Vitamin D acts in a way which to me is counterintuitive. It functionally supplemets Parathormone. It in the intestinal tract steps up calcium absorption by altering nuclear gene expression and also prevents calcium excretion in kidneys. All of this is understandable. But it also, like parathormone, steps up osteoclast action in bone (actually steps up both osteoclast and osteoblast, but the osteoclast action is increased more to result in net bone resorption). This means that Vitamin D increases blood calcium level by increasing bone resorption.

Then how does Vitamin D help in improving bone density, bone strength and prevent rickets or osteoporosis? All of these would require bone deposition rather than resorption.

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    $\begingroup$ yes there are some colflicting theories.. This article says that Vit-D actually inhibits osteoclastogenesis. What I can say about it is that the action of Vit-D should be studied in a systems perspective. It may be the effect of dynamics. It allows calcium absorption, and its deficiency would cause reduced calcium leading to reduced bone-mineralization as seen in rickets. However, it also affects resorption and active modeling of the bone. It is important to take other factors (hormones etc) into consideration. $\endgroup$
    Jan 9, 2014 at 6:26

1 Answer 1


There are two pieces to this question:

a) How does bone resorption (movement of Ca/Phos out of bone into the blood) result in net improvement in bone structure?

Bones are constantly remodeling, primarily in response to mechanical stressors. Although you clearly already realize this, I will make it explicit: osteoblasts are the cells that create new bone; osteoclasts break down (resorb) bone.

Quoting Harrison’s Internal Medicine1:

Radioisotope studies indicate that as much as 18% of the total skeletal calcium is deposited and removed each year. Thus, bone is an active metabolizing tissue.…The cycle of bone resorption and formation is a highly orchestrated process carried out by the basic multicellular unit, which is composed of a group of osteoclasts and osteoblasts

Bone mineral density (BMD) can not be equated with bone quality. (This is the difference between osteoporosis – deficient bone density – and rickets – poor bone architecture.) Thus, vitamin D’s stimulation of both osteoblast and osteoclast activity is beneficial to bone structure.

b) How does vitamin D lead to overall increased bone density?

In addition to the effects above, you mentioned that vitamin D increases serum calcium by several mechanisms. This is true. Both this increased serum calcium as well as the direct effects of Vitamin D on the parathyroid gland suppress PTH production.* As PTH has powerful actions to increase bone resorption by mobilizing calcium and phosphorus to move from the bone into the blood, the suppression on its excretion applied both directly and indirectly by Vitamin D results in a net increase in bone density.

Thus, both by its effects on bone quality and quantity, vitamin D is a net boon for the bones.

*Parathyroid hormone, a.k.a. parathormone. There is a paradox here, because drugs such as teriparatide (a.k.a. Forteo, recombinant PTH) are anabolic for bone and are used to treat osteoporosis. Although the mechanism is unresolved, intermittent administration (as in the case of drug treatment) increases BMD while chronic sustained elevations decrease BMD.2


1. Bringhurst F, Demay M.B., Krane S.M., Kronenberg H.M. (2012). Chapter 352. Bone and Mineral Metabolism in Health and Disease. In Longo D.L., Fauci A.S., Kasper D.L., Hauser S.L., Jameson J, Loscalzo J (Eds), Harrison's Principles of Internal Medicine, 18e.

2. Rosen CJ. The cellular and clinical parameters of anabolic therapy for osteoporosis. Crit Rev Eukaryot Gene Expr. 2003;13(1):25.

  • $\begingroup$ Nice answer, but I still am unclear about how suppressing parathormone will help out bone density. Since functionally, Vit D and Parathormone are complimentary, will not suppressing PTH be equivalent to negative feedback control, valid for most hormone systems? $\endgroup$ May 18, 2015 at 16:24
  • $\begingroup$ @SatwikPasani Thank you for the feedback. I have added some additional explanation. This system is more complicated than a straightforward negative feedback loop, and the two hormones, while complimentary, do not have identical functions. Hopefully my addition and the reference to the pieces that remain unresolved gets at what you're asking. $\endgroup$
    – Susan
    May 18, 2015 at 23:31

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