ArticleAmerican journal of physiology. Cell physiology2018
Recombinant sclerostin antagonizes effects of ex vivo mechanical loading in trabecular bone and increases osteocyte lacunar size.
Article in American journal of physiology. Cell physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
24 citing papers in PubMed, 35 citations in OpenAlex.
- Article
- Article
- Osteoblastic sclerostin loop3-LRP4 interaction required by sclerostin to inhibit bone formation.Bone research · 2026Article
- Impact of elevated sclerostin levels on bone resorption : unravelling structural changes and mineral metabolism disruption.Bone & joint research · 2025Article
- Treatment of large bone defects in load-bearing bone: traditional and novel bone grafts.Journal of Zhejiang University. Science. B · 2025Review
- Localized sclerostin accumulation in osteocyte lacunar-canalicular system is associated with cortical bone microstructural alterations and bone fragility inFrontiers in cell and developmental biology · 2025Article
- Culture system for longitudinal monitoring of bone dynamics ex vivo.Biotechnology and bioengineering · 2025Article
- Microvascular Disease Associates with Larger Osteocyte Lacunae in Cortical Bone in Type 2 Diabetes Mellitus.JBMR plus · 2023Article
- Osteopathy in Complex Lymphatic Anomalies.International journal of molecular sciences · 2022Review
- Osteocytes and Estrogen Deficiency.Current osteoporosis reports · 2021Review
- Potential Role of Perilacunar Remodeling in the Progression of Osteoporosis and Implications on Age-Related Decline in Fracture Resistance of Bone.Current osteoporosis reports · 2021Review
- Sclerostin Directly Stimulates Osteocyte Synthesis of Fibroblast Growth Factor-23.Calcified tissue international · 2021Article
- Changes in the intra- and peri-cellular sclerostin distribution in lacuno-canalicular system induced by mechanical unloading.Journal of bone and mineral metabolism · 2021Article
- Ex vivo Bone Models and Their Potential in Preclinical Evaluation.Current osteoporosis reports · 2021Review
- The Mechanosensory Role of Osteocytes and Implications for Bone Health and Disease States.Frontiers in cell and developmental biology · 2021Review
- Influence of the TGF-β Superfamily on Osteoclasts/Osteoblasts Balance in Physiological and Pathological Bone Conditions.International journal of molecular sciences · 2020Review
- Osteocytic Osteolysis in PTH-treated Wild-type andThe journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2020Article
- Osteocyte-Related Cytokines Regulate Osteoclast Formation and Bone Resorption.International journal of molecular sciences · 2020Review
- Review
- The Role of Sclerostin in Bone and Ectopic Calcification.International journal of molecular sciences · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sclerostin has emerged as an important regulator of bone mass. We have shown that sclerostin can act by targeting late osteoblasts/osteocytes to inhibit bone mineralization and to upregulate osteocyte expression of catabolic factors, resulting in osteocytic osteolysis. Here we sought to examine the effect of exogenous sclerostin on osteocytes in trabecular bone mechanically loaded ex vivo. Bovine trabecular bone cores, with bone marrow removed, were inserted into individual chambers and subjected to daily episodes of dynamic loading. Cores were perfused with either osteogenic media alone or media containing human recombinant sclerostin (rhSCL) (50 ng/ml). Loaded control bone increased in apparent stiffness over time compared with unloaded bone, and this was abrogated in the presence of rhSCL. Loaded bone showed an increase in calcein uptake as a surrogate of mineral accretion, compared with unloaded bone, in which this was substantially inhibited by rhSCL treatment. Sclerostin treatment induced a significant increase in the ionized calcium concentration in the perfusate and the release of β-CTX at several time points, an increased mean osteocyte lacunar size, indicative of osteocytic osteolysis, and the expression of catabolism-related genes. Human primary osteocyte-like cultures treated with rhSCL also released β-CTX from their matrix. These results suggest that osteocytes contribute directly to bone mineral accretion, and to the mechanical properties of bone. Moreover, it appears that sclerostin, acting on osteocytes, can negate this effect by modulating the dimensions of the lacunocanalicular porosity and the composition of the periosteocyte matrix.
Indexed as
Identifiers
What OpenQuestion holds
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.