Calcitonin Regulation in Bone Metabolism
Summary
Calcitonin is a peptide hormone secreted by thyroid C-cells in response to rises in circulating calcium. Its classical role is to inhibit osteoclastic bone resorption, thereby acutely reducing serum calcium levels. Beyond this pharmacological action, emerging evidence reveals a dual role for calcitonin in skeletal homeostasis, involving not only suppression of osteoclast activity but also modulation of osteoblast function via intercellular signalling. The calcitonin receptor (CTR), expressed predominantly on osteoclasts, mediates downstream effects on transporter and signalling pathways that influence the release of coupling factors. These mediators, including lipids and Wnt ligands, orchestrate a balance between bone degradation and formation. Understanding this crosstalk has global significance for the treatment of osteoporosis and other disorders of bone remodelling, as it offers routes to harness or mimic calcitonin’s osteoanabolic potential while avoiding unwanted suppression of bone turnover.
Research from Nature Portfolio
Recent studies have redefined the mechanism by which calcitonin influences bone formation. Inactivation of the calcitonin receptor in animal models unexpectedly led to increased bone mass, prompting investigations into the underlying coupling signals. It was discovered that calcitonin negatively regulates the gene encoding the S1P transporter Spns2 in osteoclasts. Loss of CTR increases extracellular sphingosine 1-phosphate (S1P) levels, which in turn activates S1P3 receptors on osteoblasts and stimulates bone formation. Genetic deletion of S1P3 normalises the high‐bone‐mass phenotype of CTR-deficient mice, and pharmacological agonism of S1P receptors enhances bone formation in wild-type animals. These findings establish S1P as an osteoanabolic lipid messenger and propose the osteoclast–osteoblast axis controlled by calcitonin as a target for novel bone therapies.
Calcitonin Regulation in Bone Metabolism publication trend
The graph below shows the total number of articles in calcitonin regulation in bone metabolism across all publications each year (not limited to Nature Index journals).
Technical terms
Calcitonin: Peptide hormone secreted by thyroid C-cells that lowers blood calcium by inhibiting bone resorption.
Osteoclast: Multinucleated cell responsible for degrading bone matrix during remodelling.
Osteoblast: Mononuclear cell that synthesises and mineralises new bone tissue.
Sphingosine 1-phosphate (S1P): Lipid mediator released by osteoclasts that stimulates osteoblast activity and bone formation.
Wnt10b: Secreted glycoprotein acting as a clastokine to promote osteoblast differentiation and enhance bone matrix deposition.
References
- Calcitonin controls bone formation by inhibiting the release of sphingosine 1-phosphate from osteoclasts. Nature Communications (2014).
- Calcitonin Induces Bone Formation by Increasing Expression of Wnt10b in Osteoclasts in Ovariectomy-Induced Osteoporotic Rats. Frontiers in Endocrinology (2020).
- A meta-analysis of the therapeutic effect of intranasal salmon calcitonin on osteoporosis. European Journal of Medical Research (2021).
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