Bone physiology Flashcards by Hannah Hutchison

bone remodeling is regulated by

biochemical markers, mechanical activity, endocrine function

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how long does the bone remodeling cycle take

~4-6 months

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annual turnover is 4% for what type of bone

cortical bone

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annual turnover is 25% for what type of bone

trabecular bone

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between puberty and 3rd decade of life, bone density increases

~3% per year

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bone loss rate after 30 years

0.3%-0.5% per year

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bone loss rate after menopause

3% per year for 10 years (rapid loss)

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bone loss rate >60 years

0.5%

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vitamin D supplementation

800

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calcium supplementation

total = 1200 (400-500 supplementation)

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who has highest risk of fractures

white, thin females

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overweight and risk of osteoporosis

decreased risk if overweight

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phases of bone remodeling

Resorption
Reversal
Formation
Mineralization

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how long is the resorption period

~10 days

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osteoclasts are derived from

hematopoietic stem cells

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osteoclasts resorb bone through secretion of

H+ and cathepsin K (digesting enzyme)

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what are osteoclasts dependent on for maturation and differentiation

cytokines

MCSF
RANKL

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MCSF bind to what cells

precursor cells –> pre osteoclasts

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on what cell in RANK found

pre osteoclasts

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RANKL binds to

RANK –> maturation and differentiation

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a decoy receptor for RANKL

osteoprotegerin (OPG)

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what stimulates OPG secretion

estrogen

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OPG/RANK ratio is high

osteoclast apoptosis

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OPG/RANK ratio is low

bone resorption

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what do osteoblasts secrete

MCSF and RANKL

what causes osteoblasts to secrete cytokines

PTH (parathyroid hormone)

osteoblasts are derived from

mesenchymal precursor

what promotes osteoblast maturation

growth factor released from RESORBED bone

what specific growth factors promote maturation of osteoblasts

IGF1 and IGF2

what do pre-osteoblasts secrete

bone morphogenic protein (BMP)

BMP is important in

differentiation of mesenchymal cells

what can a mature osteoblast become

lining cell, osteocyte, or can undergo apoptosis

what causes PTH to be released into the blood

low calcium levels

anabolic effects of PTH on bones

inhibits osteoclasts and activates osteoblasts

anabolic effects of PTH on kidneys and intestines

encourage kidneys to get more calcium from the urine instead of excreting it stimulate renal tubules to release calcitriol which works in the intestines to get more calcium

calcitriol is also called

active vitamin D

easy way to remember calcitriol

TRY all that you can to increase calcium levels

anabolic effects of PTH

PTH given in low and intermittent doses can activate the WNT pathway which promotes osteoblasts and inhibits osteoclasts

can PTH be used for osteoporosis treatment

yes -- very specific usage. low and intermittent doses

calcitriol (active vitamin D) is synthesized from

the kidneys

what is secreted in response to PTH

calcitriol

effects of calcitriol

increases osteocalcin production stimulates maturation of osteoclasts stabilizes systemic calcium levels by encouraging intestines to absorb more calcium

what type of estrogen is necessary for bone health

bioavailable/free

what percent of estrogen is free

what is bound estrogen bound to

sex hormone binding globulin

effects of estrogen and bone health

reduces apoptosis of osteoclasts and osteoblasts decreases oxidative stress increases OPG balances bone resorption with bone formation

thyroid gland can release

thyroid hormones and calcitonin

calcitonin is released in response to

high levels of circulating calcium

effects of calcitonin on bones

stimulates osteoblasts inhibits osteoclasts

T3 effects on bone

increases osteoclast activity independent of osteoblast activity stimulates bone resorption

how does T3 affect the amount of bioavailable estrogen

induces more production of sex hormone binding globulin in the liver

prolactin has what type of effects on bone remodeling

direct and indirect

where are prolactin receptors located

on osteoblasts

effects on prolactin receptors on osteoblasts

decrease osteocalcin mRNA increased RANKL expression decreased OPG expression

indirect effects on prolactin

negative feedback to HPO axis --> increased PRL --> decreased estrogen --> increased bone resorption

cortisol levels can be increased due to

stress glucocorticoid meds

effects of increased cortisol on intestines

decreased calcium absorption in intestines

effects of increased cortisol on kidneys

increased renal excretion of calcium

effects of cortisol on PTH

lowering calcium levels --> increased PTH

effects of high cortisol on GnRH

decreased GnRH --> decreased estrogen --> imbalance of RANKL and OPG

effects of cortisol on osteoclasts

increase osteoclast activity

effects of cortisol on osteoblasts

decrease osteoblast activity