Osteoblasts/clasts and PTH/calcitonin

[hellobruin]

I am thoroughly confused on this subject! Checked the previous threads, and whatnot, but couldn't quite understand the explanations.

Basically, does PTH stimulate osteoclast activity? And since calcitonin is antagonistic, does it inhibit osteoclast activity? (And would the opposite system apply to osteoblasts?)

My reasoning is that PTH increases calcium levels in the blood, which means it induces osteoclast activity because osteoclasts break down bone and subsequently release calcium in the blood. And on the other hand, because calcitonin lowers calcium levels, it would inhibit osteoclast activity because there's no way for calcium to be released into the blood.

I'd love a layman-terms explanation. Thank you!

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[jpark1800]

Your assumption is correct.

 

[IsaacYankem]

Calcitonin decreases blood Ca2+ level by increasing osteblast activity of bone building by taking blood Ca2+ --> bone formation

PTH increases blood Ca2+ by increasing osteclast activity (increased bone resorption); increase Ca2+ from bone resorption --> blood

There is a more complex process with negative feedback loops that I discovered when going through this first time, but hopefully we won't have to worry about that until BioChem in Dental School

 

[Papasmurf1234]

Sounds good to me, the reasoning is logical.

 

[jhmcknight]

Yea that sounds right to me.

Calcium in blood too low --> parathyroid make PTH --> PTH stimulates osteoclasts to release Ca2+ from the bone to the blood --> blood Ca2+ increases.

When Ca2+ goes above normal/needed levels, PTH shuts off and thyroid start to produce calcitonin --> calcitonin stimulates osteoblast activity, which causes uptake of blood Ca2+ into the bone --> this causes Ca2+ in blood to go back down.

This happened constantly in your body to regulate Ca2+ at the proper levels. Bone stores tons of Ca2+. Blood glucose levels are maintained in a similar way, but with the use of glucagon and insulin released from the pancreas.

Its basically what you typed, but typing it out helps me keep track of it too
Someone let me know if I'm off...

 

[Papasmurf1234]

Yea that sounds right to me.

Calcium in blood too low --> parathyroid make PTH --> PTH stimulates osteoclasts to release Ca2+ from the bone to the blood --> blood Ca2+ increases.

When Ca2+ goes above normal/needed levels, PTH shuts off and thyroid start to produce calcitonin --> calcitonin stimulates osteoblast activity, which causes uptake of blood Ca2+ into the bone --> this causes Ca2+ in blood to go back down.

This happened constantly in your body to regulate Ca2+ at the proper levels. Bone stores tons of Ca2+. Blood glucose levels are maintained in a similar way, but with the use of glucagon and insulin released from the pancreas.

Its basically what you typed, but typing it out helps me keep track of it too
Someone let me know if I'm off...

Ya forgot glucocorticoid hormones from the adrenal cortex for the increase in blood glucose levels.

 

[hellobruin]

Awesome! Thanks for all the input + little extra details! Antagonistic concepts like this always get me, blergh. Study on, comrades!

 

[Toofly01]

Hellobruin - how was your dat? If I recall correctly you were scheduled to take it yesterday... hope it was everything you wanted it to be!!! (Oh and if you DID take it, then we took it on the same day! I thought that was pretty cool).

 

[DDSv]

I am thoroughly confused on this subject! Checked the previous threads, and whatnot, but couldn't quite understand the explanations.

Basically, does PTH stimulate osteoclast activity? And since calcitonin is antagonistic, does it inhibit osteoclast activity? (And would the opposite system apply to osteoblasts?)

My reasoning is that PTH increases calcium levels in the blood, which means it induces osteoclast activity because osteoclasts break down bone and subsequently release calcium in the blood. And on the other hand, because calcitonin lowers calcium levels, it would inhibit osteoclast activity because there's no way for calcium to be released into the blood.

I'd love a layman-terms explanation. Thank you!

calcitonin in its long term affect!!! causes reduction of osteoclasts activity and production. as osteoclast bone resorption activates the osteoblast activity so calcitonin by reducing the osteoclasts activity will reduce the osteoblast activity as well.
PTH in its long term affect causes activition of old osteoclasts in bone and it produces new osteoclasts as well. but in its short term effect it activates the calcium channel pump on the osteocytes which pumps calciums out of the bone.

 

[DMikes]

calcitonin in its long term affect!!! causes reduction of osteoclasts activity and production. as osteoclast bone resorption activates the osteoblast activity so calcitonin by reducing the osteoclasts activity will reduce the osteoblast activity as well.
PTH in its long term affect causes activition of old osteoclasts in bone and it produces new osteoclasts as well. but in its short term effect it activates the calcium channel pump on the osteocytes which pumps calciums out of the bone.

This is from 2012.

 

[dl2501]

22. An increase in calcitonin would lead to which of the following?.
A.Increase calcium concentration in blood
B. Decrease calcium reabsorption in bones
C. Stimulate osteoblast activity
D. Stimulate osteoclast activity
E. An increase in muscle contractions

I completely understand that the answer here is C. I am just wondering why B is incorrect. The explanation said that "decreasing calcium reabsorption in bones would actually lead to an increase in serum calcium levels." This sounds counterintuitive to me, because if you decrease Ca reabsorption in bone by decreasing osteoclast activity, then wouldn't this lead to a lower Ca count in the blood?

(Sorry to bring up an old post!!!)

 

[Solipsism]

22. An increase in calcitonin would lead to which of the following?.
A.Increase calcium concentration in blood
B. Decrease calcium reabsorption in bones
C. Stimulate osteoblast activity
D. Stimulate osteoclast activity
E. An increase in muscle contractions

I completely understand that the answer here is C. I am just wondering why B is incorrect. The explanation said that "decreasing calcium reabsorption in bones would actually lead to an increase in serum calcium levels." This sounds counterintuitive to me, because if you decrease Ca reabsorption in bone by decreasing osteoclast activity, then wouldn't this lead to a lower Ca count in the blood?

(Sorry to bring up an old post!!!)

Hello!

Since osteoblast activity is increased and therefore bone formation, calcium reabsorption would also be increased to form new bone. I hope that helps!

 

[volacrity]

Necrobump here, but I'm pretty sure PTH only acts on osteoblasts, because osteoclasts don't have PTH receptors. Also, calcitonin I believe only acts on osteoclasts.

Both act as inhibitors.

source is wikipedia for PTH and calcitonin

 

[Quinque]

Necrobump here, but I'm pretty sure PTH only acts on osteoblasts, because osteoclasts don't have PTH receptors. Also, calcitonin I believe only acts on osteoclasts.

Both act as inhibitors.

source is wikipedia for PTH and calcitonin

I learned in my anatomy class that PTH stimulates osteoclasts indirectly. I recall, PTH binds to osteoblasts, which in turn secrete RANKL which bind to RANK on osteoclast precursors causing them to differentiate into mature osteoclasts.