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56 Cards in this Set
- Front
- Back
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what are the 4 stages of bone remodelling |
1. Quiescence 2. Resorption 3. Reversal 4.Formation |
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what processes occur in bone remodelling for quiescence to become resorption |
osteoclast: -recruitment -differentiation -activation |
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what processes occur in bone remodelling for resorption to become reversal |
osteoclast -apoptosis -removal |
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in terms of osteoblasts, what happens in the reversal stage of bone remodelling |
osteoblast: -recruitment -differentiation -activation |
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what happens for reversal to become formation in bone remodelling |
matrix synthesis |
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what happens for formation to become quiescence |
mineralisation |
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what ligand/receptor do osteoclast progenitor cells have |
they have receptor RANK for RANKL ligand on osteoblasts |
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what ligand/receptor do osteoblast cells have |
RANKL ligands which joins with receptors on the osteoclast progenitor cells |
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what happens when RANK on (osteoclast progenitor cells) and RANKL (on osteoblasts join) |
it initiates cell fusion as well as the formation of multi-nucleated osteoclasts. |
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what are the 2 things which regulate bone remodelling |
oestrogen and OPG |
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how does oestrogen regulate bone remodelling |
it limits the amount of RANKL expression by osteoblasts |
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what is OPG and how does it regulate bone remodelling |
it is a protein produced by osteoblasts it is a natural inhibitor of RANKL and bone resorption |
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explain how in post menopausal women, there is an increased risk of osteoarthiritis |
In post- menopausal women, there is a reduced level of oestrogen, which results in increased expression of RANKL by osteoblasts. Excessive RANKL therefore overwhelms OPG, leading to increased osteoclast activity, increase bone resorption and bone loss. Osteoblasts continue to rebuild the bone, but there may not be enough to fill all the resorption pits. |
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what are the stimulatory hormones of bone remodelling |
parathyroid hormone thyroid hormone growth hormone 1, 25 dihydroxyvitamin D |
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what are the inhibitory hormones of bone remodelling |
progesteroneoestrogens androgens calcitonin |
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which factors stimulate osteoblast expression of RANKL ligand |
PTH (parathyroid hormone) PTHrP (PTH related peptide) prostoglandin (PGE2) interleukin (-1 + -11) glucocorticoids vitamin D TNF-α
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in quiescence, what do embedded osteocytes secrete? |
sclerostin- this inhibits wnt signalling in cells near the surface wnt signalling -->(signal transduction pathways made of proteins that pass signals from outside of a cell through cell surface receptors to the inside of the cell) |
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after sudden stress causes a microcrack to appear in bone, what happens to osteocytes near the crack |
they undergo apoptosis |
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following apoptosis of osteocytes, how do the lining cells attached to the bone matrix respond |
they dissattach from the bone matrix and form a canopy which merges with blood vessels |
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what are stromal cells basically (kind of..) |
the connective tissue cells of any organ
In cell biology, stromal cells are connective tissue cells of any organ, for example in the uterine mucosa (endometrium), prostate, bone marrow, and the ovary. They are cells that support the function of the parenchymal cells of that organ. |
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whilst the "cell canopy" is forming, what happens stromal cells |
they are released from sclerostin inhibition and/or exposed to other factors like interleukin-1 |
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when stromal cells are released from sclerostin inhibition and/or exposed to interleukin-1, what happens? |
they generate pre-ostebloasts and secrete M-CSF
M-CSF is macrophage colony stimulating factor, it helps generate pre-osteoclasts
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as pre-osteoblasts proliferate, what 3 factors do they secrete |
wnt interleukins bone morphogenic proteins |
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after pre-osteoblast proliferation, what forms on pre-osteoblasts and pre-osteoclasts |
pre-osteoblasts start to express RANK-L on their surfaces pre-osteoclasts start to express RANK receptors on their surfaces |
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after this pre- osteoclasts enlarge and fuse into mature osteoclasts |
after this pre- osteoclasts enlarge and fuse into mature osteoclasts |
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when osteoclasts bind to the bone matrix with integrins what do they secrete and why? also... what bone derived growth factors are released |
they secrete acid and cathepsin K, this is to resorb the bone IGF and TGF-B(beta) are released |
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eventually osteoclasts undergo apoptosis, what controls their life span? |
oestrogen and other factors |
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when pre-osteoblasts mature into osteoblasts, how does this block the activation of pre-osteoclasts? |
when they mature into osteoblasts, they stop making RANKL and secrete OPG (osteoprotegerin). the OPG binds to RANKL as a decoy receptor and therefore blocks the activation of pre-osteoclasts |
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what happens to the excess osteoblasts in bone remodelling |
they turn into osteocytes or undergo apoptosis |
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when is the attainment of peak bone mass for men and women |
0-28 ish |
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when is the "consolidation" stage in bone mass |
between roughly 28-41 |
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at what age does age-related bone loss usually occur in people |
41 onwards |
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what is calcium hydroxyapatite made of |
a combination of calcium phosphate and calcium hydroxide |
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which portion of bone, inorganic or organic is responsible for the "hardness" of bone |
inorganic (70%) |
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what is calcification |
Calcium phosphate combines with calcium hydroxide to form crystals of hydroxyapatite. This combines with other minerals such as calcium carbonate, magnesium, fluoride, potassium and sulphate. As these mineral salts are deposited in the framework of ECM, they crystallise and the tissue hardens. |
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primarily what type of collagen is the organic component of the bone made up of |
collagen type 1 |
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what portion of the bone is responsible for the flexibility of the bone and gives it its tensile strength and resistance to being stretched or torn apart. |
organic part of the bone (22%) |
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what specific portion of the organic bone gives it its tensile strength |
the type 1 collagen |
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what specific portion of the organic bone gives it its compressible strength |
the proteoglycans |
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what are the 2 types of bone called before and after fracture healing |
woven bone- during repair lamellar bone- mature bone |
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what are the characteristics of woven bone |
• Collagen fibres and cells are in no specific arrangement • Temporary • Healing |
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what are the characteristics of lamellar bone |
• Collagen fibres are parallel to one another • It is laid only on existing bone surface
• Cortical |
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what are the 3 most important determinants in risk calculation for osteoporosis |
-BMD -Age -previous history of fractures |
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what are the "T-scores" for the DXA BMD density test |
>-1 - normal -1 to -2.5 - osteopenia less than -2.5 - osteperosis
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define endochondral ossification |
-longitudinal creation of new bone tissue -involves cartilage as a precursor and therefore continuous cell division of chondrocytes -(most common in fracture healing) |
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define intermembranous ossification |
Intramembranous ossification is the direct laying down of bone into the primitive connective tissue (mesenchyme) (most common cause of healing after surgery etc) |
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define subperiosteal apposition |
-creation of new bone tissue - width -new layers added to outside whilst losing bone on the inside due to endosteal resorption which results in the expansion of the medullary cavity |
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what are the characteristics of osteomalacia |
softening of bones
Poorly mineralised osteoid Severe/long standing Vitamin D deficiency Reduced availability of calcium and phosphate |
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what are the characteristics of osteoperosis |
• Reduced total bone mass • Many factors |
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what are the characteristics of paget's disease |
Rapid bone turnover Both bone resorption and formation are increased Disorganised structure Reduced bone strength Risk of fracture Linked to osteosarcoma tumour suppressor gene |
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what are the characteristics of corticosteroid induced osteoperosis |
• Increased osteoclastic activity • Decreased osteoblastic activity • Impaired collagen formation • Increased bone turnover and poor bone formation and healing |
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what are the characteristics of osteopetrosis |
• ‘Failure’ of remodelling – decreased turnover • Unregulated osteoblastic activity, though not necessarily increased • Impaired osteoclastic activity • Dense but weak bones |
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what are the characteristics of flurosis |
• Defective mineralisation |
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what are the characteristics of primary hyperthyroidism |
• Unregulated PTH secretion • May retain bone mass, but in elderly or other risk factors, often osteoporosis |
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what are the characteristics of renal rickets |
High Phosphate – only type of rickets Combines with Ca – hypocalcaemia Excess phosphate excreted into gut –combines with Ca in gut 2° hyperPTH Aluminium excess – dialysis Types - Hyperdynamic (↑bone turnover). |
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what are the characteristics of osteogenesis imperfecta |
• Genetic bone disorder |
