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Musculoskeletal System > 5. BONE BIOLOGY > Flashcards

5. BONE BIOLOGY Flashcards

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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
DIFFERENCE in STRUCTURES of LAMELLAR vs WOVEN bone
LAMELLAR - BONE LAMELLAE (lines) HIGHLY ORGANISED WOVEN - Not as well structured
26
SKELETON contains approx how much of the body's CALCIUM
98%
27
the MINERAL COMPONENT of BONE is :
HYDROXYAPATITE - Ca10 (PO4)6 (OH)2 calcium phosphate salt - tiny CRYSTALS surround collagen fibres
28
what does BONE MINERAL COMPONENT - HYDROXYAPATITE PROVIDE
RIGIDITY & RESISTANCE to COMPRESSION
29
The MINERALISATION of OSTEOID DEPENDS on...
hormonally ACTIVE FORM of VITAMIN D3
30
VITAMIN D3 main source and EFFECTS of DEFICIENCY
main source: sunlight -deficiency results in FAILURE TO MINERALISE -leads to rickets in children, osteomalacia in adults (bendy bones)
31
FULL MINERALISATION takes how long
SEVERAL MONTHS
32
where is ALKALINE PHOSPHATASE (ALP)
- EXPRESSED on SURFACE of DIFFERENTIATED OSTEOBLASTS - RELEASED into EXTRACELLULAR FLUID and CIRCULATION
33
what can ALP act as
BONE FORMATION MARKER
34
what does ALP cause on various molecules
HYDROLYSIS - RELEASE INORGANIC PHOSPHATE IONS (PO4 3-)
35
how does ALP PROMOTE MINERALISATION (2 ways)
- INCREASING LOCAL CONC. of INORGANIC PHOSPHATE IONS - HYDROLYSING PYROPHOSPHATE - a key INHIBITOR of MINERALISATION hydrolysis releases 2 phosphate ions (used for mineralisation)
36
what are OSTEOCLASTS
MULTINUCLEATE, MOTILE, BONE-RESORBING CELLS (slide onto bone matrix, release proteolytic enzymes)
37
OSTEOCLASTS are formed by the FUSION of..
PROMONOCYTIC PRECURSORS present in MARROW and CIRCULATION
38
what does the 'RUFFLED BORDER' of OSTEOCLASTS SECRETE
H+ ENZYMES
39
what do OSTEOCLASTS EXPRESS/SECRETE to RESORB BONE
- '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
what do OSTEOCLASTS EXPRESS that are GOOD MARKERS for RESORPTION
TARTRATE-RESISTANT ACID PHOSPHATASE (TRAcP)
41
what ACTIVATES OSTEOCLAST FORMATION
RANK-RANKL SYSTEM
42
what do OSTEOCLAST PRECURSURS have on their SURFACE and how does this ACTIVATE them to FORM OSTEOCLASTS
- 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
when there is EXCESSIVE BONE RESORPTION which PROTEIN REGULATES this and HOW
OPG - OSTEOPROTEGRIN BINDS TO RANKL on OSTEOBLAST PREVENTS ACTIVATION of OSTEOCLAST (RANKL cannot bind to RANK)
44
BONE DISEASE - OSTEOPETROSIS caused by (aka Marble Bone Disease')
DYSFUNCTIONAL OSTEOCLASTS (MUTATIONS) characterised by INCREASED BONE MASS (little to no bone marrow) INHERITED bone disease
45
OSTEOPETROSIS can be caused by WHICH MUTATIONS and what do these cause
- 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
why do we need BONE METABOLISM
*To grow *Respond to altered mechanical requirements *Repair damage (macro / micro fractures) *Maintenance (failure prevention) *Calcium deficit *Pathological (hyperparathyroidism, cancers..)
47
SKELETON is RENEWED approx every ... years
7-10
48
what is the main SOURCE of RANKL
OSTEOCYTES
49
BONE REMODELLING CYCLE 4 STAGES
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
how long does the BONE REMODELLING CYCLE take
4-6 MONTHS
51
how long is the RESORPTION STAGE of the BONE REMODELLING CYCLE
10 DAYS
52
how long is the REVERSAL STAGE of the BONE REMODELLING CYCLE (osteoblasts forming matrix)
3 MONTHS
53
what are BONES composed of and what do these contain that supply nutrients
OSTEONS HAVERSIAN CANALS (houses nerve fibres and some capillaries)
54
what are HAVERSIAN CANALS supported by
VOLKMANN'S CANAL
55
what do OSTEOCYTES RESPOND to
MECHANICAL LOADING - MECHANOSENSITIVE CELLS
56
OSTEOCYTES PRODUCE a wide range of factors that regulate bone cells:
- PROSTAGLANDINS - NITRIC OXIDE (bone resorption) - RANKL (main source) - SCLEROSTIN (inhibits bone formation)
57
WHEN do OSTEOCYTES SECRETE SCLEROSTIN and what does this do
- EXCESSIVE BONE FORMATION (exceeds rate of resorption) - INHIBITS ACTIVATION of PRE-OSTEOBLASTS to OSTEOBLASTS therefore INHIBITS BONE FORMATION
58
consequence of LOSS of SCLEROSTIN
HIGH BONE MASS DISEASE eg VAN BUCHEM disease & SCLEROSTEOSIS Caused by SOST inactivating mutations
59
2 BONE RESORPTION MARKERS
- TRAcP (serum) - CROSSLINKS - PYRINIDIUM (Serum/Urinary)
60
3 BONE FORMATION MARKERS
- OSTEOCALCIN (serum) - TELOPEPTIDES (serum) - ALP (serum)
61
2 most COMMON BONE DISEASES:
*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
why do WOMEN have a greater DECREASE in BONE MASS DENSITY as they age
MENOPAUSE - LOSS of ESTROGEN
63
REGULATION of BONE METABOLISM by: (2)
1: Systemic Regulation by HORMONES 2: Regulation by LOCAL FACTORS
64
REGULATION pf BONE METABOLISM by which LOCAL FACTORS: (3)
- PROSTAGLANDINS - GROWTH FACTORS - CYTOKINES
65
REGULATION pf BONE METABOLISM by which LOCAL FACTORS: PROSTAGLANDINS: (what are they, what are they produced by, what do they do)
- Small FATTY ACID METABOLITES - PRODUCED by OSTEOBLASTS - INCREASE and DECREASE OSTEOCLAST ACTIVITY - mediate some actions of Growth Factors and responses to Mechanical Loading
66
what are PROSTAGLANDINS PRODUCED BY
OSTEOBLASTS
67
REGULATION pf BONE METABOLISM by which LOCAL FACTORS GROWTH FACTORS: (produced by, examples, what can they do)
- 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
REGULATION pf BONE METABOLISM by which LOCAL FACTORS CYTOKINES (produced by, what do they do, examples)
- 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
what is RHEUMATOID ARTHIRITIS
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
TYPE 1 COLLAGEN is secreted as an ... and undergoes..
IMMATURE PROTEIN undergoes CLEAVAGE of TELOPEPTIDES outside the cell

Musculoskeletal System (18 decks)

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