Cited by 69Bone health and osteoporosis researchBone Metabolism and DiseasesParathyroid Disorders and Treatments

PTH signaling mediates perilacunar remodeling during exercise

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Gardinier, Joseph D., Al-Omaishi, Salam, Morris, Michael D., Kohn, David H.·2016·Matrix Biology

Abstract

Mechanical loading and release of endogenous parathyroid hormone (PTH) during exercise facilitate the adaptation of bone. However, it remains unclear how exercise and PTH influence the composition of bone and how exercise and PTH-mediated compositional changes influence the mechanical properties of bone. Thus, the primary purpose of this study was to establish compositional changes within osteocytes' perilacunar region of cortical bone following exercise, and evaluate the influence of endogenous PTH signaling on this perilacunar adaptation. Raman spectroscopy, scanning electron microscopy (SEM), and energy dispersive X-ray spectroscopy (EDS) were used to evaluate tissue composition surrounding individual lacuna within the tibia of 19week old male mice exposed to treadmill running for 3weeks. As a result of exercise, tissue within the perilacunar region (within 0-5μm of the lacuna wall) had a lower mineral-to-matrix ratio (MMR) compared to sedentary controls. In addition, exercise also increased the carbonate-to-phosphate ratio (CPR) across both perilacunar and non-perilacunar regions (5-10μm and 10-15μm from the lacuna walls). Tibial post-yield work had a significant negative correlation with perilacunar MMR. Inhibition of PTH activity with PTH(7-34) demonstrated that perilacunar remodeling during exercise was dependent on the cellular response to endogenous PTH. The osteocytes' response to endogenous PTH during exercise was characterized by a significant reduction in SOST expression and significant increase in FGF-23 expression. The potential reduction in phosphate levels due to FGF-23 expression may explain the increase in carbonate substitution. Overall, this is the first study to demonstrate that adaptation in tissue composition is localized around individual osteocytes, may contribute to the changes in whole bone mechanics during exercise, and that PTH signaling during exercise contributes to these adaptations.

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Crossref · 10.1016/j.matbio.2016.02.010

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Authors
Gardinier, J. D., Al-Omaishi, S., Morris, M. D., & Kohn, D. H.
Affiliations
  • Henry Ford Health (US)
  • University of Michigan (US)
Corresponding author
Kohn, David H.
Venue
Matrix Biology
Publisher
Elsevier BV
Published
2016-05
Volume
52-54
Pages
162-175
ISSN
0945-053X (ISSN-L)
OpenAlex
W2286575445
Cited by
69
References
44
Citations by year
2026: 3 · 2025: 4 · 2024: 11 · 2023: 6 · 2022: 10 · 2021: 4 · 2020: 8 · 2019: 12 · 2018: 6 · 2017: 3 · 2016: 2
FWCI
9.33
Type
journal article
Language
en
Open access
Locations
  • Matrix Biology (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
Funders
National Institutes of Health (DE07057, AR064668, AR056657)
Topics
  • Health Sciences › Medicine › Orthopedics and Sports Medicine › Bone health and osteoporosis research
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Bone Metabolism and Diseases
  • Health Sciences › Medicine › Nephrology › Parathyroid Disorders and Treatments
Keywords
parathyroid hormone signaling, physical activity, bone remodeling, osteocytes, mineral-to-matrix ratio, carbonate substitution, fibroblast growth factor 23, sclerostin, bone mechanical properties, tibia, mechanical loading
MeSH terms
Fibroblast Growth Factor-23, Animals, Biomechanical Phenomena, Exercise Test, Male, Microscopy, Electron, Scanning, Parathyroid Hormone, Physical Conditioning, Animal, Spectrometry, X-Ray Emission, Spectrum Analysis, Raman, Tibia, Signal Transduction, Bone Remodeling, Mice

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