ArticleJournal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research2014
Mechanical load increases in bone formation via a sclerostin-independent pathway.
Article in Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers, 1 of them a synthesis that pooled it.
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Who cites it
64 citing papers in PubMed, 1 synthesis or guideline pooled it, 110 citations in OpenAlex.
- Methodological aspects ofJournal of musculoskeletal & neuronal interactions · 2023Pooled it
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- Exercise for Postmenopausal Bone Health - Can We Raise the Bar?Current osteoporosis reports · 2025Review
- Porcupine inhibition is a promising pharmacological treatment for severe sclerosteosis pathologies.Bone research · 2025Article
- Activation of connexin hemichannels enhances mechanosensitivity and anabolism in disused and aged bone.JCI insight · 2024Article
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- Effects of acute- and long-term aerobic exercises at different intensities on bone in mice.Journal of bone and mineral metabolism · 2024Article
- Osteoimmunology in Periodontitis and Orthodontic Tooth Movement.Current osteoporosis reports · 2023Review
- Constitutive bone marrow adipocytes suppress local bone formation.JCI insight · 2022Article
- Osteocytes regulate bone anabolic response to mechanical loading in male mice via activation of integrin α5.Bone research · 2022Article
- Lipolysis of bone marrow adipocytes is required to fuel bone and the marrow niche during energy deficits.eLife · 2022Article
- Importance of Sclerostin as Bone-Muscle Mediator Crosstalk.Annals of geriatric medicine and research · 2022Article
- Dissociation of Bone Resorption and Formation in Spaceflight and Simulated Microgravity: Potential Role of Myokines and Osteokines?Biomedicines · 2022Review
- Sclerostin and Its Involvement in the Pathogenesis of Idiopathic Scoliosis.Journal of clinical medicine · 2021Review
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- Bone health in spacefaring rodents and primates: systematic review and meta-analysis.NPJ microgravity · 2021Article
- Mechanistic Insight into Orthodontic Tooth Movement Based on Animal Studies: A Critical Review.Journal of clinical medicine · 2021Review
- Article
4 more citing papers are in PubMed but not listed here.
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Authors and funding
9 authors at 6 institutions in 3 countries.
Funding
Abstract
Sclerostin, encoded by the Sost gene, is an important negative regulator of bone formation that has been proposed to have a key role in regulating the response to mechanical loading. To investigate the effect of long-term Sclerostin deficiency on mechanotransduction in bone, we performed experiments on unloaded or loaded tibiae of 10 week old female Sost-/- and wild type mice. Unloading was induced via 0.5U botulinum toxin (BTX) injections into the right quadriceps and calf muscles, causing muscle paralysis and limb disuse. On a separate group of mice, increased loading was performed on the left tibiae through unilateral cyclic axial compression of equivalent strains (+1200 µe) at 1200 cycles/day, 5 days/week. Another cohort of mice receiving equivalent loads (-9.0 N) also were assessed. Contralateral tibiae served as normal load controls. Loaded/unloaded and normal load tibiae were assessed at day 14 for bone volume (BV) and formation changes. Loss of BV was seen in the unloaded tibiae of wild type mice, but BV was not different between normal load and unloaded Sost-/- tibiae. An increase in BV was seen in the loaded tibiae of wild type and Sost-/- mice over their normal load controls. The increased BV was associated with significantly increased mid-shaft periosteal mineralizing surface/bone surface (MS/BS), mineral apposition rate (MAR), and bone formation rate/bone surface (BFR/BS), and endosteal MAR and BFR/BS. Notably, loading induced a greater increase in periosteal MAR and BFR/BS in Sost-/- mice than in wild type controls. Thus, long-term Sclerostin deficiency inhibits the bone loss normally induced with decreased mechanical load, but it can augment the increase in bone formation with increased load.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.