Preserving bone structure in vascular calcification

Erik Merckelbach (Aachen)1, J. Jankowski (Aachen)1, S. Bhargava (Aachen)1

1Uniklinik RWTH Aachen Institut für Molekulare Herz-Kreislaufforschung (IMCAR) Aachen, Deutschland


Background: Cardiovascular health and mineral bone disease (MBD) are closely interlinked in patients suffering from chronic kidney disease (CKD). MBD frequently occurs in CKD patients, leading to bone resorption and hyperphosphatemia. Increased phosphate concentrations in serum promote vascular calcification and cardiovascular events such as atherosclerosis. The chromogranin A derived calcification blocking factor (CBF) has already been established as an inhibitor of vascular calcification, but nothing is known of its effect on bone health.

In this project MBD was investigated in animal models of vascular calcification and atherosclerosis as well as mediating effect of the chromogranin A derived calcification blocking factor (CBF) on the bone.


Methods: To investigate the effect of CKD on bone quality, a rat model of vascular calcification (VDN rats) was used. The structure and bone mineral density of tibia from VDN rats with and without CBF treatment were analyzed via micro-computed tomography (micro-CT) scans. In detail, the bone mineral density of the trabecular and cortical bone, as well as the trabecular thickness, number, and porosity were analyzed.


Results: VDN animals without additional treatment showed significant changes in bone structure and bone mineral density of the tibia. The mineral density of the trabecular bone was increased by 88 % in VDN rats compared to control animals (p=0.0061). The trabecular number of VDN rats increased by 134 % (p=0.0011). Conversely, the trabecular thickness, and porosity decreased by 25 % (p=0.0471), and 14 % (p=0.0068) respectively. The mineral density of the cortical bone decreased by 8 % (p=0.0010) and the porosity increased by 32 % (p=0.0072) in VDN rats. These changes were in all cases negated to non-significance compared to the control, when treated with CBF.


Conclusion: In our study, we were able to comprehensively show the changes in bone mineral density and bone structure in the tibia of rats suffering from vascular calcification. In addition, preventive treatment with CBF proved to inhibit any changes in bone structure and mineral density, effectively preserving the healthy state of the bone. Based on these results, CBF presents a novel mediator of not only vascular calcification but also MBD, highlighting it as a possible treatment target in cardiovascular disease


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