ArticleBone reports2018
Loss of RANKL in osteocytes dramatically increases cancellous bone mass in the osteogenesis imperfecta mouse (oim).
Article in Bone reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 38 citations in OpenAlex.
- Osteocalcin-dependent and -independent metabolic dysregulation in a mouse model of Osteogenesis imperfecta.Bone research · 2026Article
- Role of CXCL10 released from osteocytes in response to TNF-α stimulation on osteoclasts.Scientific reports · 2025Article
- Bone Quality and Mineralization and Effects of Treatment in Osteogenesis Imperfecta.Calcified tissue international · 2024Review
- Article
- AAV-based gene editing of type 1 collagen mutation to treat osteogenesis imperfecta.Molecular therapy. Nucleic acids · 2024Article
- Does Microwave Exposure at Different Doses in the Pre/Postnatal Period Affect Growing Rat Bone Development?Physiological research · 2024Article
- Regulation of the Osteocyte Secretome with Aging and Disease.Calcified tissue international · 2023Review
- Reversal of the diabetic bone signature with anabolic therapies in mice.Bone research · 2023Article
- Healthy and Osteoarthritis-Affected Joints Facing the Cellular Crosstalk.International journal of molecular sciences · 2023Review
- Distinct type I collagen alterations cause intrinsic lung and respiratory defects of variable severity in mouse models of osteogenesis imperfecta.The Journal of physiology · 2023Article
- Murine Animal Models in Osteogenesis Imperfecta: The Quest for Improving the Quality of Life.International journal of molecular sciences · 2022Review
- Collagen (I) homotrimer potentiates the osteogenesis imperfecta (oim) mutant allele and reduces survival in male mice.Disease models & mechanisms · 2022Article
- Loss of chaperone-mediated autophagy is associated with low vertebral cancellous bone mass.Scientific reports · 2022Article
- The osteocyte as a signaling cell.Physiological reviews · 2022Review
- Roles of the RANKL-RANK Axis in Immunity-Implications for Pathogenesis and Treatment of Bone Metastasis.Frontiers in immunology · 2022Review
- Effect of TNF-α on osteocyte RANKL expression during orthodontic tooth movement.Journal of dental sciences · 2021Article
- Calvaria Bone Transcriptome in Mouse Models of Osteogenesis Imperfecta.International journal of molecular sciences · 2021Article
- Increased Osteocyte Lacunae Density in the Hypermineralized Bone Matrix of Children with Osteogenesis Imperfecta Type I.International journal of molecular sciences · 2021Article
- Gender-Related Impact of Sclerostin Antibody on Bone in the Osteogenesis Imperfecta Mouse.Frontiers in genetics · 2021Article
- Osteocyte necrosis triggers osteoclast-mediated bone loss through macrophage-inducible C-type lectin.The Journal of clinical investigation · 2020Article
Corrections and comments
- Erratum issued
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Osteogenesis imperfecta (OI) is characterized by osteopenia and bone fragility, and OI patients during growth often exhibit high bone turnover with the net result of low bone mass. Recent evidence shows that osteocytes significantly affect bone remodeling under physiological and pathological conditions through production of osteoclastogenic cytokines. The receptor activator of nuclear factor kappa-B ligand (RANKL) produced by osteocytes for example, is a critical mediator of bone loss caused by ovariectomy, low-calcium diet, unloading and glucocorticoid treatment. Because OI bone has increased density of osteocytes and these cells are embedded in matrix with abnormal type I collagen, we hypothesized that osteocyte-derived RANKL contributes to the OI bone phenotype. In this study, the conditional loss of RANKL in osteocytes in oim/oim mice (oim-RANKL-cKO) resulted in dramatically increased cancellous bone mass in both the femur and lumbar spine compared to oim/oim mice. Bone cortical thickness increased significantly only in spine but ultimate bone strength in the long bone and spine was minimally improved in oim-RANKL-cKO mice compared to oim/oim mice. Furthermore, unlike previous findings, we report that oim/oim mice do not exhibit high bone turnover suggesting that their low bone mass is likely due to defective bone formation and not increased bone resorption. The loss of osteocyte-derived RANKL further diminished parameters of formation in oim-RANKL-cKO. Our results indicate that osteocytes contribute significantly to the low bone mass observed in OI and the effect of loss of RANKL from these cells is similar to its systemic inhibition.
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Registered trials
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