No Role of Osteocytic Osteolysis in the Development and Recovery of the Bone Phenotype Induced by Severe Secondary Hyperparathyroidism in Vitamin D Receptor Deficient Mice

Ludwig Boltzmann Institute of Osteology at the Hanusch Hospital of OEGK and AUVA Trauma Centre Meidling, 1st Medical Deptartment, Hanusch Hospital, 11140 Vienna, Austria

Michael Ogon Laboratory for Orthopaedic Research, Orthopaedic Hospital Vienna Speising, 1130 Vienna, Austria

Department of Biomedical Sciences, University of Veterinary Medicine, 1210 Vienna, Austria

Author to whom correspondence should be addressed.

Int. J. Mol. Sci. 2020, 21(21), 7989; https://doi.org/10.3390/ijms21217989

Received: 28 September 2020 / Revised: 16 October 2020 / Accepted: 22 October 2020 / Published: 27 October 2020

(This article belongs to the Special Issue Bone Development and Regeneration)

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Abstract

Osteocytic osteolysis/perilacunar remodeling is thought to contribute to the maintenance of mineral homeostasis. Here, we utilized a reversible, adult-onset model of secondary hyperparathyroidism to study femoral bone mineralization density distribution (BMDD) and osteocyte lacunae sections (OLS) based on quantitative backscattered electron imaging. Male mice with a non-functioning vitamin D receptor (VDR^Δ/Δ) or wild-type mice were exposed to a rescue diet (RD) (baseline) and subsequently to a low calcium challenge diet (CD). Thereafter, VDR^Δ/Δ mice received either the CD, a normal diet (ND), or the RD. At baseline, BMDD and OLS characteristics were similar in VDR^Δ/Δ and wild-type mice. The CD induced large cortical pores, osteomalacia, and a reduced epiphyseal average degree of mineralization in the VDR^Δ/Δ mice relative to the baseline (−9.5%, p < 0.05 after two months and −10.3%, p < 0.01 after five months of the CD). Switching VDR^Δ/Δ mice on the CD back to the RD fully restored BMDD to baseline values. However, OLS remained unchanged in all groups of mice, independent of diet. We conclude that adult VDR^Δ/Δ animals on an RD lack any skeletal abnormalities, suggesting that VDR signaling is dispensable for normal bone mineralization as long as mineral homeostasis is normal. Our findings also indicate that VDR^Δ/Δ mice attempt to correct a calcium challenge by enhanced osteoclastic resorption rather than by osteocytic osteolysis. View Full-Text

Keywords: vitamin D receptor; mice with a non-functioning vitamin D receptor; bone mineralization density distribution; osteocyte lacunae sections; quantitative backscattered electron imaging; osteocytic osteolysis

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Misof, B.M.; Blouin, S.; Hofstaetter, J.G.; Roschger, P.; Zwerina, J.; Erben, R.G. No Role of Osteocytic Osteolysis in the Development and Recovery of the Bone Phenotype Induced by Severe Secondary Hyperparathyroidism in Vitamin D Receptor Deficient Mice. Int. J. Mol. Sci. 2020, 21, 7989. https://doi.org/10.3390/ijms21217989

AMA Style

Misof BM, Blouin S, Hofstaetter JG, Roschger P, Zwerina J, Erben RG. No Role of Osteocytic Osteolysis in the Development and Recovery of the Bone Phenotype Induced by Severe Secondary Hyperparathyroidism in Vitamin D Receptor Deficient Mice. International Journal of Molecular Sciences. 2020; 21(21):7989. https://doi.org/10.3390/ijms21217989

Chicago/Turabian Style

Misof, Barbara M., Stéphane Blouin, Jochen G. Hofstaetter, Paul Roschger, Jochen Zwerina, and Reinhold G. Erben 2020. "No Role of Osteocytic Osteolysis in the Development and Recovery of the Bone Phenotype Induced by Severe Secondary Hyperparathyroidism in Vitamin D Receptor Deficient Mice" International Journal of Molecular Sciences 21, no. 21: 7989. https://doi.org/10.3390/ijms21217989

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No Role of Osteocytic Osteolysis in the Development and Recovery of the Bone Phenotype Induced by Severe Secondary Hyperparathyroidism in Vitamin D Receptor Deficient Mice

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