The main storage house of calcium is the bone. This is the place where calcium gets into the bones, and this happens through the trabeculae and the rate at which the calcium is cleared by the bone is approximately 50%. Calcium gets into the bone and is used as an ion in the solution and it goes through a phase, where it is changed into a solid and this happens as soon as it gets into contact with surface of the bone. The bone cells ensure that calcium is removed and also redistributed and this is mainly ruled by the osteoclasts and the osteoblasts. Absorption in the intestines ensures greater calcium entry and calcium normally leaves the body through the urine and the stool. Sometimes there are chances that around one in four percent calcium content is lost in the urine and stool. Sometimes lead impediments the deposition of calcium and the way it is transported. It is required that the rate of led in the body is parallel to the rate at which calcium is present. It is modified by binding affinities and also by interactions with the molecules. The ion concentration of extra cellular fluid calcium in the vertebrates is regulated and it is also seen that bone is the main mineral reserve and gives the calcium replenishment in times of calcium loss. Now how exactly bone contributes to calcium homeostasis and how the reserve of bone’s function is combined with the condition, is to be understood.
There haCalcium Homeostasisve been studies of bone histomorphometry and calcium tracer kinetics have shown that the calcium traffic occurs in al the three mechanisms and it is seen that exchange is the largest of the three mechanisms. So the problems is not whether calcium movement is there or not or how great the magnitude is.
So to put all the possible mechanisms to use, it is necessary to understand the size of the perturbations to which the condition of homeostasis shows effects. If the perturbation of ECF calcium is around 1% or 10 mg then the impact on the calcium in the skeleton calcium is very negligible. So then the distinguishing factor of the three mechanisms are not longer important. But continuous perturbations have their own sizes and also the impacts.
It has been noticed that the thyro parthryodiectomized dogs are given replacement thyroxin and they are seen to show a lot of wild swings in the serum calcium that ranges from 5 to 15 mg / dL. Metabolic and kinetic measurements have shown that the human beings are always exposed to some excess drains that are not balanced. This sometimes leads to around 10 -30% of the total ECF calcium and many on a continuous basis. So the ECF calcium homeostasis should also be inclusive of a capacity to handle a lot of continuing perturbations.
A heteroionic exchange is inclusive where the bone composition sometimes changes when the non calcium cation is substituted. This kind of mechanism sometimes could lead to a release of calcium from the bone or uptake to the bone. But if it is seen that it is usually involved with the condition of calcium homeostasis there would a lot of excess of non calcium catiions not only in the ECF but also in the bone. There is probably not enough mineral cations on any side of the ECF bone. If this kind of mechanism is found to offset a lower rate of ECF calcium by making a substitution of bone calcium with serum magnesium. Then this would result in a condition called hypomagnesemia. But this doesn’t seem to occur. The bone can be given electrical neutrality if there is enough sodium that is sufficient enough. But if this sodium is to be substituted for calcium then sodium wouldn’t fit into the hydroxyapatite crystal lattice. Then there would be a requirement for the sodium atoms in the bone to be replaced with calcium.
This is not seen to happen sometimes and thus it is seen that the changes in the sodium content of the bone are seen to concentration of sodium in the hydration shell.
So it is seen that bone and calcium homeostasis is related to the concentration of sodium in the bone and its related calcium content in the bone.