Research Paper Volume 9, Issue 10 pp 2190—2208
Degeneration of the osteocyte network in the C57BL/6 mouse model of aging
- 1 Department of Oral and Craniofacial Sciences, School of Dentistry, University of Missouri Kansas City, Kansas City, MO 64108, USA
- 2 Departments of Anatomy and Cell Biology and Orthopaedic Surgery, School of Medicine, Indiana University, Indianapolis, IN 46202, USA
received: July 19, 2017 ; accepted: October 15, 2017 ; published: October 26, 2017 ;https://doi.org/10.18632/aging.101308
How to Cite
Copyright: Tiede-Lewis et al. This is an open‐access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Age-related bone loss and associated fracture risk are major problems in musculoskeletal health. Osteocytes have emerged as key regulators of bone mass and as a therapeutic target for preventing bone loss. As aging is associated with changes in the osteocyte lacunocanalicular system, we focused on the responsible cellular mechanisms in osteocytes. Bone phenotypic analysis was performed in young-(5mo) and aged-(22mo) C57BL/6 mice and changes in bone structure/geometry correlated with alterations in osteocyte parameters determined using novel multiplexed-3D-confocal imaging techniques. Age-related bone changes analogous to those in humans were observed, including increased cortical diameter, decreased cortical thickness, reduced trabecular BV/TV and cortical porosities. This was associated with a dramatic reduction in osteocyte dendrite number and cell density, particularly in females, where osteocyte dendricity decreased linearly from 5, 12, 18 to 22mo and correlated significantly with cortical bone parameters. Reduced dendricity preceded decreased osteocyte number, suggesting dendrite loss may trigger loss of viability. Age-related degeneration of osteocyte networks may impair bone anabolic responses to loading and gender differences in osteocyte cell body and lacunar fluid volumes we observed in aged mice may lead to gender-related differences in mechanosensitivity. Therapies to preserve osteocyte dendricity and viability may be beneficial for bone health in aging.