BONE ORGANIC COMPONENT is a COMPLEX MIXTURE of: (5)

A
  • GROWTH FACTORS
  • OSTEOCALCIN (secreted by osteoblasts, marker of bone formation)
  • OSTEONECTIN
  • OSTEOPONTIN
  • GLYCOPROTEINS
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18
Q

COLLAGEN SYNTHESIS from which 2 GENES and what do they ENCODE

A
  • COL1A1
    encodes for ALPHA1 CHAIN
  • COL1A2
    encodes for ALPHA2 CHAIN
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19
Q

stages of COLLAGEN SYNTHESIS (7)

A
  1. COL1A1 encodes for ALHPHA1 CHAIN
    COL1A2 encodes for ALPHA2 CHAIN
  2. 2x ALPHA1 CHAIN and 1X ALPHA2 CHAIN form TRIPLE HELICLE PROCOLLAGEN
  3. SECRETED into EXTRACELLULAR SPACE
  4. CLEAVAGE of N & C -TERMINAL PROPEPTIDES

form COLLAGEN MOLECULE

  1. CROSS LINKING (PYRINIDIUM) to STABILISE
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20
Q

in COLLAGEN SYNTEHSIS how do we get the PREMATURE form of COLLAGEN: TRIPLE HELICAL PROCOLLAGEN

A

2 ALPHA1 CHAINS
1 ALPHA2 CHAIN
combine

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21
Q

in COLLAGEN SYNTHESIS what happens to the TRIPLE HELICLE PROCOLLAGEN (2) to from COLLAGEN MOLECULE

A

SECRETED into EXTRACELLULAR SPACE

and CLEAVED at N & C - TERMINAL PROPEPTIDES

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22
Q

in COLLAGEN SYNTHESIS what happens to the MATURE COLLAGEN and why

A

PYRIDINIUM CROSS LINKING

  • STABILISES
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23
Q

why are the PYRIDINIUM CROSS LINKS of COLLAGE useful

A

MARKERS for BONE RESORPTION
- as they are NOT BROKEN DOWN in RESORPTION

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24
Q

what is LAMELLAR versus WOVEN/PRIMARY BONE

A

LAMELLAR - several day DELAY before OSTEOID MINERALISES

WOVEN/PRIMARY - Matrix IMMEDIATELY MINERALISED after secretion - RAPID FORMATION

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25
Q

DIFFERENCE in STRUCTURES of LAMELLAR vs WOVEN bone

A

LAMELLAR - BONE LAMELLAE (lines)
HIGHLY ORGANISED

WOVEN - Not as well structured

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26
Q

SKELETON contains approx how much of the body’s CALCIUM

A

98%

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27
Q

the MINERAL COMPONENT of BONE is :

A

HYDROXYAPATITE
- Ca10 (PO4)6 (OH)2
calcium phosphate salt

  • tiny CRYSTALS surround collagen fibres
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28
Q

what does BONE MINERAL COMPONENT - HYDROXYAPATITE PROVIDE

A

RIGIDITY & RESISTANCE to COMPRESSION

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29
Q

The MINERALISATION of OSTEOID DEPENDS on…

A

hormonally ACTIVE FORM of VITAMIN D3

30
Q

VITAMIN D3 main source and EFFECTS of DEFICIENCY

A

main source: sunlight

-deficiency results in FAILURE TO MINERALISE

-leads to rickets in children, osteomalacia in adults
(bendy bones)

31
Q

FULL MINERALISATION takes how long

A

SEVERAL MONTHS

32
Q

where is ALKALINE PHOSPHATASE (ALP)

A
  • EXPRESSED on SURFACE of DIFFERENTIATED OSTEOBLASTS
  • RELEASED into EXTRACELLULAR FLUID and CIRCULATION
33
Q

what can ALP act as

A

BONE FORMATION MARKER

34
Q

what does ALP cause on various molecules

A

HYDROLYSIS

  • RELEASE INORGANIC PHOSPHATE IONS (PO4 3-)
35
Q

how does ALP PROMOTE MINERALISATION (2 ways)

A
  • INCREASING LOCAL CONC. of INORGANIC PHOSPHATE IONS
  • HYDROLYSING PYROPHOSPHATE - a key INHIBITOR of MINERALISATION
    hydrolysis releases 2 phosphate ions (used for mineralisation)
36
Q

what are OSTEOCLASTS

A

MULTINUCLEATE, MOTILE, BONE-RESORBING CELLS

(slide onto bone matrix, release proteolytic enzymes)

37
Q

OSTEOCLASTS are formed by the FUSION of..

A

PROMONOCYTIC PRECURSORS
present in MARROW and CIRCULATION

38
Q

what does the ‘RUFFLED BORDER’ of OSTEOCLASTS SECRETE

A

H+ ENZYMES

39
Q

what do OSTEOCLASTS EXPRESS/SECRETE to RESORB BONE

A
  • ‘ruffled border’ secretes H+ ENZYMES
  • HIGH LEVELS of enzyme CARBONIC ANHYDRASE
    for H+ GENERATION

CREATES ACIDIC MICRO ENVIRONMENT which causes DEGRADATION of HYDROXYAPATITE/BONE

40
Q

what do OSTEOCLASTS EXPRESS that are GOOD MARKERS for RESORPTION

A

TARTRATE-RESISTANT ACID PHOSPHATASE (TRAcP)

41
Q

what ACTIVATES OSTEOCLAST FORMATION

A

RANK-RANKL SYSTEM

42
Q

what do OSTEOCLAST PRECURSURS have on their SURFACE and how does this ACTIVATE them to FORM OSTEOCLASTS

A
  • RANK (receptor activator of NFkB)
  • RANKL (RANK LIGAND) on OSTEOBLAST BINDS to RANK on OSTEOBLAST
  • ACTIVATES NF kB (nuclear factor kB)
  • ACTIVATION of PRECURSURE, DIFFERENTIATION to MATURE OSTEOCLAST
43
Q

when there is EXCESSIVE BONE RESORPTION which PROTEIN REGULATES this and HOW

A

OPG - OSTEOPROTEGRIN

BINDS TO RANKL on OSTEOBLAST

PREVENTS ACTIVATION of OSTEOCLAST (RANKL cannot bind to RANK)

44
Q

BONE DISEASE - OSTEOPETROSIS caused by

(aka Marble Bone Disease’)

A

DYSFUNCTIONAL OSTEOCLASTS (MUTATIONS)

characterised by INCREASED BONE MASS (little to no bone marrow)
INHERITED bone disease

45
Q

OSTEOPETROSIS can be caused by WHICH MUTATIONS and what do these cause

A
  • CA II MUTATIONS
    inhibits CARBONIC ANHYDRASE (enzyme for H+)
  • TCIRG1 MUTATIONS
    Deficient PROTEIN PUMP for H+
  • CLCN7 MUTATIONS
    no CHLORIDE CHANNEL, Cl- forms HCL for ACIDIC ENVIRONMENT
  • CAT K MUTATIONS
    CATHEPSIN K enzyme not secreted
46
Q

why do we need BONE METABOLISM

A

*To grow
*Respond to altered mechanical requirements
*Repair damage (macro / micro fractures)
*Maintenance (failure prevention)
*Calcium deficit
*Pathological (hyperparathyroidism, cancers..)

47
Q

SKELETON is RENEWED approx every … years

A

7-10

48
Q

what is the main SOURCE of RANKL

A

OSTEOCYTES

49
Q

BONE REMODELLING CYCLE
4 STAGES

A
  1. QUIESCENCE
  2. RESORPTION:
    when DAMAGE: OSTEOCLAST RECRUITMENT to site
    10 DAYS
  3. REVERSAL:
    OSTEOBLASTS ACTIVATED - produce BONE MATRIX to fill area
    3 MONTHS
  4. FORMATION
    MINERALISATION
    Osteoblasts become OSTEOCYTES
50
Q

how long does the BONE REMODELLING CYCLE take

A

4-6 MONTHS

51
Q

how long is the RESORPTION STAGE of the BONE REMODELLING CYCLE

A

10 DAYS

52
Q

how long is the REVERSAL STAGE of the BONE REMODELLING CYCLE (osteoblasts forming matrix)

A

3 MONTHS

53
Q

what are BONES composed of and what do these contain that supply nutrients

A

OSTEONS

HAVERSIAN CANALS (houses nerve fibres and some capillaries)

54
Q

what are HAVERSIAN CANALS supported by

A

VOLKMANN’S CANAL

55
Q

what do OSTEOCYTES RESPOND to

A

MECHANICAL LOADING

  • MECHANOSENSITIVE CELLS
56
Q

OSTEOCYTES PRODUCE a wide range of factors that regulate bone cells:

A
  • PROSTAGLANDINS
  • NITRIC OXIDE (bone resorption)
  • RANKL (main source)
  • SCLEROSTIN (inhibits bone formation)
57
Q

WHEN do OSTEOCYTES SECRETE SCLEROSTIN and what does this do

A
  • EXCESSIVE BONE FORMATION (exceeds rate of resorption)
  • INHIBITS ACTIVATION of PRE-OSTEOBLASTS to OSTEOBLASTS

therefore INHIBITS BONE FORMATION

58
Q

consequence of LOSS of SCLEROSTIN

A

HIGH BONE MASS DISEASE

eg VAN BUCHEM disease & SCLEROSTEOSIS

Caused by SOST inactivating mutations

59
Q

2 BONE RESORPTION MARKERS

A
  • TRAcP (serum)
  • CROSSLINKS - PYRINIDIUM (Serum/Urinary)
60
Q

3 BONE FORMATION MARKERS

A
  • OSTEOCALCIN (serum)
  • TELOPEPTIDES (serum)
  • ALP (serum)
61
Q

2 most COMMON BONE DISEASES:

A

*Osteoporosis
Most common cause: Low E2 after MENOPAUSE (estrogen)
Main cause of bone loss: Increased bone resorption

*Paget’s disease
*Due to overactive osteoclasts

62
Q

why do WOMEN have a greater DECREASE in BONE MASS DENSITY as they age

A

MENOPAUSE
- LOSS of ESTROGEN

63
Q

REGULATION of BONE METABOLISM by: (2)

A

1: Systemic Regulation by HORMONES

2: Regulation by LOCAL FACTORS

64
Q

REGULATION pf BONE METABOLISM by which LOCAL FACTORS: (3)

A
  • PROSTAGLANDINS
  • GROWTH FACTORS
  • CYTOKINES
65
Q

REGULATION pf BONE METABOLISM by which LOCAL FACTORS:
PROSTAGLANDINS:
(what are they, what are they produced by, what do they do)

A
  • Small FATTY ACID METABOLITES
  • PRODUCED by OSTEOBLASTS
  • INCREASE and DECREASE OSTEOCLAST ACTIVITY
  • mediate some actions of Growth Factors and responses to Mechanical Loading
66
Q

what are PROSTAGLANDINS PRODUCED BY

A

OSTEOBLASTS

67
Q

REGULATION pf BONE METABOLISM by which LOCAL FACTORS
GROWTH FACTORS:
(produced by, examples, what can they do)

A
  • PRODUCED by OSTEOBLASTS,
    DEPOSITED in BONE MATRIX (often in large amounts)
  • Transforming growth factor ß, bone morphogenetic
    proteins,
  • insulin-like growth factors I &II,, fibroblast growth factors
  • platelet-derived growth factor
  • may mediate some hormone actions
68
Q

REGULATION pf BONE METABOLISM by which LOCAL FACTORS
CYTOKINES

(produced by, what do they do, examples)

A
  • normal PRODUCTS of IMMUNE CELLS and BONE CELLS
  • mainly INCREASE OSTEOCLAST RECRUITMENT & ACTIVITY
    therefore BONE LOSS
  • eg interleukins-1,2,3,4,6,10,11,13; tumour necrosis
    factor TNF, RANK ligand; colony-stimulating factors

*some interleukins may MEDIATE PTH, 1,25(OH)2-VITAMIN D3 ACTIONS

*SEX STEROIDS may INHIBIT PRODUCTION of some INTERLEUKINS like IL6

69
Q

what is RHEUMATOID ARTHIRITIS

A

INFLAMMATORY JOINT DISEASE - BONE LOSS DUE TO INFLAMMATION

  • Features: joint swelling, cartilage and bone erosions

-Both local and systemic bone loss

  • Affects about 1% of the population
  • Women are affected three times as frequently as men
  • Onset is usually in the patients’ thirties and forties
70
Q

TYPE 1 COLLAGEN is secreted as an … and undergoes..

A

IMMATURE PROTEIN
undergoes CLEAVAGE of TELOPEPTIDES outside the cell

Musculoskeletal System (18 decks)

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